Classification overview
1. Orofacial pain associated with disorders of dentoalveolar and associated structures
1.1 Dental pain
1.1.1 Pulpal pain
1.1.1.1. Pulpal pain attributed to hypersensitivity
1.1.1.1.1 Pulpal pain attributed to a crack in the enamel
1.1.1.1.2 Pulpal pain attributed to exposed dentin
1.1.1.1.2.1 Pulpal pain attributed to tooth wear or abrasion
1.1.1.1.2.2 Pulpal pain attributed to fracture resulting in exposed dentin
1.1.1.1.2.3 Pulpal pain attributed to developmental dental hard tissue defect
1.1.1.1.3 Pulpal pain attributed to hypersensitivity associated with dental procedures
1.1.1.1.3.1 Pulpal pain attributed to recent extensive removal of dentin
1.1.1.1.3.2 Pulpal pain attributed to recent placement of a restoration
1.1.1.1.3.3 Pulpal pain attributed to hypersensitivity due to hyperocclusion or-articulation following dental restorative procedures
1.1.1.1.4 Pulpal pain attributed to central sensitization
1.1.1.1.5 Pulpal pain attributed to other cause
1.1.1.2 Pulpal pain attributed to pulp exposure due to dental trauma
1.1.1.3 Pulpal pain attributed to pulpitis (pulpal inflammation)
1.1.1.3.1 Pulpal pain attributed to reversible pulpitis due to infection of dentin
1.1.1.3.1.1 Pulpal pain attributed to caries that does not extend to the pulp
1.1.1.3.1.2 Pulpal pain attributed to reversible pulpitis due to fracture of enamel, rootcementum, dentin or any combination thereof, resulting in exposure of dentin
1.1.1.3.1.3 Pulpal pain attributed to reversible pulpitis due to a tooth crack withoutevidence of missing tooth substance
1.1.1.3.2 Pulpal pain attributed to irreversible pulpitis due to infection of dentin
1.1.1.3.2.1 Pulpal pain attributed to caries which may extend to the pulp
1.1.1.3.2.2 Pulpal pain attributed to irreversible pulpitis due to dental hard tissuefracture without pulp exposure
111.1.1.3.2.3 Pulpal pain attributed to irreversible pulpitis due to visible crack in theenamel without evidence of missing tooth substance
1.1.1.3.3 Pulpal pain attributed to irreversible pulpitis due to infection of the dental pulp
1.1.1.3.3.1 Pulpal pain attributed to caries extending to the pulp
1.1.1.3.3.2 Pulpal pain attributed to irreversible pulpitis due to dental hard tissue fracturewithout pulp exposure
1.1.1.3.4 Pulpal pain attributed to pulpitis due to external cervical root resorption
1.1.1.3.5 Pulpal pain attributed to pulpitis due to other cause
1.1.1.4 Pulpal pain attributed to systemic cause
1.1.2 Periodontal pain
1.1.2.1 Periodontal pain attributed to periodontitis (periodontal inflammation of theperiodontium)
1.1.2.1.1 Periodontal pain attributed to traumatically induced periodontal infammation
1.1.2.1.1.1 Periodontal pain attributed to hyperocclusion or -articulation
1.1.2.1.1.2 Postoperative periodontal pain
1.1.2.1.1.3 Periodontal pain attributed to accidental dental trauma
1.1.2.1.1.4 Periodontal pain attributed to other trauma or injury
1.1.2.1.2 Periodontal pain attributed to apical periodontitis due to endodontic disease
1.1.2.1.2.1 Periodontal pain attributed to pulpal inflammation
1.1.2.1.2.2 Periodontal pain attributed to endodontic infection
1.1.2.1.2.2.1 Periodontal pain attributed to intraradicular endodontic infection
1.1.2.1.2.2.2 Periodontal pain attributed to extraradicular endodontic infection
1.1.2.1.3 Periodontal pain attributed to periodontal disease
1.1.2.1.3.1 Periodontal pain attributed to chronic periodontitis
1.1.2.1.3.2 Periodontal pain attributed to aggressive periodontitis
1.1.2.1.3.3 Periodontal pain attributed to periodontitis as a manifestation of systemicdisorder known to cause periodontitis
1.1.2.1.3.3.1 Periodontal pain attributed to a hematological disorder
1.1.2.1.3.3.2 Periodontal pain attributed to a genetic disorder
1.1.2.1.3.3.3 Periodontal pain attributed to an unspecified systemic disorder
1.1.2.1.3.4 Periodontal pain associated with necrotizing ulcerative periodontitis (NUP)
1.1.2.1.3.5 Periodontal pain associated with periodontal abscess
1.1.2.1.4 Periodontal pain attributed to apical and marginal periodontitis due to combinedendodontic infection and periodontal disease
1.1.2.1.5 Periodontal pain attributed to peri-implantitis due to peri-implant infection
1.1.2.2 Periodontal pain attributed to a local non-inflammatory cause
1.1.3 Gingival pain
1.1.3.1 Gingival pain attributed to gingivitis (gingival inflammation)
1.1.3.1.1 Gingival pain attributed to trauma
1.1.3.1.2 Gingival pain attributed to infection
1.1.3.1.2.1 Gingival pain attributed to bacterial infection
1.1.3.1.2.2 Gingival pain attributed to viral infection
1.1.3.1.2.3 Gingival pain attributed to fungal infection
1.1.3.1.3 Gingival pain attributed to autoimmunity
1.1.3.1.4 Gingival pain attributed to allergic reaction
1.1.3.1.5 Gingival pain attributed to gingival inflammation due to other cause
1.1.3.2 Gingival pain attributed to malignant lesion
1.1.3.3 Gingival pain attributed to neuropathy
1.1.3.4 Idiopathic gingival pain
1.2 Non-dental pain
1.2.1 Oral mucosal pain
1.2.1.1 Oral mucosal pain attributed to oral mucosal inflammation
1.2.1.1.1 Oral mucosal pain associated with trauma
1.2.1.1.1.1 Oral mucosal pain attributed to mechanical, thermal, or chemical injury
1.2.1.1.1.2 Oral mucosal pain attributed to surgical or other iatrogenic injury
1.2.1.1.1.3 Oral mucosal pain attributed to radiation or chemotherapy
1.2.1.1.2 Oral mucosal pain attributed to infection
1.2.1.1.2.1 Oral mucosal pain attributed to bacterial infection
1.2.1.1.2.2 Oral mucosal pain attributed to viral infection
1.2.1.1.2.3 Oral mucosal pain attributed to fungal infection
1.2.1.1.3 Oral mucosal pain attributed to autoimmunity
1.2.1.1.4 Oral mucosal pain attributed to allergic reaction
1.2.1.1.5 Oral mucosal pain attributed to oral mucosal inflammation due to other cause
1.2.1.2 Oral mucosal pain attributed to malignant lesion
1.2.1.3 Oral mucosal pain attributed to neuropathy
1.2.1.4 Idiopathic oral mucosal pain
1.2.2 Salivary gland pain
1.2.2.1 Salivary gland pain attributed to obstructive cause
1.2.2.2 Salivary gland pain attributed to infection
1.2.2.2.1 Salivary gland pain attributed to viral infection
1.2.2.2.2 Salivary gland pain attributed to bacterial infection
1.2.2.3 Salivary gland pain attributed to non-infectious cause
1.2.2.3.1 Salivary gland pain attributed to recurrent juvenile parotitis
1.2.2.3.2 Salivary gland pain attributed to immunologically mediated disorder
1.2.2.3.3 Salivary gland pain attributed to other cause
1.2.3 Jaw bone pain
1.2.3.1 Jaw bone pain attributed to infection
1.2.3.1.1 Jaw bone pain attributed to bacterial infection
1.2.3.1.2 Jaw bone pain attributed to viral infection
1.2.3.1.3 Jaw bone pain attributed to fungal infection
1.2.3.2 Therapy related jaw bone pain
1.2.3.3 Jaw bone pain attributed to a local benign lesion
1.2.3.4 Jaw bone pain attributed to a malignant lesion
1.2.3.4.1 Jaw bone pain attributed to a primary malignant lesion
1.2.3.4.2 Jaw bone pain secondary to a malignant lesion
1.2.3.5 Jaw bone pain attributed to systemic disease
1.2.3.6 Jaw bone pain attributed to traumatic injury
2. Orofacial pain associated with regional muscles
2.1. Primary myofascial pain
2.1.1. Acute primary myofascial pain
2.1.2. Chronic primary myofascial pain
2.1.2.1. Chronic infrequent primary myofascial pain
2.1.2.2. Chronic frequent primary myofascial pain
2.1.2.2.1. Chronic frequent primary myofascial pain without pain referral
2.1.2.2.2. Chronic frequent primary myofascial pain with pain referral
2.1.2.3. Chronic persistent primary myofascial pain
2.1.2.3.1. Chronic persistent primary myofascial pain without pain referral
2.1.2.3.2. Chronic persistent primary myofascial pain with pain referral
2.2. Secondary myofascial pain
2.2.1. Secondary myofascial pain due to tendonitis
2.2.2. Secondary myofascial pain due to myositis
2.2.3. Secondary myofascial pain due to muscle spasm
3. Orofacial pain associated with disorders of the Temporomandibular Joint (TMJ)
3.1. Primary TMJ arthralgia
3.1.1. Acute primary TMJ arthralgia
3.1.2. Chronic primary TMJ arthralgia
3.1.2.1. Chronic infrequent primary TMJ arthralgia
3.1.2.2. Chronic frequent primary TMJ arthralgia
3.1.2.2.1. Chronic frequent primary TMJ arthralgia without referred pain
3.1.2.2.2. Chronic frequent primary TMJ arthralgia with referred pain
3.1.2.3. Chronic persistent primary TMJ arthralgia
3.1.2.3.1. Chronic persistent primary TMJ arthralgia without referred pain
3.1.2.3.2. Chronic persistent primary TMJ arthralgia with referred pain
3.2. Secondary TMJ arthralgia
3.2.1. TMJ arthralgia attributed to arthritis
3.2.1.1. TMJ arthralgia attributed to arthritis, non-systemic
3.2.1.2. TMJ arthralgia attributed to arthritis, systemic
3.2.2. TMJ arthralgia attributed to disc displacement with reduction
3.2.3. TMJ arthralgia attributed to disc displacement with reduction with intermittentlocking
3.2.4. TMJ arthralgia attributed to disc displacement without reduction
3.2.5. TMJ arthralgia attributed to degenerative joint disease
3.2.6. TMJ arthralgia attributed to subluxation
4. Orofacial pain associated with lesion/disorders of the cranial nerves and other regionalnerve structures
4.1. Pain caused by a lesion or disease of the trigeminal nerve
4.1.1. Trigeminal neuralgia
4.1.1.1. Classical trigeminal neuralgia 4.1.1.1.1. Classical trigeminal neuralgia, purely paroxysmal
4.1.1.1.2. Classical trigeminal neuralgia with concomitant continuous pain
4.1.1.2. Secondary trigeminal neuralgia
4.1.1.2.1. Trigeminal neuralgia attributed to multiple sclerosis
4.1.1.2.2. Trigeminal neuralgia attributed to space-occupying lesion
4.1.1.2.3. Trigeminal neuralgia attributed to other demonstrable causes
4.1.1.3. Idiopathic trigeminal neuralgia
4.1.1.3.1. Idiopathic trigeminal neuralgia, purely paroxysmal
4.1.1.3.2. Idiopathic trigeminal neuralgia with concomitant continuouspain
4.1.2. Trigeminal neuropathic pain other than
4.1.1. Clinically established trigeminalneuralgia
4.1.2.1. Trigeminal neuropathic pain attributed to herpes Zoster
4.1.2.2. Trigeminal postherpetic neuralgia
4.1.2.3. Post-traumatic trigeminal neuropathic pain
4.1.2.3.1. Probable post-traumatic trigeminal neuropathic pain
4.1.2.4. Trigeminal neuropathic pain attributed to another disorder
4.1.2.4.1. Probable trigeminal neuropathic pain attributed to anotherdisorder
4.1.2.5. Idiopathic trigeminal neuropathic pain
4.1.2.5.1. Probable idiopathic trigeminal neuropathic pain
4.2. Pain caused by a lesion or disease of the glossopharyngeal nerve
4.2.1. Clinically established glossopharyngeal neuralgia
4.2.1.1. Classical glossopharyngeal neuralgia
4.2.1.2. Secondary glossopharyngeal neuralgia
4.2.1.3. Idiopathic glossopharyngeal neuralgia
4.2.2. Glossopharyngeal neuropathic pain
4.2.2.1. Glossopharyngeal neuropathic pain attributed to a known cause
4.2.2.2. Idiopathic glossopharyngeal neuropathic pain
5. Orofacial pain resembling presentations of primary headaches
5.1. Orofacial migraine
5.1.1. Orofacial migraine
5.1.2. Chronic orofacial migraine
5.1.3 Neurovascular Orofacial Pain
5.1.3.1 Shortlasting Neurovascular Orofacial Pain
5.1.3.2 Longlasting Neurovascular Orofacial Pain
5.2. Tension-type orofacial pain
5.3. Trigeminal autonomic orofacial pain
5.3.1. Orofacial cluster attacks
5.3.1.1. Episodic orofacial cluster attacks
5.3.1.2. Chronic orofacial cluster attacks
5.3.2. Paroxysmal hemifacial pain
5.3.2.1. Episodic paroxysmal hemifacial pain5.3.2.2. Chronic paroxysmal hemifacial pain
5.3.3. Short-lasting unilateral neuralgiform facial pain attacks with autonomic signs(SUNFA)
5.3.3.1. Episodic SUNFA
5.3.3.2. Chronic SUNFA
5.3.4. Hemifacial continuous pain with autonomic signs
5.3.5 Constant Unilateral Facial Pain with Attacks (CUFPA)
6. Idiopathic orofacial pain
6.1. Burning mouth syndrome (BMS)
6.1.1. Burning mouth syndrome associated with somatosensory changes
6.1.2. Burning mouth syndrome not associated with somatosensory changes
6.2. Persistent idiopathic facial pain (PIFP)
6.2.1. Persistent idiopathic facial pain associated with somatosensory changes
6.2.2. Persistent idiopathic facial pain not associated with somatosensory changes
6.3. Persistent idiopathic dentoalveolar pain
6.3.1. Persistent idiopathic dentoalveolar pain associated with somatosensory changes
6.3.2. Persistent idiopathic dentoalveolar pain not associated with somatosensory changes
7. Psychosocial Assesment
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Format: AbstractSend to
Expert Rev Neurother. 2012 May;12(5):569-76. doi: 10.1586/ern.12.40.
The classification and differential diagnosis of orofacial pain.
Renton T1, Durham J, Aggarwal VR.
Author information
1
Department Oral Surgery, Kings College London Dental Institute, Denmark Hill Campus, Bessemer Road, London SE5 9RS, UK. tara.renton@kcl.ac.uk
Abstract
There are currently four main pain classification systems relevant to orofacial pain (OFP): the International Association for the Study of Pain, International Classification of Headache Disorders, the American Academy of Orofacial Pain and the Research Diagnostic Criteria for Temporomandibular Disorders. Of the four, the Research Diagnostic Criteria for Temporomandibular Disorders is the most biopsychosocial system, with the remaining three focusing more on the biomedical aspects. Unsurprisingly, clinical scientists and clinicians have both reported perceived deficiencies in the published systems and have proposed further modified classifications and nomenclature for OFP. Establishing a standardized biopsychosocial classification of OFP is essential for ensuring continuity for patient care since it creates a standardized language with which to communicate healthcare information, thus enabling improved and more specific (epidemiological) research and patient care. Despite ongoing attempts, an accepted overarching classification of OFP is still a work in progress. There is an urgent need for a robust classification system for OFP. This review aims to highlight the recent debate and continued struggle to attain a consensus on a classification of OFP and highlight some recent developments that assist differential diagnosis of these conditions.
PMID: 22550985 DOI: 10.1586/ern.12.40
Orofacial pain classification—A new milestone and new implications:
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1Dear Reader,ICHD-3 thoroughly classifies primary and secondary headaches but such an internationallyaccepted version for primary and secondary facial pains was until now lacking. A collaborativegroup consisting of members of the Orofacial and Head Pain Special Interest Group (OFHP SIG)of the International Association for the Study of Pain (IASP), the International Network forOrofacial Pain and Related Disorders Methodology (INfORM), the American Academy ofOrofacial Pain (AAOP) and the International Headache Society (IHS) has worked over the past 3years to present such a classification for facial pain which is herewith attached.Before publishing this first edition (which will change and adapt over time, just like ICHD) weseek advise and suggestion from researchers and clinicians worldwide. Such advice andsuggestions will be considered if backed up by publications (i.e. not just based on a clinicalimpression).Please send such comments and a list of references to the following email contact:a.may@uke.uni-hamburg.de or benolira@sdm.rutgers.eduand we will foreward these to the respective section heads who are also listed page 3.We hope you will find the reading inspiring.
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2International Classification of Orofacial PainICOPVersion 1.0 beta2019
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3Classification committeeCo-chairpersonsRafael Benoliel, USA; Peter Svensson, DenmarkMembers of individual classification working groups in alphabetical order other than chair.1. Orofacial pain associated with disorders of dentoalveolar and associated structuresMaria Pigg, Sweden (Chair); Alan Law, USA; Donald Nixdorf, USA; Tara Renton, UK; YairSharav, Israel2. Orofacial pain associated with regional musclesPeter Svensson, Denmark (Chair); Malin Ernberg, Sweden; Chris Peck, Australia3. Orofacial pain associated with disorders of the TMJPer Alstergren, Sweden (Chair); Ghabi Kaspo, USA; Frank Lobbezoo, Netherlands; AmbraMichelotti, Italy4. Orofacial pain associated with lesion/disorders of the cranial nerves and other regional nervestructuresLene Baad-Hansen, Denmark (Chair); Eli Eliav, USA; Yoshiki Imamura, Japan5. Orofacial pain resembling presentations of Primary HeadachesRafael Benoliel, USA (Chair); Paulo Conti, Brazil; Arne May, Germany6. Idiopathic orofacial painThomas List, Sweden (Chair); Justin Durham, England; Jean-Paul Goulet, Canada; SatuJääskeläinen, Finland7. Psychosocial AssessmentRichard Ohrbach, USA
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4Table of ContentsPreface .................................................................................................................................. 5Using ICOP .......................................................................................................................... 7Classification with diagnostic criteria ......................................................................................... 191. Orofacial pain due to disorders of dentoalveolar and associated structures ............................ 192. Orofacial pain associated with regional muscles .................................................................... 1363. Orofacial pain associated with disorders of the TMJ ............................................................ 1465. Orofacial pain resembling presentations of primary headaches ............................................ 1886. Idiopathic orofacial pain ....................................................................................................... 2046. Idiopathic orofacial pain (v2) ................................................... Fehler! Textmarke nicht definiert.Bibliography ......................................................................... Fehler! Textmarke nicht definiert.7. Psychosocial Assessment ....................................................................................................... 212Definitions of terms ........................................................................................................... 224Pain Terminology .............................................................................................................. 227
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5PrefaceWe are proud to present the first International Classification of Orofacial Pain (ICOP). Whileanatomically the face is clearly part of the head we have found far too many cases ofmisdiagnosis where a clear diagnostic classification may have helped avoid misdiagnosis andresultant mis-directed treatment. Anatomical boundaries, and associated medical specialtyboundaries, contribute to the problem. For example, the International Headache Society definesfacial pain as “pain below the orbitomeatal line, anterior to the pinnae and above the neck”.Other definitions for facial pain include the forehead as an additional area, while orofacial pain(OFP) would necessarily include all of the structures in the oral cavity.In clinical practice ‘headaches’ often refer to ‘orofacial’ regions and vice versa. At times‘headaches’ may be located exclusively around the ‘orofacial’ region and may cause significantdiagnostic difficulties. OFPs refer to the head presenting a complex clinical phenotype. Inparticular, dental pain due to local dental pathology is often blamed for primary orofacial andhead pains. There is no comprehensive internationally accepted classification that deals withorofacial pain. These were some of the factors that made it clear to us that a classification fororofacial pains was needed. A fundamental principle in this first classification of orofacial painsis that the disorders, not the location of head vs. face, should guide the new conceptualizationand diagnostic criteria.While creating ICOP we were cognizant that the ICHD-3 thoroughly classifies primary andsecondary headaches and we refer the reader to the current version of ICHD-3 for those entities.Moreover, to make ICOP a useful tool for researchers and clinicians accustomed to using ICHD-3 we have adopted the hierarchical design and classification style of ICHD-3. The DiagnosticCriteria for Temporomandibular Disorders (DC/TMD) is a well-tested and establishedclassification that includes regional myalgias and TMJ arthralgia. We have adopted the DC/TMDcriteria, only including the painful TMDs and modifying the presentation style of the criteria tothat of ICHD-3. Overall, the ICOP is also aligned to the ICD-11/IASP criteria for orofacial painsand headaches.The aim is therefore to create a tool that will enhance research and clinical management oforofacial pain. Additionally, we are confident that methodology we have adopted will bring
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6professionals working on head, orofacial, eye, nose, sinus and neck pain closer and encourageactive collaboration.The road to ICOP began in 2016 when we first met at the World Congress of the IASP inYokohama, Japan. In the one day meeting we discussed the structure and establishedworkgroups. A follow up meeting was held in Rutgers School of Dental Medicine, USA in 2017where we examined the evidence, or lack of, to establish the individual entities making up ICOP.The result is a classification that is backed in many areas by strong evidence and in others byexpert opinion that will encourage and guide research. The members of the classificationcommittee represent the major associations involved in orofacial and head pain and are a trueinternational group, strengthening the future of ICOP.R. Benoliel, P. Svensson
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7Using ICOPBecause ICOP is modelled on ICHD-3 the instructions for use of ICOP are similar. Many ICHD-3 users will therefore find ICOP easy to use. Like ICHD-3 the document is intended as a tool toconsult particularly for research, but also for the clinical diagnosis and management of OFP.ICOP will serve as a comprehensive research and diagnostic manual and will be particularlyuseful when the diagnosis is uncertain, or when the clinician is unaware that such a clinicalpresentation exists. So, we do recommend that practitioners and researchers read through theclassification. Moreover, ICOP joins ICHD-3 and IASP/ICD-11 in establishing clearterminology that will allow communication and data sharing in an unambiguous manner. Forresearch, the classification is indispensable: every patient entered into a research project, be it adrug trial or a study of pathophysiology or biochemistry, must fulfil a set of establisheddiagnostic criteria.This classification is hierarchical, allowing the user to establish a diagnosis from only the first-digit level or extending to the fifth or even seventh digit. The level of resolution in diagnosticcoding clearly depends on the intended use. In general practice, only the first- or second-digitdiagnoses are usually applied, while in specialist practice and headache centres a diagnosisincluding a fourth- or fifth-digit (and even sixth or seventh digit) levels is appropriate.We deal with primary and secondary orofacial pains (OFP) within the same sections. This is inour opinion a more efficient manner of presenting the various disorders, in part because primaryand secondary designations become difficult to differentiate in these overlapping disorders.1.For most purposes, patients receive a diagnosis according to currently present pain or fromwithin the last year. For genetic research and some other uses, occurrence during the entirelifetime is used.2. Each distinct type, subtype or subform of OFP and headache that the patient has must beseparately diagnosed and coded. For example, a severely affected patient may receivemultiple diagnoses and codes: 2.1.2.3.2. Chronic persistent primary myofascial pain withpain referraland 3.1.4.1. Chronic primary TMJ arthralgia without referred pain andpossibly 1.1 Migraine without aura from ICHD-3.
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83.When a patient receives more than one diagnosis, these should be listed in the order ofimportance to the patient. i.e. establish which of the diagnoses is causing the most sufferingand disability in the patient’s view?4.When it is unclear which type of OFP a particular patient is experiencing, other availableinformation should be used in addition to the diagnostic criteria to decide the more likelydiagnosis. This could include the longitudinal pain history (how and when did the painstart?), the family history, the effect of drugs, menstrual relationship, age, gender and arange of other features.5.To receive a particular OFP diagnosis the patient must, in many cases, experience aminimum number of attacks of or number of days with that pain. This number is oftenspecified in the diagnostic criteria for the OFP type. The OFP diagnoses must fulfil anumber of other requirements described within the criteria under separate letter headings:A, B, C etc. Some letter headings are monothetic: that is, they express a singlerequirement. Other letter headings are polythetic, requiring for example any two out of fourlisted characteristics. This structure has been adopted from ICHD-3.6.The frequency of OFP disorders varies widely, from occurring only every 1–2 years todaily pain. The severity of attacks also varies. Other than for myofascial and TMJarthralgia, ICOP does not provide a possibility to code for frequency. None of thediagnostic criteria include routine assessment of severity and frequency, but werecommend that frequency and severity be assessed and specified.7.Primary or secondary OFP or both: When a new OFP occurs for the first time in closetemporal relation to another disorder known to cause OFP (e.g. trauma), the new OFP iscoded as secondary and attributed or associated to the causative disorder. This remains trueeven when the OFP has the characteristics of a primary disorder (myofascial pain,arthralgia). When a pre-existing OFP becomes chronic in close temporal relation to such acausative disorder, both the primary and the secondary diagnoses should be given. When apre-existing primary OFP is made significantly worse (usually meaning a two-fold orgreater increase in frequency and/or severity) in close temporal relation to such a causativedisorder, both the primary and the secondary diagnoses should be given, provided thatthere is good evidence that the disorder can cause OFP.
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98.The last criterion for almost every headache disorder is “Not better accounted for byanother ICOP or ICHD-3 diagnosis”. Consideration of other possible diagnoses (thedifferential diagnosis) is a routine part of the clinical diagnostic process. When an OFPappears to fulfil the criteria for a particular disorder, this last criterion is a reminder alwaysto consider other diagnoses that might better explain the OFP. In particular this applies toassessing whether OFP is secondary or primary. In order to accomplish this goal ofdifferential diagnosis, the clinical diagnostic process may need to consider other disordersoutside of the ICOP framework, elaborate on the pain history, and use clinical tests beyondthose implied in the ICOP criteria. Referred pain from one structure to the other in theorofacial pain region is extremely common but classifying all of these is beyond the scopeof ICOP.9.Many patients with a diagnosed OFP disorder may report occasional pain episodes that arenot typical of that diagnosed specific disorder. This can be due to treatment, inability torecall symptoms exactly, or other factors. The clinician should assist the patient indescribing typical, untreated or unsuccessfully-treated attacks and the clinician shoulddetermine if there have been enough of these to establish the diagnosis. Any less-typicalattacks should also be considered when describing attack frequency.10. When a patient is suspected of having more than one OFP, it is highly recommended thatthey complete a diagnostic daily pain diary. It has been shown that such pain diariesimprove diagnostic accuracy as well as lead to a more precise judgement of medicationconsumption. Diaries are typically recommended for a month, during which, for each painepisode, the important characteristics are recorded. Additionally, the diary helps in judgingthe balance between different OFP types or subtypes. Finally, using the diary is animportant tool in explaining to the patient how to distinguish between different OFPs, to beaware of medication consumption, to note triggering factors, and become a more reliablesource of follow-up information.
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10Classification overview1. Orofacial pain associated with disorders of dentoalveolar and associated structures1.1 Dental pain1.1.1 Pulpal pain1.1.1.1. Pulpal pain attributed to hypersensitivity1.1.1.1.1 Pulpal pain attributed to a crack in the enamel1.1.1.1.2 Pulpal pain attributed to exposed dentin1.1.1.1.2.1 Pulpal pain attributed to tooth wear or abrasion1.1.1.1.2.2 Pulpal pain attributed to fracture resulting in exposed dentin1.1.1.1.2.3 Pulpal pain attributed to developmental dental hard tissue defect1.1.1.1.3 Pulpal pain attributed to hypersensitivity associated with dental procedures1.1.1.1.3.1 Pulpal pain attributed to recent extensive removal of dentin1.1.1.1.3.2 Pulpal pain attributed to recent placement of a restoration1.1.1.1.3.3 Pulpal pain attributed to hypersensitivity due to hyperocclusion or-articulation following dental restorative procedures1.1.1.1.4 Pulpal pain attributed to central sensitization1.1.1.1.5 Pulpal pain attributed to other cause1.1.1.2 Pulpal pain attributed to pulp exposure due to dental trauma1.1.1.3 Pulpal pain attributed to pulpitis (pulpal inflammation)1.1.1.3.1 Pulpal pain attributed to reversible pulpitis due to infection of dentin1.1.1.3.1.1 Pulpal pain attributed to caries that does not extend to the pulp1.1.1.3.1.2 Pulpal pain attributed to reversible pulpitis due to fracture of enamel, rootcementum, dentin or any combination thereof, resulting in exposure of dentin1.1.1.3.1.3 Pulpal pain attributed to reversible pulpitis due to a tooth crack withoutevidence of missing tooth substance1.1.1.3.2 Pulpal pain attributed to irreversible pulpitis due to infection of dentin1.1.1.3.2.1 Pulpal pain attributed to caries which may extend to the pulp1.1.1.3.2.2 Pulpal pain attributed to irreversible pulpitis due to dental hard tissuefracture without pulp exposure
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111.1.1.3.2.3 Pulpal pain attributed to irreversible pulpitis due to visible crack in theenamel without evidence of missing tooth substance1.1.1.3.3 Pulpal pain attributed to irreversible pulpitis due to infection of the dental pulp1.1.1.3.3.1 Pulpal pain attributed to caries extending to the pulp1.1.1.3.3.2 Pulpal pain attributed to irreversible pulpitis due to dental hard tissue fracturewithout pulp exposure1.1.1.3.4 Pulpal pain attributed to pulpitis due to external cervical root resorption1.1.1.3.5 Pulpal pain attributed to pulpitis due to other cause1.1.1.4 Pulpal pain attributed to systemic cause1.1.2 Periodontal pain1.1.2.1 Periodontal pain attributed to periodontitis (periodontal inflammation of theperiodontium)1.1.2.1.1 Periodontal pain attributed to traumatically induced periodontal infammation1.1.2.1.1.1 Periodontal pain attributed to hyperocclusion or -articulation1.1.2.1.1.2 Postoperative periodontal pain1.1.2.1.1.3 Periodontal pain attributed to accidental dental trauma1.1.2.1.1.4 Periodontal pain attributed to other trauma or injury1.1.2.1.2 Periodontal pain attributed to apical periodontitis due to endodontic disease1.1.2.1.2.1 Periodontal pain attributed to pulpal inflammation1.1.2.1.2.2 Periodontal pain attributed to endodontic infection1.1.2.1.2.2.1 Periodontal pain attributed to intraradicular endodontic infection1.1.2.1.2.2.2 Periodontal pain attributed to extraradicular endodontic infection1.1.2.1.3 Periodontal pain attributed to periodontal disease1.1.2.1.3.1 Periodontal pain attributed to chronic periodontitis1.1.2.1.3.2 Periodontal pain attributed to aggressive periodontitis1.1.2.1.3.3 Periodontal pain attributed to periodontitis as a manifestation of systemicdisorder known to cause periodontitis
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121.1.2.1.3.3.1 Periodontal pain attributed to a hematological disorder1.1.2.1.3.3.2 Periodontal pain attributed to a genetic disorder1.1.2.1.3.3.3 Periodontal pain attributed to an unspecified systemic disorder1.1.2.1.3.4 Periodontal pain associated with necrotizing ulcerative periodontitis (NUP)1.1.2.1.3.5 Periodontal pain associated with periodontal abscess1.1.2.1.4 Periodontal pain attributed to apical and marginal periodontitis due to combinedendodontic infection and periodontal disease1.1.2.1.5 Periodontal pain attributed to peri-implantitis due to peri-implant infection1.1.2.2 Periodontal pain attributed to a local non-inflammatory cause1.1.3 Gingival pain1.1.3.1 Gingival pain attributed to gingivitis (gingival inflammation)1.1.3.1.1 Gingival pain attributed to trauma1.1.3.1.2 Gingival pain attributed to infection1.1.3.1.2.1 Gingival pain attributed to bacterial infection1.1.3.1.2.2 Gingival pain attributed to viral infection1.1.3.1.2.3 Gingival pain attributed to fungal infection1.1.3.1.3 Gingival pain attributed to autoimmunity1.1.3.1.4 Gingival pain attributed to allergic reaction1.1.3.1.5 Gingival pain attributed to gingival inflammation due to other cause1.1.3.2 Gingival pain attributed to malignant lesion1.1.3.3 Gingival pain attributed to neuropathy1.1.3.4 Idiopathic gingival pain1.2 Non-dental pain1.2.1 Oral mucosal pain1.2.1.1 Oral mucosal pain attributed to oral mucosal inflammation1.2.1.1.1 Oral mucosal pain associated with trauma1.2.1.1.1.1 Oral mucosal pain attributed to mechanical, thermal, or chemical injury1.2.1.1.1.2 Oral mucosal pain attributed to surgical or other iatrogenic injury
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131.2.1.1.1.3 Oral mucosal pain attributed to radiation or chemotherapy1.2.1.1.2 Oral mucosal pain attributed to infection1.2.1.1.2.1 Oral mucosal pain attributed to bacterial infection1.2.1.1.2.2 Oral mucosal pain attributed to viral infection1.2.1.1.2.3 Oral mucosal pain attributed to fungal infection1.2.1.1.3 Oral mucosal pain attributed to autoimmunity1.2.1.1.4 Oral mucosal pain attributed to allergic reaction1.2.1.1.5 Oral mucosal pain attributed to oral mucosal inflammation due to other cause1.2.1.2 Oral mucosal pain attributed to malignant lesion1.2.1.3 Oral mucosal pain attributed to neuropathy1.2.1.4 Idiopathic oral mucosal pain1.2.2 Salivary gland pain1.2.2.1 Salivary gland pain attributed to obstructive cause1.2.2.2 Salivary gland pain attributed to infection1.2.2.2.1 Salivary gland pain attributed to viral infection1.2.2.2.2 Salivary gland pain attributed to bacterial infection1.2.2.3 Salivary gland pain attributed to non-infectious cause1.2.2.3.1 Salivary gland pain attributed to recurrent juvenile parotitis1.2.2.3.2 Salivary gland pain attributed to immunologically mediated disorder1.2.2.3.3 Salivary gland pain attributed to other cause1.2.3 Jaw bone pain1.2.3.1 Jaw bone pain attributed to infection1.2.3.1.1 Jaw bone pain attributed to bacterial infection1.2.3.1.2 Jaw bone pain attributed to viral infection1.2.3.1.3 Jaw bone pain attributed to fungal infection1.2.3.2 Therapy related jaw bone pain
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141.2.3.3 Jaw bone pain attributed to a local benign lesion1.2.3.4 Jaw bone pain attributed to a malignant lesion1.2.3.4.1 Jaw bone pain attributed to a primary malignant lesion1.2.3.4.2 Jaw bone pain secondary to a malignant lesion1.2.3.5 Jaw bone pain attributed to systemic disease1.2.3.6 Jaw bone pain attributed to traumatic injury2. Orofacial pain associated with regional muscles2.1. Primary myofascial pain2.1.1. Acute primary myofascial pain2.1.2. Chronic primary myofascial pain2.1.2.1. Chronic infrequent primary myofascial pain2.1.2.2. Chronic frequent primary myofascial pain2.1.2.2.1. Chronic frequent primary myofascial pain without pain referral2.1.2.2.2. Chronic frequent primary myofascial pain with pain referral2.1.2.3. Chronic persistent primary myofascial pain2.1.2.3.1. Chronic persistent primary myofascial pain without pain referral2.1.2.3.2. Chronic persistent primary myofascial pain with pain referral2.2. Secondary myofascial pain2.2.1. Secondary myofascial pain due to tendonitis2.2.2. Secondary myofascial pain due to myositis2.2.3. Secondary myofascial pain due to muscle spasm3. Orofacial pain associated with disorders of the Temporomandibular Joint (TMJ)3.1. Primary TMJ arthralgia
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153.1.1. Acute primary TMJ arthralgia3.1.2. Chronic primary TMJ arthralgia3.1.2.1. Chronic infrequent primary TMJ arthralgia3.1.2.2. Chronic frequent primary TMJ arthralgia3.1.2.2.1. Chronic frequent primary TMJ arthralgia without referred pain3.1.2.2.2. Chronic frequent primary TMJ arthralgia with referred pain3.1.2.3. Chronic persistent primary TMJ arthralgia3.1.2.3.1. Chronic persistent primary TMJ arthralgia without referred pain3.1.2.3.2. Chronic persistent primary TMJ arthralgia with referred pain3.2. Secondary TMJ arthralgia3.2.1. TMJ arthralgia attributed to arthritis3.2.1.1. TMJ arthralgia attributed to arthritis, non-systemic3.2.1.2. TMJ arthralgia attributed to arthritis, systemic3.2.2. TMJ arthralgia attributed to disc displacement with reduction3.2.3. TMJ arthralgia attributed to disc displacement with reduction with intermittentlocking3.2.4. TMJ arthralgia attributed to disc displacement without reduction3.2.5. TMJ arthralgia attributed to degenerative joint disease3.2.6. TMJ arthralgia attributed to subluxation4. Orofacial pain associated with lesion/disorders of the cranial nerves and other regionalnerve structures4.1. Pain caused by a lesion or disease of the trigeminal nerve4.1.1. Trigeminal neuralgia4.1.1.1. Classical trigeminal neuralgia
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164.1.1.1.1. Classical trigeminal neuralgia, purely paroxysmal4.1.1.1.2. Classical trigeminal neuralgia with concomitant continuous pain4.1.1.2. Secondary trigeminal neuralgia4.1.1.2.1. Trigeminal neuralgia attributed to multiple sclerosis4.1.1.2.2. Trigeminal neuralgia attributed to space-occupying lesion4.1.1.2.3. Trigeminal neuralgia attributed to other demonstrable causes4.1.1.3. Idiopathic trigeminal neuralgia4.1.1.3.1. Idiopathic trigeminal neuralgia, purely paroxysmal4.1.1.3.2. Idiopathic trigeminal neuralgia with concomitant continuouspain4.1.2. Trigeminal neuropathic pain other than 4.1.1. Clinically established trigeminalneuralgia4.1.2.1. Trigeminal neuropathic pain attributed to herpes Zoster4.1.2.2. Trigeminal postherpetic neuralgia4.1.2.3. Post-traumatic trigeminal neuropathic pain4.1.2.3.1. Probable post-traumatic trigeminal neuropathic pain4.1.2.4. Trigeminal neuropathic pain attributed to another disorder4.1.2.4.1. Probable trigeminal neuropathic pain attributed to anotherdisorder4.1.2.5. Idiopathic trigeminal neuropathic pain4.1.2.5.1. Probable idiopathic trigeminal neuropathic pain4.2. Pain caused by a lesion or disease of the glossopharyngeal nerve4.2.1. Clinically established glossopharyngeal neuralgia4.2.1.1. Classical glossopharyngeal neuralgia
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174.2.1.2. Secondary glossopharyngeal neuralgia4.2.1.3. Idiopathic glossopharyngeal neuralgia4.2.2. Glossopharyngeal neuropathic pain4.2.2.1. Glossopharyngeal neuropathic pain attributed to a known cause4.2.2.2. Idiopathic glossopharyngeal neuropathic pain5. Orofacial pain resembling presentations of primary headaches5.1. Orofacial migraine5.1.1. Orofacial migraine5.1.2. Chronic orofacial migraine5.1.3 Neurovascular Orofacial Pain5.1.3.1 Shortlasting Neurovascular Orofacial Pain5.1.3.2 Longlasting Neurovascular Orofacial Pain5.2. Tension-type orofacial pain5.3. Trigeminal autonomic orofacial pain5.3.1. Orofacial cluster attacks5.3.1.1. Episodic orofacial cluster attacks5.3.1.2. Chronic orofacial cluster attacks5.3.2. Paroxysmal hemifacial pain5.3.2.1. Episodic paroxysmal hemifacial pain5.3.2.2. Chronic paroxysmal hemifacial pain5.3.3. Short-lasting unilateral neuralgiform facial pain attacks with autonomic signs(SUNFA)
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185.3.3.1. Episodic SUNFA5.3.3.2. Chronic SUNFA5.3.4. Hemifacial continuous pain with autonomic signs5.3.5 Constant Unilateral Facial Pain with Attacks (CUFPA)6. Idiopathic orofacial pain6.1. Burning mouth syndrome (BMS)6.1.1. Burning mouth syndrome associated with somatosensory changes6.1.2. Burning mouth syndrome not associated with somatosensory changes6.2. Persistent idiopathic facial pain (PIFP)6.2.1. Persistent idiopathic facial pain associated with somatosensory changes6.2.2. Persistent idiopathic facial pain not associated with somatosensory changes6.3. Persistent idiopathic dentoalveolar pain6.3.1. Persistent idiopathic dentoalveolar pain associated with somatosensory changes6.3.2. Persistent idiopathic dentoalveolar pain not associated with somatosensorychanges7. Psychosocial Assesment
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19Classification with diagnostic criteria1. Orofacial pain due to disorders of dentoalveolar and associated structuresGeneral commentsPain originating in dentoalveolar and associated structures is the most common reason for thecomplaint of pain in the orofacial region. The category includes pain caused by diseases, injuriesand normal functioning of the tooth pulp, periodontium, gingivae, oral mucosa, salivary glands,and jaw bone tissue. In general, the pain is nociceptive and/or inflammatory in nature, andusually acute, meaning that it lasts less than 3 months. When the underlying disorder isadequately treated, the symptom of pain does not remain for a prolonged period of time, but thismay not always be the case. The frequency of pain may be continuous, recurrent or occasional.In many cases, the natural history of the underlying disorders allows for fluctuation in allsymptoms, including pain, which means this type of pain may be sometimes described asepisodic (occurring less than 15 days per month, but being present more than 3 months). If thepain is present for more than 3 months, and at least 15 days per month, it is considered aschronic.Since pain associated with dentoalveolar and associated structures is mainly a symptom of anacute disease or disorder, it might also appear relevant to categorize pain in relation to treatment.If the pain-inducing underlying disorder is not treated at all, the acute pain will usually remainand eventually become chronic. The same occurs if the underlying disorder isineffectively/insufficiently treated, since the disorder (such as a local infection, neoplasm orsystemic disorder) and the accompanying pain also might remain for longer than 3 months.In general, the distinction between acute and chronic pain is important, since chronic pain oftenrequires different management and has a less favorable prognosis. However, it is unknownwhether the acute, episodic and chronic forms of dentoalveolar pain (and other types dealt withhere) differ in any clinically meaningful aspect except duration. Based on the lack of datasupporting that a distinction is relevant from the perspective of treatment or prognosis, the issueof acute/chronic is not reflected in this section of the ICOP. For research aiming to compare e.g.dentoalveolar pain of short versus long duration, it its recommended to use the distinction ofacute, episodic or chronic pain described above, consistent with IASP/ICD11 and ICHD-3.
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20If evidence of important differences emerges in the future, the decision not to separate painconditions based on time in this section must be re-evaluated.Diagnostic criteria1.1 Dental painDental pain includes pain attributed to conditions affecting the tooth and its immediatelysurrounding and supporting structures, i.e. the tooth pulp, periodontium, and gingiva.1.1.1 Pulpal painDescription:Dental pain caused by a disorder involving the tooth pulpDiagnostic criteria:A. Any pain fulfilling criteria B through EB. Localized to the dental region of the pulpal disorder or lesion but may refer or radiateto other ipsilateral orofacial locations.C. Clinical, laboratory, imaging and/or anamnestic evidence of a lesion, disease, ortrauma1known to produce pulpal painD. Familiar pain is exacerbated by physical stimulus2applied to the affected tooth.E. Not better accounted for by another ICOP diagnosis.Notes:1as specified per sub-diagnosis2mechanical, thermal, or chemical; as specified per sub-diagnosis
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21Comments:Pulpal pain can be associated with all types of pulpal injury or disease. The pain ispredominantly inflammatory and secondary to external or internal events.1.1.1.1Pulpal pain attributed to hypersensitivityDescription:Pulpal pain occurring in association with a clinically normal pulp.Diagnostic criteria:A. The pain fulfills criteria for 1.1.1 Pulpal pain, and fulfills at least one of B-D andcriterion EB. Is a sharp, deep sensation evoked by external stimuli (hot, cold and/or sweet)C. Subsides within a few secondsD. Is poorly localized;a. often only to an approximate area within two or three teeth adjacent to the affectedtooth,b. occasionally the patient is unable to distinguish whether the pain originates from themandible or the maxilla (Sharav et al, 1984; Falace et al 1996)E. Not better accounted for by another ICOP or ICHD-3 diagnosis.
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221.1.1.1.1Pulpal pain attributed to a crack in the enamelDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.1 Pulpal pain attributed to hypersensitivityB. The tooth has been diagnosed with a tooth crack/incomplete fracture involving theenamel based on a and at least one of b-d:a. visual identification1of crack linesb. sharp pain upon bitingc. pain on release of occlusal biting pressure or external application of forced. cold hypersensitivityC. Not better accounted for by another ICOP or ICHD-3 diagnosis.Notes:1if needed, visual identification can be aided by magnification, light enhancement andvisualization with dye1.1.1.1.2Pulpal pain attributed to exposed dentinDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.1 Pulpal pain attributed to hypersensitivityB. A dentin surface is exposedC. The pain may be reproduced by scratching the exposed dentin with a dental explorer orby air blasting
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23D. Not better accounted for by another ICOP or ICHD-3 diagnosis1.1.1.1.2.1 Pulpal pain attributed to tooth wear or abrasionDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.1.2 Pulpal pain attributed to exposed dentinB. Clinical evidence of tooth wear or abrasion; smooth, flat surfaces that are not contoured withthe natural shape of the anatomic crown of the tooth (von Toil et al, 2002)C. Not better accounted for by another ICOP or ICHD-3 diagnosis1.1.1.1.2.2 Pulpal pain attributed to fracture resulting in exposed dentinDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.1.2 Pulpal pain attributed to exposed dentinB. The tooth has been diagnosed with a fracture involving the enamel, root cementum, dentin orany combination thereof based on clinical and/or radiographic observationsC. Not better accounted for by another ICOP or ICHD-3 diagnosis1.1.1.1.2.3 Pulpal pain attributed to developmental dental hard tissue defectDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.1.2 Pulpal pain attributed to exposed dentinB. The tooth has been diagnosed with a developmental defect involving the enamel, rootcementum, and/or dentin
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24a. local hypomineralization/hypomaturation of enamelb. amelogenesis imperfectac. dentinogenesis imperfectad. other developmental defectC. Not better accounted for by another ICOP or ICHD-3 diagnosis1.1.1.1.3Pulpal pain attributed to hypersensitivity associated with dental proceduresDescription:The pain occurs subsequent to a dental procedure. It originates in dentin with a sharp, deepsensation evoked by external stimuli that subsides within a few seconds. Hot, cold, and sweet areamong the external stimuli that may produce pain. Pain is poorly localized, often only to anapproximate area within two or three teeth adjacent to the affected tooth. Occasionally, thepatient is unable to distinguish whether the pain originates from the mandible or the maxilla.(Sharav et al, 1996; Falace et al, 1996)Diagnostic criteria:A. The pain fulfills criteria for 1.1.1.1 Pulpal pain attributed to hypersensitivityB. The tooth has recently1been subject to dental treatmentC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1hours to days from dental procedure to pain onset
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251.1.1.1.3.1 Pulpal pain attributed to recent extensive removal of dentinDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.1.3 Pulpal pain attributed to hypersensitivityassociated with dental proceduresB. Pain onset upon recent1removal of dentin fulfilling either or both of a and ba. deep (i.e. in close proximity to the pulp)b. wide (i.e. opening up dentinal tubules in a large area)C. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1hours to days1.1.1.1.3.2 Pulpal pain attributed to recent placement of a restorationDiagnostic criteria:A. The pain fulfils criteria for 1.1.1.1.3 Pulpal pain attributed to hypersensitivityassociated with dental proceduresB. Pain onset upon recent1placement of a direct or indirect dental restorationC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:
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261hours to days1.1.1.1.3.3 Pulpal pain attributed to hypersensitivity due to hyperocclusion or -articulationfollowing recent dental restorative proceduresDiagnostic criteria:A. The pain fulfils criteria for 1.1.1.1.3 Pulpal pain attributed to hypersensitivityassociated with dental proceduresB. The tooth is in hyperocclusion and/or hyperarticulation as a result of recent1restorativeprocedures2C. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1hours to days2such as temporization, dental restoration or prosthodontic replacement1.1.1.1.4Pulpal pain attributed to central sensitizationDescription:Pulpal pain attributed to central sensitization can present in several teeth simultaneously, oftenstarting in one tooth and then spreading to other teeth. This pain can be continuous or recurrent,and be present for long periods, often it is chronic. Successful treatment of other pain conditions
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27and associated psychological symptoms often leads to reduced tooth pain. Desensitizing dentaltreatment may in some cases lead to pain reduction or relief.Diagnostic criteria:A. The pain fulfils criteria for 1.1.1.1 Pulpal pain attributed to hypersensitivityB. Signs of central sensitization1are presentC. The patient is diagnosed with another orofacial, neck or widespread bodily paincondition, and the tooth paina. may present spontaneouslyb. may co-present and co-fluctuate with other painsD. Local anesthesia and peripherally acting analgesics do not consistently provide painrelief (Glick et al, 1962)E. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1such as pain referral, temporal pain summation and/or allodynia1.1.1.1.5Pulpal pain attributed to other causeDiagnostic criteria:A. The pain fulfils criteria for 1.1.1.1 Pulpal pain attributed to hypersensitivity
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28B. The pain does not fulfil criteria for 1.1.1.1.1 – 1.1.1.1.4C. Not better accounted for by another ICOP or ICHD-3 diagnosis1.1.1.2Pulpal pain attributed to pulp exposure due to dental traumaDescription:The pain is mild to moderate and exacerbation is typically evoked by air, liquids, or pressure onexposed pulp tissue secondary to dental trauma. When evoked, the pain typically subsides whenthe stimulus ceases. In the immediate post-trauma period, there is a lack of temperaturesensitivity, spontaneous pain, or radiating pain, as these symptoms typically occur later and areassociated with inflammation.Diagnostic criteria:A. The pain fulfills criteria for 1.1.1 Pulpal painB. The tooth has been diagnosed with a recent1traumatic injury (a-c) exposing vital pulptissuea. fracture involving enamel, dentin and pulp (complicated crown fracture)b. fracture involving root cementum, dentin and pulp (complicated root fracture)c. fracture involving enamel, root cementum, dentin and pulp (complicated crown-rootfracture)C. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:
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291minutes to hours1.1.1.3Pulpal pain attributed to pulpitis (pulpal inflammation)Description:Pain associated with pulpitis can vary from mild to severe and can be related to the severity ofthe inflammation (Hargreaves and Seltzer, 2002; Byers and Närhi, 2002). However, severepulpal inflammation can also be asymptomatic (Hasler and Mitchell, 1970; Tyldesley andMumford, 1970; Michaelson and Holland, 2012).Diagnostic criteria:A. The pain fulfils criteria for 1.1.1 Pulpal painB. The tooth has been diagnosed with pulpal inflammation1, i.e. pulpitisC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1due to trauma or infection; as specified by subcategories1.1.1.3.1Pulpal pain attributed to reversible pulpitis due to infection of dentinDescription:Reversible pulpitis pain has been described as typically mild, not spontaneous, and provoked bychanges in temperature. When evoked, pain is typically short-lasting and does not outlast thestimulus. (Garfunkel et al 1973). The suggested diagnostic criteria for reversible/irreversible
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30pulpitis presented below have not been scientifically validated, and the presence andcharacteristics of symptoms appear poorly related to the condition of the pulp (Mejàre et al2012). When associated with caries, pulpitis is therefore considered potentially reversible as longas a zone of functionally intact dentin separates the bacterial front from the vital pulp tissue.Diagnostic criteria:A. The pain fulfils criteria for 1.1.1.3 Pulpal pain attributed to pulpitisB. The dentin is infected1C. The tooth has been diagnosed with reversible pulpitis based on the following:a. clinical and/or radiographic evidence of a zone of intact dentin covering the pulpb. pain may occur spontaneously but is not continuousc. absence of prolonged pain2after stimulation3of the pulpd. absence of severe pain intensitye. the pain responds to peripheral analgesics (NSAIDS)D. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1As evidenced by presence of caries or dentin exposed to the microbiota of the oral cavity for aperiod of time2> a few seconds3thermal (cold, heat) or mechanical (probing, drilling)
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311.1.1.3.1.1 Pulpal pain attributed to caries that does not extend to the pulpDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.3.1 Pulpal pain attributed to reversible pulpitis dueto infection of dentinB. The tooth has been diagnosed with caries that is unlikely to extend to the pulp basedon clinical and/or radiographic observationsC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:In addition to thermal sensitivity, the pain may be evoked by pressure on the carious dentin.(Sigurdsson, 2008)1.1.1.3.1.2 Pulpal pain attributed to reversible pulpitis due to fracture of enamel, root cementum,dentin or any combination thereof, resulting in exposure of dentinDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.3.1 Pulpal pain attributed to reversible pulpitis dueto infection of dentinB. The tooth has been diagnosed with a traumatic injury exposing dentinC. Not better accounted for by another ICOP or ICHD-3 diagnosis
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32Comments:In addition to thermal sensitivity, the pain may be evoked by scratching the surface of theinfected dentin. (Smulson and Sieraski, 1996; Abbott and Yu, 2007).1.1.1.3.1.3 Pulpal pain attributed to reversible pulpitis due to a tooth crack without evidenceof missing tooth substanceDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.3.1 Pulpal pain attributed to reversible pulpitis dueto infection of dentinB. The tooth has been diagnosed with a tooth crack/incomplete fracture involving theenamel or enamel and dentin based on:a. visual identification1of crack linesb. sharp pain upon bitingc. pain on release of occlusal biting pressure or external application of forced. cold hypersensitivityC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1visual identification can be aided by magnification, light enhancement and visualization withdye
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33Comments:The duration of the pain should not outlast the application of the stimulus. Cracked teeth oftenhave deep probing depths associated with the crack (Kang et al, 2016).1.1.1.3.2Pulpal pain attributed to irreversible pulpitis due to infection of dentinDescription:The pain can be exacerbated by changes in temperature. Pain may also be associated with bitingor percussion sensitivity. (Abbott and Yu, 2007). When evoked, the pain outlasts the duration ofthe stimulus. (Sigurdsson, 2008, Berman and Hartwell, 2006). The suggested diagnostic criteriafor reversible/irreversible pulpitis presented below have not been scientifically validated and thepresence and characteristics of symptoms appear poorly related to the condition of the pulp(Mejàre et al 2012). When associated with caries, pulpitis is therefore considered potentiallyirreversible when no zone of functionally intact dentin separates the bacterial front from the vitalpulp tissue.Diagnostic criteria:A. The pain fulfils criteria for 1.1.1.3 Pulpal pain attributed to pulpitisB. The dentin is infected1C. The tooth has been diagnosed with irreversible pulpitis based on the following:a. clinical and/or radiographic evidence that no zone of intact dentin covers the pulpb. spontaneous pain that may be continuousc. prolonged pain2after stimulation3of the pulp
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34d. severe pain intensitye. the pain responds poorly to NSAIDSD. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1As evidenced by presence of caries or dentin exposed to the oral cavity microbiota for a periodof time2> a few seconds3thermal (cold, heat) or mechanical (probing, drilling)1.1.1.3.2.1 Pulpal pain attributed to caries which may extend to the pulpDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.3.2 Pulpal pain attributed to irreversible pulpitis dueto infection of dentinB. The tooth has been diagnosed with deep caries that is likely to extend to the pulp basedon clinical and/or radiographic observationsC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:The presence of pain is poorly correlated to the status of the pulp. The value of symptoms todetermine the condition of the pulp (reversibly/irreversibly inflamed) is debated andcontroversial, and scientific evidence is scarce (Mejàre et al. 2012). Severe continuous pain that
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35does not respond to analgesics (NSAID) may indicate irreversible inflammation and need forinvasive treatment.1.1.1.3.2.2 Pulpal pain attributed to irreversible pulpitis due to dental hard tissue fracturewithout pulp exposureDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.3.2 Pulpal pain attributed to irreversible pulpitis dueto infection of dentinB. Clinical and/or radiographic evidence of a fracture of dental hard tissue (a-c) withoutexposure of vital pulp tissuea. fracture involving enamel and dentin (uncomplicated crown fracture)b. fracture involving root cementum and dentin (uncomplicated root fracture)c. fracture involving enamel, root cementum and dentin (uncomplicated crown-rootfracture)C. Not better accounted for by another ICOP or ICHD-3 diagnosisComments: In addition to thermal sensitivity, the pain may be evoked by scratching the surfaceof the infected dentin. (Smulson and Sieraski, 1996; Abbott and Yu, 2007)
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361.1.1.3.2.3 Pulpal pain attributed to irreversible pulpitis due to a tooth crack withoutevidence of missing tooth substanceDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.3.2 Pulpal pain attributed to irreversible pulpitis dueto infection of dentinB. Clinical evidence of a crack in the enamel or enamel and dentin based on thefollowing:a. visual identification1of crack linesb. sharp pain upon bitingc. pain on release of occlusal biting pressure or external application of forced. cold hypersensitivityC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1visual identification can be aided by magnification, light enhancement and visualization withdyeComments:Cracked teeth may result in sharp pain upon biting, unexplained cold sensitivity, pain on releaseof pressure, or deep probing depths associated with the crack (Kang et al, 2016). The duration ofthe pain typically outlasts the application of the stimulus.
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371.1.1.3.3Pulpal pain attributed to irreversible pulpitis due to infection of the dental pulpDescription:The diagnostic criteria for reversible/irreversible pulpitis have not been scientifically validated,and the presence and characteristics of symptoms appear poorly related to the condition of thepulp (Mejàre et al 2012). When the pulp has been directly exposed the oral microbiota for aperiod of time, it lacks the ability to heal and pulpitis is considered to be irreversible.Diagnostic criteria:A. The pain fulfils criteria for 1.1.1.3 Pulpal pain attributed to pulpitisB. The pulp is infected1C. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1has been exposed to the microbiota of the oral cavity for a period of time1.1.1.3.3.1 Pulpal pain attributed to caries extending to the pulpDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.3.3 Pulpal pain attributed to irreversible pulpitis dueto infection of the dental pulpB. The tooth has been diagnosed with caries that is likely to extend to the pulp based onclinical and/or radiographic observationsC. Not better accounted for by another ICOP or ICHD-3 diagnosis
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38Comments:Histological studies indicate that when the carious lesion (bacterial front) reaches the pulp,inflammation is likely to be irreversible. The assessment is based on clinical and radiographicappearance. If a zone of intact, functional dentin is not seen between the carious dentin and thepulp, it can be concluded that the microflora is in direct contact with and has infected the pulptissue, resulting in severe inflammation. It should be noted that in many cases, this condition maybe symptom free (Michaelson and Holland, 2002).1.1.1.3.3.2 Pulpal pain attributed to irreversible pulpitis due to dental hard tissue fracturewith pulp exposureDiagnostic criteria:A. The pain fulfills criteria for 1.1.1.3.3 Pulpal pain attributed to irreversible pulpitis dueto infection of the dental pulp.B. Clinical and/or radiographic evidence of a fracture of dental hard tissue and exposureof vital pulp tissuea. fracture involving enamel, dentin, and pulp (complicated crown fracture)b. fracture involving root cementum, dentin, and pulp (complicated root fracture)c. fracture involving enamel, root cementum, dentin, and pulp (complicated crown-rootfracture)C. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:
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39In addition to thermal sensitivity, the pain may be evoked by mechanical stimulation of theexposed pulp or adjacent dentin.1.1.1.3.4Pulpal pain attributed to pulpitis due to external cervical root resorptionDescription:Cervical root resorption is a process where dentin is resorbed by osteoclastic activity. Thecondition is often asymptomatic until the resorptive process reaches the pulp. Secondaryinfection in the resorbed area stimulates an inflammatory response in the adjacent pulp.In addition to thermal sensitivity, the pain may be evoked by pressure on the resorptive defectdentin. It should be noted that teeth with external cervical resorptions are usually asymptomatic(Patel et al, 2009).Diagnostic criteria:A. The pain fulfils criteria for 1.1.1.3 Pulpal pain attributed to pulpitisB. The tooth has been diagnosed with external cervical root resorption based on clinicaland/or radiographic observationsC. Not better accounted for by another ICOP or ICHD-3 diagnosis1.1.1.3.5Pulpal pain attributed to pulpitis due to other causeDiagnostic criteria:A. The pain fulfils criteria for 1.1.1.3 Pulpal pain attributed to pulpitisB. The pain does not fulfill criteria for 1.1.1.3.1–1.1.1.3.4C. Not better accounted for by another ICOP or ICHD-3 diagnosis.
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40Comments:As an example, some reports in the literature indicate that pulpitis and pulpal pain may occursecondary to neurovascular events (neurogenic inflammation). Pain symptoms may range fromdentinal hypersensitivity to lingering pain, indicative of pulpitis, and are often accompanied byautonomic signs. Pain symptoms may range from that of dentinal pain to pulpitis and oftenaccompanied by autonomic signs (see 5.1 Orofacial migraine). Pain responds to acute as well aschronic antimigraine medication (Obermann et al 2007, Benoliel et al 2010, Sharav et al 2015,2017).1.1.1.4Pulpal pain attributed to systemic causeDescription:Pulpal pain can be the result of a systemic disease causing a change in the pulp condition. Forexample, sickle cell anemia crises might result in dental pain (da Fonseca et al, 2007). Pulpalnecrosis, presumed secondary to vaso-occlusive infarcts, has been reported in patients with sicklecell anemia (Costa et al. 2013). The phenomenon of “sickle cell toothache” may occur if sicklecells become trapped in the pulpal vascular supply and impede blood flow to the pulpal tissue.This leads to hypoxia, symptoms of pulpitis, cell death, and ultimately loss of tooth vitality.Diagnostic criteria:A. The pain fulfills the criteria for 1.1.1 Pulpal painB. The patient has been diagnosed with a systemic disorder or disease known to be ableto cause pulpal pain, e.g. sickle cell anemia.C. Not better accounted for by another ICOP or ICHD-3 diagnosis
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411.1.2 Periodontal painDescription:Dental pain caused by a disorder involving the periodontium, meaning the periodontal ligamentand the adjacent alveolar (periradicular) bone tissue.Diagnostic criteria:A. Any pain fulfilling criteria B through EB. Localized to the site of the periodontal lesion, but may also refer or radiate to otheripsilateral orofacial locationsC. Clinical, laboratory, imaging and/or anamnestic evidence of a lesion, disease ortrauma1known to be able to cause periodontal painD. Familiar pain is exacerbated by physical stimulus2applied to the affected tooth(horizontally or vertically) or to the tissue overlying the rootE. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1as specified per sub-diagnosis2mechanical, thermal, or chemical; as specified per sub-diagnosisComments:Periodontal pain can be associated with all types of periodontal injury or disease. The pain ispredominantly inflammatory and secondary to external or internal events.
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421.1.2.1 Periodontal pain attributed to periodontitis (periodontal inflammation)Description:Periodontal inflammation (marginal as well as apical) is most frequently asymptomatic but canalso present with pain and sometimes observable swelling. In such cases, pain is evoked bymechanical stimulation such as biting or chewing and is typically easy for the patient to localize.There may also be spontaneous pain, which is typically ongoing for hours. The intensity may bemild to severe. The pain can be reproduced by percussion or by applying pressure to the tooth.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2 Periodontal painB. The tooth has been diagnosed with periodontal inflammation1C. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1due to trauma or infection; as specified by subcategoriesComments:Periodontal pain attributed to periodontal inflammation is further subcategorized according tocause of inflammation.In association with this type of pain, gingival pain may also occur.
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431.1.2.1.1Periodontal pain attributed to traumatically induced periodontal inflammationDescription:Traumatic injury of periodontal tissues causes acute inflammation of the periodontium and canbe painful to a varying degree. Causes for this type of pain include accidental dental injuries butalso micro-trauma caused by for example changes in occlusion or articulation following dentaltreatment, and iatrogenic periodontal damage such as periodontal surgery. The condition isfurther subcategorized according to type of trauma or injury. The pain may be mild to severe andis exacerbated by mechanical provocation of the tooth. Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1 Periodontal pain attributed to periodontitisB. The history reveals a recent1trauma or injury2involving the periodontal tissuesC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1minutes to days2 accidental, self-inflicted or iatrogenicComments:Accidental dental trauma/injury affects approximately 10–30% of the population, and almostexclusively occurs in incisors (maxilla 75–80% and mandible 20–25%). The incidence has beenreported to 2–3 injured teeth/100 schoolchildren/year, and the prevalence of traumatizedpermanent teeth in children and adolescents is reported to 6–34% (Bastone et al. 2000).
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44Epidemiologic data suggest that while mild trauma is most prevalent, approximately 3% ofpermanent incisors in a population aged 6–50 years have been afflicted with a traumatic injurysevere enough to be painful (Kaste et al. 1996).1.1.2.1.1.1 Periodontal pain attributed to hyperocclusion or -articulationDescription:Periodontal pain attributed to occlusal factors involves sensitization of periodontal nociceptorsand an inflammatory response due to the excessive loading of the tooth. The history involvesrecent dental restoration, tooth extraction, or other change in occlusion or articulation. Thepatient may report that the tooth feels elevated. Clinically, a primary contact in occlusion orarticulation is observed. The pain can be reproduced by percussion or by applying pressure to thetooth. The tooth may have increased mobility, and if so, radiographic examination may showwidening of the periodontal space.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.1 Periodontal pain attributed to traumaticallyinduced periodontal inflammationB. The pain has developed in close temporal relation1to a change in occlusal conditionsinvolving the painful toothC. Mechanical provocation2reproduces the painD. Hyperocclusion or hyperarticulation on the tooth is identified based on the following:a. primary contactb. hypermobilityE. Not better accounted for by another ICOP or ICHD-3 diagnosis
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45Notes:1hours to days2pressure, percussion1.1.2.1.1.2 Postoperative periodontal painDescription:Postoperative periodontal pain is iatrogenic and caused by surgically induced tissue damage andsubsequent inflammation. The pain is typically mild to moderate and may co-occur withclinically observable swelling and occasionally pus formation.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.1 Periodontal pain attributed to traumaticallyinduced periodontal inflammationB. The pain has developed in close temporal relation1to a surgical intervention involvingthe periodontiumC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1hours to days
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46Comments:If physiologic (primary) healing occurs normally, the pain duration is typically short (1–2weeks). Prolonged pain due to secondary healing and/or postoperative infection is occasionallyobserved but usually does not exceed 3 months.1.1.2.1.1.3 Periodontal pain due to accidental dental traumaDescription:Dental trauma frequently causes periodontal pain. The clinical and radiographic presentation,and the characteristics and severity of pain, depends on the nature and severity of the traumaticinjury. Below follows a brief description of the trauma diagnoses in used in dental practice (refThe Dental Trauma Guide).Periodontal pain due to concussion is caused by accidental injury to the periodontium andsubsequent inflammation. The tooth displays normal mobility and is not displaced from itsalveolar socket. Unless previously root-canal treated, the tooth typically shows evidence of avital pulp. Imaging shows normal periradicular conditions.Periodontal pain due to subluxation is caused by accidental injury to the periodontium andsubsequent inflammation. The tooth displays increased mobility but is not displaced from itsalveolar socket. Clinical findings include bleeding from the gingival sulcus. The tooth respondsto pulp vitality testing in about 50% of cases. Radiographic examination may show a widening ofthe periodontal space.Periodontal pain due to lateral luxation is caused by accidental injury to the periodontium andsubsequent inflammation. The tooth is laterally displaced from its alveolar socket in combinationwith comminution or fracture of the buccal or lingual/palatal alveolar bone. The periodontalligament is partially or totally separated and bleeding is seen from the sulcus. The tooth usuallydisplays decreased mobility and may interfere with the occlusion and/or articulation. The toothusually does not respond to pulp vitality testing. Radiographic examination shows variation inperiodontal space width depending on the projection.
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47Periodontal pain due to intrusion is caused by accidental injury to the periodontium andsubsequent inflammation. The tooth is axially displaced into the alveolar bone, and thus appearsshorter than the adjacent teeth. The injury is accompanied by comminution or fracture of thealveolus. Other clinical findings may include decreased mobility and high percussion sound. Thetooth usually does not respond to pulp vitality testing. Radiographic examination shows absenceof (or decreased width of) the periodontal ligament space in all or part of the tooth.Periodontal pain due to extrusion is caused by accidental injury to the periodontium andsubsequent inflammation. The tooth is axially displaced and partially out of its socket, and thusappears elongated. The periodontal ligament is partially or totally separated and there is bleedingfrom the sulcus, but the alveolar socket bone is intact. The tooth has increased mobility and mayinterfere with occlusion/articulation. The tooth usually does not respond to pulp vitality testing.Radiographic examination shows increased width of the periodontal ligament space.Periodontal pain due to avulsion is caused by accidental injury to the periodontium andsubsequent inflammation. The tooth is completely displaced out of its socket, which is foundempty or filled with a coagulum. The surrounding alveolar bone may be fractured.Periodontal pain due to root fracture is caused by dislocation or fragments and/or subsequentinfection causing periodontal inflammation. The history may or may not reveal an accidentaltraumatic event. The coronal fragment may be displaced and the tooth may appear longer thanthe adjacent teeth, may display increased mobility, and may interfere with occlusion/articulation.A local deep periodontal pocket may be present. Imaging shows a vertical or horizontal fractureconfined to the root. If not previously root-filled, the tooth may or may not respond to pulpvitality testing.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.1 Periodontal pain attributed to traumaticallyinduced periodontal inflammation
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48B. The history reveals a recent1accidental2trauma affecting the toothC. The tooth has been diagnosed with a traumatic injury (a-g) based on clinical and/orradiographic observationsa. concussionb. subluxationc. lateral luxationd. intrusione. extrusionf. avulsiong. root fracture3D. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1minutes to days2or caused by violence (in the case of root fracture, excessive loading of the tooth is also apossible cause)3horizontal or verticalComments:Accidental dental trauma/injury affects approximately 10–30% of the population, and almostexclusively occurs in incisors (maxilla 75–80% and mandible 20–25%). The incidence has been
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49reported to 2–3 injured teeth/100 schoolchildren/year, and the prevalence of traumatizedpermanent teeth in children and adolescents is reported to 6–34% (Bastone et al. 2000).Epidemiologic data suggest that while mild trauma is most prevalent, approximately 3% ofpermanent incisors in a population aged 6–50 years have been afflicted with a traumatic injurysevere enough to be painful (Kaste et al. 1996).Concussion, subluxation and extrusion trauma may also include pulpal injury and the periodontalpain may co-occur with pulpal pain, see section 1.1.1 Pulpal pain.Lateral luxation and intrusion trauma also induce pulpal and alveolar bone injuries and theperiodontal pain may co-occur with pulpal pain and jaw bone pain, see sections 1.1.1 Pulpal painand 1.2.3 Jaw bone pain.Avulsion trauma may also include alveolar bone injury and the periodontal pain may co-occurwith 1.2.3 Jaw bone painA root fracture is a hard tissue injury that may or may not reach the pulp space. If the pulp isinvolved, it is directly exposed to bacterial assault from the oral cavity and quickly becomesinflamed. If the pulp is vital, the pain may coincide with 1.1.3.3.2 Pulpal pain attributed to dentalhard tissue fracture with direct pulp exposure. In addition to accidental trauma, other commonreasons for root fracture include excessive loading of a root-canal treated tooth, typically with apost-and-core.1.1.2.1.1.4 Periodontal pain attributed to other trauma or injuryDescription:Minor trauma or injury to the periodontium can also cause pain. By anamnestic, clinical orradiographic or other imaging findings, a trauma known to be able to cause periodontalinflammation can be identified, such as insufficient cooling during dental restorative procedures,interdental foreign body impaction (including food impaction), defective dental restoration, orapically extruded endodontic material. Clinical findings may include clinical signs of acuteinflammation (swelling, pus, redness), increased tooth mobility, and local deep periodontal
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50pocket. Unless root-canal treated, the tooth typically shows evidence of a vital pulp. Imagingmay display local marginal bone loss, which may or may not include the periapical region.Diagnostic criteria:A. The pain fulfills criteria for 1.1.2.1.1 Periodontal pain attributed to traumaticallyinduced periodontal inflammationB. The painful tooth does not fulfill criteria for any of the dental trauma diagnosesincluded in 1.1.2.1.1.3C. Not better accounted for by another ICOP or ICHD-3 diagnosis1.1.2.1.2Periodontal pain attributed to apical periodontitis due to endodontic diseaseDescription:Periodontal pain due to endodontic disease is pain associated with pulpal, periapical,juxtaradicular or periradicular inflammation. Endodontic disease, i.e. pulpal and periapicaldisease, is frequently associated with pain that may be mild to severe. A broken barrier againstthe oral cavity, most often caused by caries, and subsequent bacterial invasion of the pulp androot canal system is the main cause for inflammation of the pulp and periapical tissues.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1 Periodontal pain attributed to periodontitisB. The tooth has been diagnosed with endodontic diseaseC. Not better accounted for by another ICOP or ICHD-3 diagnosis
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51Comments:This type of pain may also affect the gingivae.Endodontic disease, including periapical, juxtaradicular or periradicular inflammation, may alsobe present without any clinical symptoms.1.1.2.1.2.1 Periodontal pain attributed to pulpal inflammationDescription:Periodontal pain secondary to pulpal inflammation is associated with symptomatic pulpitis. Theperiodontal inflammation is centered to the periapical region. The pulp is vital and thus the toothtypically responds to pulp vitality testing. The tooth is often tender to percussion. Clinicalfindings may include deep caries, deep/defective restoration, or external cervical root resorption.Imaging may or may not show evidence of diffuse local periapical bone resorption or sclerosis.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.2 Periodontal pain attributed to apical periodontitisdue to endodontic diseaseB. The tooth has been diagnosed with pulpitis1based on the following:a. vital pulp evidenced by response to pulp vitality testingb. evidence of dental disorder known to be able to cause pulpal inflammationC. Not better accounted for by another ICOP or ICHD-3 diagnosis
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52Notes:1reversible pulpitis or symptomatic irreversible pulpitisComments:According to the literature, the association is weak between the actual state of the pulp and theperiodontium (histology) and diagnostic findings including present and historical symptoms suchas characteristics of tooth pain, clinical observations, and test results (Levin et al. 2009, Gutmannet al. 2009, Mejàre et al. 2012). Current diagnostics are largely based on expert opinion and fewstudies with quality deficits.Teeth with periodontal pain secondary to pulpal inflammation frequently also fulfil the criteriafor 1.1.1.3 Pulpal pain attributed to pulpitis.1.1.2.1.2.2 Periodontal pain attributed to endodontic infectionDescription:Periodontal pain due to endodontic infection is associated with non-vital pulp (or previously rootfilled tooth) and infection of the pulp space. The pulp is totally or partially necrotic (unless thetooth is previously root canal treated), thus the tooth typically does not respond to pulp vitalitytesting. Although localized, the pain frequently refers to other orofacial sites on the same side,especially if the pain is severe. The pain can be reproduced by percussion or by applyingpressure on the tooth and/or the adjacent periapical vestibular region. Imaging typically showsevidence of local periapical bone resorption.Diagnostic criteria:
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53A. The pain fulfils criteria for 1.1.2.1.2 Periodontal pain attributed to apical periodontitisdue to endodontic diseaseB. The tooth has been diagnosed with partial or total pulp necrosis and endodonticinfection based on at least two of the following findings:a. non-vital pulp evidenced by direct inspection or non-response to pulp vitality testing,orb. previously debrided1root canal, andc. clinical2and/or radiographic3evidence of apical inflammation4C. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1previously treated or previously initiated therapy2such as tenderness to percussion/pressure and/or apical palpation3apical or juxtaradicular radiolucency or sclerosis4symptomatic apical periodontitis or acute apical abscessComments:The inflammatory response in the periapical tissues is caused by root canal infection with amixed flora. An increased incidence of pain and swelling in apical periodontitis is associatedwith presence of specific anaerobes: Porphyromonas, Peptostreptococcus, and Prevotella species(Yoshida et al. 1987, Gomes et al. 1996). Upon local infection spread, a periapical abscess mayform.
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541.1.2.1.2.2.1 Periodontal pain attributed to intraradicular endodontic infectionDescription:In periodontal pain due to intra-radicular infection, the infectious agent causing the periodontalinflammation is contained within the root-canal system. Successful infection treatment usuallyresults in pain resolution.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.2.2 Periodontal pain attributed to endodonticinfectionB. The tooth has a root canal infection1C. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1bacterial, viral, fungal, or otherComments:In most teeth with infected necrotic pulp, the infection is confined to the root canal system.1.1.2.1.2.2.2 Periodontal pain attributed to extraradicular endodontic infectionDescription:
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55In periodontal pain due to extra-radicular infection, the infectious agent causing the periodontalinflammation resides on the external root surface, apically or in association with accessory canalorifices, or in the periapical tissues. The pain typically does not resolve after successfuldisinfection of the root canal system. Imaging occasionally reveals signs of external apical rootresorption (Laux et al. 2000).Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.2.2 Periodontal pain attributed to endodonticinfectionB. The tooth has an extraradicular infection1C. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1bacterial, viral, fungal, or otherComments:Extraradicular endodontic infection may occur with or without intraradicular infection (Ricucciet al. 2015). In such cases, the microbes colonize the external apical foramen and root surface,forming a biofilm (Ricucci et al. 2010). Anaerobic species such as Actinomyces andPropionibacterium also have the ability to form colonies in the periapical tissues at some distancefrom the root (Tronstad et al. 1987, Sjögren et al 1988), and this has been associated withremaining symptoms, including pain, after root canal treatment.1.1.2.1.3Periodontal pain attributed to periodontal diseaseDescription:
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56Periodontal pain due to plaque-induced periodontal disease can be acute or chronic in nature anddepending on type the pain intensity ranges from mild to severe.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1 Periodontal pain attributed to periodontitisB. The tooth has been diagnosed with periodontal disease1C. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1as specified per sub-diagnosisComments:The disease can be localized or generalized in the dentition. A number of intrinsic (diabetes,pregnancy, puberty, menopause) and extrinsic (smoking, medications, nutritional deficienciese.g. avitaminosis-C) factors are considered as disease modifiers (Kinane and Chestnutt, 2000;Armitage 1999). In addition, medications known to be associated with gingival hyperplasia (e.g.phenytoin, ciclosporin, calcium channel blockers, bisphosphonates, and oral contraceptives) maypromote periodontal breakdown due to difficulties to maintain proper oral hygiene. (Heasman &Hughes, 2014)1.1.2.1.3.1 Periodontal pain attributed to chronic periodontitisDescription:
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57Periodontal pain due to chronic periodontitis may present in association with increased toothmobility and oral hygiene routines and is typically mild. The pain typically appears only onprovocation and does not linger. Most cases of chronic periodontitis are not painful, but maybecome painful on inflammatory exacerbation (see 1.1.2.1.3.5 Periodontal pain associated withperiodontal abscess).Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.3 Periodontal pain attributed to periodontal diseaseB. The tooth has been diagnosed with chronic periodontitisC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:The disease form is characterized by slow progression of attachment loss, sometimes withperiods of more rapid progression. The absence or low level of pain in chronic periodontitis hasbeen attributed to the mainly chronic inflammatory cell infiltrates surrounding the infectioussource, and functional drainage.1.1.2.1.3.2 Periodontal pain attributed to aggressive periodontitisDescription:Periodontal pain due to aggressive periodontitis may present in association with increased toothmobility and oral hygiene routines and is typically mild to moderate. The pain typically appearsonly on provocation and does not linger.
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58Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.3 Periodontal pain attributed to periodontal diseaseB. The tooth has been diagnosed with aggressive periodontitisC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:The disease form is characterized by rapid progression of attachment loss and sometimes earlyonset.1.1.2.1.3.3 Periodontal pain attributed to periodontitis as a manifestation of systemic disorderDescription:Periodontal pain associated with periodontitis due to a systemic disorder may present inassociation with increased tooth mobility and oral hygiene routines. The pain is typically mild tomoderate, appears only on provocation and does not linger.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.3 Periodontal pain attributed to periodontal diseaseB. The tooth has been diagnosed with a systemic disorder1known to be able to causeperiodontitisC. Not better accounted for by another ICOP or ICHD-3 diagnosis
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59Notes:1Hematological, genetic or other; specified per sub-diagnosisComments:In addition to the more common plaque-induced periodontal disease, a number of systemicdisorders manifests as periodontitis. The disorders listed here are considered as causative factorsfor periodontitis. They may also alter the course of plaque-induced periodontitis from chronic toaggressive. Reports in on to what degree periodontitis as a manifestation of a systemic disorder isassociated with pain are essentially lacking the literature.1.1.2.1.3.3.1 Periodontal pain attributed to a hematological disorderDescription:Periodontal pain associated with periodontitis due to a hematological disorder may present inassociation with increased tooth mobility and oral hygiene routines and is typically mild tomoderate. The pain typically appears only on provocation and does not linger.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.3.3 Periodontal pain attributed to periodontitis as amanifestation of systemic disorderB. The patient has been diagnosed with a hematological disorder known to be able tocause periodontitis (Armitage, 1999)a. acquired neutropeniab. leukemia
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60c. other hematological disorderC. Not better accounted for by another ICOP or ICHD-3 diagnosis1.1.2.1.3.3.2 Periodontal pain attributed to a genetic disorderDescription:Periodontal pain associated with periodontitis due to a genetic disorder may present inassociation with increased tooth mobility and oral hygiene routines and is typically mild tomoderate. The pain typically appears only on provocation and does not linger.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.3.3 Periodontal pain attributed to periodontitis as amanifestation of systemic disorderB. The patient has been diagnosed with a genetic disorder known to be able to causeperiodontitis (Armitage, 1999):a. familial and cyclic neutropeniab. Down syndromec. leukocyte adhesion deficiency syndromesd. Papillon-Lefèvre syndromee. Chediak-Higashi syndromef. histiocytosis syndromesg. glycogen storage diseaseh. Infantile genetic agranulocytosis
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61i. Cohen syndromej. Ehler-Danlos syndrome (types IV and VIII)k. hypophosphatasial. other hematological disorderC. Not better accounted for by another ICOP or ICHD-3 diagnosis1.1.2.1.3.3.3 Periodontal pain attributed to an unspecified systemic disorderDescription:Periodontal pain associated with periodontitis due to an unspecified systemic disorder maypresent in association with increased tooth mobility and oral hygiene routines and is typicallymild to moderate. The pain typically appears only on provocation and does not linger.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.3.3 Periodontal pain attributed to periodontitis as amanifestation of systemicB. The patient has been diagnosed with a systemic disorder (other than hematological orgenetic) known to be able to cause periodontitisC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Systemic disorders associated with periodontitis are not currently well described in the literature.
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621.1.2.1.3.4 Periodontal pain associated with necrotizing ulcerative periodontitis (NUP)Description:Periodontal pain due to necrotizing ulcerative periodontitis is typically severe. Pain is provokedby physical stimuli applied to the affected tooth or surrounding tissue. Pain also occursspontaneously.Clinically, necrotic soft tissue lesions and loss of attachment can be observed.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.3 Periodontal pain attributed to periodontal diseaseB. The patient has been diagnosed with necrotizing ulcerative periodontitisC. The pain has developed in close temporal relation1to the onset of the ulcerations.D. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1hours to daysComments:Necrotizing ulcerative periodontitis is a rare oral infection, a more severe form of Necrotizing(ulcerative) gingivitis which besides soft tissue destruction also includes loss of clinicalattachment and alveolar bone. The two conditions are often conflated to Necrotizing periodontaldiseases (NPD) and are associated with diminished systemic resistance and immune dysfunction.
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63The predisposing factors include severe stress, sleep deprivation, alcohol, smoking, and HIVinfection (Horning & Cohen, 1995).1.1.2.1.3.5 Periodontal pain associated with periodontal abscessDescription:A periodontal abscess is an exacerbation of chronic periodontitis or aggressive periodontitis, andpain due to this is acute condition is usually severe. In addition to swelling, other clinicalfindings include plaque and/or calculus deposit on the root surface, usually with increased toothmobility and a local deep periodontal pocket. Unless previously root-canal treated, the toothtypically shows evidence of a vital pulp. Although localized, the pain frequently refers to otherorofacial sites on the same side, especially if the pain is severe. The pain can be reproduced bypercussion or by applying pressure on the tooth and/or the adjacent periapical vestibular region.Imaging shows evidence of marginal and periradicular bone resorption, which may or may notinclude the periapical region.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.3 Periodontal pain attributed to periodontal diseaseB. The patient has been diagnosed with a periodontal abscess based ona. clinical signs of acute inflammation1and loss of attachment2b. radiographic evidence of marginal and periradicular bone resorptionC. The pain has developed in close temporal relation3to the appearance of the abscess.D. Not better accounted for by another ICOP or ICHD-3 diagnosis
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64Notes:1Swelling, pus, redness, tenderness2Increased mobility, local deep periodontal pocket3Usually hours to days before appearance of the abscess1.1.2.1.4Periodontal pain attributed to apical and marginal periodontitis due to combinedendodontic infection and periodontal diseaseDescription:Periodontal pain due to combined endodontic and periodontal lesion may be symptom free. Ifpresent, the pain is typically moderate to severe, and other clinical findings may include clinicalsigns of acute inflammation (swelling, pus, redness), plaque and/or calculus deposit on the rootsurface, increased tooth mobility, and deep periodontal pocket(s). If not previously root-canaltreated, the tooth shows no or inconclusive evidence of pulp vitality. Although localized, the painfrequently refers to other orofacial sites on the same side, especially if the pain is severe. Thepain can be reproduced by percussion or by applying pressure on the tooth and/or the adjacentperiapical vestibular region. Imaging shows evidence of marginal and periradicular boneresorption that includes the periapical region.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1.3 Periodontal pain attributed to periodontal diseaseB. The tooth has been diagnosed with partial or total pulp necrosis, or is previously rootcanal treatedC. The tooth has been diagnosed with periodontal disease based on clinical andradiographic observations
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65D. Not better accounted for by another ICOP or ICHD-3 diagnosis1.1.2.1.5Periodontal pain attributed to peri-implantitis due to peri-implant infectionDescription:Periodontal pain due to inflammation surrounding a dental implant is most frequently painless,but if pain occurs it is typically moderate to severe. Other clinical findings may include clinicalsigns of acute inflammation (swelling, pus, redness), plaque and/or calculus deposit on theimplant surface, implant mobility, and local deep pocket. Imaging shows poor bony integrationof the implant and evidence of horizontal marginal bone loss or localized peri-implant boneresorption.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2.1 Periodontal pain attributed to periodontitis with theexception that it involves an implant and not a natural toothB. Clinical1and/or radiographic2evidence of a peri-implant infectionC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1signs of acute inflammation (swelling, pus, redness) and/or attachment loss (increased mobility,deep pocket2radiolucency partially or totally surrounding the implantComments:
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66Patients diagnosed with periodontal pain attributed to peri-implantitis due to peri-implantinfection are also likely to be affected by gingival pain.1.1.2.2Periodontal pain attributed to a local non-inflammatory causeDescription:Periodontal pain due to a local non-inflammatory cause is usually mild to moderate. Periodontalcysts, radicular cysts, and tumors are frequently asymptomatic, but following expansionsymptoms such as pain, localized swelling and displacement of one or more teeth may occur. Insuch cases, pain is occasionally evoked by external mechanical stimulation such as biting orchewing and is typically easy for the patient to localize. There may also be spontaneous pain,which is seldom severe.Diagnostic criteria:A. The pain fulfils criteria for 1.1.2 Periodontal painB. The patient has been diagnosed with a non-infectious disorder1known to be able to causeperiodontal pain based on clinical, imaging, and/or histological examinationC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1periodontal cyst, tumor1.1.3 Gingival pain
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67Description:Pain caused by a disorder involving the gingival tissues.Diagnostic criteria:A. Any pain fulfilling criteria B through EB. Pain is localized to the site of the gingivae, but may refer to other ipsilateral orofaciallocationsC. Clinical, laboratory, imaging and/or anamnestic evidence of a lesion or disease of the gingivaltissues, known to be able to cause painD. Evidence of causation demonstrated by the following:1. Pain has developed in temporal relation to the onset or appearance of the lesion2. Familiar pain is exacerbated by manipulation of the affected gingival tissueE. Not better accounted for by another ICOP or ICHD-3 diagnosis.1.1.3.1Gingival pain attributed to gingivitis (gingival inflammation)Description:Pain associated with gingivitis (i.e. inflammation of the gingivae).Inflammation may be caused by infection due to specific or non-specific microbial organisms,trauma (may be physical, thermal, radiation or chemical), autoimmunity, or allergic reaction.Diagnostic criteria:A. The pain fulfills criteria for 1.1.3 Gingival pain
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68B. The patient has been diagnosed with gingival inflammation1based on the clinical observationof inflammation signs in the gingivae (i.e. tumor, dolor, rubor, and calor)C. Not better accounted for by another ICOP or ICHD-3 diagnosis.Notes:1due to trauma, infection or systemic disorder; as specified by subcategories1.1.3.1.1Gingival pain associated with traumaDescription:Traumatic injury of gingival tissues causes acute inflammation and can be painful to a varyingdegree. Traumatic ulceration of the gingiva may be acute or chronic in nature with the latterdiagnostically more challenging due to underlying fibrosis and clinical appearance of neoplasticinduration. A thorough clinical history will often alert the clinician to a traumatic aetiology orburns caused by warm food or chemicals. The pain may be mild to severe and is exacerbated bymechanical provocation of the gingivae. Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfils criteria for 1.1.3.1 Gingival pain attributed to gingivitisB. The history reveals a recent1trauma2or injury3involving the gingival tissuesC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1minutes to days
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692mechanical, thermal or chemical3accidental, self-inflicted or iatrogenicComments:Causes for this type of pain include accidental dental injuries but also micro-trauma caused byfor example during eating or drinking overly hot foods or drinks, following dental treatment,trauma due to tooth brushing or flossing or other interdental instruments. Examination mayreveal the causative factor, such as a sharp broken tooth or restoration or an ill-fitting denture.Ulceration due to local anaesthetic injection most often occurs in the hard palate, the combinedresult of pressure and ischemic necrosis. Poorly fitting dentures may cause painful ulcerations.Over-erupted dentition or parafunctional habits may also cause local occlusal gingival traumawith resultant inflammation and pain. Iatrogenic gingival damage occurs during most dentalsurgery for example dental extraction, gingival or periodontal surgery, or dental restorativetherapy. Chemical burns may be related to misuse of anti-inflammatory tablets or occur due todental treatment. Self-harm may be a rare cause of gingival trauma.Dental trauma may also cause gingival inflammatory pain, see also 1.1.2.1.1 Periodontal painattributed to traumatically induced periodontal inflammation.1.1.3.1.2Gingival pain attributed to infectionDescription:Infection of the gingival tissues causes acute inflammation and can be painful to a varyingdegree. The pain may be mild to severe and is exacerbated by mechanical provocation of thegingivae. Spontaneous pain can occur. The condition is further subcategorized according tocategory of causative microorganism.Diagnostic criteria:A. The pain fulfils criteria for 1.1.3.1 Gingival pain attributed to gingivitis
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70B. The patient has been diagnosed with an infection1of the gingival tissues based on anamnesticinformation, clinical observations, and/or microbiological analysisC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1bacterial, viral, or fungalComment:Acquired or congenital immunosuppression may lead to increased risk of gingival infection.Patients on immunosuppressive therapy may develop a variety of opportunistic infectionsincluding pseudomembraneous candidosis, other fungal and viral infections. TNF-α therapyincreases the risk of tuberculosis (TB). Patients on infliximab and adalimumab with combinedimmunomodulatory therapy may be at increased risk of TB, histoplasmosis, coccidiomyinfections. Antirheumatic drugs including methotrexate, abatacept and alefacept have increasedthe risk of herpes simplex and herpes zoster infections and TB.1.1.3.1.2.1 Gingival pain attributed to bacterial infectionDiagnostic criteria:A. The pain fulfills criteria for 1.1.3.1.2 Gingival pain attributed to infectionB. The patient has been diagnosed with a bacterial infection of the gingival tissuesC. Not better accounted for by another ICOP or ICHD-3 diagnosis
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71Comments:Bacterial infections are the most common oral infections and gingival pain may be associatedwith underlying dental pathology, such as periodontal infection or endodontic infections thatmay present as swelling, inflammation and pain of the overlying gingivae.Acute necrotizing ulcerative gingivitis (ANUG) (or necrotising ulcerative gingivitis [NUG],necrotizing ulcerative periodontitis [NUP], or necrotizing ulcerative stomatitis [NUS]) is anopportunistic gingival infection caused by an array of bacteria in malnourished children, youngadults and immune deficient patients. NUG is often the initial presentation, proceeding intoNUP, NUS and ultimately noma. Necrosis and ulceration of the interdental gingival papilla,excruciating pain, severe halitosis, regional lymphadenopathy, malaise and fever differentiatesthis form of ulceration from others (Feller et al 2014).Pericoronitis (inflammation around a tooth crown) causing pain is most often associated withpartially erupted third molars. Other dentition, both permanent and deciduous, may have mildpericoronitis during eruption. If the tooth is impacted and unable to fully erupt, continued orrecurrent infection may ensue. Pain results from the individual's immune inflammatory responseto anaerobic bacteria colonized in biofilm that cannot be shed from third molars partially coveredby soft tissue (Kay 1966).Gingival pain can occur in association with conditions that mainly affects other oral tissues, andis not categorized in this section. For these types of pain, refer to the corresponding sections:- Gingival pain associated with alveolar osteitis (dry socket), see 1.2.3.2 Therapy related jawbone pain (c)- Gingival pain associated with periodontitis, see 1.1.2.1 Periodontal pain attributed toperiodontitis (periodontal inflammation)- Gingival pain associated with apical periodontitis, see 1.1.2.1.2 Periodontal pain attributed toapical periodontitis due to endodontic disease
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72- Palatal gingival pain associated with acute necrotizing sialadenitis, see 1.2.2.2.2 Salivary glandpain attributed to bacterial infection1.1.3.1.2.2 Gingival pain attributed to viral infectionDiagnostic criteria:A. The pain fulfills criteria for 1.1.3.1.2 Gingival pain attributed to infectionB. The patient has been diagnosed with a viral infection of the gingival tissuesC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Viral infections of the gingival tissues include HSV, VZV, HPV, CMV, Coxsackievirus and HIVinfection.The infected gingival tissues may often be ulcerated and painful to touch. Severe local pain isoften associated with eating or drinking acidic or hot or cold foods or drinks, which may causethe individual to be unable to eat or drink and become dehydrated.Herpes simplex (HSV) is the most common virus to affect the oral mucosa. Herpeticgingivostomatitis, the primary HSV-1 infection, mostly affects children and presents either asasymptomatic infection or with mucosal vesicles followed by painful ulceration affecting bothkeratinised and non-keratinised mucosa and gingivae. Adults with primary infection suffersymptomatic herpetic pharyngotonsillitis initiated as vesicles that rapidly break down intopainful shallow ulcerations (Fourie & Boy, 2016)1.1.3.1.2.3 Gingival pain attributed to fungal infectionDiagnostic criteria:
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73A. The pain fulfills criteria for 1.1.3.1.2 Gingival pain attributed to infectionB. The patient has been diagnosed with a fungal infection of the gingival tissuesC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Gingival pain associated with fungal infection is probably rare, and reports in the literature isessentially lacking. The painful manifestations of oral fungal infection usually affect oralmucosa.1.1.3.1.3Gingival pain attributed to autoimmunityDescription:Inflammation of the gingival tissues causes acute inflammation and can be painful to a varyingdegree. The condition is further subcategorized according to category of autoimmune disease.The pain may be mild to severe and is exacerbated by mechanical provocation of the gingivae.Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfils criteria for 1.1.3.1 Gingival pain attributed to gingivitisB. The patient has been diagnosed with an autoimmune disease or disorder1known to beable to cause gingival painC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1such as mucous membrane pemphigoid, Sjögren’s syndrome, pemphigus, or otherComments:
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74Several dermatological immune-mediated vesiculo-ulcerative lesions conditions may presentwith oral mucosal involvement, either concurrent with the skin pathology, as the initialpresentation or sometimes as the only clinical presentation (Bascones-Martinez et al. 2015).Mucous membrane pemphigoid (MMP) is a common systemic autoimmune blistering diseasewith preferential involvement of mucosal membranes. The antibodies are directed at the proteinsof keratinocyte to connective tissue matrix adhesion or hemi-desmosomes (BP180 and laminin-332) causing the epithelium to split away from its underlying connective tissue bed. Thesubepithelial nature of the split results in thick roofed vesicles which may still be intact onexamination. Rupture of the vesicles leave ulcerative lesions devoid of any epithelium, coveredby yellow-white slough. Desquamative gingivitis (erythematous and friable gingiva withepithelial destruction) is a frequent finding (Hasan 2014).Sjögren's syndrome is a systemic autoimmune disease that frequently presents concomitantlywith other systemic connective tissue or organ-specific autoimmune diseases. The association iswell described for systemic lupus erythematosus and rheumatoid arthritis. The gingival tissuescan become abraded and even cut with dry foods, and sore. The presence of Sjögren's syndromeinfluences the expression of the other autoimmune disease to some degree, for instance byincreasing fatigue and lymphoma risk (Theander & Jacobsson 2008)Pemphigus, a group of immune mediated subepithelial bullous dermatoses, is mediated by auto-antibodies directed at the proteins of keratinocyte adhesion (desmosomes) causing acantholysis.Pemphigus vulgaris most commonly affects the oral cavity, with autoantibodies mainly directedagainst desmoglein 1 and 3 (mucocutaneous forms) or only 3 (mucosal forms). Gingival pain dueto pemphigus is infrequent, since the disease mostly affects oral mucosa (Harman et al. 2003).1.1.3.1.4Gingival pain attributed to allergic reactionDescription:Inflammation of the gingival tissues causes acute inflammation and can be painful to a varyingdegree. The condition is further subcategorized according to category of hypersensitive or
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75allergic condition. The pain may be mild to severe and is exacerbated by mechanical provocationof the gingivae. Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfils criteria for 1.1.3.1 Gingival pain attributed to gingivitisB. The patient has been diagnosed with hypersensitivity or an allergic reaction in thegingival tissues associated witha. dental material (such as temporary/permanent restorative or impression material)b. oral hygiene productc. topical drugd. systemic druge. food or additivef. other factorC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Allergic reactions and oral mucosal hypersensitivity reactions are less common than cutaneousones ascribed to the possible allergen dilution and the continuous rinsing effects of normal salivaflow (Venables et al. 2016). Lesions may present with non-specific tissue oedema, erythema,cracking, ulceration, hyperkeratotic white plaques or mucosal desquamation. Lesions may startlong after the introduction of a drug and may remain for months after cessation thereofcomplicating diagnosis and management.A hypersensitivity reaction to either a systemic drug or direct contact with an offending agentmay result in clinical and histological features reminiscent of lichen planus. The term ‘orallichenoid drug reaction’ (OLDR) or ‘oral lichenoid contact lesion’ (OLCL) is used respectively,and both may present with significant ulceration, usually with erythema and white striations at
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76the periphery of the ulceration. A temporal or spatial association with an offending agent canusually be identified. Amalgam is often implicated in OLCL, confirmed by patch testing formercury or amalgam sensitivity. OLDR is encountered with some frequency in patients treatedwith angiotensin-converting enzyme (ACE) inhibitors, nonsteroidal anti-inflammatory drugs(NSAIDs) and oral hypoglycaemic drugs (Al-Hashimi et al. 2007).Potential drug reactions causing oral mucogingival reactions have been well summarised (Yuan& Woo 2015). Fixed drug eruption (FDE) is a form of hypersensitivity remarkable for its fixedanatomical nature and has been described with NSAID’s and other oxicam drugs (Andrade et al.2011), gabapentin (Gupta et al. 2009), fluconazole (Benedix et al. 2008), and systemicantibacterial and antifungal drugs (Savin 2001). FDE should be suspected in cases with atemporal association of drug ingestion, may be confirmed through patch testing or oralprovocation tests, and managed through drug avoidance or substitution, while the acute lesionscan be treated with topical or systemic steroids.Allergic contact stomatitis. Although rare, this form of mucositis has been reported in associationwith dental impression materials (Batchelor & Todd 2010), dental restorative materials(Venables et al. 2016), topical benzocaine application, and more commonly cinnamon intoothpastes, mouth rinses, and chewing gum (Kind et al. 2010). Lesions may appear as mixed redand white patches with ulceration, swelling of the cheeks and desquamation appearing on thelips, cheeks, tongue and gingiva as localised or widely distributed lesions (Calapai et al. 2014).Drug induced fibrosis epithelial hyperplasia or fibrovascular hyperplasia may occasionally beassociated with painful presentation, likely due to underlying periodontal infection due todifficulty with oral hygiene in these conditions.1.1.3.1.5Gingival pain attributed to gingival inflammation due to other causeDescription:Inflammation of the gingival tissues may occur associated with systemic disease, disorder, orcondition, or with the treatment of such diseases or disorders, and can be painful to a varying
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77degree. The pain may be mild to severe, and is exacerbated by mechanical provocation of thegingivae. Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfils criteria for 1.1.3.1 Gingival pain attributed to gingivitisB. The patient has been diagnosed with a systemic disease or condition, or receivedtherapy known to be able to cause oral mucosal paina. endocrine disorders or alterationsb. dietary deficiencyc. haematological diseasesd. gastrointestinal diseasese. dermatological diseasesf. drug induced disorders (not attributable to hypersensitivity or allergy)g. other disease, disorder or treatmentC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Alteration of physiological state such as pregnancy and menopause may cause endocrine changesthat manifest as gingival discomfort and pain. Systemic disorders that can cause gingivitisinclude endocrine disease (hypothyroidism, diabetes mellitus); dietary deficiencies (Fe, vitaminB complex, zinc); anaemia; gastrointestinal disorders (gastro-esophageal reflux disease; GERD),and drug induced and genetic disorders.
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78Epulis is a hyperplastic, non-neoplastic lesion which originates mainly from gingival tissues.Several histologic types occur, of which the prevalent type during pregnancy is thegranulomatous type, a form of pyogenic granuloma (Shailesh et al. 2010). The growth iscomposed mainly of capillary vessels and endothelial proliferation and appears usually on thefrontal part of the maxilla during the third trimester, sometimes referred to as "pregnancy tumor".The lesion usually causes no symptoms apart from its very presence, but may become painfulbecause of interference with e.g. occlusion or denture wear. Etiologic factors are impropermaintenance of oral hygiene which lead to chronic gingivitis and high gingival levels of activeprogesterone which acts in a yet undefined mechanism.Antineoplastic therapy-induced mucositis associated with chemotherapy and radiation mainlyaffects oral mucosa, but can also affect the gingivae and cause gingival pain. See 1.2.1.1.5 Oralmucosal pain attributed to systemic disorder.Benign hyperplastic lesions or tumors involving gingivae are usually not directly associated withpain, but may become painful if traumatized and/or infected due to interference with e.g.occlusion or dentures. See 1.1.3.1.1 Gingival pain attributed to trauma and 1.1.3.1.2 Gingivalpain attributed to infection.1.1.3.2Gingival pain attributed to malignant lesionDescription:Gingival pain related to a malignant disease can be painful to a varying degree. The pain may bemild to severe and is exacerbated by mechanical provocation of the gingivae. Spontaneous paincan occur.Diagnostic criteria:
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79A. The pain fulfils criteria for 1.1.3 Gingival painB. The patient has been diagnosed with a malignant lesion1known to be able to causegingival painC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1neoplasia of the gingival tissuesComments:The gingiva may be affected by an array of both primary and metastatic malignancies which mayall present as non-specific ulcers. Oral squamous cell carcinoma (OSCC) is the most common,frequently presenting as ulceration with clinical induration, fixation to the underlying tissues,rolled exophytic margins, and pain and/or numbness (Warnakulasuriya et al 2007).1.1.3.3Gingival pain attributed to neuropathy; see 4.1 Pain attributed to a lesion ordisease of the trigeminal nerveComments:Trigger points of trigeminal neuralgia may be located in the gingiva, and light touch will elicitthe typical intense paroxysmal pain attacks affecting the whole dermatome corresponding to theaffected nerve branch. As a result, patients may find it impossible to wear a denture in the region.For description and diagnostic criteria, see 4.1.1 Clinically established trigeminal neuralgia.Gingival pain may also occur as part of the early clinical presentation of trigeminal neuralgia, thediffuse deep pain, “pre-trigeminal neuralgia pain”, that sometimes precedes the onset ofcharacteristic paroxysmal pain.
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80Peripheral neuropathy may be associated with gingival pain. For description and diagnosticcriteria, see 4.1.2 Trigeminal neuropathic pain other than 4.1.1 Clinically established trigeminalneuralgia.1.1.3.4Idiopathic gingival pain; see 6 Idiopathic orofacial painComments:Burning mouth syndrome (BMS) may also affect the gingivae presenting as localized or morewidely distributed gingival pain. For description and diagnostic criteria, refer to 6.1 Burningmouth syndrome (BMS).Persistent idiopathic dentaoalveolar pain (PIDAP) is frequently associated with localized pain inthe gingivae. For description and diagnostic criteria, refer to 6.3 Persistent idiopathicdentoalveolar pain.Consideration must be given to patients presenting with chronic widespread pain or othermultiple pain conditions which may be attributable to central sensitization or other mechanisms.1.2 Non-dental painDescription:Non-dental pain includes pain attributed to conditions affecting the non-dental oral tissues, i.e.the oral mucosa, the salivary glands, and the jaw bone tissue. Pain arising from lymph tissue,muscles, joints, skin and sinuses have not been included, and are in part covered elsewhere.1.2.1 Oral mucosal painDescription:
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81Pain involving the oral mucosa which may be attributed to a local or distant cause. Oral mucosalpain is often characterized by a burning, stinging or sore sensation. Various mucosal lesions likeulcers, erosions and vesicles are common causes of oral mucosal pain, and these lesions canoccur due to a large variety of local mucosal and systemic diseases. The terms stomatitis and oralmucositis are often used as synonyms, but they do not reflect identical processes. Stomatitisrefers to any inflammatory condition of oral mucosa which occurs due to local infections orinjuries or underlying systemic diseases. Mucositis occurs due to radiation or chemotherapeuticagents (Scully et al. 2000).A large variety of local mucosal and systemic diseases are associated with pain due to formationof ulcers or erosions. Theses lesions differ with regard to extension in the oral mucosa:• A mucosal ulcer is defined as a loss of surface tissue with disintegration and necrosis ofepithelial tissue. It involves damage to both epithelium and lamina propria. It penetrates theepithelial-connective tissue border, and has its base at a deep level in the submucosa, and insome cases even within the muscle or periosteum• A mucosal erosion is defined as a superficial break on the mucous membrane with loss of thesuperficial epithelial cells and minor damage to the underlying lamina propria.Diagnostic criteria:A. Any pain fulfilling criteria B through EB. Pain is localized to the site of the oral mucosa, but may refer to other ipsilateralorofacial locationsC. Clinical, laboratory, imaging and/or anamnestic evidence of a lesion or disease of theoral mucosal tissues, known to be able to cause painD. Evidence of causation demonstrated by the following:1. Pain has developed in temporal relation to the onset or appearance of the lesion2. Familiar pain is exacerbated by manipulation of the affected oral mucosa
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82E. Not better accounted for by another ICOP or ICHD-3 diagnosis.1.2.1.1Oral mucosal pain attributed to oral mucosal inflammationDiagnostic criteria:A. The pain fulfills criteria for 1.2.1 Oral mucosal painB. The patient has been diagnosed with inflammation of the oral mucosa based on the clinicalobservation of inflammation signs in the oral mucosa (i.e. tumor, dolor, rubor, and calor)C. Not better accounted for by another ICOP or ICHD-3 diagnosis.Comment:Mucosal pain associated with ulcers or other lesions is often associated with high levels of pain-related unpleasantness. The burning pain is often severe, and oral function (eating, talking),quality of life and sleep are frequently impaired (Abdalla-Aslan et al. 2016).1.2.1.1.1Oral mucosal pain associated with traumaDiagnostic criteria:A. The pain fulfils criteria for 1.2.1.1 Oral mucosal pain attributed to oral mucosalinflammationB. The history reveals a recent1trauma or injury2involving the oral mucosal tissuesC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1minutes to days
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832accidental, self-inflicted or iatrogenic1.2.1.1.1.1 Oral mucosal pain attributed to mechanical, thermal, or chemical damageDescription:Traumatic injury of the oral mucosa causes acute inflammation and can be painful to a varyingdegree. Traumatic ulceration of the oral mucosa may be acute or chronic in nature with the latterdiagnostically more challenging due to underlying fibrosis and clinical appearance of neoplasticinduration. A thorough clinical history will often alert the clinician to a traumatic aetiology orburns caused by warm food or chemicals. The pain may be mild to severe and is exacerbated bymechanical provocation of the oral mucosa. Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfils criteria for 1.2.1.1 Oral mucosal pain attributed to oral mucosalinflammationB. The history reveals a recent1trauma or injury2, involving the oral mucosal tissuesC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1minutes to days2accidental, self-inflicted or iatrogenicComments:
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84Causes for this type of pain include accidental dental injuries but also micro-trauma caused byfor example during eating or drinking overly hot foods or drinks, following dental treatment,trauma due to tooth brushing or flossing or other interdental instruments. Examination mayreveal the causative factor such as an underlying mandibular or maxillary or dentoalveolarfracture, tooth root fracture or solely a soft tissue injury. Ulceration due to local anaesthetic mostoften occurs in the hard and soft palate, the combined result of pressure and ischemic necrosis.Poorly fitting dentures may cause painful ulcerations. Over-erupted dentition or parafunctionalhabits may also cause local oral mucosal trauma with resultant inflammation and pain. Chemicalburns may be related to misuse of anti-inflammatory tablets or eating or drinking overly hotdrinks or food. Self-harm may be a rare cause of oral mucosal trauma. In patients with dystoniaor oral neuropathy injury may be recurrent.1.2.1.1.1.2 Oral mucosal pain attributed to surgical or other iatrogenic injuryDescription:Iatrogenic oral mucosa injury occurs during most dental surgery for example dental extractions,gingival or periodontal surgery.Diagnostic criteria:A. The pain fulfils criteria for 1.2.1.1 Oral mucosa pain attributed to oral mucosalinflammationB. The history reveals a recent1surgery involving the oral mucosal tissuesC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1minutes to days
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851.2.1.1.1.3 Oral mucosal pain attributed to radiation or chemotherapyDescription:Oral mucositis refers to erythematous and ulcerative lesions of the oral mucosa that may occur inpatients who receive anticancer radiotherapy to head and neck cancer involving the oral cavity orchemotherapy. The lesions typically manifest as very painful erythema or ulcerations thatcompromise nutrition and oral hygiene as well as increased risk for local and systemic infection.The condition may also be accompanied by taste disturbances and xerostomia.Diagnostic criteria:A. The pain fulfils criteria for 1.2.1.1 Oral mucosal pain attributed to oral mucosalinflammationB. The history reveals recent1radiation involving the oral mucosal tissues, or recentchemotherapyC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1days to monthsComments:Oral mucositis describes inflammation of oral mucosa resulting from chemotherapeutic agents orionizing radiation. The frequency and severity can vary significantly with the type and dose oftherapy. The pathogenesis of oral mucositis is multifactorial; a complex five-stage model isproposed in the development of mucositis (Treister & Sonis 2007, Mravak-Stipetić 2010)
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86Mucositis may be exacerbated by local factors and infections. Infections associated with the oralmucositis lesions can cause life-threatening systemic sepsis during periods of profoundimmunosuppression. When uncomplicated by infection mucositis heals within 2 to 4 weeks aftercessation of cytotoxic chemotherapy. While oral complications primarily are associated withdiscomfort and interference with oral function, and quality of life (Duncan et al. 2005) in patientswho are also immunocompromised or debilitated, these complications can become lifethreatening. Thus, management of mucositis pain is a primary component of any mucositismanagement strategy (Sonis et al. 2004, Vera-Llonch et al. 2007).1.2.1.1.2Oral mucosal pain attributed to infectionDescription:Infection of the oral mucosal tissues causes acute inflammation and can be painful to a varyingdegree. The pain may be mild to severe and is exacerbated by mechanical provocation of the oralmucosa. Spontaneous pain can occur. The condition is further subcategorized according tocategory of causative microorganism.Diagnostic criteria:A. The pain fulfils criteria for 1.2.1.1 Oral mucosal pain attributed to oral mucosalinflammationB. The patient has been diagnosed with an infection1of the oral mucosa based on anamnesticinformation, clinical observations, and/or microbiological analysisC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1bacterial, viral, or fungal
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871.2.1.1.2.1 Oral mucosal pain attributed to bacterial infectionDescriptionBacterial infection of the oral mucosal tissues causes acute inflammation and can be painful to avarying degree. The pain may be mild to severe and is exacerbated by mechanical provocation ofthe oral mucosa. Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfills criteria for 1.2.1.1.2 Oral mucosal pain attributed to bacterialinfectionB. The patient has been diagnosed with a bacterial infection of the oral mucosaC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Bacterial infections are the most common oral infections and oral mucosa pain is oftenassociated with underlying dental pathology with periodontal infection or dental periapicalinfections may present as swelling, inflammation and pain of the overlying oral mucosae.Acute necrotizing ulcerative gingivitis (ANUG) or Necrotising ulcerative gingivitis (NUG) /periodontitis (NUP)/ stomatitis (NUS) is an opportunistic Oral mucosa infection caused by anarray of bacteria in malnourished children, young adults and immune deficient patients. NUG isoften the initial presentation, proceeding into NUP, NUS and ultimately noma. Necrosis andulceration of the oral mucosa, exquisite pain, severe halitosis, regional lymphadenopathy,malaise and fever differentiate this form of ulceration from others. When the alveolar bonebecomes exposed, necrotic bone sequestrae may develop and should be removed with theassociated teeth (Feller et al. 2014).Syphilis is caused by Treponema pallidum infection and continues to be widespread, withincreasing rates among men who have sex with men. The primary lesion presents at the first site
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88of mucosal inoculation, frequently the oral mucosa. A highly infective, painless, solitary ulcerwith indurated margins and ipsilateral lymphadenopathy is the most common, with healingwithin three weeks. Non-characteristic mucous patches alerts to the development of secondarysyphilis frequently accompanied by a maculo-papular rash of the palmo-plantar surfaces of thehands and feet, and generalised lymphadenopathy (Hertel et al. 2014).Gonorrhea lesions may occur in mouth at site of inoculation or secondarily by hematogenousspread from a primary focus elsewhere. Earliest symptoms are burning or itching sensation,dryness or heat in mouth followed by acute pain on eating or speaking. Tonsils and oropharynxare most frequently involved, and oral tissues may be diffusely inflamed or ulcerated. Salivadevelops increased viscosity and fetid odor. In severe cases, submaxillary lymphadenopathy withfever occurs.Tuberculosis (TB). The emergence of multidrug-resistant Mycobacterium tuberculosis and thehigh numbers of HIV-infected individuals in South Africa has resulted in an increase of TB casesurging inclusion in the differential diagnoses of orofacial pathology. Secondary TB in the formof painful, deep irregular ulcers with indurated appearance, undermined edges and thick mucus-like material at the base of any aspect of the tongue are typical. Haematogenous spread frompulmonary TB or secondary inoculation of a traumatic ulcer with infected sputum is the mostcommon pathogenesis. Primary oral TB is distinctly rare, usually associated with Mycobacteriumbovis. Ulcers resemble chronic traumatic ulceration and even malignancy urging a diagnosticbiopsy (von Arx & Husain, 2001; Jain & Jain 2014). Associated symptoms of pain, fever,lymphadenopathy, hoarseness of voice and weight loss frequently accompany the ulcerations.Acquired or congenital immunosuppression may lead to increased risk of gingival infection.Patients on immunosuppressive therapy may develop a variety of opportunistic infectionsincluding pseudomembraneous candidosis, other fungal and viral infections. TNF-α therapyincreases the risk of tuberculosis (TB). Patients on infliximab and adalimumab with combinedimmunomodulatory therapy may be at increased risk of TB, histoplasmosis, coccidiomyinfections. Antirheumatic drugs including methotrexate, abatacept and alefacept have increasedthe risk of herpes simplex and herpes zoster infections and TB.
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891.2.1.1.1.2 Oral mucosal pain attributed to viral infectionDescription:Viral infection of the oral mucosal tissues causes acute inflammation and can be painful to avarying degree. The pain may be mild to severe and is exacerbated by mechanical provocation ofthe oral mucosa. Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfills criteria for 1.2.1.1.1 Oral mucosal pain attributed to infectionB. The patient has been diagnosed with a viral infection of the oral mucosa as evidencedby1. A mucosal eruption in the area of pain2. PCR identification of the virus from swabs taken from the areaC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Viral infections of the oral mucosa include HSV, VZV, HPV, CMV, Coxsackie virus and HIVinfection. Note that ICHD-3 has a specific set of criteria for Herpes Zoster Virus (Chapter 13,13.1.2.1 Painful trigeminal neuropathy attributed to acute Herpes zoster). We have modelledcriteria to reflect these.The infected oral mucosa tissues may often be ulcerated and painful to palpation. Severe localpain is often noted, in eating or drinking acidic or hot or cold foods or drinks. Pain is elicited oneating and may be so severe that the individual may be unable to eat or drink and becomedehydrated.Herpes simplex (HSV) is the most common virus to affect the oral mucosa. Herpeticgingivostomatitis, the primary HSV-1 infection, mostly affects children and presents either as
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90asymptomatic infection or with mucosal vesicles followed by quickly developing painfululcerations affecting both keratinised and non-keratinised mucosa and gingivae. Fever, malaise,foul odor and cervical lymphadenopathy often accompanies the pain. Adults with primaryinfection suffer symptomatic herpetic pharyngotonsillitis initiated as vesicles that rapidly breakdown into painful shallow ulcerations (Fourie & Boy, 2016).Recurrent manifestations of the virus in the form of herpes labialis are most commonly initiatedby various factors including, but not limited to, stress, UV exposure or dental local anaesthetic.Initial prodromal stinging or burning is followed by a cluster of approximately five small fluid-filled vesicles on erythematous mucosa that ruptures to leave painful shallow ulcers whichcoalesce and crusts.Herpangina (Hand-Foot-Mouth Disease) caused by Coxsackie virus, ECHO virus, and otherenteroviruses. It typically affects children below 10 years. Red macules or vesicles are followedby self-limiting ulcerations, approximately 5mm in diameter, on the anterior tonsillar pillars, softpalate, uvula, and/or tonsils. Pyrexia, sore throat and headaches are common. Ulcers heal within4-6 days.Varicella zoster virus (VZV or HHV-3) infection is well-known for its pruritic, vesicular skinrash, ulceration and crusting, all occurring concurrently. Crusting is absent in the oral mucosawhich instead present as ulcerating papules.Herpes zoster (shingles) signifies reactivation of dormant VZV infection, mostly affecting oldand debilitated patients, and follows the dermatome of the ganglion in which the virusestablished latency. Severe burning or stinging pain to the affected dermatome is followed byfluid filled vesicles that rupture to leave painful shallow ulcerations that may coalesce to formlarge denuded areas. Oral manifestations signify involvement of the mandibular or maxillarydivisions of the trigeminal nerve with pathognomonic abrupt termination of lesions along themidline. Osteonecrosis with tooth exfoliation has been reported, especially in immune deficientindividuals. The infection often involves several locations in the anatomical distribution of theaffected nerve branch. See also 4.1.2.1 Trigeminal neuropathic pain attributed to herpes zosterand 4.1.2.2 Trigeminal post-herpetic neuralgia.
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91Human papilloma virus may cause single or multiple papillary lesions. These lesions are rarelypainful unless traumatized.Epstein-Barr virus causes mononucleosis, which may involve sore throat and numerous smallulcers that precede lymphadenopathy. Gingival bleeding, petechiae at the border between softand hard palate are other clinical features.1.2.1.1.1.3 Oral mucosal pain attributed to fungal infectionDescription:Fungal infection of the oral mucosal tissues causes acute inflammation and can be painful to avarying degree. The pain may be mild to severe and is exacerbated by mechanical provocation ofthe oral mucosa. Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfills criteria for 1.2.1.1.1 Oral mucosal pain attributed to infectionB. The patient has been diagnosed with a fungal infection of the oral mucosaC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:In recent times, the prevalence of oral fungal infections other than candidiasis has been on therise. Immunodeficiency diseases such as HIV infection and AIDS, immunosuppressive therapy,or prolonged usage of broad-spectrum antibiotics and corticosteroids are some of the notablereasons for disease emergence which occurs when the oral homeostasis is disturbed. Diabetesand salivary gland hyperfunction are other predisposing factors. The most common oral fungalinfection is Candida albicans. Erythematous candidiasis presents with generalised erythema andpain. Median rhomboid glossitis affects the tongue and has three main types: pseudomembranoustype presenting with white patches that are easily wiped off leaving erythematous, bleeding, soresurface; erythematous type with red macular lesions, often with a burning sensation; and angular
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92cheilitis type which is characterized by sore cracks and redness at angle of mouth. Xerostomia,burning, stinging and itching sensations, and metal taste are accompanying symptoms.Other mycoses to be considered in the context of gingival pain include mucormycosis,aspergillosis, histoplasmosis, blastomycosis, and paracoccidioidomycosis. Aspergillus andMucorales infections, albeit uncommon, are the most commonly encountered and follows theinhalation of the spores from soil, manure, grain, cereal and mouldy flour (Perusquia-Ortiz et al.2012) Both are superficial and invasive opportunistic fungal infections, encountered in the oralcavity of especially immunocompromised patients.1.2.1.1.3Oral mucosal pain attributed to autoimmunityDescription:Inflammation of the oral mucosa or stomatitis tissues causes pain to a varying degree. Thecondition is further subcategorized according to category of autoimmune disease. The pain maybe mild to severe and is exacerbated by mechanical provocation of the oral mucosa. Both elicitedand spontaneous pain may occur.Diagnostic criteria:A. The pain fulfils criteria for 1.2.1.1 Oral mucosal pain attributed to oral mucosalinflammationB. The patient has been diagnosed with an autoimmune disease known to be able to causeoral mucosal paina. pemphigusb. mucus membrane pemphigoidc. recurrent aphthous stomatitis
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93d. oral lichen planuse. erythema multiformef. Sjögren’s syndromeg. Behçets diseaseh. graft versus host diseasei. lupus erythematosus, systemic or discoid typej. erythema migransk. Crohn’s diseasel. ulcerative colitism. coeliac diseasen. other autoimmune disease or disorderC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:The prognosis for the pain depends on the outcome of treatment of the underlying autoimmunedisorder.Several dermatological immune-mediated vesiculo-ulcerative lesions conditions may presentwith oral mucosal involvement, either concurrent with the skin pathology, as the initialpresentation or sometimes as the only clinical presentation (Bascones-Martinez et al. 2015). Theprognosis for the pain depends on the outcome of treatment of the underlying autoimmunedisorder.
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94Pemphigus, a group of immune mediated subepithelial bullous dermatoses, is mediated by auto-antibodies directed at the proteins of keratinocyte adhesion (desmosomes) causing acantholysis.PV most commonly affects the oral cavity, it’s autoantibodies mainly directed againstdesmoglein 1 and 3 (mucocutaneous forms) or only 3 (mucosal forms). Patients, typically 40-60years of age, present with thin-roofed, flaccid intra-epithelial bullae which rupture promptly afterdevelopment resulting in large irregular areas of painful mucosal ulceration (Harman et al. 2003)Mucous membrane pemphigoid (MMP) is a common systemic autoimmune blistering diseasewith preferential involvement of mucosal membranes. The antibodies are directed at the proteinsof keratinocyte to connective tissue matrix adhesion or hemi-desmosomes (BP180 and laminin-332) causing the epithelium to split away from its underlying connective tissue bed. Thesubepithelial nature of the split results in thick roofed vesicles which may still be intact onexamination. Rupture of the vesicles leave ulcerative lesions devoid of any epithelium, coveredby yellow-white slough (Hasan 2014).Recurrent aphthous stomatitis (RAS) represents the most common form of oral mucosalulceration encountered in healthy individuals (Scully 2006; Akintoye & Greenberg 2014). Theterm should be reserved for recurrent ulcers of the oral mucosa, not associated with any systemicdisease and which typically commence in childhood or adolescence. Non-keratinised mucosa ofthe buccal mucosa, lips and soft palate is most commonly affected. A variety of local andsystemic factors including immunologic, allergic, nutritional, microbial organisms, psychosocialstress as well as immunosuppressive drugs, have been proposed as possible etiological factors.Increased prevalence in close family members also indicate a possible genetic background(Slebioda et al. 2013). RAS has an atypical clinical presentation in HIV-infected patients andshould always be considered as differential diagnosis of oral mucosal ulceration in them(Shiboski et al. 2009). When RAS starts later in life, additional mucosal surfaces may be affectedand a comprehensive physical examination and medical history should be considered to rule outinflammatory gastrointestinal disease such as Crohn’s disease, coeliac disease, Behçet’ssyndrome, Sweet’s syndrome, cyclic neutropenia, HIV infection and drug reactions in whichcase “aphthous-like ulcers” is a more appropriate term. Clinically RAS is subclassified into RASminor; the most common variant which typically presents with 1-5 ulcers, less than 10mm indiameter surrounded by a bright red inflammatory halo, and healing spontaneously within 10-14
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95days; and RAS major (Sutton disease) which present as deeper, larger, persistent ulcerations withirregular borders. The ulcers are larger, usually >10mm in diameter, and typically take weeks ormonths to heal.Oral lichen planus (OLP) is a rather common, chronic inflammatory disorder affecting mainlymiddle-aged females. The pathogenesis remains uncertain but various subsets of T-lymphocytesand mast cells play a role in the basal membrane damage (Firth et al. 2015). The disease maypresent with a diverse clinical spectrum which includes the atrophic, erosive, ulcerative and lesscommonly, bullous variants (Gorouhi et al 2014). The lesions typically affect the oral mucosabilaterally and are fairly symmetric, presenting as either solely an oral mucosal disease or beaccompanied by desquamative gingivitis and/or cutaneous manifestations. In the case of theerosive and ulcerative types, painful pseudomembrane covered ulcerations bordered by faintwhite striae are seen in a multifocal distribution. Recent meta-analyses determined the overallmalignant transformation rate of OLP to be around 1%, most commonly affecting the tongue ofolder females (Fitzpatrick et al. 2014, van der Waal 2014), but the issue remains contentious.Erythema multiforme (EM) is a T-cell-mediated type IV cytotoxic immune reaction to a varietyof antigens (viral, bacterial, pharmacological, or chemical) that result in apoptosis-mediatedepithelial cell death. Anti-desmoplakin I and II antibodies were recently demonstrated as apossible instigator of the cytotoxic reaction (Fukiwake et al 2007). EM mostly affects young,otherwise healthy individuals and is often recurrent and temporal with recurrent HSV infections(Carrozzo et al. 1999). Oral lesions may either represent the start of further mucocutaneousinvolvement or may appear in isolation, classically with swollen, cracked, haemorrhagic andcrusted lips with or without mucosal blisters and ulcerations (Farthing et al 2005).Sjögren's syndrome is a systemic autoimmune disease that frequently presents concomitantlywith other systemic connective tissue or organ-specific autoimmune diseases. This association iswell described for systemic lupus erythematosus and rheumatoid arthritis. The oral mucosaltissues can become abraded and even cut with dry foods, and sore. The presence of Sjögren'ssyndrome influences the expression of the other autoimmune disease to some degree, forinstance by increasing fatigue and lymphoma risk (Theander & Jacobsson 2008).
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96Behçet’s Disease is an autoimmune multisystem disease of unknown aetiology. It ischaracterised by oral ulcers, genital ulcers and eye inflammation. There may be dermatologicsymptoms along with neurological and vascular involvement. The oral lesions ulcers are painfuland characterized by cyclic presentation affecting the lips, buccal mucosa, soft palate and tonguewith an appearance resembling aphthous lesions, a few millimeters to centimeters in diameter.The incidence of the disease is higher in Mediterranean and Asian populations, especially inTurkey (Saccucci et al. 2018).Graft versus host disease is characterized by lichenoid, papular and erythematous lesions, andoccasionally ulcerations and desquamation on the buccal and labial mucosa, the palate and dorsalpart of the tongue. The oral lesions are often accompanied by fever, malaise, nausea, andxerostomia. The oral findings may be caused by a combination of radiotherapy, chemotherapy,immunosuppressive medications, and secondary infections.More than half of patients with systemic lupus erythematosus (SLE) may present with orallesions, most frequently ulceration and pain of the buccal mucosa and lips during the early,active disease phase (Khatibi et al. 2012). Ulcerative lesions and erythematous lesions with orwithout radiating white striae may also be seen as part of the clinical spectrum of discoid lupuserythematosus (DLE). DLE is considered a potentially malignant disorder of the oral mucosa dueto the increased prevalence of oral squamous cell carcinoma among this population, especiallyinvolving the lower lip.Erythema migrans (geographic tongue, benign migratory glossitis) is a common oralinflammatory condition of unknown etiology with an estimated prevalence of 1–3%. About 30 %have oral discomfort, burning and stinging sensation. It usually affects the tongue, although otheroral sites may be involved. Presentation may include circular erythematous areas, often sharplydefined by elevated, whitish border zones, located at the lateral, dorsal, anterior, and/or ventralparts of the tongue. The erythematous appearance is due to atrophy and loss of filiform papillaelesions. The most commonly suggested associations are atopy and psoriasis. The disorder shouldnot be confused with the characteristic rash of early Lyme disease.
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97Crohn’s disease presents with multifocal, linear, nodular, or diffuse mucosal thickenings in thelabial and buccal mucosa and the mucobuccal folds. They may be associated with painful,persistent aphthous-like ulcerations and atrophic glossitis.Ulcerative colitis presents with scattered, clumped or linearly oriented pustules on anerythematous mucosa at multiple oral sites. Some patients exhibit painful oral aphthous-likelesions in addition to the pustular lesions.Coeliac disease may present with mucosal pain, commonly associated with aphthous-like ulcers.Malabsorption of iron and vitamin B may lead to burning, stinging sensations in the tongue.Other rare autoimmune or idiopathic causes of oral mucosal ulceration causing pain andsensitivity include; eosinophilic ulcer, giant cell arteritis hypereosinophilic syndrome,necrotising sialometaplasia, polyarteritis nodosa, reactive arthritis (Reiter’s syndrome), acutefebrile neutrophilic dermatosis (Sweet syndrome), and Wegener's granulomatosis.1.2.1.1.4Oral mucosal pain attributed to allergic reactionDescription:Inflammation of the oral mucosa or stomatitis tissues related to allergy or hypersensitivity causespain to a varying degree. The condition is further subcategorized according to category ofhypersensitive or allergic condition. The pain may be mild to severe and is exacerbated bymechanical provocation of the oral mucosae. Both elicited and spontaneous pain may occur.Oral allergy syndrome (OAS) usually occurs in individuals who are allergic to pollen from trees,grasses or weeds. Fresh fruit, raw vegetables and raw nuts are common causes of OAS. Thesymptoms including itching sensation and/or swelling of all or part of the lips, tongue, mouth orthroat, but this can on occasions be severe and also include nausea and vomiting. Dentalmaterials, oral hygiene products and food additives may cause contact allergic reactions in themouth with varied clinical presentation including stomatitis, lichenoid lesions, erosions, blistersand ulcerations. Elicited and spontaneous pain may occur.
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98Diagnostic criteria:A. The pain fulfils criteria for 1.2.1.1 Oral mucosal pain attributed to oral mucosalinflammationB. The patient has been diagnosed with hypersensitivity or an allergic reaction in the oralmucosa associated witha. dental material (temporary/permanent restorative or impression material)b. oral hygiene productc. topical drugd. systemic druge. food or additivef. other factorC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Allergic reactions and oral mucosal hypersensitivity reactions are less common than cutaneousones ascribed to the possible allergen dilution and the continuous rinsing effects of normal salivaflow (Venables et al. 2016). Lesions may present with non-specific tissue oedema, erythema,cracking, ulceration, hyperkeratotic white plaques or mucosal desquamation. Lesions may startlong after the introduction of a drug and may remain for months after cessation thereofcomplicating diagnosis and management.Allergic contact stomatitis. Although rare, this form of mucositis has been reported in associationwith dental impression materials (Batchelor & Todd 2010), dental restorative materials
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99(Venables et al. 2016), topical benzocaine application, and more commonly cinnamon intoothpastes, mouth rinses, and chewing gum (Kind et al. 2010). Lesions may appear as mixed redand white patches with ulceration, swelling of the cheeks and desquamation appearing on thelips, cheeks, tongue and gingiva as localized or widely distributed lesions (Calapai et al. 2014).A hypersensitivity reaction to either a systemic drug or direct contact with an offending agentmay result in clinical and histological features reminiscent of lichen planus. The term ‘orallichenoid drug reaction’ (OLDR) or ‘oral lichenoid contact lesion’ (OLCL) is used respectively,and both may present with significant ulceration, usually with erythema and white striations atthe periphery of the ulceration. A temporal or spatial association with an offending agent canusually be identified. Amalgam is often implicated in OLCL, confirmed by patch testing formercury or amalgam sensitivity. OLDR is encountered with some frequency in patients treatedwith angiotensin-converting enzyme (ACE) inhibitors, nonsteroidal anti-inflammatory drugs(NSAIDs) and oral hypoglycaemic drugs (Al-Hashimi et al. 2007).Fixed drug eruption (FDE) is a form of hypersensitivity remarkable for its fixed anatomicalnature and has been described with NSAID’s and other oxicam drugs (Andrade et al. 2011),gabapentin (Gupta et al. 2009), fluconazole (Benedix et al. 2008), and systemic antibacterial andantifungal drugs (Savin 2001). FDE should be suspected in cases with a temporal association ofdrug ingestion, may be confirmed through patch testing or oral provocation tests, and managedthrough drug avoidance or substitution, while the acute lesions can be treated with topical orsystemic steroids.Drug induced fibrosis epithelial hyperplasia or fibrovascular hyperplasia may occasionally beassociated with painful presentation, likely due to underlying periodontal infection due todifficulty with oral hygiene in these conditions.1.2.1.1.5Oral mucosal pain attributed to oral mucosal inflammation due to other causeDescription:
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100Inflammation of the oral mucosa may occur associated with systemic disease, disorder, orcondition, or with the treatment of such diseases or disorders, and can be painful to a varyingdegree. The pain may be mild to severe, and is exacerbated by mechanical provocation of theoral mucosa. Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfils criteria for 1.2.1.1 Oral mucosal pain attributed to oral mucosalinflammationB. The patient has been diagnosed with a systemic disease or condition, or receivedtherapy known to be able to cause oral mucosal paina. endocrine disorders or alterationsb. dietary deficiencyc. haematological diseasesd. gastrointestinal diseasese. dermatological diseasesf. drug induced disorders (not attributable to hypersensitivity or allergy)g. other disease, disorder or treatmentC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Alteration of physiological state such as pregnancy and menopause may cause endocrine changesthat manifest as oral mucosal discomfort and pain. Systemic disorders that can cause oral
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101mucosal inflammation and pain include endocrine disease (hypothyroidism, diabetes mellitus);dietary deficiencies (Fe, vitamin B complex, zinc); gastrointestinal disorders, and drug induceddisorders (not attributable to hypersensitivity or allergy).Iron, vitamin B12 and folate deficiency can cause atrophic glossitis in which the filiform papillaof the dorsum of the tongue undergo atrophy, leaving a smooth, erythematous tongue. Otherparts of the oral mucosa may also appear atrophic and red. Aphthous-like ulcers are common insevere cases. Burning, stinging sensation may precede clinically detectable oral lesions. Severecases of vitamin B12 may also be associated with paresthesia. Patients may have a predispositionto develop angular cheilitis.Haematological disorders such as anaemia, gammopathies, haematinic deficiencies, leukemia,myelodysplastic syndrome, neutropenia and other white cell dyscrasias may result in friable oralmucosa with resultant ulceration and pain.Gastrointestinal disorders such as gastroesophageal reflux disorder (GERD) and peptic ulcerationmay lead to malabsorption and related dietary deficiencies and subsequent related oral mucosalpain.Dermatological causes of painful mucosal lesions include dermatitis herpetiformis, linear IgAdisease, epidermolysis bullosa and chronic ulcerative stomatitis.Antineoplastic therapy-induced mucositis involves a complex cascade of events which isinitiated by reactive oxygen species with extensive inflammation, atrophy, swelling, erythemaand ulceration (Raber-Durlacher et al. 2010). This includes chemotherapy induced mucositis aswell as radiation lesions (Rosenthal & Trotti 2009). Radiation lesions correspond to the exposedsurfaces while chemotherapy induced mucositis affects the entire alimentary tract. The type anddosage of systemic cytotoxic agents, and the dosage and field of radiation will affect thepresence and severity of mucositis. Evidence based guidelines for the management of cancertherapy induced oral mucositis was established and should be referred to in all cases of patientsreceiving these agents.Benign hyperplastic lesions or tumors involving oral mucosa are usually not directly associatedwith pain, but may become painful if traumatized and/or infected due to interference with e.g.
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102occlusion or dentures. See 1.2.1.1.1 Oral mucosal pain associated with trauma and 1.2.1.1.2Oral mucosal pain attributed to infection.1.2.1.2Oral mucosal pain attributed to a malignant lesionOral mucosal pain related to a malignant disease can be painful to a varying degree. The painmay be mild to severe and is exacerbated by mechanical provocation of the gingivae.Spontaneous pain can occur.Diagnostic criteria:A. The pain fulfils criteria for 1.2.1 Oral mucosal painB. The patient has been diagnosed with a malignant lesion1known to be able to causeoral mucosal painC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1neoplasia of the oral mucosaComments:The oral mucosa may be affected by an array of both primary and metastatic malignancies whichmay all present as non-specific ulcers. Oral squamous cell carcinoma (OSCC) is the mostcommon, frequently presenting as ulceration with clinical induration, fixation to the underlyingtissues, rolled exophytic margins, pain and/or numbness (Warnakulasuriya et al 2007).
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1031.2.1.3Oral mucosal pain attributed to neuropathy; see 4.1 Pain attributed to a lesion ordisease of the trigeminal nerveComments:Trigger points of trigeminal neuralgia may be located in the oral mucosa, and light touch willelicit the typical intense paroxysmal pain attacks affecting the whole dermatome correspondingto the affected nerve branch. As a result, patients may find it impossible to wear a denture in theregion. For description and diagnostic criteria, see 4.1.1 Trigeminal neuralgia.Oral mucosal pain may occur as part of the early clinical presentation of trigeminal neuralgia, thediffuse deep pain, “pre-trigeminal neuralgia pain", that sometimes precedes the onset ofcharacteristic paroxysmal pain.Peripheral neuropathy and may be associated with pain in the oral mucosa. For description anddiagnostic criteria, see 4.1.2 Trigeminal neuropathic pain other than 4.1.1 Trigeminal neuralgia.1.2.1.4Idiopathic oral mucosal pain; see 6 Idiopathic orofacial painComments:Burning mouth syndrome (BMS) presents as localized or more widely distributed oral mucosalpain. For description and diagnostic criteria, see 6.1 Burning mouth syndrome (BMS).Persistent idiopathic dentoalveolar pain (PIDAP) is sometimes associated with localized pain inthe adjacent oral mucosa. For description and diagnostic criteria, see 6.3 Persistent idiopathicdentoalveolar pain.Consideration must be given to patients presenting with chronic widespread pain or othermultiple pain conditions which may be attributable to central sensitization or other mechanisms.
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1041.2.2 Salivary gland painDescription:Pain caused by a disorder involving the salivary glands.Diagnostic criteria:A. Any pain fulfilling criteria B through EB. Pain is localized to the site of the salivary gland lesion, but may refer to otheripsilateral orofacial locationsC. Clinical, laboratory, imaging and/or anamnestic evidence of a lesion or disease of thesalivary glands1known to be able to cause painD. Evidence of causation demonstrated by either or both of the following:1. Pain has developed in temporal relation to the onset or appearance of the lesion2. Familiar pain is exacerbated by pressure applied to the affected salivary glandE. Not better accounted for by another ICOP or ICHD-3 diagnosis.Notes:1as specified per sub-diagnosis1.2.2.1Salivary gland pain attributed to obstructive causeDiagnostic criteria:A. The pain fulfils criteria for 1.2.2 Salivary gland pain
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105B. The patient has been diagnosed with a condition causing obstruction of the salivaryducta. sialolithiasisb. mucus plugc. space occupying lesiond. traumatic or iatrogenic injury of the salivary gland or salivary ductC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Patients with obstruction of the salivary duct most commonly present with history of acuteintermittent pain and swelling of the affected major salivary gland. The degree of pain andswelling is dependent on the extent of salivary duct obstruction and the presence of secondaryinfection.Iatrogenic causes include therapy-related injury, e.g. I131 mediated. Salivary gland function isaffected after high-activity radioiodine ablation therapy in patients with differentiated thyroidcancer (Klein Hesselink et al. 2016). Radioactive iodine is actively accumulated in salivary glandtissue, and sialadenitis is a common sequela along with decreased saliva secretion andxerostomia leading to salivary gland infection and pain.1.2.2.2Salivary gland pain attributed to infectionDiagnostic criteria:A. The pain fulfils criteria for 1.2.2 Salivary gland painB. The patient has been diagnosed with an infection of the salivary gland (or glands)
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106C. Not better accounted for by another ICOP or ICHD-3 diagnosis1.2.2.2.1Salivary gland pain attributed to viral infectionDiagnostic criteria:A. The pain fulfills criteria for 1.2.2.2 Salivary gland pain attributed to infectionB. The patient has been diagnosed with a viral infection of the salivary gland (or glands)C. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Viral infections of the salivary glands include mumps, HIV, and CMV infection, which cancause pain in addition to swelling.Mumps mostly affects the parotid gland, with bilateral sudden enlargement, painful to palpation,but up to 25% may involve unilateral swelling. Severe local pain is often noted, in moving thejaws in talking and chewing, especially if partial duct obstruction occurs. It typically affectschildren 4–6 years of age.1.2.2.2.2Salivary gland pain attributed to bacterial infectionDiagnostic criteria:A. The pain fulfills criteria for 1.2.2.2 Salivary gland pain attributed to infectionB. The patient has been diagnosed with a bacterial infection of the salivary gland (orglands)C. Not better accounted for by another ICOP or ICHD-3 diagnosis
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107Comments:The most common bacterial cause is Staphylococcus infection.Bacterial sialadenitis can be either acute or chronic. Decreased saliva flow rate is the primarypredisposing factor, and this allows retrograde microbial colonization of the duct, which mayresult in the development of acute or chronic suppurative infection. Acute sialadenitis ischaracterized by a painful swelling of a single salivary gland, commonly affecting the parotidgland. A purulent discharge may be expressed from the salivary duct orifice, and the patient maypresent with redness of the overlying skin or even abscess formation within the inflamed glandtissue, malaise, fever, and cervical lymphadenopathy. Bacterial sialadenitis often occurs inimmunocompromised patients and in elderly patients who suffer from salivary glandhypofunction due to systemic diseases, medication intake, or dehydration, or it may be associatedwith obstruction of the salivary ducts by deposition of calculi, mucus plugs, and tumor growth orby trauma. Chronic sialadenitis may develop following acute sialadenitis if the predisposingfactors cannot be eliminated. Staphylococcus aureus is the most common pathogen isolated frompurulent sialadenitis (Brook 2009).1.2.2.3 Salivary gland pain attributed to non-infectious causeDescription:Other causes of salivary gland pain may include pain attributed to allogeneic transplantation witha graft versus host disease (GVHD). Salivary glands are a major target of GVHD and manifest ashyposalivation and xerostomia (Bassim et al. 2015), infection and subsequent pain.Diagnostic criteria:A. The pain fulfills criteria for 1.2.2 Salivary gland pain
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108B. The pain does not fulfill criteria for 1.2.2.1–1.2.2.2C. Not better accounted for by another ICOP or ICHD-3 diagnosis1.2.2.3.1Salivary gland pain attributed to recurrent juvenile parotitisDiagnostic criteria:A. The pain fulfills criteria for 1.2.2.3 Salivary gland pain attributed to non-infectiouscauseB. The patient has been diagnosed with recurrent juvenile parotitisC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Juvenile recurrent parotitis is a common condition of the salivary glands in children, which ischaracterized by intermittent swelling of the parotid glands on one or both sides, with or withoutpain, and generally associated with nonobstructive sialectasis of the parotid gland, as well assalivary gland hypofunction (Leerdam et al. 2005). It has a biphasic age distribution, with peaksat 2–5 years and 10 years of age. The most common symptoms are swelling, pain and fever.Symptoms are limited to about 3 days and may be frequent, with about 8 episodes per year. It isdiagnosed from the medical history and confirmed by sialography or ultrasonography. Theetiology is unclear, but in most patients juvenile parotitis resolves during adulthood.1.2.2.3.2Salivary gland pain attributed to immunologically mediated disorderDiagnostic criteria:
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109A. The pain fulfills criteria for 1.2.2.3 Salivary gland pain attributed to non-infectiouscauseB. The patient has been diagnosed with an immunologically mediated disordera. Sjögren’s syndromeb. Other immunologically mediated disorderC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Immunologically mediated salivary gland pain includes Sjögren’s syndrome, an autoimmunedisease that results in salivary gland dysfunction. Symptoms include recurrent or persistentswelling of the salivary glands, dryness of the mouth, difficulty of chewing, pain and burningsensation of oral mucosa, chronic sore throat and pain with swallowing.1.2.2.3.3Salivary gland pain attributed to other causeDiagnostic criteria:A. The pain fulfills criteria for 1.2.2.3 Salivary gland pain attributed to non-infectiouscauseB. The pain does not fulfill criteria for 1.2.2.3.1–1.2.2.3.2C. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Infrequent causes for salivary gland pain may include benign and malignant tumors of thesalivary glands. These are usually not directly associated with pain (Guzzo et al. 2010), but
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110secondary pain may occur related to obstruction of the gland or duct (see 1.2.2.1 Salivary glandpain attributed to obstructive cause) or, for malignant tumors, to nerve impingement (see 4.1.2Trigeminal neuropathic pain).1.2.3 Jaw bone painDescription:Pain caused by a disorder involving the jaw bone tissue.Diagnostic criteria:A. Any pain fulfilling criteria B through EB. Pain is localized to the site of the jaw bone lesion, but may refer to other ipsilateralorofacial locationsC. Clinical, laboratory, imaging and/or anamnestic evidence of a lesion or disease of thejaw bone1known to be able to cause painD. Evidence of causation demonstrated by either or both of the following:1. Pain has developed in temporal relation to the onset or appearance of the jaw bonelesion2. Familiar pain is exacerbated by pressure applied to the jaw bone lesionE. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1as specified per sub-diagnosis
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1111.2.3.1Jaw bone pain attributed to infectionDiagnostic criteria:A. The pain fulfils criteria for 1.2.3 Jaw bone painB. The patient has been diagnosed with an infection of the jaw bone tissueC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Intra-bony bacterial, viral and fungal infections may cause jaw bone pain. The most commonones are bacterial infections.Infection can occur secondary to osteo(radio)necrosis of the jaws, which may contribute to thepain associated with osteonecrosis, see 1.2.3.2 Therapy related jaw bone pain.1.2.3.1.1Jaw bone pain attributed to bacterial infectionDiagnostic criteria:A. The pain fulfils criteria for 1.2.3.1 Jaw bone pain attributed to infectionB. The patient has been diagnosed with a bacterial infection of the jaw bone tissueC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:
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112Bacterial infections of the jaw bone tissue include osteomyelitis. Odontogenic infections canspread and cause osteomyelitis of the jaw, but osteomyelitis secondary to odontogenic infectionis relatively uncommon. Severe mandibular pain is a common symptom of jaw osteomyelitis andcan be accompanied by anesthesia or hypoesthesia on the affected side. In protracted cases,mandibular trismus may develop.1.2.3.1.2Jaw bone pain attributed to viral infectionDiagnostic criteria:A. The pain fulfils criteria for 1.2.3.1 Jaw bone pain attributed to infectionB. The patient has been diagnosed with a viral infection of the jaw bone tissueC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Viral infections of the jaw bone tissue include herpes zoster induced osteonecrosis.Herpes zoster (HZ) (shingles) results due to reactivation of Varicella zoster virus. Unusual dentalcomplications like osteonecrosis, exfoliation of teeth, periodontitis, and calcified and devitalizedpulps, periapical lesions, and resorption of roots as well as developmental anomalies such asirregular short roots and missing teeth may arise secondary to involvement of 2nd or 3rd divisionof trigeminal nerve by HZ (Gupta et al 2015).1.2.3.1.3Jaw bone pain attributed to fungal infectionDiagnostic criteria:A. The pain fulfils criteria for 1.2.3.1 Jaw bone pain attributed to infection
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113B. The patient has been diagnosed with a fungal infection of the jaw bone tissueC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:The most common fungal infections of the jaw bone tissue are aspergillosis and mucormycosis.Aspergillosis of the oral cavity is an uncommon condition which most frequently occurs inimmunocompromised patients, such as those with hematological malignancies. Osteomyelitiscaused by Aspergillus species is an infection that is often neglected. Invasive oral aspergillosis,though rare, is a potentially lethal disease and it should be considered in immunosuppressedpatients with oral lesions (Gabrielli et al. 2014).Mucormycosis is a rare opportunistic infection invariably affecting immunocompromisedpatients, but it may affect rarely healthy individuals after tooth extraction (Nilesh and Vande2018). The organism implicated to cause mucormycosis is a saprophytic fungus, mainly rhizopusor mucor. It is the most deadly and rapidly progressing form of fungal infection affectinghumans.1.2.3.2Therapy related jaw bone painDiagnostic criteria:A. The pain fulfils criteria for 1.2.3 Jaw bone painB. The pain has developed in close temporal relation1to a therapeutic intervention knownto be able to cause jaw bone paina. medication related osteonecrosis of the jaws (MRONJ)b. osteoradionecrosisc. alveolar osteitis (dry socket)
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114d. other therapeutic interventionC. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:1normally hours to weeks; see sub-diagnosesComments:Medication-related osteonecrosis of the jaw is defined by the presence of necrotic bone (that isexposed or can be probed through a sinus tract) for more than 8 weeks in the maxillofacial regionof an individual treated with bisphosphonate or other anti-resorptive (e.g. denosumab) or anti-angiogenic (e.g. bevacizumab) medications. MRONJ typically presents as pain, infection, andnecrotic bone in the mandible or maxilla in patients receiving these agents. Dentoalveolarsurgery is a major risk factor.Osteoradionecrosis is a complication of radiation therapy (RT) due to vascular obliteration anddecreased vascular supply of the irradiated tissues. Symptoms of osteoradionecrosis can includepain, bad breath, dysgeusia, dysesthesia or anesthesia, trismus, difficulty with chewing andswallowing, speech difficulties, fistula formation, pathologic fracture, and infection. The time toonset of osteoradionecrosis is quite variable. In some cases, it may be diagnosed shortly aftercompletion of RT, while in other patients it may not be diagnosed for years after the originalcancer treatment. The mandible is the most frequently affected bone while maxillaryosteoradionecrosis is rare.Alveolar osteitis (dry socket) is a complication of dental extractions and occurs more commonlyin extractions involving mandibular molar teeth. It is associated with severe pain developing 2 to3 days postoperatively. A socket that may be partially or totally devoid of blood clot is oftenfound and some patients experience halitosis.
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1151.2.3.3Jaw bone pain attributed to a local benign lesionDescription:Benign bone tumors often are asymptomatic and discovered incidentally during evaluation fortrauma or another condition. When they are symptomatic, benign bone tumors may present withlocalized pain, swelling, deformity, or pathologic fracture. Most benign bone tumors havecharacteristic radiographic features. Advanced imaging techniques (e.g, computed tomography,magnetic resonance imaging) may be necessary to fully characterize bone tumors.Diagnostic criteria:A. The pain fulfils criteria for 1.2.3 Jaw bone painB. The patient has been diagnosed with a local benign lesion known to be able to causejaw bone tissue paina. giant cell tumorb. osteoid osteomac. osteoblastomad. other benign lesionC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:
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116Giant cell tumor of bone (GCTB) is a relatively rare, benign osteolytic skeletal neoplasm ofyoung adults. The most common presentation of GCTB is pain and swelling. Skull andcraniofacial bones are less commonly involved sites.Patients with osteoid osteoma typically complain of progressively increasing pain that is worse atnight and unrelated to activity. The pain is relieved by aspirin or other nonsteroidal anti-inflammatory medications (NSAID), usually within 20 to 25 minutes. Lack of relief by agentsshould prompt consideration of other diagnoses.Patients with osteoblastoma typically complain of chronic, continuous pain. The radiographicfindings of osteoblastoma are variable, and advanced imaging (e.g., CT or MRI) often is requiredfor identification. Pain is not relieved by aspirin or NSAID.1.2.3.4Jaw bone pain attributed to a malignant lesionDescription:Jaw bone pain attributed to malignant lesions, whether primary or metastatic, may present withlocalized pain that may increase and wane over a few weeks' or months' duration. Pain may bedue to direct mass effect of primary or metastatic tumor, or due to paraneoplastic effect inmetastatic cases.Diagnostic criteria:A. The pain fulfills criteria for 1.2.3 Jaw bone painB. The patient has been diagnosed with a malignant lesion1C. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes:
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1171primary or secondary1.2.3.4.1Jaw bone pain attributed to a primary malignant lesionDiagnostic criteria:A. The pain fulfils criteria for 1.2.3.4 Jaw bone pain attributed to a malignant lesionB. The patient has been diagnosed with a primary malignant lesion known to be able tocause jaw bone tissue paina. osteosarcomab. Langerhans’ cell histiocytosisc. non-Hodgkin lymphomad. multiple myelomae. other primary malignant lesionC. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Osteosarcoma is an uncommon tumor, but by far the most common primary malignant tumorarising in bone (myeloma excluded). The majority of patients with osteosarcoma present withlocalized pain, typically of several months' duration. Pain frequently begins after an injury andmay wax and wane over of a few weeks' or months' duration. Systemic symptoms such as fever,weight loss, and malaise are generally absent. Osteosarcomas are often considered secondaryneoplasms, attributed to sarcomatous transformation of Paget disease of bone, or some otherbenign bone lesions. The most common sites of involvement are distal femur, proximal tibia, andproximal femur, presence in the jaw bones is rather rare.
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118In Langerhans cell histiocytosis (LCH), radiologic studies typically demonstrate a lytic,"punched out" appearance, sometimes with an accompanying soft tissue mass. Pain in the jawand loose teeth may be a presenting symptom. Although bone lesions may be asymptomatic insome areas, those in the mouth are especially troublesome because of tooth loss and a highrecurrence rate. Posterior regions of the jawbones are affected more often than anterior regions.Non-Hodgkin lymphoma is a lymphatic system tumor originating from either B or Tlymphocytes and shows a high malignant potential. Non-specific symptoms, such as unclearprimary dental pain and unresolved periapical swelling, can make an accurate diagnosis of Non-Hodgkin lymphoma difficult, which frequently lead to delayed diagnosis. A CT or cone beamcomputed tomography (CBCT) scan of the jaws and immunohistochemical staining of the biopsyspecimen is recommended (Zou H et al. 2018). When the lesion affects the bones of the jaws, itis rare in the mandible when compared to the maxilla. In the reported cases, only 0.6% is foundin the mandible.Multiple myeloma is a condition where plasma cells proliferate in the bone marrow and oftenresults in extensive skeletal destruction with osteolytic lesions, osteopenia, and/or pathologicfractures. Bone pain, particularly in the back or chest, and less often in the extremities, is presentat the time of diagnosis in approximately 60 percent of patients.1.2.3.4.2Jaw bone pain secondary to a malignant lesionDiagnostic criteria:A. The pain fulfils criteria for 1.2.3.4 Jaw bone pain attributed to a malignant lesionB. The patient has been diagnosed with a malignant lesion known to be able to causesecondary jaw bone tissue pain by direct or indirect mechanismsa. direct mass effect of metastatic tumorb. paraneoplastic effect
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119C. Not better accounted for by another ICOP or ICHD-3 diagnosisComments:Direct mass effects of a metastatic tumor include nerve compression and periosteal stretch.A paraneoplastic effect is a remote effect with no metastatic spread to the jaws.1.2.3.5Jaw bone pain attributed to systemic diseaseDescription:Some systemic diseases may present with repeated vaso-occlusive pain episodes, characterizedby diffuse bone pain, punctuated by painful crises that often result in osteonecrosis (avascularnecrosis).Diagnostic criteria:A. The pain fulfils criteria for 1.2.3 Jaw bone painB. The patient has been diagnosed with a systemic disease known to be able to cause jawbone paina. sickle cell diseaseb. Gaucher’s diseasec. Paget's diseased. other systemic diseaseC. Not better accounted for by another ICOP or ICHD-3 diagnosis
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120Comments:Sickle cell disease (SCD) is characterized by a marked heterogeneity in clinical and hematologicseverity, with repeated vaso-occlusive pain episodes as the hallmark of SCD. Pain episodes mayoccur as often as every week, or individuals with SCD may go with long stretches of timewithout any pain events. Pain episodes can lead to bone infarcts, necrosis, and, over time,degenerative changes in marrow-containing bone, leading to a chronic state of pain in addition tothe more acute painful episodes.Gaucher disease (GD) is an inborn error of metabolism that affects the recycling of cellularglycolipids, being one of the most common lysosomal storage diseases. Skeletal disease ischaracterized by diffuse bone pain, punctuated by painful crises that often result in osteonecrosis(avascular necrosis).Paget disease of bone (PDB) is also known historically as osteitis deformans. PDB is a focaldisorder of bone metabolism, characterized by an accelerated rate of bone remodeling, resultingin overgrowth of bone at single (monostotic PDB) or multiple (polyostotic PDB) sites.Commonly affected areas include the skull, spine, pelvis, and long bones of the lower extremity.Similar to osteosarcomas, they may present with localized pain and swelling and typically occurin patients with polyostotic disease.1.2.3.6Jaw bone pain attributed to traumatic injuryDescription:Jaw bone pain attributed to traumatic injury includes jaw fracture. Sports, e.g. football, baseball,and hockey, and motor vehicle collisions account for a high percentage of facial injuries amongyoung adults. Chin lacerations in particular are associated with mandibular fractures. A mandiblefracture may be present if the patient experiences restricted or abnormal mouth-opening;malocclusion also suggests the presence of a mandibular fracture, as does numbness of the chinthat is present immediately following trauma.
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121Diagnostic criteria:A. The pain fulfils criteria for 1.2.3 Jaw bone painB. The patient has been diagnosed with a traumatic injury of the jawC. Not better accounted for by another ICOP or ICHD-3 diagnosis
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122References(pulpal pain)Abbott PV, Yu C. A clinical classification of the status of the pulp and the root canal system.Austral Dent J 2007;52(Suppl):S17–31.Benoliel R, Sharav Y and Eliav E. Neurovascular orofacial pain. J Am Dent Assoc 2010; 141:1094–1096.Berman LH, Hartwell GR. Diagnosis. In: Cohen S, Hargreaves KM, eds. Pathways of the pulp.9th ed. St Louis: Mosby-Elsevier; 2006:2–39.Byers MR, Narhi MVO. Nerve supply of the pulpodentin complex and response to injury. In:Hargreaves KM, Goodis HE (eds). Seltzer and Bender’s Dental Pulp. Chicago: Quintessence,2002:151–179.Falace DA, Reid K, Rayens MK. The influence of deep (odontogenic) pain intensity, quality, andduration on the incidence and characteristics of referred orofacial pain. J Orofac Pain1996;10:232–239.Garfunkel A, Sela J, Ulmansky M. Dental pulp pathosis: clinicopathologic correlations based on109 cases. Oral Surg Oral Med Oral Pathol 1973;35:110–7.Glick DH. Locating referred pulpal pains. Oral Surg Oral Med Oral Pathol 1962;15:613–623.Hargreaves KM, Seltzer S. Pharmacologic control of dental pain. In: Hargreaves KM, GoodisHE (eds). Seltzer and Bender’s Dental Pulp. Chicago: Quintessence, 2002:205–225.Hasler JE, Mitchell DF. Painless pulpitis. J Am Dent Assoc 1970;81:671–7.Kang, SH, Kim BS, Kim, Y. Cracked teeth: Distribution, characteristics, and survival after rootcanal treatment. J Endod 2016;42:557–562.Mejare IA, Axelsson S, Davidson T, Frisk F, Hakeberg M, Kvist T, et al. Diagnosis of thecondition of the dental pulp: a systematic review. Int Endod J 2012 Jul;45(7):597-613.
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123Michaelson PL, Holland GR. Is pulpitis painful? Int Endod J 2002;35:829–832.Obermann M, Mueller D, Yoon MS, et al. Migraine with isolated facial pain: A diagnosticchallenge. Cephalalgia 2007; 27: 1278–1282.Patel S, Kanagasingam S, Pitt Ford T. External Cervical Resorption: A Review. J Endod2009;35:616–625.Seo DG, Yi YA, Shin SJ, Park JW. Analysis of factors associated with cracked teeth. J Endod2012;38:288–292.Sharav Y, Katsarava Z and Benoliel R. Migraine and possible facial variants: Neurovascularorofacial pain. In: Sharav Y, Benoliel R (eds) Orofacial Pain and Headache. Chicago:Quintessence Books, 2015, pp.319–362.Sharav Y, Katsarava Z, Charles A. Facial presentations of primary headache disordersCephalalgia. 2017 Jun;37(7):714-719Sharav Y, Leviner E, Tzukert A, McGrath PA. The spatial distribution, intensity andunpleasantness of acute dental pain. Pain 1984;20:363–370.Sigurdsson A. Clinical manifestations and diagnosis. In: Ørstavik D, Pitt-Ford TR, eds. Essentialendodontology. 2nd ed. Oxford: Blackwell Munksgaard; 2008: 235–61.Smulson MH, Sieraski SM. Histophysiology and diseases of the dental pulp. In: Weine FS, ed.Endodontic therapy. 5th ed. St Louis: Mosby; 1996:84–165.Tyldesley WR, Mumford JM. Dental pain and the histological condition of the pulp. Dent PractDent Rec 1970;20:333–336.von Troil B, Needleman I, Sanz M. A systematic review of the prevalence of root sensitivityfollowing periodontal therapy. J Clin Periodontol 2002;29(3, suppl):173–177.(periodontal pain)
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124Andreasen JO, Andreasen FM. Classification, etiology and epidemiology of traumatic dentalinjuries. In: Andreasen JO. Textbook and color atlas of traumatic injuries to the teeth. 3rded. Munksgaard, Copenhagen; 1994:151–177Armitage GC. Development of a Classification System for Periodontal Diseases and Conditions.Ann Periodontol 1999;4(1):1-6.Bastone EB, Freer TJ, McNamara JR. Epidemiology of dental trauma: A review of the literature.Aust Dent J 2000;45(1):2-9Costa CPS, Thomaz EBAF, Souza S de FC. Association between sickle cell anemia and pulpnecrosis. J Endod. 2013;39(2):177–81.Gomes BP, Lilley JD, Drucker DB. Associations of endodontic symptoms and signs withparticular combinations of specific bacteria. Int End J 1996;29:69-75Gutmann JL, Baumgartner JC, Gluskin AH, Hartwell GR, Walton RE. Identify and Define AllDiagnostic Terms for Periapical/Periradicular Health and Disease States. J Endod 2009;35(12):1658-74Heasman PA, Hughes FJ. Drugs, medications and periodontal disease. Br Dent J2014;217(8):411-8Horning GM, Cohen ME. Necrotizing ulcerative ginigivitis, periodontitis, and stomatitis: clinicalstaging and predisposing factors. J Periodontol. 1995;66(11):990-8Kaste, LM, Gift, HC, Bhat, M, Swango, PA. Prevalence of incisor trauma in persons 6 to 50years of age: United States 1988–1991. J Dent Res. 1996;75:696-705 (Special Issue)Kinane JF, Chestnutt IG. Smoking and periodontal disease. Crit Rev Oral Biol Med2000;11(3):356-365Laux M, Abbott PV, Pajarola G, Nair PN. Apical inflammatory root resorption: a correlativeradiographic and histological assessment. Int Endod J. 2000;33(6):483-93.
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125Levin LG, Law AS, Holland GR, Abbott PV, Roda RS. Identify and Define All DiagnosticTerms for Pulpal Health and Disease States. J Endod 2009; 35(12):1645-57Mejàre IA, Axelsson S, Davidson T, Frisk F, Hakeberg M, Kvist T, Norlund A, Petersson A,Portenier A, Sandberg H, Tranæus S, Bergenholtz G. Diagnosis of the condition of the dentalpulp: a systematic review. Int Endod J 2012;45:597–613Ricucci D, Siqueira JF Jr. Biofilms and apical periodontitis: study of prevalence and associationwith clinical and histopathologic findings. Endod. 2010;36(8):1277-88Ricucci D, Siqueira JF Jr, Lopes WS, Vieira AR, Rôças IN. Extraradicular infection as the causeof persistent symptoms: a case series.J Endod. 2015 Feb;41(2):265-73.Sharav Y, Benoliel R. Acute orofacial pain. In: Orofacial pain and headache. 2nded.Quintessence; 2015Sjögren U, Happonen RP, Kahnberg K-E, Sundqvist G. Survival of Arachnia propionica inperiapical tissue. Int Endodont J1988;21:277-82The Dental Trauma Guide – an online evidence-based treatment guide produced in cooperationwith the Resource Centre for Rare Oral Diseases and Department of Oral and MaxillofacialSurgery, Copenhagen University Hospital. www.dentaltraumaguide.org/Tronstad L, Barnett F, Riso K, Slots J. Extraradicular endodontic infections. Endod DentTraumatol 1987;3(2):86-90Yoshida M, Fukushima H, Yamamoto K, Ogawa, K, Toda T, SagawaH. Correlation between clinical symptoms and microorganisms isolated from root canals of teethwith periapical pathosis. J Endod 1987;13(1)24-28(gingival pain)Akintoye SO, Greenberg MS. Recurrent aphthous stomatitis. Dent Clin North Am.2014;58(2):281-97
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126Al-Hashimi I, Schifter M, Lockhart PB, Wray D, Brennan M, Migliorati CA, et al. Oral lichenplanus and oral lichenoid lesions: diagnostic and therapeutic considerations. Oral Surg Oral MedOral Pathol Oral Radiol Endod. 2007;103 Suppl:S25 e1-12Andrade P, Brinca A, Goncalo M. Patch testing in fixed drug eruptions--a 20-year review.Contact Dermatitis. 2011;65(4):195-201Bascones-Martinez A, Garcia-Garcia V, Meurman JH, Quena-Caballero L. Immune-mediateddiseases: what can be found in the oral cavity? Int J Dermatol. 2015;54(3):25Batchelor JM, Todd PM. Allergic contact stomatitis caused by a polyether dental impressionmaterial. Contact Dermatitis. 2010;63(5):296-7Benedix F, Schilling M, Schaller M, Rocken M, Biedermann T. A young woman with recurrentvesicles on the lower lip: fixed drug eruption mimicking herpes simplex. Acta Derm Venereol.2008;88(5):491-4Calapai G, Miroddi M, Mannucci C, Minciullo P, Gangemi S. Oral adverse reactions due tocinnamon-flavoured chewing gums consumption. Oral Dis. 2014;20(7):637-43Carrozzo M, Togliatto M, Gandolfo S. Erythema multiforme. A heterogeneous pathologicphenotype]. Minerva Stomatol. 1999;48(5):217-26Farthing P, Bagan JV, Scully C. Mucosal disease series. Number IV. Erythema multiforme. OralDis. 2005;11(5):261-7Feller L, Altini M, Chandran R, Khammissa RA, Masipa JN, Mohamed A, Lemmer J. Noma(cancrum oris) in the South African context. J Oral Pathol Med. 2014 Jan;43(1):1-6Firth FA, Friedlander LT, Parachuru VP, Kardos TB, Seymour GJ, Rich AM. Regulation ofimmune cells in oral lichen planus. Arch Dermatol Res. 2015;307(4):333-9Fitzpatrick SG, Hirsch SA, Gordon Sc. The malignant transformation of oral lichen planus andoral lichenoid lesions: a systematic review. J Am Dent Assoc. 2014;145(1):45-56
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128Perusquia-Ortiz AM, Vazquez-Gonzalez D, Bonifaz A. Opportunistic filamentous mycoses:aspergillosis, mucormycosis, phaeohyphomycosis and hyalohyphomycosis. J Dtsch DermatolGes. 2012;10(9):611-21Raber-Durlacher JE, Elad S, Barasch A. Oral mucositis. Oral Oncol. 2010;46(6):452-6Rosenthal DI, Trotti A. Strategies for managing radiation-induced mucositis in head and neckcancer. Semin Radiat Oncol. 2009;19(1):29-34Savin JA. Current causes of fixed drug eruption in the UK. Br J Dermatol. 2001;145(4):667-8Scully C. Clinical practice. Aphthous ulceration. N Engl J Med. 2006;355(2):165-72Shiboski CH, Patton LL, Webster-Cyriaque JY, Greenspan D, Traboulsi RS, Ghannoum M, et al.The Oral HIV/AIDS Research Alliance: updated case definitions of oral disease endpoints. JOral Pathol Med. 2009;38(6):481-8Slebioda Z, Szponar E, Kowalska A. Recurrent aphthous stomatitis: genetic aspects of etiology.Postepy Dermatol Alergol. 2013;30(2):96-102Theander E, Jacobsson LT. Relationship of Sjögren's syndrome to other connective tissue andautoimmune disorders. Rheum Dis Clin North Am. 2008 Nov;34(4):935-47van der Waal I. Oral potentially malignant disorders: is malignant transformation predictable andpreventable? Med Oral Patol Oral cir Bucal. 2014;19(4):e386-90Venables ZC, Narayana K, Johnston GA. Two unusual cases of allergic contact stomatitis causedby methacrylates. Contact Dermatitis. 2016;74(2):126-7von Arx DP, Husain A. Oral tuberculosis. Br Dent J. 2001 Apr 28;190(8):420-2Warnakulasuriya S, Johnson NW, van der Waal I. Nomenclature and classification of potentiallymalignant disorders of the oral mucosa. J Oral Pathol Med. 2007;36(10):575-80Yuan A, Woo SB. Adverse drug events in the oral cavity.Oral Surg Oral Med Oral Pathol OralRadiol. 2015 Jan;119(1):35-47
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129(oral mucosal pain)Abdalla-Aslan R, Benoliel R, Sharav Y, Czerninski R. Characterization of pain originating fromoral mucosal lesions. Oral Surg Oral Med Oral Pathol Oral Radiol. 2016 Mar;121(3):255-61Akintoye SO, Greenberg MS. Recurrent aphthous stomatitis. Dent Clin North Am.2014;58(2):281-97 DOUBLEAl-Hashimi I, Schifter M, Lockhart PB, Wray D, Brennan M, Migliorati CA, et al. Oral lichenplanus and oral lichenoid lesions: diagnostic and therapeutic considerations. Oral Surg Oral MedOral Pathol Oral Radiol Endod. 2007;103 Suppl:S25 e1-12Andrade P, Brinca A, Goncalo M. Patch testing in fixed drug eruptions--a 20-year review.Contact Dermatitis 2011;65(4):195-201Bascones-Martinez A, Garcia-Garcia V, Meurman JH, Quena-Caballero L. Immune-mediateddiseases: what can be found in the oral cavity? Int J Dermatol. 2015;54(3):25 DOUBLEBatchelor JM, Todd PM. Allergic contact stomatitis caused by a polyether dental impressionmaterial. Contact Dermatitis 2010;63(5):296-7 DOUBLEBenedix F, Schilling M, Schaller M, Rocken M, Biedermann T. A young woman with recurrentvesicles on the lower lip: fixed drug eruption mimicking herpes simplex. Acta Derm Venereol.2008;88(5):491-4 DOUBLECalapai G, Miroddi M, Mannucci C, Minciullo P, Gangemi S. Oral adverse reactions due tocinnamon-flavoured chewing gums consumption. Oral Dis. 2014;20(7):637-43 DOUBLECarrozzo M, Togliatto M, Gandolfo S. Erythema multiforme. A heterogeneous pathologicphenotype. Minerva Stomatol. 1999;48(5):217-26 DOUBLEDuncan GG, Epstein JB, Tu D, et al. Quality of life, mucositis, and xerostomia fromradiotherapy for head and neck cancers: a report from the NCIC CTG HN2 randomized trial ofan antimicrobial lozenge to prevent mucositis. Head Neck. 2005;27(5):421–8
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130Farthing P, Bagan JV, Scully C. Mucosal disease series. Number IV. Erythema multiforme. OralDis. 2005;11(5):261-7Firth FA, Friedlander LT, Parachuru VP, Kardos TB, Seymour GJ, Rich AM. Regulation ofimmune cells in oral lichen planus. Arch Dermatol res. 2015;307(4):333-9Fitzpatrick SG, Hirsch SA, Gordon SC. The malignant transformation of oral lichen planus andoral lichenoid lesions: a systematic review. J Am Dent Assoc. 2014;145(1):45-56 DOUBLEFourie J, Boy SC. Oral mucosal ulceration - a clinician’s guide to diagnosis and treatment. SADJNovember 2016, Vol 71 no 10 p500 - p508 DOUBLEFukiwake N, Moroi Y, Urabe K, Ishii N, Hashimoto T, Furue M. Detection of autoantibodies todesmoplakin in a patient with oral erythema multiforme. Eur J Dermatol. 2007;17(3):238-41Gorouhi F, Davari P, Fazel N. Cutaneous and mucosal lichen planus: a comprehensive review ofclinical subtypes, risk factors, diagnosis, and prognosis. Scientific World Journal.2014;2014:742-826Gupta S, Gupta S, Mittal A, David S. Oral fixed drug eruption caused by gabapentin. J Eur AcadDermatol Venereol. 2009;23(10):1207-8 DOUBLEHarman KE, Albert S, Black MM. British Association Guidelines for the management ofpemphigus vulgaris. Br J Dermatol. 2003;149(5):926-37Hertel M, Matter D, Schmidt-Westhausen AM, Bornstein Oral syphilis: a series of 5 cases. JOral Maxillofac Surg. 2014;72(2):338-45)Jain P, Jain I. Oral Manifestations of tuberculosis: Step towards early Diagnosis. J Clin DiagnRes. 2014;8(12): ZE18-21 DOUBLEKhatibi M, Shakoorpour Ah, Jahromi ZM, Ahmadzadeh A. The prevalence of oral mucosallesions and related factors in 188 patients with systemic lupus erythematosus. Lupus.2012;21(12):1312-5 DOUBLE
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131Kind F, Scherer K, Bircher AJ. Allergic contact stomatitis to cinnamon in chewing gummistaken as facial angioedema. Allergy 2010;65(2):276-7Mravak-Stipetić M. Differential diagnostics of painful conditions of oral mucosa anticancertherapy. Rad 507. Medical Sciences, 34(2010):55-73 M.Perusquia-Ortiz AM, Vazquez-Gonzalez D, Bonifaz A. Opportunistic filamentous mycoses:aspergillosis, mucormycosis, phaeohyphomycosis and hyalohyphomycosis. J Dtsch DermatolGes. 2012;10(9):611-21 DOUBLERaber-Durlacher JE, Elad S, Barasch A. Oral mucositis. Oral Oncol. 2010;46(6):452-6 DOUBLERosenthal DI, Trotti A. Strategies for managing radiation-induced mucositis in head and neckcancer. Semin Radiat Oncol. 2009;19(1):29-34 DOUBLESaccucci M, Di Carlo G, Bossù M, Giovarruscio F, Salucci A, Polimeni A. AutoimmuneDiseases and Their Manifestations on Oral Cavity: Diagnosis and Clinical Management. JImmunol Res. 2018 May 27;2018:6061825 DOUBLESavin JA. Current causes of fixed drug eruption in the UK. Br J Dermatol. 2001;145(4):667-8DOUBLEScully C. ABC of oral health: mouth ulcers and other causes of orofacial soreness and pain. BritMed J. 2000;321:162-265Scully C. Clinical practice. Aphthous ulceration. N Engl J Med. 2006;355(2):165-72 DOUBLEShiboski CH, Patton LL, Webster-Cyriaque JY, Greenspan D, Traboulsi RS, Ghannoum M, et al.The Oral HIV/AIDS Research Alliance: updated case definitions of oral disease endpoints. JOral Pathol Med. 2009;38(6):481-8 DOUBLESlebioda Z, Szponar E, Kowalska A. Eecurrent aphthous stomatitis: genetic aspects of etiology.Postepy Dermatol Alergol. 2013;30(2):96-102 DOUBLE
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132Sonis ST, Elting LS, Keefe D, et al. Perspectives on cancer therapy-induced mucosal injury:pathogenesis, measurement, epidemiology, and consequences for patients. Cancer. 2004:100(9Suppl):1995-2025Theander E, Jacobsson LT. Relationship of Sjögren's syndrome to other connective tissue andautoimmune disorders. Rheum Dis Clin North Am. 2008 Nov;34(4):935-47 DOUBLETreister N, Sonis S. Mucositis: biology and management. Curr Opin Otolaryngol Head NeckSurg. 2007;15(2):123–9van der Waal I. Oral potentially malignant disorders: is malignant transformation predictable andpreventable? Med Oral Pathol Oral cir Bucal. 2014;19(4):e386-90 DOUBLEVenables ZC, Narayana K, Johnston GA. Two unusual cases of allergic contact stomatitis causedby methacrylates. Contact Dermatitis 2016;74(2):126-7 DOUBLEVera-Llonch M, Oster G, Ford CM, Lu J, Sonis S. Oral mucositis and outcomes of allogeneichematopoietic stem-cell transplantation in patients with hematologic malignancies. Support CareCancer. 2007;15(5):491–6von Arx DP, Husain A. Oral tuberculosis. Br Dent J. 2001;190(8):420-2 DOUBLEWarnakulasuriya S, Johnson NW, van der Waal I. Nomenclature and classification of potentiallymalignant disorders of the oral mucosa. J Oral Pathol Med. 2007;36(10):575-80 DOUBLEYuan A, Woo SB. Adverse drug events in the oral cavity. Oral Surg Oral Med Oral Pathol OralRadiol. 2015 Jan;119(1):35-47 DOUBLE(salivary gland pain)Bassim CW, Fassil H, Mays JW, Edwards D, Baird K, Steinberg SM, Cowen EW, Naik H,Datiles M, Stratton P, Gress RE, Pavletic SZ. Oral disease profiles in chronic graft versus hostdisease. J Dent Res. 2015;94:547–54.
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133Brook I. The bacteriology of salivary gland infections. Oral Maxillofac Surg Clin North Am.2009;21:269–74.Guzzo M, Locati LD, Prott FJ, Gatta G, McGurk M, Licitra L Major and minor salivary glandtumors. Crit Rev Oncol Hematol. 2010;74(2):134.Klein Hesselink EN, Brouwers AH, de Jong JR, van der Horst-Schrivers AN, Coppes RP,Lefrandt JD, Jager PL, Vissink A, Links TP. Effects of radioiodine treatment on salivary glandfunction in patients with differentiated thyroid carcinoma: a prospective study. J Nucl Med.2016;57:1685–91.Leerdam CM1, Martin HC, Isaacs D. Recurrent parotitis of childhood. J Paediatr ChildHealth. 2005 Dec;41(12):631-4.Napeñas JJ1, Rouleau TS. Oral complications of Sjögren's syndrome. Oral Maxillofac Surg ClinNorth Am. 2014 Feb;26(1):55-6.Shiboski SC, Shiboski CH, Criswell L et al. American College of Rheumatology classificationcriteria for Sjögren's syndrome: a data-driven, expert consensus approach in the Sjögren'sInternational Collaborative Clinical Alliance cohort. Arthritis Care Res (Hoboken). 2012Apr;64(4):475-87.Wilson KF, Meier JD, Ward PD. Salivary gland disorders. Am Fam Physician. 2014 Jun1;89(11):882-8.(bone tissue pain)Annibali S, Cristalli MP, Solidani M, et al. Langerhans cell histiocytosis: oral/periodontalinvolvement in adult patients. Oral Dis. 2009;15(8):596.Campanacci M, Baldini N, Boriani S, et al. Giant-cell tumor of bone. J Bone Joint Surg Am.1987;69(1):106.
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134Caparrotti F, Huang SH, Lu L, Bratman SV, et al. Osteoradionecrosis of the mandible in patientswith oropharyngeal carcinoma treated with intensity-modulated radiotherapy. Cancer.2017;123(19):3691. Epub 2017 Jun 13.Caputo ND, Raja A, Shields C, et al. Re-evaluating the diagnostic accuracy of the tongue bladetest: still useful as a screening tool for mandibular fractures? J Emerg Med. 2013 Jul;45(1):8-12.Epub 2013 Mar 13.Chopra S, Kamdar D, Ugur OE, et al. Factors predictive of severity of osteoradionecrosis of themandible. Head Neck. 2011;33(11):1600.Copley L, Dormans JP. Benign pediatric bone tumors. Evaluation and treatment. Pediatr ClinNorth Am. 1996;43(4):949.da Fonseca M1, Oueis HS, Casamassimo PS. Sickle cell anemia: a review for the pediatricdentist. Pediatr Dent. 2007 Mar-Apr;29(2):159-69.Daly B, Sharif MO, Newton T, et al. Local interventions for the management of alveolarosteitis (dry socket). Cochrane Database Syst Rev. 2012 Dec 12;12:CD006968.D'Ambrosio N, Soohoo S, Warshall C, et al. Craniofacial and intracranial manifestations oflangerhans cell histiocytosis: report of findings in 100 patients. AJR Am J Roentgenol.2008;191(2):589.Erdmann D, Follmar KE, Debruijn M, et al. A retrospective analysis of facial fracture etiologies.Ann Plast Surg. 2008;60(4):398.Gabrielli E, Fothergill AW, Brescini L, Sutton DA, Marchionni E, Orsetti E, StaffolaniS, Castelli P, Gesuita R, Barchiesi F.Osteomyelitis caused by Aspergillus species: a review of310 reported cases. Clin Microbiol Infect. 2014 Jun;20(6):559-65.Grabowski GA, Andria G, Baldellou A, et al. Pediatric non-neuronopathic Gaucher disease:presentation, diagnosis and assessment. Consensus statements. Eur J Pediatr. 2004;163(2):58.Epub 2003 Dec 16.
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135Grabowski GA. Recent clinical progress in Gaucher disease. Curr Opin Pediatr. 2005;17(4):519.Greenspan A. Benign bone-forming lesions: osteoma, osteoid osteoma, and osteoblastoma.Clinical, imaging, pathologic, and differential considerations. Skeletal Radiol. 1993;22(7):485Gupta S, Sreenivasan V, Patil PB. Dental complications of herpes zoster: Two case reports andreview of literature. Indian J Dent Res 2015;26:214-9.Jones AC, Prihoda TJ, Kacher JE, et al. Osteoblastoma of the maxilla and mandible: a report of24 cases, review of the literature, and discussion of its relationship to osteoid osteoma ofthe jaws. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006 Nov;102(5):639-50Kyle RA, Gertz MA, Witzig TE, et al. Review of 1027 patients with newly diagnosed multiplemyeloma. Mayo Clin Proc. 2003;78(1):21.Mirabello L, Troisi RJ, Savage SA. Osteosarcoma incidence and survival rates from 1973 to2004: data from the Surveillance, Epidemiology, and End Results Program. Cancer.2009;115(7):1531.Nilesh K, Vande AV. Mucormycosis of maxilla following tooth extraction in immunocompetentpatients: Reports and review. Clin Exp Dent. 2018 Mar 1;10(3):e300-e305.Platt OS, Thorington BD, Brambilla DJ, et al. Pain in sickle cell disease. Rates and risk factors.N Engl J Med. 1991;325(1):11.Prasad KC, Prasad SC, Mouli N, et al. Osteomyelitis in the head and neck. Acta Otolaryngol.2007;127(2):194.Ruggiero SL, Dodson TB, Fantasia J, et al. American Association of Oral and MaxillofacialSurgeons. American Association of Oral and Maxillofacial Surgeons position paper onmedication-related osteonecrosis of the jaw: 2014 update. J Oral MaxillofacSurg. 2014;72(10):1938-56.Sharif MO, Dawoud BE, Tsichlaki A, et al. Interventions for the prevention of dry socket: anevidence-based update. Br Dent J. 2014 Jul 11;217(1):27-30.
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136van Staa TP, Selby P, Leufkens HG, et al. Incidence and natural history of Paget's disease ofbone in England and Wales. J Bone Miner Res. 2002 Mar;17(3):465-71.Wyers MR. Evaluation of pediatric bone lesions. Pediatr Radiol. 2010;40(4):468.Yildiz C, Erler K, Atesalp AS, et al. Benign bone tumors in children. Curr Opin Pediatr.2003;15(1):58.Zou H, Yang H, Zou Y, Lei L, Song LPrimary diffuse large B-cell lymphoma in the maxilla: Acase report. Medicine (Baltimore). 2018 May;97(20):e107072. Orofacial pain associated with regional musclesGeneral commentsTemporomandibular disorders (TMD) is a term used to describe a number of painful and non-painful disorders affecting the muscles of mastication, the temporomandibular joint andcontiguous structures. The Diagnostic Criteria for Temporomandibular disorders (DC/TMD)published by INfORM are reliable and universally accepted (Schiffman et al., 2014, Peck et al.2014). Nevertheless, controversy remains regarding terminology of chronic muscle pain. TheDC/TMD (1) uses “myalgia” and “myofascial pain” and other suggestions have been e.g.“persistent orofacial muscle pain” (2). We here propose to use the overarching label “orofacialpain associated with regional muscles” and for the specific diagnosis listed below to adhere tothe term “myofascial” in recognition of the lack of concrete evidence to link pain to specificstructures or tissues in the muscle. The same caution is noted in the overarching label by the useof the word “associated”. Furthermore, the term TMD is being maintained to align with theDC/TMD diagnosis.Diagnostic criteria2.1. Primary myofascial pain2.1.1. Acute primary myofascial painDiagnostic criteria
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137A. Single or repeated days of myofascial pain occurring within the past 3 months andfulfilling criteria B-DB. Lasting from at least 2 hours daily to days, or unremittingC. Positive for both of the following41. Pain in the jaw, temple, in the ear or in front of ear2. Pain modified with jaw movement, function or parafunctionD. Positive for both of the following51. Confirmation of pain location(s) in the temporalis or masseter muscle(s)2. Report of familiar pain in the temporalis or masseter muscle(s) with at leastone of the following provocation tests: Palpation of the temporalis or massetermuscle(s) OR maximum unassisted or assisted opening movement(s)E. Not better accounted for by another ICOP or ICHD-3 diagnosis.2.1.2. Chronic primary myofascial pain2.1.2.1. Chronic infrequent primary myofascial painDiagnostic criteriaA. At least 10 episodes of myofascial pain occurring on <1 1-14="" 10="" 1382.="" 138="" 2="" accounted="" and2.="" and="" another="" assisted="" at="" average="" b-db.="" better="" both="" by="" chronic="" confirmation="" criteria="" criteriaa.="" daily="" day="" days="" diagnosis.2.1.2.2.="" ear="" episodes="" familiar="" following1.="" following="" for="" frequent="" from="" front="" fulfilling="" function="" hours="" ichd-3="" icop="" in="" jaw="" lasting="" least="" leastone="" location="" masseter="" massetermuscle="" maximum="" modified="" monthon="" monthonaverage="" movement="" muscle="" myofascial="" not="" occurring="" of="" opening="" or="" page="" pain2.1.2.2.1.="" pain="" palpation="" parafunctiond.="" per="" positive="" primary="" provocation="" referraldiagnostic="" report="" s="" temple="" temporalis="" tests:="" the="" to="" unassisted="" unremittingc.="" with="" without="" year=""> 3 months (>12 and < 180 days per year) and fulfilling criteria B-DB. Lasting from at least 2 hours daily to days, or unremittingC. Positive for both of the following1. Pain in the jaw, temple, in the ear or in front of ear AND2. Pain modified with jaw movement, function or parafunctionD. Positive for both of the following1. Confirmation of pain location(s) in the temporalis or masseter muscle(s) AND2. Report of familiar pain in the temporalis or masseter muscle(s) with at leastone of the following provocation tests: Palpation of the temporalis or massetermuscle(s) OR maximum unassisted or assisted opening movement(s)E. Not better accounted for by another ICOP or ICHD-3 diagnosis.2.1.2.2.2. Chronic frequent primary myofascial pain with pain referralDiagnostic criteriaA. Myofascial pain occurring with at least 10 episodes and 1-14 days permonth on average for > 3 months (>12 and < 180 days per year) and fulfilling
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139criteria B-DB. Lasting from at least 2 hours daily to days, or unremittingC. Positive for both of the following1. Pain in the jaw, temple, in the ear or in front of ear AND2. Pain modified with jaw movement, function or parafunctionD. Positive for all of the following1. Confirmation of pain location(s) in the temporalis or masseter muscle(s) AND2. Report of familiar pain with palpation of the temporalis or masseter muscle(s)AND3. Report of pain at a site beyond the boundary of the muscle being palpatedE. Not better accounted for by another ICOP or ICHD-3 diagnosis.2.1.2.3. Chronic persistent primary myofascial pain2.1.2.3.1 Chronic persistent primary myofascial pain without pain referralDiagnostic criteriaA. Myofascial pain occurring on >15 days per month on average for >3months (>180 days per year), fulfilling criteria B-DB. Lasting from at least 2 hours daily to days, or unremittingC. Positive for both of the following1. Pain in the jaw, temple, in the ear or in front of ear AND2. Pain modified with jaw movement, function or parafunctionD. Positive for both of the following1. Confirmation of pain location(s) in the temporalis or masseter muscle(s) AND
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1402. Report of familiar in the temporalis or masseter muscle(s) with at least one ofthe following provocation tests: Palpation of the temporalis or massetermuscle(s) OR maximum unassisted or assisted opening movement(s)E. Not better accounted for by another ICOP or ICHD-3 diagnosis.2.1.2.3.2. Chronic persistent primary myofascial pain with pain referralDiagnostic criteriaA. Myofascial pain occurring on >15 days per month on average for >3months (>180 days per year), fulfilling criteria B-DB. Lasting from at least 2 hours daily to days, or unremittingC. Positive for both of the following1. Pain in the jaw, temple, in the ear or in front of ear AND2. Pain modified with jaw movement, function or parafunctionD. Positive for all of the following:1. Confirmation of pain location(s) in the temporalis or masseter muscle(s) AND2. Report of familiar pain with palpation of the temporalis or masseter muscle(s)AND3. Report of pain at a site beyond the boundary of the muscle being palpatedE. Not better accounted for by another ICOP or ICHD-3 diagnosis.2.2. Secondary myofascial painDescriptionMyofascial pain attributed to persistent inflammation (due to e.g. infection, crystal deposition orautoimmune disorders), structural changes (such as osteoarthritis or spondylosis), injury, ordiseases of the nervous system.Diagnostic criteria
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141A. Any myofascial pain according to 2.1.1-4 and fulfilling criterion CB. The parent disorder meets its respective diagnostic criteriaC. Evidence of causation demonstrated by at least two of the following:1. Myofascial pain has developed, or substantially worsened, in temporalrelation to the onset of the presumed causative disorder2. Myofascial pain has significantly worsened in parallel with progression of thepresumed causative disorder3. Myofascial pain has significantly improved or resolved in parallel withimprovement in or resolution of the presumed causative disorderD. Not better accounted for by another ICOP or ICHD-3 diagnosis.2.2.1 Secondary myofascial pain due to tendonitisDiagnostic criteriaA. Myofascial pain of tendon origin occurring in any masticatory muscle during the last30 days fulfilling criteria B-DB. Evidence of causation demonstrated by at least two of the following:1. Myofascial pain has developed in temporal relation to onset of tendonitis2. Myofascial pain has significantly worsened in parallel with progression oftendonitis3. Myofascial pain has significantly improved or resolved in parallel withimprovement in or resolution of of tendonitisC. Positive for all of the following1. Pain in the jaw, temple, in the ear or in front of ear2. Pain modified with jaw movement, function or parafunction3. Confirmation of pain location(s) in the affected muscle
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1424. Report of familiar pain with at least one of the following provocation tests:Palpation of the affected tendon OR maximum unassisted or assisted openingmovement(s)D. Not better accounted for by another ICOP or ICHD-3 diagnosis.2.2.2 Secondary myofascial pain due to myositisDiagnostic criteriaA. Myofascial pain occurring in any masticatory muscle during the last 30 days fulfillingcriteria B-EB. Evidence of causation demonstrated by at least two of the following:1. Myofascial pain has developed in temporal relation to onset of inflammation,infection or trauma2. Myofascial pain has significantly worsened in parallel with progression ofinflammation, infection or trauma3. Myofascial pain has significantly improved or resolved in parallel withimprovement in or resolution of inflammation, infection or traumaC. Positive for all of the following1. Pain in the jaw, temple, in the ear or in front of ear2. Pain modified with jaw movement, function or parafunction3. Confirmation of pain location(s) in the affected muscle(s)4. Report of familiar pain in the muscle with at least one of the followingprovocation tests: Palpation of the muscle OR maximum unassisted or assistedopening movement(s)5. Presence of edema, erythema, and/or increased temperature over the muscleD. Serologic tests may reveal elevated enzyme levels (e.g., creatine kinase), markers ofinflammation and the presence of autoimmune diseases.
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143E. Not better accounted for by another ICOP or ICHD-3 diagnosis.2.2.3 Secondary myofascial pain due to muscle spasmDiagnostic criteriaA. Myofascial pain occurring in any masticatory muscle during the last 30 days fulfillingcriteria BEB. Evidence of causation demonstrated by at least two of the following:1. Myofascial pain has developed in immediate temporal relation to onset ofspasm2. Myofascial pain has significantly worsened in parallel with progression ofspasm3. Myofascial pain has significantly improved or resolved in parallel withimprovement in or resolution of spasmC. Positive for all of the following1. Pain in the jaw, temple, in the ear or in front of ear2. Pain modified with jaw movement, function or parafunction3. Confirmation of pain location(s) in the affected muscle(s)4. Report of familiar pain in the affected muscle with at least one of thefollowing provocation tests: Palpation of muscle OR maximum unassisted orassisted opening movement(s)5. Limited range of jaw motion in direction that elongates affected muscle; (i.efor jaw closing muscles, opening will be limited to <40 1-14="" 10="" 144="" 144e.="" 145="" 145implications="" 146="" 146references1.schiffman="" 147="" 147arthralgia.="" 148="" 148a.="" 1493.="" 149="" 1="" 2011="" 2014="" 2015="" 2017="" 2="" 3="" 5="" 5s="" a="" aboutthe="" absence="" accepted="" according="" accounted="" aclassification="" activity="" acute="" addition="" adhere="" al.="" all="" also="" alsobe="" alstergren="" although="" anatomicalstructure.="" and="" anderson="" andmasseter="" another="" appear="" appears="" applicable="" applications:recommendations="" applied="" are="" area="" around="" arthralgia3.1.1.="" arthralgia3.1.2.1.="" arthralgia3.1.2.2.1.="" arthralgia="" arthralgiadiagnostic="" arthritis="" as="" assisted="" associated="" asuda="" at="" attributed="" aul="" average="" aziz="" b-db.="" b="" baad-hansen="" barke="" based="" be="" beapplied="" because="" been="" being="" 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generalprinciples="" giamberardino="" gm="" go="" goldberg="" good="" goulet="" greenbergm="" group.="" group="" has="" hasextensive="" have="" haythornthwaite="" he="" headache="" headaches.="" heir="" higher="" highly="" hollender="" homme="" hopefully="" hours.="" hours1daily="" however="" i.e.="" iasp="" icd-11.="" ichd-3="" icholas="" icop="" idiopathic="" if="" ifthere="" iida="" implemented="" implications.whereas="" implies="" importance="" important="" in="" include="" included.="" indeedbe="" individuals="" infavor="" infection.="" inflammatoryprocesses="" infrequent="" inhealthy="" innerup="" instead="" instructions="" interest="" international="" into="" intothe="" intramuscular="" ipsilateral="" is="" isemphasized="" isperceived="" it="" j-p="" j="" jan="" jaw="" jawmuscles="" jensen="" john="" jointdisease="" jp="" jw="" kaasa="" katz="" kawara="" keepthe="" kg="" klasser="" know="" known="" komiyama="" kosek="" l="" laat="" laid="" lasting="" lateral="" 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researchtopics="" respect="" restricted="" restriction.="" restriction="" reveal="" rief="" right="" rimary="" s.l="" s="" same="" sameprinciples="" scale="" schiffman="" scholz="" schug="" secondary="" seconds="" sensations="" sensitivity="" sensitize="" separate="" sf.="" short="" should="" show="" showselevated="" significance="" significantknowledge="" single="" sirois="" site="" sj.="" smith="" solid="" some="" specific="" specificetiology="" specificity="" spread="" stage="" standardization="" standardized="" stimulus="" strong="" studies.in="" studies="" sub-diagnoses="" subdivide="" subgroups="" subluxation="" substantial="" such="" sufficient="" suggested="" suggestion="" support.="" support="" svensson="" swallowingmuscles.="" systemic="" t.="" t="" taxonomy="" temporal="" temporalis="" temporalsum="" temporomandibular="" temporomandibulardisorders="" tension-type="" term="" terms="" tests:a.="" than="" that="" thattreatment="" the="" theclinician="" thediagnostic="" 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Lasting from at least 2 hours1daily to days, or unremittingC. All of the following characteristics:1. Pain in front of the ear, or in the ear2. Pain modified with jaw movement, function or parafunction.3. Examiner confirmation of pain location in the area of the TMJ(s).4. Report of familiar pain in the TMJ with at least one of the following provocation tests:a. Palpation of the lateral pole or around the lateral poleb. Maximum unassisted or assisted opening, right or left lateral movements, orprotrusive movements
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150c. pain with TMJ palpation with pain localized to the immediate site of thepalpationD. Not better accounted for by another ICOP or ICHD-3 diagnosis.Comment1The pain does not have to be continuous for at least 2 hours. This could be also the temporalsum of episodes that may occur during the day.3.1.2.2.2. Chronic frequent primary TMJ arthralgia with referred painDiagnostic criteriaA. TMJ pain occurring with at least 10 episodes and 1-14 days per month on average for > 3months (>12 and < 180 days per year) and fulfilling criteria B-DB. Lasting from at least 2 hours1daily to days, or unremittingC. All of the following characteristics:1. Pain in front of the ear, or in the ear2. Pain modified with jaw movement, function or parafunction.3. Examiner confirmation of pain location in the area of the TMJ(s).4. Report of familiar pain in the TMJ with at least one of the following provocation tests:a. Palpation of the lateral pole or around the lateral poleb. Maximum unassisted or assisted opening, right or left lateral movements, orprotrusive movementsc. pain with TMJ palpation beyond the location of the TMJD. Not better accounted for by another ICOP or ICHD-3 diagnosis.Comment
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1511The pain does not have to be continuous for at least 2 hours. This could be also the temporalsum of episodes that may occur during the day.3.1.2.3. Chronic persistent primary TMJ arthralgia3.1.2.3.1. Chronic persistent primary TMJ arthralgia without referred painDiagnostic criteriaA.TMJ pain occurring on >15 days per month on average for >3 months (>180 days per year),fulfilling criteria B-DB. Lasting from at least 2 hours1daily to days, or unremittingC. All of the following characteristics:1. Pain in front of the ear, or in the ear2. Pain modified with jaw movement, function or parafunction.3. Examiner confirmation of pain location in the area of the TMJ(s).4. Report of familiar pain in the TMJ with at least one of the following provocation tests:a. Palpation of the lateral pole or around the lateral poleb. Maximum unassisted or assisted opening, right or left lateral movements, orprotrusive movementsc. pain with TMJ palpation with pain localized to the immediate site of thepalpationD. Not better accounted for by another ICOP or ICHD-3 diagnosis.Comment1The pain does not have to be continuous for at least 2 hours. This could be also the temporalsum of episodes that may occur during the day.3.1.2.3.2. Chronic persistent primary TMJ arthralgia with referred painDiagnostic criteria
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152A.TMJ pain occurring on >15 days per month on average for >3 months (>180 days per year),fulfilling criteria B-DB. Lasting from at least 2 hours1daily to days, or unremittingC. All of the following characteristics:1. Pain in front of the ear, or in the ear2. Pain modified with jaw movement, function or parafunction.3. Examiner confirmation of pain location in the area of the TMJ(s).4. Report of familiar pain in the TMJ with at least one of the following provocation tests:a. Palpation of the lateral pole or around the lateral poleb. Maximum unassisted or assisted opening, right or left lateral movements, orprotrusive movementsc. pain with TMJ palpation beyond the location of the TMJD. Not better accounted for by another ICOP or ICHD-3 diagnosis.Comment1The pain does not have to be continuous for at least 2 hours. This could be also the temporalsum of episodes that may occur during the day.3.2. Secondary TMJ arthralgiaDescriptionTMJ pain attributed to persistent inflammation (due to e.g. trauma, infection, crystal depositionor autoimmune disorders), sensitization of the tissues, structural changes (such as osteoarthrosis,disc displacement or subluxation), injury or diseases of the nervous system.Diagnostic criteriaA. Any TMJ arthralgia according to 3.1.1-2 and fulfilling criteria C-DB. The parent disorder1meets its respective diagnostic criteria2C. Evidence of causation demonstrated by at least two of the following:
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1531. TMJ pain has developed in temporal relation to the onset or substantial worsening of thepresumed causative disorder2. TMJ pain has significantly worsened in parallel with progression of the presumedcausative disorder3. TMJ pain has significantly improved or resolved in parallel with improvement in orresolution of the presumed causative disorderD. Not better accounted for by another ICOP OR ICHD-3 diagnosis.3.2.1. TMJ arthralgia attributed to arthritisDiagnostic criteriaA. TMJ pain occurring the last 30 days fulfilling criteria B-E
B. Probable TMJ arthritis diagnosis2by fulfilling both of the following:1. TMJ pain on maximum mouth opening2. Contralateral laterotrusion < 8 mmC. If TMJ arthritis is to be associated with a systemic inflammatory condition,evidence of association demonstrated by at least two of the following:1. TMJ pain has developed in close temporal relation to other symptomsand/or clinical or biological signs of onset of the systemic inflammatorycondition or has led to the diagnosis of the condition2. Either or both of the following:a. TMJ pain has significantly worsened in parallel with worseningof the conditionb. TMJ pain has significantly improved or resolved with treatmentof the conditionD. All of the following characteristics:
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1541. Pain in the jaw, temple, in front of the ear, or in the ear2. Pain modified with jaw movement, function or parafunction3. Confirmation of pain location in the area of the TMJ(s)4. Report of familiar pain in the TMJ with at least one of the followingprovocation tests:a. Palpation of the lateral pole or around the lateral pole
b. Maximum unassisted or assisted opening, right or left lateralmovements, or protrusive movementsE. Not better accounted for by another ICOP or ICHD-3 diagnosisNote2Alstergren et al. 20183.2.1.1. TMJ arthralgia attributed to arthritis, non-systemicDiagnostic criteriaA. TMJ pain occurring the last 30 days fulfilling criteria B-D
B. Positive for “3.2.1 TMJ arthralgia attributed to arthritis”C. Rheumatologic consultation, when needed, negative for rheumatologic diseaseD. Not better accounted for by another ICOP or ICHD-3 diagnosis3.2.1.2. TMJ arthralgia attributed to arthritis, systemicDiagnostic criteriaA. TMJ pain occurring the last 30 days fulfilling criteria B-D
B. Positive for “3.2.1 TMJ arthralgia attributed to arthritis”C. Rheumatologic diagnosis of a systemic inflammatory joint disease
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155D. Not better accounted for by another ICOP or ICHD-3 diagnosis3.2.2. TMJ arthralgia attributed to disc displacement with reductionDiagnostic criteriaA. TMJ pain occurring the last 30 days fulfilling criteria C-E
B. TMJ disc displacement with reduction has been diagnosed by fulfilling thefollowing:1. Positive for at least one of the following:a. In the last 30 days any TMJ noise(s) present with jaw movementor functionb. Patient report of any noise present during the examination2. Positive for at least one of the following:a. Clicking, popping and/or snapping noise detected during bothopening and closing, with palpation during at least 1 of 3repetitions of jaw opening and closingORb1. Clicking, popping and/or snapping noise detected withpalpation during at least 1 of 3 repetitions of opening or closingANDb2. Clicking, popping and/or snapping noise detected withpalpation during at least 1 of 3 repetitions of right or left lateralmovements, or protrusive movementsC. Evidence of association demonstrated by at least two of the following:1. TMJ pain has developed in close temporal relation to onset of the disc
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156displacement or has led to the diagnosis of the condition2. TMJ pain present exactly when the clicking sound occurs3. Either or both of the following:a. TMJ pain has significantly worsened in parallel with worsening of theconditionb. TMJ pain has significantly improved or resolved with treatment of theconditionD. All of the following characteristics:
1. Pain in the jaw, temple, in front of the ear, or in the ear2. Pain modified with jaw movement, function or parafunction3. Confirmation of pain location in the area of the TMJ(s)4. Report of familiar pain in the TMJ with at least one of the followingprovocation tests:a. Palpation of the lateral pole or around the lateral pole
b. Maximum unassisted or assisted opening, right or left lateralmovements, or protrusive movementsE. Not better accounted for by another ICOP or ICHD-3 diagnosis.3.2.3. TMJ arthralgia attributed to disc displacement with reduction with intermittent lockingDiagnostic criteriaA. TMJ pain occurring the last 30 days fulfilling criteria C-E
B. TMJ disc displacement with reduction with intermittent locking has beendiagnosed by fulfilling the following:1. Positive for at least one of the following:
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157a. In the last 30 days any TMJ noise(s) present with jaw movementor functionb. Patient report of any noise present during the examination2. In the last 30 days, jaw locks with limited mouth opening, even for amoment, and then unlocks.3. Positive for at least one of the following:a. Clicking, popping and/or snapping noise detected during bothopening and closing, with palpation during at least 1 of 3repetitions of jaw opening and closingORb1. Clicking, popping and/or snapping noise detected withpalpation during at least 1 of 3 repetitions of opening or closingANDb2. Clicking, popping and/or snapping noise detected withpalpation during at least 1 of 3 repetitions of right or left lateralmovements, or protrusive movementsC. Evidence of association demonstrated by at least two of the following:1. TMJ pain has developed in close temporal relation to onset of the discdisplacement or has led to the diagnosis of the condition2. TMJ pain present exactly when the clicking sound occurs3. Either or both of the following:a. TMJ pain has significantly worsened in parallel with worseningof the conditionb. TMJ pain has significantly improved or resolved with treatment
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158of the conditionD. All of the following characteristics:
1. Pain in the jaw, temple, in front of the ear, or in the ear2. Pain modified with jaw movement, function or parafunction.3. Confirmation of pain location in the area of the TMJ(s)4. Report of familiar pain in the TMJ with at least one of the followingprovocation tests:a. Palpation of the lateral pole or around the lateral pole
b. Maximum unassisted or assisted opening, right or left lateralmovements, or protrusive movementsE. not better accounted for by another ICOP OR ICHD-3 diagnosis.3.2.4. TMJ arthralgia attributed to disc displacement without reductionDiagnostic criteriaA. TMJ pain occurring the last 30 days fulfilling criteria C-E
B. TMJ disc displacement without reduction has been diagnosed by fulfilling thefollowing:1. Jaw locked or caught so that the mouth would not open all the way2. Limitation in jaw opening severe enough to limit jaw opening andinterfere with ability to eat.C. Evidence of association demonstrated by either or both of the following:1. TMJ pain has significantly worsened in parallel with worsening of thecondition2. TMJ pain has significantly improved or resolved with treatment of the
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159conditionD. All of the following characteristics:
1. Pain in the jaw, temple, in front of the ear, or in the ear2. Pain modified with jaw movement, function or parafunction3. Confirmation of pain location in the area of the TMJ(s)4. Report of familiar pain in the TMJ with at least one of the followingprovocation tests:a. Palpation of the lateral pole or around the lateral pole
b. Maximum unassisted or assisted opening, right or left lateralmovements, or protrusive movementsE. Not better accounted for by another ICOP or ICHD-3 diagnosis3.2.5. TMJ arthralgia attributed to degenerative joint diseaseDiagnostic criteriaA. TMJ pain occurring the last 30 days fulfilling criteria C-E
B. TMJ degenerative joint disease has been diagnosed by fulfilling the following:1. Positive for at least one of the following:a. In the last 30 days any TMJ noise(s) present with jaw movementor functionb. Patient report of any noise present during the examination2. Crepitus detected with palpation during maximum unassisted opening,maximum assisted opening, lateral, or protrusive movementsC. Evidence of association demonstrated by either or both of the following:1. TMJ pain has significantly worsened in parallel with worsening of the
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160condition2. TMJ pain has significantly improved or resolved with treatment of theconditionD. All of the following characteristics:
1. Pain in the jaw, temple, in front of the ear, or in the ear2. Pain modified with jaw movement, function or parafunction.3. Confirmation of pain location in the area of the TMJ(s)4. Report of familiar pain in the TMJ with at least one of the followingprovocation tests:a. Palpation of the lateral pole or around the lateral pole
b. Maximum unassisted or assisted opening, right or left lateralmovements, or protrusive movementsE. Not better accounted for by another ICOP or ICHD-3 diagnosis3.2.6. TMJ arthralgia attributed to subluxationDiagnostic criteriaA. Fulfills criteria for 3.1 TMJ arthralgia as well as criteria C-F
B. Positive for both of the following:1. In last 30 days, jaw locking or catching in a wide open mouth position,even for a moment, so could not close from the wide-open position2. Inability to close the mouth without a specific manipulative maneuverC. Although no exam findings are required, when this disorder is presentclinically, examination is positive for:1. Inability to return to a normal closed mouth position without the patient
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161performing a specific manipulative maneuverD. evidence of association demonstrated by either or both of the following:1. TMJ arthralgia has significantly worsened in parallel with worsening ofthe condition2. TMJ arthralgia has significantly improved or resolved with treatment ofthe conditionE. All of the following characteristics:
1. Pain in the jaw, temple, in front of the ear, or in the ear2. Pain modified with jaw movement, function or parafunction.3. Confirmation of pain location in the area of the TMJ(s)4. Report of familiar pain in the TMJ with at least one of the followingprovocation tests:a. Palpation of the lateral pole or around the lateral pole
b. Maximum unassisted or assisted opening, right or left lateralmovements, or protrusive movementsF. Not better accounted for by another ICOP or ICHD-3 diagnosisComments1Parent disorder can be inflammatory conditions, mechanical impingements, articular tissuesensitization (of peripheral and/or central genesis) that may contribute to TMJ pain diagnosed byadequate diagnostic criteria.2For diagnostic criteria regarding TMJ arthritis, see Alstergren et al. 2018 (1). For diagnosticcriteria regarding disc displacement with reduction, disc displacement with reduction withintermittent locking, disc displacement without reduction with limited mouth opening, discdisplacement without reduction without limited mouth opening, degenerative joint disease andsubluxation, see the DC/TMD definitions in Schiffman et al. 2014 (2).
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162The temporal distinction of TMJ arthralghia is novel to the DC/TMD but follows the generalprinciples from ICHD-3 for tension-type headaches. The same criteria with regard to episodefrequency have been implemented in the current classification. While there may be debates aboutthe clinical significance of infrequent TMJ arthralgia there appears to be solid evidence in favorto separate more frequently occurring pain conditions from less frequently occurring painconditions. Future studies using the proposed temporal distinction between TMJ arthralgia mayreveal the therapeutic implications.Foot notesIt is widely recognized and accepted that both acute and chronic types of TMJ pains can beassociated with the clinical phenomenon of pain referral, i.e., pain is perceived at a different sitethan the origin of the nociceptive or noxious stimulus (3). The pathophysiological significance ofthis remains unclear as well as do the therapeutic implications (4); however, from a diagnosticpoint of view it remains clinically important to distinguish pain referrals from local pains. As aconsequence, TMJ arthralgia diagnoses can be divided into two categories based on the presenceor absence of pain referral during palpation. The DC/TMD alo operates with a category of painspread which in contrast to pain referral remains within the boundary of the anatomical structure.For further research purposes the specific criteria for TMJ arthralgia with pain spread accordingto the DC/TMD can be applied, if needed.Based on the IASP classification of chronic pain conditions (5), there is a distinction betweenprimary and secondary pain conditions. Primary pain conditions mean that the specific etiologyor cause cannot be determined, i.e., they are idiopathic although significant knowledge may existto their pathophysiological mechanisms. Secondary pain conditions mean that the pain conditionis secondary or attributed to a known medical condition or cause. Based on these definitions theproposed category of acute TMJ arthralgia may indeed be a secondary TMJ pain condition due toacute nociceptive and inflammatory processes in the TMJ caused by a mechanical, chemicaltrauma or infection. The infrequent, frequent and more frequently occurring TMJ arthralgiaconditions (3.2. - 3.4.) may fit into the primary pain category.References
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1631. Alstergren P, Pigg M, Kopp S. Clinical diagnosis of temporomandibular joint arthritis. J OralRehabil. 2018 Apr;45(4):269-2812. Schiffman E, Ohrbach R, Truelove E, Look J, Anderson G, Goulet J-P, List T, Svensson P,Gonzalez Y, Lobbezoo F, Michelotti A, Brooks S.L, Ceusters W, Drangsholt M, Ettlin D,Gaul C, Goldberg L, Haythornthwaite J, Hollender L, Jensen R, John MT, de Laat A,deLeeuw R, Maixner W, van der Meulen M, Murray GM, Nixdorf DR, Palla S, Petersson A,Pionchon P, Smith B, Visscher CM, Zakrzewska J, Dworkin SF. Diagnostic Criteria forTemporomandibular Disorders (DC/TMD) for Clinical and Research Applications:Recommendations of the International RDC/TMD Consortium Network and Orofacial PainSpecial Interest Group. J Oral Facial Pain Headache 2014;28:6-27.3. Masuda M, Iida T, Exposto FG, Baad-Hansen L, Kawara M, Komiyama O, Svensson P.Referred pain and sensations evoked by standardized palpation of the masseter muscle inhealthy participants. J Oral Facial Pain Headache 2017 (In press).4. Svensson P, Michelotti A, Lobbezoo F, List T. The many faces of persistent orofacial musclepain. J Oral Facial Pain Headache 2015;29:207-208.5. Treede RD, Rief W, Barke A, Aziz Q, Bennett MI, Benoliel R, Cohen M, Evers S, FinnerupNB, First MB, Giamberardino MA, Kaasa S, Kosek E, Lavandʼhomme P, Nicholas M, PerrotS, Scholz J, Schug S, Smith BH, Svensson P, Vlaeyen JW, Wang SJ. A classification ofchronic pain for ICD-11. Pain 2015;156:1003-1007.4. Orofacial pain associated with lesion/disorders of the cranial nerves and other regionalnerve structuresGeneral commentsThis section is based in large part on ICHD-3 and IASP/ICD11. Some small changes have beenmade. Idiopathic conditions, i.e., Persistent Idiopathic Facial Pain and Burning Mouth Syndromehave been placed in the section dealing with idiopathic pain, as there is not yet sufficientevidence to support that these are unequivocally neuropathic pain. In certain disorders we haveused the term ‘neuropathic pain’ in preference to ‘painful neuropathy’ to comply with theIASP/ICD11 criteria. The ICHD-3 would support the latter but much of the pain literature andthe IASP/ICD11 is shifting to the use of ‘neuropathic pain’. Those conditions in chapter 13 of
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164the ICHD-3, where pain is present outside the orofacial region, are only mentioned in the ICOPand the readers are referred to the ICHD-3 for specific criteria.4.1. Pain attributed to a lesion or disease of the trigeminal nerve4.1.1. Trigeminal neuralgiaDescriptionA disorder characterized by recurrent unilateral brief electric shock-like pains, abrupt in onsetand termination, limited to the distribution of one or more divisions of the trigeminal nerve andtriggered by innocuous stimuli. It may develop without apparent cause or be a result of anotherdisorder. Additionally, there may or may not be concomitant continuous pain of moderateintensity within the affected division(s).Previously used termsTic douloureux, primary trigeminal neuralgiaDiagnostic criteriaA. Recurrent paroxysms of unilateral facial pain in the distribution(s) of one or moredivision of the trigeminal nerve, with no radiation beyond1, and fulfilling criteria B and CB. The pain has all of the following characteristics:1. Lasting from a fraction of a second to 2 minutes22. Severe intensity33. Electric shock-like, shooting, stabbing or sharp in qualityC. Precipitated by innocuous stimuli within the affected trigeminaldistribution4D. Not better accounted for by another ICOP or ICHD-3 diagnosis.Notes1In a few patients pain may radiate to another division, but remains within the trigeminaldermatomes
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1652. Duration can change over time, with paroxysms becoming more prolonged. A minority ofpatients will report attacks predominantly lasting for >2 minutes.3. Pain may become more severe over time.4. Some attacks may be, or appear to be, spontaneous, but there must be a history or finding ofpain provoked by innocuous stimuli to meet this criterion. Ideally, the examining clinicianshould attempt to confirm the history by replicating the triggering phenomenon. However, thismay not always be possible because of the patient’s refusal, awkward anatomical location of thetrigger and/or other factorsComments1. Other than the triggering phenomenon, most patients with trigeminal neuralgia fail to showsensory abnormalities within the trigeminal territory unless advanced methods are used (e.g.,quantitative sensory testing). However, in some patients, clinical neurological examination mayshow sensory deficits. These should prompt neuroimaging investigations to explore possiblecause. Diagnosis of subforms such as 4.1.1.1 Classical trigeminal neuralgia, 4.1.1.2. Secondarytrigeminal neuralgia or 4.1.1.3. Idiopathic trigeminal neuralgia is then possible.When very severe, the pain often evokes contraction of the muscles of the face on the affectedside (tic douloureux). Mild autonomic symptoms such as lacrimation and/ or redness of theipsilateral eye may be present. Following a painful paroxysm there is usually a refractory periodduring which pain cannot be triggered.4.1.1.1 Classical trigeminal neuralgiaDescription: Trigeminal neuralgia developing without apparent cause other than neurovascularcompression.Diagnostic criteriaA. Recurrent paroxysms of unilateral pain fulfilling the criteria for 4.1.1 Trigeminalneuralgia
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166B. Demonstration on MRI or during surgery of neurovascular compression (not simplycontact), with morphological changes1in thetrigeminal nerve rootNote’1.Typically atrophy or displacement.Comments: Nerve root atrophy and/or displacement due to neurovascular compression areindependently associated with signs and symptoms of 4.1.1 Trigeminal neuralgia. When theseanatomic changes are present, the condition is diagnosed as 4.1.1.1. Classical trigeminalneuralgia.The common site of compression is at the root entry zone with compression by an arterymoreclearly associated with symptoms than compression by a vein. MRI techniques tomeasurevolume and crossectional area of the root are available. Atrophic changes may includedemyelination, neuronal loss, changes in microvasculature and other morphological changes.While the exact mechanisms of how atrophic changes in the trigeminal nerve contribute to thegeneration of pain, some evidence suggest that, when present preoperatively, they predict a goodoutcome following microvascular decompression.4.1.1.1.1 Classical trigeminal neuralgia, purely paroxysmalDescription: Classical trigeminal neuralgia without persistent background pain.Diagnostic criteriaA. Recurrent paroxysms of unilateral facial pain fulfilling criteria for 4.1.1.1 Classicaltrigeminal neuralgiaB. Pain-free between attacks in the at´ffected trigeminal distribution.Comment: 4.1.1.1.1. Classical trigeminal neuralgia, purely paroxysmal is usually responsive, atleast initially, to pharmacotherapy (especially carbamazepine or oxcarbazepine).
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1674.1.1.1.2 Classical trigeminal neuralgia with concomitant continuous painPreviously used terms: Atypical trigeminal neuralgia; trigeminal neuralgia type 2Description: Classical trigeminal neuralgia with persistent background pain.Diagnostic criteriaA. Recurrent paroxysms of unilateral facial pain fulfillingcriteria for 4.1.1.1 Classicaltrigeminal neuralgiaB. Concomitant continuous or near-continuous pain between attacks in theipsilateral trigeminal distribution.CommentsPeripheral or central sensitization may account for the continuous pain.4.1.1.2 Secondary trigeminal neuralgiaDescription: Trigeminal neuralgia caused by an underlying disease. Clinical examination showssensory changes in a significant percentage of these patients.Diagnostic criteriaA. Recurrent paroxysms of unilateral pain fulfilling the criteria for 4.1.1. Trigeminalneuralgia, either purely paroxysmal or associated with concomitant continuous ornear-continuous pain.B. An underlying disease has been demonstrated known that it is able to cause, andexplaining, the neuralgia1C. Not better accounted for by another ICOP or ICHD-3 diagnosis2Notes:1. Recognized causes are tumour in the cerebello-pontine angle, arteriovenous malformationand multiple sclerosis
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1682. MRI is best rquipped to detect an underlying cause for 4.1.1.2 Secondary trigeminalneuralgia. Other investigations may include neurophysiological recording of trigeminalreflexes and trigeminal evoked potentials, suitable for patients who cannot undergo MRI.4.1.1.2.1 Trigeminal neuralgia attributed to multiple sclerosisDescription: Trigeminal neuralgia caused by a multiple sclerosis (MS) plaque or plaques in thepons or trigeminal root entry zone, and associated with other synptoms and/or clinical orlaboratory findings of MS.Diagnostic criteriaA. Recurrent paroxysms of unilateral facial pain fulfilling the criteria for 4.1.1Trigeminal neuralgiaB. Both of the following:1. Multiple sclerosis (MS) has been diagnosed2. An MS plaque at the trigeminal root entry zone or in the pons affecting theintrapontine primary afferents has been demonstrated by MRI, or its presence issuggested by routine electrophysiological studies1showing impairment of thetrigeminal pathways.C. Not better accounted for by another ICOP or ICHD-3 diagnosisNote:1. Blink reflex or trigeminal evoked potentials.Comments:4.1.1.2.1 Trigeminal neuralgia attributed to multiple sclerosis occurs in 2–5% of patients withmultiple sclerosis (MS), sometimes bilaterally. Conversely, MS is detected in only 2–4% ofcases of 4.1.1 Trigeminal neuralgia. Symptoms of trigeminal neuralgia are rarely a presentingfeature of MS. The lesion in the pons affects the intrapontine central terminals of the trigeminalafferents projecting to the trigeminal brainstem nuclei. Pontine lesions aff ecting the secondorder neurones of the trigeminothalamic tract usually lead to non-paroxysmal pain and/or
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169dysaesthesias and should be classified as Central neuropathic pain attributed to multiplesclerosis (13.13.1 in the ICHD-3). Some patients with MS are found to have neurovascularcompression of the trigeminal root. It is thought that MS increases the susceptibility of the nerveroot tothe effects of compression, leading more readily to painful paroxysms. Patients with 4.1.1.2.1Trigeminal neuralgia attributed to multiple sclerosis benefit less from pharmacological andsurgical interventions than those with 4.1.1.1 Classical trigeminal neuralgia.4.1.1.2.2 Trigeminal neuralgia attributed to space-occupying lesionDescription: Trigeminal neuralgia caused by contact between the affected trigeminal nerve anda space-occupying lesion.Diagnostic criteriaA. Recurrent paroxysms of unilateral facial pain fulfilling the criteria of 4.1.1 TrigeminalneuralgiaB. Both of the following:1. A space-occupying lesion in contact with theaffected trigeminal nerve has been demonstrated by imaging.2. Pain has developed after identification of the lesion, or led to its discovery.C. Not better accounted for by another ICOP or ICHD-3 diagnosisCommentsPatients with 4.1.1.2.2 trigeminal neuralgia attributed to space-occupying lesion may or may nothave clinically detectable sensory signs, while electrophysiological tests such as trigeminalbrainstem reflexes show abnormalities in nearly all cases.4.1.1.2.3 Trigeminal neuralgia attributed to other demonstrable causesDescription:
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170Trigeminal neuralgia caused by an underlying disease other than those described above.Diagnostic criteriaA. Recurrent paroxysms of unilateral facial pain fulfilling the criteria for 4.1.1 Trigeminalneuralgia either purely paroxysmal or associated with comcomitant continuous or near-continuous pain, but not necessarily unilateralB. Both of the following:1. A disorder, other than those described above, butknown to be able to cause trigeminal neuralgia, has been diagnosed12. Pain has developed after onset of the disorder, or led to its discoveryC. Not better accounted for by another ICOP or ICHD-3 diagnosisNote:Recognized causes are skull-base bone deformity, connective tissue disease, arteriovenousmalformation, dural arteriovenous fistula and genetic causes of neuropathy or nervehyperexcitability.4.1.1.3 Idiopathic trigeminal neuralgiaDescriptionTrigeminal neuralgia with neither electrophysiological tests nor MRI showing significantabnormalities.Diagnostic criteriaA. Recurrent paroxysms of unilateral pain fulfilling the criteria for 4.1.1Trigeminal neuralgia, either purely paroxysmal or associated with concomitantcontinuous or near-continous pain.
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171B. Neither 4.1.1.1 Classical trigeminal neuralgia or 4.1.1.2 Secondary trigeminalneuralgia has been confirmed by adequate investigations including electrophysiologicaltests or MRI1.C. Not better accounted for another ICHD-3 or ICOP diagnosisNote:1. A contact between a blood vessel and the trigeminal nerve and/or nerve root is a commonfinding on neuroimaging in healthy subjects. When such a contact is found in thepresence of 4.1.1. Trigeminal neuralgia but without evidence of morphological changes(e.g., atrophy or displacement) in the nerve root, the criteria for 4.1.1.1. Classicaltrigeminal neuralgia are not fulfilled and the condition is considered idiopathic.4.1.1.3.1 Idiopathic trigeminal neuralgia, purely paroxysmalDiagnostic criteriaA. Recurrent paroxysms of unilateral facial pain fulfilling the criteria for 4.1.1.3Idiopathic trigeminal neuralgiaB. Pain-free between attacks in the affected trigeminal distribution.4.1.1.3.2 Idiopathic trigeminal neuralgia with concomitant continuous painDiagnostic criteriaA. Recurrent paroxysms of unilateral facial pain fulfilling the criteria for 4.1.1.3Idiopathic trigeminal neuralgiaB. Concomitant continuous or near-continuous pain between attacks in the affectedtrigeminal distribution.4.1.2. Trigeminal neuropathic pain, other than 4.1.1. Trigeminalneuralgia
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172DescriptionFacial pain in the distribution of one or more branches of the trigeminal nerve caused by anotherdisorder and indicative of neural damage. The primary pain is usually continuous or near-continuous, and commonly described as burning, squeezing, aching or likened to pins andneedles. Superimposed brief pain paroxysms may occur but these are not the predominant paintype. This combination is distinct from that of 4.1.1 Trigeminal neuralgia. There are clinicallydetectable somatosensory changes within the trigeminal distribution, and mechanical allodyniaand cold hyperalgesia/allodynia are common, fulfilling the IASP criteria for neuropathic pain.Allodynic areas may be much larger than the punctate trigger zones present in trigeminalneuralgia.CommentSee also 1.1.3.2 Neuropathic gingival pain4.1.2.1. Trigeminal neuropathic pain attributed to herpes zosterDescriptionUnilateral facial pain of less than 3 months’ duration in the distribution of one or more branchesof the trigeminal nerve, caused by and associated with other symptoms and/or clinical signs ofacute herpes zoster.Diagnostic criteriaA. Unilateral facial pain in the distribution(s) of a trigeminal nerve branch or branches,lasting <3 10="" 173="" 173c.="" 25="" 3="" 4.1.2.1.="" 80="" a="" about="" accompanied="" accounted="" affects="" allodynia.="" an="" and="" another="" antigen="" assay="" associated="" at="" attributed="" base="" be="" been="" better="" branch="" branches="" burning="" by="" cases="" caused="" cells="" cerebrospinal="" chain="" changes="" common="" confirmed="" cranial="" criteriaa.="" cutaneous="" detected="" diagnosis="" diagnosiscommentherpes="" direct="" distribution2.="" distribution="" divisionbeing="" dna="" eruption="" facial="" fluid.="" fluid="" followed="" following:1.="" for="" from="" ganglion="" has="" herpes="" herpete="" herpetic="" hodgkin="" ichd-3="" icop="" immunocompromisedpatients="" immunofluorescence="" in="" is="" ivth="" least="" lesions="" lymphoma="" may="" months="" monthsb.="" more="" nerve="" nervebranches="" neuralgiapreviously="" neuropathydescriptionunilateral="" not="" obtained="" occurred="" occurring="" of="" one="" ophthalmic="" or="" oraching="" ormore="" out="" page="" pain="" palsies.="" patients.="" patients="" pcr="" persisting="" polymerase="" positive="" post-herpetic="" rarely="" rash="" reaction="" reactiondetection="" recurring="" s="" sametrigeminal="" sdisease.4.1.2.2.="" sensory="" shooting="" sine="" singled="" some="" stabbing="" such="" term:="" the="" those="" tingling="" to="" trigeminal="" trigeminalneuropathic="" unilateral="" used="" usually="" variable="" varicella="" virus="" vith="" vzv="" vzvdna="" with="" withiiird="" zoster.diagnostic="" zoster="">3 months and fulfilling criterionCB. Herpes zoster has affected the same trigeminal nerve branch or branchesC. Pain developed in temporal relation to the acute herpes zoster infection1D. Not better accounted for by another ICOP or ICHD-3 diagnosisNote:
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1741. Usually, pain will have developed while the rash was still active, but on occasion later,after rash has healed. In such cases, pale or light purple scars may be present as sequelaeof the herpetic eruption.CommentDespite its long-preferred name, post-herpetic neuralgia is actually a neuropathy orneuronopathy: significant pathoanatomical changes have been shown in the nerve, ganglion andnerve root. In 4.1.2.2. Trigeminal post-herpetic neuralgia, there is also evidence of theinflammation extending into the trigeminal brainstem complex.Following acute herpes zoster, post-herpetic neuralgia is more prevalent in the elderly.The first division of the trigeminal nerve is most commonly affected in 4.1.2.2. Trigeminal post-herpetic neuralgia, but the second and third divisions can be involved also.Typically, the pain of post-herpetic neuralgia is burning and itching – the latter sometimes veryprominent and extremely bothersome. Also, typically, patients with postherpetic neuralgia showa clear sensory deficit and brush-evoked mechanical allodynia in the territory involved. Manypatients, however, show little sensory loss and instead demonstrate heightened responses tothermal and/or punctate stimuli.4.1.2.3 Post-traumatic trigeminal neuropathic painPreviously used termsAnaesthesia dolorosa, Painful post-traumatic trigeminal neuropathyDescriptionUnilateral or bilateral facial or oral pain following and caused by trauma to the trigeminalnerve(s), with other symptoms and/or clinical signs of trigeminal nerve dysfunction.For the diagnosis of post-traumatic trigeminal neuropathic pain (PTNP), pain must persist orrecur for ≥ 3 months and fulfill all criteria below.Diagnostic criteria
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175A. The pain is characterized by all of the following:1. History of a mechanical, thermal, radiation or chemical injurywith possible peripheral trigeminal nerve involvement12. Pain onset in close temporal relation to the injury23. Pain distribution neuroanatomically plausibleB. Pain is associated with somatosensory signs in the same neuroanatomically plausibledistributionC. Diagnostic test confirming the lesion of a peripheral trigeminal nerve(or nerves) explaining the painD. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes1The severity of nerve injuries may range from mild to severe. These include external trauma andiatrogenic injuries from dental treatments such as local anesthetic injections, root canal therapies,extractions, oral surgery, dental implants, orthognathic surgery and other invasive procedures.2Pain appears no later than 6 months after nerve injuryCommentsThe structure of the diagnostic criteria deviates from the ICHD-3 for this particular diagnosis inorder to comply with IASP criteria.Pain duration ranges widely from paroxysmal to constant, and may be mixed. Specificallyfollowing radiation-induced postganglionic injury, neuropathic pain may appear after more than3 months.Somatosensory signs may be negative (hypoesthesia and/ or hypoalgesia) and/or positive(hyperalgesia and/or allodynia). Note that positive somatosensory signs are not specific toneuropathy. Negative or positive somatosensory signs consistent with the distribution of the painmay be sufficient to indicate the presence of a lesion of the trigeminal nerve. The clinicalexamination is supplemented by laboratory tests, e.g., quantitative sensory testing.
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176Tests that reveal a relevant lesion or disease affecting the trigeminal nerve may, e.g., consist ofsurgical or radiological confirmation of nerve compression or lesion, nerve conduction study,laser-evoked potentials, blink reflex, or skin biopsy confirmation of reduced nerve fiberterminals. Positive findings in these investigations may provide important diagnostic hints at thesource of pain. However, all clinical and diagnostic aspects of the pain need to be considered.There may seem to be a partial overlap to “persistent idiopathic dentoalveolar pain associatedwith somatosensory changes” 6.3.1. but in this condition there may be no clear temporalrelationship and the somatosensory changes may not be limited to a neuroanatomically confinedarea in contrast to the criteria for “post-traumatic trigeminal neuropathic pain”.Neuroablative procedures for trigeminal neuralgia, aimed at the trigeminal ganglion or nerveroot, may result in neuropathic pain involving one or more trigeminal divisions and should becoded as 4.1.2.3 Post-traumatic trigeminal neuropathic pain. Such pain may in some casescoexist with trigeminal neuralgia, e.g. when the latter recurs following remission.4.1.2.3 Post-traumatic trigeminal neuropathic pain rarely, if ever, crosses the midline. Overtime, 4.1.2.3 Post-traumatic trigeminal neuropathic pain may in some cases become morediffusely distributed.4.1.2.3.1 Probable post-traumatic trigeminal neuropathic painDiagnostic criteriaA. Pain fulfilling all but criterion C for 4.1.2.3 post-traumatic trigeminal neuropathicpain.4.1.2.4 Trigeminal neuropathic pain attributed to another disorderDescriptionUnilateral or bilateral facial or oral pain in the distribution(s) of one or more branches of thetrigeminal nerve, caused by a disorder other than those described above, with other symptomsand/or clinical signs of nerve dysfunction.
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177Diagnostic criteriaFor the diagnosis of trigeminal neuropathic pain attributed to another disorder, pain must persistor recur for ≥ 3 months and fulfill all criteria below.A. The pain is characterized by all of the following:1. Pain has developed after onset of a disorder known to be capableof causing trigeminal neuropathic pain, or it has led to itsdiscovery2. Pain distribution neuroanatomically plausibleB. Pain is associated with somatosensory signs in the same neuroanatomically plausibledistributionC. Diagnostic test confirming the diagnosis of the disorder or a lesion of thesomatosensory system explaining the painD. Not better accounted for by another ICOP or ICHD-3 diagnosis.CommentTrigeminal neuropathic pain may develop secondary to multiple sclerosis, space-occupyinglesion or systemic disease, with only the clinical characteristics (quality of spontaneous pain,evoked pain and presence of sensory deficits) distinguishing between 4.1.1.2. Secondarytrigeminal neuralgia and 4.1.2. Trigeminal neuropathic pain, other than 4.1.1. Trigeminalneuralgia.4.1.2. Trigeminal neuropathic pain, other than 4.1.1. Trigeminal neuralgia caused by aconnective tissue disease or hereditary disorders is usually bilateral but may beginasymmetrically and occasionally present with paroxysmal pain superimposed on the backgroundpain. Patients will eventually develop bilateral sensory deficits and continuous pain, whichclarifies the diagnosis. MRI is normal, but trigeminal reflexes are invariably delayed or absent.4.1.2.4.1 Probable trigeminal neuropathic pain attributed to another disorder
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178Diagnostic criteriaA. Pain fulfilling all but C for 4.1.2.4 trigeminal neuropathic pain attributedto another disorder.4.1.2.5 Idiopathic trigeminal neuropathic painDescriptionUnilateral or bilateral facial pain in the distribution(s) of one or more branches of the trigeminalnerve indicative of neural damage but of unknown etiologyDiagnostic criteriaFor the diagnosis of idiopathic trigeminal neuropathic pain, pain must persist or recur for ≥ 3months and fulfill all criteria below.A. The pain is characterized by all of the following:1. No history of trauma or disorder with possible peripheral trigeminal nerveinvolvement2. Pain distribution neuroanatomically plausibleB. Pain is associated with somatosensory signs in the same neuroanatomically plausibledistributionC. Diagnostic test confirming the lesion of a peripheral trigeminal nerve (or nerves)explaining the painD. Not better accounted for by another ICOP or ICHD-3 diagnosis.4.2. Pain caused by a lesion or disease of the glossopharyngeal nerve4.2.1 Glossopharyngeal neuralgiaPreviously used termVagoglossopharyngeal neuralgia
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179DescriptionA disorder characterised by unilateral brief stabbing pain, abrupt in onset and termination, in thedistributions not only of the glossopharyngeal nerve but also of the auricular and pharyngealbranches of the vagus nerve. Pain is experienced in the ear, base of the tongue, tonsillar fossaand/or beneath the angle of the jaw. It is commonly provoked by swallowing, talking orcoughing and may remit and relapse in the fashion of trigeminal neuralgia.Diagnostic criteriaA. Recurring paroxysmal attacks of unilateral pain in the distribution of theglossopharyngeal nerve1and fulfilling criterion BB. Pain has all of the following characteristics:1. Lasting from a few seconds to 2 minutes.2. Severe intensity3. Electric shock-like, shooting, stabbing or sharp in quality4. Pain is precipitated by swallowing, coughing, talking or yawningC. Not better accounted for by another ICOP or ICHD-3 diagnosisNote1. Within the posterior part of the tongue, tonsillar fossa, pharynx or angle of the lower jawand/or in the ear.Comments4.2.1. Glossopharyngeal neuralgia can occur together with 4.1.1. Trigeminal neuralgia.The superior laryngeal nerve is a branch of the vagus. Neuralgia of the superior laryngeal nervepresents similarly to 4.2.1. Glossopharyngeal neuralgia in its location and clinically can bedifficult to distinguish from it.Imaging may show neurovascular compression of the glossopharyngeal nerve.Prior to development of 4.2.1. Glossopharyngeal neuralgia, unpleasant sensations may be felt inaffected areas for weeks to several months.
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180The pain in 4.2.1. Glossopharyngeal neuralgia may radiate to involve the eye, nose, chin orshoulder. It can be severe enough for patients to lose weight. In rare cases, attacks of pain areassociated with vagal symptoms such as cough, hoarseness or syncope and/or bradycardia. Someauthors propose distinguishing between a pharyngeal, otalgic and a vagal subforms of neuralgia,and have suggested the term ‘‘vagoglossopharyngeal’’ neuralgia, when pain is accompanied byasystole, convulsions and syncope.Clinical examination usually fails to show sensory changes in the nerve distribution but if mildsensory deficits are encountered, they do not invalidate the diagnosis. Major changes or areduced/missing gag reflex should prompt aetiological investigations.4.2.1. Glossopharyngeal neuralgia is usually responsive, at least initially, to pharmacotherapy(especially carbamazepine or oxcarbazepine). It has been suggested that application of localanaesthetic to the tonsil and pharyngeal wall can prevent attacks for a few hours.4.2.1.1 Classical glossopharyngeal neuralgiaDiagnostic criteriaA. Recurrent paroxysms of unilateral pain fulfilling the criteria for 4.2.1glossopharyngeal neuralgiaB. Demonstration on MRI or during surgery of neurovascular compression of theglossopharyngeal nerve root4.2.1.2 Secondary glossopharyngeal neuralgiaDescriptionGlossopharyngeal neuralgia caused by an underlying disease.Diagnostic criteriaA. Recurrent paroxysms of unilateral pain fulfilling the criteria for 4.2.1Glossopharyngeal neuralgia
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181B. An underlying disease has been demonstrated known to be able to cause, andexplaining the neuralgia.1Note1. There are single reports of 4.2.1.2. secondary glossopharyngeal neuralgia caused by necktrauma, multiple sclerosis, tonsillar or regional tumours, cerebello-pontine angle tumours,and Arnold-Chiari malformation.4.2.1.3 Idiopathic glossopharyngeal neuralgiaDiagnostic criteriaA. Recurrent attacks of unilateral pain fulfilling the criteria for 4.2.1Glossopharyngeal neuralgiaB. Criteria for 4.2.1.1 Classical glossopharyngeal neuralgia or 4.2.1.2Secondary glossopharyngeal neuralgia are not fulfilledC. Not better accounted for by another ICOP or ICHD-3 diagnosis4.2.2. Glossopharyngeal neuropathic painDescriptionPain within the distribution of the glossopharyngeal nerve, (posterior part of the tongue, tonsillarfossa, pharynx or beneath the angle of the lower jaw). In addition, pain is commonly perceived inthe ipsilateral ear. The primary pain is usually continuous or near-continuous, and commonlydescribed as burning, squeezing, or likened to pins and needles. Brief paroxysms may happensuperimposed but they are not the predominant pain type. This combination distinguishes 4.2.2.Glossopharyngeal neuropathic pain from that of 4.2.1 Glossopharyngeal neuralgia. Sensorydeficits may be present in the ipsilateral posterior part of the tongue and tonsillar fossa, and thegag reflex may be weak or missing.
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1824.2.2.1. Glossopharyngeal neuropathic pain attributed to a known causeDescriptionUnilateral continuous or near-continuous pain, with or without superimposed brief paroxysms, inthe distribution of the glossopharyngeal nerve and caused by another identified disorder.Diagnostic criteriaA. Unilateral continuous or near-continous pain1in the distribution of theglossopharyngeal nerve and fulfilling criterion CB. A disorder known to be able to cause glossopharyngeal neuropathic pain, has beendiagnosed2C. Evidence of causation demonstrated by both of the following:1. Pain is ipsilateral to the glossopharyngeal nerve affected by the disorder2. Pain has developed after onset of the disorder or led to its discovery.D. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes1. Brief paroxysms may be superimposed but they are not the predominant pain type2. Tumours of the cerebellopontine angle and iatrogenic injury during procedures have beenreported to cause glossopharyngeal neuropathic pain4.2.2.2 Idiopathic glossopharyngeal neuropathic painDescriptionUnilateral continuous or near-continuous pain, with or without superimposed brief paroxysms, inthe distribution(s) of the glossopharyngeal nerve and of unknown aetiology.A. Unilateral continuous or near-continuous pain1in the distribution of theglossopharyngeal nerve
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183B. No cause has been identifiedC. Not better accounted for by another ICOP or ICHD-3 diagnosisNote1. Brief paroxysms may be superimposed but are not the predominant pain type.For the following, less common clinical entities, where pain mainly presents outside theorofacial region, the reader is referred to the current version of ICHD-3.4.3. Pain caused by a lesion or disease of nervus intermedius4.4. Occipital neuralgia4.5. Neck-tongue syndrome4.6. Painful optic neuritis4.7. Headache attributed to ischaemic ocular motor nerve palsy4.8. Tolosa-Hunt syndrome4.8. Paratrigeminal oculosympathetic (Raeder’s) syndrome4.9. Recurrent painful ophthalmoplegic neuropathy4.10. Central neuropathic pain
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184References4.1 Pain caused by a lesion or disease of the trigeminal nerveScholz J, Finnerup NB, Attal N, Aziz Q, Baron R, Bennett MI, Benoliel R, Cohen M, Cruccu G,Davis KD, Evers S, First M, Giamberardino MA, Hansson P, Kaasa S, Korwisi B, Kosek E,Lavandʼhomme P, Nicholas M, Nurmikko T, Perrot S, Raja SN, Rice ASC, Rowbotham MC,Schug S, Simpson DM, Smith BH, Svensson P, Vlaeyen JWS, Wang SJ, Barke A, Rief W,Treede RD; Classification Committee of the Neuropathic Pain Special Interest Group(NeuPSIG). The IASP classification of chronic pain for ICD-11: chronic neuropathic pain. Pain.2019 Jan;160(1):53-59. doi: 10.1097/j.pain.0000000000001365.Benoliel R, Svensson P, Evers S, Wang SJ, Barke A, Korwisi B, Rief W, Treede RD; IASPTaskforce for the Classification of Chronic Pain. The IASP classification of chronic pain forICD-11: chronic secondary headache or orofacial pain. Pain. 2019 Jan;160(1):60-68. doi:10.1097/j.pain.0000000000001435.Headache Classification Committee of the International Headache Society (IHS) TheInternational Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018 Jan;38(1):1-211. doi: 10.1177/0333102417738202.4.1.1. Trigeminal neuralgiaBenoliel R, Eliav E and Sharav Y. Self-reports of pain-related awakenings in persistent orofacialpain patients. J Orofac Pain 2009; 23: 330–338.Cruccu G, Finnerup NB, Jensen TS, Scholz J, Sindou M, Svensson P, Treede R-D, ZakrzweskaJM, Nurmikko T. Trigeminal neuralgia: new classification and diagnostic grading for clinicalpractice and research. Neurology 2016;87:220-8Drangsholt M and Truelove E. Trigeminal neuralgia mistaken as temporomandibular disorder. JEvid Base Dent Pract 2001; 1: 41–50.Fromm GH, Graff-Radford SB, Terrence CF and Sweet WH. Pre-trigeminal neuralgia.Neurology 1990; 40: 1493–1495.Haviv Y, Khan J, Zini A, Almoznino G, Sharav Y, Benoliel R. Trigeminal Neuralgia (part I).Revisiting the clinical phenotype. Cephalalgia 2016;36;730-746.Koopman JSHA, Dieleman JP, Huygen FJ, de Mos N, Martin CGM, Sturkenboom MCJM.Incidence of facial pain in the general population. Pain 2009;147:122-7Mueller D, Obermann M, Yoon MS, et al. Prevalence of trigeminal neuralgia and persistentidiopathic facial pain: A population-based study. Cephalalgia 2011; 31: 1542–1548.
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185Obermann M, Yoon MS, Ese D, et al. Impaired trigeminal nociceptive processing in patientswith trigeminal neuralgia. Neurology 2007; 69: 835–841.Pareja JA, Cuadrado ML, Caminero AB, et al. Duration of attacks of first division trigeminalneuralgia. Cephalalgia 2005; 25: 305–308.Rasmussen P. Facial pain. II. A prospective survey of 1052 patients with a view of: character ofthe attacks, onset, course, and character of pain. Acta Neurochir (Wien) 1990; 107: 121–128.Rasmussen P. Facial pain. III. A prospective study of the localization of facial pain in 1052patients. Acta Neurochir (Wien) 1991; 108: 53–63.Rasmussen P. Facial pain. IV. A prospective study of 1052 patients with a view of: precipitatingfactors, associated symptoms, objective psychiatric and neurological symptoms. Acta Neurochir(Wien) 1991; 108: 100–109.4.1.1.1 Classical trigeminal neuralgiaAntonini G, Di Pasquale A, Cruccu G, et al. Magnetic resonance imaging contribution fordiagnosing symptomatic neurovascular contact in classical trigeminal neuralgia: a blinded case-control study and meta-analysis. Pain 2014;155:1464-1471.Bowsher D, Miles JB, Haggett CE, Eldridge PR. Trigeminal neuralgia: a quantitative sensoryperception threshold study in patients who had not undergone previous invasive procedures. JNeurosurg 1997;86:190-2.Leal PR, Barbier C, Hermier M, Souza MA, Cristino-Filho G, Sindou M. Atrophic changes inthe trigeminal nerves of patients with trigeminal neuralgia due to neurovascular compression andtheir association with the severity of compression and clinical outcomes. J Neurosurg2014;120:1484-1495.Maarbjerg S, Wolfram F, Gozalov A, Olesen J, Bendtsen L. Significance of neurovascularcontact in classical trigeminal neuralgia. Brain 2015;48:311-319.4.1.1.2.1 Trigeminal neuralgia attributed to multiple sclerosisCruccu G, Biasiotta A, Di RS, et al. Trigeminal neuralgia and pain related to multiple sclerosis.Pain 2009; 143: 186–191.O’Connor AB, Schwid SR, Herrmann DN, et al. Pain associated with multiple sclerosis:systematic review and proposed classification. Pain 2008; 137: 96–111.Truini A, Prosperini L, Calistri V, et al. A dual concurrent mechanism explains trigeminalneuralgia in patients with multiple sclerosis. Neurology 2016;86:2094-9.4.1.1.2.2 Trigeminal neuralgia attributed to space-occupying lesionCheng TM, Cascino TL and Onofrio BM. Comprehensive study of diagnosis and treatment oftrigeminal neuralgia secondary to tumors. Neurology 1993; 43: 2298–2302.
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186Wei Y, Zhao W, Pu C, et al. Clinical features and long-term surgical outcomes in 39 patientswith tumor-related trigeminal neuralgia compared with 360 patients with idiopathic trigeminalneuralgia. Br J Neurosurg 2016 Sep 20:1-6. [Epub ahead of print] PMID: 276488614.1.1.2.3 Trigeminal neuralgia attributed to other demonstrable causesCoffey RJ, Fromm GH. Familial trigeminal neuralgia and Charcot-Marie-Tooth neuropathy.Report of two families and review. Surg Neurol 1991;35:49-53Yip V, Michael BD, Nahser HC, Smith D. Arteriovenous malformation: a rare cause oftrigeminal neuralgia identified by magnetic resonance imaging with constructive interference insteady state sequences. QJM 2012;105:895-98.De Paula Lucas C, Zabramski JM. Dural arteriovenous fistula of the transverse-sigmoid sinuscausing trigeminal neuralgia. Acta Neurochir 2007;149:1249-53.Tanaka BS, Zhao P, Dib-Hajj FB, Morisset V, Tate S, Waxman SG, Dib-Hajj SD. A gain-of-function mutation in Nav1.6 in a case of trigeminal neuralgia. Mol Med 2016 Aug 3;22. doi:10.2119/molmed.2016.00131. [Epub ahead of print]4.1.1.3 Idiopathic trigeminal neuralgiaLee A, McCartney S, Burbidge C, Raslan AM, Burchiel KJ. Trigeminal neuralgia occurs andrecurs in the absence of neurovascular compression. J Neurosurg 2014;120:1048-1054.4.1.2.1. Painful trigeminal neuropathy attributed to herpes ZosterDworkin RH and Portenoy RK. Pain and its persistence in herpes zoster. Pain 1996; 67: 241–252.Haanpää M, Dastidar P, Weinberg A, Levin M, Miettinen A, Lapinlampi A-M, Laippala P,Nurmikko T. Characteristics of cerebrospinal fluid and magnetic resonance imaging findings inpatients with acute herpes zoster. Neurology 1998;51:1405-1411.Liesegang TJ. Herpes Zoster Ophthalmicus. Natural history, risk factors, clinical presentation,and morbidity. Ophthalmology 2008;115(2Suppl):S3-12.4.1.2.2. Trigeminal postherpetic neuralgiaAlvarez FK, de Siqueira SR, Okada M, et al. Evaluation of the sensation in patients withtrigeminal post-herpetic neuralgia. J Oral Pathol Med 2007; 36: 347–350.Truini A, Haanpaa M, Provitera V, et al. Differential myelinated and unmyelinated sensory andautonomic skin nerve fiber involvement in patients with ophthalmic postherpetic neuralgia. FrontNeuroanat 2015;9:105.Truini A, Galeotti F, Haanpaa M, et al. Pathophysiology of pain in postherpetic neuralgia: Aclinical and neurophysiological study. Pain 2008;140:405-10.
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1874.1.2.3. Post-traumatic trigeminal neuropathic painBenoliel R, Birenboim R, Regev E, Eliav E. Neurosensory changes in the infraorbital nervefollowing zygomatic fractures. Oral Surg 99: 657-65. 2005.Benoliel R, Zadik Y, Eliav E and Sharav Y. Peripheral painful traumatic trigeminal neuropathy:Clinical features in 91 cases and proposal of novel diagnostic criteria. J Orofac Pain 2012; 26:49–58.Finnerup NB, Haroutounian S, Kamerman P, Baron R, Bennett DL, Bouhassira D, Cruccu G,Freeman R, Hansson P, Nurmikko T, Raja SN, Rice AS, Serra J, Smith BH, Treede RD, JensenTS. Neuropathic pain: an updated grading system for research and clinical practice. Pain2016;157:1599-606Jääskeläinen S K, Teerijoki-Oksa T and Forssell H. Neurophysiologic and quantitative sensorytesting in the diagnosis of trigeminal neuropathy and neuropathic pain. Pain 2005; 117: 349–357.Polycarpou N, Ng YL, Canavan D, et al. Prevalence of persistent pain after endodontic treatmentand factors affecting its occurrence in cases with complete radiographic healing. Int Endod J2005; 38: 169–178.Queral-Godoy E, Figueiredo R, Valmaseda-Castellon E, Berini-Aytes L, Gay-Escoda C.Frequency and evolution of lingual nerve lesions following lower third molar extraction. J OralMaxillofac Surg 2006; 64: 402–407.Renton T and Yilmaz Z. Profiling of patients presenting with posttraumatic neuropathy of thetrigeminal nerve. J Orofac Pain 2011; 25: 333–344.4.1.2.4. Trigeminal neuropathic pain attributed to another disorderKlasser GD, Balasubramaniam R, Epstein J. Topical Review—Connective Tissue Diseases:Orofacial Manifestations Including Pain J Orofac Pain 2007;21:171-84Cruccu G, Penisi EM, Antonini G, et al. Trigeminal isolated sensory neuropathy (TISN) andFOSMN syndrome: despite a dissimilar disease course do they share commonpathophysiological mechanisms? BMC Neurol 2014;14:248.4.2.1 Glossopharyngeal neuralgiaBlumenfeld A, Nikolskaya G. Glossopharyngeal neuralgia. Curr Pain and Headache Rep2013;17:343.Huynh-Le P, Matsishima T. Hisada K. Matsumoto K. Glossopharyngeal neuralgia due to anepidermoid tumour in the cerebellopontine angle. J Clin Neurosci 2004;11:758-60.Kandan SR, Khan S,. Jeyaretna DS, Lhatoo S, Patel NK, Coakham HB. Neuralgia of theglossopharyngeal and vagal nerves: long-term outcome following surgical treatment andliterature review. Br J Neurosurg 2010;24:441-6.
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188Minagar A, Sheremata WA. Glossopharyngeal neuralgia and MS. Neurology 2000;54:1368-70.Patel A, Kassam A, Horowitz M, Chang YF. Microvascular decompression in the managementof glossopharyngeal neuralgia: Analysis of 217 cases. Neurosurgery 2002;50:705-10.Peet MM. Glossopharyngeal neuralgia. Ann Surg 1935;101:256-8.Saman Y, Whitehead D, Gleeson M. Jugular foramen schwannoma presenting withglossopharyngeal neuralgia syncope syndrome. J Laryngol Otol 2010;124:1305-8.Tanrikulu L, Hastreiter P, Dorfler A, Buchfelder M, Naraghi R. Classification of neurovascularcompression in glossophgaryngeal neuralgia: three-dimensional visualiztion of theglossopharyngeal nerve. Surg Neurol Int 2015;6:189.4.2.2 Painful glossopharyngeal neuropathyKalladka M, Nasri-Heir C, Eliav E, Ananthan S, Viswanath A, Heir G. Continuous neuropathicpain secondary to endoscopic procedures: report of two cases and review of the literature. OralSurg Oral Med Oral Pathol Oral Radiol 2016;122:e55-e59Shin HY, Park HJ, Choi YC, Kim SM. Clinical and electromyographic features of radiation-induced lower cranial neuropathy. Clin Neurophysiol 2013;124:598-602.Bakar B. The jugular foramen schwannomas : Review of the large surgical series. J KorNeurosurg Soc 2008;44:285-94.5. Orofacial pain resembling presentations of primary headachesIntroductionIn clinical practice we often see three types of patients that seem to typify the crossroads betweenheadache and orofacial pain.Type 1: Headache patients who report additional facial pain during and usually ipsilateral tothe headache attacks.Type 2: Headache patients whose headache attacks have stopped and have been replaced byfacial pain attacks of the same quality, length and severity including the occurrence ofassociated symptoms of the former headache.
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189Type 3: Headache naïve patients who develop de-novo facial pain attacks which resembleone of the primary headache types in pain character, duration and severity with or withoutassociated symptoms of such headache types.This section in the new classification is for patients in the 3rdcategory. Pain exclusivelyoccurring in the facial region resembling primary headaches but with NO head pain. All othersshould be coded as the primary headache as per ICHD-3.5.1. Orofacial migraine5.1.1 Orofacial migraineDescriptionRecurrent orofacial pain attacks lasting 4–72 hours. Typical characteristics of the pain areunilateral location, pulsating quality, moderate or severe intensity, aggravation by routinephysical activity and association with nausea and/or photophobia and phonophobia.Diagnostic criteriaA. At least five attacks fulfilling criteria B–DB. Facial and/or oral pain attacks lasting 4-72 hours (untreated or unsuccessfullytreated)C. Facial and/or oral pain has at least two of the following four characteristics:1. Unilateral location2. Pulsating quality3. Moderate or severe pain intensity4. Aggravation by, or causing avoidance of routine physical activity (e.g.walking or climbing stairs)D. During facial and/or oral pain at least one of the following:1. Nausea and/or vomiting2. Photophobia and phonophobia
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190E. Not better accounted for by another ICOP or ICHD-3 diagnosisCommentsBilateral orofacial migraine has until today not been described. Exclusive orofacial migraine(Type 3 above) seems to be very rare. A group of patients with attacks of intraoral pain ofvarying length with atypical migraine-like features have been described and may be unrelated tomigraine which is why they are described below under neurovascular orofacial pain.Orofacial migraine with aura has not been extensively described and has been excluded until dataaccumulates.5.1.2 Chronic orofacial migraineDescriptionFacial and/or oral pain occurring on 15 or more days per month for more than 3 months, whichhas the features of migraine headache on at least 8 days per month.Diagnostic criteriaA. Facial and/or oral migraine-like pain on ≥15 days per month for >3 months2andfulfilling criteria B and CB. Occurring in a patient who has had at least five lifetime attacks fulfilling criteria B-Dfor 1.1 Orofacial MigraineC. On ≥ 8 days per month for >3 months, fulfilling any of the following3:1. Criteria C and D for 1.1 Orofacial Migraine2. Believed by the patient to be migraine at onset and relieved by a triptan or ergotderivative, or beta blockerD. Not better accounted for by another ICOP or ICHD-3 diagnosis.CommentsCharacterization of frequently recurring orofacial pain generally requires a pain diary to recordinformation on pain and associated symptoms day-by- day for at least 1 month.References
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191[1-12]5.1.3 Neurovascular Orofacial PainVarious studies have suggested that a specific entity is recognizable that is similar in phenotypeto the migraines and to TACs [13-15] . In spite of these similarities it seems to be a separateentity that deserves investigation.DescriptionThe essential features are attacks of various length of severe intraoral pain, often accompaniedby ‘toothache’ like symptoms, with mild autonomic and/or migrainous symptomatology. Withinthis group there are patients with relatively short attacks (1-4 hours) and those with longerattacks (> 4 hours).5.1.3.1 Shortlasting Neurovascular Orofacial PainDiagnostic CriteriaA. At least 5 attacks of facial pain fulfilling criteria B-EB. Moderate to Severe, intraoral pain1C. At least one of the following characteristics:1. Toothache with no local pathology22. Throbbing painD. Episodic pain lasting 1 to 4 hoursE. Clinical and radiographic examination are normal and no local cause may explain the painF. Accompanied by at least one of the following:1. ipsilateral lacrimation and/or conjunctival injection2. ipsilateral rhinorrhea and/or nasal congestion3. ipsilateral cheek swelling
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1924. photo and/or phonophobia5. nausea and/or vomitingG. Not better accountedfor by another ICOP or ICHD-3 diagnosisComments:Although existing in the literature since 1997 this entity needs thorough and prospectiveexamination. Although essentially anintraoral pain there may be be referral to adjacent sitesparticularly when pain is severe. This phenomenon needs to be craefuly followed anddocumented. There are reports of abnormal sensitivity to cold both interictally and duringattacks. This finding needs to be investigared thoroughly as it would be a useful tests and maylink the entitity to migraine where mechanical allodynia occurs during attacks. To obtain all theneeded parameters above the use of pain diaries is essential.5.1.3.2 Longlasting Neurovascular Orofacial PainDiagnostic CriteriaA. At least 5 attacks of facial pain fulfilling criteria B-EB. Moderate to Severe, intraoral pain1C. At least one of the following characteristics:1. Toothache with no local pathology22. Throbbing painD. Clinical and radiographic examination are normal and no local cause may explain the painE. Episodic pain lasting > 4 hoursF. Accompanied by at least one of the following:1. ipsilateral lacrimation and/or conjunctival injection2. ipsilateral rhinorrhea and/or nasal congestion3. ipsilateral cheek swelling
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1934. photo and/or phonophobia5. nausea and/or vomitingG. Not better accounted for by another ICOP or ICHD-3 diagnosis[13-15]Comments:Although existing in the literature since 1997 this entity needs thorough and prospectiveexamination. Although essentially an intraoral pain there may be be referral to adjacent sitesparticularly when pain is severe. This phenomenon needs to be craefuly followed anddocumented. There are reports of abnormal sensitivity to cold both interictally and duringattacks. This finding needs to be investigared thoroughly as it would be a useful tests and maylink the entitity to migraine where mechanical allodynia occurs during attacks. To obtain all theneeded parameters above the use of pain diaries is essential.5.2 Tension-type orofacial painCommentsThere are great similarities in signs, symptoms epidemiology and treatment response betweenTTH here and myofascial pain in section 2 of ICOP. At this point, there is insufficient evidenceto establish any type of relationship between themThere may exist a facial pain that is unrelated to TMD and is described as “facial muscletension” only occurring during rest, which resolves with voluntary muscle activity, e.g.mastication. At this time there is insufficient evidence that such symptoms form a separategroup.5.3 Trigeminal autonomic orofacial pain5.3.1 Orofacial cluster attacksDescription
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194Attacks of severe, strictly unilateral facial and/or oral pain, lasting 15–180 minutes and occurringfrom once every other day to eight times a day. The pain is associated with ipsilateralconjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating,miosis, ptosis and/or eyelid oedema, and/or with restlessness or agitation. To reiterate the generalapproach of this classification: The pain attacks are exclusively in the facial area and not in thehead. If headache occurs, these syndromes should be coded “cluster headache” with facialcomponent).Diagnostic criteriaA. At least five attacks fulfilling criteria B–DB. Severe or very severe unilateral facial and/or oral pain lasting 15–180 minutes (whenuntreated)C. Either or both of the following:1. At least one of the following symptoms or signs, ipsilateral to the headache:a. Conjunctival injection and/or lacrimationb. Nasal congestion and/or rhinorrhoeac. Eyelid oedemad. Forehead and facial sweatinge. Forehead and facial flushingf. Sensation of fullness in the earg. Miosis and/or ptosis2. A sense of restlessness or agitationD. Attacks have a frequency between one every other day and eight per day for more thanhalf of the time when the disorder is activeE. Not better accounted for by another ICOP or ICHD-3 diagnosis.Comment
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195Autonomic symptoms in facial cluster headach might be alleviated or different from autonomicsymptoms associated with headache. At this time there is insufficient evidence that this is indeedthe case and further research is needed. A group of patients with facial and/or oral pain withatypical cluster-like features have been described. At this time there is insufficient evidence thatthese form a separate group.5.3.1.1 Episodic orofacial cluster attacksDescriptionOrofacial Cluster attacks occurring in periods lasting from 7 days to 1 year, separated by pain-free periods lasting at least 3 month.Diagnostic criteriaA. Attacks fulfilling criteria for 5.3.1 Orofacial cluster attacks and occurring in bouts(cluster periods)B. At least two cluster periods lasting from 7 days to 1 year (when untreated) andseparated by pain-free remission periods of 3 month.5.3.1.2 Chronic orofacial cluster attacksDescriptionUnilateral facial and/or oral pain occurring for more than 1 year without remission, or withremission periods lasting less than 3 month.Diagnostic criteriaA. Attacks fulfilling criteria for 5.3.1.1 Orofacial cluster attacks, and criterion B belowB. Occurring without a remission period, or with remissions lasting <1 10="" 14="" 16-24="" 16-25="" 1965.3.1.2="" 196="" 1972.="" 197="" 198="" 198references="" 199="" 199the="" 1="" 1stand="" 2005.3.4="" 200="" 20="" 27="" 28-32="" 2="" 2ndor="" 30minutes.="" 3="" 3rdtrigeminalpain="" 5.3.1.1="" 5.3.1.2="" 5.3.2.2="" 5.3.2="" 5.3.3="" 7="" a="" above="" absolute="" absolutely="" accompanied="" accompanying="" accounted="" active.e.="" additional="" al="" and="" andoccurring="" andredness="" another="" are="" arise="" as="" associated="" at="" atleast="" attack.references="" attack="" attacks.diagnostic="" attacks="" autonomic="" b-eb.="" b="" be="" been="" below.diagnostic="" belowb.="" better="" between="" both="" bouts="" boutsb.="" by="" bypain-free="" cause="" cb.="" change="" chronic="" chronicorofacial="" clearlyestablished.="" cluster="" congestion="" conjunctival="" constant="" continua="" continuous="" cranial="" criteria="" criteriaa.="" criterion="" daily="" data="" day.="" day="" days="" de="" described="" determine="" diagnosis.commentsthere="" diagnosiscomment="" diagnostic="" differ="" difficulties.references="" distinct="" distribution="" doses="" dull="" ear7.="" earg.="" either="" episodic="" equivalent="" escription:constant="" escriptionattacks="" et="" evolve="" eye="" eyelid="" face="" facial="" facialstructures="" features="" five="" flushing6.="" flushingf.="" following:1.="" following="" for="" forehead="" frequency="" from="" fulfilling="" fullness="" further="" general="" group.the="" group="" half="" has="" have="" headache="" hemicrania="" hemifacial="" ichd-3="" icop="" if="" in="" indeed="" indomethacin.d.="" indomethacin="" injection="" intensity="" into="" ipsilateral="" is="" isolated="" lacrimation2.="" lacrimation="" lacrimationb.="" lasting="" least1="" least="" less="" local="" location="" mandible="" maxilla="" may="" mayhave="" migrainoid="" mild="" minutes="" minutesc.="" miosis="" moderate="" month="" months.5.3.3.2.="" months.="" months.diagnostic="" months="" more="" nasal="" needed="" needs="" neither="" neuralgiform="" no="" nor="" not="" novo="" number="" occur="" occurrence="" occurring="" occurs="" oedema.diagnostic="" oedema4.="" oedemad.="" of="" once="" one="" or="" oral="" oreyelid="" ormany="" orofacial="" other="" page="" pain-free="" pain-freeperiods="" pain:a.="" pain="" painattacks="" paindescriptionattacks="" paroxysmal="" patients="" patternc.="" paucity="" per="" period="" periods="" periodslasting="" pifp="" press="" prevented="" previously="" previouslysecondary="" primarychronic="" prominent="" ptosis="" ptosisd.="" quality="" recurring="" referral="" referred="" regionand="" related="" remission="" remissionperiods="" remissions="" reports="" representative="" response="" rhinorrhoea3.="" rhinorrhoea="" rhinorrhoeac.="" ryvenko="" same="" saw="" seconds="" sensation="" separate="" separated="" series="" several="" severe="" short-lasting="" signs.="" signs="" signsexacerbations="" single="" some="" stabs="" strictly="" studied.in="" sunct="" sunfa="" sunfadescriptionattacks="" sweating5.="" sweating="" sweatinge.="" symptoms="" syndromes.="" than="" the="" thedisorder="" thepain:1.="" therapeutic="" there="" these="" throughout="" time.e.="" time="" times="" to="" tominutes="" tooth="" trigeminal="" two="" typical="" unclearand="" unestablished.5.3.2.1="" unilateral="" untreated="" usually="" when="" which="" with="" withconstant="" within="" without="" withremission="" year.="" year.comment="" year="" yearreferences="" yet="">2 hours perday for >3 monthsC. ≥2 additional distinct attacks per day of moderate to severe pain exacerbations in thesame location lasting 10 to 30 minutesD. Clinical and radiographic examination are normal and no local cause may explain thepainE. Not better accounted for by another ICOP or ICHD-3 diagnosisComment
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201Autonomic symptoms should be absent, but do not exclude CUFPA. A response to Indomethacinshould rather lead to the diagnosis of 5.3.2 Paroxysmal hemifacial pain. At the moment there arenot enough data availaibale to discuss episodic and chronic types.The additional attacks have to be clearly distinct from the constant pain and patients shoulddescribe the pain consisting of two components, otherwise the diagnosis of 5.3.2 Paroxysmalhemi facial pain or 6.2 Persistent idiopathic facial pain (PIFP) should be considered.References1.Alvarez, M., et al., Unilateral nasal pain with migraine features. Cephalalgia, 2013.33(12): p. 1055-8.2.Hussain, A., M.A. Stiles, and M.L. Oshinsky, Pain remapping in migraine: a novelcharacteristic following trigeminal nerve injury. Headache, 2010. 50(4): p. 669-71.3.Obermann, M., et al., Migraine with isolated facial pain: a diagnostic challenge.Cephalalgia, 2007. 27(11): p. 1278-82.4.Gaul, C., et al., Orofacial migraine. Cephalalgia, 2007. 27(8): p. 950-2.5.Eross, E., D. Dodick, and M. Eross, The Sinus, Allergy and Migraine Study (SAMS).Headache, 2007. 47(2): p. 213-24.6.Schreiber, C.P., et al., Prevalence of migraine in patients with a history of self-reportedor physician-diagnosed "sinus" headache. Arch Intern Med, 2004. 164(16): p. 1769-72.7.Penarrocha, M., et al., Lower-half facial migraine: a report of 11 cases. J Oral MaxillofacSurg, 2004. 62(12): p. 1453-6.8.Lipton, R.B., et al., Migraine diagnosis and treatment: results from the AmericanMigraine Study II. Headache, 2001. 41(7): p. 638-45.9.Yoon, M.S., et al., Prevalence of facial pain in migraine: a population-based study.Cephalalgia : an international journal of headache, 2010. 30(1): p. 92-6.10. Daudia, A.T. and N.S. Jones, Facial migraine in a rhinological setting. Clin OtolaryngolAllied Sci, 2002. 27(6): p. 521-5.11. Debruyne, F. and L. Herroelen, Migraine presenting as chronic facial pain. Acta NeurolBelg, 2009. 109(3): p. 235-7.12. Dodick, D.W., Migraine with isolated facial pain: a diagnostic challenge. Cephalalgia,2007. 27(11): p. 1199-200.13. Benoliel, R., et al., The International Classification of Headache Disorders: accuratediagnosis of orofacial pain? Cephalalgia, 2008. 28(7): p. 752-62.14. Benoliel, R., H. Elishoov, and Y. Sharav, Orofacial pain with vascular-type features.Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 1997. 84(5): p. 506-12.15. Czerninsky, R., R. Benoliel, and Y. Sharav, Odontalgia in vascular orofacial pain. JOrofac Pain, 1999. 13(3): p. 196-200.16. Sanchez Del Rio, M., et al., Errors in recognition and management are still frequent inpatients with cluster headache. Eur Neurol, 2014. 72(3-4): p. 209-12.
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20217. Van Alboom, E., et al., Diagnostic and therapeutic trajectory of cluster headachepatients in Flanders. Acta Neurol Belg, 2009. 109(1): p. 10-7.18. Gaul, C., et al., Orofacial cluster headache. Cephalalgia, 2008. 28(8): p. 903-5.19. Bahra, A. and P.J. Goadsby, Diagnostic delays and mis-management in cluster headache.Acta Neurol Scand, 2004. 109(3): p. 175-9.20. van Vliet, J.A., et al., Features involved in the diagnostic delay of cluster headache. JNeurol Neurosurg Psychiatry, 2003. 74(8): p. 1123-5.21. Cademartiri, C., et al., Upper and lower cluster headache: clinical and pathogeneticobservations in 608 patients. Headache, 2002. 42(7): p. 630-7.22. Bahra, A., A. May, and P.J. Goadsby, Cluster headache: a prospective clinical study withdiagnostic implications. Neurology, 2002. 58(3): p. 354-61.23. Gross, S.G., Dental presentations of cluster headaches. Curr Pain Headache Rep, 2006.10(2): p. 126-9.24. Larner, A.J., Unnecessary extractions. Br Dent J, 2007. 203(8): p. 442.25. Bittar, G. and S.B. Graff-Radford, A retrospective study of patients with clusterheadaches. Oral Surg Oral Med Oral Pathol, 1992. 73(5): p. 519-25.26. May, A., The exceptional role of the 1st division of the trigeminal nerve. Pain, 2018. 159:p. S81-S84.27. Bartsch, T., Y.E. Knight, and P.J. Goadsby, Activation of 5-HT(1B/1D) receptor in theperiaqueductal gray inhibits nociception. Ann Neurol, 2004. 56(3): p. 371-81.28. Delcanho, R.E. and S.B. Graff-Radford, Chronic paroxysmal hemicrania presenting astoothache. J Orofac Pain, 1993. 7(3): p. 300-6.29. Graff-Radford, S.B., Paroxysmal hemicrania. Oral Surg Oral Med Oral Pathol OralRadiol Endod, 1998. 86(2): p. 138.30. Moncada, E. and S.B. Graff-Radford, Benign indomethacin-responsive headachespresenting in the orofacial region: eight case reports. J Orofac Pain, 1995. 9(3): p. 276-84.31. Benoliel, R. and Y. Sharav, Paroxysmal hemicrania. Case studies and review of theliterature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 1998. 85(3): p. 285-92.32. Cittadini, E., M.S. Matharu, and P.J. Goadsby, Paroxysmal hemicrania: a prospectiveclinical study of 31 cases. Brain : a journal of neurology, 2008. 131(Pt 4): p. 1142-55.33. Cohen, A.S., M.S. Matharu, and P.J. Goadsby, Short-lasting unilateral neuralgiformheadache attacks with conjunctival injection and tearing (SUNCT) or cranial autonomicfeatures (SUNA)--a prospective clinical study of SUNCT and SUNA. Brain, 2006. 129(Pt10): p. 2746-60.34. Benoliel, R. and Y. Sharav, SUNCT syndrome: case report and literature review. OralSurg Oral Med Oral Pathol Oral Radiol Endod, 1998. 85(2): p. 158-61.35. Brown, R.S. and B. Pass, Orofacial pain due to trigeminal autonomic cephalgia withfeatures of short-lasting neuralgiform headache attacks with conjunctival injection andtearing: a case report. Oral Surg Oral Med Oral Pathol Oral Radiol, 2012. 114(4): p.e13-9.36. Goadsby, P.J., E. Cittadini, and A.S. Cohen, Trigeminal autonomic cephalalgias:paroxysmal hemicrania, SUNCT/SUNA, and hemicrania continua. Semin Neurol, 2010.30(2): p. 186-91.
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20337. Prakash, S., N.D. Shah, and B.V. Chavda, Unnecessary extractions in patients withhemicrania continua: case reports and implication for dentistry. J Orofac Pain, 2010.24(4): p. 408-11.38. Rossi, P., et al., Diagnostic delay and suboptimal management in a referral populationwith hemicrania continua. Headache, 2009. 49(2): p. 227-34.39. Viana, M., et al., Diagnostic and therapeutic errors in trigeminal autonomic cephalalgiasand hemicrania continua: a systematic review. J Headache Pain, 2013. 14: p. 14.40. Benoliel, R., et al., Hemicrania continua. J Orofac Pain, 2002. 16(4): p. 317-25.41. Hryvenko, I., et al., Hemicrania continua: Case series presenting in an orofacial painclinic. Cephalalgia, 2018.42. Ziegeler, C. and A. May, Constant Unilateral Facial Pain with Attacks (CUFPA). 2018.
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2046. Idiopathic orofacial pain6.1 Burning mouth syndrome (BMS)Previously used termsStomatodynia, or glossodynia when confined to the tongue. Primary burning mouth syndrome.DescriptionAn intraoral burning or dysaesthetic sensation, recurring daily for more than 2 hours per day overmore than 3 months, without evident causative lesions on clinical examination and investigation.Diagnostic criteriaA. Oral pain fulfilling criteria B and CB. Recurring daily for >2 hours per day for >3 months1C. Pain has both of the following characteristics:1. Burning quality2. Felt superficially in the oral mucosaD. Oral mucosa is of normal appearance and no local or systemic causes may explain thepain.2E. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes1It is possible to diagnose burning mouth syndrome prior to 3 months if all exclusions forsecondary burning mouth symptoms have been made.2Quantitative sensory testing is often abnormal, whereas clinical sensory examination very rarelyreveals slight sensory deficits.6.1.1 Burning mouth syndrome associated with somatosensory changesDiagnostic criteriaA-C. Oral pain fulfilling criteria for 6.1 for burning mouth syndrome
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205D. Both of the following1. Oral mucosa is of normal appearance and no local or systemic causes may explain thepain2. Somatosensory changes are present on qualitative or quantitative somatosensorytesting1.Notes1Negative or positive sensory signs.6.1.2 Burning mouth syndrome not associated with somatosensory changesDiagnostic criteriaA-C. Oral pain fulfilling criteria for 6.1 for burning mouth syndromeD. Both of the following1. Oral mucosa is of normal appearance and no local or systemic causes may explainthe pain2. Somatosensory changes are not present on qualitative or quantitativesomatosensory testing.CommentsThe pain of 6.1 burning mouth syndrome (BMS) is usually bilateral, but can on rare occasion beunilateral, and its intensity fluctuates. The most common site is the tip of the tongue. Subjectivexerostomia (~2/3 of cohort), dysaesthesia and altered taste (~2/3 of cohort) are often present.There is a high preponderance in menopausal women, and some studies show psychosocialcomorbidities similar to other persistent pain conditions. Recent data point to varying levels ofchanges in somatosensory function in BMS patients. These findings encourage further researchinto BMS as a possible neuropathic pain condition.
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206Burning mouth symptoms may occur as a secondary phenomenon attributed to a local conditionsuch as candidiasis, lichen planus, hyposalivation and contact mucosal reactivity. It has also beenattributed to systemic disorders such as medication induced, anaemia, deficiencies of vitaminB12 or folic acid, Sjögren´s syndrome, diabetes. Oral burning related to these conditions havepreviously been known as “secondary burning mouth syndrome”, but burning mouth syndrome(6.1) here only refers to burning symptoms that have had all local and systemic causes excluded(previously “primary burning mouth syndrome”). The diagnosis secondary BMS falls within thedomain of oral mucosal pain with a known local or systematic cause covered in section 1.2.6.2 Persistent idiopathic facial pain (PIFP)Previously used termAtypical facial pain.DescriptionPersistent facial pain, with varying presentations but recurring daily for more than 2 hours perday, over more than 3 months, without neurological deficits in clinical examination or closetemporal preceding event.Diagnostic criteriaA. Facial pain fulfilling criteria B and CB. Recurring daily for >2 hours per day for >3 monthsC. Pain has both of the following characteristics:1. Poorly localized, and not following the distribution of a peripheral nerve12. Dull, aching or nagging quality2D. Clinical and radiographic examination are normal and no local cause may explain thepainE. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes
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2071Pain may be described as either deep or superficial and may radiate from face to mouth or viceversa. With time, it may spread to a wider area of the craniocervical region.2A wide variety of words are used to describe the character and the pain can have exacerbations,and be aggravated by stress.3Clinical neurological somatosensory assessment with pin prick or light touch perception mayvery rarely reveal slight somatosensory changes. Nociplastic pain reflecting altered processing inthe somatosensory system may be present and related to alteration in the modulatory paininhibitory system.6.2.1 Persistent idiopathic facial pain associated with somatosensory changesDiagnostic criteriaA-C. Facial pain fulfilling criteria for 6.2 for persistent idiopathic facial painD. Both of the following:1. Clinical and radiographic examinations are normal and no local and/or distantcause may explain the pain.2. Somatosensory changes are present on qualitative or quantitativesomatosensorytesting1.Notes1Negative or positive sensory signs.6.2.2 Persistent idiopathic facial pain not associated with somatosensory changesDiagnostic criteriaA-C. Oral pain fulfilling criteria for 6.2 for persistent idiopathic facial painD. Both of the following:
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2081. Clinical and radiographic examinations are normal and no local and/or distantcause may explain the pain.2. Somatosensory changes are not present on qualitative or quantitativesomatosensory testing.CommentsIn the previous version of ICHD-3 two disorders were treated as one entity: Persistent idiopathicfacial pain and atypical odontalgia. These new criteria give an overarching categorization ofpersistent idiopathic facial pain and define two distinct entities: Persistent idiopathic facial painand persistent idiopathic dentoalveolar pain. These two conditions cause either facial ordentoalveolar pain of a fairly constant nature that may be prone to exacerbations.Patients with Persistent idiopathic facial pain may report a minor operation or injury to the face,maxillae, teeth or gums but upon clinical and radiographic examination there is no demonstrablelocal cause. Persistent idiopathic facial pain may be comorbid with other pain conditions such aschronic widespread pain and irritable bowel syndrome. In addition, it can present withpsychosocial comorbidities similar to other persistent pain conditions.6.3 Persistent idiopathic dentoalveolar painPreviously used termAtypical odontalgia, Primary PDAP, Phantom tooth painDescriptionUnilateral, or rarely multiple sites of intra-oral dentoalveolar pain with varying presentations butrecurring daily for more than 2 hours per day, over more than 3 months without close temporalpreceding event.Diagnostic criteriaA. Unilateral, or rarely multiple sites of intra-oral dentoalveolar pain fulfilling criterion Band CB. Recurring daily for >2 hours per day for >3 months
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209C. Pain has both of the following characteristics:1. Localized to dentoalveolar site or sites (tooth or alveolar bone)12. Deep, dull, pressure-like quality2D. Clinical and radiographic examination are normal and no local cause may explain thepain3.E. Not better accounted for by another ICOP or ICHD-3 diagnosisNotes1Pain may be described as either deep or superficial. With time, it may spread to a wider area ofthe craniocervical region.2A wide variety of words are used to describe the character and the pain can have exacerbations,and be aggravated by stress. Adjunctive symptom description may also be used.3Clinical neurological somatosensory assessment with pin prick or light touch perception onlyvery rarely reveals sensory abnormalities Nociplastic pain reflecting altered processing in thesomatosensory system may be present and related to alteration in the modulatory pain inhibitorysystem.CommentSee also 1.1.3.3 Idiopathic gingival pain6.3.1 Persistent idiopathic dentoalveolar pain associated with somatosensory changesDiagnostic criteriaA-C. Oral pain fulfilling criteria for 6.3 for persistent idiopathic dentoalveolar painD. Both of the following:1. Clinical and radiographic examinations are normal and no local and/or distantcause may explain the pain.
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2102. Somatosensory changes are present on qualitative or quantitativesomatosensorytesting1.Notes1Negative or positive sensory signs present but not spatially confined to a neuroanatomicalrelevant area in contrast to post-traumatic trigeminal neuropathic pain 4.1.2.3.6.3.2 Persistent idiopathic dentoalveolar pain not associated with somatosensory changesDiagnostic criteriaA-C. Oral pain fulfilling criteria for 6.3 for persistent idiopathic dentoalveolar painD. Both of the following;1. Clinical and radiographic examinations are normal and no local and/or distantcause may explain the pain.2. Somatosensory changes are not present on qualitative or quantitativesomatosensory testing.ReferencesBaad-Hansen, L. (2008) Atypical odontalgia - pathophysiology and clinical management. J OralRehabil, 35, 1-11.Baad-Hansen, L. et al. (2008) Comparison of clinical findings and psychosocial factors inpatients with atypical odontalgia and temporomandibular disorders. Journal of Orofacial Pain,22, 7-14.Baad-Hansen, L. et al. (2013) Intraoral somatosensory abnormalities in patients with atypicalodontalgia--a controlled multicenter quantitative sensory testing study. Pain, 154, 1287-1294.Benoliel, R. & Gaul, C. (2017) Persistent idiopathic facial pain. Cephalalgia, 37, 680-691.
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211Durham, J. et al. (2013) Persistent dentoalveolar pain: the patient’s experience. Journal ofOrofacial Pain, 27, 6-13.Forssell, H. et al. (2015) An update on pathophysiological mechanisms related to idiopathic oro-facial pain conditions with implications for management. J Oral Rehabil, 42, 300-322.Forssell, H. et al. (2007) Differences and similarities between atypical facial pain and trigeminalneuropathic pain. Neurology, 69, 1451-1459.Grémeau-Richard, C. et al. (2010) Effect of lingual nerve block on burning mouth syndrome(stomatodynia): a randomized crossover trial. Pain, 149, 27-32.Hagelberg, N. et al. (2004) Striatal dopamine D2 receptors in modulation of pain in humans: areview. European Journal of Pharmacology, 500, 187-192.Häggman-Henrikson, B. et al. (2017) Pharmacological treatment of oro-facial pain - healthtechnology assessment including a systematic review with network meta-analysis. J OralRehabil, 44, 800-826.Jääskeläinen, S.K. (2012) Pathophysiology of primary burning mouth syndrome. ClinNeurophysiol, 123, 71-77.Jääskeläinen, S.K. & Woda, A. (2017) Burning mouth syndrome. Cephalalgia, 37, 627-647.Kolkka-Palomaa, M. et al. (2015) Pathophysiology of primary burning mouth syndrome withspecial focus on taste dysfunction: a review. Oral Dis, 21, 937-948.Lang, E. et al. (2005) Persistent idiopathic facial pain exists independent of somatosensory inputfrom the painful region: findings from quantitative sensory functions and somatotopy of theprimary somatosensory cortex. Pain, 118, 80-91.List, T., Leijon, G. & Svensson, P. (2008) Somatosensory abnormalities in atypical odontalgia: Acase-control study. Pain, 139, 333-341.McMillan, R. et al. (2016) Interventions for treating burning mouth syndrome. CochraneDatabase Syst Rev, 11, CD002779.Nixdorf, D.R. et al. (2012) Classifying orofacial pains: a new proposal of taxonomy based onontology. J Oral Rehabil, 39, 161-169.
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212Puhakka, A. et al. (2016) Peripheral nervous system involvement in primary burning mouthsyndrome--results of a pilot study. Oral Dis, 22, 338-344.Scala, A. et al. (2003) Update on burning mouth syndrome: overview and patient management.Crit Rev Oral Biol Med, 14, 275-291.7. Psychosocial Assessment1IntroductionThe biopsychosocial model incorporates psychological and social factors in order to morecomprehensively understand and manage both disease (as related to the traditional medicalfactors) and illness across time and circumstance. Major psychological factors associated withpain disorders include anxiety, catastrophizing, depression, physical symptom reporting, andfear-avoidance; and major social factors include access to medical care, stigma, and support fromfamily and friends. Each of these factors has extensive empirical support for their associationwith pain disorders, and evidence clearly supports the significance of the biopsychosocial modelas critical for understanding the complexity of pain processing in general [4] as well as related toorofacial pain disorders.[6; 21; 22; 31; 39] Notably, the implementation of the biopsychosocialmodel into both research and clinical pain medicine remains variable; further detail isavailable,[10; 35; 36] and new taxonomies for chronic pain of all types clearly highlight thecentral importance of both physical criteria for the disorders as well as assessment ofpsychosocial factors.[16]For present purposes, recommendations for best research practices in support of the intent of theICOP taxonomy are presented for the orofacial pain field broadly and follow previouslyestablished recommendations for the RDC/TMD [14] and the DC/TMD [47; 48] which specifyappropriate constructs and instruments for the assessment of musculoskeletal pain (e.g., painfulTMDs). While these recommendations emerge from substantial research on the TMDs, a subsetof orofacial pains, no evidence exists at this time to suggest that pain from the non-TMDorofacial pain conditions is any different from the pain associated with the TMDs in terms of
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213pain processing models. Consequently, research at this stage of development of ICOP shouldinclude equivalent attention to the full biopsychosocial model and thereby include assessment ofrecommended psychosocial constructs. Subsequent structured and systematic evidence willpermit a more empirically supported assessment model for the non-TMD OFPs and lead torevision of these initial recommendations.Levels of psychosocial assessmentTwo levels of psychosocial assessment are defined by the DC/TMD [48] and one more wasdeveloped in response to specific clinical request. See Table 1 for summary. The brief screeningversion is intended for research (and clinical) settings where only the briefest biopsychosocialassessment using the fewest number of questions can be incorporated.[42] Interestingly, the samecomponents of this brief screening have been informally described by other colleagues,suggesting a convergence into a core minimal set of psychosocial assessment domains. TheInstrument# itemsComprehensiveassessmentStandard screening Brief screeningPain drawing1444GCPS v2.08444JFLS (long form)204JFLS (short form)84PHQ-45*44PHQ-910*4GAD-78*4PHQ-15154OBC2044
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214standard screening version incorporates two more instruments. Both forms of screening shouldbe recognized as very limited.Table 1. Different levels of psychosocial assessment. See text for detailsTable Comments: * Item count includes reflective question regarding functional impact of anyreported symptoms.GCPS: Graded Chronic Pain Scale; JFLS: Jaw Functional Limitation Scale; PHQ: PatientHealth Questionnaire; GAD: Generalized Anxiety Disorder; OBC: Oral Behaviors ChecklistThe comprehensive assessment is intended specifically for clinical researchers so that they canmore reliably measure all constructs of interest, thereby permitting full stratification of theirsamples based on a psychosocial profile. All of these instruments are freely available withinterpretation guides for the scoring at the following website: www.rdc-tmdinternational.org. Inaddition, a few other instruments are recommended below for consideration.Pain- and function-related constructs and instruments for OFPExtent of painThe pain drawing (also known as a “body manikin”) provides ready identification of all painlocation(s), known to be one major risk determinant for pain chronicity.[37] All pain disorders,regardless of putative nociceptive mechanism, appear to be similarly affected in terms of theextent of pain.Pain intensity and pain-related disabilityThe Graded Chronic Pain Scale (GCPS, v 2.0) is a widely used and validated instrumentexamining pain persistence, pain intensity and pain-related disability also called graded chronicpain status, which has utility to stratify patients for levels of care.[12; 13; 15] Graded chronicpain status is also an indicator of prognosis in that higher graded chronic pain status predictsgreater chance of pain chronicity.[55]
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215Functional limitationThe person’s experience of impaired functional ability is known as functional limitation.[33] TheJaw Functional Limitation Scale (JFLS) has 2 versions, an 8-item version which yields a globalscore; and a 20-item version which measures three domains: limitation in chewing, jaw opening,and verbal and emotional expression.[38; 40] Both versions are equally reliable, valid, andsensitive to change. While functional limitation is central to musculoskeletal pain (and therebyself-evident for relevance to TMD), functional consequences are assumed to occur in response tothe non-TMD OFPs; the nature of those consequences is suspected [40] and warrants furtherinvestigation in order to be understand the full dimensionality of pain in the orofacial region.Over-use behavioursThe Oral Behaviors Checklist (OBC) contains a list of 21 oral region activities individuals mayengage in, such as clenching the teeth, bracing the mandible, or talking. Psychometric propertiesare strong [24; 29; 41] and OBC values are associated with TMD.[5; 18-20; 34; 37] Whetherthese behaviours are specifically associated with the OFPs remains unknown; however, guardingbehaviours are known to affect non-musculoskeletal back pain,[32] suggesting applicability fornon-TMD OFPs.Psychosocial constructs and instruments for OFPDepression and anxietyThe PRIME-MD project (PRIMary care Evaluation of Mental Disorders) [50] was anchoredinitially in psychiatric disorders and aimed to develop psychosocial instruments for theassessment of five of the most common mental health problems presenting to primary care:anxiety, depression, somatoform, alcohol, and eating disorders.[27] Particularly relevant for paindisorders are the 9-item Patient Health Questionnaire (PHQ-9) for depression and 7-itemGeneralized Anxiety Disorder scale (GAD-7) for anxiety; each of these instruments will permitreliable and valid measurement of the respective core constructs. Each instrument contributes 2questions to create the brief PHQ-4 depression and anxiety screening instrument, oftenconsidered to assess “distress” and which is widely used across North America and Europe.Depression (measured with PHQ-9, PHQ-4) is a mood state known to be affected by the
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216presence of persistent pain and known to affect pain processing, and it appears to be highlyrelevant to OFP.[11] Anxiety (measured with GAD-7, PHQ-4) in a medical context oftenmanifests as worry and general sympathetic nervous system activation, and it is associated withpain perception [46] and hypervigilance.[7] Anxiety pervades medical settings, and it appears tobe highly relevant to OFP.[1]Somatoform disordersThe PRIME-MD project also yielded the Patient Health Questionnaire-15 (PHQ-15) for somaticsymptom severity. Physical symptoms not accompanied by appropriate signs supportive of adisease diagnosis remain a considerable challenge across all medical domains; such findings areappropriately termed somatic symptom disorder, functional disorders, medically unexplainedsymptoms, and symptoms without medical utility,[25; 45] yet none of these terms are fullysatisfactory for what appears to be a more complex construct than previously assumed. Whilethere are several proposed mechanisms underlying physical symptom reporting,[8; 9; 45] all areconsistent with the various symptoms that accompany the persistent OFPs.[1; 43] An extensionof this phenomenon involves occlusal dysesthesia,[30] which has potential relevance to at least afew of the OFPs within the ICOP.CatastrophizingCatastrophizing about pain is “characterized by the tendency to magnify the threat value of painstimulus and to feel helpless in the context of pain, and by a relative inability to inhibit pain-related thoughts in anticipation of, during or following a painful encounter” [44]. Higher levelsof catastrophizing are linked to increased utilization of healthcare, increased expression of pain,and poorer treatment outcomes. [3; 28; 52] Catastrophizing is not included as a standard measurewithin the DC/TMD framework because the evidence for the relevance of catastrophizing toTMD was not sufficiently strong when the DC/TMD Axis II recommendations were formulated.The situation has since changed and, moreover, its relevance to any pain disorder is nowappropriate for this construct to be included as a recommended domain within the ICOP.Appropriate validated measures include the Pain Catastrophizing Scale [51] and the CopingStrategies Questionnaire.[23]Fear avoidance
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217The fear-avoidance model emerged from operant models pertaining to low back pain,[17]specifically, behavioural observations that individuals reported pain incongruent with physicalfindings. The fear-avoidance model has since had extensive supporting research.[54] In themodel, having no fear of injury-related new onset pain leads to engaging in the appropriatebehaviours that will result in recovery from the injury. In contrast, having fear of that pain leadsto catastrophizing about that pain, avoidance of circumstances that may cause pain, andconsequent disuse, depression, and disability. Disability then feeds forward to further painexperience, avoidant behaviour, and the absence of recovery; as such this model is clearlyrelevant to motor behaviour, and support of this construct for TMD is slowly emerging. Themodel, however, is a person-level model with regard to the effects of behaviour and beliefs onthe central nervous system and thereby assumed to be linked to pain processing. Consequently,the clearly plausible hypotheses relating fear of movement to recovery amongst those with injuryto the masticatory system and the probable emergence of chronic pain among some of thoseindividuals warrant investigation,[56] and present data suggest that this perspective is applicableto OFP as well.Fear of pain is measured via several instruments, of which the Tampa Scale for Kinesiophobia(TSK) [26] is the best known and has very strong utility for back pain.[2] The TSK was adaptedfor the masticatory system, the TSK-TMD,[53] and it appears to capture both the somaticexperience as well as avoidant behaviours that OFP may precipitate.Conclusions and Future DirectionsFurther research of the biopsychosocial model and its clinical as well as research relevance toOFP is clearly needed. As the criteria for the disorders within the ICOP are better developed andrefined, a similar progression should occur regarding our understanding of the persons with thesepain disorders. Consequently, as taxonomy and diagnosis improve, improved understanding ofpain mechanisms as well as sound treatment recommendations should emerge. Multi-modalapproaches are clearly needed to augment the potential therapeutic yield of standard biomedicaltherapies such as pharmacological or surgical approaches.[49] For the present time, consistentuse of a standardized format for psychosocial assessment of the individual with orofacial pain is
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218strongly recommended in parallel with use of the stated criteria (and their extensions for researchpurposes) of the disorders within the ICOP.Acknowledgement:This chapter is an adaptation from Ohrbach R and Durham J, Biopsychosocialaspects of orofacial pain. In: Farah CS, Balasubramaniam R, and McCullough MJ (editors).Contemporary Oral Medicine. Heidelberg, Germany: Springer Meteor. 2018.References[1] Aggarwal VR, McBeth J, Zakrzewska JM, Lunt M, Macfarlane GJ. The epidemiology ofchronic syndromes that are frequently unexplained: do they have common associated factors?International Journal of Epidemiology 2006;35(2):468-476.[2] Boersma K, Linton SJ. Expectancy, fear and pain in the prediction of chronic pain anddisability: a prospective analysis. European Journal of Pain: Ejp 2006;10(6):551-557.[3] Brister H, Turner JA, Aaron LA, Mancl L. Self-efficacy is associated wtih pain, functioning,and coping in patients with chronic temporomandibular disorder pain. Journal of Orofacial Pain2006;20:115-124.[4] Campbell CM, Edwards RR. Mind–body interactions in pain: the neurophysiology of anxiousand catastrophic pain-related thoughts. Translational Research 2009;153(3):97-101.[5] Carlsson GE, Egermark I, Magnusson T. Predictors of bruxism, other oral parafunctions, andtooth wear over a 20-year follow-up period. Journal of Orofacial Pain 2003;17(1):50-57.[6] Ceusters W, Michelotti A, Raphael KG, Durham J, Ohrbach R. Perspectives on next steps inclassification of oro-facial pain -- part 1: role of ontology. Journal of Oral Rehabilitation2015;42:926-941.[7] Cioffi I, Michelotti A, Perrotta S, Chiodini P, Ohrbach R. Effect of somatosensoryamplification and trait anxiety on experimentally induced orthodontic pain. European journal oforal sciences 2016.[8] Craig AD. How do you feel? Interoception: the sense of the physiological condition of thebody. Nat Rev Neurosci 2002;3(8):655-666.
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219[9] Craig AD. A new view of pain as a homeostatic emotion. Trends in Neurosciences2003;26(6):303-307.[10] Durham J, Ohrbach R. Commentary on disability and dental education. Journal of OralRehabilitation 2010;37(6):490-494.[11] Durham J, Raphael KG, Benoliel R, Ceusters W, Michelotti A, Ohrbach R. Perspectives onnext steps in classification of oro-facial pain -- part 2: role of psychosocial factors. Journal ofOral Rehabilitation 2015.[12] Durham J, Shen J, Breckons M, Steele JG, Araujo-Soares V, Exley C, Vale L. HealthcareCost and Impact of Persistent Orofacial Pain: The DEEP Study Cohort. Journal of DentalResearch 2016;95(10):1147-1154.[13] Dworkin SF, Huggins KH, Wilson L, Mancl L, Turner J, Massoth D, LeResche L, TrueloveE. A randomized clinical trial using research diagnostic criteria for temporomandibulardisorders-axis II to target clinic cases for a tailored self-care TMD treatment program. Journal ofOrofacial Pain 2002;16:48-63.[14] Dworkin SF, LeResche L. Research Diagnostic Criteria for Temporomandibular Disorders:Review, Criteria, Examinations and Specifications, Critique. Journal of CraniomandibularDisorders, Facial and Oral Pain 1992;6(4):301-355.[15] Dworkin SF, Turner JA, Mancl L, Wilson L, Massoth D, Huggins KH, LeResche L,Truelove E. A randomized clinical trial of a tailored comprehensive care treatment program fortemporomandibular disorders. Journal of Orofacial Pain 2002;16:259-276.[16] Fillingim RB, Bruehl S, Dworkin RH, Dworkin SF, Loeser JD, Turk DC, Widerstrom-NogaE, Arnold L, Bennett RM, Edwards RR, Freeman R, Gewandter J, Hertz S, Hochberg M, KraneE, Mantyh PW, Markman J, Neogi T, Ohrbach R, Paice JA, Porreca F, Rappaport BA, SmithSM, Smith TJ, Sullivan MD, Verne GN, Wasan AD, Wesselmann U. The ACTTION-AmericanPain Society Pain Taxonomy (AAPT): An evidence-based and multidimensional approach toclassifying chronic pain conditions. Journal of Pain 2014;15(3):241-249.[17] Fordyce WE. Behavioral Methods for Chronic Pain and Illness. Saint Louis: C.V. MosbyCompany, 1976.
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220[18] Glaros AG, Burton E. Parafunctional clenching, pain, and effort in temporomandibulardisorders. Journal of Behavioral Medicine 2004;27(1):91-100.[19] Glaros AG, Marszalek JM, Williams KB. Longitudinal multilevel modeling of facial pain,muscle tension, and stress. J Dent Res 2016;95(4):416-422.[20] Glaros AG, Williams K. Tooth contact versus clenching: oral parafunctions and facial pain.Journal of Orofacial Pain 2012;26(3):176-180.[21] Greene CS, Mohl ND, McNeill C, Clark GT, Truelove EL. Temporomandibular disordersand science: a response to the critics. jpd 1998;80:214-215.[22] Greene CS, Obrez A. Treating temporomandibular disorders with permanent mandibularrepositioning: is it medically necessary? Oral Surgery, Oral Medicine, Oral Pathology and OralRadiology 2015;119(5):489-498.[23] Harland N, Georgieff K. Development of the coping strategies questionnaire 24, a clinicallyutilitarian version of the coping strategies questionnaire. Rehabil Psychol 2003;48(4):296-300.[24] Kaplan SEF, Ohrbach R. Self-report of waking-state oral parafunctional behaviors in thenatural environment. Journal of Oral & Facial Pain and Headache 2016;30:107-119.[25] Kirmayer LJ, Robbins JM. Functional somatic syndromes. In: LJ Kirmayer, JM Robbins,editors. Current concepts of somatization: research and clinical perspectives. Washington, DC:American Psychiatric Press, 1991. pp. 79-106.[26] Kori SH, Miller RP, Todd DD. Kinisophobia: a new view of chronic pain behavior. PainManagement 1990;3:35-43.[27] Kroenke K, Spitzer RL, Williams JB, Löwe B. The patient health questionnaire somatic,anxiety, and depressive symptom scales: a systematic review. General Hospital Psychiatry2010;32(4):345-359.[28] Litt MD, Porto FB. Determinants of Pain Treatment Response and Nonresponse:Identification of TMD Patient Subgroups. The Journal of Pain 2013;14(11):1502-1513.[29] Markiewicz MR, Ohrbach R, McCall WD, Jr. Oral Behaviors Checklist: Reliability ofPerformance in Targeted Waking-state Behaviors. Journal of Orofacial Pain 2006;20(4):306-316.
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221[30] Melis M, Zawawi KH. Occlusal dysesthesia: a topical narrative review. Journal of OralRehabilitation 2015:n/a-n/a.[31] Michelotti A, Alstergren P, Goulet JP, Lobbezoo F, Ohrbach R, Peck C, Schiffman E, ListT. Next steps in development of the diagnostic criteria for temporomandibular disorders(DC/TMD): Recommendations from the International RDC/TMD Consortium Networkworkshop. Journal of Oral Rehabilitation 2016;ePrint.[32] O’Sullivan P. Diagnosis and classification of chronic low back pain disorders: maladaptivemovement and motor control impairments as underlying mechanism. Manual Therapy2005;10(4):242-255.[33] Ohrbach R. Disability assessment in temporomandibular disorders and masticatory systemrehabilitation. Journal of Oral Rehabilitation 2010;37:452-480.[34] Ohrbach R, Bair E, Fillingim RB, Gonzalez Y, Gordon SM, Lim PF, Ribeiro-Dasilva M,Diatchenko L, Dubner R, Greenspan JD, Knott C, Maixner W, Smith SB, Slade GD. Clinicalorofacial characteristics associated with risk of first-onset TMD: the OPPERA prospectivecohort study. Journal of Pain 2013;14(12, supplement 2):T33-T50.[35] Ohrbach R, Durham J. Biopsychosocial aspects of orofacial pain. In: CS Farah, RBalasubramaniam, MJ McCullough, editors. Contemporary Oral Medicine. Heidelberg,Germany: Springer Meteor, 2018. pp. 1-21.[36] Ohrbach R, Dworkin SF. The Evolution of TMD Diagnosis: Past, Present, Future. Journalof Dental Research 2016;95(10):1093-1101.[37] Ohrbach R, Fillingim RB, Mulkey F, Gonzalez Y, Gordon S, Gremillion H, Lim P-F,Ribeiro-Dasilva M, Greenspan JD, Knott C, Dubner R, Maixner W, Slade GD. Clinical findingsand pain symptoms as potential risk factors for chronic TMD: Descriptive data and empiricallyidentified domains from the OPPERA case-control study. Journal of Pain 2011;12(11,Supplement 3):T27-T45.[38] Ohrbach R, Granger CV, List T, Dworkin SF. Pain-related Functional Limitation of the Jaw:Preliminary Development and Validation of the Jaw Functional Limitation Scale. CommunityDental and Oral Epidemiology 2008;36:228-236.
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222[39] Ohrbach R, Greene C. Temporomandibular joint diagnosis: striking a balance between thesufficiency of clinical assessment and the need for imaging. Oral Surgery Oral Medicine OralPathology Oral Radiology 2013;116(1):124-125.[40] Ohrbach R, Larsson P, List T. The Jaw Functional Limitation Scale: Development,reliability, and validity of 8-item and 20-item versions. Journal of Orofacial Pain 2008;22:219-230.[41] Ohrbach R, Markiewicz MR, McCall WD, Jr. Waking-state oral parafunctional behaviors:specificity and validity as assessed by electromyography. European Journal of Oral Sciences2008;116(5):438-444.[42] Ohrbach R, Michelotti A. Psychological Considerations. TMD and Orthodontics: Springer,2015. pp. 49-61.[43] Peters S, Goldthorpe J, McElroy C, King E, Javidi H, Tickle M, Aggarwal VR. Managingchronic orofacial pain: A qualitative study of patients', doctors', and dentists' experiences. BritishJournal of Health Psychology 2015;20(4):777-791.[44] Quartana PJ, Campbell CM, Edwards RR. Pain catastrophizing: a critical review. Expertreview of neurotherapeutics 2009;9(5):745-758.[45] Rief W, Broadbent E. Explaining medically unexplained symptoms-models andmechanisms. Clinical Psychology Review 2007;27(7):821-841.[46] Robinson ME, Wise EA, Gagnon C, Fillingim RB, Price DD. Influences of gender role andanxiety on sex differences in temporal summation of pain. Journal of Pain 2004;5:77-82.[47] Schiffman E, Ohrbach R. Executive summary of the Diagnostic Criteria forTemporomandibular Disorders for clinical and research applications. Journal of the AmericanDental Association 2016;147(6):438-445.[48] Schiffman E, Ohrbach R, Truelove E, Look J, Anderson G, Goulet J-P, List T, Svensson P,Gonzalez Y, Lobbezoo F, Michelotti A, Brooks SL, Ceusters W, Drangsholt M, Ettlin D, GaulC, Goldberg L, Haythornthwaite J, Hollender L, Jensen R, John MT, deLaat A, deLeeuw R,Maixner W, van der Meulen M, Murray GM, Nixdorf DR, Palla S, Petersson A, Pionchon P,Smith B, Visscher CM, Zakrzewska J, Dworkin SF. Diagnostic Criteria for TemporomandibularDisorders (DC/TMD) for Clinical and Research Applications: Recommendations of the
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223International RDC/TMD Consortium Network and Orofacial Pain Special Interest Group.Journal of Oral & Facial Pain and Headache 2014;28(1):6-27.[49] Spencer CJ, Neubert JK, Gremillion H, Zakrzewska JM, Ohrbach R. Case Reviews in Pain:Toothache or trigeminal neuralgia: Treatment dilemmas. Journal of Pain 2008;9:767-770.[50] Spitzer RL, Kroenke K, Williams JBW. Validation and utility of a self-report version ofPRIME-MD: The PHQ Primary Care Study. JAMA 1999;282:1737-1744.[51] Sullivan M, Bishop S, Pivik J. The pain catastrophising scale: development and validation.Psychological Assessment 1995;7(4):524-532.[52] Turner JA, Brister H, Huggins KH, Mancl L, Aaron LA, Truelove EL. Catastrophizing isassociated with clinical examination findings, activity interference, and health care use amongpatients with temporomandibular disorders. Journal of Orofacial Pain 2005;19:291-300.[53] Visscher CM, Ohrbach R, van Wijk AJ, Wilkosz M, Naeije M. The Tampa Scale forKinesiophobia for Temporomandibular Disorders (TSK-TMD). Pain 2010;150(492-500).[54] Vlaeyen JW, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletalpain: a state of the art. Pain 2000;85(3):317-332.[55] Von Korff M, Dunn KM. Chronic pain reconsidered. Pain 2008;138(2):267-276.[56] Wall PD. On the relation of injury to pain. Pain 1979;6:253-264.
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224Definitions of termsAttributed to: This term in ICOP is in accordance with ICHD-3 and describes the relationshipbetween a secondary pain and the disorder believed to cause it. It requires fulfilment of criteriaestablishing an accepted level of evidence of causation.Chronic: In pain terminology, chronic signifies long-lasting, specifically over a period exceeding3 months. In headache terminology, For primary headache disorders that are more usuallyepisodic (qv), chronic is used whenever attacks of headache (qv) occur on more days than notover a period longer than 3 months. The trigeminal autonomic cephalalgias are the exception: inthese disorders, chronic is not used until the disorder has been unremitting for more than oneyear with less than 3 months attack free. Results from research based on ICOP will allow us toestablish how applicable these criteria are to orofacial pain (see also Benoliel et al 2010)Duration of attack: Time from onset until termination of an attack of headache (or pain) (qv)meeting criteria for a particular headache type or subtype. After migraine or cluster headache, alow-grade non-pulsating headache without accompanying symptoms may persist, but this is notpart of the attack and is not included in duration. If the patient falls asleep during an attack andwakes up relieved, duration is until time of awakening. If an attack of migraine is successfullyrelieved by medication but symptoms recur within 48 hours, these may represent a relapse of thesame attack or a new attack. Judgement is required to make the distinction (see also Frequencyof attacks).Episodic: Recurring and remitting in a regular or irregular pattern of attacks of headache (orpain) (qv) of constant or variable duration. Through long usage the term has acquired specialmeaning in the context of episodic cluster headache, referring to the occurrence of clusterperiods (qv) separated by cluster remission periods (qv) rather than to attacks. Similar usage hasbeen adopted for paroxysmal hemicrania and short-lasting unilateral neuralgiform headacheattacks.Facial pain: Pain below the orbitomeatal line, anterior to the pinnae and above the neck.Focal neurological symptoms: Either negative signs of one or more cranial nerves, or centralsymptoms of focal brain (usually cerebral) disturbance such as occur in migraine aura (qv).Frequency of attacks: The rate of occurrence of attacks of headache (or pain) (qv) per timeperiod (commonly one month). Successful relief of a migraine attack with medication may befollowed by relapse within 48 hours. The IHS Guidelines for Controlled Trials of Drugs in
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225Migraine, 3rd edition, recommend as a practical solution, especially in differentiating attacksrecorded as diary entries over the previous month, to count as distinct attacks only those that areseparated by at least 48 hours headache-free.Headache: Pain (qv) located in the head, above the orbitomeatal line and/or nuchal ridge.Headache days: Number of days during an observed period of time (commonly one month)affected by headache for any part or the whole of the day.Intensity of pain: Level of pain may be scored on a four-point numerical rating scale (0-3)equivalent to no, mild, moderate and severe pain, or on a visual analogue scale (commonly 10cm). It may also be scored on a verbal rating scale expressed either on a scale from 0-10 or interms of its functional consequence: 0, no pain; 1, mild pain, does not interfere with usualactivities; 2, moderate pain, inhibits but does not wholly prevent usual activities; 3, severe pain,prevents all activities.Persistent: This term, used in the context of certain secondary headaches, describes headache,initially acute and caused by another disorder, that fails to remit within a specified time interval(usually 3 months) after that disorder has resolved. In many such cases, the headache isrecognized as a distinct subtype or subform, with evidence of causation depending upon earlierfulfilment of the criteria for diagnosis of the acute type, and persistence of the same headache.Phonophobia: Hypersensitivity to sound, even at normal levels, usually causing avoidance.Photophobia: Hypersensitivity to light, even at normal levels, usually causing avoidance.Primary pain (disorder): Pain (OFP or headache) not caused by or attributed to another disorder.It is distinguished from secondary OFP and headache disorders.Refractory period: The time following resolution of an attack of pain (qv) during which a furtherattack cannot be triggered.Sidelocked: Unilateral occurrence of pain that never changes sides.Unilateral: On either the right or the left side, not crossing the mid line. Unilateral headache doesnot necessarily involve all of the right or left side of the head, but may be frontal, temporal oroccipital only. When used for sensory or motor disturbances of migraine aura, the term includescomplete or partial hemidistribution.References
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226The International Classification of Headache Disorders. Cephalalgia. 38(1); 1-211Benoliel R, Eliav E, Sharav Y. Classification of chronic orofacial pain: applicability of chronicheadache criteria. Oral Surg 110:729-737. 2010
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227Pain TerminologyPainAn unpleasant sensory and emotional experience associated with actual or potential tissue damage, ordescribed in terms of such damage.Note: The inability to communicate verbally does not negate the possibility that an individual isexperiencing pain and is in need of appropriate pain-relieving treatment. Pain is always subjective.Each individual learns the application of the word through experiences related to injury in early life.Biologists recognize that those stimuli which cause pain are liable to damage tissue. Accordingly,pain is that experience we associate with actual or potential tissue damage. It is unquestionably asensation in a part or parts of the body, but it is also always unpleasant and therefore also anemotional experience. Experiences which resemble pain but are not unpleasant, e.g., pricking, shouldnot be called pain. Unpleasant abnormal experiences (dysesthesias) may also be pain but are notnecessarily so because, subjectively, they may not have the usual sensory qualities of pain. Manypeople report pain in the absence of tissue damage or any likely pathophysiological cause; usuallythis happens for psychological reasons. There is usually no way to distinguish their experience fromthat due to tissue damage if we take the subjective report. If they regard their experience as pain, andif they report it in the same ways as pain caused by tissue damage, it should be accepted as pain. Thisdefinition avoids tying pain to the stimulus. Activity induced in the nociceptor and nociceptivepathways by a noxious stimulus is not pain, which is always a psychological state, even though wemay well appreciate that pain most often has a proximate physical cause.AllodyniaPain due to a stimulus that does not normally provoke pain.Note: The stimulus leads to an unexpectedly painful response. This is a clinical term that does notimply a mechanism. Allodynia may be seen after different types of somatosensory stimuli applied tomany different tissues.The term allodynia was originally introduced to separate from hyperalgesia and hyperesthesia, theconditions seen in patients with lesions of the nervous system where touch, light pressure, ormoderate cold or warmth evoke pain when applied to apparently normal skin. Allo means "other" inGreek and is a common prefix for medical conditions that diverge from the expected. Odynia isderived from the Greek word "odune" or "odyne," which is used in "pleurodynia" and "coccydynia"and is similar in meaning to the root from which we derive words with -algia or -algesia in
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228them. Allodynia was suggested following discussions with Professor Paul Potter of the Department ofthe History of Medicine and Science at The University of Western Ontario.The words "to normal skin" were used in the original definition but later were omitted in order toremove any suggestion that allodynia applied only to referred pain. Originally, also, the pain-provoking stimulus was described as "non-noxious." However, a stimulus may be noxious at sometimes and not at others, for example, with intact skin and sunburned skin, and also, the boundaries ofnoxious stimulation may be hard to delimit. Since the Committee aimed at providing terms forclinical use, it did not wish to define them by reference to the specific physical characteristics of thestimulation, e.g., pressure in kilopascals per square centimeter. Moreover, even in intact skin there islittle evidence one way or the other that a strong painful pinch to a normal person does or does notdamage tissue. Accordingly, it was considered to be preferable to define allodynia in terms of theresponse to clinical stimuli and to point out that the normal response to the stimulus could almostalways be tested elsewhere in the body, usually in a corresponding part. Further, allodynia is taken toapply to conditions which may give rise to sensitization of the skin, e.g., sunburn, inflammation, ortrauma.It is important to recognize that allodynia involves a change in the quality of a sensation, whethertactile, thermal, or of any other sort. The original modality is normally nonpainful, but the response ispainful. There is thus a loss of specificity of a sensory modality. By contrast, hyperalgesia (q.v.)represents an augmented response in a specific mode, viz., pain. With other cutaneousmodalities, hyperesthesia is the term which corresponds to hyperalgesia, and as with hyperalgesia,the quality is not altered. In allodynia, the stimulus mode and the response mode differ, unlike thesituation with hyperalgesia. This distinction should not be confused by the fact that allodynia andhyperalgesia can be plotted with overlap along the same continuum of physical intensity in certaincircumstances, for example, with pressure or temperature.See also the notes on hyperalgesia and hyperpathia.AnalgesiaAbsence of pain in response to stimulation which would normally be painful.Note: As with allodynia (q.v.), the stimulus is defined by its usual subjective effects.DysesthesiaAn unpleasant abnormal sensation, whether spontaneous or evoked.
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229Note: Compare with pain and with paresthesia. Special cases of dysesthesia include hyperalgesia andallodynia. A dysesthesia should always be unpleasant and a paresthesia should not be unpleasant,although it is recognized that the borderline may present some difficulties when it comes to decidingas to whether a sensation is pleasant or unpleasant. It should always be specified whether thesensations are spontaneous or evoked.Hyperalgesia*Increased pain from a stimulus that normally provokes pain.Note: Hyperalgesia reflects increased pain on suprathreshold stimulation. This is a clinical term thatdoes not imply a mechanism. For pain evoked by stimuli that usually are not painful, theterm allodynia is preferred, while hyperalgesia is more appropriately used for cases with anincreased response at a normal threshold, or at an increased threshold, e.g., in patients withneuropathy. It should also be recognized that with allodynia the stimulus and the response are indifferent modes, whereas with hyperalgesia they are in the same mode. Current evidence suggeststhat hyperalgesia is a consequence of perturbation of the nociceptive system with peripheral orcentral sensitization, or both, but it is important to distinguish between the clinical phenomena, whichthis definition emphasizes, and the interpretation, which may well change as knowledge advances.Hyperalgesia may be seen after different types of somatosensory stimulation applied to differenttissues.HyperesthesiaIncreased sensitivity to stimulation, excluding the special senses.Note: The stimulus and locus should be specified. Hyperesthesia may refer to various modes ofcutaneous sensibility including touch and thermal sensation without pain, as well as to pain. Theword is used to indicate both diminished threshold to any stimulus and an increased response tostimuli that are normally recognized.Allodynia is suggested for pain after stimulation which is not normallypainful. Hyperesthesia includes both allodynia and hyperalgesia, but the more specific terms shouldbe used wherever they are applicable.HyperpathiaA painful syndrome characterized by an abnormally painful reaction to a stimulus, especially arepetitive stimulus, as well as an increased threshold.
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230Note: It may occur with allodynia, hyperesthesia, hyperalgesia, or dysesthesia. Faulty identificationand localization of the stimulus, delay, radiating sensation, and aftersensation may be present, andthe pain is often explosive in character.HypoalgesiaDiminished pain in response to a normally painful stimulus.Note: Hypoalgesia was formerly defined as diminished sensitivity to noxious stimulation, making it aparticular case of hypoesthesia (q.v.). However, it now refers only to the occurrence of relatively lesspain in response to stimulation that produces pain. Hypoesthesia covers the case of diminishedsensitivity to stimulation that is normally painful.HypoesthesiaDecreased sensitivity to stimulation, excluding the special senses.Note: Stimulation and locus to be specified.NeuralgiaPain in the distribution of a nerve or nerves.Note: Common usage, especially in Europe, often implies a paroxysmal quality, but neuralgia shouldnot be reserved for paroxysmal pains.NeuritisInflammation of a nerve or nerves.Note: Not to be used unless inflammation is thought to be present.Neuropathic pain*Pain caused by a lesion or disease of the somatosensory nervous system.Note: Neuropathic pain is a clinical description (and not a diagnosis) which requires a demonstrablelesion or a disease that satisfies established neurological diagnostic criteria. The term lesion iscommonly used when diagnostic investigations (e.g. imaging, neurophysiology, biopsies, lab tests)reveal an abnormality or when there was obvious trauma. The term disease is commonly used whenthe underlying cause of the lesion is known (e.g. stroke, vasculitis, diabetes mellitus, geneticabnormality). Somatosensory refers to information about the body per se including visceral organs,rather than information about the external world (e.g., vision, hearing, or olfaction). The presence ofsymptoms or signs (e.g., touch-evoked pain) alone does not justify the use of the term neuropathic.
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231Some disease entities, such as trigeminal neuralgia, are currently defined by their clinicalpresentation rather than by objective diagnostic testing. Other diagnoses such as postherpeticneuralgia are normally based upon the history. It is common when investigating neuropathic pain thatdiagnostic testing may yield inconclusive or even inconsistent data. In such instances, clinicaljudgment is required to reduce the totality of findings in a patient into one putative diagnosis orconcise group of diagnoses.Central neuropathic pain*Pain caused by a lesion or disease of the central somatosensory nervous system. See neuropathicpain note.Peripheral neuropathic pain*Pain caused by a lesion or disease of the peripheral somatosensory nervous system. See neuropathicpain note.Neuropathy*A disturbance of function or pathological change in a nerve: in one nerve, mononeuropathy; inseveral nerves, mononeuropathy multiplex; if diffuse and bilateral, polyneuropathy.Note: Neuritis (q.v.) is a special case of neuropathy and is now reserved for inflammatory processesaffecting nerves.Nociception*The neural process of encoding noxious stimuli.Note: Consequences of encoding may be autonomic (e. g. elevated blood pressure) or behavioral(motor withdrawal reflex or more complex nocifensive behavior). Pain sensation is not necessarilyimplied.Nociceptive pain*Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation ofnociceptors.Note: This term is designed to contrast with neuropathic pain. The term is used to describe painoccurring with a normally functioning somatosensory nervous system to contrast with the abnormalfunction seen in neuropathic pain.Nociceptive stimulus*
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232An actually or potentially tissue-damaging event transduced and encoded by nociceptors.Nociceptor*A high-threshold sensory receptor of the peripheral somatosensory nervous system that is capable oftransducing and encoding noxious stimuli.Nociplastic pain*Pain that arises from altered nociception despite no clear evidence of actual or threatened tissuedamage causing the activation of peripheral nociceptors or evidence for disease or lesion of thesomatosensory system causing the pain.Note: Patients can have a combination of nociceptive and nociplastic painNoxious stimulus*A stimulus that is damaging or threatens damage to normal tissues.Pain threshold*The minimum intensity of a stimulus that is perceived as painful.Note: Traditionally the threshold has often been defined, as we defined it formerly, as the leaststimulus intensity at which a subject perceives pain. Properly defined, the threshold is really theexperience of the patient, whereas the intensity measured is an external event. It has been commonusage for most pain research workers to define the threshold in terms of the stimulus, and that shouldbe avoided. However, the threshold stimulus can be recognized as such and measured. Inpsychophysics, thresholds are defined as the level at which 50% of stimuli are recognized. In thatcase, the pain threshold would be the level at which 50% of stimuli would be recognized as painful.The stimulus is not pain (q.v.) and cannot be a measure of pain.Pain tolerance level*The maximum intensity of a pain-producing stimulus that a subject is willing to accept in a givensituation.Note: As with pain threshold, the pain tolerance level is the subjective experience of the individual.The stimuli which are normally measured in relation to its production are the pain tolerance levelstimuli and not the level itself. Thus, the same argument applies to pain tolerance level as to painthreshold, and it is not defined in terms of the external stimulation as such.
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233ParesthesiaAn abnormal sensation, whether spontaneous or evoked.Note: Compare with dysesthesia. After much discussion, it has been agreed to recommendthat paresthesia be used to describe an abnormal sensation that is not unpleasant while dysesthesia beused preferentially for an abnormal sensation that is considered to be unpleasant. The use of one term(paresthesia) to indicate spontaneous sensations and the other to refer to evoked sensations is notfavored. There is a sense in which, since paresthesia refers to abnormal sensations in general, it mightinclude dysesthesia, but the reverse is not true. Dysesthesia does not include all abnormal sensations,but only those that are unpleasant.Sensitization*Increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of aresponse to normally subthreshold inputs.Note: Sensitization can include a drop in threshold and an increase in suprathreshold response.Spontaneous discharges and increases in receptive field size may also occur. This is aneurophysiological term that can only be applied when both input and output of the neural systemunder study are known, e.g., by controlling the stimulus and measuring the neural event. Clinically,sensitization may only be inferred indirectly from phenomena such as hyperalgesia or allodynia.Central sensitization*Increased responsiveness of nociceptive neurons in the central nervous system to their normal orsubthreshold afferent input.Note: See note for sensitization and nociceptive neuron above. This may include increasedresponsiveness due to dysfunction of endogenous pain control systems. Peripheral neurons arefunctioning normally; changes in function occur in central neurons only.Peripheral sensitization*Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to thestimulation of their receptive fields.Note: See note for sensitization above.References
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234Part III: Pain Terms, A Current List with Definitions and Notes on Usage" (pp 209-214)Classification of Chronic Pain, Second Edition, IASP Task Force on Taxonomy, edited by H.Merskey and N. Bogduk, IASP Press, Seattle, 1994 (updated December 14, 2017. Accessed8/8/2018: http://www.iasp-pain.org/Education/Content.aspx?ItemNumber=1698)1. Orofacial pain associated with disorders of dentoalveolar and associated structures
1.1 Dental pain
1.1.1 Pulpal pain
1.1.1.1. Pulpal pain attributed to hypersensitivity
1.1.1.1.1 Pulpal pain attributed to a crack in the enamel
1.1.1.1.2 Pulpal pain attributed to exposed dentin
1.1.1.1.2.1 Pulpal pain attributed to tooth wear or abrasion
1.1.1.1.2.2 Pulpal pain attributed to fracture resulting in exposed dentin
1.1.1.1.2.3 Pulpal pain attributed to developmental dental hard tissue defect
1.1.1.1.3 Pulpal pain attributed to hypersensitivity associated with dental procedures
1.1.1.1.3.1 Pulpal pain attributed to recent extensive removal of dentin
1.1.1.1.3.2 Pulpal pain attributed to recent placement of a restoration
1.1.1.1.3.3 Pulpal pain attributed to hypersensitivity due to hyperocclusion or-articulation following dental restorative procedures
1.1.1.1.4 Pulpal pain attributed to central sensitization
1.1.1.1.5 Pulpal pain attributed to other cause
1.1.1.2 Pulpal pain attributed to pulp exposure due to dental trauma
1.1.1.3 Pulpal pain attributed to pulpitis (pulpal inflammation)
1.1.1.3.1 Pulpal pain attributed to reversible pulpitis due to infection of dentin
1.1.1.3.1.1 Pulpal pain attributed to caries that does not extend to the pulp
1.1.1.3.1.2 Pulpal pain attributed to reversible pulpitis due to fracture of enamel, rootcementum, dentin or any combination thereof, resulting in exposure of dentin
1.1.1.3.1.3 Pulpal pain attributed to reversible pulpitis due to a tooth crack withoutevidence of missing tooth substance
1.1.1.3.2 Pulpal pain attributed to irreversible pulpitis due to infection of dentin
1.1.1.3.2.1 Pulpal pain attributed to caries which may extend to the pulp
1.1.1.3.2.2 Pulpal pain attributed to irreversible pulpitis due to dental hard tissuefracture without pulp exposure
111.1.1.3.2.3 Pulpal pain attributed to irreversible pulpitis due to visible crack in theenamel without evidence of missing tooth substance
1.1.1.3.3 Pulpal pain attributed to irreversible pulpitis due to infection of the dental pulp
1.1.1.3.3.1 Pulpal pain attributed to caries extending to the pulp
1.1.1.3.3.2 Pulpal pain attributed to irreversible pulpitis due to dental hard tissue fracturewithout pulp exposure
1.1.1.3.4 Pulpal pain attributed to pulpitis due to external cervical root resorption
1.1.1.3.5 Pulpal pain attributed to pulpitis due to other cause
1.1.1.4 Pulpal pain attributed to systemic cause
1.1.2 Periodontal pain
1.1.2.1 Periodontal pain attributed to periodontitis (periodontal inflammation of theperiodontium)
1.1.2.1.1 Periodontal pain attributed to traumatically induced periodontal infammation
1.1.2.1.1.1 Periodontal pain attributed to hyperocclusion or -articulation
1.1.2.1.1.2 Postoperative periodontal pain
1.1.2.1.1.3 Periodontal pain attributed to accidental dental trauma
1.1.2.1.1.4 Periodontal pain attributed to other trauma or injury
1.1.2.1.2 Periodontal pain attributed to apical periodontitis due to endodontic disease
1.1.2.1.2.1 Periodontal pain attributed to pulpal inflammation
1.1.2.1.2.2 Periodontal pain attributed to endodontic infection
1.1.2.1.2.2.1 Periodontal pain attributed to intraradicular endodontic infection
1.1.2.1.2.2.2 Periodontal pain attributed to extraradicular endodontic infection
1.1.2.1.3 Periodontal pain attributed to periodontal disease
1.1.2.1.3.1 Periodontal pain attributed to chronic periodontitis
1.1.2.1.3.2 Periodontal pain attributed to aggressive periodontitis
1.1.2.1.3.3 Periodontal pain attributed to periodontitis as a manifestation of systemicdisorder known to cause periodontitis
1.1.2.1.3.3.1 Periodontal pain attributed to a hematological disorder
1.1.2.1.3.3.2 Periodontal pain attributed to a genetic disorder
1.1.2.1.3.3.3 Periodontal pain attributed to an unspecified systemic disorder
1.1.2.1.3.4 Periodontal pain associated with necrotizing ulcerative periodontitis (NUP)
1.1.2.1.3.5 Periodontal pain associated with periodontal abscess
1.1.2.1.4 Periodontal pain attributed to apical and marginal periodontitis due to combinedendodontic infection and periodontal disease
1.1.2.1.5 Periodontal pain attributed to peri-implantitis due to peri-implant infection
1.1.2.2 Periodontal pain attributed to a local non-inflammatory cause
1.1.3 Gingival pain
1.1.3.1 Gingival pain attributed to gingivitis (gingival inflammation)
1.1.3.1.1 Gingival pain attributed to trauma
1.1.3.1.2 Gingival pain attributed to infection
1.1.3.1.2.1 Gingival pain attributed to bacterial infection
1.1.3.1.2.2 Gingival pain attributed to viral infection
1.1.3.1.2.3 Gingival pain attributed to fungal infection
1.1.3.1.3 Gingival pain attributed to autoimmunity
1.1.3.1.4 Gingival pain attributed to allergic reaction
1.1.3.1.5 Gingival pain attributed to gingival inflammation due to other cause
1.1.3.2 Gingival pain attributed to malignant lesion
1.1.3.3 Gingival pain attributed to neuropathy
1.1.3.4 Idiopathic gingival pain
1.2 Non-dental pain
1.2.1 Oral mucosal pain
1.2.1.1 Oral mucosal pain attributed to oral mucosal inflammation
1.2.1.1.1 Oral mucosal pain associated with trauma
1.2.1.1.1.1 Oral mucosal pain attributed to mechanical, thermal, or chemical injury
1.2.1.1.1.2 Oral mucosal pain attributed to surgical or other iatrogenic injury
1.2.1.1.1.3 Oral mucosal pain attributed to radiation or chemotherapy
1.2.1.1.2 Oral mucosal pain attributed to infection
1.2.1.1.2.1 Oral mucosal pain attributed to bacterial infection
1.2.1.1.2.2 Oral mucosal pain attributed to viral infection
1.2.1.1.2.3 Oral mucosal pain attributed to fungal infection
1.2.1.1.3 Oral mucosal pain attributed to autoimmunity
1.2.1.1.4 Oral mucosal pain attributed to allergic reaction
1.2.1.1.5 Oral mucosal pain attributed to oral mucosal inflammation due to other cause
1.2.1.2 Oral mucosal pain attributed to malignant lesion
1.2.1.3 Oral mucosal pain attributed to neuropathy
1.2.1.4 Idiopathic oral mucosal pain
1.2.2 Salivary gland pain
1.2.2.1 Salivary gland pain attributed to obstructive cause
1.2.2.2 Salivary gland pain attributed to infection
1.2.2.2.1 Salivary gland pain attributed to viral infection
1.2.2.2.2 Salivary gland pain attributed to bacterial infection
1.2.2.3 Salivary gland pain attributed to non-infectious cause
1.2.2.3.1 Salivary gland pain attributed to recurrent juvenile parotitis
1.2.2.3.2 Salivary gland pain attributed to immunologically mediated disorder
1.2.2.3.3 Salivary gland pain attributed to other cause
1.2.3 Jaw bone pain
1.2.3.1 Jaw bone pain attributed to infection
1.2.3.1.1 Jaw bone pain attributed to bacterial infection
1.2.3.1.2 Jaw bone pain attributed to viral infection
1.2.3.1.3 Jaw bone pain attributed to fungal infection
1.2.3.2 Therapy related jaw bone pain
1.2.3.3 Jaw bone pain attributed to a local benign lesion
1.2.3.4 Jaw bone pain attributed to a malignant lesion
1.2.3.4.1 Jaw bone pain attributed to a primary malignant lesion
1.2.3.4.2 Jaw bone pain secondary to a malignant lesion
1.2.3.5 Jaw bone pain attributed to systemic disease
1.2.3.6 Jaw bone pain attributed to traumatic injury
2. Orofacial pain associated with regional muscles
2.1. Primary myofascial pain
2.1.1. Acute primary myofascial pain
2.1.2. Chronic primary myofascial pain
2.1.2.1. Chronic infrequent primary myofascial pain
2.1.2.2. Chronic frequent primary myofascial pain
2.1.2.2.1. Chronic frequent primary myofascial pain without pain referral
2.1.2.2.2. Chronic frequent primary myofascial pain with pain referral
2.1.2.3. Chronic persistent primary myofascial pain
2.1.2.3.1. Chronic persistent primary myofascial pain without pain referral
2.1.2.3.2. Chronic persistent primary myofascial pain with pain referral
2.2. Secondary myofascial pain
2.2.1. Secondary myofascial pain due to tendonitis
2.2.2. Secondary myofascial pain due to myositis
2.2.3. Secondary myofascial pain due to muscle spasm
3. Orofacial pain associated with disorders of the Temporomandibular Joint (TMJ)
3.1. Primary TMJ arthralgia
3.1.1. Acute primary TMJ arthralgia
3.1.2. Chronic primary TMJ arthralgia
3.1.2.1. Chronic infrequent primary TMJ arthralgia
3.1.2.2. Chronic frequent primary TMJ arthralgia
3.1.2.2.1. Chronic frequent primary TMJ arthralgia without referred pain
3.1.2.2.2. Chronic frequent primary TMJ arthralgia with referred pain
3.1.2.3. Chronic persistent primary TMJ arthralgia
3.1.2.3.1. Chronic persistent primary TMJ arthralgia without referred pain
3.1.2.3.2. Chronic persistent primary TMJ arthralgia with referred pain
3.2. Secondary TMJ arthralgia
3.2.1. TMJ arthralgia attributed to arthritis
3.2.1.1. TMJ arthralgia attributed to arthritis, non-systemic
3.2.1.2. TMJ arthralgia attributed to arthritis, systemic
3.2.2. TMJ arthralgia attributed to disc displacement with reduction
3.2.3. TMJ arthralgia attributed to disc displacement with reduction with intermittentlocking
3.2.4. TMJ arthralgia attributed to disc displacement without reduction
3.2.5. TMJ arthralgia attributed to degenerative joint disease
3.2.6. TMJ arthralgia attributed to subluxation
4. Orofacial pain associated with lesion/disorders of the cranial nerves and other regionalnerve structures
4.1. Pain caused by a lesion or disease of the trigeminal nerve
4.1.1. Trigeminal neuralgia
4.1.1.1. Classical trigeminal neuralgia 4.1.1.1.1. Classical trigeminal neuralgia, purely paroxysmal
4.1.1.1.2. Classical trigeminal neuralgia with concomitant continuous pain
4.1.1.2. Secondary trigeminal neuralgia
4.1.1.2.1. Trigeminal neuralgia attributed to multiple sclerosis
4.1.1.2.2. Trigeminal neuralgia attributed to space-occupying lesion
4.1.1.2.3. Trigeminal neuralgia attributed to other demonstrable causes
4.1.1.3. Idiopathic trigeminal neuralgia
4.1.1.3.1. Idiopathic trigeminal neuralgia, purely paroxysmal
4.1.1.3.2. Idiopathic trigeminal neuralgia with concomitant continuouspain
4.1.2. Trigeminal neuropathic pain other than
4.1.1. Clinically established trigeminalneuralgia
4.1.2.1. Trigeminal neuropathic pain attributed to herpes Zoster
4.1.2.2. Trigeminal postherpetic neuralgia
4.1.2.3. Post-traumatic trigeminal neuropathic pain
4.1.2.3.1. Probable post-traumatic trigeminal neuropathic pain
4.1.2.4. Trigeminal neuropathic pain attributed to another disorder
4.1.2.4.1. Probable trigeminal neuropathic pain attributed to anotherdisorder
4.1.2.5. Idiopathic trigeminal neuropathic pain
4.1.2.5.1. Probable idiopathic trigeminal neuropathic pain
4.2. Pain caused by a lesion or disease of the glossopharyngeal nerve
4.2.1. Clinically established glossopharyngeal neuralgia
4.2.1.1. Classical glossopharyngeal neuralgia
4.2.1.2. Secondary glossopharyngeal neuralgia
4.2.1.3. Idiopathic glossopharyngeal neuralgia
4.2.2. Glossopharyngeal neuropathic pain
4.2.2.1. Glossopharyngeal neuropathic pain attributed to a known cause
4.2.2.2. Idiopathic glossopharyngeal neuropathic pain
5. Orofacial pain resembling presentations of primary headaches
5.1. Orofacial migraine
5.1.1. Orofacial migraine
5.1.2. Chronic orofacial migraine
5.1.3 Neurovascular Orofacial Pain
5.1.3.1 Shortlasting Neurovascular Orofacial Pain
5.1.3.2 Longlasting Neurovascular Orofacial Pain
5.2. Tension-type orofacial pain
5.3. Trigeminal autonomic orofacial pain
5.3.1. Orofacial cluster attacks
5.3.1.1. Episodic orofacial cluster attacks
5.3.1.2. Chronic orofacial cluster attacks
5.3.2. Paroxysmal hemifacial pain
5.3.2.1. Episodic paroxysmal hemifacial pain5.3.2.2. Chronic paroxysmal hemifacial pain
5.3.3. Short-lasting unilateral neuralgiform facial pain attacks with autonomic signs(SUNFA)
5.3.3.1. Episodic SUNFA
5.3.3.2. Chronic SUNFA
5.3.4. Hemifacial continuous pain with autonomic signs
5.3.5 Constant Unilateral Facial Pain with Attacks (CUFPA)
6. Idiopathic orofacial pain
6.1. Burning mouth syndrome (BMS)
6.1.1. Burning mouth syndrome associated with somatosensory changes
6.1.2. Burning mouth syndrome not associated with somatosensory changes
6.2. Persistent idiopathic facial pain (PIFP)
6.2.1. Persistent idiopathic facial pain associated with somatosensory changes
6.2.2. Persistent idiopathic facial pain not associated with somatosensory changes
6.3. Persistent idiopathic dentoalveolar pain
6.3.1. Persistent idiopathic dentoalveolar pain associated with somatosensory changes
6.3.2. Persistent idiopathic dentoalveolar pain not associated with somatosensory changes
7. Psychosocial Assesment
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Format: AbstractSend to
Expert Rev Neurother. 2012 May;12(5):569-76. doi: 10.1586/ern.12.40.
The classification and differential diagnosis of orofacial pain.
Renton T1, Durham J, Aggarwal VR.
Author information
1
Department Oral Surgery, Kings College London Dental Institute, Denmark Hill Campus, Bessemer Road, London SE5 9RS, UK. tara.renton@kcl.ac.uk
Abstract
There are currently four main pain classification systems relevant to orofacial pain (OFP): the International Association for the Study of Pain, International Classification of Headache Disorders, the American Academy of Orofacial Pain and the Research Diagnostic Criteria for Temporomandibular Disorders. Of the four, the Research Diagnostic Criteria for Temporomandibular Disorders is the most biopsychosocial system, with the remaining three focusing more on the biomedical aspects. Unsurprisingly, clinical scientists and clinicians have both reported perceived deficiencies in the published systems and have proposed further modified classifications and nomenclature for OFP. Establishing a standardized biopsychosocial classification of OFP is essential for ensuring continuity for patient care since it creates a standardized language with which to communicate healthcare information, thus enabling improved and more specific (epidemiological) research and patient care. Despite ongoing attempts, an accepted overarching classification of OFP is still a work in progress. There is an urgent need for a robust classification system for OFP. This review aims to highlight the recent debate and continued struggle to attain a consensus on a classification of OFP and highlight some recent developments that assist differential diagnosis of these conditions.
PMID: 22550985 DOI: 10.1586/ern.12.40
Web results
Using ICOP. 135. Rules of use. 135. Classification overview. 141. 1. Orofacial pain attributed to disorders of dentoalveolar and anatomically related structures.
Orofacial Pain (AAOP) and the International Headache Society (IHS) has worked over the past 3 years to present such a classification for facial pain which is ...
Jan 30, 2020 - For example, the International Headache Society (IHS) defines facial pain as 'pain below the orbitomeatal line, anterior to the pinnae and above the neck'. Other definitions of facial pain additionally include the forehead, while the term 'orofacial pain' necessarily includes all the structures in the oral cavity.
Orofacial pain classification—A new milestone and new implications:
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