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ABSTRACT Persistent facial Persistent facial conditions pain conditions

Persistent facial , especially temporoman- dibular disorders (TMD), are common condi- Heli Forssell , associate professor, ph.d., Department of Oral and Max- tions. As dentists are responsible for the treat- illofacial Surgery, Institute of Dentistry, University of Turku, Finland ment of most of these disorders, up-to date Per Alstergren, associate professor, med.dr., ph.d., Department of knowledge on the latest advances in the field and Jaw Function, Orofacial Pain Unit, Faculty of Od- is essential for successful diagnosis and man- ontology, Malmö University, Malmö, Sweden; Skåne University Hospi- tal, Specialized Pain Rehabilitation, Lund, Sweden and Scandinavian agement. The review covers TMD, and differ- Center for Orofacial Neurosciences (SCON). ent neuropathic or putative neuropathic facial Merete Bakke, associate professor, dr.odont., ph.d., Department of pains such as persistent idiopathic facial pain Odontology, Faculty of Health and Medical Sciences, University of Co- and atypical odontalgia, trigeminal penhagen, Denmark and painful posttraumatic trigeminal neuropa- Tore Bjørnland, professor and chair, ph.d., Department of Oral Surgery thy. The article presents an overview of TMD and Oral Medicine, Institute of Clinical Dentistry, Faculty of Dentistry, University of Oslo, Norway pain as a biopsychosocial condition, its preva- lence, clinical features, consequences, central Satu K. Jääskeäinen, professor and chair, ph.d., Department of Clinical and peripheral mechanisms, diagnostic criteria Neurophysysiology, Turku University Hospital and University of Turku, Finland (DC/TMD), and principles of management. For each of the neuropathic facial pain entities, the definitions, prevalence, clinical features, and diagnostics are described. The current under- ersistent facial pains, especially temporomandibular standing of the pathophysiology of these enti- disorders (TMD), are common conditions; their prev- ties is presented, and a description of the evi- alence is in the range of 8-15%. As patients often pre- dence based treatment methods is provided. sent complaints of facial pain to their dentist, it is im- Pportant that dentists are familiar with these conditions. Many advances have been made during recent decades in the under- standing of chronic facial pain, such as increased knowledge of the peripheral and central neural processes involved in differ- ent facial pain entities, recognition of the multidimensional na- ture of pain, and improvements in evidence-based treatments, both physical and behavioural, for different conditions. The present article aims to provide up-to-date information on dif- ferent chronic facial pain entities to enhance their recognition and proper treatment or referral.

Temporomandibular disorders Temporomandibular disorders (TMD) are recognized as a group of musculoskeletal and neuromuscular conditions that involve the temporomandibular joints (TMJs), the masticatory muscles, and associated tissues (1). The most common of TMD are orofacial pain and impaired jaw function. TMD patients often suffer from other painful disor- ders, and other comorbidities, such as sleep

EMNEORD disorders. The chronic forms of TMD pain

Temporomandibular may lead to absence from or impairment of disorders; idiopathic work or social interactions, resulting in an facial pain; neuropathic overall reduction in the quality of life. facial pain; trigeminal Communication with author: neuralgia; pain patho- TMD is common in the adult population Heli Forssell, e-mail: [email protected] physiology and seem to affect women more than men

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(2), and the prevalence is reported to be between 5-12 % (3). central modulation of pain (13,14). Aberrant activation pat- The prevalence is lowest in children, and symptoms and clinical terns have been demonstrated in response to painful stimuli in findings increase through adolescence, peak in adulthood and chronic pain states such as (15), a chronic pain seem to decrease in the elderly. Muscle disorders, disc displace- condition often associated with TMD. ments, and other joint disorders are frequent findings in the pa- The multidimensionality of pain perception is supported tients. As in other joints there may be pathological changes of by activation of brain areas not only associated with the per- the TMJs both because of localized degenerative joint diseases ception of sensory features (e.g. somatosensory cortices) but or systemic diseases. However, most disorders are primary and even more so regions associated with emotional and cognitive localized, and can be divided into non-infectious inflamma- aspects of pain (16). These regions are known to play critical tory disorders, and disc displacements and degenerative joint roles in various aspects of pain experiences. In addition, brain disorders. The conditions may be associated with a feeling of areas involved in the regulation of the autonomic nervous sys- tenderness, stabbing or radiant pain from the joints during tem and endogenous pain modulation are affected. In an fMRI rest and shooting pain during jaw function. In addition the jaw study, during periods of ongoing low only brain re- movements may be restricted, irregular or asymmetric and as- gions of importance for emotional and cognitive aspects of pain sociated with TMJ clicking or crepitation, and secondarily the were activated (17). These findings indicate that the perception chewing pattern may be changed and the bite force reduced of chronic, ongoing pain requires only limited involvement of (4). Disorders of the masticatory muscles often start gradually the somatosensory areas. Central sensitization is still difficult as episodes of fatigue, tension and stiffness, which may evolve to clinically assess and quantify but may impact all levels of the into more persistent dull and pressing pain localized to the biopsychosocial model of chronic pain: biological changes, psy- cheeks, jaws, temples or even . chological aspects and social aspects.

Central and peripheral mechanisms Diagnosis of TMD in general and specialist practice The pathophysiology and aetiology of TMD are not yet well The recently published Diagnostic Criteria for Temporoman- understood. Peripheral and central sensitization seems to con- dibular Disorders (DC/TMD; 18) provides a simple and highly tribute synergistically to this condition, which may explain why accurate methodology to diagnose TMD. DC/TMD comprises many of these patients need multidisciplinary and multimodal two axes; Axis I that provides a diagnosis of the clinical con- approaches to diagnostics and therapy (5). dition (orofacial pain of myogenous or arthrogenous origin, The relation between peripheral pathology and pain mani- headache attributed to TMD as well as disc displacement and festations is often weak in chronic orofacial pain. For exam- degenerative joint disease) while Axis II provides a biopsycho- ple, clinical signs and symptoms of TMD do not discriminate social estimate of the degree of psychosocial distress. The DC/ between treatment responders and non-responders (6). TMD TMD is currently available in English and Swedish but transla- patients seem to be more sensitive than TMD-free controls tions into at least 25 more languages are ongoing. For Finnish, to experimental pain, both in the orofacial areas as well as in Dutch and German the translation process is very near comple- other parts of the body (7,8). While central mechanisms have tion and these translations may very well be available at this been implicated in this increased sensitivity, there is also a role time. Please see www.rdc-tmdinternational.org for details. of peripheral sensitization that contributes to changes in noci- DC/TMD diagnostics is divided into three levels: screen- ceptive and sensory input. Experimental injections of algesic ing, a short version for general dentistry and a comprehensive substances like bradykinin, serotonin and glutamate into jaw version to be used in specialist clinics. The aim of the screen- muscle tissue result in muscle pain similar to that observed in ing is to identify patients with potential TMD symptoms. This patients with chronic myalgia of the masticatory muscles (8,9). is possible by asking each patient two questions with a “Yes” There is also convincing evidence that peripheral changes in or “No” alternative: i) Do you have pain in the temples, face, the levels of certain mediators in the TMJ and masticatory mus- temporomandibular joints or jaws once a week or more often? cle are related to pain. In particular, mediators like cytokines and ii) Do you have pain when you open your mouth or chew and serotonin have been investigated in both the TMJ and mus- once a week or more often? If the patient answers “Yes” on one cle tissues (10). or two questions, it is highly likely that the patient has a DC/ Central sensitization refers to neurofunctional changes of TMD diagnosis (sensitivity: 0.98, specificity 0.83 for the two the somatosensory system in the spinal cord, brain stem and first questions; 19). The majority of patients identified with this the brain pain matrix (11). There is substantial evidence that instrument request treatment for their problems, making this central pain mechanisms are disturbed in chronic orofacial instrument clinically relevant and useful (20). pain. For example, reduced cognitive ability predicts treatment The clinical DC/TMD examination may lead to one or more outcome (6). Furthermore, chronic orofacial pain patients Axis I diagnoses and will provide information about psychoso- show increased spatial distribution of TMD pain, increased cial factors of importance in Axis II. Axis I diagnostics uses in- temporal summation in remote body areas (12) and impaired formation from a questionnaire as well as findings in the struc-

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tured clinical examination. The clinical examination is strictly appliances, thermal physical therapy and temporary use of an- specified, including commands to the patient and palpation algesics, non-steroidal anti-inflammatory drugs (NSAIDs), and sites. Axis II evaluation of psychosocial factors uses validated intra-articular injections with glucocorticoid (26). In severe questionnaires with established cut-offs. The questionnaires and complicated TMD, a team approach, usually consisting of a recommended in DC/TMD cover most aspects of pain and its dentist, psychologist, and a physiotherapist, is needed. The ef- consequences as well as risk factors for chronic pain (18). The ficacy of different TMD treatment methods, as well as the mul- purpose is to assess to what degree psychosocial factors con- tidisciplinary/multimodal management of patients with severe tribute, and to use this information to guide treatment planning symptoms is described in other articles of the Nordic Theme and to evaluate prognosis. In general practice, these instru- 2016. ments can also guide whether to refer the patient or to begin Regarding TMJ surgery, numerous articles over the past 35 treatment. years have dealt with interventions of the TMJ from injections The DC/TMD does not cover all chronic orofacial pain and to open surgery, but these interventions have not yet been suffi- jaw dysfunction conditions. The Expanded DC/TMD Taxonomy ciently evaluated except for ankylosis cases or severe functional (21) attempts to broaden the list of conditions, including gen- disturbances (27). Controlled trials have been sparse and com- eralized pain conditions involving the orofacial region. Condi- parison of different treatment strategies is therefore important. tions not covered by the current DC/TMD, like neuropathic or Schiffman et al (28) found no difference between treatment cervicogenic types of pain, arthritis, fibromyalgia etc., so far strategies relative to any treatment outcome of medical treat- need to be assessed and diagnosed according to other diagnos- ment; non-surgical rehabilitation, arthroscopic surgery and tic methodologies and criteria. open TMJ surgery. Further studies are needed to evaluate the long-term effects of different treatment modalities. To compare Principles of management the outcome of different treatments it is necessary to use stand- As TMD is considered to be a complex, multisystem disorder ardized evaluation methods such as diagnostic criteria for TMD with multiple causes and comorbidities, and a strong genetic (28) or surgical classifications for TMD (29). susceptibility (22), management rather than cure is the realis- tic approach to the treatment of this disorder. The general goal Persistent idiopathic facial pain and atypical odontalgia of management is to alleviate pain, minimize the consequences Persistent idiopathic facial pain (PIFP), also known as atypical of the chronic pain on the patient and restore normal jaw func- facial pain (AFP), is defined as a chronic facial pain in which tions. Unless there are specific and justifiable indications to the signs of structural pathology or other specific causes of pain are contrary, treatment of TMD patients should be based on the use not identified. The term atypical odontalgia (AO) is used when of conservative, reversible therapeutic modalities as studies of chronic pain is felt in a tooth region. AO is considered a sub- the natural history of many TMDs suggest that they tend to im- category of PIFP (30). Prevalence and incidence estimates of prove or resolve over time (1). The fact that widely differing PIFP and AO are limited, but both are rare conditions. Clinical treatment modalities produce comparable treatment effects, case series indicate a preponderance of middle-aged or older suggesting that the positive outcomes of treatment are prob- women among PIFP patients, and chronicity of the symptoms. ably at least partially due to non-specific factors, also speaks for PIFP is usually felt as deep, poorly localized continuous the use of simple methods. When planning treatment several pain. Up to one third may experience bilateral pain. The pain factors, such as physical symptoms and findings, psychosocial is aching, throbbing, or pressing, and the intensity varies from status of the patient, the impact of pain, pain chronicity, the moderate to severe. AO patients report persistent, moderately presence of comorbid pain conditions, and the presence of co- intense, usually well localized intraoral pain. The pain can morbid disorders need to be taken into account. A special focus include any tooth or mucosa of an extraction site, and it may should be on person-specific or Axis II factors, as these are very move from tooth to tooth following dental procedures. Many important in terms of affecting disease course and response to PIFP and AO patients report that the onset of pain is related treatment (23). According to a recent study, most primary care to some type of trauma or surgical procedure, e.g. endodontic TMD patients report mild symptoms and are psychosocially treatment, extraction of teeth, or sinus surgery (31). well functioning, while only about 10% of patients report se- The diagnoses of PIFP and AO can only be made after care- vere symptoms and pain-related psychosocial distress (24). ful exclusion of pathology in teeth or adjacent structures, As there is evidence showing that functional TMD patients neurological disorders, and related systemic diseases, which can be helped by simple means such as counselling, self-care may demand collaboration with several medical specialties. and jaw exercises (25), most TMD patients can be easily treated A thorough clinical and radiological examination is essential. by primary care dentists. Thus TMD pain may be reduced and Examination of trigeminal sensory function with neurophysi- jaw mobility, chewing function and bite force restored with ologic recordings and quantitative sensory tests (QST) are rec- conservative therapy in terms of reassurance and counselling, ommended to improve diagnostic accuracy, as well as head MRI therapeutic home exercises and relaxation of the jaw, occlusal examination to exclude intracranial pathology. As always in

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cases of chronic pain, attention should also be paid to possible CLINICAL RELEVANCE psychological distress (31). In recent years, clinical neurophysiology, QST, and func- tional brain imaging have provided sensitive tools for detailed Persistent facial pains, es- dental practitioner to have investigation of pain mechanisms (32). Clinical neurophysi- pecially temporomandibular knowledge of the diagnosis ological studies have revealed nerve fibre dysfunction in PIFP disorders are common condi- and treatment of different and AO (33,34). Damage to the large tactile nerve fibres and tions in the adult population. persistent facial pain condi- the trigeminal brainstem complex may also occur in both con- Their symptoms may be quite tions in order to avoid misdi- ditions. PET scanning of the brain dopamine system has sug- similar to pain arising from the agnosis and to give the right gested that PIFP may be associated with striatal dopaminergic teeth and periodontium. It is treatment for the various pain hypofunction (35). The current evidence supports the concept therefore important for the conditions. that in the majority of patients with PIFP and AO, the condition is a subclinical trigeminal arising from minor peripheral nerve trauma or a more central trigeminal system lesion (31). There are no curative treatments available for PIFP and AO, cal specialists. When the diagnosis of TN is suspected, the pa- and patients frequently have difficulties in accepting these di- tient should be sent to neurologists for the confirmation of the agnoses and their management, seeking help from different diagnosis, and necessary further examinations. Brain MRI is specialists, and therefore potentially receiving unnecessary in- considered a routine examination for TN patients. Very rarely, vasive dental and surgical treatments, which carry a high risk of posterior fossa tumours may cause typical TN pain. In younger pain aggravation. This stresses the need for patient education, patients with TN symptoms, the possibility of multiple sclerosis and management should be multidisciplinary as the pain is of- should be considered, as TN may be the first manifestation of ten complicated by physical and psychiatric co-morbidity (31). the disease. Randomized controlled trials performed on PIFP and AO are Dentists should know the characteristic features of TN, espe- scarce. However, the experience gained in treatment of other cially because it is important to differentiate the brief, intense, neuropathic pain conditions (36) can be transferred to PIFP and shooting type of pain in TN from pain of dental origin, because AO. The recommended pharmacologic treatment of PIFP and of the similarities between TN and dental conditions such as AO includes tricyclic and gabapentinoids. Be- and . As a result patients with havioural therapies are beneficial complements to biomedical TN may be treated with ineffective dental treatments. The pain approaches. provoking factors aid in differential diagnostics: TN is provoked by tactile stimuli such as touching the skin or brushing the teeth, whereas tooth pain is provoked by thermal (cold or hot) Trigeminal neuralgia (TN) is neuropathic pain with specific and sweet stimuli or percussion or pressure on the teeth. characteristics. The classical type of TN is a sudden, unilat- The aetiology of TN is considered to be due to compression eral, superficial, shooting or electric-shock like pain occurring of the root by a vascular loop in the posterior repeatedly within the distribution of one or more branches of fossa. This is thought to lead to local changes, such as disruption the trigeminal nerve (30). TN is most common in the maxillary of myelin sheet, ephaptic conduction, and secondary hyperex- and mandibular branch, and the paroxysms usually last some citability, which can explain most of the characteristics of TN seconds, but may persist up to 2 minutes. The attacks are often (38). initiated by non-painful physical stimulation of specific areas, The treatment of TN is usually pharmacological. Standard trigger points. The frequency of the paroxysms varies from a treatment is with , and the first choice is usually few to even hundreds per day, but there may also be remission carbamazepine, but the efficacy may be compromised by poor periods with days or even months without attacks. In addition tolerability and pharmacokinetic interactions. A better-toler- to the classical paroxysmal pain attacks, TN patients may also ated alternative is oxcarbazepine with similar efficacy. Other suffer from continuous background pain, especially those with anticonvulsants may be used as add-on medications (39). Neu- more (30). rosurgical procedures, preferably microvascular decompres- TN is a rare; the presented incidence rates range from 12.6/ sion surgery should be considered in case of poor response to 100 000 person years to 28.9/100,000 person years (37). The pharmacotherapy or because of intolerable side effects caused incidence increases with age, and is highest in patients older by medication (40). than 60 years. The diagnosis of TN can only be made on clinical grounds, Painful posttraumatic trigeminal neuropathy and is based on the patient’s pain description, and may there- Trigeminal neuropathic pain may arise from intra- or extra- fore be mistaken for tooth pain, by patients, dentists and medi- cranial lesions within the trigeminal system or general diseases

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causing such as diabetes, connective PPTTN is described as moderate to severe pain, which usu- tissue diseases, or herpes zoster . The most important ally occurs consistently or daily. The pain is often characterized form of trigeminal neuropathic pain which dentists, and espe- as burning, lancinating, stubbing, pressing or tingling (44), and cially oral- and maxillofacial surgeons, should be aware of is, is accompanied by sensory alterations, in most cases in the form however, neuropathic pain caused by iatrogenic nerve damage. of reduced function. Diagnosis of PPTTN can in some cases be This entity belongs to peripheral painful posttraumatic trigemi- straightforward when a patient after a procedure reports senso- nal neuropathies (PPTTN). These are defined by a history of an ry symptoms and pain that persists beyond the normal healing identifiable traumatic event to the trigeminal nerve with clini- time of tissue injury. However, after minor nerve injuries, sen- cally or neurophysiologically evident signs of sensory altera- sory signs may not be obvious in clinical examination. There- tion, and pain which is located within the affected trigeminal fore thorough history taken with respect to previous surgery distribution and has developed within 3-6 months of the trau- and trauma is important. Clinical sensory tests should be done matic event (30). carefully, testing different sensory modalities, but they are too Many dental and surgical procedures, such as orthognathic crude to detect minor or old nerve injuries (41). Clinical neuro- surgery, third molar extraction, implant surgery, root canal physiology offers many sensitive methods such as neurography, therapy, and even local anaesthesia carry a risk of trigeminal blink reflex test, QST and contact heat or laser evoked potential nerve damage. Fortunately, neuropathic pain evolves in only a recordings to confirm the diagnosis, to localize the lesion, and minority of these. The incidence of PPTTN has been reported to to assess the type and profile of nerve fibre damage, which form vary from 3 % to 6 % after endodontic treatment, and to be 5 the prerequisite for reliable appraisal of the prognosis (41). The % after surgical endodontics, 5 % after mandibular sagittal os- tests are available in major hospitals of Nordic countries and teotomy, and 3 % after facial fractures. The prognosis of nerve they offer objective means to diagnose nerve damage, which is damage greatly depends on the type of the damage; injuries in especially valuable in litigation cases. which only the myelin sheath is involved usually recover com- The treatment of neuropathic pain relies mainly on pharma- pletely within four months, whereas the recovery of axonal cotherapy, but thorough patient information, and helping pa- injuries is much slower, and mostly incomplete. Posttraumatic tients to cope with the pain are essential parts of the treatment neuropathic pain has been particularly related to axonal nerve process, too. Surgical procedures are usually of no use, and damage of the small fibre system (41). Other risk factors for de- can exacerbate the pain. First line drugs to treat neuropathic velopment of neuropathic pain include genetic factors, comor- pain include tricyclic antidepressants, serotonin-noradrenaline bid pain or psychosocial distress (42,43). reuptake inhibitors, gabapentin and pregabalin (36). Thera-

Facial pain conditions

Pain Other symptoms, Location Duration Provoking/ag- character findings gravating factors

TMD Aching, pressing, Muscle/joint Cheek, temple, Varying, often con- Jaw opening, stabbing tenderness, TMJ region tinuous chewing functional disturbances, joint sounds

PIFP/AO Aching, pressing Usually none, subtle Varying/ tooth Continuous Psychological sensory symptoms region factors possible

TN Sharp, brief, electric Usually none Trigeminal nerve Seconds – a few Tactile stimuli shock like distribution minutes

Neuropathic pain Burning, tingling, Sensory alterations Trigeminal nerve Continuous, may Often: Tactile/ aching distributions fluctuate in intensity thermal stimuli

TMD; temporomandibular disorder, TMJ; temporomandibular joint, PIFP; persistent idiopathic facial pain, AO; atypical odontalgia, TN; Trigeminal neuralgia

Table 1. Frequent features of different facial pain conditions.

Tabel 1. Karakteristiske træk ved faciale smertetilstande.

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peutic brain stimulation (transcranial magnetic stimulation cial pains. However, many aspects of facial pain are still poorly and motor cortex stimulation) offers a novel treatment line for understood, and much needs to be done to validate many of treatment-resistant neuropathic pain within the orofacial re- the methods used to treat facial pain, and to develop new im- gion (45). proved, more effective treatment approaches with fewer side effects. Differential diagnostics Science is advancing rapidly in the field of pain, including Correct diagnosis is the sine qua non of successful treatment. facial pain. The special areas of interest in facial pain research Table 1, which features the most common or typical signs of include molecular biology, biomarkers, imaging, genetics, and different facial pain conditions, aims to provide a basis for the pain and psychological comorbidities, among others. It is to be diagnostic work-up of chronic facial pain conditions. expected that increased understanding of the pain mechanisms and other aspects of facial pain will in the future bring some Concluding remarks and future scenarios novel therapeutic possibilities. For our patients a correct treat- Considerable progress has been made during the last decades ment is of uttermost importance. Treatment of chronic pain in the understanding of the processes involved in facial pain. disorders have to be based on correct diagnosis and evidence The complexity and multidimensionality of pain is increasingly based treatment modalities. The future will most probably also comprehended, and more insights have been gained into the witness the rise of personalized pain medicine, where treat- risk factors predisposing to chronic pain. In addition, improved ments are customized to fit each patient’s pain and psychoso- and more reliable diagnostic systems and approaches have cial, as well as genetic characteristics. In the light of rapid ad- been introduced, and some advances have been made in the vances in the field of pain, much more emphasis should be put treatment of certain facial pain entities, such as neuropathic fa- on pain education in the dental curriculums.

ABSTRACT (DANSK)

Persisterende faciale smertetilstande trigeminusneuralgi og smertefuld posttraumatisk trigeminus Kroniske ansigtssmerter er en almindeligt forekommende li- neuropati. Artiklen giver et overblik over TMD-smerter som en delse, i særdeleshed i forbindelse med temporomandibulær biopsykosocial tilstand, dens prævalens, karakteristika, cen- dysfunktion (TMD). Da tandlæger er ansvarlige for behand- trale og perifere mekanismer, diagnostik (DC/TMD) og prin- lingen af de fleste af disse tilstande, er opdateret viden om cipper for behandling. Ligeledes beskrives definitioner, præ- de nyeste fremskridt inden for området helt afgørende for valens, karakteristika og diagnostik for hver af de forskellige at kunne foretage vellykket diagnostik og behandling. Denne typer af neuropatiske ansigtssmerter. Den aktuelle forståelse oversigt omfatter TMD og forskellige typer af neuropatiske af patofysiologien af disse neuropatiske tilstande præsente- eller formodede neuropatiske ansigtssmerter i form af ved- res, og der gives en beskrivelse af de evidensbaserede be- varende idiopatiske ansigtssmerter og atypisk odontalgia, handlingsmetoder.

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