International Headache Society (IHS) code and diagnosis: 11.6 Headache attributed to disorders of teeth, jaws, and related structures

World Health Organization (WHO) code: G44.846

The most common cause of intraoral pain is dental disease. Inflammatory dental disease may be pulpal, periodontal, or a combination of both. With limited capacity for repair, inflamed or damaged pulpal tissue frequently becomes necrotic. The management of irreversible pulpitis is root canal therapy (amputation of the symptomatic pulp) or extraction. Symptoms generally resolve, but postoperative persistent pain or dysesthesia can ensue. Periodontal disorders involve the supporting structures of the teeth: the bone, periodontal ligament, and cementum.

Acute dental pain may spread unilaterally but (unlike headache) rarely crosses the midline. Convincing research on the epidemiology and qualitative characteristics of dental pain is lacking. However, acute dental pain is intense, throbbing, poorly localized, and generally provoked by stimulation of the offending tooth (58). Differentiation from comorbid headache pain does not usually pose a significant diagnostic dilemma. However, there are occasions where primary headache disorders such as migraine or cluster or paroxysmal hemicrania are located in the lower half of the face and mimic acute dental disease. Diagnostic problems are sometimes associated with a condition called “cracked tooth syndrome.” A crack that extends through enamel and dentine into pulpal tissue may arise during mastication or external trauma. Pain is usually poorly localized and radiographs are not sufficiently sensitive to identify a fracture (26).

Periodontal disease is normally associated with chronic discomfort/pain. It is clearly localized to the affected teeth (unlike pulpal pain), a characteristic attributed to the proprioceptive and mechanoreceptive sensibility of the periodontium. Acute periodontal conditions can arise but they are generally limited in duration and rarely associated with, or misdiagnosed as, headache. Chronic periodontal disease may lead to pulpal involvement and this progression naturally alters symptom presentation. Although chronic periodontal disease is the most frequent cause of tooth loss in adults, the exact relationship between headache and chronic periodontal disease is unclear.

Pain associated with pulpal or periodontal disease is managed with conventional dental therapies and is not a cause of long-term disability. However, this view was challenged recently when approximately 12% of patients treated in a specialist endodontic unit reported persistent pain, despite clinical and radiographic absence of dental disease (46). This raises the question of possible change in the peripheral or central nervous system (CNS) following amputation of the pulpal tissue.

Persistent tooth site/jaw pain in the absence of dental disease, or “atypical facial pain,” does not have the characteristics of the cranial neuralgias and is not associated with physical signs or a demonstrable organic cause (47,60) (Table 124-1).

The diagnosis of atypical facial pain is controversial and not even recognized in the International Association for the Study of Pain (IASP) Chronic Pain Classification (64). Furthermore, data on its cause and epidemiology remains scarce and unconvincing. Suggestions that atypical facial pain is psychogenic in origin are unfounded. A hypothesis implying neurovascular mechanisms in the genesis of atypical facial pain is supported partially by the success of tricyclics and the 5HT₁ agonist sumatriptan (24).

Atypical odontalgia (AO), which is considered a sub-category of atypical facial pain, is defined as a localized pain in a tooth or tooth site (62) and is linked to head pain (Table 124-2). Neurovascular (59) and differentiation mechanisms are some hypotheses on the pathogenesis of AO (20,36,37,59). Others have implicated the sympathetic nervous system due to the high frequency of associated trauma, the equivocal effect of somatic block, and the positive effects of sympathetic block (20,21).

IHS code and diagnosis: 11.7 Headache or facial pain attributed to temporomandibular joint (TMJ) disorder

WHO code: G44.846

Temporomandibular disorders (TMDs) are a collection of clinical problems that involve the masticatory musculature or the TMJ and associated structures (46).

Other terms: Other terms have included Costen syndrome (7), craniomandibular disorders, oromandibular dysfunction (46), temporomandibular joint syndrome, and facial arthromyalgia (23).

Epidemiologic data on facial pain in general are weak. Available evidence fails to differentiate headache from facial pain, which further confuses the relationship between TMD and headache. Also, studies lack conformity in diagnostic criteria, data collection, and interpretation. One Swedish study indicated that 12% of patients report pain on wide opening of the mouth, 7% reported limitation of mouth opening, 39% had noise on opening the mandible, and 2% complained of joint pain and stiffness (3). Facial pain and headache were reported by 24% of respondents (3). Generally, women report more headache, TMJ clicking, TMJ tenderness, and muscle tenderness than men (2,32,51).

No evidence exists to implicate genetic factors in the cause of functional disorders of the TMJs.

The TMJ is unique in its bilateral location with an upper and lower compartment separated by a fibrocartilaginous disc. This diarthrodial structure allows for both rotatory and translational movement of the mandible. This relatively simple anatomic scheme underlies masticatory movements that require complex neuromuscular control for adequate function. Although the TMJ is subject to the same pathologic disorders that may affect other synovial joints, it is unique in certain anatomic aspects. Both joints move as a functional unit and are lined by a fibrous connective tissue that is more resistant to degenerative change and has a greater capacity for repair. The masticatory system includes the articulation of the upper and lower dentition, which in itself may limit or support joint function and stability. TMDs are generally divided into those that are joint related (arthrogenous) and those that are muscular (myogenous). Clinically, the two frequently occur together but this arbitrary separation facilitates research and discussion.

Sensory innervation of the TMJ is mediated through the mandibular division of the trigeminal nerve. Pain-sensitive elements within the TMJ include the joint capsule, the posterior attachment tissues, and the discal ligaments. The posterior attachment is highly innervated, richly vascularized, and frequently implicated in the pathophysiology of joint pain. In contrast, the intra-articular disc is largely devoid of neural or vascular tissue, but plays a vital role in maintaining condylar stability during mandibular movement. Trauma to the TMJ may result in acute capsulitis, but this inflammatory process tends to resolve quickly without complication. Chronic joint disorders are more frequently
associated with painful derangement of the TMJ. Articular disc displacement frequently underlies the mechanism of joint derangement, but the cause is unclear.

The remarkable adaptive capacity of the TMJ is well documented (30,53). Failure of this mechanism may lead to tissue breakdown and disc displacement. This may be affected by age, stress, gender, systemic illness, and previous trauma. However, acute and chronic disc displacement is not always painful. Indeed, a magnetic resonance imaging (MRI) study indicated that 32% of anterior disc displacements are asymptomatic (31).

Although the cause of muscle pain is unclear, putative mechanisms underlying the transition from acute to chronic muscle pain include:

Chronic sensitization of nociceptors

Changes in innervation density

Reflex within the CNS

Neuroplasticity

Disturbance of the antinociceptive system

Psychosomatic interactions

Aggravating and perpetuating factors

Myofascial pain, which is considered a regional pain syndrome, is the most common form of TMD (40). However, the recognition of this entity as a specific disease of the masticatory system is debated. Myofascial pain is characterized by discrete tender areas (trigger points) that reproduce classical patterns of pain referral when palpated. Muscle tenderness may cause headache (19,29,34) by a mechanism that remains elusive (40). This is the case in many patients with tension-type headache whose pain frequency increases with increasing degrees of tenderness (29). However, such a relationship is not seen in migraine (28,44).

Tenderness and pain in masticatory muscles are the most frequently reported symptoms and signs of TMD. These symptoms may represent dysfunction of the trigeminal nervous system, rather than a musculoskeletal disorder. Indeed, a central origin of the myofascial trigger point syndrome is supported by referred pain, dysesthesias, hypesthesias, autonomic symptoms, and disturbance of motor function. These particular characteristics are commonly observed in the orofacial area.