Temporomandibular Disorders. Part 1: Anatomy, Aetiology, Diagnosis and Classification

Anatomy

The temporomandibular joint is an atypical synovial joint that permits a hinging movement and a gliding motion of the surfaces.³ The left and right condyles articulate with the temporal bone but are unable to move independently of each other.³ The TMJ shares some commonalities with other synovial joints such as a disc, fibrous capsule, fluid, synovial membrane and ligaments. However, the features that make the TMJ unique are its articular surface covered by fibrocartilage rather than hyaline cartilage.⁴

The anatomy of the joint can be considered in three parts: the joint; the ligaments; and the muscles.

The joint (Figure 1)

The two articular surfaces, the condylar head and the glenoid (mandibular) fossa, which are lined by a synovial membrane, never actually come into contact with one another. They are separated by the articular disc which divides the joint into two spaces, superior and inferior. The articular disc is a biconcave fibrocartilaginous structure that functions to accommodate the hinging and gliding actions of the condyle. The disc itself is described as having two bands, anterior and posterior. The anterior band attaches to the joint capsule and the superior head of the lateral pterygoid. The posterior band attaches to the fossa and is referred to as the retrodiscal tissue. Unlike the disc itself, the retrodiscal tissue is highly innervated and vascular. As a result, it is often a major contributor to the pain experienced in some disc dysfunctions⁴.

The fibrous capsule is a dense fibrous connective tissue that completely surrounds the joint. It attaches to the articular eminence, the articular disc and the condylar neck.⁵

The ligaments

There are several ligaments that act to provide stability and proprioception to the TMJ. The main three are the temporomandibular ligament (collateral ligament), the sphenomandibular ligament and the stylomandibular ligament.

The temporomandibular ligament arises from the outer surface of the articular eminence and inserts into the neck of the condyle. It anchors the disc to the condyle and prevents posterior dislocation of the joint (Figure 2). The sphenomandibular ligament (Figure 3) originates from the sphenoid spine, and inserts into the lingula of the mandible. It helps to prevent excessive translation of the condyle. The stylomandibular ligament (Figure 3) arises from the styloid process of the temporal bone and inserts into the angle of the mandible; its function is unclear.⁴

The muscles and movements

Movements of the TMJ are produced by the muscles of mastication and the supra- and infra-hyoid muscles. Their actions are summarized in Figure 4 and Table 1. The muscles of mastication are the primary depressors (opening) and elevators (closing) of the mandible. They are also used to produce protrusive and lateral movements.⁴

Table 1. Summary of the anatomy and actions of the muscles of mastication.

Muscle	Origin	Insertion	Action
Masseter	Zygomatic arch	Angle of mandible	Closing
Temporalis	Temporal fossa	Coronoid process	Closing
Lateral pterygoid	Sphenoid bone (superior belly)Pterygoid plate (inferior belly)	Articular capsule (superior belly)Condylar neck (inferior belly)	OpeningProtrusionLateral deviation
Medial pterygoid	Pterygoid bone (deep head)Pyramidal process of palatine bone (superficial head)	Medial angle of mandible	ClosingProtrusion

Epidemiology

TMD constitutes the third most common musculoskeletal pain complaint, behind chronic back pain and headaches, and are the most common causes of chronic pain in the orofacial region.⁶ The reported prevalence of TMD is between 5–50% as the majority of patients do not report or seek help for their symptoms, with peak incidence occurring in the second and third decades.^6,7 The prevalence appears to be only marginally higher in females in the general population,⁸ rising to 4: 1 in a clinical setting, as females are more likely to seek advice and treatment.⁶ TMD can be associated with other chronic pain conditions such as fibromyalgia and chronic pain syndrome. In addition, they are often comorbid with bruxism, depressive illnesses and chronic fatigue.^9,10

TMD has a significant impact on an individual's daily activities, psychosocial functioning and quality of life that is difficult to quantify. Furthermore, chronic pain has significant cost implications for patients, the health service and the economy.¹¹ Individual responses to pain vary considerably, but for those living with chronic pain as a permanent feature of their lives, its effects on psychosocial wellbeing can be far reaching.¹²

Understanding the complexities of TMD pain and manifestations is best explained by the biopsychosocial model of pain, which recognizes the dynamic interaction of the biological, psychological and social components of pain.¹³ First introduced by Engel in 1977, the model proposes that the concept of chronic pain cannot be broken down into discrete physical or psychosocial elements. Rather, it is the interwoven relationship between these elements that is seen to modulate the individual's perception of pain and resultant disability.¹⁴

Aetiology

The cause of TMD is complex and multifactorial in nature, with interaction of different biological and psychosocial factors.¹³ In isolation, factors may be considered as predisposing, precipitating or perpetuating, although it is difficult to make such distinctions in reality.¹⁵ Review of the evidence shows that the multifactorial nature of the disease involves multiple mechanisms at the level of muscles, peripheral nervous system and central nervous system. Table 2 summarizes the various factors that have been investigated in relation to the development of TMD. It is important to note that these factors help increase our understanding at a population level, but do not always explain the experiences of the individual.¹⁶

Psychosocial upset can be involved in the onset and perpetuation of TMD, and may also significantly impact on patient compliance with, and outcomes of, treatment.¹⁷ The inability to employ coping strategies in response to pain and the recruitment of maladaptive strategies, such as catastrophizing, have a positive correlation with increased experience of TMD-related pain.^13,17,18 Depression, lack of sleep and stress-related disorders may underlie or contribute to the development of chronic TMD.^13,17,18

Patients with TMD are frequently found to experience other pain-related comorbidities such as fibromyalgia, headaches, chronic back pain, and irritable bowel syndrome.^17,19,20 There are indications that these comorbidities share similar altered pain regulation features and psychosocial risk factors with TMD.¹⁷ Furthermore, patients with TMD have been shown to have lower pain thresholds at the site of pain and at other sites. This suggests both peripheral and central pain sensitization.⁷

The relationship between TMD and parafunctional habits (bruxism and clenching) has historically been reported as a significant cause and effect relationship. However, the association between them is highly inconsistent.¹⁷ The literature is unable to demonstrate a dose–response between bruxism and TMD because most bruxists do not report intense levels of TMD pain.^21,22 However, this is not to say that parafunctional activity is not of significance in some patients.

Similarly, occlusal interferences, malocclusions and orthodontics seem to be of minor importance in the aetiology of TMD.²³ No consistent pattern between occlusal variables and TMD have been shown,¹⁷ in fact, there is some evidence to suggest that it is the adaptive capacity of the patient in relation to occlusal changes that influences the development of TMD.²⁴ Similarly, the possibility that orthodontic treatment may lead to the initiation or deterioration of TMD, or that orthodontic tooth movement can be used to improve TMD, has been refuted by scientific evidence.²⁵

Trauma, in the form of macrotrauma to the head and neck (eg head injury), or microtrauma (eg dental treatment) may contribute to the development of TMD in predisposed patients.²⁶ Acute myofascial pain following a dental intervention from direct muscle damage or stretch injuries can be managed conservatively if the intervention is early.¹⁷ However, chronic TMD can develop if inflammatory or degenerative changes occur and the patient has other biopsychosocial risk factors.²⁶

Clinical features

Imaging

The role of imaging in the diagnosis and management of TMD is generally adjunctive to the clinical diagnosis as opposed to a definitive diagnostic tool.¹⁶ For most patients, imaging is not required.

Where there is suspected bone pathology, the initial imaging modality of choice should be plain radiography, normally a panoramic radiograph (sectional, if appropriate).³⁷ Acute fractures, dislocations and severe degenerative disease are often visible in this way.³⁸ Computed tomography, traditional or cone beam, is superior to plain radiography in detecting more subtle bony changes.³⁹

Magnetic resonance imaging (MRI) is the optimal modality for comprehensive joint assessment, allowing detailed examination of the soft tissues. MRI should be reserved for specific cases where:

Before considering the use of any form of imaging, it is important to remember that in a significant proportion of cases there will be no visible pathological anatomical changes, and therefore the use of ionizing radiation must be justified given that it may have no effect on the patient's management. Furthermore, some changes noted on imaging are not always of clinical relevance, especially if function is not affected.^16,39 For example, flattening of the condylar head or increase in joint space.

Diagnosis and classification

The DC/TMD identifies three main diagnostic groups:²

Myofascial pain tends to be the most common presenting diagnosis of a painful TMD. Disc displacements with reduction (clicking joints), with or without pain, are also common complaints. Non-reducing disc displacements are less frequent. Where there is pain in the TMJ without myalgia, and because the cause of pain is difficult to distinguish (eg synovitis, capsulitis, retrodiscitis), it is termed arthralgia. Crepitus with and without pain can indicate degenerative diseases such as osteoarthritis and osteoarthrosis, respectively¹⁶. It is also important to note an individual may present with multiple diagnoses at any one time.

The flow diagrams (Figure 5) may help the practitioner to arrive at a diagnosis and implement the appropriate management.

Acute and chronic TMD

It is important to differentiate between acute and chronic TMD, as it influences the resultant management plan¹⁶.

Acute TMD often has an identifiable cause, such as a stressful life event or mechanical trauma (eg localized myofascial pain with limited opening following a difficult lower third molar extraction). It is often of short duration and self-limiting, and normally resolves following rest, a soft diet and simple analgesia.¹.

Chronic TMD relates to pain that normally exceeds 3–months duration. The pain may become biopsychosocially destructive, result in depression, or the development of chronic pain behaviours and disability.¹⁶

It is therefore important to prevent acute TMD from becoming chronic by identifying patients who are more at risk of developing chronic pain. Potential vulnerabilities and comorbidities may include female gender, more widespread non-specific symptoms, existing psychosocial diagnoses (eg anxiety and depression), and high pain intensities.^7,10,18

Conclusion

Temporomandibular joint disorders represent the most common orofacial pain conditions, and can have an overwhelmingly negative impact on an individual's psychosocial wellbeing. They contribute to the high economic burden of managing and living with chronic pain. The accepted biopsychosocial pathophysiology of the disease and significant associations with other chronic pain conditions suggest that early detection and a holistic management approach, which encourages self-management and development of coping mechanisms, can offer good long-term outcomes. The general dental or general medical practitioner are often the first people to whom a patient experiencing TMD will present, and as such, it is hoped that the primary care practitioner will be able to recognize the various TMDs, the associated risk factors and instigate timely management or referral, in keeping with the evidence presented in this series.