Abstract

Temporomandibular disorders (TMD) represent the collective phrase for a cluster of musculoskeletal conditions involving discomfort, dysfunction, or both, in the masticatory muscles, temporomandibular joints (TMJ), and their associated structures. The etiology of prevalent painful TMD is biopsychosocial and multifaceted. Early recognition and treatment of TMD are apt to significantly enhance prognosis and quality of life, and diminish healthcare and economic expenditures. Certain sinister or noteworthy diagnoses may manifest with akin symptoms to TMD; practitioners should be cognizant of these 'red flags.' Conservative methods demonstrate effectiveness in TMD management. When warranted, particular patients may derive advantages from specialist referral and multidisciplinary management.¹

Introduction

Osteoarthritis stands as the most prevalent joint ailment, encompassing the entire joint, including not solely the articular cartilage and subchondral bone, but also the joint capsule, synovial membrane, ligaments, and even neighboring muscles. The temporomandibular joint (TMJ) serves as a synovial articulation linking the mandibular condyle to the glenoid fossa of the temporal bone, with its internal space segregated into two compartments by a fibrocartilaginous TMJ disc. Additionally, it has been regarded as a bilateral diarthrodial joint due to its hinge and slide movements and involvement in vital life-sustaining activities such as mastication, deglutition, and articulation.^2,3

Causes

While it's acknowledged that biological, psychological, and societal factors combine to predispose, initiate, or perpetuate painful TMD, the precise Pathophysiology remains uncertain. Various mechanisms have been proposed that might interact with each other to contribute to painful TMD. The mechanisms proposed below can also elucidate the presence of painful and non-painful comorbidities in individuals with TMD.Pro- and anti- inflammatory cytokines have also been identified as contributors to the pathophysiology of TMD in genetically susceptible individuals. Specifically, elevated circulating levels of pro-inflammatory monocyte chemotactic protein (MCP-1), decreased transcription of anti-inflammatory transforming growth factor-1 (TGF-1) were observed in patients with painful TMD. Additionally, calcitonin gene- related peptide (CGRP), a neuropeptide discharged from trigeminal nerves, mediates neurogenic inflammation. Elevated CGRP levels within the joint capsule, observed in individuals with TMD, are believed to induce inflammation and pain through stimulation of peripheral and central sensitization.

These particular pathways and mechanisms that might predispose, initiate, or perpetuate persistent painful TMD within an individual don't function autonomously. They are likely to interact, resulting in heightened excitability and synaptic efficacy of neurons in peripheral and central nociceptivepathways. This phenomenon is termed peripheral and central sensitization, and for TMD, it has been demonstrated to manifest as sensitization of trigeminal neurons and intensified pain signaling. Patients with heightened peripheral and central sensitization are also more prone to experiencing other forms of persistent pain, including headache and fibromyalgia; thus, these conditions frequently coexist in individuals with TMD.

Catecholamine-O-methyltransferase (COMT) activity has been discovered to substantially impact pain sensitivity and TMD onset via adrenergic pathways. This enzyme possesses diverse biological roles, including the regulation of catecholamines and enkephalins, which are implicated in numerous neurological functions. Females with specific genetic variations (haplotypes) causing reduced COMT activity were identified to have significantly heightened pain sensitivity and be 2.3 times more predisposed to developing TMD.

An investigation into single-nucleotide polymorphisms (SNP) disclosed associations between genetic susceptibility factors for clinical, psychological, and sensory phenotypes and the emergence of TMD. A total of 3295 SNP representing 358 genes linked to pain perception were scrutinized, and five SNP were determined to be significantly prognostic of TMD and pain onset.¹

Clinical presentation

Individuals with TMD may exhibit any or all of the subsequent indicators and manifestations: discomfort in the TMJ or muscles of mastication that might radiate or refer to local or distant structures; clicking, locking, or crepitus of the TMJ during any of its motions with or without joint locking; headache in the temporal area; and otalgia or tinnitus or both without aural ailment. Symptoms have a tendency to recur in the majority of individuals (65%) and are associated with the orofacial region (71.1%), although a significant proportion (23%) solely present with headache.^4,5

Diagnosis

Throughout recent decades, various forms of evaluations have been suggested for TMD. The most extensively acknowledged among these diagnostic instruments is the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD). The DC/TMD strives to deliver a standardized and operationalized instrument that incorporates physical inspection of the masticatory structures (axis I) and screening for psychosocial and accompanying factors (axis II) to facilitate diagnosis of TMD.⁶

Management

Global consensus advocates for employing reversible conservative therapies as the primary approach to treating TMD. This recommendation is grounded in evidence indicating that between 75% and 90% of patients will respond to less invasive therapeutic methods. As TMD are characterized by intricate multifactorial causation, often a treatment strategy encompassing biological, psychological, and societal facets of care are necessary. Additionally, it is understood that the presence of psychosocial elements can forecast a poorer long-term prognosis and heightened likelihood of persistent pain development; thus, the identification and timely management of psychosocial distress are advisable.⁶

Conclusion

TMD represents a complex array of disorders that frequently result in persistent pain. As advancements in research emerge, a deeper comprehension of the multifaceted causation of painful TMD is evolving. This is likely to culminate in the development of enhanced TMD prevention, diagnosis, and treatment strategies targeting individual mechanisms and contributing factors. A biopsychosocial framework of care is recommended for addressing TMD, involving a multidisciplinary approach through a unified integrated treatment pathway. Evidence suggests that establishing specialized regional centers for orofacial pain could offer a more streamlined and cost-efficient management approach within secondary or tertiary care.