Temporomandibular disorders (TMDs), characterized by pain and/or dysfunction of the Temporomandibular joints (TMJs), masticatory muscles, and supporting structures, are the second most common musculoskeletal condition after chronic lower backache [1]. According to the Diagnostic Criteria for TMDs (DC/TMD) standard, TMDs can be broadly divided into pain-related and intra-articular conditions. While pain-related TMDs (PT) include TMJ pain (arthralgia), masticatory muscle pain (myalgia), and TMD-related headaches, intra-articular TMDs (IT) consists primarily of TMJ disc displacements (DDs) and degenerative joint disease (DJD) [2]. TMJ DJD is typified by progressive articular tissue deterioration with concurrent osseous changes in condyles and/or articular eminence [3]. The prevalence of TMJ DJD in the general adult population is about 10% and ranges from 18 to 85% among TMD patients [4, 5]. TMJ DJD and DDs are intricately linked and half of TMD patients with DDs have DJD. The occurrence of TMJ DJD is higher in DD without reduction (66%) than in DD with reduction (36%) [6]. Whilst the natural course of TMJ DJD is generally favourable [7], it can lead to morphological condylar changes, decreased ramal height, and progressive mandibular asymmetry or retrusion when advanced [8]. Dentofacial deformities and bite derangements might eventually develop resulting in jaw functional limitations, compromised facial appearance, psychosocial impairments, and diminished quality of life [9, 10].
Though the exact etiopathogenesis of TMJ DJD has not been established [11], sustained local and systemic inflammation appears to play an important role [12–14]. Biomechanical overloading and metabolic changes can degrade articular cartilage tissues. The degraded cartilage tissues are theorized to trigger foreign body reactions within synovial cells resulting in the production of inflammatory cytokines, matrix metalloproteases, and prostaglandins that contribute to further cartilage destruction and subchondral bone re-modelling [13, 14]. The innate immune system and activated macrophages have also been implicated in DJD progression [14]. Risk factors for TMJ DJD include genetics, age, macro and micro TMJ trauma, systemic conditions, congenital as well as developmental abnormalities [10, 11]. TMJ DJD normally involves three phases with periods of remission and repair [10, 15]. The initial phase is associated with TMJ clicking and intermittent locking whereas the intermediate phase is often accompanied by TMJ pain, opening difficulty/limitation, and crepitus (grating sounds). In the final or “burnout” phase, degenerative activity ceases and the joint is relatively stable. The entire process from initiation to the final “burnout” phase takes about 5.5 years [15].
Following the DC/TMD protocol, TMJ DJD is inferred when there is a history of TMJ sounds with jaw movement/function and TMJ crepitus on palpation during jaw movements. However, adjunctive imaging is needed to render a definitive diagnosis as symptom history and physical examination by themselves generally have inadequate diagnostic validity for intra-articular conditions [2]. Cone-beam computed tomography (CBCT) is particularly useful for TMJ imaging due to its superior accuracy for the three-dimensional assessment of hard tissues/bone [16, 17]. Hilgenberg-Sydney et al. reviewed the diagnostic validity of CBCT and concluded that it provided good images for evaluating DJD progression over time but should not be employed as a screening tool for individuals with healthy joints [18]. In a recent systematic review, Wu et al. examined the association between TMD symptoms/signs and bony changes on CBCT images in patients with TMJ DJD [19]. Only nine studies were available and all had modest sample sizes (varying from 30 to 198 patients) with a total of 697 subjects. TMJ sounds and pain were reported to have the strongest relation to various CBCT findings. Additionally, they suggested that patients with primary muscle pain should not be routinely prescribed CBCT. Given the limited studies detailing both symptoms and signs, the relatively small sample sizes of earlier work, as well as the infrequent use of standardized assessment/diagnostic protocols, further research involving larger patient samples and based on the DC/TMD is warranted.
With the aforesaid premises, the objective of this study was to investigate the relationships between CBCT findings, clinical symptoms, and signs in a large sample of TMD patients with TMJ DJD. More specifically it compared the type of TMD symptoms/signs in individuals with no, early, and late TMJ DJD, and determined the agreement between TMD symptoms and signs. The research hypotheses were: (a) substantial variances in the prevalence of TMD symptoms/signs exist among participants with no, early, and late TMJ osseous changes, and (b) the agreement between patient-reported symptoms and clinician-established signs is moderately good.