3D osteoarthritic changes in TMJ condylar morphology correlates with specific systemic and local biomarkers of disease

Abstract

Objective To assess 3D morphological variations and local and systemic biomarker profiles in subjects with a diagnosis of temporomandibular joint osteoarthritis (TMJ OA). Design Twenty-eight patients with long-term TMJ OA (39.9 ± 16 years), 12 patients at initial diagnosis of OA (47.4 ± 16.1 years), and 12 healthy controls (41.8 ± 12.2 years) were recruited. All patients were female and had cone beam CT scans taken. TMJ arthrocentesis and venipuncture were performed on 12 OA and 12 age-matched healthy controls. Serum and synovial fluid levels of 50 biomarkers of arthritic inflammation were quantified by protein microarrays. Shape Analysis MANCOVA tested statistical correlations between biomarker levels and variations in condylar morphology. Results Compared with healthy controls, the OA average condyle was significantly smaller in all dimensions except its anterior surface, with areas indicative of bone resorption along the articular surface, particularly in the lateral pole. Synovial fluid levels of ANG, GDF15, TIMP-1, CXCL16, MMP-3 and MMP-7 were significantly correlated with bone apposition of the condylar anterior surface. Serum levels of ENA-78, MMP-3, PAI-1, VE-Cadherin, VEGF, GM-CSF, TGFβb1, IFNγg, TNFαa, IL-1αa, and IL-6 were significantly correlated with flattening of the lateral pole. Expression levels of ANG were significantly correlated with the articular morphology in healthy controls. Conclusions Bone resorption at the articular surface, particularly at the lateral pole was statistically significant at initial diagnosis of TMJ OA. Synovial fluid levels of ANG, GDF15, TIMP-1, CXCL16, MMP-3 and MMP-7 were correlated with bone apposition. Serum levels of ENA-78, MMP-3, PAI-1, VE-Cadherin, VEGF, GM-CSF, TGFβ1, IFNγ, TNFα, IL-1α, and IL-6 were correlated with bone resorption.

IL‐1β‐regulating angiogenic factors expression in perforated temporomandibular disk cells via NF‐κB pathway

“…The predominant pathogenesis and progression of TMJ OA is joint inflammatory condition . Interleukin (IL)‐1β and several other inflammatory factors, including IL‐6, IL‐12 and tumor necrosis factor (TNF)‐α, are increased in the synovial fluid of patient with TMJ OA . Recent evidence has revealed IL‐1β as a pivotal molecule linking inflammation and angiogenesis because of promoting MMP s, TIMP s , and lumican gene expressions in TMJ disk cells.…”

The many faces of genetic contributions to temporomandibular joint disorder: An updated review

“…Is the hallmark of early degenerative changes in internal derangement of TMJ and inflammatory symptoms, correlated with bone apposition and resorption, and has decreased expression in condylar hyperplasia…”

Evaluation of the relationships between contrast-enhanced magnetic resonance characteristics and joint pain in patients with temporomandibular disorders

“…In clinical settings, perforations of the disk and posterior disk attachment are frequently observed in the lateral and latero-central portions. Therefore, osteoarthritis and inflammatory changes in the bony and soft tissues of the TMJ mostly occur in the lateral and central portions of the disk, posterior disk attachment, and mandibular condyle [62]. Recently, several finite element stimulations of the TMJ have been applied for clinical studies [62][63][64].…”

“…Therefore, osteoarthritis and inflammatory changes in the bony and soft tissues of the TMJ mostly occur in the lateral and central portions of the disk, posterior disk attachment, and mandibular condyle [62]. Recently, several finite element stimulations of the TMJ have been applied for clinical studies [62][63][64]. In the symptomatic model, the highest stresses are located at the lateral portion of the disk throughout clenching [63,64].…”