Local and systemic inflammatory mediators and their relation to pressure-pain threshold and pain of the temporomandibular joint

The first aim of this investigation was to investigate the validity of TMJ pressure-pain threshold for assessment of pain conditions of inflammatory nature in the TMJ. Pressure-pain threshold was recorded from the palpable lateral pole of the TMJ condyle with a hand-held electronic pressure algometer (Somedic Production AB, Sollentuna, Sweden). TMJ pressure-pain threshold is systemically modulated and not modulated by the investigated inflammatory mediators (5-HT, TNFα, IL-1sRII) in the TMJ synovial fluid. TMJ pressure-pain threshold is therefore not valid as a tool for assessment of intra-articular pain conditions of inflammatory nature.

The second aim was to investigate differences in pressure-pain threshold between genders in healthy individuals and RA patients as well as between healthy females and female RA patients with clinical signs of TMJ involvement. TMJ pressure-pain threshold in female RA patients is lower than in male RA patients as well as in healthy females. No difference between healthy females and males was observed.

The third aim of was to investigate the influence of synovial fluid and blood levels of 5-HT and TNFα on the effects by intra-articular injections of glucocorticoid regarding pressure-pain threshold and on pain of the TMJ in patients with chronic inflammatory TMJ disorders. The glucocorticoid was injected into the upper joint compartment of the TMJ. TMJ synovial fluid samples were obtained before and after treatment. Patients with detectable pretreatment levels of synovial fluid 5-HT experienced a larger reduction of TMJ pain intensity at rest and on maximum mouth opening after treatment with intra-articular glucocorticoid. Patients with detectable pretreatment levels of synovial fluid TNFα experience a larger reduction of TMJ pain on maximum mouth opening than those without after treatment. Pretreatment presence of TNFα or 5-HT in the synovial fluid predicts reduction of TMJ pain by intra-articular injection of glucocorticoid in patients with chronic inflammatory TMJ disorders.

The fourth and final aim was to investigate the relative importance of systemic and local inflammatory mediators (5-HT, TNFα, IL-1sRII) in the modulation of pressurepain threshold and other pain entities in patients with seropositive or seronegative RA involving the TMJ and whether these pain entities are related to each other. TMJ synovial fluid samples were obtained from all patients. TMJ pressure-pain threshold as well as other TMJ pain entities were recorded. The results indicate that TMJ pressure-pain threshold is modulated by systemic rather than local inflammatory mediators and is unrelated or weakly related to other TMJ pain entities in RA patients. TMJ pain intensity at rest is mainly locally modulated but with an additional systemic influence. TMJ movement pain is mainly modulated by systemic mediators in the seropositive patients and mainly by local mediators in the seronegative patients. Tenderness and pain reflex to palpation are modulated mainly by systemic mediators in both groups, where TNFα dominate in seropositive and 5-HT in seronegative patients.

List of scientific papers

I. Fredriksson L, Alstergren P, Kopp S (2000). Absolute and relative facial pressure-pain thresholds in healthy individuals. J Orofac Pain. 14(2): 98-104.
https://pubmed.ncbi.nlm.nih.gov/11203752

II. Fredriksson L, Alstergren P, Kopp S (2003). Pressure pain thresholds in the craniofacial region of female patients with rheumatoid arthritis. J Orofac Pain. 17(4): 326-32.
https://pubmed.ncbi.nlm.nih.gov/14737877

III. Fredriksson L, Alstergren P, Kopp S (2005). Serotonergic mechanisms influence the response to glucocorticoid treatment in TMJ arthritis. Mediators Inflamm. 2005(4): 194-201.
https://doi.org/10.1155/MI.2005.194

IV. Fredriksson L, Alstergren P, Kopp S (2006). Tumor necrosis factor in temporomandibular joint synovial fluid predicts treatment effect on pain of intra-articular glucocorticoid treatment. Mediators of Inflammation. [Accepted]
https://doi.org/10.1155/MI/2006/59425

V. Alstergren P, Fredriksson L, Kopp S (2006). Temporomandibular joint pressure-pain threshold is modulated by systemic inflammatory mechanisms and only weakly related to other temporomandibular joint pain entities in rheumatoid arthritis. [Submitted]