Insufficient endogenous control of tumor necrosis factor-α contributes to temporomandibular joint pain and tissue destruction in rheumatoid arthritis

Objective. To investigate whether pain and tissue destruction in the temporomandibular joint (TMJ) of patients with rheumatoid arthritis (RA) are influenced by plasma levels of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) or the soluble receptor TNFsRII. Methods. Fifty-one patients with RA were included. TMJ resting pain intensity, pain intensity upon mandibular movement, tenderness to palpation, pressure-pain threshold,and presence of anterior open bite were assessed. Venous blood was obtained for analysis of TNF-alpha, TNFsRII, and inflammatory markers. Results. A total of 29 patients had TMJ pain and 22 patients had anterior open bite. In the group of patients with TMJ pain, 12 had anterior open bite and 17 did not. In the patients without TMJ pain 10 patients had anterior open bite and 12 did not. Patients with or without anterior open bite did not differ regarding any investigated variable. Plasma TNF-alpha and TNFsRII were positively correlated in the total patient sample. TNFsRII was negatively correlated with degree of anterior open bite in patients with TMJ pain but positively correlated with TMJ pressure-pain threshold in patients with elevated plasma TNF-alpha. Conclusion. Our results indicate that insufficient systemic endogenous control of TNF-alpha seems to contribute to TMJ pain and tissue destruction in RA.