Immunohistochemical Expression of IL-1 in the Disks of Patients With Temporomandibular Joint Dysfunction

Objectives: The fibrocartilaginous disk in the temporomandibular joint (TMJ) consists of collagen fibers and fibroblast-like cells. It plays an important role in pressure distribution. When a disk is chronically overloaded, it may undergo structural changes with pathological consequences. Cytokines have been shown to be present in synovial fluid of patients with internal derangement and osteoarthritis. Interlukin 1 (IL-1) acts as a pro-inflammatory cytokine. It is produced by many cell types, including macrophages, monocytes and fibroblasts. In patients with internal derangements, fibroblasts may release IL-1 as a protective mechanism. The majority of studies have been performed with synovial fluid, animal models or cadavers. Therefore, the objective of this study is to determine the association of IL-1 expression in the disks of patients with TMJ dysfunctions using an immunihistochemcial approach to evaluate the joint disk.
Methods: A total of 45 human TMJ samples were collected, 36 samples in the test group (patients with anterior disk displacement with reduction (n=29) and without reduction (7) and nine samples in the control group. The discs will be immunostained with monoclonal IL-1 antibodies diluted 1:50 in phosphate-buffered sailne. They will be histochemically analyzed and statistically compared to the control group.
Results: There will be a difference in the expression of IL-1 betweeen the control group and the displacement groups. The experimental groups will express higher levels of IL-1 compared to the group without reduction. IL-1 will be expressed the most in the group with patients who had anterior disc displacement without reduction.
Conclusions: The chronic mechanical stress generated during jaw movement in patients with disc displacement activates the inflammatory process in the disk. The higher expression of IL-1 found in disks of patients with disc displacement with and without reduction is due to a chronic inflammatory process. This is the body's attempt to remodel the TMJ to correct the joint dysfunction.