Osteoarthritis-like damage of cartilage in the temporomandibular joints in mice with autoimmune inflammatory arthritis.

摘要: Summary Objective To study temporomandibular joint (TMJ) involvement in an autoimmune murine model of rheumatoid arthritis (RA), a disease characterized by inflammatory destruction the synovial joints. Although TMJ dysfunction is frequently found RA, RA remains unclear, and pathology has not been studied systemic animal models RA. Methods Proteoglycan (PG) aggrecan-induced (PGIA) was generated genetically susceptible BALB/c mice. TMJs tissues/cartilage were harvested for histological immunohistochemical analyses RNA isolation quantitative polymerase chain-reaction. Serum cytokine levels measured mice with acute or chronic arthritis, non-arthritic control animals. Results Despite development destructive synovitis limbs, little no inflammation PGIA. However, arthritic showed evidence aggrecanase- matrix metalloproteinase-mediated loss glycosaminoglycan-containing aggrecan, most severe cases, structural damage cartilage. pro-inflammatory cytokines, including interleukin (IL)-1β, elevated Expression IL-1β gene also high inflamed but essentially normal TMJs. Local expression genes encoding matrix-degrading enzymes (aggrecanases stromelysin) upregulated to similar degree both limbs Conclusion We propose that constantly catabolic such as IL-1β, circulation (released from joints) create milieu within TMJ, causing local upregulation proteolytic subsequent aggrecan