Psoriasis vulgaris caused by ceramic inserts used in total hip replacement.

BACKGROUND: Ceramics are inorganic nonmetallic materials and are used as bioinert components in joint replacement surgeries. Ceramics are known to be low allergenic. We experienced a ceramic-induced psoriasis. OBJECTIVE: We report a first case of possible ceramic-induced psoriasis caused by a ceramic insert. METHODS: A 55-year-old female received an implanted ceramic-on-ceramic total hip replacement for osteoarthritis of the right hip joint. Following surgery, she developed psoriatic lesions, which continued for 10 years. We suspected that psoriasis was caused by a ceramic insert and removed it surgically. RESULTS: When the ceramic insert was replaced with a polyethylene-on-metal hip joint, the psoriatic lesions completely disappeared. CONCLUSION: The pathogenesis of psoriasis is still an enigma, although deregulation of nuclear factor κB signaling and resulting abnormal cytokine secretion are speculated to be involved. Ceramics may affect these signaling events and cause the onset of psoriasis.

Downregulation of RCAS1 and upregulation of cytotoxic T cells affects synovial proliferation and apoptosis in rheumatoid arthritis.

OBJECTIVE: The main histological change in rheumatoid arthritis (RA) is the villous proliferation of synovial lining cells. This seems to be the result of the proliferation and apoptosis induced by immune balance. We studied the involvement of RCAS1 and the infiltration of cytotoxic T lymphocytes (CTL), and examined the synovium immunohistochemically to determine the involvement of proliferation and apoptosis in synovial lining cells, and their relationship with the activity of RATreg cells in the germinal center. METHODS: We used double-immunological staining of Ki-67 and caspase-3 to investigate proliferation and apoptosis. We analyzed CTL, regulatory T cells (Treg), and receptor-binding cancer antigen expressed on SiSo cells (RCAS1), recently recognized to play a role in immune evasion. Proliferation and apoptosis were more frequently encountered in synovial lining cells in RA than in those in osteoarthritis (OA) that were used as a control. RESULTS: High expression of RCAS1 was detected more frequently in the synovial lining cells of OA, but CTL infiltration into the synovium was rarely found. In RA, on the other hand, CTL were observed, while RCAS1 expression was lacking. We compared the presence of Foxp3-positive cells with the level of C-reactive protein (CRP) that served as an active inflammatory marker. Foxp3-positive cells in the germinal center and in CRP showed possible correlation in terms of the range of inflammatory states. CONCLUSION: In RA, the lack of RCAS1 is thought to induce CTL infiltration through loss of the ability to evade immune attack, thus leading to apoptosis of the synovial lining cells. In addition, Treg cells may play a role in the downregulation of activated T cells.