In practice, this effect might impair the healing of repaired meniscal roots to the tibial bone.

Objective. To study the expression of small ubiquitin-like modifier 1 (SUMO-1) in aseptic loosening of prosthesis implants and to investigate its role in regulating the susceptibility of prosthesis-loosening fibroblastlike synoviocytes (FLS) to Fas-induced apoptosis.Methods. Specimens of aseptically loosened tissue were obtained at revision surgery, and the expression of SUMO-1 was analyzed by in situ hybridization. SUMO-1 levels in FLS were determined by quantitative polymerase chain reaction and Western blot analysis. Immunohistochemistry and confocal microscopy were used to study the subcellular localization of SUMO-1. The functional role of SUMO-1 in Fas-induced apoptosis of prosthesis-loosening FLS was investigated by small interfering RNA-mediated knockdown of SUMO-1 and by gene transfer of the nuclear SUMO-specific protease SENP1.Results. SUMO-1 was expressed strongly in aseptically loosened tissue and was found prominently at sites adjacent to bone. Prosthesis-loosening FLS expressed levels of SUMO-1 similar to the levels expressed by rheumatoid arthritis (RA) FLS, with SUMO-1 being found mainly in promyelocytic leukemia protein nuclear bodies. Knockdown of SUMO-1 had no effect on spontaneous apoptosis but significantly increased the susceptibility of prosthesis-loosening FLS to Fas-induced apoptosis. Gene transfer of the nuclear SUMO-specific protease SENP1 reverted the apoptosis-inhibiting effects of SUMO-1. Conclusion. These data suggest that SUMO-1 is involved in the activation of both RA FLS and prosthesis-loosening FLS by preventing these cells from undergoing apoptosis. Modification of nuclear proteins by SUMO-1 contributes to the antiapoptotic effects of SUMO-1 in prosthesis-loosening FLS, providing evidence for the specific activation of sumoylation during their differentiation. Therefore, SUMO-1 may be an interesting target for novel strategies to prevent aseptic prosthesis loosening.Aseptic loosening of prosthetic implants is a major long-term complication of joint replacement surgery. It is characterized by the development and destructive growth of a synovium-like membrane at the interface between the implanted prosthesis and bone (1,2). Synovium-like membrane formation is widely considered a foreign body reaction initiated by wear debris particles from the prosthesis. However, the cellular and molecular mechanisms that initiate development of this membrane and promote its growth remain incompletely understood. Multiple data suggest that in addition to macrophages, fibroblasts of the synovium-like membrane play an important role in aseptic loosening, and there is evidence that the synovial membrane in rheuSupported in part by the DFG (grants Pa689/2 and Pa689/3) and the Arbeitsgemeinschaft Rheumaorthopädie of the German Society of Rheumatology.

The pedicle subtraction osteotomy represents a powerful surgical technique for correction of a sagittal spinal imbalance.