[Hip resurfacing arthroplasty]. / Hüftgelenk-Oberflächenersatzendoprothesen.

In comparison to stemmed total hip replacements, hip resurfacing offers advantages especially in joint stability and amount of femoral bone resection. After the poor results achieved with this concept that were mainly caused by failure of the materials used, reintroduction of the metal-on-metal bearing initiated a renaissance. This bearing, the cementless cup, and the improved surgical technique led to better short- to medium-term results. Revision and complication rates are now comparable to conventional total hip replacements. The functional capacity of the method is higher. Because long-term results are not available, however, questions remain, for instance, the consequences of the higher metal ion serum concentrations or the impossibility of changing the inlay when femoral revision becomes necessary.

[Functional results after surface replacement of the hip: comparison between dysplasia and idiopathic osteoarthritis]. / Funktionelle Behandlungsergebnisse nach Oberflächenersatz am Hüftgelenk: Vergleich zwischen Dysplasie- und idiopathischer Koxarthrosen.

AIM: To determine if there are differences in function after resurfacing arthroplasty of the hip in patients with primary osteoarthritis compared to patients with secondary osteoarthritis due to developmental dysplasia of the hip. METHOD: In a controlled prospective study of Birmingham Hip Resurfacing (BHR) we included all patients with primary osteoarthritis (n = 54, average age 48.4 years) and osteoarthritis due to high grade dysplasia (Eftekhar B, n = 34, average age 55.8 years). Standardized clinical (Harris hip score) and radiographic examinations were performed 6 weeks, 3 months and 6 months and then every year after the operation. RESULTS: All patients could be followed up to 1.5 years (1-4 years) after surgery. The average Harris hip score improved to 82-95 points in both groups 3 months postoperatively. Statistically significant differences could be found in the subscales "function" and "limp", where patients with dysplastic hips showed somewhat lower results after 6 (function) to 12 weeks (limp) postoperatively. This is probably attributable to extended non-weight-bearing after acetabular reconstruction in these cases, as the difference disappeared with full weight-bearing. Radiographically determined neck-shaft angles are slightly higher in dysplastic hips (142 degrees versus 135 degrees ), but we did not recognize any significant differences in implant positioning. CONCLUSION: The short- to mid-term results showed no clinically relevant functional differences after surface replacement in patients with primary osteoarthritis of the hip and patients with secondary osteoarthritis due to higher grade dysplasia. Long-term observation is necessary, however, to determine if these positive functional results are reflected by appropriate radiographic survival.

Expression of the VEGF receptor-3 in osteoarthritic chondrocytes: stimulation by interleukin-1 beta and association with beta 1-integrins.

Recent studies have demonstrated enhanced expression of vascular endothelial growth factor and vascular endothelial growth factor receptor (VEGFR)-1 and -2 in chondrocytes of rheumatoid and osteoarthritic cartilage. Since expression of VEGFR-3 ( Flt-4) in chondrocytes has not yet been investigated, we studied the distribution of VEGFR-3 in osteoarthritic cartilage samples by immunohistochemistry and immunoelectron microscopy. Furthermore, we looked for functional colocalization of VEGFR-3 with the signal transduction receptor beta(1)-integrin. Superficial osteoarthritic chondrocytes exhibited VEGFR-3 expression in the cytoplasm and on the cell membrane. Using western blotting we could demonstrate that interleukin-1 beta (IL-1 beta) stimulates the expression of VEGFR-3 in chondrocytes in vitro in a dose-dependent manner. By coimmunoprecipitation assay we found a functional complex between the beta(1)-integrin and VEGFR-3 in IL-1 beta-stimulated chondrocytes indicating that activated VEGFR-3 may interact with beta(1)-integrin and associated subcellular pathways in osteoarthritic chondrocytes. Taken together with results of previous studies showing that beta(1)-integrins were also associated with other surface receptors and proteins in chondrocytes that cause cartilage destruction in arthritis (for example, urokinase-type plasminogen activator receptor and matrix metalloproteinases), we can hypothesize that signal transduction by these receptor complexes via beta(1)-integrins may play a crucial role in pathogenesis of osteoarticular disorders. Further work needs to be done to elucidate downstream signaling events activated by these receptors.

Expression of the urokinase-type plasminogen activator receptor in human articular chondrocytes: association with caveolin and beta 1-integrin.

The urokinase-type plasminogen activator (uPA) in concert with other proteolytic enzymes plays a critical role in cartilage degradation during osteoarthritis. Urokinase receptor (uPAR), a glycosyl-phosphatidylinositol-linked glycoprotein present on the cell surface of various cell types such as cancer cells, fibroblasts, synoviocytes, and chondrocytes, is a key regulator of the plasmin-mediated pericellular proteolysis. Recently, in arthritic synovial tissue increased uPAR expression has been detected. By immunohistochemical analysis we observed, in addition, enhanced expression of uPAR in chondrocytes of arthritic samples of human cartilage compared to non-arthritic controls. Using in vitro cultured human chondrocytes, we analyzed whether uPAR is associated with structural proteins, which are known to be involved in cell signaling and activation. uPAR in phorbol-12-myristate-13-acetate-stimulated chondrocytes colocalized with caveolin as well as beta 1-integrin, as demonstrated by double immunostaining with specific antibodies. Furthermore, uPAR was present in caveolae-like structures of chondrocytes as detected by immunoelectron microscopy. Finally, both caveolin and beta 1-integrin were coprecipitated with uPAR-specific antibodies from cell extracts suggesting that these proteins may form functional complexes in human chondrocytes. The localization of uPAR in caveolae and its close association with caveolin and beta 1-integrin points to a significance of uPAR-mediated signaling pathways in human chondrocytes.