The weight-QTL coincide with previously described genes and QTL involved in fatty acid metabolism and offer a plausible explanation for the observed phenotype in STR/ort mice. The exact match of the COMP-QTL and the COMP gene itself suggests a regulatory polymorphism to account for elevated serum levels in STR/ort mice and questions the robustness of serum COMP as a prognostic marker in human knee OA. The newly identified QTL associated with degenerative changes of the knee joints support the concept of OA resulting from a defective chondrocyte metabolism and/or altered apoptosis rate. However, we also discuss the unlikelihood of one QTL being responsible for OA in STR/ort mice and the inherent limitations of microsatellite analyses for complex genetic diseases.
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