Absence of or mutation in any matrix component will result in cartilage that cannot fully resist mechanical loads. Significant defects in type II collagen or aggrecan cause chondrodys-plasias and defective skeletal growth [80,85]; as a result, animals do not live long enough to develop OA. However, smaller defects in the type II collagen gene have been linked to early-onset OA in humans [46,96]. In mice created with additional copies of a transgene with a small deletion of type II collagen, the resulting synthesis of a truncated type II collagen, added to the normal gene, leads to osteoarthritic-like lesions as the mice age. The reason is that expression of the transgene causes deposition of a structurally inferior collagen network . Indeed, it is the absence of minor components that is associated with OA, presumably because the small matrix defect will become apparent only with time. Mice lacking alpha 1
(IX) collagen develop noninflammatory degenerative joint disease . Mice deficient in both biglycan and fibromodulin develop severe and premature knee OA , even though the cartilage defect may be secondary to tendon defects that cause subluxation of the joints. Genetic defects in the minor matrix components may cause OA in some instances, but not for most OA patients.
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