Our previous studies demonstrated that the residual collagen in osteoporotic bone was not normal but possessed higher levels of lysine hydroxylation and modified cross-linking. However, the mechanism for these changes was not clear. In the current investigation, an assessment of bone collagen metabolism in osteoporosis (OP) revealed an increase in the overall metabolism of collagen relative to age-matched controls. The increased metabolism accounts for the observed post-translational modifications of collagen which lead to a more fragile bone matrix. The rate of bone metabolism is therefore an important aspect of the pathogenesis of osteoporosis, the greater the turnover the greater the propensity of a more fragile tissue. Clearly, the quality of bone tissue does not depend solely on adequate bone density but also on the state of the collagenous matrix.