Abstract
Evidence has accumulated that collagen cross-links play important roles in bone strength. We have demonstrated that the quantitative and qualitative deterioration of lysyl oxidase controlled and non-enzymatic cross-links (Advanced glycation end products, AGEs, Pentosidine) of collagen in patients with osteoporotic femoral neck fracture cases might be affected by hyperhomocysteinemia, oxidative stress and B-group vitamins insufficiency. Recently, Shiraki et al. demonstrated that a functional polymorphism in methylenetetrahydrofolate reductase (MTHFR) polymorphism, T allele (C677T), may be a risk factor for future fracture in addition to the traditional risk factors. In addition, we have reported that a higher urinary pentosidine was an independent risk factor, for vertebral fracture in a 5-year prospective study in Japanese post-menopausal women. If confirmed in large, prospective trials, measurement of serum homocysteine and serum or urinary excretion of pentosidine might be characterized as markers reflecting bone collagen deterioration.
