Osteoporosis

One of the common degenerative diseases of aging is osteoporosis. Bone density is decreased in an age-dependent fashion after it reaches its peak at young adulthood. The prevalence of osteoporosis and fractures increases with age. In women, estrogen withdrawal accompanying menopause plays a major role in the first 10 years. Diabetes also is associated with increased risk of fracture of the hip, proximal humerus, and foot (Inzerillo and Epstein, 2004; Schwartz, 2003). Type 1 diabetes is associated with modest reductions in bone mineral density (BMD), but type 2 diabetes often is characterized by elevated BMD (Inzerillo and Epstein, 2004). The paradoxically increased fracture risk in type 2 diabetes may be explained by a combination of factors, including more frequent falls and poorer bone quality.

The precise cause for the osteopenia or poor bone quality of diabetes is not known. Potential mechanisms contributing to reduced bone mass in diabetes include nutritional deficiencies, alterations in vitamin D metabolism and possibly alterations in the microenvironment of bone as a result of microvascular disease, and increased glycation of key structural proteins such as collagen. In addition, increased cytokine production in diabetes may also contribute to osteopenia. Finally, it has been suggested that decreasing leptin level with peroxisome proliferators-activated receptor (PPAR) gamma agonist treatment is associated with prevention of bone loss in type 2 diabetes (Watanabe et al., 2003). Indeed, leptin-deficient mice have higher bone mass, and the thiazolidi-nedione drugs have been shown to inhibit the formation of bone-resorbing osteoclasts in vitro and to decrease bone resorption markers in vivo.

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