Diabetes and skeletal health

Abstract

Osteoporosis and diabetes affect a large proportion of the elderly population. The prevalence of diabetes and osteoporosis is increasing. Compared with individuals without diabetes, both men and women with diabetes have a higher risk of fractures, particularly at the hip, with consequent significant morbidity and mortality. Type 1 diabetes is associated with decreased bone mass and although bone mass data for Type 2 diabetes may or may not be decreased, there is evidence of altered bone quality in diabetes. The mechanisms involved include effects of insulin, insulin-like growth factor 1, cytokines, advanced glycation end products, and altered calcium homeostasis. In addition, a drug-induced increase in the incidence of fractures has been noted with the use of thiazolidinediones (TZDs). TZDs improve insulin sensitivity and have multitude other beneficial effects. Osteoblasts and adipocytes are derived from a common multipotential mesenchymal stem cell progenitor, with activation of peroxisome proliferator-activated receptor γ2 by both currently available TZDs (i.e. rosiglitazone and pioglitazone) stimulating adipogenesis and inhibiting osteoblastogenesis. The use of both rosiglitazone and pioglitazone is associated with an increased fracture risk, with changes in bone turnover markers and decreased bone mineral density.