Peter Vestergaard
Diabetes – both type 1 (T1D) and type 2 (T2D) has profound effects on the skeleton. Bone turnover is reduced, i.e. bone biopsies show a reduced bone formation with reduced mineralisation, and a reduced number of bone cells. Biochemical markers of bone turnover show a reduction in both formation and resoprtion. Bone mineral density (BMD) is reduced in T1D, whereas an increased BMD is seen in T2D. Despite this, an increased risk of hip fractures is seen in both T1D and T2D, the increase in risk of fractures being more pronounced in T1D than in T2D. This discrepancy between BMD and fracture risk along with evidence from animal studies of a reduced bone biomechanical competence in diabetes suggest that the bone tissue is weakened in patients with diabetes. This weakening may be related to glycation of collagen and formation of advanced glycation end-products (AGE), which together with their receptor (RAGE) lead to a decreased activity of the bone cells and thus a reduced turnover and a reduced de-novo formation of bone. The reduced competence despite normal BMD makes the diagnosis of osteoporosis difficult as standard bone scans (DXA) may not truly reflect bone strength. Regarding anti-diabetic treatment, most such drugs improve glucose control and thus reduce the detrimental effects of diabetes on the skeleton. However, the thiazolidinediones (rosiglitazone and pioglitazone) are associated with a decreased BMD and an increased fracture risk through an effect on the stem cells in the bone marrow leading to formation of adipocytes rather than osteoblasts. Anti-resoprtive treatment for osteoporosis seem equally effective in diabetes patients as in non-diabetics despite the reduced bone turnover in diabetes. In conclusion diabetes has many effects on bone and bone-turnover, and more research is needed.
