Diabetes mellitus is an enormous menace to public health globally. This
chronic disease of metabolism will adversely affect the skeleton if not controlled. Both
type 1 diabetes mellitus (T1DM) and
type 2 diabetes mellitus (T2DM) are associated with an increased risk of
osteoporosis and fragility fractures. Bone mineral density is reduced in T1DM, whereas patients with T2DM have normal or slightly higher bone density, suggesting impaired bone quality is involved. Detrimental effects of T1DM on the skeleton are more severe than T2DM, probably because of the lack of osteo-
anabolic effects of
insulin and other
pancreatic hormones. In both T1DM and T2DM, low bone quality could be caused by various means, including but not limited to
hyperglycemia, accumulation of advanced glycosylation end products (AGEs), decreased serum levels of
osteocalcin and
parathyroid hormone. Risk for
osteoarthritis is also elevated in diabetic population. How diabetes accelerates the deterioration of cartilage remains largely unknown.
Hyperglycemia and
glucose derived AGEs could contribute to the development of
osteoarthritis. Moreover, it is recognized that oral
antidiabetic medicines affect bone metabolism and turnover as well.
Insulin is shown to have
anabolic effects on bone and
hyperinsulinemia may help to explain the slightly higher bone density in patients with T2DM.
Thiazolidinediones can promote bone loss and
osteoporotic fractures by suppressing osteoblastogenesis and enhancing osteoclastogenesis.
Metformin favors bone formation by stimulating osteoblast differentiation and protecting them against diabetic conditions such as
hyperglycemia. Better knowledge of how diabetic conditions and its treatments influence skeletal tissues is in great need in view of the growing and aging population of patients with
diabetes mellitus.