Skeletal involvement in patients with diabetes mellitus

Studies on skeletal involvement in patients with diabetes mellitus have generated conflicting results, largely because of the pathogenetic complexity of the condition. Several mechanisms may contribute to skeletal damage, including the increased urinary excretion coupled with the lower intestinal absorption of calcium, the inappropriate homeostatic response in terms of parathyroid hormone secretion, and also the complex alteration of vitamin D regulation. Decreased or increased insulin and IGF-1 concentrations and the effects of the accumulation of glycation endproducts on the bone tissue could also play a role. A possible genetic predisposition is also currently under investigation. Finally, the role of fat tissue in type 1 and type 2 diabetes and that of diabetic complications also deserve note. As far as bone mass is concerned, in adult patients with type 1 diabetes a moderately reduced bone mineral density has been shown in both axial and appendicular skeleton. On the contrary, patients with type 2 diabetes seem to have higher bone mineral density in respect to healthy control subjects, especially when overweight women are considered. No clear relationship between bone mass measurements and biochemical parameters of mineral metabolism has been shown in the different types of diabetes. Cohort studies recently carried out on large samples indicate that diabetic patients (with both type 1 and type 2 disease) have a higher risk for fracture, in particular for hip fracture, the most dangerous osteoporotic complication. This seems to be dependent both on qualitative and quantitative alterations of the bone, as well as on extra-skeletal factors due to the neuropathic and microangiopathic complications of the disease. Copyright © 2004 John Wiley & Sons, Ltd

Cyclical changes of vertebral body heights and bone loss in healthy women after menopause

Annual changes in vertebral body heights (VHs) and lumbar bone mineral density (LBMD) were evaluated in 120 healthy pre- and post-menopausal women aged 45-74 years. Subjects were divided into groups according to menstrual status and years since menopause (YSM). Vertebral heights were evaluated, using radiological morphometry as the sum of anterior vertebral body heights (AVHs) from T4 to L5 at baseline and exactly 12 months later. Results indicate that the sum of VHs is inversely correlated with advancing age, and the decrease in VHs is not a constant process over time but rather exhibits cyclical damping oscillations. When log-linear trend of VH decrease was transformed into a constant considering annual percentage changes, the presence of a cyclical component of 7 years was evident. Employing a harmonic regression model, the cyclical component was also statistically significant on baseline data. The cyclical decrease of VHs corresponds to an analogous cyclical behavior of LBMD values. These results suggest that a lack of estrogen acts as a synchronizer on bone remodeling, triggering a latent cyclical rhythm of bone loss, accompanied by cyclical bone microarchitecture deterioration and consequent vertebral body deformities, which after menopause persists throughout life. The existence of a chronobiological rhythm of bone loss and trabecular bone strength reduction at vertebral level after menopause, if confirmed, could have important clinical implications. (c) 2005 Elsevier Inc. All rights reserved