Osteoporosis and risk of fracture in patients with diabetes: an update

Abstract

Diabetes mellitus (DM) and osteoporotic fractures are two of the most important causes of mortality and morbidity in older subjects. Recent data report a close association between fragility fracture risk and DM of both type 1 (DM1) and type 2 (DM2). However, DM1 is associated with reduced bone mineral density (BMD), whereas patients with DM2 generally have normal or increased BMD. This apparent paradox may be explained by the fact that, at a given level of BMD, diabetic patients present lower bone quality with respect to non-diabetics, as shown by several studies reporting that diabetes may affect bone tissue by means of various mechanisms, including hyperinsulinemia, deposition of advanced glycosylation endproducts (AGEs) in collagen, reduced serum levels of IGF-1, hypercalciuria, renal failure, microangiopathy and inflammation. In addition, the propensity to fall and several comorbidities may further explain the higher fracture incidence in DM patients with respect to the general population. It is reasonable to expect that close metabolic control of diabetes may improve bone status, although its effect on reduction of fracture risk has not yet been demonstrated. However, metformin has a direct effect on bone tissue by reducing AGE accumulation, whereas insulin acts directly on osteoclast activity, and thiazolidinediones (TZD) may have a negative effect by switching mesenchymal progenitor cells to adipose rather than bone tissue. New prospects include the incretins, a class of antidiabetic drugs which may play a role linking nutrition and bone metabolism. Better knowledge on how diabetes and its treatments influence bone tissue may lie at the basis of effective prevention of bone fracture in diabetic patients. Thus, close glycemic control, adequate intake of calcium and vitamin D, screening for low BMD, and prevention and treatment of diabetic complications are key elements in the management of osteoporosis in both DM1 and DM2. Attention should be paid to treating diabetes with TZD in women with DM2, particularly if elderly. Lastly, patients with osteoporosis and diabetes should be offered the same pharmacological treatments as non-diabetics, although specific trials on the effects of anti-osteoporotic drugs in the diabetic population are lacking.

Status of Bone Mineral Density in Children with Type 1 Diabetes Mellitus and Its Related Factors

“…Osteoporosis, which is usually asymptomatic until a fracture occurs, is known as an alarming health problem throughout the world (4). Given the importance and high incidence of osteoporosis and bone fractures in patients with type 1 DM, researchers investigate different pathological mechanisms that reduce bone density in these patients (5)(6)(7)(8). Bone marrow derived endothelial progenitor cells (EPCs) play an important role in bone repair, and diabetes leads to decreased expression of these cells through different paths, which ultimately reduces ossification at the fracture site (9).…”

Reciprocal Regulation of Adipocyte and Osteoblast Differentiation of Mesenchymal Stem Cells byEupatorium japonicumPrevents Bone Loss and Adiposity Increase in Osteoporotic Rats

“…As expected, OVX induced significant changes in the BMD of the right femur (0.116 g/cm 2 ) compared to that of the sham group (0.127 g/cm 2 ; Fig. 4).…”

“…1 Osteoporosis is more common with increasing age and is associated with metabolic diseases such as diabetes and obesity. 2 Thus, the prevalence of osteoporosis is forecasted to increase worldwide due to the increase in the aging population and in the incidence of metabolic diseases. 3 Estrogen deficiency, particularly in elderly women, often leads to rapid bone loss.…”

The effect of caffeine on some indicators of bone metabolism in rats

“…Conlisk and Galuska [22] conducted the effect of caffeine intake in doses of 100 mg/dl on bone tissue of young women. BMD was decreased of femoral neck and lumbar vertebral column 0.0069 g/cm 2 and 0.0119 g/cm 2 , respectively. There was an association between caffeine consumption and elevated risk of fractures after menopause in women aged 50-59 who intake caffeine with a dose of 400 mg/dl [23].…”

“…The intake of caffeine-containing beverages has unwanted health consequences but it can also produce several conceivable health benefits. Caffeine, is associated with a significant increase of periodontal diseases, induce loss of bone mineral density (BMD) with 5 mg net loss of calcium per cup of coffee [2], increased risk of fractures and negative influence on calcium retention [3,4]. Direct effect of caffeine on protein expression of the vitamin D receptor and osteoblast activity may be indicating a probable molecular mechanism for the role of caffeine in osteoporosis [5].…”