No abstract

As the popularity of bariatric surgery to treat morbid obesity has risen, so has a concern of increased skeletal fragility secondary to accelerated bone loss following bariatric procedures. We reviewed cross-sectional and prospective literature reporting bone density outcomes following bariatric surgical treatment for morbid obesity. Prospective research provides evidence of hip and lumbar spine areal bone mineral density (aBMD) reductions primarily in women despite calcium and vitamin D supplementation. Femoral neck aBMD declines of 9-11% and lumbar spine aBMD reductions up to 8% were observed at the first post-operative year following malabsorptive procedures. Mean T- and Z-scores up to 25 years following surgery remained within normal and healthy ranges. Of those studies reporting development of osteoporosis following gastric bypass, one woman became osteoporotic after 1 year. Despite observed bone loss in the hip region post-surgery, data do not conclusively support increased incidence of osteoporosis or increased fracture risk in post-bariatric patients. However, given the limitations of dual energy X-ray absorptiometry technology in this population and the relative lack of long-term prospective studies that include control populations, further research is needed to provide conclusive evidence regarding fracture outcomes in this population.

Bariatric surgery is the most effective therapeutic approach to morbid obesity, resulting in substantial weight loss and improved cardiometabolic profiles; however, a growing body of evidence suggests that bariatric procedures increase both skeletal fragility and the risk of related future fracture secondary to excessive bone loss. Prospective evidence shows that areal bone mineral density (BMD) assessed by dual energy X-ray absorptiometry (DXA) declines by as much as 14% in the proximal femoral regions, including the femoral neck and total hip, 12 months postoperatively. Lumbar spine areal BMD outcomes show greater 12-month postoperative variability across surgical procedures (-8 to +6%) and contrast with no change in volumetric BMD outcomes measured by quantitative computed tomography. Diminished mechanical loading, micronutrient deficiency and malabsorption, along with neurohormonal alterations, offer plausible underlying mechanisms to explain these observed post-bariatric bone changes, but most remain largely unsubstantiated in this population. Importantly, DXA-based skeletal imaging may have limited utility in accurately detecting bone change in people undergoing bariatric surgery; partly because excessive tissue overlying bone increases the variability of areal BMD outcomes. Moreover, a paucity of fracture and osteoporosis incidence data raises questions about whether marked post-bariatric surgery bone loss is clinically relevant or a functional adaptation to skeletal unloading. Future studies that use technology which is able to accurately capture the site-specific volumetric BMD and bone architectural changes that underpin bone strength in people undergoing bariatric surgery, that consider mechanical load, and that better quantify long-term fracture and osteoporosis incidence are necessary to understand the actual skeletal effects of bariatric surgery.

No abstract

Factors that contribute to bone fragility in type 2 diabetes are not well understood. We assessed the effects of intensive glycemic control, thiazolidinediones (TZDs), and A1C levels on bone geometry and strength at the radius and tibia. In a substudy of the Action to Control Cardiovascular Risk in Diabetes trial, peripheral quantitative computed tomographic (pQCT) scans of the radius and tibia were obtained 2 years after randomization on 73 participants (intensive n = 35, standard n = 38). TZD use and A1C levels were measured every 4 months during the trial. Effects of intervention assignment, TZD use, and A1C on pQCT parameters were assessed in linear regression models. Intensive, compared with standard, glycemic control was associated with 1.3 % lower cortical volumetric BMD at the tibia in men (p = 0.02) but not with other pQCT parameters. In women, but not men, each additional year of TZD use was associated with an 11 % lower polar strength strain index (SSIp) at the radius (p = 0.04) and tibia (p = 0.002) in models adjusted for A1C levels. In women, each additional 1 % increase in A1C was associated with an 18 % lower SSIp at the ultradistal radius (p = 0.04) in models adjusted for TZD use. There was no consistent evidence of an effect of intensive, compared with standard, glycemic control on bone strength at the radius or tibia. In women, TZD use may reduce bone strength at these sites. Higher A1C may also be associated with lower bone strength at the radius, but not tibia, in women.