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The
th Annual Meeting of April 8-9, 2017 The Endocrine Society and The Diabetes Association of the R.O.C. (Taiwan)
MD-1
PATHOGENESIS OF OSTEOPOROSIS AND OSTEOPOROTIC FRACTURES IN PATIENTS WITH DIABETES J-F KUO Division of Endocrinology and Metabolism, Department of Internal Medicine, Changhua Christian Hospital, Taiwan, ROC
Both type 1 (T1DM) and 2 diabetes (T2DM) are associated with an increased risk of fracture. Although bone mineral density (BMD) is decreased in T1DM, BMD in T2DM is often normal or even slightly elevated compared with an age-matched control population. On the other hand, bone loss as determined by Dual-energy X-ray absorptiometry (DXA) occurs more rapidly in type 2 diabetic postmenopausal women. Fracture risk in T2DM is higher for a given BMD T-score and age or for a given Fracture Risk Assessment Tool (FRAX) score. Bone strength consists of BMD and bone quality, which suggests that factors other than BMD play a major role in bone quality in diabetes. The skeletal system seems to be an additional target of diabetes-mediated damage, leading to the development of diabetes- induced osteoporosis. Mechanisms of diabetes- induced bone fragility including low bone turnover, accumulation of advanced glycation end products (non-enzymatic glycosylation of collagen) with micro and macro-architecture alterations (increased cortical porosity) that cause reduced resistance to mechanical stress, pro-inflammatory state with increased oxidative VWUHVV DGLSRNLQHV G\VUHJXODWLRQ LQVXOLQ GH¿FLHQF\ RU DOWHUHG LQVXOLQ VLJQDOLQJ ORZ OHYHO RI LQVXOLQ like growth factor 1, loss of incretin effect, increased marrow fat. Complications of DM increase the risk of falls and fracture including peripheral neuropathy, orthostatic hypotension, sarcopenia, YLVLRQ LPSDLUPHQW DQG IUHTXHQW K\SRJO\FDHPLF HYHQWV 9LWDPLQ ' GH¿FLHQF\ K\SRJRQDGLVP XVH RI DQWLGLDEHWLF PHGLFDWLRQV WKLD]ROLGLQHGLRQHV FDQDJOLÀR]LQ PLJKW DOVR FRQWULEXWH WR LQFUHDVHG IUDFWXUH risk.
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