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Cognitive decline and osteoporosis often coexist and some evidence suggests a causal link. However, there are no data on the longitudinal relationship between cognitive decline, bone loss and fracture risk, independent of aging. This study aimed to determine the association between: (i) cognitive decline and bone loss; and (ii) clinically significant cognitive decline (>= 3 points) on Mini Mental State Examination (MMSE) over the first 5 years and subsequent fracture risk over the following 10 years. A total of 1741 women and 620 men aged >= 65 years from the population-based Canadian Multicentre Osteoporosis Study were followed from 1997 to 2013. Association between cognitive decline and (i) bone loss was estimated using mixed-effects models; and (ii) fracture risk was estimated using adjusted Cox models. Over 95% of participants had normal cognition at baseline (MMSE >= 24). The annual % change in MMSE was similar for both genders (women -0.33, interquartile range [IQR] -0.70 to +0.00; and men -0.34, IQR: -0.99 to 0.01). After multivariable adjustment, cognitive decline was associated with bone loss in women (6.5%; 95% confidence interval [CI], 3.2% to 9.9% for each percent decline in MMSE from baseline) but not men. Approximately 13% of participants experienced significant cognitive decline by year 5. In women, fracture risk was increased significantly (multivariable hazard ratio [HR], 1.61; 95% CI, 1.11 to 2.34). There were too few men to analyze. There was a significant association between cognitive decline and both bone loss and fracture risk, independent of aging, in women. Further studies are needed to determine mechanisms that link these common conditions. (c) 2021 American Society for Bone and Mineral Research (ASBMR).

Cognitive decline and osteoporosis often coexist and some evidence suggests a causal link. However, there are no data on the longitudinal relationship between cognitive decline, bone loss and fracture risk, independent of aging. This study aimed to determine the association between: (i) cognitive decline and bone loss; and (ii) clinically significant cognitive decline (>= 3 points) on Mini Mental State Examination (MMSE) over the first 5 years and subsequent fracture risk over the following 10 years. A total of 1741 women and 620 men aged >= 65 years from the population-based Canadian Multicentre Osteoporosis Study were followed from 1997 to 2013. Association between cognitive decline and (i) bone loss was estimated using mixed-effects models; and (ii) fracture risk was estimated using adjusted Cox models. Over 95% of participants had normal cognition at baseline (MMSE >= 24). The annual % change in MMSE was similar for both genders (women -0.33, interquartile range [IQR] -0.70 to +0.00; and men -0.34, IQR: -0.99 to 0.01). After multivariable adjustment, cognitive decline was associated with bone loss in women (6.5%; 95% confidence interval [CI], 3.2% to 9.9% for each percent decline in MMSE from baseline) but not men. Approximately 13% of participants experienced significant cognitive decline by year 5. In women, fracture risk was increased significantly (multivariable hazard ratio [HR], 1.61; 95% CI, 1.11 to 2.34). There were too few men to analyze. There was a significant association between cognitive decline and both bone loss and fracture risk, independent of aging, in women. Further studies are needed to determine mechanisms that link these common conditions. (c) 2021 American Society for Bone and Mineral Research (ASBMR).

PURPOSE OF REVIEW: Diabetes mellitus (DM) is associated with increased fracture risk. The aim of this systematic review was to examine the effects of different classes of glucose-lowering drugs on fracture risk in patients with type 2 DM. The heterogeneity of the included studies did not allow formal statistical analyses.RECENT FINDINGS: Sixty studies were included in the review. Metformin, dipeptidylpeptidase-IV inhibitors, glucagon-like peptide-1 receptor agonists, and sodium-glucose cotransporter 2-inhibitors do not appear to increase fracture risk. Results for insulin and sulphonylureas were more disparate, although there may be an increased fracture risk related to hypoglycemia and falls with these treatments. Glitazones were consistently associated with increased fracture risk in women, although the evidence was sparser in men. New glucose-lowering drugs are continuously being developed and better understanding of these is leading to changes in prescription patterns. Our findings warrant continued research on the effects of glucose-lowering drugs on fracture risk, elucidating the class-specific effects of these drugs.

Introduction: Cortical bone thinning and a rarefaction of the trabecular architecture represent possible causes of increased femoral neck (FN) fracture risk. Due to X-ray exposure limits, the bone microstructure is rarely measurable in the FN of subjects but can be assessed at the tibia. Here, we studied whether changes of the tibial cortical microstructure, which were previously reported to be associated with femur strength, are also associated with structural deteriorations of the femoral neck.Methods: The cortical and trabecular architectures in the FN of 19 humans were analyzed ex vivo on 3D microcomputed tomography images with 30.3 mu m voxel size. Cortical thickness (Ct.Th-tibia), porosity (Ct.Po-tibia) and pore size distribution in the tibiae of the same subjects were measured using scanning acoustic microscopy (12 mu m pixel size). Femur strength during sideways falls was simulated with homogenized voxel finite element models.Results: Femur strength was associated with the total (vBMD(tot); R-2 = 0.23, p <0.01) and trabecular (vBMD(trab); R-2 = 0.26, p <0.01) volumetric bone mineral density (vBMD), with the cortical thickness (Ct.Th-FN; R-2 = 0.29, p <0.001) and with the trabecular bone volume fraction (Tb.BV/TVFN; R-2 = 0.34, p <0.001), separation (Tb.Sp(FN); R-2 = 0.25, p <0.01) and number (Tb.N-FN; R-2 = 0.32, p <0.001) of the femoral neck. Moreover, smaller Ct.Th-tibia was associated with smaller CLThFN (R-2 = 0.31, p <0.05), lower Tb.BV/TVFN (R-2 = 0.29, p <0.05), higher Tb.Sp(FN) (R-2 = 0.33, p <0.05) and lower Tb.N-FN (R-2 = 0.42, p <0.01). A higher prevalence of pores with diameter > 100 mu m in tibial cortical bone (relCt.Po100 mu m-tibia) indicated higher Tb.Sp(FN) (R-2 = 0.36, p <0.01) and lower Tb.N-FN (R-2 = 0.45, p <0.01).Conclusion: Bone resorption and structural decline of the femoral neck may be identified in vivo by measuring cortical bone thickness and large pores in the tibia.

PURPOSE OF REVIEW: Diabetes mellitus (DM) is associated with increased fracture risk. The aim of this systematic review was to examine the effects of different classes of glucose-lowering drugs on fracture risk in patients with type 2 DM. The heterogeneity of the included studies did not allow formal statistical analyses.RECENT FINDINGS: Sixty studies were included in the review. Metformin, dipeptidylpeptidase-IV inhibitors, glucagon-like peptide-1 receptor agonists, and sodium-glucose cotransporter 2-inhibitors do not appear to increase fracture risk. Results for insulin and sulphonylureas were more disparate, although there may be an increased fracture risk related to hypoglycemia and falls with these treatments. Glitazones were consistently associated with increased fracture risk in women, although the evidence was sparser in men. New glucose-lowering drugs are continuously being developed and better understanding of these is leading to changes in prescription patterns. Our findings warrant continued research on the effects of glucose-lowering drugs on fracture risk, elucidating the class-specific effects of these drugs.

Introduction: Cortical bone thinning and a rarefaction of the trabecular architecture represent possible causes of increased femoral neck (FN) fracture risk. Due to X-ray exposure limits, the bone microstructure is rarely measurable in the FN of subjects but can be assessed at the tibia. Here, we studied whether changes of the tibial cortical microstructure, which were previously reported to be associated with femur strength, are also associated with structural deteriorations of the femoral neck.Methods: The cortical and trabecular architectures in the FN of 19 humans were analyzed ex vivo on 3D microcomputed tomography images with 30.3 mu m voxel size. Cortical thickness (Ct.Th-tibia), porosity (Ct.Po-tibia) and pore size distribution in the tibiae of the same subjects were measured using scanning acoustic microscopy (12 mu m pixel size). Femur strength during sideways falls was simulated with homogenized voxel finite element models.Results: Femur strength was associated with the total (vBMD(tot); R-2 = 0.23, p <0.01) and trabecular (vBMD(trab); R-2 = 0.26, p <0.01) volumetric bone mineral density (vBMD), with the cortical thickness (Ct.Th-FN; R-2 = 0.29, p <0.001) and with the trabecular bone volume fraction (Tb.BV/TVFN; R-2 = 0.34, p <0.001), separation (Tb.Sp(FN); R-2 = 0.25, p <0.01) and number (Tb.N-FN; R-2 = 0.32, p <0.001) of the femoral neck. Moreover, smaller Ct.Th-tibia was associated with smaller CLThFN (R-2 = 0.31, p <0.05), lower Tb.BV/TVFN (R-2 = 0.29, p <0.05), higher Tb.Sp(FN) (R-2 = 0.33, p <0.05) and lower Tb.N-FN (R-2 = 0.42, p <0.01). A higher prevalence of pores with diameter > 100 mu m in tibial cortical bone (relCt.Po100 mu m-tibia) indicated higher Tb.Sp(FN) (R-2 = 0.36, p <0.01) and lower Tb.N-FN (R-2 = 0.45, p <0.01).Conclusion: Bone resorption and structural decline of the femoral neck may be identified in vivo by measuring cortical bone thickness and large pores in the tibia.