The use of routine magnetic resonance imaging (MRI) to potentially assess skeletal fragility has been widely studied in osteoporosis. The aim of this study was to evaluate bone texture attributes (TA) from routine lumbar spine (LS) MRI and their correlation with vertebral fragility fractures (VFF) and bone mineral density (BMD). Sixty-four post-menopausal women were submitted to LS densitometry, total spine radiographs, and routine T2-weighted LS MRI. Twenty-two TA were extracted with the platform IBEX from L3 vertebra. The statistical difference was evaluated using ANOVA and Duncan's post-test. Correlation analyses were performed using Spearman's coefficient. Statistical significance was considered when P<0.05. The results did not show a significant difference in BMD between the women with and without fractures. Two bone TA (cluster tendency and variance) were significantly lower in the fracture group. Cluster tendency with VFF in osteopenia was 1.54±1.37 and in osteoporosis was 1.11±58. Cluster tendency without VFF in osteopenia was 2.23±1.38 and in osteoporosis was 1.88±1.14). Variance with VFF in osteopenia was 1.44±1.37 and in osteoporosis was 1.13±59. Variance without VFF in osteopenia was 2.34±1.38 and in osteoporosis was 1.89±1.14. There was a significant correlation between BMD and cluster prominence (r=0.409), cluster tendency (r=0.345), correlation (r=0.570), entropy (r=0.364), information measure corr1 (r=0.378), inverse variance (r=0.449), sum entropy (r=0.320), variance (r=0.338), sum average (r=-0.274), and sum variance (r=-0.266). Our results demonstrated the potential use of TA extracted from routine MRI as a biomarker to assess osteoporosis and identify the tendency of skeletal fragility vertebral fractures. (MRI (TA (LS (VFF BMD. . (BMD) Sixtyfour Sixty four postmenopausal post menopausal densitometry radiographs T2weighted Tweighted T2 weighted T Twentytwo Twenty two L vertebra Duncans Duncan s posttest. posttest test. test post-test Spearmans Spearman coefficient P005 P 0 05 P<0.05 group 154137 1 54 37 1.54±1.3 11158 11 58 1.11±58 223138 2 23 38 2.23±1.3 1.88±1.14. 188114 1.88±1.14 88 14 1.88±1.14) 144137 44 1.44±1.3 11359 13 59 1.13±59 234138 34 2.34±1.3 189114 89 1.89±1.14 r=0.409, r0409 r r=0.409 , 409 (r=0.409) r=0.345, r0345 r=0.345 345 (r=0.345) r=0.570, r0570 r=0.570 570 (r=0.570) r=0.364, r0364 r=0.364 364 (r=0.364) corr r=0.378, r0378 r=0.378 378 (r=0.378) r=0.449, r0449 r=0.449 449 (r=0.449) r=0.320, r0320 r=0.320 320 (r=0.320) r=0.338, r0338 r=0.338 338 (r=0.338) r=0.274, r0274 r= 0.274 274 (r=-0.274) r=0.266. r0266 0.266 266 (r=-0.266) (BMD P00 P<0.0 15413 5 3 1.54±1. 1115 1.11±5 22313 2.23±1. 18811 1.88±1.1 8 14413 4 1.44±1. 1135 1.13±5 23413 2.34±1. 18911 1.89±1.1 r040 r=0.40 40 (r=0.409 r034 r=0.34 (r=0.345 r057 r=0.57 57 (r=0.570 r036 r=0.36 36 (r=0.364 r037 r=0.37 (r=0.378 r044 r=0.44 (r=0.449 r032 r=0.32 32 (r=0.320 r033 r=0.33 33 (r=0.338 r=0.274 r027 0274 0.27 27 (r=-0.274 r=0.266 r026 0266 0.26 26 (r=-0.266 P0 P<0. 1541 1.54±1 111 1.11± 2231 2.23±1 1881 1.88±1. 1441 1.44±1 113 1.13± 2341 2.34±1 1891 1.89±1. r04 r=0.4 (r=0.40 r03 r=0.3 (r=0.34 r05 r=0.5 (r=0.57 (r=0.36 (r=0.37 (r=0.44 (r=0.32 (r=0.33 r=0.27 r02 027 0.2 (r=-0.27 r=0.26 026 (r=-0.26 P<0 154 1.54± 1.11 223 2.23± 188 1.88±1 144 1.44± 1.13 234 2.34± 189 1.89±1 r0 r=0. (r=0.4 (r=0.3 (r=0.5 r=0.2 02 0. (r=-0.2 P< 15 1.54 1.1 22 2.23 18 1.88± 1.44 2.34 1.89± r=0 (r=0. (r=-0. 1.5 1. 2.2 1.88 1.4 2.3 1.89 (r=0 (r=-0 2. 1.8 (r= (r=- (r

Bone loss is a potential adverse consequence of rapid and sustained weight loss after bariatric surgery. The aim of the present study was to evaluate the bone mass, body fat distribution, and metabolic parameters in women submitted to Roux-en-Y gastric bypass (RYGB). The study included the following three groups: one group of lean women (control [C] group) and two groups of obese women, one evaluated one year (B1) and the other five years (B5) after RYGB. Dual-energy X-ray absorptiometry and magnetic resonance imaging were used to determine bone mineral density (BMD; lumbar spine, total hip, and femoral neck) and abdominal fat content (subcutaneous [SAT] and visceral [VAT] adipose tissues, and intrahepatic lipids [IHL]). The BMD/body mass index ratio was lower in the B5 compared with the C group at all sites. Serum C-terminal telopeptide of type I collagen (CTX) levels were higher in the B1 and B5 groups compared with the C group. Individuals submitted to RYGB showed greater SAT but similar VAT and IHL values compared with those in the C group. However, the B5 group had higher mean parathyroid hormone levels compared with the other two groups. Individuals submitted to RYGB presented increased levels of CTX and low BMD for body weight than those in the C group, suggesting that bone catabolism is a persistent alteration associated with RYGB. In conclusion, the long-lasting metabolic benefits obtained with RYGB in obesity are counterbalanced by a persistent catabolic effect of the procedure on bone and mineral metabolism.

Osteoporosis is a major complication of chronic cholestatic liver disease (CCLD). We evaluated the efficacy of using disodium pamidronate (1.0 mg/kg body weight) for the prevention (Pr) or treatment (Tr) of cholestasis-induced osteoporosis in male Wistar rats: sham-operated (Sham = 12); bile duct-ligated (Bi = 15); bile duct-ligated animals previously treated with pamidronate before and 1 month after surgery (Pr = 9); bile duct-ligated animals treated with pamidronate 1 month after surgery (Tr = 9). Rats were sacrificed 8 weeks after surgery. Immunohistochemical expression of IGF-I and GH receptor was determined in the proximal growth plate cartilage of the left tibia. Histomorphometric analysis was performed in the right tibia and the right femur was used for biomechanical analysis. Bone material volume over tissue volume (BV/TV) was significantly affected by CCLD (Sham = 18.1 ± 3.2 vs Bi = 10.6 ± 2.2%) and pamidronate successfully increased bone volume. However, pamidronate administered in a preventive regimen presented no additional benefit on bone volume compared to secondary treatment (BV/TV: Pr = 39.4 ± 12.0; Tr = 41.2 ± 12.7%). Moreover, the force on the momentum of fracture was significantly reduced in Pr rats (Sham = 116.6 ± 23.0; Bi = 94.6 ± 33.8; Pr = 82.9 ± 22.8; Tr = 92.5 ± 29.5 N; P < 0.05, Sham vs Pr). Thus, CCLD had a significant impact on bone histomorphometric parameters and pamidronate was highly effective in increasing bone mass in CCLD; however, preventive therapy with pamidronate has no advantage regarding bone fragility.

We assessed the effect of chronic hyperglycemia on bone mineral density (BMD) and bone remodeling in patients with type 2 diabetes mellitus. We investigated 42 patients with type 2 diabetes under stable control for at least 1 year, 22 of them with good metabolic control (GMC: mean age = 48.8 ± 1.5 years, 11 females) and 20 with poor metabolic control (PMC: mean age = 50.2 ± 1.2 years, 8 females), and 24 normal control individuals (CG: mean age = 46.5 ± 1.1 years, 14 females). We determined BMD in the femoral neck and at the L2-L4 level (DEXA) and serum levels of glucose, total glycated hemoglobin (HbA1), total and ionic calcium, phosphorus, alkaline phosphatase, follicle-stimulating hormone, intact parathyroid hormone (iPTH), 25-hydroxyvitamin D (25-OH-D), insulin-like growth factor I (IGFI), osteocalcin, procollagen type I C propeptide, as well as urinary levels of deoxypyridinoline and creatinine. HbA1 levels were significantly higher in PMC patients (12.5 ± 0.6 vs 7.45 ± 0.2% for GMC and 6.3 ± 0.9% for CG; P < 0.05). There was no difference in 25-OH-D, iPTH or IGFI levels between the three groups. BMD values at L2-L4 (CG = 1.068 ± 0.02 vs GMC = 1.170 ± 0.03 vs PMC = 1.084 ± 0.02 g/cm²) and in the femoral neck (CG = 0.898 ± 0.03 vs GMC = 0.929 ± 0.03 vs PMC = 0.914 ± 0.03 g/cm²) were similar for all groups. PMC presented significantly lower osteocalcin levels than the other two groups, whereas no significant difference in urinary deoxypyridine was observed between groups. The present results demonstrate that hyperglycemia is not associated with increased bone resorption in type 2 diabetes mellitus and that BMD is not altered in type 2 diabetes mellitus.