TBS correlates with bone density and microstructure at trabecular and cortical bone evaluated by HR-pQCT.

INTRODUCTION: Trabecular bone score (TBS) estimates bone microstructure, which is directly measured by high-resolution peripheral quantitative computed tomography (HRpQCT). We evaluated the correlation between these methods and TBS influence on fracture risk assessed by FRAX. MATERIALS AND METHODS: We evaluated 129 individuals (82 women, 43 postmenopausal) 20 to 82.3 years without prevalent clinical or non-clinical morphometric vertebral fractures, using DXA (spine and hip), HR-pQCT at distal radius (R) and tibia (T) and TBS which classifies bone microarchitecture as normal (TBS ≥ 1.350), partially degraded (1.200 < TBS < 1.350), or degraded (TBS ≤ 1.200). RESULTS: Spine and hip BMD and HR-pQCT parameters at cortical bone: area (T), density (R,T) thickness (T) and trabecular bone: density (R,T), number (T) and thickness (R) were significantly better in the 78 individuals with normal TBS (group 1) versus the 51 classified as partially degraded (n = 42) or degraded microarchitecture (n = 9) altogether (group 2). TBS values correlated with age (r = - 0.55), positively with spine and hip BMD and all cortical and trabecular bone density and microstructure parameters evaluated, p < 0.05 all tests. Binary logistic regression defined age (p = 0.008) and cortical thickness (p = 0.018) as main influences on TBS, while ANCOVA demonstrated that HR-pQCT data corrected for age were not different between TBS groups 1 and 2. TBS adjustment increased FRAX risk for major osteoporotic fractures and hip fractures. CONCLUSION: We describe significant association between TBS and both trabecular and cortical bone parameters measured by HR-pQCT, consistent with TBS influence on fracture risk estimation by FRAX, including hip fractures, where cortical bone predominates.

Low Energy Availability Interferes With Exercise-Associated Bone Effects in Female Long-Distance Triathletes as Detected by HR-pQCT.

Female Athlete Triad, initially described as the association of disordered eating, amenorrhea and osteoporosis, was further redefined to focus on low energy availability (EA), which has a central role in development of hypoestrogenism and low bone mineral density (BMD). However, the contribution of each variable, that is, low EA and hypoestrogenism, for bone derangements is still an open question. To evaluate body composition and bone status in long-distance triathletes without hypoestrogenism, as compared to non-athletes, using DXA and HR-pQCT, and the influence of EA. Population comprised 23 triathletes who had completed at least one long-distance race in the previous year, and 17 non-athletic healthy controls. The athletes denied previous oligo-amenorrhea and had spontaneous regular menses or were on hormonal contraceptives. Control patients also had regular menses. Energy deficiency (low EA) was defined as energy intake below the recommended level for athletes, that is, 45 kcal/kg free fat mass/day. Only femoral neck BMD Z-score measured by DXA trended higher in athletes (p = 0.05), whereas high-resolution peripheral quantitative computed tomography detected significantly higher values of entire bone and trabecular bone area, cortical perimeter, trabecular vBMD and trabecular bone volume/tissue volume, and lower trabecular separation and trabecular inhomogeneity in athletes. No difference was found between athletes with spontaneous menses and those on hormone contraceptives in respect to all parameters. The effects of exercise on bone were not so pronounced in athletes with low EA, although they still had better bone parameters than controls. Stress fractures were reported by 4:12 athletes with low EA and by 2:11 athletes with adequate EA. Long-distance female triathletes without hypoestrogenism show higher values of cortical perimeter, bone area, volumetric density and trabecular microstructure, but low EA interferes with exercise-associated bone effects. These innovative findings reinforce the importance of adequate EA in female athletes to guarantee skeletal health.

Vitamin D deficiency is associated with cortical bone loss and fractures in the elderly.

INTRODUCTION: The role of vitamin D on bone microarchitecture and fragility is not clear. OBJECTIVE: To investigate whether vitamin D deficiency (25(OH)D <20 ng/mL) increases cortical bone loss and the severity of fractures. DESIGN: Cross-sectional study of 287 elderly women with at least one prevalent low-impact fracture. METHODS: Biochemistry, X-rays to identify vertebral fractures (VFs) and to confirm non-vertebral fractures (NonVFs), and high-resolution peripheral quantitative computed tomography (HR-pQCT) to evaluate bone microstructure. RESULTS: Serum 25(OH)D levels were associated with body mass index (BMI: r = -0.161, P = 0.006), PTH (r = -0.165; P = 0.005), CTX (r = -0.119; P = 0.043) and vBMD at cortical bone (Dcomp: r = 0.132; P = 0.033) and entire bone (D100: r = 0.162 P = 0.009) at the distal radius, but not at the tibia. Age and PTH levels were potential confounding variables, but in the multiple linear regressions only BMI (95% CI: 0.11-4.16; P < 0.01), 25(OH)D (95% CI: -0.007 to 1.70; P = 0.05) and CTX (95% CI: -149.04 to 21.80; P < 0.01) predicted Dcomp, while BMI (95% CI: 1.13-4.18; P < 0.01) and 25(OH)D (95% CI: 0.24-1.52; P < 0.01) predicted D100. NonVFs predominated in patients with 25(OH)D <20 ng/mL (P = 0.013). Logistic regression analysis showed a decrease in the likelihood of presenting grade 2-3 VFs/NonVFs for every increase in 25(OH)D (OR = 0.962, 95% CI: 0.940-0.984; P = 0.001), BMI (OR = 0.932, 95% CI: 0.885-0.981; P = 0.007) and D100 at radius (OR = 0.994, 95% CI: 0.990-0.998; P = 0.005). CONCLUSION: In elderly patients with prevalent fractures, vitamin D deficiency was associated with cortical bone loss and severity of fractures.