Journal of Bone and Mineral Metabolism最新文献

Introduction: The association between serum zinc (SZn) concentration and fracture risk in postmenopausal women was investigated.

Materials and methods: Women (n = 851) with a history of natural, premature, or surgical menopause who had completed data, including SZn concentrations at baseline (2009-2011), were included and followed through March 2018 for the incidence of any fracture requiring inpatient care. Potential non-linear and dose-response associations between SZn and fracture risk were assessed using a restricted cubic spline model (RCS) in Cox regression with the likelihood ratio test (LRT). Multivariable Cox proportional hazard models were used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) of fractures across the categories of SZn [< 86, 86-135 (as reference), and ≥ 135 μg/dL].

Results: During a median follow-up period of 8.8 years (interquartile range: 8.1-9.2 years), 4.3% of postmenopausal women (with a mean age of 61.4 ± 8.6 years) experienced a new incident fracture. The mean of baseline SZn concentration was 113 ± 39.3 μg/dL. The LRT indicated no significant non-linear association (P = 0.176) and no evidence of a dose-response relationship (P = 0.448) between SZn and fracture risk. Using the categorical approach, the multivariable-adjusted Cox model showed that postmenopausal women with SZn concentrations below 86 μg/dL had a significantly increased risk of fracture compared to those within the reference range (86-135 μg/dL), with an HR of 2.29 (95% CI = 1.02-5.16, P = 0.044). SZn concentrations exceeding the reference range (≥ 135 μg/dL) were not associated with risk of fractures (HR = 1.47, 95% CI = 0.61-3.58).

Conclusions: Suboptimal SZn levels, indicative of inadequate zinc status, may contribute to an increased risk of bone fractures in postmenopausal women.

Introduction: Administration of an anti-sclerostin antibody enhances Wnt/β-catenin signaling, resulting in a significant increase in bone mass by stimulating bone formation and suppressing bone resorption. Wnt/β-catenin signaling upregulates the expression of osteoprotegerin (Opg), a key regulator that inhibits osteoclast differentiation and suppresses bone resorption. However, sclerostin-knockout (Sost-KO) mice exhibit increased bone formation without a corresponding suppression of bone resorption. Therefore, the role of Opg in Sost deficiency remains unclear.

Materials and methods: To determine whether the osteogenic effects of Sost deficiency depend on the presence of Opg, we compared femoral bone mass among Sost/Opg double-knockout (DKO), Sost-KO, Opg-KO, and C57BL/6 (WT) mice.

Results: High-resolution imaging and histological analysis revealed that cortical bone mass was significantly higher in DKO mice compared with WT and Opg-KO mice. In contrast, trabecular bone mass was reduced in DKO mice compared with WT mice, and the number of TRAP-positive osteoclasts and serum CTX levels, a bone resorption marker, were significantly higher in DKO mice compared with Sost-KO mice. To further examine the role of bone resorption in DKO mice, an anti-RANKL antibody was administered to these mice. This treatment markedly increased both trabecular and cortical bone mass. Bone resorption was almost completely suppressed in antibody-treated DKO mice compared with vehicle-treated mice, while bone formation markers, including the mineral apposition rate, were maintained at approximately one-third the levels of vehicle-treated mice.

Conclusion: These findings indicate that the enhanced bone formation in DKO mice primarily increases cortical bone mass without inhibiting bone resorption. The osteogenic effects of Sost deficiency are independent of Opg.

Introduction: Bone loss is most common around the knee region in spinal cord injury (SCI) population. However, bone mineral density (BMD) measurement and T score in the knee region, which indicate osteoporosis, are not clear. This study aimed to examine BMD, T and Z scores at hip and knee including femoral neck (FN), total hip (TH), proximal tibia (PT), and distal femur (DF) in individuals with SCI, to investigate the relationship between BMD of the knee and hip, and to define DF and PT T scores thresholds that predict osteoporosis at the hip.

Materials and methods: This cross-sectional study used dual-energy x-ray absorptiometry to assess BMD in 94 SCI individuals. The medial and lateral parts of the PT and DF were defined as PT-1 and PT-2, DF-1 and DF-2, respectively. T and Z scores of PT and DF were calculated with a tool recommended by ISCD.

Results: All knee BMD values showed positive correlations with the hip BMD. Applying a PT-1 T-score threshold of - 1.55, the overall specificity was 83.9% and the sensitivity was 84.2% in detecting osteoporosis at FN or TH.

Conclusion: Low hip BMD values are associated with low knee BMD values in SCI individuals. A T score of -1.55 in PT-1 probably indicates osteoporosis of the hip. However, there is a prompt need for standardization of the T-cut off value in the knee region, where the risk of fracture risk is high. Body mass index, time since injury, wheelchair use, and injury severity were associated with bone loss in the PT-1.

Qi et al. presented a prognostic model for hip refracture survival, identifying age, comorbidities, lymphocyte count, and surgery as key predictors. Although clinically relevant, the model lacks external validation and uses suboptimal predictor handling. The selection bias and underpowered subgroup analysis limit the generalizability of the results. Further robust multicenter studies are needed to refine risk stratification in this high-risk population.

Introduction: Hip fracture (HF) is one of the leading causes of mortality and disability in older populations. Hip refracture (HRF) is more serious than HF. We examined the survival rates of patients with HRFs at the Affiliated Dongyang Hospital of Wenzhou Medical University and developed a prediction model for their survival outcomes.

Materials and methods: This study involved identifying and analyzing patients with HRFs from January 2013 to August 2023. Utilizing our hospital's database, we systematically extracted these patients' information. We monitored the survival time and constructed Kaplan-Meier (K-M) survival curve. Through Cox proportional hazards regression analyses, independent risk factors were identified. Based on these factors, a survival prediction model was developed and its reliability was evaluated by the receiver operating characteristic (ROC) curve. In addition, patients who refused surgery were excluded, the eligible patients were divided into a long waiting group (> 48 h) and a short waiting group (≤ 48 h). According to a similar process, independent risk factors were identified. Another nomogram chart and ROC curve were conducted.

Results: Data from 174 patients were used, presenting a median survival time of 40 months. Both univariate and multivariate analyses identified age (HR = 1.71, 95% CI: 1.26-2.32), surgical intervention (HR = 0.34, 95% CI: 0.21-0.55), number of comorbidities (HR = 1.44, 95% CI: 1.09-1.92) and lymphocyte levels (HR = 0.75, 95% CI: 0.61-0.92) as independent influence factors. Based on these factors, a nomogram chart was constructed. The areas under the ROC curve for predicting 1-year, 2-year, and 3-year survival rates were 0.748, 0.794 and 0.806 respectively. Additionally, through regression analysis of surgical patients, some factors (age, number of comorbidities and lymphocyte levels) were supported as independent influence factors.

Conclusion: Advanced age, non-surgical management, multiple comorbidities and lower lymphocyte levels showed a higher risk of all-cause mortality among the patients with HRFs, and these factors were associated with a poor prognosis in this patient population. This study may be useful for improving these patients' prognosis.

Introduction: Few studies assessed comprehensive effects of composite unhealthy lifestyles on aging and musculoskeletal health. This study aimed to address such issues with the UK Biobank datasets.

Materials and methods: An unhealthy lifestyle score (UHLS) was constructed based on 9 lifestyle behaviors. Aging indicators were calculated from 18 clinical traits. General linear and Cox proportional hazards regression models were used to analyze associations between UHLS, aging, and musculoskeletal morbidity. Mendelian randomization (MR) analysis was performed for causal relationship exploration.

Results: Among 396,037 participants, 54.5% and 3.3% of them were designated to the low (scored 0-2) and high UHLS (scored 6-9) groups, respectively. Increasing UHLS was associated with elevated aging acceleration (AA) based on biological age (0.343 per unit; 95% CI: 0.331, 0.355) and phenotypic age (AA_PA) (0.408 per unit; 95% CI: 0.394, 0.422), and higher morbidity of low grip strength (HR = 1.025; 95% CI: 1.001, 1.050), slow walking pace (HR = 1.134; 95% CI: 1.074, 1.198), osteoporosis (HR = 1.077; 95% CI: 1.063, 1.091), fracture (HR = 1.059; 95% CI: 1.048, 1.069) and osteoarthritis (HR = 1.036; 95% CI: 1.030, 1.042). Unhealthy lifestyles in conjunction with AA jointly increased musculoskeletal morbidity. Besides, AA mediated UHLS effects on slow walking pace, osteoporosis and fracture, with mediating proportion of 4.85%-12.79%. MR analyses revealed causal relationships between UHLS and low grip strength, osteoarthritis, and reduced femoral neck bone mineral density. In addition, AA_PA suggestively mediated the UHLS-osteoarthritis association.

Conclusions: Composite unhealthy lifestyles accelerate aging and impair musculoskeletal health. Both mediating and joint effects of AA showed unhealthy lifestyle-associated musculoskeletal morbidity.