PKP治疗骨质疏松性椎体压缩骨折的预后评价及继发危险因素分析

目的:分析椎弓根入路行椎体后凸成形术(PKP)治疗骨质疏松性椎体压缩骨折的预后评价及继发危险因素分析。方法:选择2016年2月-2018年2月我院收治的骨质疏松性椎体压缩骨折患者85例纳入本次研究,采用随机数表法分为观察组(n=43)和对照组(n=42)。对照组使用经皮椎体成形术进行治疗,观察组采用PKP进行治疗。比较两组患者手术情况、术后情况、椎体前缘高度丢失率、Cobb角、继发性骨折发生情况及分析骨质疏松性椎体压缩骨折患者术后继发骨折的危险因素。结果:观察组手术时间、透视次数、骨水泥注入量、术中出血量均显著低于对照组,差异显著(P0.05);观察组疼痛缓解时间、下地时间及住院时间均显著低于对照组,差异显著(P0.05);治疗前,两组椎体前缘高度丢失率、Cobb角比较,无显著差异;治疗后,两组患者的椎体高度丢失率明显下降,但两组术后7 d、术后6月两组椎体前缘高度丢失率、Cobb角比较无显著差异;观察组术后12月椎体前缘高度丢失率、Cobb角低于对照组,差异显著(P0.05);所有患者均随访12月,其中22例(25.88%)发生继发性椎体骨折,进行单因素分析,结果发现,两组患者性别、骨折部位、局部矢状面后凸角度、骨水泥量、椎体高度恢复、术后抗骨质疏松治疗差异无统计学意义(P0.05);骨质疏松原因、骨水泥椎间隙渗漏、术后支具佩戴、原发骨折类型与骨质疏松性椎体压缩骨折患者术后发生继发骨折相关(P0.05)。多因素Logistic分析显示,骨质疏松原因、骨水泥椎间隙渗漏、术后支具佩戴、原发骨折类型均是骨质疏松性椎体压缩骨折患者术后发生继发骨折的独立危险因素(P0.05)。结论:在骨质疏松性椎体压缩骨折患者中应用PKP可有效改善手术情况,随着时间的延长,PKP更有利于维持患者椎体高度;骨质疏松原因、骨水泥椎间隙渗漏、术后支具佩戴、原发骨折类型是骨质疏松性椎体压缩骨折患者术后发生继发骨折的危险因素,临床上对于具有危险因素的患者引起重视,并采取干预措施。     

单球囊双侧扩张后凸成形术治疗不同程度骨质疏松性椎体压缩骨折的疗效

目的:观察单球囊双侧交替扩张后凸成形术治疗老年骨质疏松性椎体压缩骨折的疗效。方法:选择我院2014年7月-2015年5月收治的老年骨质疏松性椎体压缩骨折患者60例,按照椎体塌陷程度分为重度骨折组和轻度骨折组,每组各30例。两组患者均接受单球囊双侧交替扩张后凸成形术治疗,观察治疗效果和椎体变化等。结果:与轻度骨折组比较,重度骨折组手术时间长、骨水泥注射量少,且椎体前缘高度恢复率、椎体中部高度恢复率、Cobb角矫正度高(P0.05)。治疗后,两组患者VAS评分均优于治疗前(P0.05),但两组间差异无统计学意义(P0.05)。与治疗前比较,两组治疗后椎体前缘高度、椎体中部高度、Cobb角均有所改善(P0.05),轻度骨折组的椎体前缘高度、椎体中部高度明显大于重度骨折组(P0.05),但两组Cobb角比较,差异无统计学意义(P0.05)。结论:单球囊双侧交替扩张后凸成形术治疗老年骨质疏松性椎体压缩骨折具有较好的临床疗效,可以明显纠正椎体塌陷和Cobb角度。     

Effect of vertebral body stiffness before and after vertebroplasty on intradiscal pressure]

Fractures of osteoporotic vertebral bodies are increasingly stabilized with bone cement. The effects of vertebral-body stiffness before and after augmentation with bone cement and of wedge-shaped vertebral body fractures on intradiscal pressure are insufficiently known. In a finite element model of the lumbar spine the elastic modulus of cancellous bone as well as the amount and the elastic modulus of bone cement were varied and the dependency of intradiscal pressure on these parameters was calculated. In addition, a wedge-shaped vertebral-body fracture was simulated. The bulge of the vertebral-body endplate and thus the intradiscal pressure depends strongly on the grade of osteoporosis in the vertebral body. The influence of amount and elastic modulus of bone cement on intradiscal pressure is small. A wedge-shaped vertebral-body fracture causes an anterior shift of upper-body centre of gravity. If this shift is not compensated, it leads to an increased flexion moment that has to be balanced by muscle forces. In addition, this shift leads to a stronger increase of intradiscal pressure than the augmentation of the vertebral body with bone cement.     

Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in TallyHo/JngJ mice

Increasing evidence that decreased bone density and increased rates of bone fracture are associated with abnormal metabolic states such as hyperglycemia and insulin resistance indicates that diabetes is a risk factor for osteoporosis. In this study, we observed that TallyHo/JngJ (TH) mice, a polygenic model of type II diabetes, spontaneously developed bone deformities with osteoporotic features. Female and male TH mice significantly gained more body weight than control C57BL/6 mice upon aging. Interestingly, bone density was considerably decreased in male TH mice, which displayed hyperglycemia. The osteoblast-specific bone forming markers osteocalcin and osteoprotegerin were decreased in TH mice, whereas osteoclast-driven bone resorption markers such as IL-6 and RANKL were significantly elevated in the bone marrow and blood of TH mice. In addition, RANKL expression was prominently increased in CD4+ T cells of TH mice upon T cell receptor stimulation, which was in accordance with enhanced IL-17 production. IL-17 production in CD4+ T cells was directly promoted by treatment with leptin while IFN-γ production was not. Moreover, blockade of IFN-γ further increased RANKL expression and IL-17 production in TH-CD4+ T cells. In addition, the osteoporotic phenotype of TH mice was improved by treatment with alendronate. These results strongly indicate that increased leptin in TH mice may act in conjunction with IL-6 to preferentially stimulate IL-17 production in CD4+ T cells and induce RANKL-mediated osteoclastogenesis. Accordingly, we propose that TH mice could constitute a beneficial model for osteoporosis.     

IL-6, IL-1β及TNF-α与大鼠骨质疏松形成的关系

目的:研究白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)及肿瘤坏死因子-α(TNF-α)与大鼠骨质疏松形成的关系,为研究细胞因子与骨质疏松之间的相关作用机制提供参考。方法:选择2015年1月至2015年11月我院采购的90只雌性大鼠作为研究对象,按照数字随机法将大鼠分成观察组(n=45)以及对照组(n=45)。观察组制成骨质疏松模型,对照组不作处理,对比两组局部骨密度,成骨细胞,骨小梁以及破骨细胞在视野面积中的比例,骨组织相关细胞因子水平,分析IL-6、IL-1β以及TNF-α水平与大鼠骨质疏松的相关性。结果:观察组椎体骨密度(BD)和椎间盘BD以及小关节BD均明显低于对照组,差异均有统计学意义(P0.05);观察组骨小梁和成骨细胞在视野面积中的比例明显低于对照组,而破骨细胞在视野面积中的比例明显高于对照组,差异均有统计学意义(P0.05);观察组IL-6和IL-1β以及TNF-α均明显高于对照组,差异有统计学意义(P0.05)。IL-6、IL-1β以及TNF-α水平与大鼠椎体BD、椎间盘BD以及小关节BD均呈明显负相关。结论:去卵巢大鼠的细胞因子与其骨质疏松具有紧密联系,表现在IL-6、IL-1β以及TNF-α水平与大鼠椎体BD、椎间盘BD以及小关节BD均呈明显负相关。     

网袋强化椎体成形术在骨质疏松椎体骨折治疗中的经验教训

摘要 目的：探讨和总结使用网袋强化椎体成形术在骨质疏松椎体骨折围手术期的注意事项及相关对策。方法：回顾性分析2017年6月到2020年6月3年时间内,使用网袋强化椎体成形术治疗骨质疏松性椎体骨折患者共计112例。统计和比较患者在围手术期的各项指标,分析穿刺失败的原因及相关危险因素。结果：112例患者共涉及138个椎体。其中一期穿刺失败率（骨水泥分布不佳）为47个,占34.0%。骨水泥注入3 mL以下者为19个,占13.8%。骨水泥渗漏为36个,占26.1%。所有患者在术后3天及3月复查, VAS评分和ODI评分较前均有显著改善(P<0.05)。所有患者均未出现严重并发症(P>0.05)。结论：网袋强化椎体成形术在骨质疏松性椎体骨折的治疗中是一种理想的治疗方式,但在具体过程中仍有相关的经验和教训需要整理和总结。     

金天格在老年骨质疏松性椎体骨折术后的应用及临床分析

目的:探讨和分析金天格胶囊在老年骨质疏松症导致的椎体骨折术后的作用和临床疗效。方法:将2013.01-2015.01来我院明确诊断为骨质疏松症导致的椎体骨折共计136人经纳入标准和排除标准筛选后,使用随机数字表将其随机分为2组。实验组给予经皮椎体成形术(PVP)+钙剂+维生素D+唑来磷酸+金天格胶囊治疗。对照组则不给予金天格进行治疗。所有患者均至少接受了12个月的系统随访观察。观察和进行比较的指标主要为疼痛(VAS),骨密度,Macnab腰椎功能评分以及血液肝肾功等指标。结果:在术后3月和12个月,两组患者在疼痛、骨密度及腰椎功能评分等方面较术前均有显著改善(P0.05)。两组之间在上述指标中有统计学显著性差异。而在血液肝肾功等指标的比较中,则未发现疼显著统计学差异(P0.05)。结论:金天格胶囊在骨质疏松性椎体骨折术后的应用,能够有效地提高治疗效果,安全程度较高,在临床中可进一步的进行推广应用。     

Melphalan exposure induces an interleukin-6 deficit in bone marrow stromal cells and osteoblasts

Bone marrow stromal cells (BMSC) and osteoblasts are critical components of the microenvironment that support hematopoietic recovery following bone marrow transplantation. Aggressive chemotherapy not only affects tumor cells, but also influences additional structural and functional components of the microenvironment. Successful reconstitution of hematopoiesis following stem cell or bone marrow transplantation after aggressive chemotherapy is dependent upon components of the microenvironment maintaining their supportive function. This includes secretion of soluble factors and expression of cellular adhesion molecules that impact on development of hematopoietic cells. In the current study, we investigated the effects of chemotherapy treatment on BMSC and human osteoblast (HOB) expression of interleukin-6 (IL-6) as one regulatory factor. IL-6 is a pleiotropic cytokine which has diverse effects on hematopoietic cell development. In the current study we demonstrate that exposure of BMSC or HOB to melphalan leads to decreases in IL-6 protein expression. Decreased IL-6 protein is the most pronounced following melphalan exposure compared to several other chemotherapeutic agents tested. We also observed that melphalan decreased IL-6 mRNA in both BMSC and HOB. Finally, using a model of BMSC or HOB co-cultured with myeloma cells exposed to melphalan, we observed that IL-6 protein was also decreased, consistent with treatment of adherent cells alone. Collectively, these observations are of dual significance. First, suggesting that chemotherapy induced IL-6 deficits in the bone marrow occur which may result in defective hematopoietic support of early progenitor cells. In contrast, the decrease in IL-6 protein may be a beneficial mechanism by which melphalan acts as a valuable therapeutic agent for treatment of multiple myeloma, where IL-6 present in the bone marrow acts as a proliferative factor and contributes to disease progression. Taken together, these data emphasize the responsiveness of the microenvironment to diverse stress that is important to consider in therapeutic settings.     

Osteoporosis Treatment After Osteoporotic Fractures: Data From a Single Medical Center

ObjectiveMost patients do not receive osteoporosis treatment after osteoporotic fracture. This study reviewed osteoporosis treatment after osteoporotic fractures in a center without a Fracture Liaison Service.MethodsWe identified all patients with hip, vertebral, humeral or radial fractures, evaluated in Meir Medical Center, in 2017. The exclusion criteria were not a Clalit Health Services member, high-energy fracture or 30-day postoperative mortality. The primary endpoint was osteoporosis drugs issued within 12 months of fracture. Secondary endpoints included bone densitometry and 1-year mortality.ResultsFive-hundred-eighty-two patients (average age 78.6 ± 11.1 years, 75.8% women) were included. There were 321 (55.5%) hip, 84 (14.1%) humeral, 33 (5.6%) vertebral, and 144 (24.7%) radial fractures. Osteoporosis drugs were issued to 26.5% of the patients; those with humeral fractures received the least (21.4%) and vertebral, the most (30.3%; P = .51). Bone densitometry was performed in 23.2% of patients. One-year mortality after hip fracture was 12.1%, followed by humeral (3.6%; P < .05). Logistic regression showed that previous treatment (odds ratio [OR] = 7.4; 95% confidence interval [CI] 3.6–15.2), bone densitometry (OR = 4.4; 95% CI 2.6–7.4) and endocrinology visit (OR = 2.6; 95% CI, 1.4–4.6) were the most important factors associated with treatment.ConclusionFewer than one third of patients received pharmacotherapy within 1 year after fracture. Because pharmacotherapy reduces future fractures and mortality, we recommend that medical staff who care for patients with fracture adopt practical and effective strategies to increase treatment rates among patients with osteoporotic fractures.     

椎体静脉稀疏区注入骨水泥对PVP术中骨水泥渗漏的影响

目的:探讨椎体静脉稀疏区注入骨水泥对骨质疏松椎体压缩性骨折患者行经皮穿刺椎体成形术(percutaneous vertebroplasty,PVP)术中骨水泥渗漏的影响。方法:选择西安交通大学第二附属医院2014年1月至2018年6月收治的61例骨质疏松椎体压缩性骨折患者,根据骨水泥注入区域的不同,将所有患者分为A组(30例)及B组(31例),A组骨水泥注入区域为椎体静脉密集区(椎体中1/3平面处),B组骨水泥注入区域为椎体静脉稀疏区(椎体上1/3及下1/3平面处),对比两组的骨水泥渗漏率,术前、术后6个月时的视觉模拟评分(Visual analogue scale,VAS),治疗中的骨水泥用量、椎体高度恢复率及cobb角恢复度数。结果:B组的骨水泥渗漏率及骨水泥用量均明显低于A组(P0.05)。两组的VAS评分、椎体高度恢复率、cobb角恢复情况对比差异无统计学意义(P0.05)。结论:与椎体静脉密集区相比,在椎体静脉稀疏区注入骨水泥可显著降低骨质疏松椎体压缩性骨折患者PVP术中骨水泥渗漏率,椎体静脉稀疏区可作为PVP术中骨水泥注射的一个相对安全区域。     

GPX7 Facilitates BMSCs Osteoblastogenesis via ER Stress and mTOR Pathway

Emerging evidence indicates extensive oxidative stress is a consequence of obesity which impairs bone formation. Glutathione peroxidase 7 (GPX7) is a conserved endoplasmic reticulum (ER) retention protein, lacking of which causes accumulation of reactive oxygen species (ROS) and promotes adipogenesis. Since the imbalance between osteogenic and adipogenic differentiation of bone marrow mesenchymal stem cell (BMSC) leads to severe bone diseases such as osteoporosis, it is critical to investigate the potential protective role of Gpx7 in osteogenesis. Here, we provide evidence that deficiency of Gpx7 reduces osteogenesis, but increases adipogenesis in both human BMSCs (hBMSCs) and mouse mesenchymal stem cell line. Interestingly, further studies indicate this defect can be alleviated by the ER stress antagonist, but not the ROS inhibitor, unveiling an unexpected finding that, unlike adipogenesis, lacking of Gpx7 inhibits osteogenesis mediating by induced ER stress instead of enhanced ROS. Furthermore, the mTOR signalling pathway is found down-regulation during osteogenic differentiation in Gpx7-deficient condition, which can be rescued by relief of ER stress. Taken together, for the first time we identify a novel function of Gpx7 in BMSCs’ osteogenic differentiation and indicate that Gpx7 may protect against osteoporotic deficits in humans through ER stress and mTOR pathway interplay.     

The GDF11-FTO-PPARγ axis controls the shift of osteoporotic MSC fate to adipocyte and inhibits bone formation during osteoporosis

During osteoporosis, the shift of bone mesenchymal stem cell (BMSC) lineage commitment to adipocyte leads to the imbalance between bone mass and fat, which increases the risk of fracture. The mechanism underlying this process is not fully understood. Fat mass and obesity-associated protein (FTO) is an RNA demethylase that demethylates various methylated nucleic acids and participates in various physiological and pathological processes. Here we identified FTO as a regulator for BMSC fate determination during osteoporosis. FTO was up-regulated in bone marrow during aging or osteoporosis in human and mice in a GDF11(growth differentiation factor 11)-C/EBPα-dependent mechanism. The expression of FTO was also up-regulated during adipocyte differentiation of BMSCs whereas its expression was down-regulated during osteoblast differentiation. Gain-of-function and loss-of-function experiments showed that FTO favored the BMSCs to differentiate to adipocytes rather than osteoblasts. Further mechanism study demonstrated that FTO bound and demethylated the mRNA of the Peroxisome proliferator-activated receptor gamma (Pparg), leading to the increase in the expression of Pparg mRNA. Reversely, Pparg knockdown blocked the function of GDF11-FTO during osteoblast differentiation of BMSCs. Furthermore, conditionally genetic knockout of Fto in osteoblasts inhibited the development of osteopenia in mice. Collectively, our findings demonstrated that GDF11-FTO-Pparg axis promoted the shift of osteoporotic BMSC fate to adipocyte and inhibited bone formation during osteoporosis.     

Gelatin microspheres containing calcitonin gene-related peptide or substance P repair bone defects in osteoporotic rabbits

Objectives

To investigate the therapeutic effect of gelatin microspheres containing different concentrations of calcitonin gene-related peptide (CGRP) or substance P on repairing bone defects in a rabbit osteoporosis model.

Results

Gelatin microspheres containing different concentrations of CGRP or substance P promoted osteogenesis after 3 months in a rabbit osteoporotic bone defective model. From micro-computed tomography imaging results, 10 nM CGRP was optimal for increasing the trabecular number and decreasing the trabecular bone separation degree; similar effects were observed with the microspheres containing 1 µM substance P. Histological analysis showed that the gelatin microspheres containing CGRP or substance P, regardless of the concentration, effectively promoted osteogenesis, and the highest effect was achieved in the groups containing 1 µM CGRP or 1 µM substance P.

Conclusions

Gelatin microspheres containing CGRP or substance P effectively promoted osteogenesis in a rabbit osteoporotic bone defect model dose-dependently, though their effects in repairing human alveolar ridge defects still need further investigation.

     

AR/PCC herb pair inhibits osteoblast pyroptosis to alleviate diabetes-related osteoporosis by activating Nrf2/Keap1 pathway

Osteoporosis is a prevalent complication of diabetes, characterized by systemic metabolic impairment of bone mass and microarchitecture, particularly in the spine. Anemarrhenae Rhizoma/Phellodendri Chinensis Cortex (AR/PCC) herb pair has been extensively employed in Traditional Chinese Medicine to manage diabetes; however, its potential to ameliorate diabetic osteoporosis (DOP) has remained obscure. Herein, we explored the protective efficacy of AR/PCC herb pair against DOP using a streptozotocin (STZ)-induced rat diabetic model. Our data showed that AR/PCC could effectively reduce the elevated fasting blood glucose and reverse the osteoporotic phenotype of diabetic rats, resulting in significant improvements in vertebral trabecular area percentage, trabecular thickness and trabecular number, while reducing trabecular separation. Specifically, AR/PCC herb pair improved impaired osteogenesis, nerve ingrowth and angiogenesis. More importantly, it could mitigate the aberrant activation of osteoblast pyroptosis in the vertebral bodies of diabetic rats by reducing increased expressions of Nlrp3, Asc, Caspase1, Gsdmd and IL-1β. Mechanistically, AR/PCC activated antioxidant pathway through the upregulation of the antioxidant response protein Nrf2, while concurrently decreasing its negative feedback regulator Keap1. Collectively, our in vivo findings demonstrate that AR/PCC can inhibit osteoblast pyroptosis and alleviate STZ-induced rat DOP, suggesting its potential as a therapeutic agent for mitigating DOP.     

Dexamethasone shifts bone marrow stromal cells from osteoblasts to adipocytes by C/EBPalpha promoter methylation

Dexamethasone (Dex)-induced osteoporosis has been described as the most severe side effect in long-term glucocorticoid therapy. The decreased bone mass and the increased marrow fat suggest that Dex possibly shifts the differentiation of bone marrow stromal cells (BMSCs) to favor adipocyte over osteoblast, but the underlying mechanisms are still unknown. In this paper, we established a Dex-induced osteoporotic mouse model, and found that BMSCs from Dex-treated mice are more likely to differentiate into adipocyte than those from control mice, even under the induction of bone morphogenetic protein-2 (BMP2). We also discovered both in vitro and in vivo that the expression level of adipocyte regulator CCAAT/enhancer-binding protein alpha (C/EBPalpha) is significantly upregulated in Dex-induced osteoporotic BMSCs during osteoblastogenesis by a mechanism that involves inhibited DNA hypermethylation of its promoter. Knockdown of C/EBPalpha in Dex-induced osteoporotic cells rescues their differentiation potential, suggesting that Dex shifts BMSC differentiation by inhibiting C/EBPalpha promoter methylation and upregulating its expression level. We further found that the Wnt/beta-catenin pathway is involved in Dex-induced osteoporosis and C/EBPalpha promoter methylation, and its activation by LiCl rescues the effect of Dex on C/EBPalpha promoter methylation and osteoblast/adipocyte balance. This study revealed the C/EBPalpha promoter methylation mechanism and evaluated the function of Wnt/beta-catenin pathway in Dex-induced osteoporosis, providing a useful therapeutic target for this type of osteoporosis.     

Podoplanin Immunopositive Lymphatic Vessels at the Implant Interface in a Rat Model of Osteoporotic Fractures

Insertion of bone substitution materials accelerates healing of osteoporotic fractures. Biodegradable materials are preferred for application in osteoporotic patients to avoid a second surgery for implant replacement. Degraded implant fragments are often absorbed by macrophages that are removed from the fracture side via passage through veins or lymphatic vessels. We investigated if lymphatic vessels occur in osteoporotic bone defects and whether they are regulated by the use of different materials. To address this issue osteoporosis was induced in rats using the classical method of bilateral ovariectomy and additional calcium and vitamin deficient diet. In addition, wedge-shaped defects of 3, 4, or 5 mm were generated in the distal metaphyseal area of femur via osteotomy. The 4 mm defects were subsequently used for implantation studies where bone substitution materials of calcium phosphate cement, composites of collagen and silica, and iron foams with interconnecting pores were inserted. Different materials were partly additionally functionalized by strontium or bisphosphonate whose positive effects in osteoporosis treatment are well known. The lymphatic vessels were identified by immunohistochemistry using an antibody against podoplanin. Podoplanin immunopositive lymphatic vessels were detected in the granulation tissue filling the fracture gap, surrounding the implant and growing into the iron foam through its interconnected pores. Significant more lymphatic capillaries were counted at the implant interface of composite, strontium and bisphosphonate functionalized iron foam. A significant increase was also observed in the number of lymphatics situated in the pores of strontium coated iron foam. In conclusion, our results indicate the occurrence of lymphatic vessels in osteoporotic bone. Our results show that lymphatic vessels are localized at the implant interface and in the fracture gap where they might be involved in the removal of lymphocytes, macrophages, debris and the implants degradation products. Therefore the lymphatic vessels are involved in implant integration and fracture healing.     

France Verus Wales

Assessment of roentgenographic measurements of cortical bone of the radius in 196 elderly females, including 63 diabetics, revealed that: (1) in the non-diabetic group there was a significant loss of cortical bone relative to the number of years after the menopause and to body weight; (2) although there was a significant loss of cortical bone relative to years postmenopausal in a group of diabetic patients the cortex in the diabetic group was better preserved than in those non-diabetic controls in whom no vertebral compressions were diagnosed in the roentgenograms; no correlation between bone loss and body weight was found among the diabetics; (3) the thinnest cortical bone and the lowest average body weight was found in the 34 non-diabetics with vertebral compression deformities. It thus appears that involutional osteoporosis will be less prevalent among old women suffering from diabetes mellitus than in comparable non-diabetic subjects, and more prevalent among non-diabetics of low body weight than in old women who are obese or of normal weight.     

Bone Mineral Density of the 1/3 Radius Refines Osteoporosis Diagnosis,Correlates With Prevalent Fractures,and Enhances Fracture Risk Estimates

ObjectiveTo investigate the added value of 1/3 radius (1/3R) for the diagnosis of osteoporosis by spine and hip sites and its correlation with prevalent fractures and predicted fracture risk.MethodsFracture Risk Assessment Tool (FRAX) scores for hip and major osteoporotic fractures (MOF) with/without trabecular bone score were considered proxy for fracture risk. The contribution of 1/3R to risk prediction was depicted via linear regression models with FRAX score as the dependent variable—first only with central and then with radius T-score as an additional covariate. Significance of change in the explained variance was compared by F-test.ResultsThe study included 1453 patients, 86% women, aged 66 ± 10 years. A total of 32% (n = 471) were osteoporotic by spine/hip and 8% (n = 115) by radius only, constituting a 24.4% increase in the number of subjects defined as osteoporotic (n = 586, 40%). Prior fracture prevalence was similar among patients with osteoporosis by spine/hip (17.4%) and radius only (19.1%) (P = .77).FRAX prediction by a regression model using spine/hip T-score yielded explained variance of 51.8% and 49.9% for MOF and 39.8% and 36.4% for hip (with/without trabecular bone score adjustment, respectively). The contribution of 1/3R was statistically significant (P < .001) and slightly increased the explained variance to 52.3% and 50.4% for MOF and 40.9% and 37.4% for hip, respectively.ConclusionReclassification of BMD results according to radius measurements results in higher diagnostic output. Prior fractures were equally prevalent among patients with radius-only and classic-site osteoporosis. FRAX tool performance slightly improved by incorporating radius BMD. Whether this approach may lead to a better fracture prediction warrants further prospective evaluation.     

The prevention and treatment of osteoporosis: a review

Osteoporosis is a disorder characterized by reduced bone strength, diminished bone density, and altered macrogeometry and microscopic architecture. Adult bone mass is the integral measurement of the bone mass level achieved at the peak minus the rate and duration of subsequent bone loss. There is clearly a genetic predisposition to attained peak bone mass, which occurs by a person's mid-20s. Bone loss with age and menopause are universal, but rates vary among individuals. Both peak bone mass and subsequent bone loss can be modified by environmental factors, such as nutrition, physical activity, and concomitant diseases and medications. Osteoporosis prevention requires adequate calcium and vitamin D intake, regular physical activity, and avoiding smoking and excessive alcohol ingestion. Risk of fracture determines whether medication is also warranted. A previous vertebral or hip fracture is the most important predictor of fracture risk. Bone density is the best predictor of fracture risk for those without prior adult fractures. Age, weight, certain medications, and family history also help establish a person's risk for osteoporotic fractures. All women should have a bone density test by the age of 65 or younger (at the time of menopause) if risk factors are present. Guidelines for men are currently in development. Medications include both antiresorptive and anabolic types. Antiresorptive medications--estrogens, selective estrogen receptor modulators (raloxifene), bisphosphonates (alendronate, risedronate, and ibandronate) and calcitonins--work by reducing rates of bone remodeling. Teriparatide (parathyroid hormone) is the only anabolic agent currently approved for osteoporosis in the United States. It stimulates new bone formation, repairing architectural defects and improving bone density. All persons who have had osteoporotic vertebral or hip fractures and those with a bone mineral density diagnostic of osteoporosis should receive treatment. In those with a bone mineral density above the osteoporosis range, treatment may be indicated depending on the number and severity of other risk factors.