骨质疏松症与维生素D受体基因ApaI多态性的相关性分析

目的分析骨质疏松症与维生素D受体基因ApaI多态性的相关性。方法选择70例骨质疏松症患者作为实验组1,70例骨质疏松性骨折患者作为实验组2,另选同期82例骨密度正常者作为对照组。检测三组血钙磷、血糖指标,经过双能量X线检测不同部位(腰椎、股骨颈、Ward三角、大转子、股骨干)骨密度值,观察年龄和体质量指数与不同部位的骨密度的相关性,比较实验组1与对照组、实验组2与对照组基因型和等位基因分布频率。结果腰椎、股骨颈、Ward三角、大转子、股骨干骨密度分别为(21.6±2.2)、(21.5±2.3)、(21.4±2.4)、(21.5±2.2)、(22.0±1.9)g/cm2,年龄和不同部位的骨密度呈负相关(P<0.05),体质量指数和不同部位的骨密度呈正相关(P<0.05)。实验组2与对照组aa基因型、a等位基因分布频率比较,差异无统计学意义(P>0.05)。实验组1aa基因型、a等位基因分布频率均高于对照组,差异有统计学意义(P<0.05)。结论维生素D受体基因ApaI多态性与骨质疏松症有关,维生素D受体基因多态性在决定骨质疏松症的遗传易感性方面具有显著价值。     

类风湿关节炎和骨质疏松关系的探讨

目的了解类风湿关节炎（RA）患者骨密度（BMD）的变化和骨质疏松（OP）的发生情况。方法采用双能X线骨密度仪（DEXA）对40例RA患者和45例年龄、性别与RA组匹配的健康对照者进行腰椎（L2～L4）、左股骨上端（股骨颈、Ward’s三角区、大转子）骨密度测定。结果 RA组腰椎及股骨上端的骨密度值分别为（0.75＋0.12）g/cm2及（0.59＋0.11）g/cm2;对照组腰椎及股骨上端的骨密度值分别为（0.97＋0.13）g/cm2及（0.78＋0.12）g/cm2。RA组无论腰椎或股骨上端的骨量丢失较健康对照组有显著性差异（P〈0.05）。结论类风湿关节炎患者存在明显的骨量丢失。     

比较腰椎定量CT与双能X线骨密度检测骨质疏松症患者的价值

目的 分析腰椎定量CT与双能X线检测方法用来诊断骨质疏松症患者的效果。方法 选取我院进行健康体检者80例,均接受腰椎定量CT与双能X线检查,分析两种方法对骨质疏松患者的检出情况、对不同年龄骨质疏松的检出情况、骨密度检测结果以及对不同性别骨质疏松的检出情况。结果 腰椎定量CT检测对骨量减少以及骨质疏松的检出率均高于双能X线检测(P<0.05);腰椎定量CT对≥60岁人群骨量减少以及骨质疏松的检出率较高于40～60岁(P<0.05);40～60岁组骨密度大于≥60岁组骨密度值(P<0.05);腰椎定量CT对女性人群骨量减少以及骨质疏松的检出率较高于男性(P<0.05)。结论 采用腰椎定量CT对骨质疏松症患者实施骨密度检测的检出率相较于双能X线骨密度检测更高,且腰椎定量CT下不同年龄及性别的检出率也有所不同,在骨质疏松症骨密度检测中有较高应用价值。     

上海某社区146例低骨量女性骨密度及骨丢失现况调查

目的：了解上海某社区低骨量（包括骨量低下及骨质疏松）女性患者的骨密度现况及不同年龄段骨丢失情况。方法：2010年2月至2010年12月采用双能X线骨密度仪对146例50～75岁的低骨量女性患者进行骨密度测量,并于2012年12月至2013年1月再次测量骨密度,按每5岁为一个年龄组将患者分为5组,比较不同年龄段患者的骨丢失情况。结果：低骨量女性患者身高随年龄增长呈下降趋势;各年龄段腰椎及左、右股骨颈骨密度值随年龄增加下降,以50~岁及65~岁组下降明显（P＜0.05）。在未经任何干预情况下,各年龄段各部位总骨丢失率下降趋势明显,其中50~岁组L1-4的总骨丢失率为50%,为所有年龄组中最高。结论：骨量低下作为骨质疏松症的前期,应早期进行规范干预,以减少骨量的丢失。     

伊班膦酸钠联合治疗类固醇性骨质疏松症26例临床观察

目的 探讨伊班膦酸钠联合碳酸钙D3片及骨化三醇胶丸治疗类固醇性骨质疏松症的安全性及疗效.方法 对26例类固醇性骨质疏松症患者进行前后自身对照研究.患者年龄31～76(平均52±4.6)岁,口服碳酸钙D3片0.6 g/d,骨化三醇胶丸0.25 μg,每隔3个月静脉滴注伊班磷酸钠2 mg,总疗程l2个月,对比治疗前后的骨密度变化.结果 治疗12个月后,患者腰椎、股骨颈、大转子及Ward's三角骨密度显著增加(均P<0.05),增幅分别达6.5%、4.3%、3.8%及3.2%.结论 伊班磷酸钠联合碳酸钙D3片及骨化三醇胶丸治疗类固醇性骨质疏松症安全、有效、方便.     

长期酒精摄入对中老年男性骨密度与骨代谢及抗骨折能力的影响

目的探讨长期酒精摄入对中老年男性骨密度、骨代谢指标及抗骨折能力的影响。方法以在我院查体中心进行体检的982例45～79岁的中老年男性为调查对象,如有饮酒史则至少5年,按酒精摄入量分为4个等级：不饮酒,少量饮酒（〈50g／d）,中等量饮酒（50g～100g／d）,大量饮酒（〉100g／d）;按开始饮酒年龄分为〈20岁、20～30岁、〉30岁3个等级。采用统一的问卷进行调查,测定血钙磷及碱性磷酸酶（ALP）,放射免疫法测定骨钙素（BGP）,酶联免疫吸附法测定尿脱氧吡啶啉（DPD）,采用双能x线吸收法测量腰椎和股骨颈骨密度。结果①与不饮酒组相比,饮酒者血ALP和骨钙素水平明显降低,且随日酒精摄入量的增加以及开始饮酒年龄的提前而降低更为明显（P〈0．05）。②受试者各组间腰椎骨密度无显著差别,〈50g／d组受试者的股骨颈、Ward’s三角区和大转子骨密度亦无显著改变（P〉0．05）,但50～100g／d、〉100g／d组和〈20岁、20～30岁组受试者的股骨颈、Ward’s三角区和大转子骨密度显著降低（P〈0．01）,且其抗骨折能力和下肢最大肌力亦显著降低（P〈0．01）。③982例受试者髋部骨密度测定共检出骨质疏松者为423例（47．5％）,50～100g／d组和〉100g／d组骨质疏松患病率明显高于不饮酒组和〈50g／d组（P〈0．05）;〈20组骨质疏松患病率明显高于小饮酒组、〉30岁组和20～30岁组（P〈0．01）。结论长期大量饮酒可抑制中老年男性骨的转换,降低股骨颈骨密度,从而降低股骨颈的抗骨折能力。     

阿仑膦酸钠治疗绝经后骨质疏松症的效果观察

目的 观察阿仑膦酸钠治疗绝经后骨质疏松症的效果.方法 选取本院2015年1月~2016年1月收治的58例绝经后骨质疏松患者作为研究对象,随机分为实验组与对照组各29例.对照组给予钙尔奇联合安慰剂治疗,实验组患者给予钙尔奇/阿法骨化醇联合阿仑膦酸钠治疗.观察两组患者治疗前后骨密度(BDM)增加情况、身高变化情况、不良反应发生情况,以骨密度增加情况为准,判定治疗效果.结果 治疗前,两组患者骨密度、身高无统计学差异,治疗后,实验组患者腰椎2~4、股骨颈、Ward′s三角区、大转子部位功能,与对照组相比,改善情况更加明显(P<0.05),用药对两组患者身高无影响,实验组不良反应发生率更低(0),治疗有效率(96.55%)更高.结论 应将阿仑膦酸钠用于绝经后骨质疏松症的治疗.     

老年男性109例骨密度影响因素调查分析

目的探讨老年男性骨质疏松症发病相关危险因素及防治骨质疏松的策略。方法对109例老年男性采用骨质疏松危险因素相关的健康生活方式情况调查表作问卷调查，并应用美国XR-36型双能X线骨密度仪测定左股骨颈、大转子及Ward三角区骨密度。结果老年男性股骨骨量减少（骨质疏松症）的检出率高于腰椎；骨密度与年龄呈负相关（P〈0．01），与体重指数（BMI）呈正相关（P〈0．05）。结论年龄是骨量减少的独立危险因子，运动及BMI是骨量减少的保护因子，健康的生活方式可延缓骨质疏松症的发展和预防骨折的发生。     

唑来膦酸注射液联合碳酸钙D3片治疗老年女性骨质疏松症的疗效观察

目的:探讨唑来膦酸注射液联合碳酸钙D3片治疗老年女性骨质疏松症的临床疗效。方法:以2013年1月至2018年5月赤峰市医院收治的老年女性骨质疏松症患者192例作为研究对象,采用随机数字表分为唑来膦酸组(给予唑来膦酸注射液治疗)、碳酸钙D3组(给予碳酸钙D3片治疗)及联合用药组(给予唑来膦酸注射液联合碳酸钙D3片治疗),每组64例。比较三组患者治疗前后血磷和血钙的含量、骨密度(包括Ward三角区、股骨大转子、股骨颈和腰椎L2—4骨密度)、骨代谢相关生化指标[骨特异性碱性磷酸酶(BAP)、骨钙素(BGP)、人抗酒石酸酸性磷酸酶5b(TRAP-5b)和Ⅰ型胶原羟基端肽β降解产物(β-CTX)]含量及临床疗效的差异。结果:随着时间迁移,三组患者血磷、血钙、BAP及BGP含量,股骨大转子、股骨颈及腰椎L2—4骨密度呈显著升高趋势;而TRAP-5b、β-CTX含量呈显著降低趋势。治疗后,三组患者血磷、血钙、BAP、BGP、TRAP-5b及β-CTX含量,股骨大转子、股骨颈及腰椎L2—4骨密度的差异均有统计学意义(P<0.05)。治疗后,联合组患者血磷、血钙、BAP及BGP含量,股骨大转子、股骨颈及腰椎L2—4骨密度明显高于唑来膦酸组和碳酸钙D3组,TRAP-5b含量明显低于唑来膦酸组和碳酸钙D3组,差异均有统计学意义(P<0.05)。联合组患者的总有效率为92.19%(59/64),明显优于唑来膦酸组的79.69%(51/64)和碳酸钙D3组的78.13%(50/64),差异均有统计学意义(P<0.05)。结论:唑来膦酸注射液和碳酸钙D3片对老年女性骨质疏松症有一定的疗效,二者联合治疗的效果更好。     

急性首发脑梗死患者合并骨质疏松的临床研究

目的了解并探讨急性首发脑梗死患者骨质疏松的发生情况和骨代谢的改变特点。方法急性首发脑梗死患者167例,全部为偏瘫患者按头颅CT或MRI结果分为单发脑梗死组和多发脑梗死组；按病情程度分为轻度、中度和重度脑梗死组。应用双能X线骨密度仪测定脑梗死组和对照组双侧股骨颈、大转子、Ward’s三角区及L2-L4椎体骨密度,并用放射免疫法测定2组的骨代谢指标。结果单发脑梗死患者骨质疏松发生率为28.57%,多发组为39.72%,2组比较差异无统计学意义（P〉0.05）。单发与多发脑梗死组患侧髋关节骨密度及骨代谢指标的测定结果比较差异均无显著性（P〉0.05）。轻、中、重度脑梗死患者骨质疏松的发生率分别为28.42%、47.16%和63.20%,差异有显著性（P〈0.05）。结论脑急性首发梗死患者易发生骨质疏松,骨质疏松以瘫痪侧肢体为重,股骨颈、Ward’s三角骨量丢失明显。     

一期自体骨钻孔骨屑植骨在预防四肢长骨骨折骨不连中的应用

随着现代交通、工业、农业的发展,四肢创伤骨折的发生率明显增多。切开复位钢板内固定是临床治疗四肢骨折的常用方法。但在临床治疗过程中骨不连或骨延迟愈合时有发生。植骨是临床上预防,治疗骨不连或骨延迟愈合的有效方法之一,依植骨的有效性及病人的自身考虑,1989年1月～2003     

Demineralized bone matrix in bone repair: History and use

Demineralized bone matrix (DBM) is an osteoconductive and osteoinductive commercial biomaterial and approved medical device used in bone defects with a long track record of clinical use in diverse forms. True to its name and as an acid-extracted organic matrix from human bone sources, DBM retains much of the proteinaceous components native to bone, with small amounts of calcium-based solids, inorganic phosphates and some trace cell debris. Many of DBM's proteinaceous components (e.g., growth factors) are known to be potent osteogenic agents. Commercially sourced as putty, paste, sheets and flexible pieces, DBM provides a degradable matrix facilitating endogenous release of these compounds to the bone wound sites where it is surgically placed to fill bone defects, inducing new bone formation and accelerating healing. Given DBM's long clinical track record and commercial accessibility in standard forms and sources, opportunities to further develop and validate DBM as a versatile bone biomaterial in orthopedic repair and regenerative medicine contexts are attractive.     

Bisphosphonates in bone diseases

Bisphosphonates are a class of drugs which are strongly attracted to the bone where they influence the calcium metabolism, mainly by inhibition of the osteoclast-mediated bone resorption. This property makes these compounds suited for the treatment of several diseases of the bone. In Paget's disease, several bisphosphonates can reduce bone pain and decrease the bone turnover 6070%. Cyclical oral etidronate and daily oral alendronate both proved to reduce the vertebral fracture rate for postmenopausal osteoporotic woman, while most investigated bisphosphonates can increase spinal bone mass in osteoporosis. Bisphosphonates can help lowering serum calcium and reverse skeletal complications in malignancy mediated bone diseases. Oral and intravenous administration of therapeutic doses is relatively safe. In general, gastrointestinal disturbances are described most often and the oldest, least potent, bisphosphonate etidronate can induce osteomalacia. The various characteristics of bisphosphonates: physicochemical, biological, therapeutic and toxicological, vary greatly depending on the structure of the individual bisphosphonate. Even small changes in the structure can lead to enormous differences in potency. Overall, this class of drugs offers several prospects for the future.     

Glutamate signalling in bone

The identification of novel signalling pathways in a tissue provides new avenues for pharmacological manipulation of tissue function. Where the pathway concerned is one that has been the subject of extensive research in another body system, progress towards new therapies can be rapid. The discovery that glutamate has functions in bone that share striking similarities with its role in synaptic neurotransmission opens the way to manipulate skeletal pathophysiology using modulators of glutamate release, uptake or receptor function. The purpose of this review is to describe the way that a role for glutamate as a signalling molecule in bone was discovered, to summarise the evidence for this role. In addition, it will identify points that are unresolved, to highlight areas where new research could provide significant advances. Furthermore, it will indicate how studies already performed but analysed without consideration of the non-neuronal functions of modulators of glutamate signalling, could contain information of significant value for the advance of therapeutic approaches to bone diseases.     

Receptor tyrosine kinase inhibition causes simultaneous bone loss and excess bone formation within growing bone in rats

During postnatal skeletal growth, adaptation to mechanical loading leads to cellular activities at the growth plate. It has recently become evident that bone forming and bone resorbing cells are affected by the receptor tyrosine kinase (RTK) inhibitor imatinib mesylate (STI571, Gleevec®). Imatinib targets PDGF, ABL-related gene, c-Abl, c-Kit and c-Fms receptors, many of which have multiple functions in the bone microenvironment. We therefore studied the effects of imatinib in growing bone. Young rats were exposed to imatinib (150 mg/kg on postnatal days 5-7, or 100 mg/kg on postnatal days 5-13), and the effects of RTK inhibition on bone physiology were studied after 8 and 70 days (3-day treatment), or after 14 days (9-day treatment). X-ray imaging, computer tomography, histomorphometry, RNA analysis and immunohistochemistry were used to evaluate bone modeling and remodeling in vivo. Imatinib treatment eliminated osteoclasts from the metaphyseal osteochondral junction at 8 and 14 days. This led to a resorption arrest at the growth plate, but also increased bone apposition by osteoblasts, thus resulting in local osteopetrosis at the osteochondral junction. The impaired bone remodelation observed on day 8 remained significant until adulthood. Within the same bone, increased osteoclast activity, leading to bone loss, was observed at distal bone trabeculae on days 8 and 14. Peripheral quantitative computer tomography (pQCT) and micro-CT analysis confirmed that, at the osteochondral junction, imatinib shifted the balance from bone resorption towards bone formation, thereby altering bone modeling. At distal trabecular bone, in turn, the balance was turned towards bone resorption, leading to bone loss.     

GDF8 inhibits bone formation and promotes bone resorption in mice

Growth Differentiation Factor 8 (GDF8), also called myostatin, is a member of the transforming growth factor (TGF)‐β super‐family. As a negative regulator of skeletal muscle growth, GDF8 is also associated with bone metabolism. However, the function of GDF8 in bone metabolism is not fully understood. Our study aimed to investigate the role of GDF8 in bone metabolism, both in vitro and in vivo. Our results showed that GDF8 had a negative regulatory effect on primary mouse osteoblasts, and promoted receptor activator of nuclear factor κB ligand (RANKL)‐induced osteoclastogenesis in vitro. Intraperitoneal injection of recombinant GDF8 repressed bone formation and accelerated bone resorption in mice. Furthermore, treatment of aged mice with a GDF8 neutralizing antibody stimulated new bone formation and prevented bone resorption. Thus, our study showed that GDF8 plays a significant regulatory role in bone formation and bone resorption, thus providing a potential therapeutic pathway for osteoporosis.     

羟基磷灰石生物微晶玻璃人工骨充填长骨骨囊肿临床体会

从1990年6月—1993年12月采用控基磷灰石生物微晶玻璃人工骨(HBG)充填骨囊肿腔或 HBG 与游离自体骨混合充填骨囊肿腔14例。除1例股骨上1/3骨囊胂伴病理骨折术后过早负重而致髋内翻畸形外,其他经随访观察疗效满意,无复发。本人着重强调术中彻底刮除囊肿腔壁后以2份 HBG 与1份游离自体骨充填囊肿腔。术后观察无一例发生惑染。HBG 及游离自体骨与宿主骨嵌合生长良好。     

Short- to mid-term effects of ovariectomy on bone turnover, bone mass and bone strength in rats

To determine the short- to mid-term effects of ovariectomy on bone turnover, bone mass and bone strength in rats. SD rats aged 12 weeks were randomly divided into No-treatment, Sham and OVX groups. The rats were sacrificed for sample collection at week 0, week 4 and week 18 after surgical operation. Chemistries in serum and urine were measured by standard colorimetric methods and bone turnover markers were measured by ELISA kits. Bone mass and bone strength were determined using pQCT system and three-point bending tests, respectively. At week 4, OVX rats showed drastic increase in the level of urine Ca, P and DPD. At week 18, in OVX rats the levels of serum ALP, urine DPD and Ca were much higher and the level of serum Ca was much lower when comparing with Sham rats. Ovariectomy produced significant reduction in cancellous BMD, total BMD and SSI of proximal tibial metaphysis rapidly at week 4 and continuously at week 18 after surgical operation. However, no marked changes of bone mass and bone strength were found in the diaphysis of tibia and femur, respectively. The current study concluded that ovariectomy induced the uncoupling of bone turnover, and the proximal metaphysis of long bone was the sensitive site for the short- to mid-term effect of ovariectomy, demonstrated as the markers of bone mass and stress strain index.