血清甲状旁腺素和降钙素水平对骨代谢影响的临床研究

骨质疏松症(osteoporosis,OP)是一种以骨量降低、骨组织微结构破坏、骨脆性增加及易发生骨折为特征的全身性代谢性疾病。2001年由美国国立卫生研究院(NIH)提出OP的定义为以骨强度下降和骨折风险增加为特征的骨骼系统疾病,骨强度反映骨骼的2个方面,即骨质量及骨矿密度。根据世界卫生组织(WHO)分类,OP有3种类型,包括原发性OP、继发性OP和特发性OP。     

温补肾阳单味中药及其有效成分防治骨质疏松症的可能分子机制研究进展

骨质疏松症(osteoporosis,OP)是一种代谢性骨病,以骨量下降、骨微结构损坏为主要临床特征,发病率呈现逐渐上升的趋势。中医学将OP纳入“骨痿”“骨枯”“骨极”等疾病范畴,中医药被用于治疗OP由来已久,具有简、便、廉、验等优势。随着中西医结合医学学科的深入融合发展,基础研究发现多种温补肾阳类单味中药及其有效成分可能通过调控Wnt/β-连环蛋白(β-catenin)、骨形态生成蛋白(BMP)/Smads、磷脂酰肌醇-3磷酸激酶/AKT/雷帕霉素靶蛋白信号通路(PI3K/Akt/mTOR)等骨代谢相关信号通路以达到防治OP的目的,这有可能从分子机制上肯定了中医药治疗OP的科学性。该文综述杜仲、骨碎补等常见代表性温补肾阳类中药及其有效成分防治OP的可能分子机制,以期为中医药临床治疗OP的进一步研究应用提供参考。     

骨质疏松症的规范性治疗策略

骨质疏松症(OP)是一种以低骨量、骨微结构破坏导致骨密度降低、骨脆性增加、易发生骨折为特征的全身性骨病。中国成年人OP患病率约为7%,其中50岁以上女性的发病率50.1%,预计2020—2050年中国患有OP和骨量减少的人数分别为2.87亿和5.33亿。在中国发生骨质疏松性髋部骨折后会有＞50%致残率和致畸率。基于OP可能导致的严重后果,其治疗已成为各专科医生需要掌握的基本功。本文简要介绍OP的规范性治疗策略。     

非编码RNA调控骨质疏松症骨重建机制及补肾壮骨类中医药治疗机制研究进展

非编码RNA (non-coding RNAs,ncRNAs)是一种缺乏蛋白编码功能但可以影响染色体结构、基因转录及参与表观遗传调控的特殊RNA,主要包括长链非编码RNA、微小RNA等。近年来研究发现,这些ncRNAs主要通过影响骨质疏松(osteoporosis,OP)的骨吸收与骨形成来维持其骨重建。明确ncRNAs在OP发生发展中的调控机制可能是未来治疗OP药物药效筛选的关键靶点。由于中医将OP归属于“骨痹”范畴,根据中医的“肾主骨生髓”理论,临床主要采用补肾壮骨类方药来治疗OP,且疗效显著。已有研究发现,补肾壮骨类方药可通过上调或下调ncRNA的表达来增强成骨细胞增殖或抑制破骨细胞分化,最终维持了OP骨稳态,从而发挥疗效,但其具体分子机制仍处于探索阶段。故本文通过总结近年来补肾壮骨类方药通过调控ncRNAs治疗OP的分子机制,以期为治疗OP药物药效关键靶点的筛选和中医药防治OP提供新思路。     

类风湿关节炎合并骨质疏松症的药物治疗研究进展

类风湿关节炎(RA)是一种严重的慢性全身性自身免疫性炎性反应疾病,致残率高,与局部和全身骨质疏松症(OP)密切相关.在RA的OP治疗中应同时考虑OP和RA相关因素.近年来越来越多关于RA合并OP药物的研究,包括基础药物、骨吸收抑制剂、骨形成促进剂、改善病情抗风湿药物,本文就RA的抗OP药物进行综述,为RA合并OP患者的...     

2型糖尿病合并骨质疏松的相关因素分析

方法用双能X线骨密度仪测定128例2型糖尿病患者,其中60例合并骨质疏松或骨量减少(OP),68例骨量正常,比较两组的年龄、体重、体重指数、腰围臀围、病程、空腹血糖、糖化血红蛋白、胰岛素敏感指数、血脂、24小时尿蛋白、C反应蛋白等。结果128例2型糖尿病患者中,OP发生率约46.8%。2型糖尿病合并OP组与2型糖尿病骨量正常组在体重、体重指数、病程、臀围、LDL、24小时尿蛋白比较中具有统计学上的显著性差异。而C肽在OP组明显降低,但统计学上无显著性差异。结论2型糖尿病合并骨质疏松或骨量减少与多因素有关,高龄,低体重,女性患者,病程长,肾功能损害,高脂血症为OP发生的高危因素,肾功能损害可能为OP进展的重要因素。     

老年男性2型糖尿病合并骨质疏松症的危险因素分析

目的 探讨老年男性2型糖尿病（T2DM）合并骨质疏松症（OP）患者骨生化指标改变,为早期防治（T2DM）并发骨质疏松症提供防治理论依据。方法 根据双能X线骨密度仪对腰椎及左股骨颈骨密度的检测结果 ,并根据WHO推荐的骨质疏松症诊断标准将93例老年男性2型糖尿病患者分为合并骨质疏松组（G1）和无骨质疏松组（G2）,分别检测2组血清骨形成生化指标包括骨碱性磷酸酶（BAP）、骨钙素（OC）、Ⅰ型胶原氨基端前肽（PINP）,血清骨吸收生化指标Ⅰ型胶原C端肽（CTX）、空腹血糖（FPG）、空腹胰岛素（FINS）、糖化血红蛋（HbA1C）的浓度,并进行比较。结果 OP组的BMI及FINS、骨形成指标（BAP、OC、PINP）浓度低于非OP组,FPG、HbA1c浓度及病程高于非OP组（P〈0．05）,骨吸收指标（CTX）浓度高于非OP组（P〉0．05）。OP组骨形成生化指标浓度低于骨量减少组（P〈0．05）,骨吸收指标浓度高于骨量减少组（P〉0．05）。结论 老年男性T2DM合并OP的发生与骨形成能力不足有关,在治疗T2DM的同时,应重视早期预防和治疗OP。     

骨质疏松症与血管钙化的相关性研究进展

骨质疏松症( OP)是以骨的微结构破坏、骨量减少、脆性增加、易发生骨折为特征的全身代谢性骨病。血管钙化( VC)是动脉粥样硬化的主要表现形式,是心血管疾病的主要病理基础。 OP与 VC的影响因素众多且复杂,该研究将从两方面讨论 OP与 VC的相关性:在临床上,老龄化、雌激素水平降低、血脂异常、高血糖、甲状旁腺激素上升、维生素 D3下降可导致 OP的同时也可促进 VC;在共同分子作用机制层面,骨保护素( OPG)、骨形态发生蛋白( BMP)、基质 Gla蛋白( MPG)、 Klotho因子( Klotho)、胎球蛋白 -A(FITUIN-A)表达抑制可导致 OP同时也可促进 VC,而 Wnt信号通路(Wnt)表达增加、骨桥蛋白( OPN)表达下降可以改善 OP但是会导致 VC。     

甲状旁腺素与维生素D检验在骨质疏松症中的应用进展

骨质疏松症（ osteoporosis ,OP）是一种以骨量降低和骨显微结构破坏为特征,导致骨脆性增加和易发生骨折的代谢性骨病。我国患OP的人口约有8000万,发病率为6．97％,2010年世界骨质疏松日警告说2020年我国将超过2亿人受到骨质疏松症和骨量减少的影响。在诊断与治疗 OP 中,临床常用骨密度（ BMD）检测和生化指标检测（激素、骨钙素、骨性碱性磷酸酶、I型胶原交联降解产物、骨矿物）。激素检测主要包括甲状旁腺激素（ PTH ）、维生素D 和降钙素（CT）,其中甲状旁腺激素（PTH）、维生素D在维持钙动态平衡中起重要作用,在诊断与治疗、监测OP中应用较广。     

阿仑膦酸钠联合氨基酸螯合钙治疗老年男性骨质疏松症疗效观察

骨质疏松症(osteoporosis,OP)是一种以低骨量和骨组织微结构破坏为特征导致骨脆性增加,易发生骨折的全身性疾病。国内研究多基于女性绝经后OP患者,对老年男性OP的疗效报道较少。本文报道了阿仑膦酸钠(alen-dronate,商品名福善美)治疗39例老年男性OP患者的疗效和安全性。1资料与     

绝经后妇女骨密度与骨代谢标志物的关系

目的 研究绝经后妇女骨密度(Bone mineral density,BMD)与骨代谢标志物的关系.方法 应用双能X线骨密度仪测量绝经期妇女腰椎BMD值,参照WHO的骨质疏松诊断标准,将109例绝经后妇女分为无骨质疏松(NOP)组,骨量减少组(OPl)组和骨质疏松(OP2)组,测定各组受试者BMD和电化学发光法检测骨代谢标志物包括血清骨钙素(0C)、Ⅰ型原胶原N端肽(PINP)、Ⅰ型胶原交联C-末端肽(β-CTX)、25羟维生素D(VitD-T)和甲状旁腺素(PTH)的水平.结果 随着OP程度的加重,BMD值逐渐降低,而年龄逐渐增大;然而不同骨量组患者的OC、PINP、β-CTX和PTH等比较差异均无统计学意义(均P＞ 0.05).结论 绝经后骨质疏松患者血清骨代谢标志物水平未提示与骨密度存在联系;血清OC、PINP、β-CTX和PTH只反映绝经后妇女骨转换的高低,对绝经后骨质疏松的诊断无明显意义.     

补肾阳与补肾阴中药抗骨质疏松作用的研究进展

骨质疏松症是一种由多因素引起的骨密度和骨质量降低的全身性骨病，其破坏性之大、受众面之广已严重危害人类身心健康。目前，临床上治疗骨质疏松的药物，如双磷酸盐类、雌激素类等多具有潜在的副作用，而传统中药因其安全、有效且副作用小的特点已逐渐成为治疗骨质疏松症的补充和替代药物。中医认为"肾主骨"，肾虚则骨萎，因此采用补肾中药治疗骨质疏松症更是获得越来越多国内外学者的认可。补肾中药依据其作用效果的不同又分为补肾阳中药和补肾阴中药。对近年来补肾阳和补肾阴中药治疗骨质疏松症的作用及机制进行综述，旨在探索二者在治疗特点上的异同，为补肾中药抗骨质疏松的发展提供借鉴。     

辛伐他汀对骨质疏松患者种植体周围骨的影响

目的用辛伐他汀干预骨质疏松(OP),观察在OP患者中行种植术后治疗骨质疏松药物对种植体周围骨质的影响。方法将26位OP患者随机分为2组,每组13位。共植入31枚种植体,由同一位医师完成。对照组服用安慰剂,实验组口服辛伐他汀片5mg/d,共3个月。以曲面断层片判定骨质变化。结果对照组术后3个月与术前的骨密度变化不明显,实验组术后3个月与术前的骨密度相比有明显提高。结论口服辛伐他汀可影响OP患者种植体周围骨密度,提高种植成功率。     

Osteopontin

Although osteopontin (OP) has been shown to play a role in bone mineralization and to mediate bone cell adhesion, its function in other tissues is not yet known. The sequences of OP from seven species have been reported; some of the sequences that are conserved in all seven species and their functions are mentioned. The biochemical structure of OP and the functional properties of its motifs make OP a strong candidate for regulating mineralization and/or mediating local cell dynamics. In addition to its role in mineralization, OP has also been shown to promote migration of smooth muscle cells and macrophages. OP expression is high in many tumors, and it correlates with the metastatic potential in some instances. Abundant OP has also been found in human tissue specimens from patients with clinical tuberculosis and in other granulomatous diseases. Experimental approaches in the authors' laboratory have focused on the role of OP as an autocrine motility factor in osteoclasts and human melanoma cell lines; their results suggest that posttranslational modification (phosphorylation) of OP is important in its biological functions.     

Effects of alkylphenols on bone metabolism in vivo and in vitro

Alkylphenols are endocrine disruptors that show estrogen-like effects in various wildlife species. However, little information is available about the action of these chemicals on bone metabolism. We investigated the effects of alkylphenols, such as nonylphenol (NP) and octylphenol (OP), on the formation of bone using several culture systems for osteoclasts and osteoblasts, as well as in vivo experiments. NP and OP dose-dependently inhibited the formation of tartrate-resistant acid phosphatase-positive multinucleated cells (osteoclasts) in cocultures of mouse spleen cells or mouse bone marrow cells with ST2 cells. However, beta-estradiol at 10(-9)M to 10(-6)M did not affect this process. In contrast, neither compound affected the proliferation and differentiation of rat calvarial osteoblast-like cells (ROB cells). When NP or OP (0.1mg/kg body weight) was administered subcutaneously to pregnant mice at 10 days, 12 days and 14 days post-coitus, fetuses at 17.5 days post-coitus showed stimulation of sternebrae bone calcification. Our findings suggest that alkylphenols have critical effects on the formation of bone by non-estrogenic effects.     

Bone loss and vascular calcification: A bi-directional interplay?

Vascular calcification (VC) represents a recognized adverse predictor for cardiovascular morbidity and mortality. Previously considered passive and degenerative, VC is now recognized as an active process that resembles bone formation, and shares a number of histopathological features, mineral composition, and initiation mechanisms with bone development and metabolism. Oxidative stress and inflammation are key factors in both VC and osteoporosis (OP). Biochemical factors known to be primarily involved in the healthy bone metabolism also regulate VC. These biomarkers include vitamin D, osteoprotegerin, osteopontin, matrix Gla protein, cathepsin K, fibroblast growth factor-23, and fetuin-A.A better understanding of this highly controlled regulatory network, with multiple, nested feedback loops and cross talk between organs, may help to decrease the growing prevalence of calcific vasculopathy as well as OP in the aging population, and to advance in common preventive and therapeutic interventions targeted at both conditions.     

上海市北蔡镇老年女性骨质疏松症与生理因素关系分析

目的了解上海市北蔡镇老年女性骨质疏松症（OP）与生理因素的关系,为本地区OP的防治提供参考。方法使用美国GE公司的Lunar Prodigy Advance PA＋300164型双能X线骨密度仪对398名上海市北蔡镇60—79岁老年女性正位腰椎和左股骨近端进行骨密度测定。结果将老年女性以骨密度测定结果分为：OP组、骨量正常组及骨量减少组,3组对照初潮年龄差异无统计学意义（P〉0．05）,闭经年龄、行经年限、行经天数、孕次差异有统计学意义（P〈0．05）;3组两两比较显示：骨量正常组与OP组比较在闭经年龄、行经年限、孕次方面差异有统计学意义（P〈0．05）,在行经天数方面差异无统计学意义（P〉0．05）;骨量正常组与骨量减少组比较在闭经年龄、行经年限、行经天数方面差有统计学意义（P〈0．05）;骨量减少组与OP组比较在闭经年龄、行经天数、孕次方面差异有统计学意义（P〈0．05）,在行经年限方面差异无统计学意义（P〉0．05）。结论上海市北蔡镇老年女性人群OP与女性生理因素密切相关,尤其闭经年龄早、行经年限短、行经天数少、孕次多的老年女性,应注意OP预防。     

Chemokines and bone remodeling

Bone remodeling is characterized by spatial and temporal coupling of bone resorption and formation and is necessary for skeletal growth and normal bone structure maintenance. Imbalance of this process is related to metabolic bone disorders such as osteoporosis or rheumatoid arthritis. For this reason, bone remodeling is under the control of several local and systemic factors, including molecules of the immune system. The importance of the interplay of both the skeletal and immune systems is reflected by the emerging interdisciplinary research field, called osteoimmunology, focused on common aspects of osteology and immunology. This review focuses on the role of inflammatory mediators, such as cytokines in bone remodeling and, in particular, a subfamily of chemotactic cytokines or chemokines which are involved not only in several aspects of physiological bone remodeling but also in pathological bone disorders, such as rheumatoid arthritis or osteoporosis. Understanding the role of inflammation and chemokines will provide new insights for the treatment of diseases affecting both skeletal and immune systems, by the development of new therapeutic strategies targeting common inflammatory mediators.     

雄激素对雄性骨质疏松大鼠骨代谢及骨骼生物力学的影响

目的探讨雄激素对男性骨质疏松骨代谢及骨骼生物力学的影响。方法采用15周龄雄性SD大鼠随机分为正常对照组、模型（去睾）组和雄激素治疗组（十-酸睾酮）。28周后行血尿生化、骨密度、骨骼生物力学检查。结果与正常对照组比较,模型组睾酮水平、全身及股骨中点骨密度均明显下降,碱性磷酸酶降低,24h尿羟脯氨酸、尿钙、与尿磷肌酐比值显著增高,股骨生物力学指标-最大受力负荷（Pb）及股骨最大挠度（δb）也显著下降。应用雄激素替代治疗后,上述指标好转。结论雄性大鼠去睾28周后形成了骨质疏松。雄激素在骨代谢过程中对骨形成与骨吸收均有影响,并最终影响骨骼生物力学性能,早期应用雄激素替代治疗可预防这种骨质疏松的发生。     

Subchondral bone as a key target for osteoarthritis treatment

Osteoarthritis (OA), the most common form of arthritis, is a debilitating and progressive disease that has become a major cause of disability and impaired quality of life in the elderly. OA is considered an organ disease that affects the whole joint, where the subchondral bone (SB) plays a crucial role. Regardless of whether SB alterations precede cartilage damage or appear during the evolution of the disease, SB is currently recognised as a key target in OA treatment. In fact, bone abnormalities, especially increased bone turnover, have been detected in the early evolution of some forms of OA. Systemic osteoporosis (OP) and OA share a paradoxical relationship in which both high and low bone mass conditions may result in induction and/or OA progression. Recent findings suggest that some drugs may be useful in treating both processes simultaneously, at least in a subgroup of patients with OA and OP. This review focuses on the role of SB in OA pathogenesis, describing relevant underlying mechanisms involved in the process and examining the potential activity as disease-modifying anti-osteoarthritic drugs (DMOADs) of certain SB-targeting agents currently under study.