基于“肝主筋、肾主骨”理论探讨OPG/RANKL/RANK信号轴与绝经后骨质疏松症症的筋骨相关性

中医基础理论素有“肝主筋，肾主骨”之说，肝藏血主筋，筋束骨利关节，肾为先天之本，主骨而生髓，肝肾精血同源、筋骨相关，互资互生，二者共同介导机体器官、脏腑的发育、生长与衰退过程，尤其与骨细胞生长代谢机制关系密切。随着中医药分子生物学研究的深入，发现骨保护蛋白（OPG）/核因子-kB受体活化因子（RANK）/核因子-kB受体活化因子配体（RANKL）信号轴在骨代谢中发挥关键作用。本文基于“肝主筋，肾主骨”理论，从绝经后骨质疏松症症的病因病机出发，从“肝肾论治，筋骨并重”角度将OPG/RANKL/RANK信号转导系统与骨代谢内环境稳态相结合，为中医药柔肝补肾、调筋养骨机制提供分子生物学、筋骨力学依据支撑，以期进一步指导临床论治。     

骨质疏松症的中医治疗研究进展

骨质疏松症是以骨量减少,骨质量受损及骨强度降低,导致骨脆性增加,易发生骨折为特征的全身性骨病,属中医学 “骨痿”、“骨痹”等范畴。中医药对骨质疏松症有独特的认识及治疗方法,近年来在治疗骨质疏松症方面已取得一定成果。本文基于近年来的文献研究,结合“从肾论治”、“从脾论治”、“瘀血论”等中医理论,着重从骨质疏松症的病因病机、辨证论治、专方专药、针灸疗法等方面进行探析,以期更加清楚地认识中医药治疗骨质疏松症的现状,从而更好地发挥中医药治疗本病的优势。     

抗骨吸收和促骨形成药物在骨质疏松症治疗中的联合应用

骨质疏松症是一种以骨量减少、骨组织细微结构受损,导致脆性骨折为特征的一种常见疾病。随着人类寿命延长和老年人口的增加,骨质疏松症患病率持续增高,且所致的疼痛和骨折严重影响患者的生活质量,故骨质疏松症的治疗非常重要。目前抗骨质疏松症药物的疗效和安全性比较明确,是防治骨质疏松症的主要手段,但临床上发现单药治疗作用有限,基于不同的作用机制,有学者提出抗骨质疏松症药物的联合治疗。本文针对抗骨质疏松症药物中的两类即抗骨吸收和促骨形成药物之间的联合应用进展做一综述。     

运动疗法防治骨质疏松症机制的研究进展

骨质疏松症是一类全身性、代谢性骨病，表现为持续骨量减少、骨组织微结构退变，骨的强度降低，继发骨脆性增加，引起疼痛和驼背等症状，并能极易出现病理性骨折的疾病。合理适当的运动有助于改善骨质流失而防治骨质疏松症。为更加清晰地认知运动疗法防治骨质疏松的理论基础，以帮助指导临床制定更为合理的运动治疗处方，更好发挥其防治骨质疏松症的优势，本文详细介绍了中西运动疗法在防治骨质疏松症的作用机制。例如西医注重运动机械应力对骨骼的效应作用、运动对钙的调节效应作用、运动诱导细胞调节因子、激素的变化对骨代谢的作用、运动对骨代谢信号通路的调节作用以及其他新陈代谢作用；中医则认为其病因病机主要是与肾、脾、肝三脏的关系，传统中医导引运动疗法防治骨质疏松的作用机制正是通过功法由外到内的调理三脏。中医运动疗法-导引功法与西医运动疗法比较更适合在我国的推广，临床应用中更具有独特的优势，以发挥其“简、便、廉、效”的目的。     

由“肾藏精主骨”理论探讨DNA甲基化修饰与骨质疏松症

骨质疏松症（osteoporosis，OP）是一种以骨结构退化和骨量减少为主要特征的代谢性疾病。《黄帝内经》中提出“肾藏精主骨”理论，将“肾”与“骨”之间的生理病理转化密切联系起来。近年来，随着中国传统医学与表观遗传学研究的发展，甲基化修饰在骨质疏松症发生发展中的作用已成为研究热点。中医药治疗骨质疏松症在分子水平上被证实与DNA甲基化的调控有关，本文基于中医“肾藏精主骨”理论探讨DNA甲基化对骨质疏松症的调控机制，分析DNA甲基化修饰与中医基础理论的有机结合，旨在为中医药现代化研究提供新的参考。     

从“脑为髓海”理论探讨骨质疏松症与阿尔兹海默症的相关性

目的 从“脑为髓海”理论为出发点，分析阿尔兹海默症（Alzheimer’s disease， AD）与骨质疏松症（osteoporosis，OP）的联系，探究二者的共同发病机制，以拓宽OP的防治思路。方法 通过检索中国知网、万方、PubMed等数据库中关于“脑为髓海”理论和OP、AD的中医古籍文献、临床研究与实验研究，深入探讨OP与AD的关联。结果 “脑为髓海”出自《黄帝内经》，医家们对脑与髓的认知不断加深，意识到髓海充盛滋养骨骼，筋骨强健，脑力聪慧，反应敏捷，骨与脑两个系统通过髓在生理上相互依赖，OP与AD有着共同的生理病理基础。结论 “脑为髓海”理论在指导认识AD与OP的共同发病机制上具有很高的价值，大多数医生在防治OP时都以肝、肾、脾、筋、骨、肉为导向，忽视了脑-髓的重要作用，期待以此理论为基础探究出更多的OP防治思路。     

基于肾之“精气”“阴阳”理论探析绝经后骨质疏松症的病机变化

中医学防治绝经后骨质疏松症具有完善的理论体系、确切的临床疗效,中医药的现代研究又为其防治绝经后骨质疏松症提供了客观依据。基于古代文献和中医临床立法用药规律,结合现代医学对绝经后骨质疏松症发病机制的研究,围绕肾之“精气”“阴阳”理论阐释绝经后骨质疏松症的病机变化为以肾精亏虚为先导,继而肾之阴阳平衡失调,导致骨髓失养、代谢紊乱、骨枯形伤,出现疼痛、骨量减少、骨强度下降、骨脆性增加、易于骨折等临床表现。     

腰臀筋膜炎从肝论治

腰臀筋膜炎属中医“痹症”、“伤筋”的范畴。唐·王冰注《素问》：“肝藏血,心行之,人动则血运于诸经,人静则血归于肝。”“肝主身之筋膜。”全身筋膜依赖肝血的滋养。人体肢节的运动虽然是筋的作用,但却关系于肝血的盛衰。只有肝血充盈,才能“淫气于筋”。使肢体的筋膜得到充分的濡养,从而维持正常的运动。若肝血不足,血不营筋,则出现肢体麻木,筋脉拘急。肝主疏泄,通利三焦。如肝气的疏泄功能失调,水湿内停,蕴而化热,湿热淫经,经脉灼热疼痛。跌扑损伤,恶血内留,内舍于肝,使其难司其职。肝与筋的关系密切,互相影响,临床表现出肝经的症候群。根据辨证论治的原则,从肝分型论治,效果满意。     

密骨疏治疗骨质疏松症病例报告

骨质疏松症是最为常见的代谢性骨病 ,是一种重要的老年性疾病 ,其特点为单位体积内骨组织量减少 ,骨皮质变薄 ,海绵骨骨小梁数目及大小均减少 ,髓腔增宽 ,骨荷载功能减弱 ,从而产生腰背、四肢疼痛、脊柱畸形甚至骨折。中医学把本病归属于“骨痿”“骨枯”“骨痹”“骨缩”等范畴 ,认为病机有肾虚、脾虚与血瘀 ;肾精不足则不能化生气血以荣筋养骨 ,肾阳虚衰则气血温运无力又渐可致瘀而呈本虚标实证 ,在治疗方面现代医学主要有周期应用性激素、钙剂、维生素Ｄ、二磷酸盐、降钙素和病因治疗 ,中医则按辨证论治以重在补肾兼顾脾、肝 ,佐以祛瘀为…     

基于“脾肾相关”论治疗骨质疏松症的研究进展

骨质疏松症常见于中老年人群，是由多种原因导致骨组织显微结构受损、易发脆性骨折的一种全身性骨代谢障碍疾病。中医学认为肾虚是骨质疏松症发病的重要病机，因此以补肾壮骨为主要治法已达成普遍共识。笔者通过大量文献搜索发现，脾虚在骨质疏松症的致病过程中亦起着关键作用。肾、脾两脏为先后天之本，是维持人体正常生理活动的根本所在。因此本文着眼于“脾肾相关”理论，从中医基础理论、实验研究及临床观察等角度综述其防治疗骨质疏松症的科学内涵，并试探讨中医“脾肾相关”理论防治骨质疏松症的作用机制，找寻中医基础理论在防治骨质疏松症中的理论渊源，优化中医药防治骨质疏松症的诊疗方案，为更好得将祖国医学运用于临床提供新的思路与方法。     

从肝论治甲亢性骨质疏松的相关性探讨

甲亢性骨质疏松是因甲状腺激素过多引起机体骨代谢及骨矿化紊乱而导致的继发性疾病,随着社会的节奏不断加快,其发病率也逐年升高。因其沉默性发病,临床上常常出现漏诊、误诊,耽误了治疗的最佳时机,使病情加重,病程延长,故早诊断、早治疗是治疗此病的关键。对于其治疗,现代医学尚无明确治疗方案和早期干预手段,中医药治疗甲亢性骨质疏松具有充分优势,《黄帝内经》认为"肝藏血主疏泄,调畅气机,以强筋骨",提示气血的运行、筋骨的生长与肝的疏泄功能密切相关。但目前临床治疗多集中在"肾为先天主骨生髓"方面,忽视了"从肝论治"在甲亢性骨质疏松防治中的重要性。本文旨在从中西医角度探讨"从肝论治"甲亢性骨质疏松临床研究的相关性,为甲亢性骨质疏松的防治诊疗提供新思路。     

中药通过调控短链脂肪酸防治骨质疏松症的研究进展

肠道菌群微生物是与宿主共生的一个大的生物群落，当其发生紊乱时将会导致多种疾病的发生，尤其是全身代谢性疾病。其代谢产物也对全身代谢性疾病起到重要的调控作用，尤其是骨代谢性疾病。短链脂肪酸(short chain fatty acids, SCFAs)是肠道微生物群所产生的一类代谢产物，能够很好地反映肠道菌群微生物的功能，大量的研究证明其在骨代谢性疾病中起着调控作用。中药在调控肠道菌群微生物及其代谢产物中有很大的作用，尤其是对于SCFAs的调控。笔者就单味中药及提取物与中药复方通过调控SCFAs影响骨代谢，从而在防治骨质疏松症方面的研究进行总结，以期为骨质疏松症的预防和治疗提供新思路。     

Hormonal factors in osteoporosis

Primary osteoporosis is a ubiquitous disease of unknown etiology. The condition undoubtedly has multiple causes and the metabolic pattern of bone loss may vary significantly from case to case. Five hormones, PTH, gonadal steroids, CT, T3 and T4, and glucocorticoids, and possibly a sixth, GH, have fundamental actions on bone metabolism and may therefore be causally involved in primary osteoporosis. A consideration of selected data on hormonal interactions culled from a much larger body of experimental and clinical data leads to the conclusion that in vitro studies, animal research, and data obtained in postmenopausal women with age-related bone atrophy, but not osteoporosis, have yielded considerable data relating to bone metabolism, but have failed to define the causes or treatment of primary osteoporosis. There has been excessive emphasis on hormonal reactions relating to bone metabolism and bone cell function, and too little concern for nonhormonal factors which might influence the kinetics of skeletal turnover through alterations in bone cell activity. A practical approach to the cause(s) and treatment in the only suitable model, the human with osteoporosis, is proposed with the expectation that a better insight into the pathogenesis of the condition will be achieved.     

Tendon biomechanics and mechanobiology--a minireview of basic concepts and recent advancements

Due to their unique hierarchical structure and composition, tendons possess characteristic biomechanical properties, including high mechanical strength and viscoelasticity, which enable them to carry and transmit mechanical loads (muscular forces) effectively. Tendons are also mechanoresponsive by adaptively changing their structure and function in response to altered mechanical loading conditions. In general, mechanical loading at physiological levels is beneficial to tendons, but excessive loading or disuse of tendons is detrimental. This mechanoadaptability is due to the cells present in tendons. Tendon fibroblasts (tenocytes) are the dominant tendon cells responsible for tendon homeostasis and repair. Tendon stem cells (TSCs), which were recently discovered, also play a vital role in tendon maintenance and repair by virtue of their ability to self-renew and differentiate into tenocytes. TSCs may also be responsible for chronic tendon injury, or tendinopathy, by undergoing aberrant differentiation into nontenocytes in response to excessive mechanical loading. Thus, it is necessary to devise optimal rehabilitation protocols to enhance tendon healing while reducing scar tissue formation and tendon adhesions. Moreover, along with scaffolds that can mimic tendon matrix environments and platelet-rich plasma, which serves as a source of growth factors, TSCs may be the optimal cell type for enhancing repair of injured tendons.     

Effect of hyaluronic acid/chondroitin sulfate on healing of full-thickness tendon lacerations in rabbits

Viscoat, a high-molecular-weight, highly purified hyaluronic acid (HA) and chondroitin sulfate (CS) compound, was instilled around rabbit plantaris tendon following full-thickness laceration and surgical repair. After 3 weeks of immobilization, no significant difference in adhesion strength or tensile strength of the healing tendons existed between Viscoat-treated tendons and controls. This contradicts previous studies which suggest that hyaluronic acid reduces postoperative tendon adhesions. Further studies examining tendon adhesions after less severe degrees of tendon injury and using direct, quantitative measurement techniques are warranted to demonstrate whether HA has a beneficial effect on tendon healing.     

原发性胆汁性胆管炎继发骨质疏松的研究进展

原发性胆汁性胆管炎(primary biliary cholangitis,PBC)又称原发性胆汁性肝硬化,是一种以进行性、非化脓性肝内胆管炎为病理特征,最终发展为肝硬化的慢性自身免疫性肝病。骨质疏松症(osteoporosis,OP)是一种以骨密度下降、骨结构损伤和骨折风险增加为特征的全身性疾病。骨质疏松是PBC的常见并发症,随病情进展发病率逐渐增加,发病率和骨折风险均高于普通人群,正日益受到关注。骨质疏松的危险因素包括老年、女性、吸烟、过量饮酒、低体重、早绝经、类固醇激素治疗、低体力活动、维生素D和钙摄入减少等。PBC继发骨质疏松是由多种病理机制导致的,其中严重的骨吸收和缓慢的骨形成发挥了主要作用,遗传、性腺机能减退、脂溶性维生素缺乏、高脂血症等也参与骨质疏松发病。确诊PBC后应早期开始骨质疏松的预防和治疗。目前尚无治疗PBC并发骨质疏松患者的统一方案,可按照老年性骨质疏松和绝经后骨质疏松方案治疗,包括双膦酸盐、激素替代治疗、甲状旁腺激素、调脂药物、降钙素等。本文就PBC并发骨质疏松的临床表现、危险因素、病理机制及治疗方面的研究进展进行综述。     

Tendon injury response: assessment of biomechanical properties, tissue morphology and viability following flexor digitorum profundus tendon transection.

Insertion site injuries of the flexor digitorum profundus (FDP) tendon often present for delayed treatment. Apart from gross observations made at the time of surgery, the changes that occur in the flexor tendon stump during the interval from injury to repair are unknown. These changes may include tendon softening and loss of viability, which may contribute to the poor outcomes observed clinically and experimentally. Thirty-eight FDP tendons from 23 adult dogs were transected sharply from their insertions on the distal phalanges and were not repaired. Dogs were allowed full weight bearing and were euthanized 7 or 21 days after injury. Biomechanical testing indicated that the resistance of injured tendons to pullout of a Kessler-type suture was not different from control tendons at 7 days and was increased at 21 days by 25% (p<0.05). Morphologically, at 7 and 21 days the cut surface had a smooth appearance and the end of the injured tendon was increased in thickness by 30% and 50%, respectively (p<0.05). Histologically, we observed increased cellularity and dramatic fibroblast proliferation within the injured tendon stump; there was no evidence of decreased cell viability. We conclude that during the interval from 0 to 21 days after FDP insertion-site injury, tendons cells are viable, proliferative and synthesizing new matrix. This leads to increased tendon size and enhanced resistance to suture pullout. These findings offer a scientific rationale supporting the clinical practice of surgical re-attachment within the first 3 weeks after injury.     

骨质疏松对肩袖损伤修复的影响研究进展

老年人群因合并有不同程度的骨质疏松,肩袖损伤修复再撕裂率高。为解决这一难题,手术医师尝试通过增加锚钉初始固定强度、改变局部骨质情况等方法来降低这类患者肩袖损伤的再撕裂率。组织工程学的快速发展也使生长因子的辅助应用成为可能。但在目前的临床工作中,合并有骨质疏松的肩袖损伤修复仍然是临床工作者面临的一个巨大挑战。如何更好地增加锚钉固定强度,改善腱骨愈合微环境,降低肩袖再撕裂率成为了近年来的研究热点。本文从骨质疏松与肩袖损伤的关系、骨质疏松对肩袖腱骨愈合的影响及目前采用的减少骨质疏松对腱骨愈合的不同方法3个方面进行综述,以便更好地指导临床治疗,提高患者的手术效果及术后满意率。