Article(id=1322912240176857553, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322912162913596032, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2025.01.019, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1793336456578, onlineDateStr=2026-10-30, pubDate=1736438400000, pubDateStr=2025-01-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793336456578, onlineIssueDateStr=2026-10-30, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793336456578, creator=13701087609, updateTime=1793336456578, updator=13701087609, issue=Issue{id=1322912162913596032, tenantId=1146029695717560320, journalId=1255847919539208197, year='2025', volume='43', issue='1', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1736438400000', pubDateStr='2025-01-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1793336438157, creator='13701087609', updateTime=1793340633627, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1322929760048906989, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322912162913596032, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1322929760048906990, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322912162913596032, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=102, endPage=107, ext={EN=ArticleExt(id=1322912240449487315, articleId=1322912240176857553, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Discussion on Pathogenesis of Comorbidity of Lumbar Degenerative Disc Disease and Paravertebral Sarcopenia Based on Theory of “Bone and Flesh Not Match”, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=

Lumbar degenerative disc disease(LDDD)and sarcopenia are common age-related motor system diseases in the elderly,which seriously affect the health of the elderly. The reduction of paravertebral muscle is the manifestation of sarcopenia in the spine,and clinical findings show the paravertebral sarcopenia and LDDD often present comorbidity status,mutual influence and mutual causality. Basic research suggests that the two have similar pathogenesis and pathological mechanisms. LDDD is mostly treated symptomatically in clinical practice,and there is still a lack of effective means to reverse in tervertebral disc degeneration. The common intervention methods for sarcopenia include resistance exercise and nutritional supplementation,but there is a lack of effective therapeutic drugs. Traditional Chinese medicine(TCM)classifies LDDD as “lumbago” and “spinalgia” and paravertebral sarcopenia as “Wei syndrome” and “consumptive disease”. TCM has a profound understanding of the relationship between the two,and highly summarizes the pathological state of its comorbidity with the theory of “bone and flesh notmatch”. It is believed that the deficiency of spleen and kidney is the common pathogenesis. Tonifying spleen and kidney is the basic treatment method. However,the research on traditional Chinese medicine urgently needs to adopt real-world research to enrich theories and evidence-based medicine research to verify therapeutic effects and basic experimental research to deeply reveal the mechanisms of comorbidities and explain the mechanisms of therapeutic effects,providing new ideas for deepening the relevant theories of traditional Chinese medicine and inventing new drugs.

, authors=Haijian CUI1, 2, Xiaosheng YAO2, Xiaonan QI2, Hongxin ZHENG1, Yu WANG2, Siwei WANG2, Yingtao HUANG1, authorsList=Haijian CUI, Xiaosheng YAO, Xiaonan QI, Hongxin ZHENG, Yu WANG, Siwei WANG, Yingtao HUANG, authorCompany=null, correspAuthors=Xiaosheng YAO, Hongxin ZHENG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1322912241120575958, articleId=1322912240176857553, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=基于“骨肉不相亲”理论探讨腰椎间盘退行性疾病与椎旁肌减少症共病机制, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=

腰椎间盘退行性疾病(LDDD)和骨骼肌减少症(简称肌少症)是老年人常见的增龄性运动系统疾病,严重影响老年人的健康。肌少症在脊柱区域表现为椎旁肌减少。临床发现椎旁肌减少症和LDDD常呈现共病状态,相互影响,互为因果。基础研究提示二者具有相似的发病基础和病理机制。LDDD临床上多是对症治疗,尚缺乏逆转椎间盘退变的有效手段。肌少症常见的干预手段有抗阻运动和营养补充,但缺少有效的治疗药物。中医将LDDD和肌少症分别归为“腰痛”“腰脊痛”“痿证”“虚劳”等。中医对二者相互关系有深刻认识,以“骨肉不相亲”理论高度概括其肌骨共病的病理状态。认为脾肾亏虚是其共同的发病机制,补益脾肾是基本治法。但中医药研究亟待采用真实世界研究丰富理论,循证医学研究验证疗效,基础实验研究深入揭示其共病的机理和阐释疗效的机制,为深化中医药相关理论和发明新药提供新思路。

, authors=崔海舰1, 2, 姚啸生2, 戚晓楠2, 郑洪新1, 王禹2, 王思微2, 黄英韬1, authorsList=崔海舰, 姚啸生, 戚晓楠, 郑洪新, 王禹, 王思微, 黄英韬, authorCompany=null, correspAuthors=姚啸生, 郑洪新, authorNote=

崔海舰(1991-),男,河北承德人,博士在读,研究方向:中医药防治椎间盘退变及骨伤科疾病。

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姚啸生(1969-),男,辽宁沈阳人,教授,博士研究生导师,博士,研究方向:中医药防治椎间盘退变及骨质疏松症。Email:。
郑洪新(1952-),女,辽宁沈阳人,教授,博士研究生导师,博士,研究方向:中医藏象理论及应用。E-mail:。
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崔海舰(1991-),男,河北承德人,博士在读,研究方向:中医药防治椎间盘退变及骨伤科疾病。

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崔海舰 1, 2 , 姚啸生 2 , 戚晓楠 2 , 郑洪新 1 , 王禹 2 , 王思微 2 , 黄英韬 1
中华中医药学刊 | 国家项目点击 2025,43(1): 102-107
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中华中医药学刊 |国家项目点击 2025 , 43 (1) : 102 -107
基于“骨肉不相亲”理论探讨腰椎间盘退行性疾病与椎旁肌减少症共病机制
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崔海舰(1991-),男,河北承德人,博士在读,研究方向:中医药防治椎间盘退变及骨伤科疾病。

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崔海舰(1991-),男,河北承德人,博士在读,研究方向:中医药防治椎间盘退变及骨伤科疾病。

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崔海舰1, 2, 姚啸生2 , 戚晓楠2, 郑洪新1 , 王禹2, 王思微2, 黄英韬1
作者信息
  • 1.辽宁中医药大学,辽宁 沈阳 110847
  • 2.辽宁中医药大学附属医院,辽宁 沈阳 110032
通讯作者:
姚啸生(1969-),男,辽宁沈阳人,教授,博士研究生导师,博士,研究方向:中医药防治椎间盘退变及骨质疏松症。Email:。
郑洪新(1952-),女,辽宁沈阳人,教授,博士研究生导师,博士,研究方向:中医藏象理论及应用。E-mail:。
作者简介:

崔海舰(1991-),男,河北承德人,博士在读,研究方向:中医药防治椎间盘退变及骨伤科疾病。

Discussion on Pathogenesis of Comorbidity of Lumbar Degenerative Disc Disease and Paravertebral Sarcopenia Based on Theory of “Bone and Flesh Not Match”
Haijian CUI1, 2, Xiaosheng YAO2 , Xiaonan QI2, Hongxin ZHENG1 , Yu WANG2, Siwei WANG2, Yingtao HUANG1
Affiliations
  • 1.Liaoning University of Traditional Chinese Medicine, Shenyang 110847, Liaoning, China
  • 2.The Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang 110032, Liaoning, China
出版时间: 2025-01-10 doi: 10.13193/j.issn.1673-7717.2025.01.019
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腰椎间盘退行性疾病(LDDD)和骨骼肌减少症(简称肌少症)是老年人常见的增龄性运动系统疾病,严重影响老年人的健康。肌少症在脊柱区域表现为椎旁肌减少。临床发现椎旁肌减少症和LDDD常呈现共病状态,相互影响,互为因果。基础研究提示二者具有相似的发病基础和病理机制。LDDD临床上多是对症治疗,尚缺乏逆转椎间盘退变的有效手段。肌少症常见的干预手段有抗阻运动和营养补充,但缺少有效的治疗药物。中医将LDDD和肌少症分别归为“腰痛”“腰脊痛”“痿证”“虚劳”等。中医对二者相互关系有深刻认识,以“骨肉不相亲”理论高度概括其肌骨共病的病理状态。认为脾肾亏虚是其共同的发病机制,补益脾肾是基本治法。但中医药研究亟待采用真实世界研究丰富理论,循证医学研究验证疗效,基础实验研究深入揭示其共病的机理和阐释疗效的机制,为深化中医药相关理论和发明新药提供新思路。

腰椎间盘退行性疾病  /  肌少症  /  椎旁肌减少症  /  骨肉不相亲  /  共病

Lumbar degenerative disc disease(LDDD)and sarcopenia are common age-related motor system diseases in the elderly,which seriously affect the health of the elderly. The reduction of paravertebral muscle is the manifestation of sarcopenia in the spine,and clinical findings show the paravertebral sarcopenia and LDDD often present comorbidity status,mutual influence and mutual causality. Basic research suggests that the two have similar pathogenesis and pathological mechanisms. LDDD is mostly treated symptomatically in clinical practice,and there is still a lack of effective means to reverse in tervertebral disc degeneration. The common intervention methods for sarcopenia include resistance exercise and nutritional supplementation,but there is a lack of effective therapeutic drugs. Traditional Chinese medicine(TCM)classifies LDDD as “lumbago” and “spinalgia” and paravertebral sarcopenia as “Wei syndrome” and “consumptive disease”. TCM has a profound understanding of the relationship between the two,and highly summarizes the pathological state of its comorbidity with the theory of “bone and flesh notmatch”. It is believed that the deficiency of spleen and kidney is the common pathogenesis. Tonifying spleen and kidney is the basic treatment method. However,the research on traditional Chinese medicine urgently needs to adopt real-world research to enrich theories and evidence-based medicine research to verify therapeutic effects and basic experimental research to deeply reveal the mechanisms of comorbidities and explain the mechanisms of therapeutic effects,providing new ideas for deepening the relevant theories of traditional Chinese medicine and inventing new drugs.

lumbar degenerative disc disease  /  sarcopenia  /  paravertebral sarcopenia  /  bone and flesh notmatch  /  comorbidity
崔海舰, 姚啸生, 戚晓楠, 郑洪新, 王禹, 王思微, 黄英韬. 基于“骨肉不相亲”理论探讨腰椎间盘退行性疾病与椎旁肌减少症共病机制. 中华中医药学刊, 2025 , 43 (1) : 102 -107 . DOI: 10.13193/j.issn.1673-7717.2025.01.019
Haijian CUI, Xiaosheng YAO, Xiaonan QI, Hongxin ZHENG, Yu WANG, Siwei WANG, Yingtao HUANG. Discussion on Pathogenesis of Comorbidity of Lumbar Degenerative Disc Disease and Paravertebral Sarcopenia Based on Theory of “Bone and Flesh Not Match”[J]. Chinese Archives of Traditional Chinese Medicine, 2025 , 43 (1) : 102 -107 . DOI: 10.13193/j.issn.1673-7717.2025.01.019
腰椎间盘退行性疾病(LDDD)与骨骼肌减少症(简称肌少症)是常见的增龄性运动系统疾病[1-2]。随着全球人口老龄化进程的加快,其患病率越来越高,并威胁着老年人的健康,给患者及医疗工作均带来巨大挑战,正日益受到关注[3]。骨关节疾病与肌少症共病状态是老年人运动系统退行性疾病的临床发病特点之一[2,4-6]。目前已有众多研究表明肌少症与脊柱退行性疾病、骨质疏松症(osteoporosis,OP)受许多共同因素调控,存在相似的生理病理基础,并相互影响和相互促进,共同导致了老年人的日常活动能力下降、躯体功能障碍、失能,甚至死亡等不良结局,成为了亟待解决的社会问题[7-8]。椎旁肌减少症是肌少症在脊柱区域的特殊表现,其典型表现是椎旁肌萎缩和脂肪浸润,与LDDD密切相关[9]。
“骨肉不相亲”理论最早见于《灵枢·经脉》[10],高度概括了运动系统退行性疾病发病过程中的肌骨关系。结合“骨肉相保”、肌骨同治理念,对于上述疾病的防治具有重要的指导意义。本文基于“骨肉不相亲”理论,从肌骨关系探讨LDDD与椎旁肌减少症共病的机制,为肌少症与LDDD的共同防治和研究提供新思路。
LDDD是指腰椎间盘等由于衰老、长期姿势不良、劳损、代谢障碍及创伤等因素导致的退行性疾病。病理改变主要表现为腰椎间盘退变和/或突出、韧带等增生钙化、椎管狭窄、椎体滑脱或侧弯等。包括椎间盘源性腰痛、腰椎间盘突出症(LDH)、腰椎管狭窄症(LSS)、退行性腰椎滑脱(DLS)和退行性脊柱侧凸(DS)等疾病。产生腰痛、腰椎功能障碍,以及影响神经功能等一系列临床表现的疾病群[11]。2017年世界卫生组织发布的全球疾病统计显示,在195个国家和地区的354种疾病中,LDDD相关的腰痛位居伤残首位,是造成生产损失的首要原因[12]。
肌少症是指与年龄相关的进行性、广泛性全身骨骼肌肌量减少及功能减退性疾病[13],老年人群患病率为4.1%~11.5%[14]。主要表现为骨骼肌力量减弱、质量降低和数量减少,以及躯体活动能力下降,并与跌倒、骨折、残疾和死亡等不良事件的发生密切相关[15]。目前肌少症诊断多仅以四肢骨骼肌指数(ASMI)和握力测量等为评定方法,并不包含对椎旁肌等躯干骨骼肌的评价方法和指标。因此,LDDD临床研究过程中,直接应用肌少症功能评定方法存在一定局限性。就此,KIM JC等[9]基于椎旁肌对脊柱矢状面平衡和脊柱退变的重要影响,观察到椎旁肌减少、萎缩和脂肪浸润与慢性腰痛和功能障碍关系密切,认为椎旁肌减少是导致脊柱退变的主要原因之一,进而提出了“脊柱旁骨骼肌减少症”(SarcoSpine)的概念。期望通过对椎旁肌质量和功能等进行评价来探究椎旁肌减少对脊柱影响的机制。脊柱旁骨骼肌减少症,简称椎旁肌减少症,是一种与年龄增长等相关的脊柱周围骨骼肌退行性疾病,是肌少症在脊柱的特殊类型。病理表现主要为椎旁肌萎缩,横截面积减少,脂肪浸润增加。使肌量、肌力、肌肉质量和肌功能降低,通过影响脊柱节段的稳定性,加重脊柱疼痛和功能障碍[9,16]。
脊柱生物力学平衡和运动功能的维持有赖于骨性结构和椎旁肌的共同作用[17]。其中,椎体和椎间链接结构起到了支持和运动作用。而多裂肌、竖脊肌和腰大肌等椎旁肌群对于脊柱运动和稳定性的维持具有重要意义[18-19]。PANJABI M M[20]提出脊柱稳定性的“三亚系模型”,即椎旁肌构成的主动亚系、骨骼韧带构成的被动亚系和起反馈控制作用的神经控制亚系。当三亚系彼此之间无法功能代偿时,则导致脊柱整体稳定性的破坏,继而影响脊柱序列、生理曲度、脊柱-骨盆参数,出现矢状位失衡等生物力学改变,引起椎间盘退变等,进而发生腰痛或脊柱退行性疾病[21-22]。
随着对椎旁肌及肌少症在脊柱生理病理作用中研究的逐渐深入,发现腰椎椎旁肌减少参与了LDDD相关疾病的进程[23]。研究表明,LDDD患者往往伴有椎旁肌萎缩,其横截面积随年龄增加而减少,并伴有脂肪浸润增加,腰痛患者尤为明显[24]。腰痛患者多裂肌肌电图活动减少,肌束募集时间改变,收缩能力降低[25]。同时,随着椎旁肌质量的下降,椎间盘退变等级相应提高[26]。
研究表明,衰老、肥胖和慢性低度炎症是肌少症、LDDD的共同病理基础,对其发展起促进作用[27]。椎旁肌退变造成腰痛,腰痛常诱发关节源性肌肉抑制,肌肉保护性抑制导致椎旁肌活动减少,促使椎旁肌力量、功能进一步下降,进入到肌骨互相影响的恶性循环[28]。
虽然越来越多的实验研究已证实,白细胞介素(ILs)、肌肉生长抑制素(Myostatin)、鸢尾素(Irisin)、胰岛素样生长因子Ⅰ(IGF-I)和成纤维细胞生长因子21(FGF-21)等肌因子与骨钙素(OCN)、硬骨抑素(Sclerostin)、前列腺素E2(PCE2)、转化生长因子β(TCF-β)等骨因子存在明确的相互交联作用,双向接收和分泌生化信号,从而影响骨骼肌和骨代谢[29],但肌、骨因子在椎旁肌减少症和LDDD中的交互机制尚缺少深入研究。
LDDD多以椎旁肌的改变为先导,椎旁肌减少及力量减弱影响脊柱的稳定性,可导致椎间盘退变及LDDD,是LDDD发生和发展的危险因素。同时,LDDD也会加重椎旁肌减少的程度。
在DS发生发展中,椎旁肌起到“稳定器”的作用,其通过对侧凸脊柱力学环境的代偿与适应,延缓了DS的进展。多裂肌不对称萎缩和脂肪浸润的增加,可造成DS患者生活质量的显著下降[30]。保护和改善椎旁肌是维持腰椎稳定和DS治疗中的重要策略,合理的康复训练增大了椎旁肌横截面积,缓解DS临床症状并延缓侧凸的进展[21,31]。
同时,临床观察表明,LDH患侧多裂肌的脂肪浸润和萎缩较健侧更明显[32]。LDH导致椎旁肌萎缩机制主要有疼痛、炎症、椎旁肌去神经萎缩[33-35]。而椎旁肌退变也会进一步加重LDH的症状。在腰椎管狭窄症患者中,肌少症患病率高达16%~33%,椎旁肌的横截面积明显变小,L4-L5水平多裂肌脂肪浸润率更大,且双侧椎旁肌表现出明显不对称[36],并预示更差的临床结局[2,37-39]。退行性腰椎滑脱患者中存在椎间盘高度的降低,以及双侧多裂肌横截面积减小、萎缩和脂肪浸润程度提高的表现[40]。此外,椎旁肌减少及力量减弱也影响了脊柱手术患者预后、降低生存率、增加院内并发症、住院时间及护理成本[7]。
临床发现,LDDD患者通过腰背肌功能锻炼可有效改善腰痛症状和功能评分[41-42],脊柱畸形患者进行保护性举重、自行车运动和水上运动治疗等核心肌强化可改善椎旁肌功能[43],补充维生素D和氨基酸可改善老年人的骨骼肌质量[44]。肌少症的治疗也以抗阻运动和营养补充为主,虽然睾酮、雌激素、孕酮、生长激素、血管紧张素转换酶抑制剂等可以改善肌量,但是目前还没有特定有效药物被批准用于治疗肌少症[45]。而LDDD治疗目前也仅是缓解临床症状,尚无逆转椎间盘退变的有效方法,并未彻底解决或逆转腰椎间盘退变进展[46]。因此,椎旁肌减少症的早期筛查和干预对延缓LDDD发生发展具有重要意义[47]。肌骨同治的有效药物研发是未来肌骨共病基础与临床研究方向之一。
LDDD在中医属“腰痛”“腰脊痛”“腰腿疼”等范畴。《灵枢·经脉》云:“脊痛,腰似折,髀不可曲,腘如结,端如裂,是为踝厥”[10]。清代程国彭在《医学心悟·腰痛》中描述为“腰痛拘急,牵引腿足”[48],与腰痛伴下肢放射痛的症状很相似。
“肌少症”的病名中医古籍未见记载,但关于“痿证”“虚劳”的描述和肌少症临床表现很相似[49]。《素问·痿论篇》有“肉痿”“骨痿”之分,定义为“痿谓痿弱,无力以运动”,临床表现是“肌肉不仁”“腰脊不举”[50]。明代王肯堂《证治准绳·杂病》进一步描述为“痿者,手足痿软而无力,百节缓纵而不收也”[51],这与肌少症的肌量流失、肌力下降和功能减退的表现非常相似。
《说文解字》解释“脊”为“背呂也,从从肉”[52]。“背”指脊背,“呂”呈现椎骨颗颗相承之象,“从肉”强调了骨骼肌的重要地位。故“脊”兼有骨、肉之义,提示骨与肉在脊柱的结构和功能上共同发挥着重要作用[53]。现代研究也表明,椎旁肌和脊柱、椎间盘发育的同源性决定了两者的密切关系。脊柱是由中胚层的生骨节细胞围绕脊髓和脊索发育形成。椎体源于生骨节,脊索完全退化。但椎间隙中央的脊索却保留下来,并经黏液样变性形成髓核组织。髓核周围的结缔组织分化成纤维软骨环,与髓核、终板共同构成椎间盘。因此,从起源上看,椎体、椎间盘等共同起源于中胚层生骨节,可同属于“骨”。椎旁肌起源于中胚层生骨节旁同一节段的生肌节组织,并发育成脊柱周围的骨骼肌群,属“肉”[54]。《素问·痿论篇》中“宗筋主束骨而利机关”强调了在脊柱运动中,椎旁肌的主导作用和韧带、关节囊等经筋的约束作用。
肌骨关系的生理状态,《素问·汤液醪醴论篇》描述为“精自生,形自盛,骨肉相保,巨气乃平”[50]。人体精气充足,外在表现为形体盛满,而达到“骨肉相保”的状态。与临床所见腰脊强健者外在表型肌强骨健,影像学腰椎序列良好,相应椎旁肌量和瘦肉比例正常相一致。
《内经》《难经》以“骨肉不相亲”理论高度概括了骨骼肌与骨共病关系的病理状态[55-56]。《灵枢·经脉》记载:“足少阴气绝,则骨枯……伏行而濡骨髓者也,故骨不濡,则肉不能着也;骨肉不相亲,则肉软却”[10]。《难经·第二十四难》描述为“骨髓不濡,即肉不着骨;骨肉不相亲,即肉濡而却”[57]。肾主骨生髓,肾精亏虚,则骨髓失于濡养,骨肉不相亲,骨表现不荣而枯,肌肉出现软弱,痿而无力[58]。临床上也发现,LDDD并发椎旁肌减少症患者椎旁肌的主要病理改变为肌肉减少萎缩和脂肪浸润。出现肌不附骨、骨肉分离的现象,丧失了其维持脊柱稳定的功能,进一步印证了脊柱与椎旁肌功能上相互促进,病理上相互影响的紧密关系。
“骨肉不相亲”的病机本质是脾肾功能的失常[58]。肌骨的生理病理及与脾肾二脏的关系体现在人体“生、长、壮、老、已”自然生命规律中。肾精亏虚是肌骨退行性疾病共病的本质,也是LDDD与椎旁肌减少症共病发病的共同基础。《素问·上古天真论篇》论述肾精盛满,在女子表现为“筋骨坚”“身体盛壮”,男子则为“筋骨劲强”“筋骨隆盛,肌肉满壮”。而随着肾精亏虚、肾气耗竭,则表现为“肌肉痿软无力,筋不能动,形体皆极”。可见,随着年龄增长,人体筋骨、肌肉随着肾精盛衰而同步表现为由“筋骨劲强”“筋骨隆盛”和“肌肉满壮”到“筋不能动”“骨槁齿脱”“肉痿无力”“形体皆极”的衰老状态。
但是,肌骨退变虽以肾虚为本,但脾胃为后天之本,气血生化之源,肾藏先天之精全赖后天之精充养。因此脾虚是肌骨退变的重要促进因素。《素问·痿论篇》“脾气热……肌肉不仁,发为肉痿,肾气热,则腰脊不举,骨枯而髓减,发为骨痿”。提示肉痿不仁、骨痿腰脊活动障碍等临床表现的根源在于脾肾功能失常。而且“脾主肌肉、四肢、治中央”“中央为土,病在脾,俞在脊”“脊居体中,故应土也”[50],提示脾虚是LDDD和椎旁肌减少症的共同促进因素。
《素问·脉要精微论篇》云:“腰者肾之府,转摇不能,肾将惫矣”[50],揭示LDDD导致的腰部活动障碍多为肾虚所致。《仁斋直指方论·腰》进一步阐释肾虚与腰痛的关系,指出“腰者,肾之外候……盖诸筋皆贯于肾而络于腰脊。肾气一虚……种种腰痛”[59]。《证治准绳·腰痛》曰:“有风、有湿……皆标也,肾虚其本也”[51],认为肾虚是腰痛的根本病机。
此外,关于腰脊、督脉与肾的关系,《医方考·痿痹门》中解释为“肾主督脉,督脉者,行于脊里,肾坏则督脉虚,故令腰脊不举”[60],强调肾主督脉,肾虚导致督脉虚是出现“腰脊不举”临床表现的病因。《医学衷中参西录·论腰疼治法》载“凡人之腰痛,皆脊梁处作痛,此实督脉主之……肾虚者,其督脉必虚,是以腰疼”[61]。进一步强调了肾亏督虚是腰痛的主要病因[62]。
脾与骨骼肌的生理关系在《素问·五藏生成篇》认为“脾之合肉也”[50]。张志聪注释并进一步阐释为“脾主运化水谷之精,以生养肌肉,故主肉”[63]。《四圣心源·卷一·天人解》曰:“肌肉者,脾土之所生也,脾气盛则肌肉丰满而充实”[64]。表明肌肉的盛壮全赖脾胃运化水谷充养。脾与四肢的生理关系在《素问·太阴阳明论篇》描述“四肢皆禀气于胃,而不得至经,必因于脾,乃得禀也”[50],《素问·阴阳应象大论篇》中云:“清阳实四肢”[50]。四肢为诸阳之本,人体四肢赖清阳充养,脾主升清,脾气健,清阳实,则四肢强健有力。
脾虚与肌少症的病理关系,《素问·藏气法时论篇》阐释为:“脾病者,身重善肌肉痿,足不收行”[50]。《局方发挥·卷二》总结为:“脾伤则四肢不能为用,而诸痿之病作”[65]。由此可见,肌肉萎软,身重无力的病因在于脾虚。脾虚导致肌少症的病机,《素问·太阴阳明论篇》解释为:“脾病不能为胃行其津液……筋骨肌肉,皆无气以生,故不用焉”[50]。脾胃虚弱,营卫气血生化乏源,故筋骨肌肉、关节经脉失养,肌肉羸弱,四肢不用[66]。
关于脾与脊柱的关系,古代医家分别从“五行”、经筋、脾胃的温养作用、脾肾失和的影响等多角度进行了阐释。《素问·太阴阳明论篇》云:“脾者,土也,治中央”[50]。《素问·金匮真言论篇》曰“中央为土,病在脾,俞在脊”,王冰解释为“脊居体中,故应土也”[50]。从“五行”理论可见脾脏与人体中轴——脊柱密切相关。
此外,经筋理论也揭示了脊柱与脾有密切关系。足阳明经筋“属脊”,足太阴经筋“著于脊”,手阳明经筋“挟脊”[67]。《素问·痿论篇》云:“阳明者……主润宗筋,宗筋主束骨而利机关也”[50]。提示骨骼肌、韧带和关节囊等宗筋的润养和束骨功能的发挥均有赖于脾胃。
脾胃对于骨骼肌和骨关节的温养作用在《灵枢·痈疽》中描述为“肠胃受谷,上焦出气,以温分肉,而养骨节”[10]。《灵枢·决气》“谷入气满,淖泽注于骨,骨属屈伸”则揭示了脾胃化生的精微物质灌输骨关节是保证其正常活动的物质基础[10]。《太平圣惠方·治脾胃气虚弱肌体羸瘦诸方》谓:“脾胃者,水谷之精,化为气血……润养身形,荣于肌肉也”[68]。清代医家周学海《读医随笔·气血精神论》云:“营气者,生于脾胃,以濡筋骨、肌肉、皮肤”[69],可见肌肉筋骨盛壮均赖脾胃、营气、水谷滋养,如脾胃内伤,水谷运化纳运失常,营气无以濡养肌肉、筋骨。
关于脾肾关系失调对骨关节的影响,李东垣在《脾胃论·脾胃盛衰论》指出:“脾病则下流乘肾,土克水则骨之无力,是为骨蚀,令人骨髓空虚,足不能履地”[70]。
虽然,古今医家认为肾虚是LDDD的主要病机,补肾治疗腰痛和LDDD已经成为共识。刘柏龄提出“治肾亦即治骨”的学术思想,辨证选用补肾活血中药治疗腰痛[71]。但是,古今医家同时强调补脾在治疗LDDD中的重要性。清·许豫和《怡堂散记·卷下》强调:“善补肾者,当于脾胃求之”[72]。《医门棒喝·虚损论》解释补肾治疗中补脾的原因是:“肾元亏损,禀质不足者,全赖脾胃生化以滋培”[73]。补肾的同时,兼顾补脾会增强补肾的效果[50]。因此,施杞制定了调和气血、健脾补肾填精治疗骨关节退变性疾病的治疗大法[74-76]。岳美中阐释脾肾的关系是先天与后天的关系。人始生,先成精,精旺而有脾胃;人衰老,肾精枯,累及诸脏,全赖脾胃吸收精微,滋养五脏,充养精气而祛病延年[77]。
补脾胃是治疗肌少症等“痿证”的主要治则[78-79]。脾胃为五脏六腑之海,濡养周身筋骨、肌肉,故《素问·痿论篇》强调了“治痿独取阳明”的基本治则。临床研究已证实八珍汤加减可通过健脾胃、补气血改善肌肉质量、力量、肌肉功能治疗肌少症[80-81]。但是,对于痿证的治疗,除重视脾胃外,还需根据虚实兼顾他脏他经。故《素问·痿论篇》对痿证治疗又补充了“各补其荥而通其俞,调其虚实,和其逆顺,筋脉骨肉,各以其时受月,则病已矣”的治疗理念[50]。脾的运化功能有赖于肾阳的温养,兼顾与痿证相关的经穴和脏腑,尤需补肾为重,现代医家认为治疗肌少症应脾肾并调[82]。所以在补脾的同时,应用补肾中药,以增强治疗效果。实验研究还发现补肾复方可通过调控肌肉铁死亡信号,改善肌少症模型小鼠表型,为肌少症的临床治疗提供了基础研究的支持[83]。
此外,中医将骨骼肌脂肪浸润称为“膏浊湿邪”,认为是脾虚生痰的病理产物。中医导引练功可“通其道,去其邪”,通过振奋脾肾阳气,使膏浊痰湿无法壅塞积聚,而让气血润养身形、荣于肌骨[84]。强调了锻炼在肌少症治疗中的重要性。
LDDD和椎旁肌减少症的共病状态、脾肾亏虚的病机决定了脾肾双补是其治疗大法。脾之运化功能有赖于肾阳温煦作用方可健旺,肾所藏精气亦需脾所运化精微物质营养方能充盛。《素问·逆调论篇》曰“肾不生则髓不能满”[50],可见补肾可充髓,髓满才能骨健。《灵枢·五癃津液别》曰:“五谷之津液,和合而为膏者,内渗入于骨空,补益脑髓”[10]。水谷充盈渗骨而益髓。《注解伤寒论·平脉法第二》述“脾合荣气,荣养骨髓,实肌肉,濡筋络”[85]。可见补益骨髓、荣养肌肉均需补益脾肾[86]。
古今治疗“虚劳”“痿证”“腰痛”实践均体现了脾肾双补的治则。张仲景治虚劳以补益脾肾为核心,如“虚劳诸不足,风气百疾,薯蓣丸主之。”[87]方中用薯蓣(山药)、熟地黄等补益脾肾。对于虚劳腰痛的治疗,“虚劳腰痛……八味肾气丸主之”[88],肾气丸中熟地黄、山药配伍少量附子、桂枝同温补脾肾[89]。现代数据挖掘研究痿证和腰痛治疗用药规律,也发现多以补益脾肾药物为核心药物的特点[90]。
LDDD和椎旁肌减少症的关系,目前现代医学研究尚处于在器官层面和临床上开展观察性研究的起始阶段,且二者相互关系和具体机制阐释还不全面。椎旁肌减少症尚无确切定义及系统评价手段和诊断标准。基于四肢骨骼肌质量、力量和功能评价的肌少症诊断、评定方法在LDDD和椎旁肌减少症共病研究中存在局限性。除了营养补充和抗阻运动,缺乏有效的治疗药物。中医有明确的“骨肉不相亲”理论、脾肾亏虚的病理机制、补益脾肾的治疗原则、“骨肉相保”的治疗目标,以及辨证中药和针灸导引等一系列的治疗方法,弥补了现代医学的不足,显示了广阔的发展前景。但中医存在真实世界的研究不足,缺少足够有力的说理证据、现代病理机制和治疗机制等研究不足等问题。亟待开展中西医结合研究,在中医肌骨理论的指导下,借助现代技术和设备,开展真实世界的研究,通过对椎旁肌的质量等进行调查来评估椎旁肌对脊柱的影响,明确椎旁肌减少症的概念,规范椎旁肌质量、力量和功能评定方法,制订诊断标准,并发现其与LDDD共病的微观机制,展开中医药治疗“肌少-LDDD”共病的循证医学研究,并阐释其作用机制。为进一步丰富中医理论,揭示共病机制,建立中医特色的诊疗方案,阐释中药疗效的机制,开发新药作出贡献。
  • 国家自然科学基金面上项目(82174398)
  • 国家自然科学基金青年科学基金项目(82305275)
  • 辽宁省教育厅科学技术研究青年项目(JYTQN2023456)
  • 辽宁省名中医传承工作室建设项目(辽中医药综合字〔2022〕12号)
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2025年第43卷第1期
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doi: 10.13193/j.issn.1673-7717.2025.01.019
  • 首发时间:2026-10-30
  • 出版时间:2025-01-10
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国家自然科学基金面上项目(82174398)
国家自然科学基金青年科学基金项目(82305275)
辽宁省教育厅科学技术研究青年项目(JYTQN2023456)
辽宁省名中医传承工作室建设项目(辽中医药综合字〔2022〕12号)
作者信息
    1.辽宁中医药大学,辽宁 沈阳 110847
    2.辽宁中医药大学附属医院,辽宁 沈阳 110032

通讯作者:

姚啸生(1969-),男,辽宁沈阳人,教授,博士研究生导师,博士,研究方向:中医药防治椎间盘退变及骨质疏松症。Email:。
郑洪新(1952-),女,辽宁沈阳人,教授,博士研究生导师,博士,研究方向:中医藏象理论及应用。E-mail:。
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2种不同金属材料的力学参数
科
Family
属数
Number of
genus
种数
Number of
species
占总种数比例
Percentage of
total species (%)
属
Genus
种数
Number of
species
占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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