腰椎间盘突出症发病机制研究进展

Research Progress on the Pathogenesis of Lumbar Disc Herniation

摘要: 腰椎间盘突出症(LDH)是指由腰椎间盘因素引发的腰腿痛综合征，其发病机制复杂，临床可见影像学表现与症状严重程度相分离的现象，单一学说难以完整解释其发病过程。本文以椎间盘退变为始动环节，将LDH相关机制研究归纳为两个层面：致病机制层面包括机械压迫学说、炎性反应学说与自身免疫学说，共同解释腰腿痛(尤其是神经根性疼痛)的产生；转归机制层面以突出物重吸收为核心，反映机体的自我修复与清除能力。同时，本文补充介绍了细胞衰老、自噬功能障碍、表观遗传学调控以及神经炎症、中枢敏化等方面的近期进展。笔者检索近年来国内外研究文献，对业内有关LDH的研究现状及主流发病学说进行总结。现有证据提示，在椎间盘退变基础上，突出物可对神经根产生物理压迫、化学致炎及免疫损伤而致痛，同时机体可通过重吸收进行自我修复；推拿等非手术疗法可能通过调整椎间隙与突出物–神经根相对位置、下调促炎因子并上调抗炎因子等环节干预上述过程，从而缓解腰腿痛症状，但上述作用机制目前多属假说或初步探索：相关研究多为小样本、单中心的临床疗效观察，缺乏假推拿对照与盲法评估，证据等级有限；其对重吸收微环境的调控作用尚属推测，缺乏以MRI和血清标志物为客观终点的验证。系统认识上述机制及其交互网络，有助于阐明推拿可能的起效环节，为优化治疗方案及后续验证性研究设计提供依据。

Abstract: Lumbar disc herniation (LDH) is a syndrome of low back and leg pain caused by lumbar intervertebral disc-related factors. Its pathogenesis is complex; clinically, imaging findings and symptom severity may be dissociated, and no single theory can fully explain its onset. Taking intervertebral disc degeneration as the initiating factor, this review categorizes the mechanisms of LDH into two levels: pathogenic mechanisms (mechanical compression, inflammatory response, and autoimmune injury), which jointly explain the generation of pain, and regression mechanisms (spontaneous resorption of herniated material), which reflect the body’s self-repair. Recent advances in cellular senescence, autophagy dysfunction, epigenetic regulation, neuroinflammation, and central sensitization are also summarized. By reviewing recent domestic and international literature, this article summarizes the current research status and mainstream pathogenetic theories of LDH. Current evidence suggests that, on the basis of disc degeneration, the herniated material may cause pain through physical compression, chemical inflammation, and immune injury of the nerve root, while the body may achieve self-repair through resorption. Non-surgical therapies such as Tuina may alleviate low back and leg pain by adjusting the intervertebral space and the relative position between the herniated material and the nerve root, and by downregulating pro-inflammatory and upregulating anti-inflammatory cytokines; however, these mechanisms remain largely hypothetical. Current evidence derives mainly from small-sample, single-center clinical observations without sham controls or blinded assessment, with limited evidence quality; their regulatory effect on the resorption microenvironment remains speculative and lacks validation with objective endpoints such as MRI and serum biomarkers. A systematic understanding of these mechanisms and their interplay will help clarify the putative mechanistic steps underlying Tuina and provide a basis for optimizing treatment strategies and designing confirmatory studies.