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1.天津中医药大学 第一附属医院,天津 300381
2.国家中医针灸临床医学研究中心,天津 300381
3.天津中医药大学,天津 301617
4.天津中医药研究院附属医院,天津 300120
Received:02 July 2025,
Revised:2025-09-10,
Accepted:10 September 2025,
Online First:11 September 2025,
Published:20 May 2026
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郭小静,丁久力,孙宏源等.病络理论视角下类风湿关节炎与牙周炎共病关系探析[J].中国实验方剂学杂志,2026,32(10):280-287.
GUO Xiaojing,DING Jiuli,SUN Hongyuan,et al.Analysis of Rheumatoid Arthritis and Periodontitis Multimorbidity from Perspective of Abnormal Collateral Theory[J].Chinese Journal of Experimental Traditional Medical Formulae,2026,32(10):280-287.
郭小静,丁久力,孙宏源等.病络理论视角下类风湿关节炎与牙周炎共病关系探析[J].中国实验方剂学杂志,2026,32(10):280-287. DOI: 10.13422/j.cnki.syfjx.20251741.
GUO Xiaojing,DING Jiuli,SUN Hongyuan,et al.Analysis of Rheumatoid Arthritis and Periodontitis Multimorbidity from Perspective of Abnormal Collateral Theory[J].Chinese Journal of Experimental Traditional Medical Formulae,2026,32(10):280-287. DOI: 10.13422/j.cnki.syfjx.20251741.
类风湿关节炎(RA)与牙周炎(PD)共病的现象日益受到关注,均以慢性炎症、免疫失衡与进行性骨破坏为特征。现代研究证实PD是RA发病的重要危险因素,且二者共存时互相加重病情。然目前中医理论对此复杂共病关系尚缺乏系统解释。研究基于中医学“病络”理论,深入剖析RA与PD共病的内涵,提出“病络为枢、蕴毒蚀骨”为其核心中医病机。研究阐释PD作为“病络之始”,其病原体作为毒邪循络入节,通过分子模拟等机制诱发RA。RA与PD共病的动态病理演变过程:营卫倾移在微观层面的体现为免疫异常活化,导致络脉不荣;热毒循络引发络道亢变,使得病理性血管生成;最终于病络枢纽处蕴毒蚀骨,激活核因子
κ
B受体活化因子配体(RANKL)/核因子
κ
B受体活化因子(RANK)信号通路驱动的破骨细胞分化。该理论框架创新性地整合口腔微生物、免疫炎症及骨代谢等现代发现,为理解共病的复杂性提供整体动态新视角。鉴于现有牙周治疗对RA疗效存在局限及中医复方干预共病报道较少,依据病络理论,提出“以络统病、以药调络”的系统干预思路,提出“通络、清络、荣络”的中医策略。并列举治疗共病的潜在中药,未来应聚焦完善共病患者中医证候学特征,借助组学技术深入探索,为中医药应对多病共存状态提供理论依据与研究方向。
The multimorbidity of rheumatoid arthritis (RA) and periodontitis (PD) has drawn increasing attention, as both conditions are characterized by chronic inflammation, immune dysregulation, and progressive bone destruction. Modern research confirms that PD is a significant risk factor for RA development, and their coexistence mutually exacerbates disease progression. However, traditional Chinese medicine (TCM) currently lacks a systematic theoretical explanation for this complex multimorbid relationship. This study, based on the TCM theory of abnormal collateral, thoroughly examines the intrinsic connection between RA and PD multimorbidity, proposing "abnormal collateral as the pivot, with accumulated toxins eroding bone" as the core TCM pathogenesis. The research elucidates PD as the "origin of abnormal collateral", where its pathogens act as toxic factors that invade the joints through collaterals, triggering RA via mechanisms such as molecular mimicry. The dynamic pathological progression of RA-PD multimorbidity can be described as follows: the displacement of Ying and Wei at the microscopic level manifests as immune hyperactivation, leading to collateral malnutrition; heat-toxins traversing collaterals induce collateral hyperactivity, resulting in pathological angiogenesis; ultimately, toxin accumulation at the pivotal abnormal collateral site erodes bone, activating the receptor activator of nuclear factor kappa-B ligand (RANKL)-receptor activator of nuclear factor kappa-B (RANK) signaling pathway-driven osteoclast differentiation. This theoretical framework innovatively integrates modern findings in oral microbiology, immune-inflammation, and bone metabolism, offering a holistic and dynamic perspective to understand the complexity of multimorbidity. Given the limited efficacy of current periodontal treatments for RA and the scarcity of reported TCM compound interventions for multimorbidity, the abnormal collateral theory proposes a systematic intervention strategy centered on "governing diseases through collaterals and regulating collaterals with herbs", along with TCM therapeutic principles such as "unblocking, clearing, and nourishing collaterals". Potential herbal treatments for multimorbidity are also highlighted. Future research should focus on refining TCM syndrome patterns in multimorbid patients and leveraging omics technologies for deeper exploration, thereby providing a theoretical foundation and research direction for TCM in addressing complex multimorbid conditions.
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