[Research progress on pathological changes of glenohumeral capsule in patients with recurrent shoulder anterior dislocation].

Q3 Medicine
Pai Chen, Daqiang Liang, Bing Wu, Hao Li, Haifeng Liu, Zeling Long, Yuwei Liu, Wei Lu
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引用次数: 0

Abstract

Objective: To review the research progress of pathological changes of glenohumeral capsule in patients with recurrent shoulder anterior dislocation (RSAD).

Methods: The literature on shoulder capsules, both domestic and international, was reviewed. The anatomy, histology, and molecular biology characteristics of the glenohumeral capsule in RSAD patients were summarized.

Results: Anatomically, the glenohumeral capsule is composed of four distinct parts: the upper, lower, anterior, and posterior sections. The thickness of these sections is uneven, and the stability of the capsule is further enhanced by the presence of the glenohumeral and coracohumeral ligaments. Histologically, the capsule tissue undergoes adaptive changes following RSAD, which improve its ability to withstand stretching and deformation. In the realm of molecular biology, genes associated with the regulation of structure formation, function, and extracellular matrix homeostasis of the shoulder capsule's collagen fibers exhibit varying degrees of expression changes. Specifically, the up-regulation of transforming growth factor β 1 (TGF-β 1), TGF-β receptor 1, lysyl oxidase, and procollagen-lysine, 2-oxoglutarate 5-dioxygenase 1 facilitates the repair of the joint capsule, thereby contributing to the maintenance of shoulder joint stability. Conversely, the up-regulation of collagen type Ⅰ alpha 1 (COL1A1), COL3A1, and COL5A1 is linked to the recurrence of shoulder anterior dislocation, as these changes reflect the joint capsule's response to dislocation. Additionally, the expressions of tenascin C and fibronectin 1 may play a role in the pathological processes occurring during the early stages of RSAD.

Conclusion: Glenohumeral capsular laxity is both a consequence of RSAD and a significant factor contributing to its recurrence. While numerous studies have documented alterations in the shoulder capsule following RSAD, further research is necessary to confirm the specific pathological anatomy, histological, and molecular biological changes involved.

[复发性肩关节前脱位患者肩关节囊病理改变的研究进展]。
目的:综述复发性肩前脱位(RSAD)患者肩关节囊病理变化的研究进展。方法:回顾国内外有关肩囊的文献。综述了RSAD患者肩胛囊的解剖、组织学和分子生物学特征。结果:解剖上,盂肱囊由四个不同的部分组成:上、下、前、后部分。这些部分的厚度是不均匀的,肩胛韧带和肩胛韧带的存在进一步增强了囊的稳定性。组织学上,RSAD后囊组织发生适应性变化,提高了其承受拉伸和变形的能力。在分子生物学领域,与肩囊胶原纤维的结构形成、功能和细胞外基质稳态调控相关的基因表现出不同程度的表达变化。其中,转化生长因子β 1 (TGF-β 1)、TGF-β受体1、赖氨酸氧化酶和前胶原-赖氨酸、2-氧葡萄糖酸酯5-双加氧酶1的上调促进了关节囊的修复,从而有助于维持肩关节的稳定性。相反,胶原型Ⅰα 1 (COL1A1)、COL3A1和COL5A1的上调与肩关节前脱位的复发有关,因为这些变化反映了关节囊对脱位的反应。此外,腱素C和纤维连接蛋白1的表达可能在RSAD早期发生的病理过程中发挥作用。结论:盂肱关节囊松弛既是RSAD的后果,也是导致其复发的重要因素。虽然许多研究已经记录了RSAD后肩关节囊的改变,但需要进一步的研究来证实具体的病理解剖、组织学和分子生物学变化。
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来源期刊
中国修复重建外科杂志
中国修复重建外科杂志 Medicine-Medicine (all)
CiteScore
0.80
自引率
0.00%
发文量
11334
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