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.
Humans ; Joint Capsule/metabolism* ; Shoulder Dislocation/metabolism* ; Recurrence ; Shoulder Joint/metabolism* ; Tenascin/metabolism* ; Transforming Growth Factor beta1/genetics* ; Collagen Type I/genetics* ; Extracellular Matrix/metabolism*

BACKGROUNDShoulder immobilization can induce adhesion of the joint, capsular contracture or lead to the condition of frozen shoulder. However, little is known about the histological effects of immobilization on the shoulder joint. This study aimed to explore the effect of immobility on the subscapular bursa (SSB) and the joint capsular content, including the distribution of types I and III collagen, within an immobilized rat shoulder.

METHODSForty-six Sprague-Dawley rats were randomly divided into one control group (n = 6) and four immobilization groups (n = 10 in each group), in which the left shoulders were immobilized with plaster for 1, 2, 3 and 4 weeks. At the end of each time point, 2 rats from each group were euthanized and shoulders prepared for serial histological observations of the glenohumeral joints, as well as picrosirius red and immunohistochemical observation of type III collagen. Histological sections of the remaining rat shoulders were used for the immunohistochemical detection of the capsular content of types I and III collagen.

RESULTSThe hyperplastic synovium of the anterior capsule obstructed the communication between the SSB and the glenohumeral joint cavity at 2 and 3 weeks. The adhesion of the SSB appeared at 3 and 4 weeks. The quantitative and qualitative results showed that the capsular contents of types I and III collagen progressively increased at 2, 3 and 4 weeks, and that type III collagen was distributed extensively within the joint capsule at 2 and 3 weeks.

CONCLUSIONImmobilization of the rat shoulder induced synovial hyperplasia of the joint capsule, adhesion of the SSB and an increase of the capsular content of types I and III collagen.

Animals ; Collagen ; metabolism ; Disease Models, Animal ; Immunohistochemistry ; Joint Capsule ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Shoulder Dislocation ; metabolism ; pathology ; Shoulder Joint ; metabolism ; pathology

OBJECTIVEThis study examined the distribution and expression of transforming growth factor-ß₂ (TGF-ß₂) in the hip capsule of children with developmental dysplasia (dislocation) of the hip (DDH) and non-DDH children in order to investigate the roles of TGF-ß₂ in hip joint laxity.

METHODSEight children with DDH and eight age- and gender-matched non-DDH children (control group) were enrolled. The immunohistochemical technique (S-P method) was used to examine the distribution and content of TGF-ß₂ in the hip capsule. Semiquantitative RT-PCR method was used to detect mRNA expression of TGF-ß₂ in the hip capsule. The quantitative analysis of TGF-ß₂ was performed by professional image software.

RESULTSA high expression of TGF-ß₂ was observed in the synovial layer with fibroblast regularly arranged parallel to the joint surface. There was decreased expression of TGF-ß₂ in the fibrous layer of the capsule. The percentage of positive fibroblasts and the gray-scale density in the fibrous layer in the DDH group were significantly lower than those in the control group (P < 0.01). TGF-ß₂ mRNA expression in the DDH group decreased compared with that in the control group (P < 0.05).

CONCLUSIONSThe decreased TGF-ß₂ in distribution, content and mRNA expression in the hip capsule might contribute to hip joint laxity in children with DDH.

Child ; Child, Preschool ; Female ; Hip Dislocation, Congenital ; metabolism ; Hip Joint ; chemistry ; Humans ; Immunohistochemistry ; Infant ; Joint Capsule ; chemistry ; Male ; RNA, Messenger ; analysis ; Reverse Transcriptase Polymerase Chain Reaction ; Transforming Growth Factor beta2 ; analysis ; genetics