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*

Numerous musculoskeletal disorders are caused by thickened ligament, tendon stiffness, or fibrosis of joint capsule. Relaxin, a peptide hormone, can exert collagenolytic effect on ligamentous and fibrotic tissues. We hypothesized that local injection of relaxin could be used to treat entrapment neuropathy and adhesive capsulitis. Because hormonal effect depends on the receptor of the hormone on the target cell, it is important to confirm the presence of such hormonal receptor at the target tissue before the hormone therapy is initiated. The aim of this study was to determine whether there were relaxin receptors in the ligament, tendon, and joint capsular tissues of rats and to identify the distribution of relaxin receptors in these tissues. Transverse carpal ligaments (TCLs), inguinal ligaments, anterior cruciate ligaments (ACLs), Achilles tendons, and shoulder joint capsules were obtained from male Wistar rats. Western blot analysis was used to identify relaxin receptor isoforms RXFP1 and RXFP2. The distribution of relaxin receptors was determined by immunohistochemical staining. The RXFP1 isoform was found in all tissues examined. The RXFP2 isoform was present in all tissues but the TCLs. Its expression in ACLs tissues was relatively weak compared to that in other tissues. Our results revealed that RXFP1 and RXFP2 were distributed in distinctly different patterns according to the type of tissue (vascular endothelial cells, fibroblast-like cells) they were identified.
Animals ; Blotting, Western ; *Gene Expression Regulation ; Immunohistochemistry ; Ligaments/*metabolism ; Male ; Rats ; Rats, Wistar ; Receptors, G-Protein-Coupled/*genetics/metabolism ; Receptors, Peptide/*genetics/metabolism ; Shoulder Joint/*metabolism ; Tendons/*metabolism

The term tumoral calcinosis in used to describe the deposition of nodular calcareous masses in the soft tissue around large joints, such as the hips, shoulders, and elbows. Although the cause has not yet been clearly determined, according to the hypothesis, failure of phosphorus metabolism in the proximal tubule in kidney, chronic renal disease and hyperparathyroidism may cause tumoral calcinosis. No cases of tumoral calcinosis treated with surgical resection in chronic renal failure patients on hemodialysis, so called uremic tumoral calcinosis, have been reported in Korea. The authors experienced the case of a 57-year-old woman with chronic kidney disease on hemodialysis who presented with a mass around the hip. We made a diagnosis using plain radiographs, magnetic resonance imaging, and computed tomography of tumoral calcinosis, and treated the patient successfully with surgical resection. We report on a case of uremic tumoral calcinosis with a review of the literature.
Calcinosis* ; Diagnosis ; Elbow ; Female ; Hip ; Hip Joint* ; Humans ; Hyperparathyroidism ; Joints ; Kidney ; Kidney Failure, Chronic ; Korea ; Magnetic Resonance Imaging ; Metabolism ; Middle Aged ; Phosphorus ; Renal Dialysis* ; Renal Insufficiency, Chronic ; Shoulder

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

Necrotizing fasciitis (NF) is a deep infection of the subcutaneous tissue that progressively destroys fascia and fat; it is associated with systemic toxicity, a fulminant course, and high mortality. NF most frequently develops from trauma that compromises skin integrity, and is more common in patients with predisposing medical conditions such as diabetes mellitus, atherosclerosis, alcoholism, renal disease, liver disease, immunosuppression, malignancy, or corticosteroid use. Most often, NF is caused by polymicrobial pathogens including aerobic and anaerobic bacteria. NF caused by Staphylococcus aureus as a single pathogen, however, is rare. Here we report a case of NF that developed in a healthy woman after an isolated shoulder sprain that occurred without breaking a skin barrier, and was caused by Staphylococcus aureus as a single pathogen.
*Arm ; Coagulase/metabolism ; Fasciitis, Necrotizing/*etiology/microbiology/pathology/surgery ; Female ; Humans ; Middle Aged ; Shoulder Joint/*injuries ; Sprains and Strains/*complications ; Staphylococcal Infections/*etiology/microbiology ; Staphylococcus aureus/enzymology/isolation & purification

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is a disease of the elderly and extremely rare in young individuals. If young people develop CPPD crystal deposition disease, it may be associated with metabolic diseases such as hemochromatosis, hyperparathyroidism, hypophosphatasia, hypomagnesemia, Wilson's disease, hypothyroidism, gout, acromegaly, and X-linked hypophosphatemic rickets. Therefore, in young-onset polyarticular CPPD crystal deposition disease, investigation for predisposing metabolic conditions is warranted. We report a case of a young male patient with idiopathic CPPD crystal deposition disease, who did not have any evidences of metabolic diseases after thorough evaluations. As far as we know, this is the first report of a young male patient presented with idiopathic CPPD crystal deposition disease.
Adult ; Calcium Pyrophosphate/*metabolism ; Cartilage, Articular/metabolism/pathology ; Diagnosis, Differential ; Human ; Knee Joint/*pathology ; Male ; Metabolic Diseases/metabolism/pathology ; Shoulder Joint/pathology