No abstract

These results suggest that, in addition to up-regulation of TIMP-1 gene expression, increased MMP-3 gene expression in ruptured rotator cuff tendons is associated with postoperative tendon retear. Thus, drug therapy specifically targeting MMP-3 after rotator cuff repair should be considered in the future.

Corticosteroids (CS) or hyaluronic acid (HA) is used in subacromial injection for the conservative treatment of rotator cuff tears (RCT); this study addresses the question of how CS and HA affect the tendon tissue and fibroblasts in vitro and in rats. Cell proliferation assays were performed in human tendon fibroblasts from RCT. Rats underwent surgery to create RCT, and the surgical sites were injected with CS or HA. The rotator cuff tendons were subjected to biomechanical testing, microscopic and immunohistochemical analysis of proliferating cell nuclear antigen (PCNA), and ultrastructural analysis. Cell proliferation was significantly decreased with CS in vitro (p < 0.05). Maximal load of CS-treated tendons was significantly decreased compared with that of HAtreated tendons (p < 0.05), as well as PCNA þ cells at 2 weeks (p < 0.05). Ultrastructural observations of the CS-treated rats detected apoptosis of tendon fibroblasts 24 h after surgery. Histological and biomechanical data 4 weeks after surgery were not significant among the three groups. Unlike HA, CS caused cell death, and inhibition of the proliferation of tendon fibroblasts, leading to a delay of tendon healing involved and a subsequent decrease of biomechanical strength at the surgical site. Keywords: tendon; corticosteroids; hyaluronic acids; totator cuff tears; tendon fibroblast Rotator cuff tears (RCT) occur in the middle-aged and elderly people and cause severe shoulder pain. The prevalence of RCT ranges from 5% to 40% in the general population, 1 increasing linearly with age from the third decade. [2][3][4] In clinical settings, initial treatment of RCT to alleviate shoulder pain and restore shoulder function employs subacromial injection of corticosteroids (CS), administration of nonsteroid antiinflammatory drugs, and physical therapy.

BackgroundThere is growing evidence that adiponectin, a physiologically active polypeptide secreted by adipocytes, controls not only adipose tissue but also bone metabolism. However, a role for adiponectin in bone development remains controversial.MethodsWe therefore investigated the endocrine effects of adiponectin on bone metabolism using 12-week-old male transgenic (Ad-Tg) mice with significant hyperadiponectinemia overexpressing human full-length adiponectin in the liver.ResultsIn Ad-Tg mice, the serum level of osteocalcin was significantly increased, but the levels of RANKL, osteoprotegerin, and TRAP5b were not. Bone mass was significantly greater in Ad-Tg mice with increased bone formation. In contrast, bone resorption parameters including the number of osteoclasts and eroded surface area did not differ between Ad-Tg and their littermates.ConclusionsThese findings demonstrate that hyperadiponectinemia enhances bone formation in mice.

There is a growing body of evidence supporting the use of hyaluronan (HA) in patients with adhesive capsulitis of the shoulder, although the mechanisms of the effect have not yet been clarified. This in vitro study examined the effects of HA on glenohumeral synovial/ capsular fibroblasts (GSCFs) from patients with adhesive capsulitis of the shoulder. The study subjects were seven patients with primary or secondary adhesive capsulitis of the shoulder (average age: 55 years; range: 42-65). Synovial/capsular specimens were obtained from the rotator interval of each patient during arthroscopy. Part of the tissue specimen was used for histological analysis. The remainder of the tissue was prepared for cell culture. Various concentrations of HA (0.0-4.0 mg/mL) were added to the monolayer-cultured GSCFs from these patients. Histological analysis consistently demonstrated chronic nonspecific inflammation with synovial hyperplasia, proliferation of vessels and fibroblasts, and increased amount of extracellular matrix. Treatment with HA at various concentrations significantly and dose-dependently inhibited cell proliferation and decreased the expression levels of mRNA for adhesion-related procollagens and cytokines. Pretreatment with OS/37 did not reverse the inhibitory effect of HA. These results suggest that HA modulates cell proliferation and expression of the mRNA of adhesion-related procollagens and cytokines in GSCFs, preventing the progression of adhesion formation in patients with adhesive capsulitis of the shoulder. ß