[Isolated biceps tenodesis by double row for pulley lesions].

Objective: To explore clinical outcome of isolated arthroscopic biceps tenodesis by double row for pulley lesions. Methods: Forty-nine patients with pulley lesions were treated from July 2017 to June 2018 in the Department of Sport Medicine, the Affiliated Zhongshan Hospital of Dalian University by isolated arthroscopic biceps tenodesis by double row. Patients were divided into 2 groups according to the intraoperative damage of the pulley system. In group A, there were 16 patients with isolated superior glenohumeral ligament/coracohumeral ligament (SGHL/CHL) complex lesions, including 9 males and 7 females, aged (55±6) years. In group B, there were 33 patients (15 males and 18 females, aged (57±8) years) with SGHL/CHL complex and adjacent supraspinatus tendon and/or subscapularis tendon articular-side partly tears. Patients in two groups were treated with different isolated arthroscopic biceps tenodesis by double row. Constant-Murley shoulder score and pain visual analogue scale (VAS) score were assessed before operation and 3, 6, 12 months after the operation. Postoperative complications were also recorded in two groups. The t test was used to compare the quantitative data within and between two groups. Results: All 49 patients were followed up for 12 to 24 months with an average of (17±6) months. The first-stage healing was achieved in all incisions in the two groups. No surgical complications related to revision, infection, Popeye syndrome and cramping pain were observed in either group. There was 1 case treated by secondary arthroscopy for retrauma in group B. The Constant-Murley shoulder score in group A before the operation was 46±10, and it was increased to 89±9 at the 12 months post operation(t=-22.637, P<0.05); and it was 39±10 and 87±8 before and 12 months after the operation respectively in group B (t=-44.849, P<0.05). The VAS scores in the two groups were both decreased significantly at the 12 months post operation when compared with those before the operation (0.68±0.70 vs 5.25±0.27 and 0.72±0.83 vs 5.69±0.84, respectively) (t=29.007, 37.079, both P<0.05). Conclusion: Isolated arthroscopic biceps tenodesis by double row can relieve pain, recover functions of shoulder joint effectively, and achieve a satisfactory outcome in the treatment of pulley lesions.

SIRT2 inhibits oxidative stress and inflammatory response in diabetic osteoarthritis.

OBJECTIVE: Diabetes mellitus is involved in inflammation, immunity, and metabolism during osteoarthritis (OA). It destroys the normal synthesis and degradation balance of chondrocytes (CHs) and extracellular matrix (ECM). The purpose of this study was to explore the possible way of SIRT2 influencing the progress of diabetic OA. PATIENTS AND METHODS: Proteins of diabetic OA and normal OA cartilage samples were extracted from patients undergoing knee joint operation. CHs were also isolated from the cartilage exempted from diabetes for cell culture. Glucose was used to treat CHs for imitating the microenvironment of diabetes. The expressions of SIRT2, acetylated H3K9, H3K14, and H3K56 protein were determined by Western blotting. SIRT2, 8-hydroxy-2' deoxyguanosine (8-OH), and MMP-13 expressions were analyzed using immunofluorescence. RT-PCR was performed to measure the mRNA levels of SOD1, SOD2, CAT, MMP-13, ADAMTS-4, and ADAMTS-5. Total ROS level was performed by flow cytometry assay. RESULTS: SIRT2 expression was reduced, whereas acetylated H3K9, H3K14, and H3K56 were upregulated in diabetic cartilage compared to normal. High glucose suppressed the expression of SIRT2 but accelerated the acetylation of H3K9, H3K14, and H3K56. Besides, high glucose promoted the expression of 8-OH, and inhibited SOD1, SOD2, and CAT mRNA expressions, resulting in the up-regulated ROS level of CHs. In addition, high glucose activated the inflammatory response by upregulation of MMP-13, ADAMTS-4, and ADAMTS-5 expressions. SirReal2 suppressed SIRT2 and resulted in several acetylations of H3, more ROS, less antioxidant enzymes, and stronger inflammatory response caused by high glucose. However, supplied rh-SIRT2 reversed these negative effects of high glucose in CHs. CONCLUSIONS: SIRT2 expression is reduced along with the diabetic OA process with increased acetylation of H3, oxidative stress, and inflammatory response. Suppression of SIRT2 accelerates the progress of diabetic OA and upregulation of SIRT2 alleviates diabetic OA development by suppressing oxidative stress and inflammatory response that are likely to be related to the deacetylation of H3.