Blood supply of the subacromial bursa and rotator cuff tendons on the bursal side.

PURPOSE: Vascularity of the subacromial bursa and rotator cuff tendons is key factors in the pathogenesis of subacromial bursitis and impingement syndrome, rotator cuff tendinitis, and rotator cuff tears. The purpose of this study was to investigate and describe blood supply to the cranial and caudal parts of the subacromial bursa and the vascularity of the rotator cuff tendons on the bursal side. METHODS: Fourteen fresh cadaveric shoulders from six females and eight males with a mean age of 71.7 (±10.8) years were studied. Before dissection, an arterial injection of 10% aqueous dispersion of latex was administered. Post-injection, the shoulders were fixed in an alcohol-formalin-glycerol solution. RESULTS: The cranial and caudal bursa of all specimens was mainly supplied by the thoracoacromial, suprascapular, and anterior and posterior circumflex humeral arteries. The cranial part of the bursa was supplied anteriorly by the thoracoacromial artery, and posteriorly and medially by the posterior circumflex humeral artery as far as the medial third. The caudal part received arterial blood anteriorly from the anterior circumflex humeral artery, and posteriorly and medially by the posterior circumflex humeral artery as far as the medial third of the caudal bursa. In addition, the suprascapular artery branched at the upper surface of the coracohumeral ligament, and the subcoracoid artery branched at the under surface of the same ligament. CONCLUSION: The subacromial bursa appears well vascularized. The results of the present investigation showed that blood supply to the subacromial bursa at the caudal part and rotator cuff tendons on the bursal side was linked to the same arteries. The subcoracoid artery supplied interval rotator structures close to the caudal bursa. It is the wish of the authors that this meticulous anatomical work will help surgeons in their day-to-day clinical work, e.g. to minimize the risk of complications such as perioperative bleeding.

Intrabursal vein abrasion and thrombosis. An unusual complication of femoral osteochondroma.

A 21-year-old female with right distal femoral pedunculated osteochondroma is presented. She was admitted for severe lower limb pain, and swelling of one week duration. Clinical findings supported deep vein thrombosis (DVT) but Doppler ultrasound, and venography were normal. Surgical exploration revealed a large bursa around the tumor with a big vein abraded and thrombosed inside the bursa.

Involvement of the subacromial bursa in impingement syndrome of the shoulder as judged by expression of tenascin-C and histopathology.

Our aim was to evaluate bursal involvement at different stages of the impingement syndrome as judged by conventional histopathological examination and expression of tenascin-C, which is known to reflect active reparative processes in different tissues and disorders. Samples of subacromial bursa were taken from 33 patients with tendinitis, 11 with a partial tear and 18 with a complete tear of the rotator cuff, and from 24 control shoulders. We assessed the expression of tenascin-C, the thickness of the bursa, and the occurrence and degree of fibrosis, vascularity, haemorrhage and inflammatory cells. The expression of tenascin-C was significantly more pronounced in the complete tear group (p < 0.001) than in the partial tear, tendinitis or control groups. It was more pronounced in the tendinitis group than in the control group (p = 0.06), and there was more fibrosis in all the study groups than in the control group. The changes in the other parameters were not equally distinctive. Expression of tenascin-C did not correlate with the conventional histopathological parameters, suggesting that these markers reflect different phases of the bursal reaction. Tenascin-C seems to be a general indicator of bursal reaction, being especially pronounced at the more advanced stages of impingement and this reaction seems to be an essential part of the pathology of impingement at all its stages.

The fibular collateral ligament-biceps femoris bursa. An anatomic study.

The anatomy of the fibular collateral ligament-biceps femoris bursa is described. The bursa is located lateral to the distal quarter of the fibular collateral ligament and forms an inverted "J" shape around the anterior and anteromedial portions of the ligament. Its most distal margin is just proximal to the fibular head where the fibular collateral ligament inserts, and its more proximal aspect is at the superior edge of the anterior arm of the long head of the biceps femoris muscle. We found this structure in all 50 knees dissected; there was a constant anatomic location of the fibular collateral ligament-biceps femoris bursa in all specimens. Measurement of the anatomic dimensions of the bursa revealed a mean width of 8.4 mm and a mean height of 18 mm. Knowing the prevalence, shape, size, and anatomic location of this bursa may aid the clinician in the differential diagnosis of lateral knee pain.

Immunolocalization of cytokines and their receptors in adhesive capsulitis of the shoulder.

The purpose of this study was to test the hypothesis that specific cytokines are involved in the initiation and evolution of the fibrotic process in adhesive capsulitis of the shoulder. After approval from the Institutional Review Board, biopsies of shoulder capsule and synovium were collected during shoulder arthroscopy from 19 patients with adhesive capsulitis, 14 patients with nonspecific synovitis and no fibrosis or clinical evidence of adhesive capsulitis, and seven patients undergoing surgery for another pathology who had a normal capsule and synovium. Immunohistochemical localization with monoclonal antibodies to transforming growth factor-beta and its receptor, platelet-derived growth factor and its receptor, basic fibroblast growth factor, interleukin-1 beta, tumor necrosis factor-alpha, and hepatocyte growth factor was performed using standard immunoperoxidase techniques. The frequency of cytokine staining was correlated with the clinical diagnosis. Synovial cells, fibroblasts, T-cells, and B-cells were identified with specific antibodies, and newly synthesized matrix was examined for type-I and type-III collagen by immunohistochemical staining. The predominant cell types present were synovial cells and fibroblasts. Staining for type-III collagen in adhesive capsulitis tissues indicated new deposition of collagen in the capsule. There was staining for transforming growth factor-beta and its receptor, platelet-derived growth factor and its receptor, interleukin-1 beta, and tumor necrosis factor-alpha in adhesive capsulitis and nonspecific synovitis tissues, compared with minimal staining in normal capsule. Staining was more frequent in synovial cells than in capsular cells. The frequency of cell and matrix staining for transforming growth factor-beta, platelet-derived growth factor, and hepatocyte growth factor was greater in adhesive capsulitis tissues than in those from patients with nonspecific synovitis. No difference in the frequency of staining between primary (idiopathic) and secondary adhesive capsulitis was found. The results of this study indicate that adhesive capsulitis involves both synovial hyperplasia and capsular fibrosis. Cytokines such as transforming growth factor-beta and platelet-derived growth factor may be involved in the inflammatory and fibrotic processes in adhesive capsulitis. Matrix-bound transforming growth factor-beta may act as a persistent stimulus, resulting in capsular fibrosis. Understanding the basic pathophysiology of adhesive capsulitis is an important step in the development of clinically useful antifibrotic agents that may serve as novel treatments for patients with this conditions.