The morphological and immunocytochemical features of impingement syndrome and partial-thickness rotator-cuff tear in relation to outcome after subacromial decompression.

We assessed the predictive value of the macroscopic and detailed microscopic appearance of the coracoacromial ligament, subacromial bursa and rotator-cuff tendon in 20 patients undergoing subacromial decompression for impingement in the absence of full-thickness tears of the rotator cuff. Histologically, all specimens had features of degenerative change and oedema in the extracellular matrix. Inflammatory cells were seen, but there was no evidence of chronic inflammation. However, the outcome was not related to cell counts. At three months the mean Oxford shoulder score had improved from 29.2 (20 to 40) to 39.4 (28 to 48) (p < 0.0001) and at six months to 45.5 (36 to 48) (p < 0.0001). At six months, although all patients had improved, the seven patients with a hooked acromion had done so to a less extent than those with a flat or curved acromion judged by their mean Oxford shoulder scores of 43.5 and 46.5 respectively (p = 0.046). All five patients with partial-thickness tears were within this group and demonstrated less improvement than the patients with no tear (mean Oxford shoulder scores 43.2 and 46.4, respectively, p = 0.04). These findings imply that in the presence of a partial-thickness tear subacromial decompression may require additional specific treatment to the rotator cuff if the outcome is to be improved further.

[In vitro effects of diclofenac and selective cyclooxygenase-2 inhibitors on prostaglandin release from inflamed bursa subacromialis tissue in patients with subacromial syndrome]. / Effekte von Diclofenac und selektiven Cyclooxygenase-(COX-)2-Inhibitoren auf die Prostaglandinfreisetzung aus entzündetem Bursa-subacromialis-Gewebe von Patienten mit Subakromialsyndrom in vitro.

BACKGROUND: To compare the in vitro effects of selective COX-2 inhibitors (L-745,337, NS-398 and DFU) and of COX-unspecific diclofenac on release of PGE(2 )and 6-keto-PGF(1alpha) from inflamed bursa subacromialis tissue (IBST) obtained from a total of 35 patients with shoulder impingement syndrome (SIS). PATIENTS AND METHODS: Bursal specimens were incubated in the presence of drugs (0.01-1000 microM) for 20 min and 16 h. RESULTS: After 20 min 10 microM diclofenac significantly inhibited formation of PGE(2) and 6-keto-PGF(1alpha), whereas L-745,337 and NS-398 (10-1000 microM) induced significant inhibition only at concentrations > or =100 microM. In contrast to equimolar diclofenac, DFU (0.01-10 microM) induced no inhibition of bursal PGE(2) release but a dose-dependent, although statistically not significant inhibition after 16 h. The inhibitory potency of diclofenac (0.01-10 microM) was even more increased during long-term incubation showing greater inhibition than DFU at all concentrations studied. CONCLUSION: The data suggest that in IBST in SIS in vitro the majority of PG is generated via the COX-1 pathway.

Increased interleukin-1beta production in the synovium of glenohumeral joints with anterior instability.

Macroscopic synovitis of the glenohumeral joint is frequently seen during arthroscopy in patients with anterior instability. Interleukin-1beta is known to be expressed in inflamed tissue, to correlate with the magnitude of inflammation, and to affect articular cartilage in the joint. We hypothesized that chronic synovitis may occur in the glenohumeral joint in patients with anterior instability. The purpose of this study was to examine the expression of interleukin-1beta in the synovium of the glenohumeral joint with anterior instability and to discuss its clinicopathologic significance. Specimens of synovial tissue around the greater tuberosity in the subacromial synovium (as controls) and around the rotator interval in the glenohumeral synovium were obtained from 10 patients who had anterior instability without signs of subacromial impingement. Semiquantitative reverse transcriptase-polymerase chain reaction was used to compare the levels of interleukin-1beta mRNA expression in the glenohumeral joint with those in the subacromial bursa. We also employed immunohistochemistry and in situ reverse transcriptase-polymerase chain reaction to detect the cells producing interleukin-1beta protein and mRNA. The levels of interleukin-1beta mRNA expression were significantly higher in the glenohumeral joint than in the subacromial bursa (p < 0.01). Histology showed nonspecific inflammation in all 10 samples of glenohumeral synovium, whereas no inflammation was seen in seven of 10 samples of subacromial synovium. Immunohistochemistry identified interleukin-1beta protein in the vessels and inflammatory and synovial cells (from lining to sublining layers) in synovium of the glenohumeral joint, whereas immunoreactivity was negative in seven subacromial bursa. The remaining three synovial specimens of subacromial bursa, however, showed positive immunoreactivity that was unremarkable and confined around the vessels. In situ reverse transcriptase-polymerase chain reaction was exclusively performed in the synovial specimens of the glenohumeral joint, which exhibited a positive reaction (in the same kinds of cells as seen with immunohistochemistry) in the lining and sublining layers and to a lesser extent in the stroma. Thus, our data confirmed the increased production of interleukin-1beta in the synovium of the glenohumeral joint in patients with anterior instability, suggesting the presence of chronic inflammation at the site. We conclude that this chronic synovitis may be partly associated with the development of dislocation arthropathy in the long term.