Abstract

Purpose: Bursal inflammation is thought to be a major cause of pain in degenerative rotator cuff tears (RCTs). While the expression of proinflammatory mediators, such as COX-2, TNF-α, IL-1β, and IL-6, is crucial for the pathophysiology of osteoarthritis (OA), their role in degenerative RCTs remains unknown. The aim of this study was to determine the expression of COX-2 and proinflammatory mediators in the development of RCT-induced pain by comparing their levels in patients with hip OA or RCTs. Methods: We included samples obtained from 31 shoulders of 31 patients with RCTs and samples from 30 hips of 27 patients with hip OA. The mRNA levels of COX-2, TNF-α, IL-1β, and IL-6 were determined using RT-PCR, and were compared between the subacromial bursa and hip joints. We also analyzed IL-1β-induced COX-2 expression in the subacromial bursa and synovial blast of the hip. Results: COX-2, IL-1β, and IL-6 expression levels were significantly lower in the subacromial bursa of RCTs than in hip OA samples, while no significant difference was observed for TNF-α. No significant difference in the fold increase was observed between subacromial bursa and hip OA samples, even though IL-1β-induced COX-2 expression increased in both samples. Conclusion: Our findings suggest that the main mechanism underlying pain development differs between patients with RCTs and those with hip OA.

Highlights

  • Most patients with rotator cuff tears (RCTs) first come to the hospital because of pain [1]

  • No significant difference in the fold increase was observed between subacromial bursa and hip OA samples, even though IL-1β-induced COX-2 expression increased in both samples

  • There was no significant difference in age between the groups, whereas significant differences in gender and International Cartilage Repair Society (ICRS) classification were observed

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Summary

Introduction

Most patients with rotator cuff tears (RCTs) first come to the hospital because of pain [1]. Inflammation is normally implicated as the source of shoulder pain in patients with rotator cuff impairments [2] [3]. The expression of proinflammatory mediators in degenerative RCTs remains largely unknown. Inflammatory stimuli initiate a cascade of events, including the release of cytokines and other mediators from the cartilage and synovium. These induce metabolic disturbances and enhance catabolism in joint tissues of patients with OA, which promotes joint pain [6]. Anti-inflammatory effects are related to the downregulation of cyclooxygenase-2 (COX-2) and reduced proinflammatory mediator expression, regardless of joint [7] [8]

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