Abstract

The pathophysiology of rotator cuff tendinopathy is not fully understood, particularly in terms of the local inflammatory process. This study aimed to investigate the expression of selected molecules in the tumour necrosis factor (TNF)-α transduction pathway, including TNF-α, TNF receptor 1 (TNFR1), neutral sphingomyelinase activation associated factor (NSMAF), caspase 3 (Casp3), and interleukin (IL)-8, in patients with rotator cuff tendinopathy that had undergone surgical treatment. We included 44 participants that underwent arthroscopy, due to rotator cuff tendinopathy. Samples from the injured tendon were collected during arthroscopy, and RT-PCR was performed to determine gene expression. Pearson correlation analyses or U-Mann–Whitney test were performed to identify associations with the following parameters: sex, age at admission, body mass index, the presence of night pain, previous treatment (nonsteroidal anti-inflammatory drugs and/or steroids), medical history of the shoulder injury, upper subluxation of the humeral head, and the number of tendons injured. RT-PCR showed that the selected pro-inflammatory factors involved in the TNF-α signalling pathway expression levels were expressed in the tendon tissues. However, the levels of expression varied from patient to patient. Variations were over 250-fold for TNF-α, about 130-fold for TNFR1, NSMAF, and Casp3, and 1000-fold for IL-8. We could not confirm that any of the clinical parameters investigated were associated with the level of gene expression in the TNF-α pathway and IL-8.

Highlights

  • Rotator cuff (RC) tendinopathy is one of the principal causes of shoulder pain

  • There are very limited data regarding the involvement of tumour necrosis factor (TNF)-α pathway into pathophysiology of RC tendinopathy, the present study aimed to investigate the gene expression for selected molecules in the (TNF-α) transduction pathway, including TNF-α, TNF receptor 1 (TNFR1), neutral sphingomyelinase activation associated factor (NSMAF), and caspase 3 (Casp3) and interleukin (IL)-8, in patients with RC tendinopathy that underwent surgical treatment

  • Millar et al (2009) demonstrated that pro-inflammatory cytokines and apoptotic genes were significantly upregulated in a rodent model of tendinopathy, and they confirmed these results in humans

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Summary

Introduction

Rotator cuff (RC) tendinopathy is one of the principal causes of shoulder pain. Tendinopathy is characterised by pain in and around the tendon associated with repetitive sports or daily living activities. The aetiology of RC tendinopathy that leads to a partial or full-thickness tear is complex, and the pathophysiology remains unclear (Pandey and Jaap Willems 2015). Cuff tears are either traumatic or degenerative, resulting from extrinsic or intrinsic factors (Spargoli 2018). Extrinsic factors consist of various anatomical and biomechanical alterations that lead to narrowing of the subacromial space and mechanical compression of RC tendons. One is degenerative-microtrauma, where age-related collagen fibre disorganisation and structural changes reduce the ability of the tendon to withstand repetitive microtraumas that could lead to a partial- or full-thickness tear. Other mechanisms include harmful oxidative stress around the tendon, induced by repetitive injury, followed by a reparative process or a change in vascularisation (Cipollaro et al 2019; Pandey and Jaap Willems 2015).

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