Observational study demonstrates elevated inflammatory and pain mediators in extra-articular biceps tissue, highlighting the bicipital tunnel as an active source of shoulder pain.
The pathophysiology of extra-articular biceps disease is not fully understood. The purpose of the study was to assess molecular evidence of inflammation, degradation, and nociception within the 3 separate anatomic zones of the extra-articular biceps tendon and its confining tunnel. Arthroscopic biopsies were taken from the bicipital tunnel from 11 patients with suspected biceps-labrum complex disease undergoing subdeltoid biceps transfer to the conjoint tendon. Tissue was analyzed for mRNA expression of various inflammatory mediators including interleukin-6, interleukin-1β, transforming growth factor-β (TGF-β), matrix metalloproteinase-13, and substance P precursor. Extra-articular tissue was compared with intra-articular tendon (internal control) to determine fold change in expression. Compared to intra-articular tendon, extra-articular biceps tendon and synovium have increased levels of these aforementioned mediators, significantly TGF-β (P = .012). In patients with clinical history of long head of the biceps tendon tendinopathy as well as arthroscopic findings of synovitis, tear, and loose bodies, pro-inflammatory and degenerative cytokines were upregulated in the extra-articular tendon. Inflammatory cytokines, degenerative mediators, and pain molecules associated with nociception were found within both the extra-articular long head of biceps tendon and its constraining fibro-osseous bicipital tunnel in patients with clinically evident biceps-labral complex disease.
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Campbell et al. (2020) studied this question.
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