Increased expression of macrophages and inflammatory cytokines at tendon origin in patients with chronic lateral epicondylitis.

BACKGROUND

The success of anti-inflammatory medications and corticosteroid injections in controlling chronic lateral epicondylitis symptoms suggests an underlying inflammatory pathology that is also causative of the pain experienced by patients; however, evidence regarding inflammatory mediators and cells remains inconclusive.

METHODS

We conducted a case-control study that included a total of 24 participants (10 patients and 14 controls). Extensor carpi radialis brevis tendon samples were obtained from patients, and flexor carpi radialis tendon samples were obtained from control subjects. We then performed immunohistochemical assessment to determine the expression levels of neuropeptides (substance P and calcitonin gene-related peptide), glutamate receptors (N-methyl-d-aspartate receptor type 1 and metabotropic glutamate receptor 5), inflammatory cytokines (interleukin 1α and tumor necrosis factor α), and inflammatory cells (M1 macrophages [CD68], M2 macrophages [CD163 and CD206], T-lymphocytes [CD3], and B-lymphocytes [CD20]).

RESULTS

Patients' sampled extensor carpi radialis brevis tendons showed significantly elevated expression levels of neuropeptides, glutamate receptors, and inflammatory cytokines, along with a number of macrophages, compared with controls (P < .001 or P < .0001); however, there were no differences in the number of T- and B-lymphocytes between the 2 groups.

CONCLUSION

The findings of this study showed that inflammation is involved in the pathology of chronic lateral epicondylitis.