Effects of corticosteroid on the expressions of neuropeptide and cytokine mRNA and on tenocyte viability in lateral epicondylitis

Soo Hong Han,Soon Chul Lee,Young Do Kwon,Jong Sup Shim,Ji Ye Song,Hee Jung An,Dong Eun Shin

doi:10.1186/1476-9255-9-40

Abstract

BackgroundThe purpose of this study was to determine the reaction mechanism of corticosteroid by analyzing the expression patterns of neuropeptides (substance P (SP), calcitonin gene related peptide (CGRP)) and of cytokines (interleukin (IL)-1α, tumor growth factor (TGF)-β) after corticosteroid treatment in lateral epicondylitis. In addition, we also investigated whether corticosteroid influenced tenocyte viability.MethodsThe corticosteroid triamcinolone acetonide (TAA) was applied to cultured tenocytes of lateral epicondylitis, and the changes in the mRNA expressions of neuropeptides and cytokines and tenocyte viabilities were analyzed at seven time points. Quantitative real-time polymerase chain reaction and an MTT assay were used.ResultsThe expression of SP mRNA was maximally inhibited by TAA at 24 hours but recovered at 72 hours, and the expressions of CGRP mRNA and IL-1α mRNA were inhibited at 24 and 3 hours, respectively. The expression of TGF-β mRNA was not significant. Tenocyte viability was significantly reduced by TAA at 24 hours.ConclusionsWe postulate that the reaction mechanism predominantly responsible for symptomatic relief after a corticosteroid injection involves the inhibitions of neuropeptides and cytokines, such as, CGRP and IL-1α. However the tenocyte viability was compromised by a corticosteroid.

Highlights

The purpose of this study was to determine the reaction mechanism of corticosteroid by analyzing the expression patterns of neuropeptides (substance P (SP), calcitonin gene related peptide (CGRP)) and of cytokines (interleukin (IL)-1α, tumor growth factor (TGF)-β) after corticosteroid treatment in lateral epicondylitis
Ljung BO et al [11] analyzed six patients suffering from lateral epicondylitis and six healthy volunteers using immunohistochemistry, and suggested that nerve fibers showing SP-like and CGRP-like immunoreactivity were demonstrated at the origin of the extensor carpi radialis brevis muscle, and neurogenic inflammation might be implicated in the etiology of lateral epicondylitis
Uchio Y et al [8] concluded that neuropeptides (SP, CGRP) and cytokines (interleukin (IL)-1α, tumor growth factor (TGF)-β) might contribute to the pathology of lateral epicondylitis, and suggested that further studies would be conducted to clarify the interactions between neuropeptides and cytokines

Summary

Introduction

The purpose of this study was to determine the reaction mechanism of corticosteroid by analyzing the expression patterns of neuropeptides (substance P (SP), calcitonin gene related peptide (CGRP)) and of cytokines (interleukin (IL)-1α, tumor growth factor (TGF)-β) after corticosteroid treatment in lateral epicondylitis. Recent studies have suggested that neuropeptides, such as, substance P (SP) and calcitonin gene related peptide (CGRP), are involved in its pathogenesis [8,11,12] because inflammatory responses, such as, increased. Uchio Y et al [8] concluded that neuropeptides (SP, CGRP) and cytokines (interleukin (IL)-1α, tumor growth factor (TGF)-β) might contribute to the pathology of lateral epicondylitis, and suggested that further studies would be conducted to clarify the interactions between neuropeptides and cytokines. Corticosteroid injection is often used to treat lateral epicondylitis, and high short-term success rates have been reported [13]. Several reports of tendon weakness or spontaneous rupture after corticosteroid injection have been issued [16]

Objectives

Methods

Results

Conclusion