Abstract
BackgroundThis article systematically reviews the current evidence regarding inflammation in Tendinopathy with the aim to increase understanding of a potential common pathophysiology.MethodsFollowing the PRISMA statements, the terms: (tendinopathy OR (tendons AND rupture)) AND (inflammation OR (inflammation AND cells) OR immune system OR inflammation mediators OR bacteria) were used. One thousand four hundred thirty-one articles were identified which was screened down to 53.Results39/53 studies mentioned inflammatory cells but had contradicting conclusions. Macrophages were the most common cell type and inflammatory markers were detectable in all the articles which measure them.ConclusionsThe included studies show different conclusions, but this heterogeneity is not unexpected since the clinical criteria of ‘tendinopathy’ encompass a huge clinical spectrum.Different ‘tendinopathy’ conditions may have different pathophysiology, and even the same clinical condition may be at different disease stages during sampling, which can alter the histological and biochemical picture. Control specimen sampling was suboptimal since the healthy areas of the pathological-tendon may actually be sub-clinically diseased, as could the contralateral tendon in the same subject.Detection of inflammatory cells is most sensitive using immunohistochemistry targeting the cluster of differentiation markers, especially when compared to the conventional haematoxylin and eosin staining methods. The identified inflammatory cell types favour a chronic inflammatory process; which suggests a persistent stimulus. This means NSAID and glucocorticoids may be useful since they suppress inflammation, but it is noted that they may hinder tendon healing and cause long term problems.This systematic review demonstrates a diversity of data and conclusions in regard to inflammation as part of the pathogenesis of Tendinopathy, ranging from ongoing or chronic inflammation to non-inflammatory degeneration and chronic infection. Whilst various inflammatory markers are present in two thirds of the reviewed articles, the heterogenicity of data and lack of comparable studies means we cannot conclude a common pathophysiology from this systematic review.
Highlights
This article systematically reviews the current evidence regarding inflammation in Tendinopathy with the aim to increase understanding of a potential common pathophysiology
Tendon specimens were heterogenous in terms of location and presentation of tendinopathy
The evidence level of included studies was assessed according to the Oxford Centre of Evidence based Medicine (OCEBM) [66]
Summary
This article systematically reviews the current evidence regarding inflammation in Tendinopathy with the aim to increase understanding of a potential common pathophysiology. Tendinopathy affect millions of people in both the athletic and general population, causing great socioeconomical impacts [1]. Despite the presence of various modalities of conservative and surgical treatments, more than one third of the patients do not respond and continue to present with persistent pain and disability [2, 3]. Anti-inflammatory treatments including NSAIDs and glucocorticoids form the back-bone of conservative treatments for tendinopathy. There is still an ongoing debate on the presence of active inflammation in this chronic disorder. Whether inflammation play an important role in tendinopathy is currently unclear. By reviewing the presence and pattern of inflammation in tendinopathic tendons, the current management strategies can be re-assessed
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