Are inflammatory cells increased in painful human tendinopathy? A systematic review

Abstract

The existing evidence supports the hypothesis that increased numbers of inflammatory cells are present in pathological tendons. The lack of high-quality quantitative studies in this area demonstrates a clear need for future research to better understand the role of inflammation in tendinopathy.

Inflammation and the continuum model: time to acknowledge the molecular era of tendinopathy

“…However, clear pathological and molecular evidence exists of its dysregulation throughout the spectrum of human tendon disease, while inflammatory change may help to explain the mismatch between pain and macroscopic tendon structure 4. The use of a quotation from a twitter feed as evidence that cytokines are biologically inert within the context of tendinopathy seems biased and inappropriate, considering the strong evidence base throughout landmark publications in the scientific literature demonstrating a key role of cytokines in musculoskeletal pathologies 5…”

Tendinosis in Trigger Finger

“…There are cells scattered between the collagen fibres, connected to each other, communicating and maintaining the extracellular matrix. The cells, tenocytes and tenoblasts are poorly defined, and there is no single marker for them 24,25 . The tendon matrix is a composite of collagens constituting the reinforcing skeleton, and of various proteoglycans and glycoproteins.…”

“…Notably, there is a paucity of knowledge about the tenocytes and tenoblasts, and it is also increasingly clear that the previously suggested absence of inflammatory cells is not the same as total absence of inflammation 25,[65][66][67][68] . Macrophages, T lymphocytes, B lymphocytes 69 and granulocytes 25 can now be found with immunohistochemic methods. Nevertheless, the histopathological picture of tendinosis is still dominated by typically degenerative changes.…”

“…Suggested pathogenetic models can be divided into at least four groups; 1) collagen disruption or tearing, 2) failed healing response, 3) tendon cell response or 4) inflammation 25,62,74 .…”

“…Increased levels of interleukin-1 and -6, cyclooxygenase-1 and -2, iso-forms of transforming growth factor-β or substance P have been presented in tendinosis 21 . There is now also evidence supporting an increased number of inflammatory cells in tendinosis 25,66,67,78 , but still no evidence supporting inflammation as the primary event 74 .…”