Expression of transforming growth factor‐beta isoforms and their receptors in chronic tendinosis

Chronic tendon lesions are degenerative conditions and may represent a failure to repair or remodel the extracellular matrix after repeated micro‐injury. Since TGF‐β is strongly associated with tissue repair, we investigated the expression of TGF‐β isoforms (β1, β2 and β3) and their 2 signalling receptors (TGF‐βRI and TGF‐βRII) in normal and pathological Achilles tendons. In all tissues, all 3 TGF‐β isoforms and the 2 receptors were present at sites of blood vessels. Cells in the matrix showed no staining for TGF‐β1 or β3, while TGF‐β2 was associated with cells throughout the normal cadaver tendon. Tissue from tendons with pathological lesions showed an increase in cell numbers and percentage TGF‐β2 expression. TGF‐βRII showed a wide distribution in cells throughout the tissue sections. As with TGF‐β2, there was an increase in the number of cells expressing TGF‐βRII in pathological tissue. TGF‐βRI was restricted to blood vessels and was absent from the fibrillar matrix. We conclude that despite the presence and upregulation of TGF‐β2, TGF‐β signalling is not propagated due to the lack of TGF‐βRI. This might explain why chronic tendon lesions fail to resolve and suggests that the addition of exogenous TGF‐β will have little effect on chronic tendinopathy.