Abstract

Tendons are designed to take tensile load, but excessive load can cause overuse tendinopathy. Overuse tendinopathy results in extensive changes to the cells and extracellular matrix, resulting in activated cells, increase in large proteoglycans and a breakdown of the collagen structure. Within these pathological changes, there are areas of fibrocartilaginous metaplasia, and mechanotransduction models suggest that this response could be due to compressive load. As load management is a cornerstone of treating overuse tendinopathy, defining the effect of tensile and compressive loads is important in optimising the clinical management of tendinopathy.

This paper examines the potential role of compressive loads in the onset and perpetuation of tendinopathy, and reviews the anatomical, epidemiological and clinical evidence that supports consideration of compressive loads in overuse tendinopathy.