Abstract

This presentation will synthesise and review recent findings from our laboratory and others' on inflammatory mechanisms involved in tendon overuse injuries. Tendinopathy is a state of chronic tendon thickening and pain, usually as a result of overuse. Recent work has shown that repetitive loading of human tendon-derived cells leads to upregulation of TAC1, the mRNA encoding for Substance P1—a pro-inflammatory neuropeptide which is known to contribute to tendon pain.2 In addition, previous work has found that mast cells are present in greater numbers in chronically overused tendon,3 and that they degranulate in response to SP, releasing substances that directly influence human tenocyte collagen remodelling. Thus, both SP and one of its main targets—the mast cell—are over-represented in tendinopathic tissue. Mast cells have a high affinity for human tenocytes, forming elaborate inter-cellular junctions, and releasing substances which substantially influence tenocyte behaviour that could have relevance for improving outcomes following injury or overuse. For example, inhibiting mast cells results in a reduction of TGF-beta-related genes (related to scarring) and reduces the amount of tendon thickening following injury.4 Additionally, mast cells induce a large increase in COX-2 expression by human tenocytes. It is possible that a clinical strategy which incorporates inhibitors of mast cells could improve on outcomes with standard treatment.5