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Tendinopathy -- From Basic Science to Treatment

Authors: Graham Riley, PhDFaculty and Disclosures

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Summary and Introduction

Summary

Chronic tendon pathology (tendinopathy), although common, is difficult to treat. Tendons possess a highly organized fibrillar matrix, consisting of type I collagen and various ‘minor’ collagens, proteoglycans and glycoproteins. The tendon matrix is maintained by the resident tenocytes, and there is evidence of a continuous process of matrix remodeling, although the rate of turnover varies at different sites. A change in remodeling activity is associated with the onset of tendinopathy. Major molecular changes include increased expression of type III collagen, fibronectin, tenascin C, aggrecan and biglycan. These changes are consistent with repair, but they might also be an adaptive response to changes in mechanical loading. Repeated minor strain is thought to be the major precipitating factor in tendinopathy, although further work is required to determine whether it is mechanical overstimulation or understimulation that leads to the change in tenocyte activity. Metalloproteinase enzymes have an important role in the tendon matrix, being responsible for the degradation of collagen and proteoglycan in both healthy patients and those with disease. Metalloproteinases that show increased expression in painful tendinopathy include ADAM (a disintegrin and metalloproteinase)-12 and MMP (matrix metalloproteinase)-23. The role of these enzymes in tendon pathology is unknown, and further work is required to identify novel and specific molecular targets for therapy.

Introduction

Soft-tissue disorders are the third most common rheumatologic condition in the UK, with a reported prevalence of 18 cases per 1,000 people.[1] These disorders, which primarily affect tendon, are the main reasons for a musculoskeletal consultation with a general practitioner, and comprised 30% of all such consultations in a 1-year study.[2] This is probably an under estimate of the scale of the problem, because only 40% of elderly individuals (over 70 years of age) with shoulder pain seek treatment.[3] Although many soft-tissue problems are treated by a general practitioner, often with NSAIDs, cortico steroid injection or physiotherapy, a substantial proportion of new patient consultations with rheumatologists are for soft-tissue rheumatism. Secondary referral rates vary widely, but one study reported that 17% of new patients seen in a rheumatology clinic had soft-tissue complaints.[4]

Conditions affecting tendons, which include chronic pain and rupture, are now generally referred to as ‘tendinopathies’ in preference to terms such as ‘tendinosis’ and ‘tendinitis’, because this terminology makes no assumptions about the underlying pathology. Although the role of inflammation is still debated, it has long been known that tendino pathies are primarily degenerative conditions—there is usually an absence of inflammatory cells in or around the lesion.[5] Consequently, it should be no surprise that treatment with anti-inflammatory drugs showed little benefit in controlled trials.[6] In fact, there is remarkably little evidence that any conventional therapies are effective.[7] It has taken several years for research interest to grow, but the molecular mechanisms underlying the cause and progression of tendinopathy are beginning to be elucidated. This article will review the molecular pathology of tendon, and discuss how this knowledge might provide potential new targets for the treatment of chronic tendino pathies.

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