Histopathology of common tendinopathies - Update and implications for clinical management

Citation
Km. Khan et al., Histopathology of common tendinopathies - Update and implications for clinical management, SPORT MED, 27(6), 1999, pp. 393-408
Citations number
146
Categorie Soggetti
Ortopedics, Rehabilitation & Sport Medicine
Journal title
SPORTS MEDICINE
ISSN journal
01121642 → ACNP
Volume
27
Issue
6
Year of publication
1999
Pages
393 - 408
Database
ISI
SICI code
0112-1642(199906)27:6<393:HOCT-U>2.0.ZU;2-S
Abstract
Tendon disorders are a major problem for participants in competitive and re creational sports. To try to determine whether the histopathology underlyin g these conditions explains why they often prove recalcitrant to treatment, we reviewed studies of the histopathology of sports-related, symptomatic A chilles, patellar, extensor carpi radialis brevis and rotator cuff tendons. The literature indicates that healthy tendons appear glistening white to th e naked eye and microscopy reveals a hierarchical arrangement of tightly pa cked, parallel bundles of collagen fibres that have a characteristic reflec tivity under polarised light. Stainable ground substance (extracellular mat rix) is absent and vasculature is inconspicuous. Tenocytes are generally in conspicuous and fibroblasts and myofibroblasts absent. In stark contrast, symptomatic tendons in athletes appear grey and amorphou s to the naked eye and microscopy reveals discontinuous and disorganised co llagen fibres that lack reflectivity under polarised light. This is associa ted with an increase in the amount of mucoid ground substance, which is con firmed with Alcian blue stain. At sites of maximal mucoid change, tenocytes , when present, are plump and chondroid in appearance (exaggerated fibrocar tilaginous metaplasia). These changes are accompanied by the increasingly c onspicuous presence of cells within the tendon tissue, most of which have a fibroblastic or myofibroblastic appearance (smooth muscle actin is demonst rated using an avidin biotin technique). Maximal cellular proliferation is accompanied by prominent capillary proliferation and a tendency for discont inuity of collagen fires in this area. Often, there is an abrupt discontinu ity of both vascular and myofibroblastic proliferation immediately adjacent to the area of greatest abnormality. The most significant feature is the a bsence of inflammatory cells. These observations confirm that the histopathological findings in athletes with overuse tendinopathies are consistent with those in tendinosis - a deg enerative condition of unknown aetiology. This may have implications for th e prognosis and timing of a return to sport after experiencing tendon sympt oms. As the common overuse tendon conditions are rarely, if ever, caused by 'ten dinitis', we suggest the term 'tendinopathy' be used to describe the common overuse tendon conditions. We conclude that effective treatment of athlete s with tendinopathies must target the most common underlying histopathology , tendinosis, a noninflammatory condition.