ABSTRACT

Tendon injuries can be divided into several categories on the basis of the nature of their onset and the tissues involved. Acute tendon injuries, such as laceration of the flexor tendons of the fingers, are traumatic in nature. Chronic overuse injuries are the result of multiple microtraumatic events that cause disruption of the internal structure of the tendon and degeneration of the cells and matrix, which fail to mature into normal tendon; at times, such injuries result in tendinosis35. The healing of acute tendon injuries has been studied from the perspective of the body's response to lacerations of flexor tendons as well as after operative intervention35,67.

Tendinosis is incompletely understood. Although the term tendinitis is used frequently and often indiscriminately, histopathological studies have shown that specimens of tendon obtained from areas of chronic overuse do not contain large numbers of macrophages, lymphocytes, or neutrophils26,35,59. Rather, tendinosis appears to be a degenerative process that is characterized by the presence of dense populations of fibroblasts, vascular hyperplasia, and disorganized collagen. This constellation of findings has been termed angiofibroblastic hyperplasia48. It is not clear why tendinosis is painful, given the absence of acute inflammatory cells, nor is it known why the collagen fails to mature. If it can be assumed that tendinosis has essentially the same pathogenesis regardless of where it occurs in the body, then the examination of specimens from patients who have tennis elbow can serve as a model for the investigation of pain in other regions in which tendinosis has been reported, such as the rotator cuff, the Achilles tendon, the patellar ligament, the adductors of the hip, the triceps, the flexors and extensors of the elbow, and the plantar fascia.