TENDINOSIS OF THE ROTATOR CUFF: A REVIEW

Abstract

Rotator cuff tendinosis is a disease whose etiology and pathophysiology are still under debate. Three mechanisms have been proposed as giving rise to rotator cuff disease: the intrinsic mechanism, the extrinsic mechanism and overuse. Evidence for and against each one as being the primary cause of disease abounds. The current consensus is that the etiology is probably multifactorial and each factor plays different roles in different patients. The histologic features of rotator cuff disease are fibroblast hyperplasia, collagen disorganization and neovascularization. These findings together are termed angiofibroblastic hyperplasia, believed to be a reflection of unsuccessful attempts at repair of tendon with a tendency towards degeneration. The concept supports the current view that rotator cuff disease is a tendinosis, a degenerative process, rather than a tendinitis, an inflammatory one. This poor healing response is seen in the collagen content of diseased tendon. Production of collagen fails to shift from the initial type III collagen to the mature type I collagen, causing the tendon to become weak. Most current treatment modalities fail to address the biologic processes going on within the tendon and future directions need to address these problems.