Comparative Histological and Biomechanical Effects of Prostaglandin-E2 and Bacterial Collagenase on the Rabbit Patellar Tendon

Ninety-seven percent of tendon ruptures are found in areas of chronic tendon degeneration, which is thought to be a cell-mediated process involving increased extracellular matrix turnover and remodeling [1,2]. The degenerative aspects seen within regions of tendon degeneration include collagen matrix disorganization, collagen fibril thinning, cellular hyperplasia, and neovascularization [1–3]. The etiology of tendon degeneration is unclear at this point. One theory involves the introduction of multiple mechanical insults (mechanical overuse) that act to trigger a degenerative pathway of increased matrix degradation by matrix metalloproteinases (MMP). Inflammation is not seen within regions of degenerative tendon. However, inflammatory mediators such as prostaglandin-E₂ (PGE₂) may have a role as they have been shown to be upregulated by fibroblasts as a result of mechanical over-stimulation in culture [4]. Multiple injections of PGE₂ within the midsubstance of the rabbit patellar tendon (PT) also produced collagen fibril disorganization and thinning [5].