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 . Multiple injections of PGE2 within the midsubstance of the rabbit patellar tendon (PT) also produced collagen fibril disorganization and thinning .
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Comparative Histological and Biomechanical Effects of Prostaglandin-E2 and Bacterial Collagenase on the Rabbit Patellar Tendon
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Dyment, NA, Shearn, JT, Galloway, MT, Greiwe, RM, Kenter, K, Hasan, SS, Butler, DL, & Boivin, GP. "Comparative Histological and Biomechanical Effects of Prostaglandin-E2 and Bacterial Collagenase on the Rabbit Patellar Tendon." Proceedings of the ASME 2008 Summer Bioengineering Conference. ASME 2008 Summer Bioengineering Conference, Parts A and B. Marco Island, Florida, USA. June 25–29, 2008. pp. 275-276. ASME. https://doi.org/10.1115/SBC2008-192395
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