Flexor tendon repair.
Healing canine flexor tendons treated with either total immobilization, delayed protected mobilization, or early protected mobilization was studied by biomechanical, microangiographic, biochemical, and histologic techniques at intervals through 12 weeks. The healing characteristics of the early mobilization tendons showed higher tensile strengths and improved gliding function than the delayed mobilization and immobilization tendons. Protected passive motion brought about accelerated changes in peritendinous vessel density and configuration, as well as increased repair site total DNA content. While adhesions obliterated the space between the tendon surface and the tendon sheath of the immobilized repairs, the mobilized tendons demonstrated coverage of the repair site by cells from the epitenon by 10 days, and a smooth, gliding surface that was maintained free of adhesions through 42 days. A series of in vitro studies demonstrated the cellular processes involved in the repair: phagocytosis of cellular debris and collagenous fragments by cells from the epitenon, and collagen synthesis primarily by endotenon cells.
D000818:Animals; D001696:Biomechanical Phenomena; D002645:Chickens; D004247:DNA / Q000378:metabolism; D003670:Deer; D004285:Dogs; D005260:Female; D007103:Immobilization; D066298:In Vitro Techniques; D008254:Macaca nemestrina; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D011817:Rabbits; D013708:Tendon Injuries / Q000503:physiopathology; D013710:Tendons / Q000098:blood supply / Q000502:physiology* / Q000648:ultrastructure; D013718:Tensile Strength; D013997:Time Factors; D014945:Wound Healing
D004247:DNA