Gelberman R H, Manske P R, Akeson W H, Woo S L, Lundborg G, Amiel D
J Orthop Res. 1986;4(1):119-28. doi: 10.1002/jor.1100040116.
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.
通过生物力学、微血管造影、生化和组织学技术，在12周的时间间隔内，对采用完全固定、延迟保护性活动或早期保护性活动治疗的犬屈肌腱愈合情况进行了研究。与延迟活动和固定的肌腱相比，早期活动肌腱的愈合特征表现出更高的拉伸强度和更好的滑动功能。保护性被动活动使腱周血管密度和形态发生加速变化，同时修复部位的总DNA含量增加。在固定修复的情况下，粘连会使肌腱表面与腱鞘之间的间隙消失，而活动的肌腱在10天时可见腱外膜细胞覆盖修复部位，并且在42天内保持光滑、无粘连的滑动表面。一系列体外研究证明了修复过程中涉及的细胞过程：腱外膜细胞对细胞碎片和胶原片段的吞噬作用，以及主要由腱内膜细胞进行的胶原合成。
