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Title: The cellular mechanisms of tendon repair and their strategic modification
Author: Jones, Martin Edward
Awarding Body: University of London
Current Institution: University College London (University of London)
Date of Award: 2001
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It is currently believed that tendons heal by a combination of extrinsic and intrinsic mechanisms. The contribution of each is thought to vary with site and type of the injury. The tendon is known to partly derive its nutritional requirements from a complicated vascular supply. A novel technique was developed for mapping the intricate vascular networks within the rabbit tendon model. Immunohistochemical localisation of endothelial tissue has allowed us to quantify the reduction in tendon blood supply with its passage through the digital sheath. It has highlighted intra-species variability between different anatomical sites. Healing within these relatively avascular zones is notoriously poor and the contribution of tendon surface fibroblasts in this process is still debated. A vital dye was employed to examine the distribution of surface fibroblasts up to seven days post injury of an in vitro and in vivo tendon model. In the latter experiment, the surface fibroblasts readily took up the vital dye at day 0. By day 1, dyed cells had moved into the cut. By day 3, they had migrated laterally into the core substance of the tendon. Core dyed cell counts at days 1, 3, 5 and 7 were significantly different compared with day 0 dye cell core counts (p < 0.05). It was concluded that this pathway is important in the early stages of tendon healing and indeed may be central to both the intrinsic and extrinsic classical theories. The encompassing phrase of transtrinsic healing was therefore put forward for the migration pathway observed. In an attempt to improve outcome of tendon repair by substance application at the time of tenorraphy, the role of an autologuous fibrin sealant in post surgical adhesion formation was examined. It was found in the rabbit model that Vivostat® resulted in significant reduction in postoperative adhesion formation as measured by tensiometer and histological analysis (both p < 0.05). These findings suggest that the ideal tendon repair in the future could involve the delivery of pertinent cells to the required site of healing, possibly seeded on a collagen construct. After securing the repair around this scaffold, substances such as Vivostat® could act as a barrier to prevent the build-up of detrimental adhesions. This may prove to be especially important in areas of reduced tendon vascularity.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available