Annually, approximately 30% of acute injuries in workers are to the upper extremity (National Safety Council, 1993; Kelsey Report, 1994). Among those injuries, over 350,000 require extensive tendon surgery including tendon repair and reconstruction. The incidence of adhesion formation resulting in poor digital range of motion following primary tendon repair and autogenous tendon grafting within the digital sheath has been high. Recent clinical studies have suggested that two factors, increased levels of proximal musculotendinous load and greater magnitudes of intrasynovial tendon repair site excursion, may improve the healing response of intrasynovial tendons and tendon grafts compared to controlled passive motion and immobilization rehabilitation techniques. Our central hypothesis is that primary contact tendon healing is facilitated and peripheral adhesion formation is inhibited with the use of increased levels of proximal musculotendinous load and/or greater levels of intrasynovial tendon repair site excursion. In addition, we hypothesize that the healing response is accelerated as adhesion-free neovascularization is enhanced, and tendon surface cell migration and type I collagen deposition are increased. We propose that repaired tendons and autogenous tendon autografts treated with an accelerated program of -rehabilitation heal consistently by intrinsic processes, relying on cellular survival and proliferation from the epitenon without significant contributions from peripheral cellular or vascular ingrowth sources. The objectives of this proposal are to determine the effects of variations in applied repair site force and excursion in vivo brought about by altering wrist and digital position and by muscle stimulation during the rehabilitation process. Morphological, biomechanical and biochemical changes in repaired intrasynovial tendons and autogenous tendon grafts treated with carefully selected increased loads and greater levels of gliding will be determined in vivo. Specifically, the morphological functional and structural changes occurring at the repair site and in the tendon stumps will be evaluated by light and electron microscopy, by roentgenographic evaluation, by gliding and tensile testing, and by immunohistochemical analysis of the cell's receptors (i.e. integrins) and growth factors (i.e. PDGF-BB and IGF-I) during the early term (6-18 days) post repair. Longer term effects (6-12 weeks post repair) will be evaluated biomechanically by performing gliding and tensile testing. The neovascularization response of the repaired tendons will be examined with vascular injection studies and biochemical characterization of the repaired tendon matrix will be carried out by examining collagen concentration, crosslinking collagen typing and DNA content.
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