Presently, PRP use in tendon and ligament injuries has several potential advantages, including faster recovery and, possibly, a reduction in recurrence, with no adverse reactions described. However, only 3 randomized clinical trials have been conducted.

There are currently no available options to promote nerve regeneration through chronically denervated distal nerve stumps. Here we used a rat model of delayed nerve repair asking of prior insertion of side-to-side cross-bridges between a donor tibial (TIB) nerve and a recipient denervated common peroneal (CP) nerve stump ameliorates poor nerve regeneration. First, numbers of retrogradely-labelled TIB neurons that grew axons into the nerve stump within three months, increased with the size of the perineurial windows opened in the TIB and CP nerves. Equal numbers of donor TIB axons regenerated into CP stumps either side of the cross-bridges, not being affected by target neurotrophic effects, or by removing the perineurium to insert 5-9 cross-bridges. Second, CP nerve stumps were coapted three months after inserting 0-9 cross-bridges and the number of 1) CP neurons that regenerated their axons within three months or 2) CP motor nerves that reinnervated the extensor digitorum longus (EDL) muscle within five months was determined by counting and motor unit number estimation (MUNE), respectively. We found that three but not more cross-bridges promoted the regeneration of axons and reinnervation of EDL muscle by all the CP motoneurons as compared to only 33% regenerating their axons when no cross-bridges were inserted. The same 3-fold increase in sensory nerve regeneration was found. In conclusion, side-to-side cross-bridges ameliorate poor regeneration after delayed nerve repair possibly by sustaining the growth-permissive state of denervated nerve stumps. Such autografts may be used in human repair surgery to improve outcomes after unavoidable delays.

PURPOSE: Indoleamine 2,3-dioxygenase (IDO) has a powerful role in mesenchymal stem cell (MSC)-mediated immunosuppression, as previously demonstrated by our lab. However the environmental conditions that regulate IDO expression and thereby increase MSC immunosuppression remain unknown. Here we investigate approaches to enhance the role of IDO in MSC function. We hypothesize that MSC exposure to an inflammatory environment will increase IDO expression. METHODS:MSCs derived from Lewis rat bone marrow were expanded in either normoxia or hypoxia (5% O2 or 0.5% O2). During expansion, MSCs were exposed to IFNγ and/or TNFα for either 24 hours or 1 week. IDO expression was assessed using quantitative real-time PCR. Composite tissue allografts from Brown Norway rats were seeded ex-vivo with Lewis rat MSCs and transferred to Lewis rats and local inflammatory markers were measured using quantitative real-time PCR.

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