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Enhancing MSC survival and functions in an ischemic environment
Several studies, including those of the B2OA, already demonstrated the capacity of MSCs seeded on a porous scaffold to repair large bone defect. The reproducibility of this method, however, is mediocre and, most importantly, lower than the one of the autograft, which remains the gold standard for bone repair.
This limited success may be caused, at least in part, by the massive cell death observed after MSC transplantation, with 80-90% of cells dying within the first days. This death might be explained by the fact that the cells are transplanted in an ischemic environment (deprived of oxygen and nutrient), caused by the absence of vascularization in the defects.
Survival of MSC after subcutaneous implantation
Viability of MSCs seeded in fibrin gel, loaded 
[left] or not [right] with glucose.
Reference
The lack of oxygen was thought to be the most detrimental factor for MSC survival and function. Recent work from the B2OA, however, is questioning this paradigm: glucose (main nutrient for cell metabolism) appears to also play a critical role in MSC survival in an ischemic environment. The addition of exogenous glucose, indeed, allows MSC to survive even in a near anoxic environment (complete deprivation of oxygen). 
These findings improve our knowledge of the mechanisms involved in MSC death after transplantation. Based on this better understanding, the B2OA is developing new strategies to deliver in situ exogenous glucose in order to improve post-transplantation survival and function of MSCs. These findings are of high interest not only for bone, but also for cardiac, cartilage tissue engineering.

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