One of the striking findings in the present study is that ectopic stem cells isolated from dental pulp fail to fuse into multinucleated myofiber-like structures despite exposure to chemically defined medium that is known to induce myogenic fusion of several other postnatal stem cell populations such as bone marrow or adipose. The mechanisms of cell fusion are not well understood, although several cellular. machineries including cell membrane proteins and associated signaling appear to be highly conserved for cell fusion and differentiation into myocytes. Few myogenic stem/ progenitor cells are present among heterogeneous stem cells of dental pulp in the present study: only 3 out of 42 clones showing myogenic potential. It is conceivable that the scarce myogenic cells fail to fuse with adjacent cells most of which are not myogenic and do not Cetylpyridinium chloride monohydrate express the same cell surface proteins that are putatively important for cell fusion. Conversely, myogenic clones in the present study, B6 and C3, readily fuse even without co-culture with mouse myoblast cell line, C2C12 cells which are known to fuse with other myocyte-like cells. We found a lack of statistically significant differences in mRNA expression of human PECAM by the transplanted heterogeneous DSCs and their clonal progeny cells. This appears to suggest that while myogenic clones of ectopic stem cells show advantage in myogenic capacity, they may not necessarily Pyriproxyfen elaborate more vasculature. Previous work has shown that transplanted stem/ progenitor cells are capable of co-endothlializing blood vessels with host cells. Whereas the isolated myogenic clones are capable of engrafting with host muscle fibers and yield myosin heavy chain without necessarily relying on enhanced angiogenesis. Coupled with the paucity or decreases in the expression of CD146, an endothelial progenitor marker by either heterogeneous DSCs or their myogenic clones, it is somewhat surprising that the derived myogenic clones appear to be capable of muscle repair without necessarily an accompanied enhancement in angiogenesis.