Bone-vasculature interactions in the mandible: is bone an angiogenic tissue?

Starting from early stages of craniofacial development, the leading role of vasculature, in particular endothelial progenitor cells, becomes apparent. They are probably the cells that synthesize the appropriate bone morphogenetic protein (BMP), that precedes neural crest cell migration and determines their final destination and skeletal development. During postnatal osteosynthesis in the mandible, angiogenesis similarly goes before osteosynthesis, regulates this process with the production of BMP-2 and serves as a scaffold for osteoblasts. This growth factor is involved in bone metabolism and bone injury repair. The dependence of bone from vasculature, is better understood when looking to osseous changes that result from vasculopathies and arteritides, like in diabetes mellitus and polyarteritis nodosa respectively, that affect the mandible more frequently than previously suspected. These changes are not only the result of a dysregulation of osteoblasts and osteoclasts, but of a complex network of factors that affect the vasculature, like VEGF and hypoxia. Abnormal vasculature results in qualitatively degradated bone, with an atypical architecture or even in bone necrosis. The dynamic interplay between vasculature and bone of the mandible, with the vasculature endothelium playing an initiating and regulatory role in osteosynthesis, supports the hypothesis of an angiogenic origin of bone. This hypothesis, helps in understanding of bone pathology, like avascular necrosis and of the impact of interventions and medications that affect vasculature, on bone metabolism.