Physiological and pathological changes in the arterial supply of the mandible

The inferior alveolar artery, more frequently than previously estimated, is subject to age-related degenerative changes, mostly of arteriosclerotic origin. Moreover, it appears that vasculopathies and arteritides, such as polyarteritis nodosa and giant-cell arteritis, also affect the inferior alveolar artery. The role of arterial supply is not just mechanical-passive, serving as a scaffold for osteoblasts during osteogenesis, but also regulatory, since angiogenesis precedes and initiates osteogenesis. Already at the time of craniofacial development, it is speculated that progenitor endothelial cells account for the synthesis of one particular morphogenetic protein that precedes osteosynthesis and determines the final destination of migrating neural crest cells. Similarly, in the postnatal period, angiogenesis precedes osteosynthesis and plays a vital role in bone metabolism and repair, through the synthesis of endothelial growth factors, such as morphogenetic protein-2. Thus, clinical manifestations, such as avascular necrosis, are now believed to result from a combination of chronic disorder of the mandible’s arterial supply with fibrinolysis and coagulation disorders, rather than from primary osteoblast dysfunctions. This close interplay between the vascular and bone tissues, with the vasculature playing a guiding role, supports the hypothesis of the bone being an angiogenic tissue.