H vessels are an essential link in angiogenic-osteogenic coupling and orchestrate the process of bone healing. H vessels are critically deficient in the setting of radiation-induced fractures, which have been reported to occur in up to 25% of patients undergoing radiotherapy. By increasing H-vessel proliferation, Deferoxamine (DFO) revitalizes the physiologic response to skeletal injury and accelerates irradiated fracture repair.
View Article and Find Full Text PDFIn the setting of bone defects, the injured vasculature and loss of hemodynamic inflow leads to hematoma formation and low oxygen tension which stimulates vascular expansion through the HIf-1α pathway. Most importantly, this pathway upregulates sprouting of type H vessels (CD31hiEmcnhi vessels). H vessels engage in direct interaction with perivascular osteoprogenitor cells (OPCs), osteoblasts, and preosteoclasts of bone formation and remodeling.
View Article and Find Full Text PDFBackground: Cleft palatoplasty commonly results in denuded maxillary bone in the lateral gutters and a posterior void between oral and nasal closures. Bony exposure of the anterior palate subjects the maxilla to scarring and growth restriction; scar contracture of the posterior void may result in velopharyngeal insufficiency and fistula formation. Use of the buccal fat pad flap (BFPF) at the time of palatoplasty provides vascularized tissue over these critical areas, thereby reducing the rate of secondary surgery for speech and fistula revision.
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