الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Chronic hyperglycemia in Type I diabetes mellitus has been accompanied by the occurrence of complications involving the skeletal system. Bone repair abnormalities associated with diabetes mellitus include compromised angiogenic process, inhibition of osteoblastic differentiation, and induction of osteoblast apoptosis. Thus, restoration of critical-sized bone defects that are created by injuries, infections, or resection surgeries is very challenging in clinical practice, especially in diabetics. Therefore, hyperbaric oxygen therapy (HBOT) may be combined with bone grafts to reconstruct these defects. This therapy has been associated with enhanced tissue repair, increased collagen synthesis, accelerated osteoblast differentiation, and promotion of angiogenesis.
Aim of the study: The aim of the present study was to assess, histologically and histomorphometrically, the effect of hyperbaric oxygen therapy on the regeneration of mandibular critical-sized defects in rats with induced type I diabetes mellitus.
Materials and Methods: Twenty-four adult male albino rats weighing 250-280 grams, six months of age, with induced diabetes mellitus were divided randomly into 2 main groups: group A (control group) and group B (study group). Critical-sized bone defects of 4 mm diameter were performed in the right side of the posterior mandibles of all rats and filled with β-tricalcium phosphate bone graft. group A was not treated with HBOT, while animals in group B were treated with HBOT. Animals were euthanized at 1 and 3 weeks postoperatively and the results of the defects regeneration were evaluated histologically and histomorphometrically. Angiogenesis was assessed by immunohistochemistry against vascular endothelial progenitor cell marker (CD34) and the microvessel density (MVD) was calculated in the regenerated bone.
Results: The obtained histological and immunohistochemical results revealed superior bone regeneration and angiogenesis in the study group compared to the control group at both intervals. These results were confirmed by histomorphometric analysis.
Conclusion: Exposure of diabetic animals to hyperbaric oxygen accelerated defect regeneration, qualitatively and quantitively, enhanced the regenerative effect of β-tricalcium phosphate, and increased the proliferation of endothelial cells in the defects.