The minimally invasive surgery (MIS) yields favorable clinical outcomes for periodontal regeneration therapy. However, there have been few reports on the histological analysis underlying these outcomes. In this study, we created periodontal defects for investigate two different surgical procedures by histological assessment at the early wound healing process. The maxillary second molars of Sprague-Dawley (SD) male rats at twelveweek-old were used. In the control (open flap) left maxillary, mucoperiosteal flap resection was performed on the first to third molars of both the buccal and palate sides. The right maxillary served as the experimental (minimally invasive) side and the resection was performed only on the second molar of the palatal side. Periodontal defects were then created to the palatal root of second molar at the both sides with round bur. On each of days 1, 3, and 5 after surgery, five rats were euthanized. Sections were prepared and subjected to hematoxylin-eosin staining, and immunohistochemical staining on type III collagen followed by microscopic observations and statistical analysis. In the experimental side, the inflammatory cell infiltration disappeared earlier compared to the control side. The defect area was positive for type III collagen staining in the experimental side, which were significantly greater on days 1, 3, and 5 after surgery. The results suggest that wound healing accelerated by wound stability caused by fibrous tissue generation with type III collagen formation, using minimally invasion by single flap line periodontal surgery, caused by fibrous tissue generation.

Diabetes mellitus is an important risk factor for periodontitis. Although numerous complications are associated with the disease, all of these are attributed to vascular disorders and are closely related to the potent angiogeneic factor vascular endothelial growth factor (VEGF). However, it remains unknown how diabetes mellitus/hyperglycemia-associated VEGF expression affects alveolar bone resorption in the periodontium. The aim of this study was to determine the level of adverse effect on bone resorption of diabetes mellitus-associated VEGF. Therefore, we induced experimental periodontitis with injections of the endotoxin lipopolysaccharide (LPS) from Porphyromonas gingivalis in diabetic rats, measured the level of bone resorption, and observed VEGF expression and localization of osteoclasts in the periodontium. Eight-week-old male Goto-Kakizaki (GK) rats were in the experimental group, and male Wistar rats were in the control group. Experimental periodontitis was induced by injecting P. gingivalis LPS and inserting ligatures. All rats were euthanized and underwent micro X-ray computed tomography (CT) to acquire bone resorption image, in which the distance between the cement-enamel junction and the alveolar bone crest was measured to determine the amount of bone resorption. Samples were prepared and underwent immunohistochemical staining with an anti-VEGF monoclonal antibody and tartrate-resistant acid phosphatase (TRAP) staining. The amount of bone resorption measured by micro X-ray CT images was significantly greater in the experimental group than in the control group. Immunohistochemical staining showed that VEGF expression levels on the alveolar bone surface and around microvessels in the gingival connective tissue were higher in the experimental group than in the control group. On the alveolar bone surface, localization of TRAP-positive cells and bone resorption lacunae from the same sites were observed in both groups. These results suggest that VEGF expression in the periodontium caused by hyperglycemia in rats with diabetes mellitus affects P. gingivalis LPS-induced alveolar bone resorption.