Role in Periodontal Disease

During the progression of periodontal disease, the periodontal vasculature is profoundly affected and there is evidence that inflamed tissue enhances the expression of inflammatory mediators, which in their turn may promote angiogenesis. It has been found that there are greater amounts of VEGF in gingival crevicular fluid collected from clinically diseased sites than in fluid from healthy sites. VEGF production in gingival fibroblasts and periodontal ligament fibroblasts may enhance vascular permeability and the accumulation of inflammatory cells, which is similar to the inflammatory phase of periodontal disease. Therefore, VEGF may be associated with the etiology of periodontal disease, particularly specific to the gingiva, which is characterized by swelling, edema, gingival exudation, and heavy neovascularization.

Porphyromonas gingivalis and Actinobacillus actino-mycetemcomitans are major etiologic agents of periodontal disease. They contain a number of cell surface bioactive components such as fimbriae, extracellular vesicles, lipopolysaccharide, and outer membrane protein. These components induce numerous inflammatory mediators, such as prostaglandins, IL-8, and TNF-a, from human peripheral mononuclear cells and fibroblasts in periodontal tissue and are involved in the progression of periodontal disease. Recent research shows that gingival fibroblasts and peri-odontal ligament fibroblasts express VEGF in response to periodontopathic bacteria.

The possibility that VEGF is produced by gingival fibroblast and periodontal ligament fibroblasts has important implications for the study of periodontal disease and its progression, as well as the healing process that follows peri-odontal treatment.

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