Microvasculature in gingivitis and chronic periodontitis: Disruption of vascular networks with protracted inflammation

Abstract

Gingivitis occurring when bacterial plaque accumulates in the gingival crevice provides a convenient and interesting model for chronic inflammation in humans. In some patients, gingivitis progresses to the destructive lesion of periodontitis, involving the formation of periodontal pockets. The basis for pocket formation and progression is not as yet clear, although neutrophilic polymorphonuclear leukocytes (PMN) appear to play a protective role. Vascular changes appear to either facilitate or inhibit PMN function with the effect of either protecting from, or stimulating, periodontitis. Contrary to most circumstances, high endothelial cells in periodontitis are involved with PMN rather than lymphocyte emigration. Expansion of the microvasculature through increased vascular diameter and tortuosity as well as the development of high endothelial cells appears to protect from periodontitis by increasing the supply of both plasma defense factors and PMN to the tissues. Vascular changes that may oppose this and promote periodontitis are the formation of perivascular hyaline material and accumulation of basement membrane rests. The inadequate tissue turnover that accumulation of these vascular products represents can be argued as a vascular response to a chronic inflammation that has failed to eliminate the irritant. It is suggested that these vascular changes may account for the highly localized and burst-like pattern of pocket formation in periodontitis. Finally, it is possible that the recent observation that periodontitis is an independent risk factor for systemic vascular disease may reflect stimulation of acute phase protein synthesis by cytokines released by periodontal high endothelial cells.

Gingipains fromPorphyromonas gingivalisW83 Induce Cell Adhesion Molecule Cleavage and Apoptosis in Endothelial Cells

“…Because of the degradation of proteins of epithelial cell-cell junctional complexes, P. gingivalis may be able to invade and spread in deeper structures via a paracellular pathway (38). The periodontal pocket is a highly vascularized tissue in close proximity to the bacterial biofilm (15) that is separated from endothelial cells by one to two epithelial cells and a negligible layer of extracellular matrix (71). It has been suggested that in periodontitis, proapoptotic signals, such as direct toxic effects of bacterial products from the nearby plaque, at times overwhelm the usual antiapoptotic functional signals that maintain periodontal vessels (71).…”

Gingipains from Porphyromonas gingivalis W83 Synergistically Disrupt Endothelial Cell Adhesion and Can Induce Caspase-Independent Apoptosis

“…diseased periodontal pocket, there is a close proximity between the bacterial biofilm and endothelial cells, which can lead to endothelial cell damage (59). Furthermore, there is evidence for the presence of apoptotic cells in periodontitis (19,34,51,57).…”

Quantitative Parameters of Interdental Gingiva in Chronic Periodontitis Patients with IFN-γ Gene Polymorphism

“…Chapple et al (2000) found that vascular expansion in periodontal pocket was related to CP progression and the thickened basement membrane of capillaries and venules represented an evidence of angiogenic activity during inflammation. Vascular response to inflammation includes angiogenesis and capillaries dilation (Pinchback et al, 1996;Chapple et al, 2000;Zoellner et al, 2002). The present study demonstrated that Vv of blood vessels in CP gingival tissues was significantly higher than that of healthy subjects.…”