Proliferative responses of endothelial cell populations to experimentally induced inflammatory lesions of gingival connective tissues in the cynomolgus monkey (Macaca fascicularis)

Abstract

1) Experimentally induced inflammation and connective tissue destruction in the gingival connective tissues of Cynomolgus monkeys is associated with site-specific perturbations in the turnover of endothelial cells that is closely linked to lymphocytic infiltration; 2) the vascular response is a generalized increase in endothelial cell proliferation and blood vessel numbers but not lumen size or number of endothelial cells, suggesting the existence of homeostatic controls for preservation of the whole population in a steady state.

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

“…Also, essentially identical observations were made with regard to vessel profile number adjacent to the pocket epithelium in humans by others (Bonakdar et al, 1997;Johnson et al, 1999). Nemeth et al (1994) also observed an increase in vessel profile number in the sulcular region in experimental lesions in monkeys. This was further confirmed in human periodontal disease, when advanced human periodontitis was compared with minimally inflamed tissues using more readily quantified con-focal microscopic methods (Chapple et al, 2000).…”

“…It seems reasonable to suggest that similar mechanisms are at work in inflamed gingival tissues and that extensive accumulation of vascular basement membrane material unrelated to viable endothelial cells is due to either crises during neovascularisation or loss of receptor signals to guide replacement of the original vascular template. This idea is partially supported by the work of Nemeth et al (1994) who suggested that data from endothelial cell counts, vessel profile counts, vascular volume measures, and the labeling of endothelium with tritiated thymidine in monkey lesions could be in part accounted for by endothelial cell death. In this context, the cysteine proteinases of P. gingivalis have the capacity to disrupt vascular networks formed in vitro (Fig.…”

“…Also, these authors pooled data from different parts of gingival biopsies, so that the strong changes observed in the sulcular and pocket regions (Chapple et al, 2000;Zoellner and Hunter, 1991a) may have been obscured (Brecx et al, 1992). Similarly, despite observing an increase in sulcular vessel number, Nemeth et al (1994) did not find any evidence for dilation of the vessels in experimental gingivitis and destructive lesions in monkeys, perhaps again reflecting work with relatively newly established lesions (Nemeth et al, 1994).…”

“…The basis for dilation of vessels is unclear, but it seems reasonable to conclude that dilation reflects either or both hypertrophy and spreading of individual endothelial cells or endothelial proliferation. With regard to the possible role of proliferation in this process, it is interesting to note the approximately fourfold increase in the number of endothelial cells incorporating radioactive thymidine subjacent to the sulcular epithelium in experimental inflammatory and destructive lesions in monkeys (Nemeth et al, 1994). It has been argued that microvascular dilation in chronic inflammation represents a form of angiogenesis (Thurston et al, 1998;Zoellner and Hunter, 1991a).…”

Development and degeneration of the arterial system in the mesonephros and metanephros of chicken embryos

“…New interest about vasculogenesis and angiogenesis has arisen due to their close relation to tumoral neovascularization (Folkman and Cotran, 1976;Grunt et al, 1986;Coffin and Poole, 1988;Pardanaud et al, 1989;Poole and Coffin, 1989;Rhodin and Fujita, 1989;Burri and Tarek, 1990;Arnold and West, 1991;Phillips et al, 1991) and inflammation (Bergstrom, 1992;Nemeth et al, 1994).…”