Electron microscopic features of chronically inflamed human gingiva

Freedman, Harvey L.; Listgarten, Max A.; Taichman, Norton S.

doi:10.1111/j.1600-0765.1968.tb01937.x

Cited by 171 publications

(70 citation statements)

References 20 publications

(10 reference statements)

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“…This was consistent with earlier electron microscopic studies (Freedman et al, 1968;Garant, 1976;Zoellner et al, 1989a) and indicated that this type of productive vasculopathy is not confined to the gingival sulcus and pocket wall. Vrako and Benditt (1970) studied the re-vascularization of muscle subjected to repeated freezing and repair cycles, noting that multiple layers of vascular basal lamina reflected alternate episodes of endothelial death followed by repopulation by migrating cells and it is tempting to speculate that a similar mechanism is operative in periodontitis (Zoellner and Hunter, 1989b).…”

Section: Perivascular Hyaline Materials and Vascularsupporting

confidence: 91%

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

Zoellner

Chapple

Hunter

2002

Microscopy Res & Technique

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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.

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Section: Perivascular Hyaline Materials and Vascularsupporting

confidence: 91%

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

Zoellner

Chapple

Hunter

2002

Microscopy Res & Technique

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“…Free extracellular granules have also been described in inflamed connective tissue (15), wound healing sites (16), tuberculin sensitvity reactions (17), and delayed hypersensitivity and arthus reactions (18). We report the presence of two alkaline hydrolases, alkaline phosphatase and collagenase, in a welldefined cytoplasmic body characteristic of lysosomes.…”

mentioning

confidence: 69%

Collagenase: Localization in Polymorphonuclear Leukocyte Granules in the Rabbit

Robertson

Ryel

Taylor

et al. 1972

Science

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Polymorphonuclear leukocyte granules were submitted to zonal fractionation through a discontinuous sucrose gradient. Azurophilic and specific granules were enzymatically characterized by peroxidase and alkaline phosphatase activity, respectively. The enzymes formed modal distributions like those reported by others. Collagenase activity was consistently associated with the specific granules containing alkaline phosphatase.

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“…Our results provide some information about the possible mechanism of this phenomenon. The periodontal inflammation results in disruption of gingival basement membrane and stimulation ofgrowth ofjunctional epithelial cells (Freedman et al, 1968;Takarada et al, 1974). Binding of cytokines such as the various growth factors, as well as matrix molecules, to epithelial cells could result in both re-organization ofthe cell-surface receptors and altered cell behavior.…”

Section: Methodsmentioning

confidence: 99%

Expression of Fibronectin and Integrins in Cultured Periodontal Ligament Epithelial Cells

et al. 1992

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The process of attachment of epithelial cells obtained from the porcine periodontal ligament (cell rests of Malassez) to different extracellular matrix proteins and their expression of fibronectin and integrin receptors were studied by means of immunocytochemistry, in situ hybridization, and time-lapse cinemicrography techniques. The cell lines of periodontal ligament epithelial cells (PLE cells) attached to and spread rapidly on fibronectin, vitronectin, and type I collagen. One of the cell lines also attached to laminin, while the other cell line showed poor attachment to both laminin and Matrigel, a basement membrane material. By use of the in situ hybridization technique, some PLE cells were found to express the fibronectin gene strongly. Immunocytochemical staining localized fibronectin in extracellular fibrils and intracellular granules. Fibronectin was also found in the tracks left behind by the cells migrating on the substratum. Arg-gly-asp-ser peptide inhibited the attachment of the PLE cells to fibronectin, laminin, type I collagen, and vitronectin by 47%, 43%, 83%, and 94%, respectively, suggesting that the cell-matrix interactions were partly mediated by receptors related to the integrin family. Antibodies against the beta 1-integrin subunit stained the cell bodies and the plasma membrane projections of spreading cells. After 24 h or longer in culture, beta 1-integrins were localized to the regions of cell-cell contact. Cinemicrography of the arg-gly-asp-ser-peptide-treated cells demonstrated that the spreading and migration of isolated cells were prevented by the peptide. The peptide did not appear to dissociate the cell-cell contacts or interfere with migration of spread-cell colonies.(ABSTRACT TRUNCATED AT 250 WORDS)

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Electron microscopic features of chronically inflamed human gingiva

Cited by 171 publications

References 20 publications

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

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

Collagenase: Localization in Polymorphonuclear Leukocyte Granules in the Rabbit

Expression of Fibronectin and Integrins in Cultured Periodontal Ligament Epithelial Cells

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