Host Factors in Juvenile Periodontitis

Cogen, Ronald B.; Roseman, Jeffrey M.; Al‐Joburi, W.; Louv, William C.; Acton, Ronald T.; Barger, Bruce O.; Go, Rodney C.P.; Rasmussen, Robert A.

doi:10.1177/00220345860650030401

Cited by 40 publications

(25 citation statements)

References 39 publications

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“…9). Since leukocyte emigration is known to occur primarily in post-capillary venules, this observation was consistent with both the important role of PMN in defence against periodontitis as well as the location of PHELV in postcapillary venules draining the pocket wall and sulcus (Bauer, 1946;Ciancola et al, 1977;Cogen et al, 1986;Cohen and Morris, 1961;Kalmar et al, 1987;Katsuragi et al, 1988;McMullen et al, 1981;Temple et al, 1972;Ramamurthy et al, 1979;Van Dyke et al, 1984). However, massive PMN emigration from HELV in the absence of significant lymphocyte emigration did seem inconsistent with the widely held assumption that the "high endothelial morphology" reflects specific adaptations for lymphocyte emigration.…”

Section: High Endothelial Cells In Gingivitissupporting

confidence: 57%

“…Neutrophils are thought to have a particularly important role in defending the host from periodontitis, so that defects in neutrophil production, emigration, migration, chemotaxis, and intracellular killing are associated with rapidly progressive forms of the disease in adolescents and adults (Bauer, 1946;Cainciola et al, 1977;Cogen et al, 1986;Cohen and Morris, 1961;Gainet et al, 1999;Kalmar et al, 1987;Katsuragi et al, 1987;McMullen et al, 1981;Ramamurthy et al, 1979;Temple et al, 1972;Van Dyke et al, 1984).…”

Section: Gingivitis and Periodontitis Definition Of Gingivitis And Pementioning

confidence: 99%

“…PMN defects are common to virtually all of the rapidly progressive forms of periodontitis while PMN defects are not seen in the more common chronic adult form of the disease (Bauer, 1946;Ciancola et al, 1977;Cogen et al, 1986;Cohen and Morris, 1961;Gainet et al, 1999;Kalmar et al, 1987;Katsuragi et al, 1987;McMullen et al, 1981;Ramamurthy et al, 1979;Temple et al, 1972;Van Dyke et al, 1984). From this, it is tempting to speculate that highly localized defects in PMN function are responsible for periodontitis in patients with common chronic adult periodontitis.…”

Section: Characteristics Of Periodontitis That Are Unexplained But Mmentioning

confidence: 99%

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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: High Endothelial Cells In Gingivitissupporting

confidence: 57%

Section: Gingivitis and Periodontitis Definition Of Gingivitis And Pementioning

confidence: 99%

Section: Characteristics Of Periodontitis That Are Unexplained But Mmentioning

confidence: 99%

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

Zoellner

Chapple

Hunter

2002

Microscopy Res & Technique

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“…Cogen et al . [4] reported a significant decrease in the phagocytosis and chemotactic ability of peripheral blood PMNs in both LJP and generalized juvenile periodontitis (GJP) subjects. Suzuki et al ,[16] stated that the radioisotope phagocytic indices were lower in a majority of the LJP subjects and the defect remained unchanged even after periodontal therapy.…”

Section: Discussionmentioning

confidence: 99%

“…The neutrophils could be easily differentiated and were subjected to phagocytosis without any further treatment. [4]…”

Section: Methodsmentioning

confidence: 99%

Phagocytic activity of peripheral blood and crevicular phagocytes in health and periodontal disease

Asif¹,

Kothiwale²

2010

J Indian Soc Periodontol

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Background:Neutrophils constitute the main phagocytic cell system in mammalian host defense against an infecting agent. Abnormalities in leukocyte number and function are associated with increased susceptibility to periodontal diseases. The purpose of this study is to evaluate the in vitro phagocytic properties of crevicular and peripheral blood neutrophils in healthy and periodontitis subjects.Patients and Methods:A total of 30 subjects, that is, 10 patients in each of the following three groups: healthy controls, chronic periodontitis (CP), and localized aggressive periodontitis (LAP), were included in the study. The neutrophils were isolated from the peripheral blood and gingival crevice and tested for phagocytosis of Candida albicans. The percentage of leukocytes with ingested C. albicans was determined by light microscopy.Results:A significant reduction in the phagocytic activity of crevicular fluid polymorphonuclear neutrophils (CF-PMN) of LAP subjects (mean: 54.3±7)(P<0.001) was observed, compared to healthy controls (mean: 74.2±9) and chronic periodontitis subjects (mean: 69±9)(P=0.352). The mean percentage of peripheral blood polymorphonuclear neutrophils (PMNs) with phagocytosis of opsonized C. albicans in LAP patients was significantly reduced (mean: 74.9±5)(P<0.0068) compared to the phagocytic activity of neutrophils from controls (mean:82.1±3) and chronic periodontitis subjects (mean: 82.0±5)(P=0.970). There was no significant reduction in the phagocytic activity of CF PMNs (mean: 69±9) (P=0.35) and peripheral blood PMNs (mean: 82.5)(P=0.97) in the chronic periodontitis group when compared to the control group.Conclusion:The phagocytic activity of both crevicular and peripheral neutrophils in subjects with periodontitis is altered, increasing the susceptibility to periodontitis. Thus individual susceptibility may be an additional and important modifying factor in the pathogenesis of periodontal disease.

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Thermal Regulation of FMLP Receptors on Human Neutrophils

Coles

Freer

Carchman

1989

Journal of Leukocyte Biology

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Polymorphonuclear leukocytes (PMNs) from subjects diagnosed as having juvenile periodontitis (JP) have been categorized on the basis of their chemotactic (CTX) response to f-met-leu-phe (FMLP) when assayed concurrently with PMNs from periodontally healthy subjects (HP). When PMNs from JP groups demonstrating depressed CTX were assayed for lysosomal enzyme secretion (LES) in response to FMLP, there were no significant differences with respect to rate or amount. Significant differences were observed between HP and chemotactically depressed JP cells when assessed for FMLP receptor ligand binding at 23 degrees C, but not at 4 degrees C. Receptor differences observed at 23 degrees C in HP cells included an increase in amount of total binding, number of receptors, and available displaceable binding sites, compared with the chemotactically depressed JP PMNs, whereas the receptor affinities were similar. These data suggest that differences in FMLP receptor density in JP PMN that are chemotactically depressed may be related to processes that modulate receptor mobility and/or expression.

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Host Factors in Juvenile Periodontitis

Cited by 40 publications

References 39 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

Phagocytic activity of peripheral blood and crevicular phagocytes in health and periodontal disease

Thermal Regulation of FMLP Receptors on Human Neutrophils

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