Periodontal Manifestations of Cyclic Neutropenia

Cohen, D. Walter; Morris, Alvin L.

doi:10.1902/jop.1961.32.2.159

Cited by 132 publications

(50 citation statements)

References 19 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: 61%

“…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: 61%

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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“…For example, patients with neutrophil disorders suffer from severe periodontal disease, often leading to early loss of teeth. Neutrophil disorders associated with severe forms of destructive periodontal disease include: drug-induced agranulocytosis (Bauer, 1946), cyclic neutropenia (Cohen and Morris, 1961), the Chediak-Higashi syndrome (Tempel et al, 1972;Hamilton and Giansanti, 1974), abnormality in the neutrophil surface glycoprotein receptor CR3 (Thompson et al, 1984), abnormalities in the neutrophil surface adherence protein LFA-1 (Anderson et al, 1985), and abnormalities of neutrophil glycoprotein 138 (Anderson et al, 1984). Charon et al (1985) have shown that patients with Job's syndrome, cyclic neutropenia, and chronic granulomatous disease often suffer from oral mucosal ulcerations and severe gingivitis.…”

mentioning

confidence: 99%

1985 Kreshover lecture. Molecular Factors Influencing Neutrophil Defects in Periodontal Disease

et al. 1986

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Major advances in our understanding of the role of the neutrophil in host defense against periodontal organisms have been made through studies of localized juvenile periodontitis (LJP). Several lines of evidence suggest that LJP is an infectious process closely associated with Actinobacillus (Haemophilus) actinomycetemomitans as a causative agent, although other organisms may also participate. The immunologic profile of LJP patients suggests that a cell-associated neutrophil locomotory dysfunction is a key underlying immunodeficiency resulting in increased susceptibility to periodontal infection. In addition, LJP patients often exhibit cervical lymphadenopathy and IgG-hypergammaglobulinemia, and a markedly elevated antibody response to the infecting organism, A. actinomycetemcomitans, is found in the serum and crevicular fluid of most patients. Evaluation of the locomotory properties of LJP neutrophils shows that random migration and chemokinesis are normal; however, about 70% of the LJP patients suffer from a defect in chemotaxis, with their neutrophils responding poorly to bacterial chemotactic factors, synthetic chemotactic peptides, and complement fragments (C5a). Depressed chemotaxis of LJP neutrophils is paralleled by their reduced capacity to bind the synthetic chemotactic peptide N-formylmethionylleucylphenylalanine (FMLP), as well as C5a. Furthermore, there is a reduction in the amount of glycoprotein 110, a neutrophil membrane matrix component and differentiation antigen which is associated with FMLP- and possibly also C5a-mediated chemotaxis. Reduction of C5a and of FMLP ligand binding, decreased expression of GP-110, and reduced neutrophil chemotaxis are consistent with a stem cell maturation error in LJP patients. This is further supported by studies demonstrating increased expression of CR2, the C3d/EBV receptor, on peripheral blood neutrophils of LJP patients. CR2 receptors are normally present on immature human neutrophils but are lost during the maturation process. These alterations in neutrophil surface components and their reduced chemotaxis may result from a genetically determined abnormality. Studies demonstrating the familial nature of both the neutrophil chemotactic disorder and the clinical entity represented by localized juvenile periodontitis point to a strong role for genetic determinants in the disease which affect neutrophil surface receptors.

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“…A reduction in the number of circulating neutrophils or the alteration of one or more of the neutrophil functions results in severe, rapid, precocious periodontal disease (Tempel et al, 1972;Bauer, 1946;Cohen and Morris, 1961;Arnold and Hoffman, 1979;Rabson et al, 1978;Quie, 1969;Issekutz et al, 1979;Clark et al, 1973). The clearest example of this phenomenon is in patients with localized juvenile periodontitis (LJP).…”

Section: Introductionmentioning

confidence: 99%

Neutrophil Receptor Modulation in the Pathogenesis of Periodontal Diseases

Dyke

1984

J Dent Res

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The role of the neutrophil as a primary protective cell in the pathogenesis of periodontal disease has been well established. In this paper, the role of receptor modulation on the neutrophil surface is discussed as a possible mechanism for neutrophil functional abnormalities. Using localized juvenile periodontitis (LJP) as a model, the direct inhibition of neutrophils by bacterial products is discussed as a possible mechanism for local neutrophil dysfunction. In both disease processes, neutrophil receptor modulation plays a central role.

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Periodontal Manifestations of Cyclic Neutropenia

Cited by 132 publications

References 19 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

1985 Kreshover lecture. Molecular Factors Influencing Neutrophil Defects in Periodontal Disease

Neutrophil Receptor Modulation in the Pathogenesis of Periodontal Diseases

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