Neutrophil Receptor Modulation in the Pathogenesis of Periodontal Diseases

Dyke, Thomas E. Van

doi:10.1177/00220345840630031701

Cited by 25 publications

(12 citation statements)

References 18 publications

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“…A similar low association was found with untreated bacteria in contrast to the association obtained with immune serum. P. gingivalis proteases can also destroy opsonin receptors on the surface of PMNL and thereby aect the interaction (37,38). However, the eect on the PMNL receptors is probably negligible under the present experimental conditions since the incubation time of the bacteria with PMNL was too short to allow receptor degradation and the assay mixture contained increased concentration of serum, which counteracts speci®c protein degradation by P. gingivalis proteases (23, 39).…”

Section: Discussionmentioning

confidence: 92%

Anaerobic neutrophil‐dependent killing of Actinobacillus actinomycetemcomitans in relation to the bacterial leukotoxicity

Johansson¹,

Sandström²,

Claesson³

et al. 2000

European J Oral Sciences

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The effect of leukotoxin on the interaction of Actinobacillus actinomycetemcomitans with human polymorphonuclear leukocytes (PMNL) was studied under anaerobic conditions with strains able to produce high or low amounts of leukotoxin. PMNL morphology, phagocytosis and killing were examined by transmission electron microscopy and bioassays, respectively. At ratios of > or =25 bacteria/PMNL, a highly toxic A. actinomycetemcomitans strain completely destroyed the PMNL within 7 min, resulting in bacterial survival. Lowering the bacteria/PMNL-ratio enabled phagocytosis and killing of this highly toxic strain. A. actinomycetemcomitans strains with low leukotoxicity were effectively killed by PMNL under any condition. Presence of specific antibodies against A. actinomycetemcomitans or of anti-leukotoxin serum protected PMNL from being injured and allowed phagocytosis to occur. Pre-incubation of the leukotoxic strain with Porphyromonas gingivalis, a bacterium that destroys leukotoxin, abolished lysis of PMNL and inhibited phagocytosis of A. actinomycetemcomitans. The results show that leukotoxin may protect A. actinomycetemcomitans against phagocytosis by human PMNL. The protection occurs at a population level and in relation to the bacterial load. The size of the bacterial population required to counteract phagocytosis is dependent on the leukotoxin production of the strain.

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Section: Discussionmentioning

confidence: 92%

Anaerobic neutrophil‐dependent killing of Actinobacillus actinomycetemcomitans in relation to the bacterial leukotoxicity

Johansson¹,

Sandström²,

Claesson³

et al. 2000

European J Oral Sciences

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“…Therefore, it is unlikely that receptor occupancy of less than 1 % at relatively high concentrations of fMLP (20 nM) is different on PMNs from JP and healthy control subjects. Finally, different radiolabelled chemotactic peptides have been shown to exhibit similar binding characteristics in PMNs from JP patients, suggesting a common intrinsic mechanism responsible for reduced PMN function (25).…”

Section: Discussionmentioning

confidence: 92%

Altered free cytosolic calcium changes and neutrophil chemotaxis in patients with juvenile periodontitis

Agarwal

Reynolds

Duckett

et al. 1989

J of Periodontal Research

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Nearly 70-75% of patients with localized juvenile periodontitis (JP) have abnormal polymorphonuclear leukocytic (PMN) chemotaxis. The objective of this study was to determine whether the lower chemotactic response in PMNs from JP patients is associated with a defect in intracellular signal transduction, as measured by stimulus-induced changes in free cytosolic calcium (Ca2+) mobilization. We report that peptide chemoattractants such as N-formyl-methionyl-leucyl-phenylalanine (fMLP) and the complement fragment C5a in direct comparative studies induced lower amounts of initial Ca2+ mobilization in PMNs from JP patients than healthy controls, as monitored by intracellular fura-2 fluorescence. The initial resting levels of free cytosolic Ca2+ in PMNs from JP patients and normal individuals were found to be similar. fMLP and C5a both mobilized Ca2+ in PMNs in a dose-dependent manner. Treatment of PMNs from 0.16 to 20 nM fMLP and 0.2 to 20 nM C5a resulted in elevated levels of free cytosolic Ca2+. However, above 20 nM fMLP and 5 nM C5a concentrations the extent of total Ca2+ mobilization did not differ significantly. Although fMLP and C5a caused Ca2+ mobilization in PMN cells from JP and healthy control subjects, fMLP stimulation induced higher levels of free cytosolic Ca2+ mobilization in PMN cells from healthy control subjects (141.29 +/- 25.55 nM/2 x 10(6) PMNs), than PMNs from JP patients (62.33 +/- 23.76 nM/2 x 10(6) PMNs). Similarly C5a induced higher levels of Ca2+ mobilization in PMNs from healthy control individuals (130.43 +/- 18.26 nM Ca2+/2 x 10(6) PMNs)O, when compared to JP patients (49.92 +/- 14.92 nM Ca2+/2 x 10(6) PMNs).(ABSTRACT TRUNCATED AT 250 WORDS)

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“…At around the same time that the etiologic role of microorganisms in periodontal diseases was being firmly established, an intense effort was made to understand, in greater detail, the major inflammatory ⁄ immunologic events associated with periodontal infections (53,75,102,114,130,155,156,161,173,185,186,189,198,221,236,279,280,283). From a conceptual point of view the work of Page et al was particularly important (185)(186)(187)(188)(192)(193)(194).…”

Section: Role Of Host Responses In Destruction Of Periodontal Tissuesmentioning

confidence: 99%

Learned and unlearned concepts in periodontal diagnostics: a 50‐year perspective

Armitage¹

2013

Periodontology 2000

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In the past 50 years, conceptual changes in the field of periodontal diagnostics have paralleled those associated with a better scientific understanding of the full spectrum of processes that affect periodontal health and disease. Fifty years ago, concepts regarding the diagnosis of periodontal diseases followed the classical pathology paradigm. It was believed that the two basic forms of destructive periodontal disease were chronic inflammatory periodontitis and 'periodontosis'- a degenerative condition. In the subsequent 25 years it was shown that periodontosis was an infection. By 1987, major new concepts regarding the diagnosis and pathogenesis of periodontitis included: (i) all cases of untreated gingivitis do not inevitably progress to periodontitis; (ii) progression of untreated periodontitis is often episodic; (iii) some sites with untreated periodontitis do not progress; (iv) a rather small population of specific bacteria ('periodontal pathogens') appear to be the main etiologic agents of chronic inflammatory periodontitis; and (v) tissue damage in periodontitis is primarily caused by inflammatory and immunologic host responses to infecting agents. The concepts that were in place by 1987 are still largely intact in 2012. However, in the decades to come, it is likely that new information on the human microbiome will change our current concepts concerning the prevention, diagnosis and treatment of periodontal diseases.

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Neutrophil Receptor Modulation in the Pathogenesis of Periodontal Diseases

Cited by 25 publications

References 18 publications

Anaerobic neutrophil‐dependent killing of Actinobacillus actinomycetemcomitans in relation to the bacterial leukotoxicity

Anaerobic neutrophil‐dependent killing of Actinobacillus actinomycetemcomitans in relation to the bacterial leukotoxicity

Altered free cytosolic calcium changes and neutrophil chemotaxis in patients with juvenile periodontitis

Learned and unlearned concepts in periodontal diagnostics: a 50‐year perspective

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