Neutrophil chemotactic behaviour in patients with early‐onset forms of periodontitis

Kinane, D. F.; Cullen, Connie; Johnston, Frances A.; Evans, Clive W.

doi:10.1111/j.1600-051x.1989.tb01649.x

Cited by 42 publications

(23 citation statements)

References 13 publications

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“…An other fact that may explain tiie discrepancy of results is the daily individual variability since celis for a given patient may dispiay variabie locomotory behaviour on a day-to-day basis (Kinane et al, 1989), However, it seems difficult to think that if the defect is an intrinsic one, it appears and disappears depending on time, unless the presence or the absence of certain periodotitai pathogens infiuence the results. Indeed, Hiii et ai.…”

Section: Discussionmentioning

confidence: 99%

Ex vivo studies of polymorphonuclear neutrophils from patients with early‐onset forms of periodontitis (I).

Mouynet¹,

Delamaire²,

Goff³

et al. 1994

J Clinic Periodontology

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The polymorphonuclear neutrophil (PMN) appears to be an important cell in the protection of the host from pathogenic periodontal microorganisms and, despite some reports to the contrary, it is generally assumed that early-onset forms of periodontal disease (including both juvenile and rapidly progressing periodontitis) are associated with a defect in PMN chemotactic behaviour. The purpose of the present study was to examine the peripheral PMN chemotactic behaviour, using the under agarose method, in 4 groups, namely healthy periodontium group (n = 7), gingivitis group (n = 8), early-onset periodontitis group (n = 17) and adult periodontitis group (n = 8). PMN from early-onset periodontitis patients showed normal random and chemotactic locomotory behaviour when compared with those of PMN from subjects of the other groups. No statistically significant difference could be found among the 4 studied groups, with regard to spontaneous and oriented migration.

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Section: Discussionmentioning

confidence: 99%

Ex vivo studies of polymorphonuclear neutrophils from patients with early‐onset forms of periodontitis (I).

Mouynet¹,

Delamaire²,

Goff³

et al. 1994

J Clinic Periodontology

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show abstract

“…Kinane et al. performed an extensive study of polymorphonuclear neutrophil chemotaxis from a series of these patients with aggressive periodontitis and found not only no defect, but rather an overactivation of these cells in the peripheral blood of patients with aggressive periodontitis. Thus, although polymorphonuclear neutrophils are critical in the defense of the periodontium, as evidenced by the rapid destruction in conditions such as leukocyte adhesion deficiency, a neutrophil chemotactic defect does not appear to be the key mechanism.…”

Section: Innate Immunitymentioning

confidence: 99%

Host response in aggressive periodontitis

Kulkarni¹,

Kinane²

2014

Periodontology 2000

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It is critical to understand the underlying host responses in aggressive periodontitis to provide a better appreciation of the risk and susceptibility to this disease. Such knowledge may elucidate the etiology and susceptibility to aggressive periodontitis and directly influence treatment decisions and aid diagnosis. This review is timely in that several widely held tenets are now considered unsupportable, namely the concept that Aggregatibacter actinomycetemycomitans is the key pathogen and that chemotactic defects in polymorphonuclear leukocytes are part of the etiopathology. This review also serves to put into context key elements of the host response that may be implicated in the genetic background of aggressive periodontitis. Furthermore, key molecules unique to the host response in aggressive periodontitis may have diagnostic utility and be used in chairside clinical activity tests or as population screening markers. It is becoming increasingly appreciated that the microbial etiology of aggressive periodontitis and the histopathology of this disease are more similar to than different from that of chronic periodontitis. An important therapeutic consideration from the lack of support for A. actinomycetemycomitans as a critical pathogen here is that the widely held belief that tetracycline had a role in aggressive periodontitis therapy is now not supported and that antibiotics such as those used effectively in chronic periodontitis (metronidazole and amoxicillin) are not contraindicated. Furthermore, A. actinomycetemycomitans-related molecules, such as cytolethal distending toxin and leukotoxin, are less likely to have utility as diagnosis agents or as therapeutic targets.

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“…Abnormal polymorphonuclear leukocyte chemotaxis has been demonstrated in African-American subjects with EOP, 16 whereas investigations in European Caucasian populations have failed to identify such defects. [17][18][19] Northern Ireland has a homogeneous, relatively stable, predominantly Caucasian population of 1.6 million and the province is therefore well suited to the study of conditions such as EOP. The current study investigated the phenotype of a group of subjects with early-onset forms of periodontitis as part of an ongoing investigation of the environmental and genetic factors associated with EOP in Northern Ireland.…”

mentioning

confidence: 99%