Destructive periodontitis lesions are determined by the nature of the lymphocytic response

Gemmell, E, Yamazaki, K and Seymour, GJ (2002) Destructive periodontitis lesions are determined by the nature of the lymphocytic response. Critical Reviews In Oral Biology & Medicine, 13 1: 17-34. doi:10.1177/154411130201300104

Author Gemmell, E
Yamazaki, K
Seymour, GJ
Title Destructive periodontitis lesions are determined by the nature of the lymphocytic response
Journal name Critical Reviews In Oral Biology & Medicine   Check publisher's open access policy
ISSN 1045-4411
Publication date 2002-01-01
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1177/154411130201300104
Open Access Status Not yet assessed
Volume 13
Issue 1
Start page 17
End page 34
Total pages 18
Editor OF Alvares
Place of publication USA
Publisher International and American Association for Dental Research
Language eng
Subject C1
320899 Dentistry not elsewhere classified
730112 Oro-dental and disorders
Abstract It is now 35 years since Brandtzaeg and Kraus (1965) published their seminal work entitled Autoimmunity and periodontal disease. Initially, this work led to the concept that destructive periodontitis was a localized hypersensitivity reaction involving immune complex formation within the tissues. In 1970, Ivanyi and Lehner highlighted a possible role for cell-mediated immunity, which stimulated a flurry of activity centered on the role of lymphokines such as osteoclast-activating factor (OAF), macrophage-activating factor (MAF), macrophage migration inhibition factor (MIF), and myriad others. In the late 1970s and early 1980s, attention focused on the role of polymorphonuclear neutrophils, and it was thought that periodontal destruction occurred as a series of acute exacerbations. As well, at this stage doubt was being cast on the concept that there was a neutrophil chemotactic defect in periodontitis patients. Once it was realized that neutrophils were primarily protective and that severe periodontal destruction occurred in the absence of these cells, attention swung back to the role of lymphocytes and in particular the regulatory role of T-cells. By this time in the early 1990s, while the roles of interleukin (IL)-1, prostaglandin (PG) E-2, and metalloproteinases as the destructive mediators in periodontal disease were largely understood, the control and regulation of these cytokines remained controversial. With the widespread acceptance of the Th1/Th2 paradigm, the regulatory role of T-cells became the main focus of attention, Two apparently conflicting theories have emerged. One is based on direct observations of human lesions, while the other is based on animal model experiments and the inability to demonstrate IL-4 mRNA in gingival extracts. As part of the Controversy series, this review is intended to stimulate debate and hence may appear in some places provocative. In this context, this review will present the case that destructive periodontitis is due to the nature of the lymphocytic infiltrate and is not due to periodic acute exacerbations, nor is it due to the so-called virulence factors of putative periodontal pathogens.
Keyword Dentistry, Oral Surgery & Medicine
Actinobacillus-actinomycetemcomitans Leukotoxin
Gingival Crevicular Fluid
B-cell Activation
Early-onset Periodontitis
Alveolar Bone Loss
Rapidly Progressive Periodontitis
Localized Juvenile Periodontitis
Ligature-induced Periodontitis
Messenger-rna Expression
Q-Index Code C1
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Excellence in Research Australia (ERA) - Collection
School of Dentistry Publications
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Citation counts: TR Web of Science Citation Count  Cited 132 times in Thomson Reuters Web of Science Article | Citations
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Created: Wed, 15 Aug 2007, 03:01:19 EST