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1 School of Dentistry, The University of Queensland, Brisbane 4072, Australia; and 2 Faculty of Dentistry, Niigata University, Niigata 951-8514, Japan;
* corresponding author, e.gemmell{at}mailbox.uq.edu.au
CONTROVERSY The article that follows is part of an ongoing "Controversy" series. This review presents the case that destructive periodontitis is due to the nature of the lymphocytic infiltrate. In presenting this case, the authors have highlighted several controversial issues: (1) It is the inflammatory infiltrate that causes destruction and not the bacteria—that is, the lymphocytes and not the PMNs or macrophages are the primary source of destructive cytokines; (2) that susceptible subjects are characterized by the production of non-protective antibodies; and (3) that Th1 cells are associated with the stable lesion, while Th2 cells are associated with the progressive lesion. This review is intended to stimulate debate and further research, and hence may occasionally appear to be selective rather than comprehensive.
—Olav Alvares, Editor, CROBM
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) E2, 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.
Key words. Destructive, periodontitis, lymphocytes, Th1/Th2, cytokines
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