The protective nature of host responses in periodontal diseases

Ebersole, Jeffrey L.; Taubman, Martin A.

doi:10.1111/j.1600-0757.1994.tb00021.x

Cited by 227 publications

(231 citation statements)

References 182 publications

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“…Taken together, however, these data seem to support the hypothesis that Th1 cells are associated with the stable lesion and a Th2 response with disease progression. In contrast to these studies, Ebersole and Taubman (1994) found that IFN-␥message was prominently expressed by diseased gingival tissue cells (Table). Cytokine profiles of cells extracted from six patients were consistent with Th1 cells in that they were IL-2-and IFN-␥ -positive but negative for IL-4 and IL-5.…”

Section: (B) T-cells Inperiodontal Diseasecontrasting

confidence: 47%

“…Non-susceptibility to periodontal breakdown may involve a predominantly Th1-like response, resulting in T-cell activation, cellmediated immunity, IFN-␥enhancement of innate immunity, and, if necessary, the production of protective antibodies (Fig., A). On the other hand, Ebersole and Taubman (1994) have formulated their hypothesis (Fig., B) based on their adoptive transfer experiments using the Th2 clone A3. They speculate that Th2 cells abrogate periodontal disease symptoms and Th1 cells enhance disease.…”

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confidence: 99%

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DestructivePeriodontitisLesions areDetermined by theNature of theLymphocyticResponse

Gemmell

Yamazaki²,

Seymour³

2002

Critical Reviews in Oral Biology & Medicine

177

152

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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.

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Section: (B) T-cells Inperiodontal Diseasecontrasting

confidence: 47%

mentioning

confidence: 99%

DestructivePeriodontitisLesions areDetermined by theNature of theLymphocyticResponse

Gemmell

Yamazaki²,

Seymour³

2002

Critical Reviews in Oral Biology & Medicine

177

152

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“…In all of these models, infection with P. gingivalis elicits a cell-mediated Th1 type response characterized by increased production of IFN-γ, IL-12 and TNFα, and leads to increased inflammation and bone destruction [5,6]. Similarly, high levels of Th1 cytokines in gingival tissues and mononuclear cells, and gingival crevicular fluid are associated with increased periodontal disease progression [7,8,9]. We recently showed that dental pulp infection with P. gingivalis causes extensive inflammation and bone destruction and is associated with a strong Th1 response, characterized by increased intra-lesional production of IFNγ and IL-1 [6].…”

Section: Introductionmentioning

confidence: 99%

Th1 biased response to a novel Porphyromonas gingivalis protein aggravates bone resorption caused by this oral pathogen

Leshem

Kashino²,

Gonçalves

et al. 2008

Microbes and Infection

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In previous studies we showed that biasing the immune response to Porphyromonas gingivalis antigens to the Th1 phenotype increases inflammatory bone resorption caused by this organism. Using a T cell screening strategy we identified eight P. gingivalis genes coding for proteins that appear to be involved in T-helper cell responses. In the present study we characterized the protein, encoded by PG_1841 gene and evaluated its relevance in the in bone resorption caused by P. gingivalis because subcutaneous infection of mice with this organism resulted in the induction of Th1 biased response to the recombinant PG1841 antigen molecule. Using an immunization regime that strongly biases toward the Th1 phenotype followed by challenge with P. gingivalis in dental pulp tissue, we demonstrate that mice pre-immunized with rPG1841 developed severe bone loss compared with control immunized mice. Pre-immunization of mice with the antigen using a Th2 biasing regime resulted in no exacerbation of the disease.These results support the notion that selected antigens of P. gingivalis are involved in a biased Th1 host response that leads to the severe bone loss caused by this oral pathogen.

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“…In humans, numerous studies have supported the hypothesis that Th1 cells are associated with stable lesions and Th2 cells are associated with progressive lesions [35][36][37][38][39][40]. In contrast, several studies have demonstrated that upregulation of Th1 responses or downregulation of Th2 responses are involved in periodontal tissue destruction [41][42][43]. Moreover, others have shown a comparable presence of Th1 and Th2 cytokines in human periodontitis lesions [44][45][46][47][48][49].…”

Section: Cd4mentioning

confidence: 96%

The Role of Distinct T Cell Subsets in Periodontitis—Studies from Humans and Rodent Models

Okui

Aoki-Nonaka

Nakajima

et al. 2014

Curr Oral Health Rep

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The protective nature of host responses in periodontal diseases

Cited by 227 publications

References 182 publications

DestructivePeriodontitisLesions areDetermined by theNature of theLymphocyticResponse

DestructivePeriodontitisLesions areDetermined by theNature of theLymphocyticResponse

Th1 biased response to a novel Porphyromonas gingivalis protein aggravates bone resorption caused by this oral pathogen

The Role of Distinct T Cell Subsets in Periodontitis—Studies from Humans and Rodent Models

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