Literature DB >> 3316294

Immunologic dysfunction in the pathogenesis of periodontal diseases.

B J Shenker1.   

Abstract

Despite significant progress in our understanding of the pathogenesis and etiology of periodontal diseases, the nature and contribution of the immune system to this disorder remains unclear. Several studies provide evidence for either a protective or destructive rôle. These conflicting findings are difficult to reconcile, since most interpretations tend to argue for a static contributory rôle (i.e., either protective or destructive) of the immune system. Current theories on the rôle of the immune response do not address these conflicting findings as well as the contradictory observation of a detectable immune response in the face of persistent infection in these patients. In this article, we present a model, based on available data, for the contribution of the immune system to the pathogenesis of periodontal disease. This model ascribes a dynamic rôle for the immune response. As documented in other infectious diseases, it is entirely possible, for example, that a state of immunologic dysfunction may occur in the earliest stages of periodontal disease progression; this may then be followed by a period of active immune reactivity (humoral and/or cellular) that would represent either a delayed or depressed response. This model is discussed in conjunction with recent findings that several suspected periodontal pathogens are capable of producing immunosuppressive agents. Many of the apparently contradictory clinical observations concerning the host immune response to oral pathogens and its correlation (or lack of) with both the progression and severity of periodontal disease may be accounted for in this model.

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Year:  1987        PMID: 3316294     DOI: 10.1111/j.1600-051x.1987.tb00989.x

Source DB:  PubMed          Journal:  J Clin Periodontol        ISSN: 0303-6979            Impact factor:   8.728


  12 in total

1.  Elevated CTLA-4 expression on CD4 T cells from periodontitis patients stimulated with Porphyromonas gingivalis outer membrane antigen.

Authors:  T Aoyagi; K Yamazaki; Y Kabasawa-Katoh; T Nakajima; N Yamashita; H Yoshie; K Hara
Journal:  Clin Exp Immunol       Date:  2000-02       Impact factor: 4.330

2.  Involvement of ganglioside GM3 in G(2)/M cell cycle arrest of human monocytic cells induced by Actinobacillus actinomycetemcomitans cytolethal distending toxin.

Authors:  Koji Mise; Sumio Akifusa; Shinobu Watarai; Toshihiro Ansai; Tatsuji Nishihara; Tadamichi Takehara
Journal:  Infect Immun       Date:  2005-08       Impact factor: 3.441

3.  CD4(+) T cells and the proinflammatory cytokines gamma interferon and interleukin-6 contribute to alveolar bone loss in mice.

Authors:  P J Baker; M Dixon; R T Evans; L Dufour; E Johnson; D C Roopenian
Journal:  Infect Immun       Date:  1999-06       Impact factor: 3.441

4.  Immune suppression induced by Actinobacillus actinomycetemcomitans: effects on immunoglobulin production by human B cells.

Authors:  B J Shenker; L A Vitale; D A Welham
Journal:  Infect Immun       Date:  1990-12       Impact factor: 3.441

5.  Recombinant Actinobacillus actinomycetemcomitans cytolethal distending toxin proteins are required to interact to inhibit human cell cycle progression and to stimulate human leukocyte cytokine synthesis.

Authors:  S Akifusa; S Poole; J Lewthwaite; B Henderson; S P Nair
Journal:  Infect Immun       Date:  2001-09       Impact factor: 3.441

6.  Induction of apoptotic cell death in peripheral blood mononuclear and polymorphonuclear cells by an oral bacterium, Fusobacterium nucleatum.

Authors:  A Jewett; W R Hume; H Le; T N Huynh; Y W Han; G Cheng; W Shi
Journal:  Infect Immun       Date:  2000-04       Impact factor: 3.441

7.  Fusobacterium nucleatum inhibits human T-cell activation by arresting cells in the mid-G1 phase of the cell cycle.

Authors:  B J Shenker; S Datar
Journal:  Infect Immun       Date:  1995-12       Impact factor: 3.441

8.  Immunosuppressive effects of Prevotella intermedia on in vitro human lymphocyte activation.

Authors:  B J Shenker; L Vitale; J Slots
Journal:  Infect Immun       Date:  1991-12       Impact factor: 3.441

9.  Flow cytometric approach to human polymorphonuclear leukocyte activation induced by gingival crevicular fluid in periodontal disease.

Authors:  R Biselli; C Ferlini; C Di Murro; M Paolantonio; A Fattorossi
Journal:  Inflammation       Date:  1995-08       Impact factor: 4.092

10.  The relationship between colonization and haemagglutination inhibiting and B cell epitopes of Porphyromonas gingivalis.

Authors:  C G Kelly; V Booth; H Kendal; J M Slaney; M A Curtis; T Lehner
Journal:  Clin Exp Immunol       Date:  1997-11       Impact factor: 4.330

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