Polyclonal B‐cell activating capacities of gram‐positive bacteria frequently isolated from periodontally diseased sites

Sl, Donaldson; Ph, Bick; We, Moore; Rr, Ranney; Ja, Burmeister; Jg, Tew

doi:10.1111/j.1600-0765.1982.tb01178.x

Cited by 32 publications

(17 citation statements)

References 17 publications

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“…As indicated previously by many authors, these periodontally associated bacteria, composed of both Gram-and Gram+ varieties are capable of inducing a significant degree of B-and T-cell responses in vitro (Carpenter et al 1984, Baker & Tondreau 1985. Selected varieties of these isolates were found to polyclonally induce significant levels of IgG and IgM in culture supernatants obtained from peripheral blood lymphocyte cultures (Clagett et al 1980. Donaldson et al 1982, Carpenter et al 1984.…”

Section: Discussionmentioning

confidence: 60%

Immunohistological analysis of gingival lymphocytes in adult periodontitis

Çelenligil

Kartsu²,

Ruacan

et al. 1992

J Clin Pharm Ther

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Inflammatory periodontal diseases are mediated by interactions between the dental plaque and the components of the host immune system. This study was designed to analyse the phenotypic properties of gingival lymphocytes in adult periodontitis. Biopsies were obtained from 12 patients and aged between 35 and 55 years. The tissues were processed for both histopathological and immunohistological examinations. Gingival tissue lymphocytes were identified using monoclonal and polyclonal antibodies with the immunoperoxidase technique. All speciments revealed a significant degree of CD3( + ) cell infiltration beneath the pocket epithelium, which is located adjacent to the bacterial plaque, compared to that on the oral epithelial side. CD4( + ) and CD8( + ) cells were evenly distributed within these infiltrates. Numerous HLA-DR(-I-) cells were also noted. The majority of plasma cells in the central lamina propria bore IgG isotypes. These findings suggest that T-cell mediated regulatory mechanisms play an important role in the pathogenesis of adult periodontitis.

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Section: Discussionmentioning

confidence: 60%

Immunohistological analysis of gingival lymphocytes in adult periodontitis

Çelenligil

Kartsu²,

Ruacan

et al. 1992

J Clin Pharm Ther

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“…Among bacterial products reported to act as B-cell activators in RA are bacterial peptidoglycans (Pardo et al 1984). Increased blast responses and polyclonal B-cell activation to extracts of dental plaque were observed in several studies of peripheral lymphocytes from patients with periodontitis (Patters 1976, Smith et al 1979, Bick et al 1981, Donaldson et al 1982, Osterberg et al 1983.…”

Section: Discussionmentioning

confidence: 93%

Serum antibodies and loss of periodontal bone in patients with rheumatoid arthritis

Tolo

Jorkjend

1992

J Clin Pharm Ther

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Tolo K and Jorkjend L: Serum antibodies and loss of periodontal bone in patients with rheumatoid arthritis. J Clin Periodontol 1990; 17: 288-291. Abstract. The number of teeth, % of alveolar bone loss, serum IgG, and serum antibodies to Bacteroides gingivalis, Capnocytophaga ochracea and Eubacterium saburreum were recorded in 37 patients diagnosed with rheumatoid arthritis (RA) and in an age-and sex-matched control group of 37 individuals free from RA. The RA group had a significantly increased loss of teeth and loss of alveolar bone compared to the control group. The RA patients also had a significantly increased level of serum IgG. In the total material, 26% of the variation in loss of alveolar bone was accounted for by age, diagnosis of rheumatoid arthritis, and levels of antibodies against B. gingivalis and E. saburreum. In the RA group, 48% of this variation was accounted for by age, total serum IgG and IgG antibodies to B. gingivalis and E. saburreum.

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“…[6][7][8] Stimulation of peripheral blood mononuclear cell (PBMC) cultures with periodontopathic bacteria leads to the activation of B cells, the production of polyclonal antibodies, and an increased proliferative response. 9,10 It is becoming increasingly clear that the enhanced antibody production associated with PBA seems to be of little value to the host. In fact, much of this non-protective antibody may be locally produced auto-antibodies against gingival tissue components (collagen).…”

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confidence: 99%