Polyclonal B‐cell activation in periodontitis*

Tew, John G.; Engel, David; Mangan, D F

doi:10.1111/j.1600-0765.1989.tb01787.x

Cited by 106 publications

(70 citation statements)

References 168 publications

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“…The concept that polyclonal B cell activation may be important in the pathogenesis of periodontal disease was first introduced in the early 1980s [33][34][35] and Tew et al [36] suggested that in the lesion, this would result in the expansion of B cell clones and their differentiation into immunoglobulin producing plasma cells. However, the results of the present study indicated that neither P. gingivalis nor F. nucleatum induced the production of cross-reactive antibodies to B. forsythus, P. intermedia or A. actinomycetemcomitans.…”

Section: Discussionmentioning

confidence: 99%

Effect of Fusobacterium nucleatum on the T and B cell responses to Porphyromonas gingivalis in a mouse model

Gemmell

Bird

Carter

et al. 2002

Clinical and Experimental Immunology

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Periodontal disease results from the inflammatory response to bacteria in dental plaque (reviewed in [1]). Although there are well over 300 different bacterial species in the plaque, progression to periodontitis depends not on bacterial load, but on the presence of specific periodontopathic bacteria. The major pathogens identified at the 1996 World Workshop in Periodontics as causative agents are Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans and Bacteroides forsythus [2]. P. gingivalis has been found in 15% of subjects in an Australian population, the prevalence increasing with increasing pocket depth [3]. In another study, Slots and Ting [4] found that 40-100% of adult periodontitis patients were positive for P. gingivalis. This high occurrence, together with the pathogenic potential of P. gingivalis, has made it a major pathogen of adult periodontitis [5].Immunohistological studies have established that a T cell/macrophage lesion identical to a delayed hypersensitivity 238 Effect of Fusobacterium nucleatum on the T and B cell responses toPorphyromonas gingivalis in a mouse model SUMMARYT cell cytokine profiles and specific serum antibody levels in five groups of BALB/c mice immunized with saline alone, viable Fusobacterium nucleatum ATCC 25586, viable Porphyromonas gingivalis ATCC 33277, F. nucleatum followed by P. gingivalis and P. gingivalis followed by F. nucleatum were determined. Splenic CD4 and CD8 cells were examined for intracytoplasmic interleukin (IL)-4, interferon (IFN)-gamma and IL-10 by dual colour flow cytometry and the levels of serum anti-F. nucleatum and anti-P. gingivalis antibodies determined by an ELISA. Both Th1 and Th2 responses were demonstrated by all groups, and while there were slightly lower percentages of cytokine positive T cells in mice injected with F. nucleatum alone compared with the other groups immunized with bacteria, F. nucleatum had no effect on the T cell production of cytokines induced by P. gingivalis in the two groups immunized with both organisms. However, the percentages of cytokine positive CD8 cells were generally significantly higher than those of the CD4 cells. Mice immunized with F. nucleatum alone had high levels of serum anti-F. nucleatum antibodies with very low levels of P. gingivalis antibodies, whereas mice injected with P. gingivalis alone produced anti-P. gingivalis antibodies predominantly. Although the levels of anti-F. nucleatum antibodies in mice injected with F. nucleatum followed by P. gingivalis were the same as in mice immunized with F. nucleatum alone, antibody levels to P. gingivalis were very low. In contrast, mice injected with P. gingivalis followed by F. nucleatum produced equal levels of both anti-P. gingivalis and anti-F. nucleatum antibodies, although at lower levels than the other three groups immunized with bacteria, respectively. Anti-Actinobacillus actinomycetemcomitans, Bacteroides forsythus and Prevotella intermedia serum antibody levels were also determined and found to be negligible. In conclusion, F. nucleatum ...

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Section: Discussionmentioning

confidence: 99%

Effect of Fusobacterium nucleatum on the T and B cell responses to Porphyromonas gingivalis in a mouse model

Gemmell

Bird

Carter

et al. 2002

Clinical and Experimental Immunology

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“…In parallel with the pathogenesis seen in RA, the degenerative capability of periodontitis may be initiated and maintained by the presence of endotoxins and exotoxins introduced by microbial organisms (13,32,44). It is suggested that while T lymphocytes and polymorphonuclear cells dominate in the early stages of plaque accumulation and gingivitis, B cells dominate in more advanced lesions, with a higher degree of soft tissue destruction and bone loss (9,36). As is seen in periodontal disease (5,15,20,36), B cells are activated in the synovial tissue in patients with arthritis, leading to a spontaneous secretion of Igs (IgG, IgA, and IgM) (1).…”

Section: Discussionmentioning

confidence: 99%

“…These gramnegative anaerobic bacteria possess various antigens (32,36) that provoke a host-mediated immune response to the offending species (2,36). This is a complex immunopathogenic process which involves interactions between T and B lymphocytes, neutrophils, monocytes, and phagocytes and the subsequent production of cytokines and prostaglandins (15).…”

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confidence: 99%

Immunoglobulin G and A Antibody Responses toBacteroides forsythusandPrevotella intermediain Sera and Synovial Fluids of Arthritis Patients

Moen

Brun

Madland

et al. 2003

Clin Vaccine Immunol

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The objective of the present study was to investigate immunoglobulin G (IgG) and IgA antibody immune responses to Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus, and Candida albicans in the sera of patients with rheumatoid arthritis (RA), the synovial fluid (SF) of patients with RA (RA-SF samples), and the SF of patients without RA (non-RA-SF samples). An enzyme-linked immunosorbent assay was used to determine IgG and IgA antibody levels in 116 serum samples from patients with RA, 52 RA-SF samples, and 43 non-RA-SF samples; and these were compared with those in SF samples from 9 patients with osteoarthritis (OA-SF samples) and the blood from 100 donors (the control [CTR] group). Higher levels of IgG antibodies against B. forsythus (P < 0.0001) and P. intermedia (P < 0.0001) were found in non-RA-SF samples than in OA-SF samples, and higher levels of IgG antibodies against B. forsythus (P ‫؍‬ 0.003) and P. intermedia (P ‫؍‬ 0.024) were found in RA-SF samples than in OA-SF samples. Significantly higher levels of IgA antibodies against B. forsythus were demonstrated in both RA-SF and non-RA-SF samples than in OA-SF samples. When corrected for total Ig levels, levels of IgG antibody against B. forsythus were elevated in RA-SF and non-RA-SF samples compared to those in OA-SF samples. Lower levels of Ig antibodies against B. forsythus were found in the sera of patients with RA than in the plasma of the CTR group for both IgG (P ‫؍‬ 0.003) and IgA (P < 0.0001). When corrected for total Ig levels, the levels of IgG and IgA antibodies against B. forsythus were still found to be lower in the sera from patients with RA than in the plasma of the CTR group (P < 0.0001). The levels of antibodies against P. gingivalis and C. albicans in the sera and SF of RA and non-RA patients were comparable to those found in the respective controls. The levels of IgG and IgA antibodies against B. forsythus were elevated in SF from patients with RA and non-RA-SF samples compared to those in OA-SF samples. Significantly lower levels of IgG and IgA antibodies against B. forsythus were found in the sera of patients with RA than in the plasma of the CTR group. This indicates the presence of an active antibody response in synovial tissue and illustrates a potential connection between periodontal and joint diseases.

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“…In particular, a progressive lesion has been associated with increased infiltration of B lymphocytes and plasma cells (6,7). Lymphocyte prominence in periodontal lesions prompted the suggestions that this segment of cellular influx could be responsible for regulation of immune response in periodontal tissues (1,8,9). We have developed a model of periodontitis in gnotobiotic Rowett rats (10,11) infected with Actinobacillus actinomycetemcomitans, a pathogenic microbe linked to periodontal disease.…”

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confidence: 99%

Bacterial-Responsive B Lymphocytes Induce Periodontal Bone Resorption

Han¹,

Kawai²,

Eastcott³

et al. 2006

The Journal of Immunology

116

122

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Host immune responses play a key role in periodontal diseases. We have found that B lymphocytes in human periodontal lesions bear abundant receptor activator of NF-κB ligand (RANKL), a major factor in the regulation of osteoclast differentiation. The purpose of this study was to evaluate Actinobacillus actinomycetemcomitans-responsive B lymphocytes in their level of RANKL expression and their effects on periodontal bone resorption. Congenitally athymic Rowett rats received injections of formalin-fixed A. actinomycetemcomitans into the gingival papillae, and donor B cells from normal rats immunized with A. actinomycetemcomitans were transferred via tail vein injection. We demonstrated that B cells from A. actinomycetemcomitans-immunized animals had greater levels of RANKL expression and induced a significantly higher level of osteoclast differentiation from RAW 264.7 cells than did nonimmune B cells that were not Ag specific. This activity was eliminated by incubation with the RANKL decoy receptor osteoprotegerin fusion protein. A. actinomycetemcomitans-binding B cell (ABB) and RANKL-expressing B cells were recovered from the gingival tissues of recipient rats transferred with ABB, but not from recipients of PBS nonimmune B cells or A. actinomycetemcomitans nonbinding B cells. Also, recipients of ABB exhibited increased osteoclast formation on the alveolar bone surface and significant periodontal bone resorption. This effect was antagonized by injection of osteoprotegerin fusion protein into the local gingival tissues. In summary, this study suggests that B lymphocytes can contribute to increased periodontal bone resorption in the absence of T lymphocytes. This effect is associated with the up-regulation of RANKL expression.

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Polyclonal B‐cell activation in periodontitis*

Cited by 106 publications

References 168 publications

Effect of Fusobacterium nucleatum on the T and B cell responses to Porphyromonas gingivalis in a mouse model

Effect of Fusobacterium nucleatum on the T and B cell responses to Porphyromonas gingivalis in a mouse model

Immunoglobulin G and A Antibody Responses toBacteroides forsythusandPrevotella intermediain Sera and Synovial Fluids of Arthritis Patients

Bacterial-Responsive B Lymphocytes Induce Periodontal Bone Resorption

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