Polyclonal B-cell activation: Severe periodontal disease in young adults

Smith, Steven C.; Bick, Peter H.; Miller, Glenn A.; Ranney, Richard R.; Rice, P L; Lalor, J.H.; Tew, John G.

doi:10.1016/0090-1229(80)90141-5

Cited by 85 publications

(35 citation statements)

References 31 publications

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“…This infiltrate could then acquire the characteristics of self-sustained inflammation, i.e., lymphocytic nodules with macrophages, plasma-cells, T-cells, and slightly more OKT8+ cells than OKT4+ cells, possibly in a regulatory attempt. The Bcell lesion ) would appear together with the presence of plaque and B-cell polyclonal activators (Smith et al 1980). The presence of numerous HLA 11+ cells in these tissues previously mentioned by others (Seymour & Greaves 1980, Newcomb et al 1982, and evidenced here, might also be of irnportance, since these cells are known as antigen-presenting and interleukin-1 producing cells.…”

Section: Discussionsupporting

confidence: 66%

Immunohistological identification of cell subsets in human gingival after local treatment for gingivitis or periodontitis

Jully¹,

Béné²,

Martin³

et al. 1986

J Clinic Periodontology

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The cellular infiltrate present in human diseased gingiva was analyzed in biopsies from 12 patients with gingivitis or periodontitis. The samples studied had been obtained in the course of surgery at inflammatory sites remaining after institution of periodontal treatment. Histological and immunological techniques were used to identify macrophages, B-cells, plasma-cells, T-cells and T cell subsets, as well as cells expressing class II HLA membrane antigens. T-cells appeared as the predominant population, but plasma-cells were also visualized in nearly all samples. Both OKT4+ and OKT8+ cells were seen in all cases, the latter being more numerous in periodontitis patients. Interdigitating-like cells were observed, positively labelled for class II antigens, as well as macrophages which were more numerous in periodontitis patients. These results suggest the participation of all components of the immune response in gingival disease, in a way resembling chronic recurrent inflammatory diseases.

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Section: Discussionsupporting

confidence: 66%

Immunohistological identification of cell subsets in human gingival after local treatment for gingivitis or periodontitis

Jully¹,

Béné²,

Martin³

et al. 1986

J Clinic Periodontology

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“…Although not determined in the present study, it is possible that the high level of immunoglobulin secretion detected in vitro may have been elicited, in part, by polyclonal B cell activating substances (PBAs) released by dental plaque bacteria (Smith et al 1980). Stimulation by PBAs leads to the production of heterologous antibodies (MoUer, Strom & Al-Balaghi 1980) suggesting that a proportion of the immunoglobulin detected in the present study may not have specificity for plaque components.…”

Section: Discussionmentioning

confidence: 72%

Lymphocytes from chronically inflamed human gingiva

Daly

Clancy

1983

J of Periodontal Research

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Recovery and identification in vitro of lymphocytes from gingival tissue was carried out for 20 patients with chronic marginal gingivitis. A combination of 90 min incubation in a collagenase‐containing medium followed by mechanical disruption through a stainless‐steel grid resulted in a mean yield of 2.42 × 105 (S. D. ± 1.26 × 105: n = 16) lymphocytes per 100 mg or tissue. When Ficoll density centrifugation was introduced into the recovery procedure, the mean lymphocyte yield dropped to 2. 15 × 104 (S. D. ± 0.99 × 104: n = 4) per 100 mg. Mean viability of recovered lymphocytes was 78% (S. D. ± 5%: n =16) and for Ficoll separation, 77% (S. D. ± 1%: n = 4). In cell suspensions obtained from 12 or the patients, T lymphocytes were identified by rosette formation with sheep erythrocytes, and B cells were quantitated using fluorescent identification of membrane immunoglobulin. Macrophages were identified on the basis of non‐specific esterase characteristics. Tire predominant lymphocytes round were T cells, with a mean proportion of 53.9% (S. D. ± 5.6%); the mean proportion of B cells was 32.7% (S. D. ± 5.4%). Macrophages accounted for a mean of 7.7% (S. D. ± 2.8%) or the recovered lymphoid cells. The lymphocyte‐plasma cell ratio in recovered cell suspensions was 7:1 compared with a ratio of 1.7:1 noted in histological sections.

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“…The level of this regulation is probably local as well as systemic. In addition, Smith et al (1980) have shown a hyperresponsiveness of peripheral blood B-cells to the T-dependent PBA streptococcal protein A in patients with severe periodontal disease. Although controversial, these results illustrate the possible importance of T-cell control mechanisms.…”

Section: Introductionmentioning

confidence: 98%

Invited Review: Possible Mechanisms Involved in the Immunoregulation of Chronic Inflammatory Periodontal Disease

Seymour

1987

J Dent Res

124

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It is generally agreed that immunological mechanisms are involved in the pathogenesis of periodontal disease; however, regulation of these mechanisms has hitherto received scant attention. Regulatory networks exist at both a cellular and a molecular level. At the cellular level, the existence of helper (T4-positive) and suppressor (T8-positive) T lymphocytes, the expression of Class II major histocompatibility complex antigens, and the heterogeneity of macrophage subpopulations are central to an understanding of the regulatory mechanisms involved. It is only recently that studies of these separate components, in both humans and experimental animals, have begun to provide a basis for understanding the complex interactions occurring in periodontal disease. Studies using the human experimental gingivitis model have shown an immunoregulatory picture consistent with a controlled immunological reaction with an essentially normal T4:T8 ratio of 2.0. In contrast, studies utilizing cells extracted from adult periodontitis lesions have shown a reduced T4:T8 ratio (approximately 1.0) and an inability to respond in, or to stimulate, an autologous mixed lymphocyte reaction. Animal studies using athymic nude rats have supported the concept of a central role for T-cell control in periodontal disease and the possibility of an imbalance in this control with disease progression. These results are reviewed and areas of future research explored.

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Polyclonal B-cell activation: Severe periodontal disease in young adults

Cited by 85 publications

References 31 publications

Immunohistological identification of cell subsets in human gingival after local treatment for gingivitis or periodontitis

Immunohistological identification of cell subsets in human gingival after local treatment for gingivitis or periodontitis

Lymphocytes from chronically inflamed human gingiva

Invited Review: Possible Mechanisms Involved in the Immunoregulation of Chronic Inflammatory Periodontal Disease

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