Lymphocytes from chronically inflamed human gingiva

Abstract

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.

Analysis of lymphocyte populations extracted from chronically inflamed human periodontal tissues

“…ations in the response was seen. This is in It is possible that such suppressor cells are agreement with the results of Ivanyi (1980) not only present in the population of cells and Daly et al (1983b) who also found that extracted from the tissues but may also be local anesthetic and collagenase had httle if active. Furthermore, Ivanyi (1980) and Iv-any effect, respectively.…”

“…Technical difliculties in cell handling (Suzuki et al 1983). Daly et al (1983b) have demonstrated that cells extracted from periodontal diseased tissues cannot be stimulated by PWM to produce further immunoglobulin and that the levels being produced by the unstimulated cells were similar to those produced by PWM stimulated peripheral blood lymphocytes. These results certainly suggest that the cells are maximally stimulated in vivo.…”

“…Nevertheless, interpretation is still diflicult in as much as the responsiveness of peripheral blood lymphocytes may not reflect that of the cells in the often localized lesions. Recognition of this fact has recently led to a number of studies designed to extract cells from periodontally diseased tissue (Mackler et al 1979, Sinden & Walker 1979, Ivanyi 1980, Daly, Clancy & Cripps 1983a, Daly, Cripps & Clancy 1983b. However, only one study has investigated the blastogenic response of these extracted cells (Ivanyi 1980).…”

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

“…In general, these studies have shown that approximately 50% of the lymphocytes recovered have a T-cell phenotype (Daly et al, 1983a;Seymour et al, 1985a), with approximately 30-35% being B-cells. The majority of these B-cells displayed a maturation/activation antigen identified by the monoclonal antibody FMC 7 (Seymour et al, 1985a), which is in keeping with the demonstration of high levels of immunoglobulin production by these cells in vitro without stimulation (Daly et al, 1983b). Later studies have shown that, compared with peripheral blood, there is a depressed T4:T8 ratio in cells extracted from periodontitis lesions (Taubman et al, 1984b;Cole et al, 1986).…”

Gingivitis*

“…These too, participate in host defense by enhancing microbial killing and clearance. A portion of the antibodies specific for periodontal pocket bacteria comes from the blood plasma, while another portion is produced locally by plasma cells present within the soft tissue pocket wall (Lally et al 1980, Mouton et al 1981, Schonfeld & Kagan 1982, Daly et al 1983. Although much of the immunoglobulin produced by gingival plasma cells is nonsense antibody resulting from polyclonal activation (see review.…”