Importance of Actinomyces and certain gram-negative anaerobic organisms in the transformation of lymphocytes from patients with periodontal disease

Abstract

Dental plaque deposits are known to be potent stimulants of lymphocyte transformation in patients with periodontal disease but not in normal subjects. Since plaque deposits consist mainly of whole bacteria, the cell walls of the most commonly found organisms in plaque were tested for their capacity to induce lymphocyte transformation. There was a direct correlation between the severity of peridontal disease and the amount of transformation induced by the cell walls of oral bacteria and by solubilized dental plaque. Cord blood leukocytes and lymphocytes from clinically normal people did not respond, which indicates that these stimulants are antigens rather than mitogens. Of the eleven bacteria tested, four members of the family Actinomycetaceae (Actinomyces viscosus, A. israelii, A. naeslundii, and Arachnia propionica), the related Propionibacterium acnes, and an anaerobic gram-negative anaerobic rod (27N). The high prevalence of the former organisms in the mature dental plaque that forms around the gingival crevice area and the potent efficacy with which they stimulate lymphocytes indicates that Actinomyces and certain gram-negative anaerobes may be important etiological agents in chronic periodontal inflammation in man.

Blastogenic responsiveness of peripheral blood mononuclear cells from individuals with various forms of periodontitis and effects of treatment

“…This observation is in direct conflict with the report by Lehner (!972) that cells from patients with severe periodontitis do produce lymphokine when activated. Kiger et al (1977) found no correlations between blastogenic responsiveness of PBM to plaque bacterial components and any of several measures of seventy of periodontitis, and Baker et al (1978) found ceils from patients with severe periodontitis to be anaergic to a microbial plaque extract but responsiveness appeared during and following periodontal treatment. Page et al (1978) compared the blastogenic responsiveness and lymphokine production by PBM from normal subjects and patients with adult periodontitis to homogenates of gram-positive and gram-negative plaque bacteria and found responsiveness RESPONSIVENESS OF BLOOD MONONUCLEAR CELLS…”

“…In cultures activated using the patients' own microbial plaque, responsiveness had decreased following completion of treatment. Enhanced responsiveness may be a consequence of reducing the magnitude of the bacterial challenge and the resulting release from immune suppression by an overwhelming antigenic load as suggested by Baker et al (1978), but this seems unlikely. A more plausible interpretation would be a developing immune responsiveness to bacteria!…”

“…A mass of data regarding the nature of lymphocyte activation by plaque bacterial substances and polyclonal activators has been obtained from studies of peripheral blood mononuclear cells in culture (Ivanyi & Lehner 1970, 1971a, b, 1974, Ivanyi et al 1972, 1973, Horton et al 1972, Lehner 1972, Mackler et al 1974, Patters etal. 1976, Budtz-Jorgensen et al !977, Kiger et al 1977, Lting & Smith 1977, Baker et a!. 1978, Page et al 1978, Mangan & Lopatin I98I, Tew et al 1981.…”

The immunopathogenesis of progressive chronic inflammatory periodontal disease

“…Immunoglobulins of the IgG, IgM and 'gA classes have been described in the gingival fluid (Brill & Bronnestam 1960, J^randtzaeg 1965 and in the gingival tissues (Brandtzaeg & Kraus 1965, Thonard et al 1966, Genco et al 1974. '^ost studies, in attempting to demonstrate Specificity of these immunoglobulins and nce antibody activity against plaque ''microorganisms, have however been inconclusive.…”

Microbial etiology of periodontal disease

“…A changing immune response during the course of gingivitis to a given subgingivai microorganism in the presence of a consistent response to the other subgingivai organisms may suggest a special role of this organism in the disease process and thus imply bacterial specificity in the etiology of gingivitis. With some exceptions (Kiger et al 1974, Lang & Smith 1977, Smith et al 1978 most studies have demonstrated a greater stimulation of lymphocyte transformation by a variety of plaque microorganisms in patients with gingivitis than in periodontally healthy subjects (Ivanyi & Lehner 1970, Lehner et al 1974, Baker et al 1976, Patters et al 1976, 1977, 1979. These findings therefore suggest a lack of bacterial specificity in the etiology of gingivitis.…”