Microbiological, immunological, host‐defensive, and genetic analyses were performed on a mother and daughter, both of whom had early‐onset periodontitis (rapidly progressive periodontitis in the mother; localized juvenile periodontitis in the daughter). Microscopic examination revealed a greatly elevated percentage of rod‐form bacteria in both subjects. Fusobacterium sp. and Porphyromonas gingivalis (formerly Bacteroides gingivalis) were the predominant microorganisms cultured. The humoral immune responses to F. nucleatum, P. gingivalis, and Actinobacillus actinomycetemcomitans were much higher in both subjects than those to any other periodontal bacteria examined. Functional and phenotypic analysis of the peripheral lymphocytes showed no significant abnormalities. However, investigation of neutrophil function showed that the mother had depressed neutrophil Chemotaxis and Superoxide production. The daughter had depression not only of Chemotaxis and Superoxide production, but also of neutrophil phagocytosis. Serological typing of HLA antigens revealed the same Class II HLA profile in both subjects. It was concluded that both subjects very probably had an identical condition and that these patients provided a unique model for improving our understanding of the host factors involved in periodontal disease. J Periodontol 1990; 61:755–765.
Family case studies help us identify host risk factors in periodontal disease. In this study we examine a family consisting of a mother (40 years old, with rapidly progressive periodontitis), her elder daughter (14 years old, with localized juvenile periodontitis), and younger daughter (13 years old, with simple gingivitis). We examined 1) the peripheral neutrophil functions (chemotactic migration, phagocytosis, superoxide production); 2) lymphocyte functions (proliferative activity and cytokine productivity of T cells, immunoglobulin [Ig] M productivity of B cells when stimulated with pokeweed mitogen); 3) phenotypic analyses of peripheral lymphocyte subpopulations; 4) serum IgG antibody titers against periodontopathic bacteria; and 5) serological type of HLA class II. All the subjects exhibited high T4/T8 ratios due to high percentage of CD4‐positive cells, showed high IgG titers to Actinobacillus actinomycetemcomitans, and had a HLA DQwl in common. The mother showed a slight deficiency of neutrophil chemotactic migration to N‐formyl methyonyl leucyl phenylalanin (fMLP), raised interleukin‐2 productivity of T cell, and high levels of IgG titers to Porphyromonus gingivalis and Fusobacterium nucleatum. Both daughters showed weak T cell proliferative response to anti‐CD3 monoclonal antibody and low IgM productivity. Low lymphocyte responsiveness may be involved in the pathogenesis of periodontal disease of these daughters; therefore, the lymphocyte dysfunctions shown should be considered in relation to the progression of periodontal disease. J Periodontol 1996;671:433–442.
In this cross-sectional study, we assessed the in vitro interleukin-2 (IL-2) producing capacity of peripheral blood mononuclear cells (PBMC) and lymphocytes from patients with different forms of periodontitis. 45 patients (12 with localised early onset periodontitis (LEOP), 20 with generalised early onset periodontitis (GEOP), and 13 with adult periodontitis (AP), and 20 periodontally healthy subjects (HS), participated in this study. PBMC and lymphocytes were isolated from the subjects and their cells were stimulated with an anti-CD3 monoclonal antibody (anti-CD3 MoAb) and the secreted IL-2 levels in the culture were bioassayed. No significant differences could be found in IL-2 producing activity of PBMC between the patients and HS group. There was wide interindividual variation and high and low "IL-2 producers" were noted. We found a LEOP patient who was a high producer of IL-2 (> mean + 8 SD) and 2 LEOP patients and a HS who were low producers of IL-2 (< mean - 1.5 SD) with their lymphocytes. Incidentally, the HS became a LEOP patient during 2 years after this study. The low IL-2 producing activity of their PBMC and lymphocytes against anti-CD3 MoAb could not be overcome by stimulation with phorbol myristate acetate and ionomycin. Thus, we found high and low IL-2 producing capacity by PBMC and lymphocytes in certain subjects and these subjects may be useful models in assessing the role of systemic IL-2 productivity associated with their progression of periodontal disease.
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