Clinical and Laboratory Studies on a Patient With Early Onset Periodontitis and Her Family Members. A Case Report

Abstract

Extensive clinical, microbiological, hematological, and immunological studies were performed on a patient with early onset periodontitis (EOP) and two other members of the family. The proband, a 27‐year‐old female, had early onset periodontitis and a high level of serum rheumatoid factors (RF) with no diagnosable medical disease. Her mother had lost all her teeth at the age of 50 because of advanced periodontitis, while her elder sister was unaffected by periodontitis. Neither the proband's periodontally‐affected mother nor her unaffected sister exhibited a detectable level of RF. In this study, we examined: 1) serum Immunoglobulin G (IgG) antibody titers against putative periodontal pathogenic bacteria; 2) peripheral neutrophil functions; 3) phenotypic analyses of peripheral lymphocyte subpopulations; and 4) peripheral lymphocyte functions (T cell proliferative activity, ability of cytokine [interleukin (IL)‐2, tumor necrosis factor‐α, interferon‐γ, IL‐6 and IL‐8] and IgG and IgM productivity). High antibody titers to Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Campylobacter rectus were detected in the sera of the proband, as were high serum antibody titers to P. gingivalis in the mother and to C. rectus in the unaffected sister compared to the non‐periodontitis affected subjects. The proband also showed enhanced neutrophil Chemotaxis; a high percentage of pan‐B cells; and high productivity of IL‐6, IgG, and IgM compared to individuals who were not periodontally affected. The mother showed slightly low helper/induced T cells (Th/i) suppressor/cytotoxic T cells (Ts/c) ratios due to the elevated count of Ts/c, and high IFN‐γ productivity compared to control subjects. We could not identify any common risk factor in this family, but the immunological profiles of this proband might be useful for discussing the relationship between RF and periodontal disease. J Periodontol 1995; 66:403–412.

Genetic study of families affected with aggressive periodontitis

“…There are several other interesting reports on microbiological agents and lymphocyte dysfunctions that should be considered in relation to the progression of periodontal disease (2, 85). Takahashi et al (85) found high antibody titers to A. actinomycetemcomitans, P. gingivalis and C. rectus in the serum of the proband. High serum antibody titers to P. gingivalis were found in the mother, and to C. rectus in the unaffected sister, compared with the healthy control patients.…”

“…There are several other interesting reports on microbiological agents and lymphocyte dysfunctions that should be considered in relation to the progression of periodontal disease (2, 85). Takahashi et al.…”

“…Takahashi et al. (85) found high antibody titers to A. actinomycetemcomitans , P. gingivalis and C. rectus in the serum of the proband. High serum antibody titers to P. gingivalis were found in the mother, and to C. rectus in the unaffected sister, compared with the healthy control patients.…”

T‐ and B‐cell subsets in periodontitis

“…Although fewer in number, subpopulations of T‐cells have also been investigated in patients with aggressive periodontitis . The presence of interleukin‐2, interferon gamma, interleukin‐4, interleukin‐5, interleukin‐10, interleukin‐13 and transforming growth factor beta was analyzed in CD3 + , CD4 + and CD8 + subpopulations extracted from gingival biopsies of healthy subjects, patients with gingivitis and patients with aggressive periodontitis .…”

Heterogeneity of Host Immunological Risk Factors in Patients With Aggressive Periodontitis

“…9,10 In fact, the majority of previous studies have shown that alteration in the host defensive cell functions, immunological and immunogenetic characteristics, such as neutrophil and lymphocyte dysfunctions, aberrant cytokine production and specific HLA types, are associated with the pathogenesis of some, but not all, EOP patients. 5,[11][12][13][14][15] Previous studies showing a high prevalence of EOP in certain families, [16][17][18][19] twin studies, 20 and the linkage with specific HLA types [21][22][23] suggest that susceptibility to this disease is heritable and that certain genetic risk factors may be involved. 24 Therefore, we have hypothesized that the heterogeneous nature of EOP could be explained from various host risk factors.…”