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A Family Study of a Mother and Daughter with Increased Susceptibility to Early‐Onset Periodontitis: Microbiological, Immunological, Host Defensive, and Genetic Analyses
Author(s) -
Nishimura Fusanori,
Nagai Atsushi,
Kurimoto Keiji,
Isoshima Osama,
Takashiba Shogo,
Kobayashi Mitsuharu,
Akutsu Isao,
Kurihara Hidemi,
Nomura Yoshio,
Murayama Yoji,
Ohta Hiroyuki,
Kato Keijiro
Publication year - 1990
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1990.61.12.755
Subject(s) - daughter , periodontitis , host (biology) , biology , host response , immunology , medicine , genetics , immune system , dentistry , evolutionary biology
M icrobiological, 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 .