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Clinical and Laboratory Studies of a Family with a High Prevalence of Juvenile Periodontitis
Author(s) -
Page Roy C.,
Vandesteen G. Edward,
Ebersole Jeffrey L.,
Williams Betsy L.,
Dixon Irwin L.,
Altman Leonard C.
Publication year - 1985
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.1985.56.10.602
Subject(s) - actinobacillus , eikenella corrodens , antibody , periodontitis , aggressive periodontitis , immunology , disease , biology , chemotaxis , medicine , dentistry , genetics , bacteria , receptor
The form of periodontitis with onset at puberty and affecting predominantly the first molars and incisors is called juvenile periodontitis (JP). The disease has been the object of intense study because from its analysis may come insights into understanding other, more common, forms of periodontitis. We recently had the opportunity to study an unusual family in which both parents developed JP in their teens. We did clinical examinations, measured leukocyte Chemotaxis, analyzed the pocket microflora, looked for serum antibodies against a large panel of putative periodontal pathogens and correlated the results. The couple had two affected and two unaffected children. One of the unaffected children was not available for study. Neutrophil Chemotaxis was abnormal in both parents and in the two affected children, but not in the unaffected child. Actinobacillus actinomycetemcomitans accounted for 17.5% of the pocket flora isolated from one affected child and 2.5% of that from the unaffected child, but was not detected in the remaining family members. Antibodies specific for A. actinomycetemcomitans, Hemophilus aphrophilus and Eikenella corrodens were present in the serum of both affected children and for Capnocytophaga sputigena and C. ochracea in the father, but no antibodies directed against any of the species studied were found in the mother and the unaffected child. The distribution of disease in this family was more compatible with an X‐linked dominant than with an autosomal recessive mode of inheritance. The correlations among presence or absence of disease, abnormal neutrophil Chemotaxis and presence of serum antibodies reacting with A. actinomycetemcomitans were excellent. However, the pattern of serum antibodies observed did not reflect the composition of the pocket flora, and antibodies against putative periodontal pathogens not detected in the pocket flora were also found, indicating that JP has a more complex microbial etiology than has been previously suspected.