Clinical and Laboratory Studies of a Family with a High Prevalence of Juvenile Periodontitis

Abstract

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.

Familial periodontal disease in the cayo santiago rhesus macaques

“…[Baab et al, 1985; Page et al, 1985; van der Velden, 1991; Marazita et al, 1994; Hodge et al, 2000; Modeer and Wondimu, 2000; Kinane et al, 2005; Carlsson et al, 2006; Armitage and Cullinan, 2010]. Additionally, data clearly demonstrate the familial distribution of periodontitis that affects younger individuals, termed localized or generalized periodontitis, early onset periodontitis or aggressive periodontitis [Baab et al, 1985; Page et al, 1985; Schenkein and Van Dyke, 1994; Hart and Kornman, 1997; Diehl et al, 1999; Kinane et al, 1999].…”

“…[Baab et al, 1985; Page et al, 1985; van der Velden, 1991; Marazita et al, 1994; Hodge et al, 2000; Modeer and Wondimu, 2000; Kinane et al, 2005; Carlsson et al, 2006; Armitage and Cullinan, 2010]. Additionally, data clearly demonstrate the familial distribution of periodontitis that affects younger individuals, termed localized or generalized periodontitis, early onset periodontitis or aggressive periodontitis [Baab et al, 1985; Page et al, 1985; Schenkein and Van Dyke, 1994; Hart and Kornman, 1997; Diehl et al, 1999; Kinane et al, 1999]. Some of these clinical presentations, particularly leukocyte adhesion deficiency (LAD)-associated periodontitis, have been documented to be related to genetic modifications of neutrophil functions [Van Dyke et al, 1984; Baab et al, 1985; Page et al, 1985; Waldrop et al, 1987; Schenkein and Van Dyke, 1994; Hart and Kornman, 1997; Diehl et al, 1999; Kinane et al, 1999; Gronert et al, 2004; Moutsopoulos et al, 2014] polymorphisms in Cathepsin C [Hart et al, 2000], or have an autosomal recessive gene pattern in specific families [Marazita et al, 1994].…”

“…Additionally, data clearly demonstrate the familial distribution of periodontitis that affects younger individuals, termed localized or generalized periodontitis, early onset periodontitis or aggressive periodontitis [Baab et al, 1985; Page et al, 1985; Schenkein and Van Dyke, 1994; Hart and Kornman, 1997; Diehl et al, 1999; Kinane et al, 1999]. Some of these clinical presentations, particularly leukocyte adhesion deficiency (LAD)-associated periodontitis, have been documented to be related to genetic modifications of neutrophil functions [Van Dyke et al, 1984; Baab et al, 1985; Page et al, 1985; Waldrop et al, 1987; Schenkein and Van Dyke, 1994; Hart and Kornman, 1997; Diehl et al, 1999; Kinane et al, 1999; Gronert et al, 2004; Moutsopoulos et al, 2014] polymorphisms in Cathepsin C [Hart et al, 2000], or have an autosomal recessive gene pattern in specific families [Marazita et al, 1994]. However, these potential genetic regulators are also interfaced with experimental evidence documenting the transmission of a particular periodontal pathogen, Aggregatibacter actinomycetemcomitans within the affected individuals in these families [Zambon et al, 1983; Schenkein and Van Dyke, 1994; Papapanou, 2002; Kilian et al, 2006; Teixeira et al, 2006; Dogan et al, 2008].…”

Oral and Periodontal Diseases in Consanguineous Marriages

“…Family linkage studies have informed diferent modes of inheritance such as X-linked-dominant [34], autosomal-dominant [23], autosomal-recessive [22], or both X-linked-dominant and autosomal-dominant [35].…”

Immunoglobulin G proteolytic activity of Actinobacillus actinomycetemcomitans

“…Actinobacillus actinomycetemcomitans is a Gramnegative coccobacillus, frequently associated with localized aggressive periodontitis [LAP] which is characterized by rapid and marked bone loss around the incisor and molar teeth (1,9,14,20). This organism has been also associated with a variety of non-oral infectious diseases such as endocarditis, osteomyelitis, septicemia, pneumonia, arthritis and abscesses.…”