Susceptibility to Early-Onset Periodontitis (EOP) appears to be attributable to a gene inherited in an autosomal dominant pattern. This explains why EOP clusters in families and why about half of the family members develop periodontal disease early in life. Manifestation of EOP is variable, with some patients having a localized form restricted to first molars and incisors (LJP) and others with a severe generalized form of periodontitis (SP). The extent and severity of disease is less in patients who are seropositive for Actinobacillus actinomycetemcomitans than in seronegative patients, and this relationship prompted the hypothesis that anti-A. actinomycetemcomitans helps limit disease. The dominant antibody is an IgG2 reactive with the serotype-specific carbohydrate. The incidence of the LJP form of EOP is about 10 times higher in blacks than in whites. Interestingly, blacks have higher levels of serum IgG2, a higher frequency of anti-A. actinomycetemcomitans antibody, and higher serum titers of IgG2 anti-A actinomycetemcomitans which may help explain why the disease is localized. Studies in progress suggest that smoking reduces serum IgG2 levels in SP patients and is associated with more severe periodontal destruction. In marked contrast, IgG2 does not appear to be reduced in LJP patients who smoke, and smoking does not appear to increase periodontal destruction. We think that IgG2 anti-A. actinomycetemcomitans is playing a role in limiting the extent and severity of disease in patients genetically susceptible to EOP.
- Antibodies, bacterial
- Periodontitis, early-onset/epidemiology
- Periodontitis, early-onset/etiology
- Periodontitis, early-onset/microbiology
- Racial factors
ASJC Scopus subject areas