ANTIBODY OF THE IGG2 SUBCLASS, ACTINOBACILLUS-ACTINOMYCETEMCOMITANS, AND EARLY-ONSET PERIODONTITIS

SUSCEPTIBILITY TO EARLY-ONSET PERIODONTITIS (EOP) appears to be attrib utable to a gene inherited in an autosomal dominant pattern. This expl ains why EOP clusters in families and why about half of the family mem bers develop periodontal disease early in life. Manifestation of EOP i s variable, with some patients having a localized form restricted to f irst molars and incisors (LJP) and others with a severe generalized fo rm of periodontitis (SP). The extent and severity of disease is less i n patients who are seropositive for Actinobacillus actinomycetemcomita ns than in seronegative patients, and this relationship prompted the h ypothesis that anti-A. actinomycetemcomitans helps limit disease. The dominant antibody is an IgG2 reactive with the serotype-specific carbo hydrate. 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 antib ody, and higher serum titers of IgG2 anti-A. actinomycetemcomitans whi ch may help explain why the disease is localized. Studies in progress suggest that smoking reduces serum IgG2 levels in SP patients and is a ssociated with more severe periodontal destruction. In marked contrast , IgG2 does not appear to be reduced in LJP patients who smoke, and sm oking does not appear to increase periodontal destruction. We think th at IgG2 anti-A. actinomycetemcomitans is playing a role in limiting th e extent and severity of disease in patients genetically susceptible t o EOP.