High titers of serum IgG2 reactive with Actinobacillus actinomycetemcomitans are present in early‐onset periodontitis (EOP) patients and it appears that anti‐A. actinomycetemcomitans may be protective. Smoking is associated with increased periodontal disease severity in generalized early‐onset periodontitis (G‐EOP) patients, but is not associated with periodontal disease severity in patients with localized juvenile periodontitis (LJP). Furthermore, smoking is associated with reduced serum IgG2 levels in black patients with G‐EOP but not in those with LJP. Based on this selective effect of smoking, we hypothesized that smoking would be associated with a reduction of specific IgG2 reactive with A. actinomycetemcomitans in black G‐EOP patients but not black LJP patients. In addition, we examined IgG2 responses to carbohydrate antigens from non‐periodontal pathogens including Haemophilus influenzae b Oligosaccharide antigen (Hib) and the Streptococcus pneumoniae antigen phosphocholine (PC). Smoking status was assessed from serum cotinine levels, and IgG2 specific for A. actinomycetemcomitans, Hib, and PC was assessed by ELISA. Our study revealed that smoking was correlated with a dramatic reduction in serum IgG2 anti‐A. actinomycetemcomitans in G‐EOP smokers but not in LJP smokers. In contrast, anti‐Hib IgG2 and anti‐PC IgG2 were not affected in either G‐EOP or LJP patients. In short, these results indicate that smoking is associated with a reduction in serum IgG2 antiA. actinomycetemcomitans in black G‐EOP subjects, but IgG2 reactive with other antigens may not be reduced in G‐EOP smokers. J Periodontol 1997;68:842–850.

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 serotypespecific 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. J Periodontol 1996;67:317–322.