Influence of smoking and race on immunoglobulin G subclass concentrations in early-onset periodontitis patients

Abstract

Recent data indicate that smoking is an important risk factor for the development of periodontitis. Smoking is also known to reduce serum immunoglobulin G (IgG) levels. Interestingly, patients with the localized form of early-onset periodontitis (LJP) have elevated levels of serum IgG2, and those who smoke are not clinically different from nonsmoking LJP subjects. In contrast, patients with the generalized form of early-onset periodontitis (G-EOP) who smoke have more extensive destruction than their nonsmoking counterparts. Given the effects of smoking on EOP and the association of IgG2 with less severe disease, we hypothesized that smoking might reduce serum IgG2 and that this might be most apparent in G-EOP. We therefore examined the effects of smoking on serum IgG subclass concentrations in race-matched groups: LJP, G-EOP, and agematched periodontally healthy controls (NPs). Smoking status was established from serum cotinine levels, and serum IgG subclass concentrations were determined by using radial immunodiffusion. The data indicated that the effects of smoking were remarkably selective with respect to both IgG subclass and race. Smoking did not appear to have any effect on the concentration of IgG1 or IgG3 in either black or white subjects. In contrast, smoking was associated with depressed serum IgG2 concentrations in both white NP and G-EOP subgroups. Serum IgG2 levels in black subjects did not appear to be depressed by smoking, with the single striking exception of the black G-EOP subgroup which also had depressed serum IgG4 levels. The results here confirm that smoking has effects on serum immunoglobulin levels, but the effects were both race and serum IgG subclass specific. Furthermore, the periodontal diagnosis of EOP subjects appeared to be important, as indicated by the fact that IgG2 and IgG4 levels were reduced in smoking black G-EOP subjects whereas the IgG2 and IgG4 levels in black LJP and NP subjects were not reduced by smoking.

Infection patterns in chronic and aggressive periodontitis

“…It should also be emphasized that in the present study, responsiveness to infecting bacteria was also analysed by means of infection ratios that reflect a combined measure of both colonization and ab response and are biologically more relevant than the mere study of ab titres. Obviously, we cannot rule out that part of the discrepancy between our findings and those of other studies in the literature can be ascribed to the limited size of the examined sample or be attributed to variance because of specific subject sample characteristics such as race/ethnicity or smoking habits, both of which have been shown to affect ab levels and the proportion of specific serum IgG subclasses (Quinn et al 1996, 1998, Albandar et al 2002. However, in all likelihood, the discrepancy is mainly because of the fact that, according to the current guidelines, the diagnosis of either chronic or aggressive periodontitis can be assigned to individuals of any age, rendering inferences based on patients with early-onset periodontitis not applicable.…”

Cigarette Smoking and the Periodontal Patient

“…Alterations in gingival crevicular fluid [68][69][70] and peripheral blood mononuclear cell 71 levels of various cytokines in smokers, tipping the balance in favor of tissue breakdown, have been noted. Smoking decreases salivary IgA 72 and serum IgG, 73 and specifically reduces IgG2 to A. actinomycetemcomitans. 74 The ability of tobacco products to decrease the proliferative capacity of T and B lymphocytes might contribute to this diminished production of protective antibodies.…”

Neutralizing effect of green tea epigallocatechin‐3‐gallate on nicotine‐induced toxicity and chemokine (C‐C motif) ligand 5 secretion in human oral epithelial cells and fibroblasts

“…It has been reported that smokers harbor a higher prevalence of potential periodontal pathogens. [11][12][13] In addition, smoking impairs various aspects of the innate and immune host responses, including neutrophil functions, 14,15 antibody production, 16,17 fibroblast activities, 18,19 and inflammatory mediator production. [20][21][22] It has been well documented that smokers exhibit greater bone loss and attachment loss, 23 as well as a higher prevalence of deep periodontal pockets than non-smokers.…”