Smoking and periodontal disease: discrimination of antibody responses to pathogenic and commensal oral bacteria

Abstract

SummarySmoking is an independent risk factor for the initiation, extent and severity of periodontal disease. This study examined the ability of the host immune system to discriminate commensal oral bacteria from pathogens at mucosal surfaces, i.e. oral cavity. Serum immunoglobulin (Ig)G antibody reactive with three pathogenic and five commensal oral bacteria in 301 current smokers (age range 21-66 years) were examined by enzyme-linked immunosorbent assay. Clinical features of periodontal health were used as measures of periodontitis. Antibody to the pathogens and salivary cotinine levels were related positively to disease severity; however, the antibody levels were best described by the clinical disease unrelated to the amount of smoking. The data showed a greater immune response to pathogens than commensals that was related specifically to disease extent, and most noted in black males. Significant correlations in individual patient responses to the pathogens and commensals were lost with an increasing extent of periodontitis and serum antibody to the pathogens. Antibody to Porphyromonas gingivalis was particularly distinct with respect to the discriminatory nature of the immune responses in recognizing the pathogens. Antibody responses to selected pathogenic and commensal oral microorganisms differed among racial groups and genders. The antibody response to the pathogens was related to disease severity. The level of antibody to the pathogens, and in particular P. gingivalis, was correlated with disease severity in black and male subsets of patients. The amount of smoking did not appear to impact directly serum antibody levels to these oral bacteria.

Altered Antigenic Profiling and Infectivity of Porphyromonas gingivalis in Smokers and Non‐Smokers With Periodontitis

“…Thus, while clearly facilitating impressive molecular microbiology advances, research strains of P. gingivalis may not always be the most relevant to in vivo situations. There were no statistically significant differences in the intensity of the humoral response to P. gingivalis between current smokers and non-smoking subjects with AP, in keeping with the findings of Hayman et al , who have recently reported that correlations between pathogen and commensal antibody ratios in individuals with periodontitis disappear in those with aggressive disease 7 . This may be partly explained by our finding that current smokers with AP are more likely to be currently infected with P. gingivalis than non-smokers with AP.…”

“…The great majority 5-6, 22, 25-26 , but not all 7 , have shown that smoking reduces the antibody response to P. gingivalis , particularly IgG. We show that the total IgG response mounted against low passage clinical isolates (5607, 10208C and 1052), but not laboratory strains, of P. gingivalis (33277 and W83) is significantly suppressed in smokers with CP.…”

“…Antibody responses to P. gingivalis , particularly IgG 2 , may vary significantly by race and type of periodontal disease 7, 25-26, 32 . All recruits herein were Caucasian and no tobacco-related differences in IgG subtype titers could be ascribed.…”

“…Indeed, of all tested oral bacterial species, only P. gingivalis -specific antibodies have been associated with disease severity 7-8 . In vitro, cigarette smoke extract (CSE) represents an environmental stressor to P. gingivalis 9 .…”

Lifestyle, dietary factors, and antibody levels to oral bacteria in cancer-free participants of a European cohort study

“…An association between oral bacteria and systemic antibody response is well-established in individuals who have different degrees of periodontal disease; serum antibody levels to oral pathogens, such as P. gingivalis, correlate with severity of periodontal disease 32 . However, in the general population, the association between serum antibody levels to oral pathogenic bacteria and periodontal disease status is inconsistent; other factors, such as smoking status, can influence the immune response (i.e., IgG levels) 19, 20 .…”