Variations in IgG antibody subclass responses to oral bacteria: Effects of periodontal disease and modifying factors

Abstract

Background and objective Local and systemic IgG antibodies or oral bacteria have been described with periodontitis. We extended these observations by assessing the impact of a range of intrinsic factors on serum IgG subclass antibodies to both commensal and pathogenic oral bacteria that would contribute to variations in immune protection or disease susceptibility in periodontitis have not been described. Methods Subjects (n = 278) were classified as healthy, gingivitis, or periodontitis and categorized as mild, moderate, and severe periodontitis. Demographic stratification included sex, age, race/ethnicity, smoking, and obesity. Whole formalin‐fixed bacteria were used as antigens to detect serum immunoglobulin (Ig)G subclass antibody levels using an ELISA. Results The greatest differences in variations in IgG subclasses occurred in periodontitis versus health or gingivitis to bacteria considered oral pathogens (eg, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Treponema denticola) with IgG1, IgG2, and IgG4 increased by three‐ to sevenfold with Pg. Differences in subclass levels and distribution were also observed related to disease severity, particularly related to individual subclass responses to Pg. Examination of the overall population showed that females had elevated antibody, reflected by elevated IgG2 amounts/proportions. The older group of subjects demonstrated elevated antibody to multiple oral bacteria, lacking any particular subclass pattern. IgG2 antibody to Aa and Pg was increased in smokers. Multiple IgG subclass antibody levels to oral pathogens were significantly decreased in the obese subset within this population. Conclusion This investigation identified patterns of IgG subclass antibody responses to oral bacteria and demonstrated substantial effects of disease impacting the level and subclass distribution of antibody to an array of oral bacteria. Altered subclass antibody profiles most often in IgG2 levels and for antibody to P. gingivalis were found related to sex, age, disease severity, race/ethnicity, smoking, and obesity to both pathogens and commensal bacteria.

Treatment resistance of rheumatoid arthritis relates to infection of periodontal pathogenic bacteria: a case–control cross-sectional study

“…It is well known that the carrier rate of Aa is high in young individuals and decreases with age and that of Pg changes conversely 45 . A previous study reported that in the older group of individuals, antibody titer against Pg was elevated, while that against Aa was unchanged 46 . Our study found no correlation between age and antibody titers against Aa and Pg (Supplemental Table S1 ).…”

Gingival tissue antibody gene utilization in aging and periodontitis

“…Additionally, Gunsolley et al 87 reported that IgG2 was a dominate antibody response to Aggregatibacter actinomycetemcomitans with genetic effects in juvenile periodontitis. Thus, we can also associate the Ig gene changes in the nonhuman primates with antibody data from human periodontitis and aging 88 . These findings showed the most frequent antibody response changes to oral bacteria in disease were in the IgG2 and IgG4 subclasses, while age effects were seen in IgG1, IgG2, and IgG4 antibody levels.…”

“…13,[25][26][27][28] The population differences in disease also show enhanced disease with aging, in males, and within minority populations. [29][30][31] We have recently shown significant differences in antibody diversity 19 and IgG subclass distribution response 32 that parallel this enhanced disease expression. However, how these antibody molecules may reflect and affect disease prevention and/or resolution remains to be elucidated.…”

Could AMPs and B-cells be the missing link in understanding periodontitis?

“…initially, no direct connection to osteolysis, the major concern in periodontitis, was described ( 106 ). More recently, anti-carbamylated LL37 autoantibodies have been linked to an increase in bone resorption in RA ( 107 ). Auto-immunity and periodontitis are connected in many ways.…”

“…In addition, AMPs’ participation in autoimmunity has been investigated in the past few years. High concentrations of AMPs have been found in sera of Lupus patients or the joints of RA patients ( 107 , 111 , 112 ). For now, AMPs’ immunomodulatory role in autoimmunity is not fully understood, probably due to the difficulty in overcoming AMPs/cytokines/chemokines’ roles redundancy combined with dual detrimental and protective effects ( 113 , 114 ).…”