Abstract
Chronic periodontitis (CP) is a chronic inflammatory condition which destroys the supporting tissues of teeth and increases in prevalence with age. Immune responses against heat shock proteins (HSP) can be cross-reactive among bacterial and human antigens. There is evidence that microbial HSP65 and human HSP60 are involved in periodontal disease. The aim of this study is to investigate immune responses to the human HSP60 and microbial HSP65 in patients with CP and relate these to the level of inflammation and smoking status. We collected serum samples from 30 patients with chronic gingivitis (CG) and 30 patients with CP. In each group, eight subjects were current smokers. ELISA was used to determine the levels of serum anti-HSP and C-reactive protein (CRP) in each group. Peripheral blood mononuclear cells were also isolated and stimulated with HSPs. Significant lymphoproliferation was seen in CP when stimulated with human HSP60. CRP and serum anti-human HSP60 IgG were elevated in CP compared to the CG, but not serum anti-microbial HSP 65 IgG. In view of the potential confounding effects of smoking in CP, a group of current smokers (n = 16) was also recruited to investigate whether smoking affects HSP immune responses. There was no significant difference in HSP-induced lymphoproliferation between smokers and non-smokers in either the CG or CP. There was a significant correlation between CRP and lymphoproliferative responses to Human HSP60 irrespective of smoking status. This study shows that serum anti-human HSP60 IgG and serum CRP are raised in untreated CP. In CP, serum CRP levels correlated significantly with human HSP60-induced lymphoproliferation, but not with anti-HSP antibody levels.
Highlights
Chronic periodontitis (CP) is an inflammatory disease characterised by connective tissue destruction and bone resorption, affecting 10% - 15% of the developed world population and is the major cause of tooth loss in adults [1]
This study shows that serum anti-human HSP60 IgG and serum C-reactive protein (CRP) are raised in untreated CP
The objectives of this investigation are to determine whether serum anti HSP60/65 IgG and IgA are associated with smokers or non-smokers with chronic gingivitis (CG) or CP and to determine if these responses are related to inflammation, as reflected by CRP levels, or to smoking status
Summary
Chronic periodontitis (CP) is an inflammatory disease characterised by connective tissue destruction and bone resorption, affecting 10% - 15% of the developed world population and is the major cause of tooth loss in adults [1]. There is evidence from cross-sectional studies implicating Porphyromonas gingivalis, Tannerella forsythia as well as other microbial species including Gram-negative and Gram-positive bacteria, some of which are unculturable [3]. These findings support the hypothesis that the aetiology of CP is polymicrobial. HSPs are the most highly conserved group of proteins known in phylogeny with respect to biochemical function, mode of regulation and structure [6,7] They are expressed in all eukaryotic and prokaryotic cells including Gram-positive and Gram-negative bacteria. The objectives of this investigation are to determine whether serum anti HSP60/65 IgG and IgA are associated with smokers or non-smokers with CG or CP and to determine if these responses are related to inflammation, as reflected by CRP levels, or to smoking status
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
