2001;16:290C5. or decreased after periodontal treatment, suggesting that synthesis of these antibodies might be controlled individually during the course of periodontal contamination. Although their regulatory mechanisms in chronic contamination are not comprehended, further study would provide insight not only into the role of these antibodies in the pathogenesis of periodontitis but also into the ADL5747 possible link between periodontitis and systemic diseases such as coronary heart disease. Keywords: atherosclerosis, HSP60, periodontitis, treatment INTRODUCTION Heat shock protein 60 (HSP60) belongs to a family of related proteins which have been conserved during development. Despite ADL5747 being highly homologous between prokaryotic and eukaryotic cells, HSP60s are strongly immunogenic and immune responses to microbial HSP60s are speculated to initiate chronic inflammatory diseases in humans [1]. HSP60 has been reported to be involved in the pathogenesis of a number of chronic diseases including periodontal disease. We have exhibited previously that this frequency of sero-positivity and the antibody titre to human HSP60 and GroEL, a bacterial homologue of human HSP60, were significantly higher in periodontitis patients compared with periodontally healthy control subjects. Furthermore, affinity purified serum antibodies to human HSP60 and GroEL cross-reacted with GroEL and human HSP60, respectively [2]. Recently, we exhibited that this proliferative response of peripheral blood T cells to autologous HSP60 was significantly higher in periodontitis patients ADL5747 compared with gingivitis patients. Furthermore, clonal analysis, using single-strand conformation polymorphism, exhibited clearly that Rabbit polyclonal to CCNB1 HSP60-specific T cells accumulated in the gingival lesions of periodontitis patients but not in gingivitis patients and that the T cell clones with an identical specificity to those in peripheral blood existed in periodontitis lesions [3]. In addition, human HSP60 is usually expressed abundantly in periodontitis lesions and, much like bacterial lipopolysaccharide (LPS), is able to stimulate tumour necrosis factor (TNF)- production from macrophages [4]. Thus, immune responses to HSP60 derived from either inflammatory tissue or bacteria were thought to play an important role in the periodontal disease process. However, as yet you will find no reports describing the effect of periodontal treatment around the humoral immune response to HSP60s. Recent cross-sectional epidemiological studies have shown that individuals with chronic periodontitis have a significantly increased risk of developing coronary heart disease (CHD) [5C7]. However, while the evidence linking periodontitis with an increased risk for CHD is limited [8] and any causal relationship between periodontal disease and coronary heart disease has not been clarified, there is much evidence linking chronic contamination to CHD. It is therefore not unreasonable to suggest that chronic periodontitis could contribute to the total burden of contamination and as such contribute to the ADL5747 development of atherosclerosis. Support for this has come from the concept that immune responses targeted to self-proteins located in the vessel wall are a result of molecular mimicry ADL5747 with bacterial antigens. As a number of studies have exhibited that the immune response to either endogenous (human) or bacterial HSP60 may be involved in the pathogenesis of atherosclerosis and subsequent coronary heart disease and cerebrovascular disease [9C12], we hypothesized that elevated serum antibodies to periodontopathic bacterial HSP60 during the course of periodontal contamination cross-reacts with human HSP60s expressed in either the periodontal tissues or on arterial endothelial and easy muscle cells and hence could deteriorate pre-existing atherosclerotic lesions further. Therefore, the aim of the present study was to determine whether periodontal treatment prospects to a reduction in the serum levels of antibodies to GroEL and, in turn, in the serum levels of anti-human HSP60 antibodies. MATERIALS AND METHODS Patients A total of 21 patients with moderate to advanced chronic periodontitis were included in the study. In order to exclude the confounding effects of smoking, all patients were non-smokers. The mean age of the patients was 406 years at the baseline examination. The institutional review boards of Niigata University or college Graduate School of Medical and Dental Sciences approved this study and written knowledgeable consent was obtained from all the patients before inclusion in the study. Periodontal tissue destruction was assessed as explained previously [3]. Clinical examination included plaque control record [13], probing depths, attachment levels and alveolar bone resorption. Probing depths and attachment levels were recorded at six sites around each tooth. Mean probing depth and attachment level at baseline and at reassessment were calculated by dividing the mean probing depth and attachment level of each subject by the number of subjects. Radiographs were used to measure the alveolar bone resorption around the proximal surface of each tooth [14]. Mean alveolar bone resorption was calculated the.