Accumulation of Human Heat Shock Protein 60-Reactive T Cells in the Gingival Tissues of Periodontitis Patients
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Heat shock protein 60s (hsp60) are remarkably immunogenic, and both T-cell and antibody responses to hsp60 have been reported in various inflammatory conditions. To clarify the role of hsp60 in T-cell responses in periodontitis, we examined the proliferative response of peripheral blood mononuclear cells (PBMC), as well as the cytokine profile and T-cell clonality, for periodontitis patients and controls following stimulation with recombinant human hsp60 and Porphyromonas gingivalis GroEL. To confirm the infiltration of hsp60-reactive T-cell clones into periodontitis lesions, nucleotide sequences within complementarity-determining region 3 of the T-cell receptor (TCR) beta-chain were compared between hsp60-reactive peripheral blood T cells and periodontitis lesion-infiltrating T cells. Periodontitis patients demonstrated significantly higher proliferative responses of PBMC to human hsp60, but not to P. gingivalis GroEL, than control subjects. The response was inhibited by anti-major histocompatibility complex class II antibodies. Analysis of the nucleotide sequences of the TCR demonstrated that human hsp60-reactive T-cell clones and periodontitis lesion-infiltrating T cells have the same receptors, suggesting that hsp60-reactive T cells accumulate in periodontitis lesions. Analysis of the cytokine profile demonstrated that hsp60-reactive PBMC produced significant levels of gamma interferon (IFN-gamma) in periodontitis patients, whereas P. gingivalis GroEL did not induce any skewing toward a type1 or type2 cytokine profile. In control subjects no significant expression of IFN-gamma or interleukin 4 was induced. These results suggest that periodontitis patients have human hsp60-reactive T cells with a type 1 cytokine profile in their peripheral blood T-cell pools.Periodontitis is a chronic inflammatory disease that degrades dental supporting tissues, including the alveolar bone. The global prevalence is 19%, in Sweden it is 11%. Left untreated, periodontitis can cause loss of teeth. The initial clinical manifestations of periodontitis usually start between 35 and 45 years of age. The underlying pathological mechanism is an aberrant inflammatory response to the bacteria colonizing the gingival crevice. Periodontitis has been associated with several other diseases, most prominently diabetes. The relation between periodontitis and diabetes is bidirectional in the sense that diabetes increases the risk for periodontitis and vice versa. Periodontitis also increases the risk for cardiovascular disease and cancer.
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Cigarette smoking is a risk factor for many diseases, and recent evidence indicates that smoking adversely influences periodontal health. A number of epidemiologic studies have shown strong associations between smoking and the prevalence and severity of periodontitis, as well as interproximal bone loss. Whereas the pathogenesis of periodontitis in smokers is poorly understood, there are data suggesting defects in neutrophil function, impaired serum antibody responses to periodontal pathogens, and potentially diminished gingival fibroblast function. The prevalence and severity of periodontitis in former smokers is decreased compared with current smokers, providing evidence that smoking cessation is beneficial. Smoking markedly influences response to treatment, and a subset of smokers predominates among patients with refractory periodontitis whose disease is resistant to conventional treatment. Smokers are a high-risk group for periodontitis, and smoking history is a useful clinical predictor of future disease activity. Current estimates suggest that smoking is associated with a large proportion of periodontitis cases and constitutes a major dental public health problem. A new disease category, smoking-associated periodontitis, is proposed, given the unique characteristics of smokers with periodontitis.
Pathogenesis
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To determine the association between periodontitis stage and grade with oral-health-related quality of life (OHRQoL).This cohort was derived from the Porto Alegre study. The original sample was representative of more than 3 million inhabitants of a Brazilian urban area. Full-mouth periodontal examinations at six sites per tooth were performed at baseline and 5 years later. Periodontitis grade was determined by direct evidence of progression of attachment loss over the follow-up. Stage of periodontitis and OHRQoL, determined by the oral health impact profile version 14 (OHIP-14), were recorded at the follow-up examination. Mean ratios (MRs) and 95% confidence intervals (95% CIs) were estimated adjusting for age, sex, smoking, systemic diseases, tooth loss, and baseline periodontitis diagnosis.Five-hundred and ninety-nine individuals were analysed. Individuals with periodontitis grade C + stage II (MR = 1.49; 95% CI = 1.08-2.04) and stages III/IV (MR = 1.83; 95% CI = 1.25-2.66) had significantly higher OHIP scores than those without periodontitis or with periodontitis stage I/grade B. Individuals with periodontitis stages II and III/IV + grade B did not differ from those without periodontitis or with periodontitis stage I/grade B.Severity and progression rate of periodontitis are associated with poor OHRQoL.
Clinical attachment loss
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Tooth loss
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澄清 IL-6 多型性和 periodontitis，盒子控制研究的元分析和全身的评论的协会的目的被进行。我们执行了文学的材料和方法用 PubMed 和 Medline 数据库寻找到 2009 年 5 月，没有限制。我们也从所有检索文章考察了参考书。包含 1 的六盒子控制研究 093 个 periodontitis 盒子和 574 控制被选择让元分析估计在 IL-6 多型性和 periodontitis 的风险之间的声称的协会。IL-6 −174 G/C 和 −572 C/G 多型性在在 IL-6 −6331 T/C 多型性之间的现在的元分析，和协会被包括， periodontitis 的风险足够地也被考察。结果和结论现在的元分析显示 IL-6 −174 G 等位基因不能修改长期的 periodontitis 的风险，但是增加好攻击的 periodontitis 的风险。并且 −572 C/G 多型性与 periodontitis，包括的长期的 periodontitis 或好攻击的 periodontitis 的致病被联系。
Aggressive periodontitis
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Etiology
Periodontium
Aggressive periodontitis
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Periodontitis is an inflammatory disease caused by microorganisms that induce the destruction of periodontal tissue. Inflamed and damaged tissue produces various inflammatory cytokines, which activate osteoclasts and induce alveolar bone loss and, eventually, tooth loss. Sirt6 expression suppresses inflammation and bone resorption; however, its role in periodontitis remains unclear. We hypothesized that Sirt6 has a protective role in periodontitis. To understand the role of Sirt6 in periodontitis, we compared periodontitis with ligature placement around the maxillary left second molar in 8-week-old control (C57BL/6J) male mice to Sirt6-overexpressing Tg (Sirt6Tg) mice, and we observed the resulting phenotypes using micro-CT. MDL801, a Sirt6 activator, was used as a therapy for periodontitis through oral gavage. Pro-inflammatory cytokines and increased osteoclast numbers were observed in alveolar bone tissue under periodontitis surgery. In the same condition, interestingly, protein levels from Sirt6 were the most downregulated among sirtuins in alveolar bone tissue. Based on micro-CT and CEJ-ABC distance, Sirt6Tg was observed to resist bone loss against ligature-induced periodontitis. Furthermore, the number of osteoclasts was significantly reduced in Sirt6Tg-ligated mice compared with control-ligated mice, although systemic inflammatory cytokines did not change. Consistent with this observation, we confirmed that bone loss was significantly reduced when MDL801, a Sirt6 activator, was included in the ligation mouse model. Our findings demonstrate that Sirt6 activation prevents bone loss against ligature-induced periodontitis. Thus, a Sirt6 activator may provide a new therapeutic approach for periodontitis.
Ligature
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Periodontitis is an infectious disease caused by bacteria destroying periodontal supporting tissues. As the number of patients with periodontitis is increasing, more attention is being paid to the prevention and treatment of periodontitis. The incidence of periodontitis in China is about 70%. Currently, periodontitis has been considered one of the three major diseases that endanger human oral health. Both diabetic patients and hypertensive patients have a higher risk of periodontitis disease than healthy individuals. Advanced stages of periodontitis are often accompanied by tooth loss, and tooth loss can lead to decreased chewing function, which can lead to diseases such as indigestion and gastric ulcers. Besides, A growing body of research links periodontitis to Alzheimer's disease. Periodontitis is closely related to other systemic diseases. Therefore, the prevention and treatment of periodontitis is important. The paper summarizes the treatment measures for periodontitis in different periods in the new international classification of periodontal diseases in 2018 by analyzing the relevant literature and also introduce the measures related to the prevention of periodontitis.
Tooth loss
Aggressive periodontitis
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Electroodontometric study of 756 intact teeth in 209 patients 18-65 years of age with normal periodontium and different stages of periodontal disease (periodontitis) showed that 96.8% of teeth in patients with mild periodontitis retained normal sensitivity, 68.4% -- with moderate periodontitis and 55% -- with severe periodontitis. Decreased pain threshold was detected in 3.2% of teeth of patients with mild periodontitis, 22.6% -- with moderate periodontitis and 12% -- with severe periodontitis. Increased pain threshold was not detected in teeth of patients with mild periodontitis, but in 9% with moderate periodontitis and in 29% with severe periodontitis it was obvious.
Periodontium
Aggressive periodontitis
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