The role of the microbiota in periodontal disease

The last decade has witnessed unparalleled advances in our understanding of the complexity of the oral microbiome and the compositional changes that occur in subgingival biofilms in the transition from health to gingivitis and to destructive periodontal disease. The traditional view, which has held sway for the last 2 decades, that disease is characterized by the outgrowth of a consortium, or consortia, of a limited number of potentially pathogenic organisms, has given way to an alternative paradigm. In this new view, the microbiological changes associated with disease represent whole-scale alterations to the overall microbial population structure and to the functional properties of the entire community. Thus, and in common with other microbially mediated diseases of the gastrointestinal tract, the normally balanced, symbiotic, and generally benign commensal microbiome of the tooth-associated biofilm undergoes dysbiosis to a potentially deleterious microbiota. Coincident with progress in defining the microbiology of these diseases, there have been equally important advances in our understanding of the inflammatory systems of the periodontal tissues, their control, and how inflammation may contribute both to the development of dysbiosis and, in a deregulated state, the destructive disease process. One can therefore speculate that the inflammatory response and the periodontal microbiome are in a bidirectional balance in oral health and a bidirectional imbalance in periodontitis. However, despite these clear insights into both sides of the host/microbe balance in periodontal disease, there remain several unresolved issues concerning the role of the microbiota in disease. These include, but are not limited to, the factors which determine progression from gingivitis to periodontitis in a proportion of the population, whether dysbiosis causes disease or results from disease, and the molecular details of the microbial stimulus responsible for driving the destructive inflammatory response. Further progress in resolving these issues may provide significant benefit to diagnosis, treatment, and prevention.     

The role of autophagy in the pathogenesis of periodontal disease

Periodontal disease is a chronic inflammatory disease leading to destruction of periodontal tissues. As a local inflammation, periodontopathic bacterium, pro‐inflammatory mediators, and local immune response play pivotal role in the progress of periodontal disease. Besides, cigarette smoke has long been associated with periodontal disease and tooth loss. Autophagy is an intracellular degradation process highly conserved from yeast to humans. As a lysosomal degradation pathway of self‐digestion, it is critical for maintaining cells homeostasis and development. The role of autophagy has been investigated in oral diseases, such as oral cancer, periapical lesions, and oral candidiasis. Recently, increasing studies investigated the role of autophagy in periodontal disease. In this review, we try to illustrate the effect of autophagy on periodontal disease pathogenesis from 5 aspects: autophagy affects the intracellular infection and survival of bacteria; autophagy has an interaction with periodontal inflammation; autophagy is pivotal in periodontal cells biology and periodontal tissues destruction and reconstruction; autophagy can be induced by cigarette smoke; last but not least, autophagy may affect periodontal disease via endoplasmic reticulum stress.     

Heterogeneity of systemic inflammatory responses to periodontal therapy

Aims: We investigated the effect of comprehensive periodontal therapy on the levels of multiple systemic inflammatory biomarkers.
Material and Methods: Thirty patients with severe periodontitis received comprehensive periodontal therapy within a 6-week period. Blood samples were obtained at: 1-week pre-therapy (T1), therapy initiation (T2), treatment completion (T3), and 4 weeks thereafter (T4). We assessed the plasma concentrations of 19 biomarkers using multiplex assays, and serum IgG antibodies to periodontal bacteria using checkerboard immunoblotting. At T2 and T4, dental plaque samples were analysed using checkerboard hybridizations.
Results: At T3, PAI-1, sE-selectin, sVCAM-1, MMP-9, myeloperoxidase, and a composite summary inflammatory score (SIS) were significantly reduced. However, only sE-selectin, sICAM, and serum amyloid P sustained a reduction at T4. Responses were highly variable: analyses of SIS slopes between baseline and T4 showed that approximately 1/3 and 1/4 of the patients experienced a marked reduction and a pronounced increase in systemic inflammation, respectively, while the remainder were seemingly unchanged. Changes in inflammatory markers correlated poorly with clinical, microbiological and serological markers of periodontitis.
Conclusions: Periodontal therapy resulted in an overall reduction of systemic inflammation, but the responses were inconsistent across subjects and largely not sustainable. The determinants of this substantial heterogeneity need to be explored further.     

Prevalence and severity of periodontal disease in patients with inflammatory bowel disease

Previous reports have demonstrated that oral mucosa and periodontal lesions occur in patients suffering from inflammatory bowel disease (Crohn's disease [CD] and ulcerative colitis [UC]). It is unknown whether periodontal disease is an occasional or regular finding in these patients. The purpose of this study was to assess the prevalence and severity of periodontal disease in patients with inflammatory bowel disease (IBD). The periodontal status of 107 consecutive patients seeking treatment for inflammatory bowel disease was assessed. Examination of the mid- and mesiobuccal aspects of one quadrant on one jaw and the contralateral quadrant of the opposite jaw revealed the 93.5% of the CD patients and 95.1% of UC patients had at least one site with probing attachment loss of 2 mm or greater, and a mean probing attachment loss 1.4 +/- 0.9 mm and 1.5 +/- 1.0 mm, respectively. We found that 28.3% of CD patients and 29.5% of UC patients possessed at least 1 site with a pocket probing depth of 4 mm or greater; the mean pocket probing depth in these patients was 2.4 +/- 0.2 mm and 2.3 +/- 0.2 mm, respectively. Compared with the assessment of Oral Health of United States Adults, IBD patients revealed a 11.9% higher prevalence (P less than or equal to 0.01) but 0.6 mm lower severity (P less than or equal to 0.01) of periodontal disease. The magnitudes of these differences suggest no clinical implications for the management of periodontal disease in IBD subjects.     

The defensive role of lysozyme in human gingiva in inflammatory periodontal disease

Background and Objective:  The presence of lysozyme in human gingiva has not previously been demonstrated. In this study, we looked for evidence for the potential role of lysozyme as a protector of gingival elastic fibres. The objective of this study was also to determine the ex vivo susceptibility to hydrolysis of gingival elastic fibres from patients with or without periodontal disease by human leukocyte elastase and by human cathepsin G.
Materials and Methods:  Using gingival tissue sections from eight control, 10 gingivitis and 10 periodontitis patients, we evaluated the area fraction occupied by gingival elastic fibres (after selective staining) by the use of automated image analysis. In the ex vivo experiments, serial tissue sections from four control, four gingivitis, four young periodontitis and four aged periodontitis patients were submitted to the action of human leukocyte elastase and cathepsin G, after which enzymatic activities were determined by image analysis. Indirect immunodetection of lysozyme was also done on tissue sections for all patients included in this study.
Results:  Large variations of the area fraction occupied by elastic fibres were observed in human gingiva from young and aged patients with and without periodontal disease. In control and gingivitis patients, leukocyte elastase and cathepsin G had high comparable elastin solubilizing activities. With young and aged periodontitis patients, the two serine proteinases had weak elastin solubilizing activities. Lysozyme appeared to be present at the periphery of gingival elastic fibres in periodontitis patients.
Conclusion:  Lysozyme can be considered an important natural protector of elastic fibres in pathological gingiva.     

Increased risks of dental caries and periodontal disease in Chinese patients with inflammatory bowel disease

Objectives: Inflammatory bowel disease (IBD) may be associated with oral diseases, but few relevant studies have been reported in China. This study aimed to compare the prevalence, severity and extent of dental caries and periodontal disease in Chinese IBD patients and healthy controls. Materials and methods: In this cross-sectional study, questionnaires and oral examinations were completed for 389 IBD patients [265 with Crohn’s disease (CD) and 124 with ulcerative colitis (UC)] and 265 healthy controls based on the established criteria of the World Health Organization. Tobit regression, multiple linear regression and logistic regression were performed to analyse the data. Results: After adjusting for confounders, the decayed, missing and filled surfaces indices were significantly increased in the CD and UC patients compared with those in the controls (P < 0.001). Patients with CD [odds ratio (OR) = 4.27, 95% confidence interval (95% CI): 2.63–6.95, P < 0.001] and UC (OR = 2.21, 95% CI: 1.24–3.94, P = 0.007) had significantly higher risks of dental caries than controls. Significantly higher percentages of sites with probing pocket depth ≥ 5 mm and clinical attachment loss ≥ 4 mm were observed in CD and UC patients compared with controls (P < 0.001). A fully adjusted model revealed that CD and UC were risk indicators for periodontitis (OR = 4.46, 95% CI: 2.50–7.95, P < 0.001; OR = 4.66, 95% CI: 2.49–8.71, P < 0.001, respectively). No significant differences in dental caries and periodontal disease were observed between the CD and UC patients. Conclusions: Chinese IBD patients have a higher prevalence, severity and extent of dental caries and/or periodontal disease than controls, and require oral health education and multidisciplinary treatment.Key words: Dental caries, periodontal disease, inflammatory bowel disease, Crohn’s disease, ulcerative colitis     

The role of supragingival plaque in the control of progressive periodontal disease

Abstract Levels of supragingival plaque and calculus have been related to progressive periodontal disease, and control of supragingival plaque in conjunction with professional tooth cleaning subgingivally forms the basis for the management of progressive periodontal disease. However, the contribution towards the management of progressive periodontal disease brought about by supragingival plaque control alone is not clear. There are studies which address, directly or indirectly, the contribution of supragingival plaque control alone towards the management of progressive periodontal disease. The effects of supragingival plaque control alone have been evaluated clinically, histologically and microbiologically, and taken together, the evaluations suggest that these effects may not be as marked as when professional subgingival tooth cleaning is also performed. These studies, however, given the patterns of periodontal disease found in adults in many communities, can form the basis for advocating high individual levels of supragingival plaque control as a community measure in the management of periodontal disease. Further long-term investigations into this approach may be warranted.     

Prevalence of dental caries and periodontal disease in patients with inflammatory bowel disease: a case-control study

AIM: Previous reports suggest a higher incidence of dental caries in patients with inflammatory bowel disease (IBD) and similarities in the immunopathogenesis of IBD and periodontitis. This study assessed the prevalence of periodontal disease and caries in patients with IBD. METHODS: In the present case-control study, 62 patients seeking treatment of IBD and 59 matched healthy controls of a dental practice were clinically examined. Oral soft-tissue alterations, the decayed, missing and filled tooth surface (DMF-S) index, dentine caries, plaque index (PI), bleeding on probing (BOP), probing pocket depth (PPD) and clinical attachment loss (CAL) were evaluated in each patient and in the controls. RESULTS: Patients with IBD showed a significantly higher number of oral manifestations compared with controls. The DMF-S index showed no significant differences, but there was a significantly higher number of subjects with dentine caries in patients with IBD. The mean PPD in patients with IBD was 2.08 versus 2.23 mm in controls (p=0.014). Compared with controls, patients with IBD had more sites with CAL of at least 4 mm (81% versus 64% in controls, p=0.07) and 5 mm (63% versus 46%, p=0.07), respectively. CONCLUSIONS: The results of this case-control study demonstrate a higher frequency of dentine caries in patients with IBD but the periodontal findings showed no distinct differences between cases and controls.     

Salivary nitric oxide levels in inflammatory periodontal disease - a case-control and interventional study

To cite this article: Int J Dent Hygiene 10 , 2012; 67–73
DOI: 10.1111/j.1601‐5037.2011.00508.x
Parwani SR, Chitnis PJ, Parwani RN. Salivary nitric oxide levels in inflammatory periodontal disease – A case‐control and interventional study. Abstract: Background: Biochemical markers of inflammatory periodontal disease present in saliva can partially determine the extent of periodontal disease. Furthermore, collection of salivary constituents is a simple and non‐invasive procedure. Nitric oxide (NO) has been linked to etiopathogenesis of inflammatory periodontal disease and is expressed in saliva. This study was conducted with the objective of estimating salivary NO levels in inflammatory periodontal diseases (gingivitis and periodontitis) and comparing these levels with control subjects. A re‐assessment of these levels was also made after providing appropriate treatment with a view to ascertain its diagnostic and prognostic values. Methods: This was a case–control as well as an interventional study including a total of 90 (30 control, 30 gingivitis and 30 periodontitis) subjects. Saliva samples were collected from each subject, and NO levels were assayed by Griess reaction. Results: NO levels were increased significantly in gingivitis and periodontitis subjects as compared with controls. There was a statistically significant decrease in the NO levels in each study group after the healing period (corresponding to the reduced clinical signs of inflammation). Our study also correlated probing pocket depths with salivary NO levels in periodontitis group where we found a positive correlation between the two. Conclusion: Salivary NO levels can be utilized as a good indicator of the inflammatory status of the periodontium, and evaluating its levels in saliva by Griess reaction on a photoelectric colorimeter is a reliable, accurate and faster method to estimate the level of inflammation in periodontal tissues.     

The relationship of inflammatory periodontal disease to diabetic status in insulin-dependent diabetes mellitus patients

This study was designed to evaluate the relationship of inflammatory periodontal disease to the diabetic status of the insulin-dependent diabetes mellitus (IDDM) patient. 52 IDDM patients, ages 11-22 years, were evaluated. These patients were closely monitored at regular intervals in the University of Kentucky pediatric diabetic clinic. A periodontal examination was carried out for each patient. The patients were then assigned to a periodontitis or non-periodontitis group. Moderate to advanced periodontitis was found in 5.8% of the subjects. The gingival index and sulcular bleeding index were significantly higher in the periodontitis group (P less than 0.05). There was no significant difference between groups for plaque index, age of diabetic onset, duration of diabetes, present age, insulin dosage/weight, or serum glucose (P greater than 0.05). There was a greater % of ketoacidosis, retinopathy and neuropathy in the periodontitis group. IDDM patients with neurological complications or a history of chronic infections had a significantly higher gingival index score than those without the complication (P less than 0.05).     

Correlation between periodontal disease, inflammatory alterations and pre-eclampsia

Politano GT, Passini R, Nomura ML, Velloso L, Morari J, Couto E. Correlation between periodontal disease, inflammatory alterations and pre‐eclampsia. J Periodont Res 2011; 46: 505–511. © 2011 John Wiley & Sons A/S Background and Objective: Several studies have hypothesized that periodontal disease may increase the risk of pre‐eclampsia. The correlation between the two diseases would probably be based on hypertension‐related cytokine release in the local periodontal environment. The aim of this study was to evaluate the association between periodontal disease and pre‐eclampsia, and the correlation of the two conditions with interleukin‐6 (IL‐6) and tumor necrosis factor‐α(TNFα) mRNA expression. Material and Methods: A case–control analysis of 116 pregnant women, 58 with pre‐eclampsia (cases) and 58 normotensive pregnant women (controls) was performed. In addition to collection of socio‐demographic data and periodontal evaluation, peripheral blood samples were collected for laboratory analysis of IL‐6 and TNFα mRNA expression by real‐time PCR. Results: There was an association between periodontitis and pre‐eclampsia (adjusted odds ratio 3.73; 95% confidence interval 1.32–10.58). Increased TNFα mRNA expression was observed in pre‐eclamptic women; however, there was no correlation between periodontitis and systemic cytokine expression. In the case group, systemic cytokine mRNA levels were similar in pregnant women with and without periodontitis (means ± SD): 0.73 ± 0.24 vs. 0.82 ± 0.38 for TNFα and 1.31 ± 1.49 vs. 1.09 ± 0.74 for IL‐6, respectively. Conclusion: Periodontitis was clinically related to pre‐eclampsia; however, the supposed mechanism that correlates the two diseases, i.e. a systemic inflammatory process involving cytokines TNFα and IL‐6 in the presence of periodontal disease, could not be confirmed in this study.     

Psychosocial factors in inflammatory periodontal diseases

Abstract. Reviewing the literature concerning the possible role of psychosocial factors in the aetiology of inflammatory periodontal diseases, it may be concluded that there is evidence which strongly suggests that emotional stress is one of the predisposing factors to ANUG. On the other hand, it is not clear that the scientific evidence is sufficient to substantiate the hypothesis that psychosocial factors are of aetiological importance in periodontitis. The proposed mechanisms which may mediate the putative relationship between psychosocial conditions and inflammatory periodontal diseases remain to be tested. However, psychoneuroimmunologic studies make lowered host resistance especially interesting as a possible mechanism. Although available studies do not definitively support causal relationships, they suggest that psychosocial factors may be involved in the aetiology of inflammatory periodontal diseases, which, in turn, would relate to clinical management of these conditions.     

Osteoclast activation in inflammatory periodontal diseases

OBJECTIVE: In this paper, we review the mechanisms thought to be involved in the activation of osteoclasts in periodontitis.
SUMMARY Osteoclasts are regulated by both microbial and host factors. Some factors act directly on cells of the osteoclast lineage, whereas others act indirectly through other cell types in the bone environment. The pro-inflammatory cytokines (interleukins I and 6, tumor necrosis factors) have been implicated in the stimulation of osteoclastic resorption. The roles of the immunoregul-atory cytokines (interleukins 2 and 4, interferon γ) are less clear, but decreased levels of these factors may contribute to periodontitis. A number of lipid mediators may be involved in stimulation of bone resorption. These include bacterial lipopolysaccharide and host-derived platelet-activating factor and prostaglandins. More recently, reactive oxygen intermediates and extracellular nucleo-tides, both present at sites of inflammation, have been investigated as possible modulators of osteoclast activity. The potential use of antiresorptive therapies in periodontitis is reviewed.
CONCLUSIONS: A wide range of host and bacterial factors contribute to the loss of alveolar bone in periodontitis. However, much remains to be understood about the complex mechanisms through which these factors regulate osteoclast activity. Further studies at the cellular and molecular level will lead to a better understanding of these processes and perhaps suggest new approaches for periodontal therapy.     

Plaque and chronic inflammatory Periodontal disease A question of ecology

The nature of the relationship between dental plaque and chronic inflammatory periodontal disease (CIPD) remains unclear, although there is no doubt that plaque is the direct cause. Non-specific, specific and exogenous hypotheses have been proposed to explain plaque-host relationships. Current evidence indicates that plaque is part of the natural human microflora, one of many such in nature, and that disruption of oral microbial ecology, due primarily to diet texture changes, leads to gingivitis and periodontitis. These result in increased plaque accumulation, and particularly in increased interdental effective plaque thickness. The latter leads to alterations in plaque ecology, particularly increasing anaerobiosis, with resultant shifts in proportions of its constituent species. These shifts are responsible for the increased counts of, for example, Bacteroides gingivalis, Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, Wolinella recta, spirochaetes and others, associated with chronic periodontitis in its various forms. Measures to prevent or control chronic periodontitis should aim, not to eliminate plaque, which ignores ecology and would compromise host defence, but to restore the species distribution in plaque to that compatible with health.     

牙周干预治疗对牙周炎伴冠心病患者血脂水平及炎症因子的影响

目的探讨牙周干预治疗对牙周炎伴冠心病患者血脂水平及炎症因子的影响。方法选取中、重度牙周炎伴冠心病患者进行牙周干预治疗83例(干预组)和冠心病不伴牙周炎患者50例(对照组),干预组患者采取口腔卫生指导、超声龈上洁治、龈下刮治和根面平整等干预措施,对照组不采取任何干预措施。对干预组和对照组患者牙周状况进行评估,检测患者血清和龈沟液中炎症因子。结果干预组患者干预治疗后临床附着水平、探诊深度、菌斑指数和出血指数均较低于干预治疗前(P<0.05);干预组患者干预治疗后血清和龈沟液中IL-1β、IL-6、TNF-α水平均低于干预治疗前(P<0.05);干预组患者干预治疗后血清TC、TG和LDL-C水平均较干预治疗前降低,而HDL-C和脂联素则较干预治疗前升高(P<0.05)。结论牙周干预治疗可有效改善牙周炎伴冠心病患者牙周状况,降低机体炎症反应,改善血脂代谢,从而可对冠心病病程进展产生正作用。