Periodontal diseases and health: Consensus Report of the Sixth European Workshop on Periodontology

Introduction: The remit of this group was to update the knowledge base on periodontal diseases and health.
Material and Methods: The literature was systematically searched and critically reviewed in five specific topics.
Results: Prevalence of periodontitis: The data suggest a trend towards a lower prevalence of periodontitis in recent years.
Adverse pregnancy outcome: The findings indicate a likely association between periodontal disease and an increased risk of adverse pregnancy outcomes. There is no evidence that treating periodontal disease decreases the rate of adverse pregnancy outcomes.
Prevalence and distribution of periodontal pathogens: Genetic analysis of bacteria has demonstrated an unanticipated diversity within species. Carriage rates and particular subsets of these species vary between ethnic groups. Few of these differences can be related to differences in disease prevalence.
Diabetes mellitus: Evidence on the association supports the concept of increased severity but not extent of periodontitis in subjects with poorly controlled diabetes. It is inconclusive that periodontal treatment results in improved metabolic control.
Cardiovascular diseases: Evidence suggests that having periodontitis contributes to the total infectious and inflammation burden and may contribute to cardiovascular events and stroke in susceptible subjects. The impact of periodontal therapy must be further investigated.     

The effect of periodontal therapy on serum TNF-α and HbA1c levels in type 2 diabetic patients

Background:  To determine the effect of non-surgical periodontal therapy on serum TNF-α and HbA1c levels in poorly and well-controlled type 2 diabetic patients.
Methods:  In total, 45 patients were enrolled in the study; 30 patients with type 2 diabetes mellitus with periodontitis (15 with poorly controlled diabetes, HbA1c ≥ 7%, group 1A and 15 with well-controlled diabetes, HbA1c < 7%, group 1B) and 15 patients that were systemically healthy with periodontitis (group 2). The plaque index, gingival index, probing depth, clinical attachment loss, gingival bleeding index, HbA1c value, and circulating TNF-α concentration were measured at baseline and three months after the non-surgical periodontal therapy.
Results:  All periodontal parameters and serum TNF-α levels were significantly decreased three months after the non-surgical periodontal therapy compared to the baseline values in all groups. The HbA1c values were significantly decreased only in well-controlled diabetic patients. We found no significant differences in the periodontal parameters or TNF-α levels at baseline and after three months between the two groups.
Conclusions:  Although non-surgical periodontal therapy eliminates local/systemic infection and inflammation via decreases in TNF-α, it is insufficient for significantly reducing HbA1c levels without strict glycaemic control in poorly controlled diabetic patients in a short time period.     

Periodontitis and risk for atherosclerosis: an update on intervention trials

Aims: Periodontitis has been associated with an increased risk of cardiovascular events. The nature of the association is unclear because both periodontitis and cardiovascular disease (CVD) share a host of risk factors. Intervention trials are critical to explore the relationship. If the association were causal, successful periodontal therapy will lead to an attenuation of the effect – CVD.
Material and Methods: The paper reviewed the design and the results of intervention trials aimed at improving systemic inflammation, endothelial dysfunction, carotid atherosclerosis and cardiovascular events.
Results: Early systematic reviews and a definitive controlled clinical trial indicate that intensive periodontal therapy results in a decrease in systemic inflammation and an improvement of endothelial dysfunction in systemically healthy subjects. A pilot trial has indicated the feasibility to assess the impact of periodontal therapy on carotid atherosclerosis in a primary cardiac prevention design.
Conclusions: Efforts to test causality in the relationship between periodontitis and CVD are ongoing. Evidence to date is consistent with the notion that severe generalized periodontitis causes systemic inflammation and endothelial dysfunction. Periodontitis has effects that go beyond the oral cavity and its treatment and prevention may contribute to the prevention of atherosclerosis.     

Periodontal manifestations of systemic disease

Periodontitis is a chronic bacterial infection of the supporting structures of the teeth. The host response to infection is an important factor in determining the extent and severity of periodontal disease. Systemic factors modify periodontitis principally through their effects on the normal immune and inflammatory mechanisms. Several conditions may give rise to an increased prevalence, incidence or severity of gingivitis and periodontitis. The effects of a significant number of systemic diseases upon periodontitis are unclear and often it is difficult to causally link such diseases to periodontitis. In many cases the literature is insufficient to make definite statements on links between certain systemic factors and periodontitis and for several conditions only case reports exist whereas in other areas an extensive literature is present. A reduction in number or function of polymorphonuclear leukocytes (PMNs) can result in an increased rate and severity of periodontal destruction. Medications such as phenytoin, nifedipine, and cyclosporin predispose to gingival overgrowth in response to plaque and changes in hormone levels may increase severity of plaque-induced gingival inflammation. Immuno-suppressive drug therapy and any disease resulting in suppression of the normal inflammatory and immune mechanisms (such as HIV infection) may predispose the individual to periodontal destruction. There is convincing evidence that smoking has a detrimental effect on periodontal health. The histiocytoses diseases may present as necrotizing ulcerative periodontitis and numerous genetic polymorphisms relevant to inflammatory and immune processes are being evaluated as modifying factors in periodontal disease. Periodontitis severity and prevalence are increased in diabetics and worse in poorly controlled diabetics. Periodontitis may exacerbate diabetes by decreasing glycaemic control. This indicates a degree of synergism between the two diseases. The relative risk of cardiovascular disease is doubled in subjects with periodontal disease. Periodontal and cardiovascular disease share many common risk and socio-economic factors, particularly smoking, which is a powerful risk factor for both diseases. The actual underlying aetiology of both diseases is complex as are the potential mechanisms whereby the diseases may be causally linked. It is thought that the chronic inflammatory and microbial burden in periodontal disease may predispose to cardiovascular disease in ways proposed for other infections such as with Chlamydia pneumoniae. To move from the current association status of both diseases to causality requires much additional evidence. Determining the role a systemic disease plays in the pathogenesis of periodontal disease is very difficult as several obstacles affect the design of the necessary studies. Control groups need to be carefully matched in respect of age, gender, oral hygiene and socio-economic status. Many studies, particularly before the aetiological importance of dental plaque was recognised, failed to include such controls. Longitudinal studies spanning several years are preferable in individuals both with and without systemic disease, due to the time period in which periodontitis will develop.     

Periodontal disease: associations with diabetes, glycemic control and complications

Objective:  This report reviews the evidence for adverse effects of diabetes on periodontal health and periodontal disease on glycemic control and complications of diabetes.
Design:  MEDLINE search of the English language literature identified primary research reports published on (a) relationships between diabetes and periodontal diseases since 2000 and (b) effects of periodontal infection on glycemic control and diabetes complications since 1960.
Results:  Observational studies provided consistent evidence of greater prevalence, severity, extent, or progression of at least one manifestation of periodontal disease in 13/17 reports reviewed. Treatment and longitudinal observational studies provided evidence to support periodontal infection having an adverse effect on glycemic control, although not all investigations reported an improvement in glycemic control after periodontal treatment. Additionally, evidence from three observational studies supported periodontal disease increasing the risk for diabetes complications and no published reports refuted the findings.
Conclusion:  The evidence reviewed supports diabetes having an adverse effect on periodontal health and periodontal infection having an adverse effect on glycemic control and incidence of diabetes complications. Further rigorous study is necessary to establish unequivocally that treating periodontal infections can contribute to glycemic control management and to the reduction of the burden of diabetes complications.     

Do patients with aggressive periodontitis have evidence of diabetes? A pilot study

Davies RC, Jaedicke KM, Barksby HE, Jitprasertwong P, Al‐Shahwani RM, Taylor JJ, Preshaw PM. Do patients with aggressive periodontitis have evidence of diabetes? A pilot study. J Periodont Res 2011; 46: 663–672. © 2011 John Wiley & Sons A/S Background and Objective: Complex relationships exist between diabetes and periodontal disease. Diabetes is accepted as a risk factor for periodontal disease, and recent evidence supports the existence of a bidirectional relationship between these two diseases. It has been hypothesized that inflammation, lipids and adipokines may mediate these relationships. However, research regarding the above relationships with respect to aggressive periodontitis is very limited. This pilot study aimed to investigate whether patients with aggressive periodontitis (not previously diagnosed with diabetes) have evidence of diabetes and have altered serum levels of inflammatory mediators, lipids and adipokines. Material and Methods: Glycaemic control markers (random plasma glucose and glycated haemoglobin), inflammatory mediators (high‐sensitivity C‐reactive protein, tumour necrosis factor‐α, interleukin‐1β, interleukin‐6, interferon‐γ and interleukin‐18), lipids (triglycerides, total cholesterol and high‐density lipoprotein‐cholesterol) and adipokines (leptin, adiponectin and resistin) were measured in serum samples from 30 patients with aggressive periodontitis and 30 age‐ and sex‐matched periodontally healthy control subjects, none of whom had a previous diagnosis of diabetes. Results: Levels of glycaemic control markers, inflammatory mediators, lipids and adipokines were not significantly different (p > 0.05) between the aggressive periodontitis patients and healthy subjects for unadjusted and adjusted analyses (adjusting for body mass index, smoking, ethnicity, age and sex). The p‐value for the adjusted analysis of adiponectin in female aggressive periodontitis patients compared with the female control subjects reached 0.064, the mean adiponectin level being lower in the female aggressive periodontitis patients (4.94 vs. 5.97 μg/mL). Conclusion: This pilot study provided no evidence to suggest that patients with aggressive periodontitis (not previously diagnosed with diabetes) have evidence of diabetes or altered serum levels of inflammatory mediators, lipids and adipokines.     

Prospective study of complier individuals under periodontal maintenance therapy: analysis of clinical periodontal parameters, risk predictors and the progression of periodontitis

Aim: This prospective study aimed to evaluate the progression of periodontitis and the influence of risk variables among individuals attending a programme of periodontal maintenance treatment in an academic environment.
Material and Methods: A total of 150 individuals diagnosed with chronic moderate-advanced periodontitis, and who had finished active periodontal treatment, were incorporated into the periodontal maintenance therapy. Social, demographic and biological variables of interest from subjects were collected at quarterly recalls, over a 12-month period. The effect of variables of interest and confounding on the periodontal status and progression of periodontitis was tested by univariate and multivariate logistic analysis.
Results: A total of 130 subjects (86.7%) showed stable periodontal status, whereas 20 subjects (13.3%) presented periodontitis progression. Twenty-eight subjects (18.66%) presented tooth loss that resulted in a total of 47 lost teeth (1.38%). Diabetes was not found to be associated with periodontitis progression ( p =0.67). Smoking was significantly associated with a greater progression of periodontitis (OR=2.7, 95% CI 1.01–7.22).
Conclusions: Periodontal maintenance programmes in academic environment can stabilize the periodontal condition obtained after active periodontal therapy as well as control the action of risk variables for the progression of periodontitis.     

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.     

Involvement of vascular endothelial growth factor, CD44 and CD133 in periodontal disease and diabetes: an immunohistochemical study

Aim: The aim of this study was to investigate the relationship between expression of angiogenic and regeneration markers and periodontal disease in subjects with/without diabetes mellitus.
Material and Methods: Immunohistochemical detection of vascular endothelial growth factor (VEGF), CD44 and CD133 was performed in 16 samples each of (1) healthy gingiva from non-diabetic subjects (controls), (2) gingiva from non-diabetic subjects with periodontitis, (3) gingiva from subjects with type 1 diabetes and periodontitis, (4) gingiva from subjects with type 2 diabetes and periodontitis.
Results: Diseased gingivae from patients with diabetes and periodontitis had greater clinical measures of periodontal disease than those with periodontitis only. VEGF expression was significantly enhanced in epithelial and endothelial cells from patients with periodontitis compared with controls ( p <0.05). Epithelial CD44 expression was strong in all groups, while CD44 was significantly enhanced ( p <0.05) in connective tissue cells from both diabetic groups. Epithelial and endothelial CD133 expression was comparable in all patients except those with type 2 diabetes and periodontitis, where it was not detected. Stromal CD133 expression was significantly lower in patients with type 2 diabetes and periodontitis and was increased in periodontitis patients ( p <0.05).
Conclusions: The involvement and high expression of VEGF, CD44 and CD133 in periodontal disease may predict a greater regeneration capacity of gingival tissue.     

Periodontitis prevalence and severity in Indonesians with type 2 diabetes

Background: The prevalence of diabetes mellitus type 2 (DM2) in Indonesia is high and still rising. Periodontitis is associated with DM2. No study has investigated this association in Indonesia, nor has any study investigated this association using a variety of methods to operationalize periodontitis. The present study compares prevalence and severity of periodontitis in patients with DM2 to healthy controls, using different methods to operationalize periodontitis. Methods: A total of 78 subjects with DM2 and 65 healthy control subjects underwent a full‐mouth periodontal screening assessing probing depth, gingival recession, plaque index, and bleeding on probing. Using these measurements, the prevalence and severity of periodontitis was operationalized in various ways. Differences in the prevalence and severity of periodontitis between subjects with DM2 and healthy subjects were analyzed using univariate analyses. In regression analyses, the prevalence and severity of periodontitis were predicted on the basis of DM2 presence, controlling for confounders and effect modification. Results: Prevalence of periodontitis was significantly higher in subjects with DM2 compared to healthy subjects, showing odds ratios of 5.0 and 6.1. Likewise, periodontitis severity was significantly higher in subjects with DM2. Conclusion: Indonesian subjects with DM2 had more prevalent and more severe periodontitis than healthy Indonesian subjects, independent of confounding factors or the methods used to operationalize periodontitis.     

Effect of periodontal treatment on metabolic control, systemic inflammation and cytokines in patients with type 2 diabetes

Objective: The aim of this study was to investigate the effect of periodontal therapy on the circulating concentration of high-sensitivity capsule-reactive protein (hs-CRP), fibrinogen (FIB), interleukin (IL)-4, IL-6, IL-8, IL-10 and tumour necrosis factor- α (TNF- α ) and on the metabolic control in type 2 diabetes mellitus (T2DM) patients.
Material and Methods: Twenty-three T2DM patients with chronic periodontitis were enrolled in this study. Periodontal clinical parameters, namely visible plaque index, gingival bleeding index, bleeding on probing, probing depth and clinical attachment levels, were evaluated. Blood samples for plasma were collected and assessed for the levels of hs-CRP, FIB, IL-4, IL-6, IL-8, IL-10 and TNF- α . The glycated haemoglobin (HbA_1c) and fasting plasma glucose were also measured. All parameters were evaluated before and 3 months after non-surgical periodontal therapy.
Results: All clinical parameters were significantly improved 3 months after the periodontal therapy. A univariate comparison showed a tendency towards a decrease of the measured biomarkers, most pronounced for TNF- α and FIB, after therapy. Periodontal treatment also reduced HbA_1c and hs-CRP levels, albeit not significantly.
Conclusions: The clinically successful non-surgical periodontal therapy tended to reduce systemic inflammation and the concentration of some circulating cytokines.     

Single-blind studies of the effects of improved periodontal health on metabolic control in Type 1 diabetes mellitus

Abstract Uncontrolled studies have suggested a beneficial effect of periodontal treatment on metabolic control of insulin-dependent diabetes mellitus (IDDM). We therefore conducted controlled single-blind studies, using current metabolic status indicators in IDDM subjects free of significant complications other than periodontal diseases. In the 1st study, 41 IDDM subjects with gingivitis and early periodontitis were randomly assigned to treatment (oral hygiene and scaling) or control groups. The study was completed by 16 experimental and 15 control subjects. Reassessment after 2 months showed a Hawthorne effect in the control group, and no difference between groups. However, further analysis showed a relationship between individual metabolic control variation and gingival inflammation. A 2nd study enrolled 23 IDDM subjects with advanced periodontitis, who were randomised to treatment (full initial therapy including root planing) or control groups. Only 1 subject failed to complete the study, owing to illness. In this study, a significant response to periodontal treatment was not accompanied by any improvement in metabolic control. These results support the concept that the effect of metabolic control may be predominant in the relationship between IDDM and periodontal health.     

Systemic effects of periodontitis: lessons learned from research on atherosclerotic vascular disease and adverse pregnancy outcomes

Studies conducted over the past 25 years have focussed on the role of periodontitis, an inflammatory condition of microbial aetiology that destroys the tooth‐supporting tissues, as a systemic inflammatory stressor that can act as an independent risk factor of atherosclerotic vascular disease (AVSD) and adverse pregnancy outcomes (APOs). It has been suggested that periodontitis‐associated bacteraemias and systemic dissemination of inflammatory mediators produced in the periodontal tissues may result in systemic inflammation and endothelial dysfunction, and that bacteria of oral origin may translocate into the feto‐placental unit. Epidemiological studies largely support an association between periodontitis and ASVD/APOs, independently of known confounders; indeed, periodontitis has been shown to confer statistically significantly elevated risk for clinical events associated with ASVD and APOs in multivariable adjustments. On the other hand, intervention studies demonstrate that although periodontal therapy reduces systemic inflammation and improves endothelial function, it has no positive effect on the incidence of APOs. Studies of the effects of periodontal interventions on ASVD‐related clinical events are lacking. This review summarises key findings from mechanistic, association and intervention studies and attempts to reconcile the seemingly contradictory evidence that originates from different lines of investigation.     

运用牙周特色治疗改善重度牙周炎的临床效果（附1例6年诊治随访观察报告）

 牙周炎是最常见的失牙原因之一，不仅严重影响口腔健康，也是多种全身性疾病的风险因素。完善的牙周检查及系统的治疗计划是消除炎症、控制疾病进展、恢复口腔功能和美观的关键。如何尽最大可能保留存在牙周组织严重破坏的天然牙并维持其功能是口腔医生面临的挑战。文章展示了1例重度牙周炎病例的综合诊疗过程，通过完善的牙周基础治疗和恰当的手术治疗，控制了牙周炎症进展，并采用可摘局部义齿修复缺失牙，恢复口腔功能，同时定期行牙周维护治疗，随访6年，获得良好的治疗效果。基于此病例，文章探讨了重度牙周炎患牙的治疗决策，重度牙周炎诊疗中基础治疗和手术治疗的临床效果以及菌斑控制对长期维护治疗效果的作用，总结了本病例临床处理中的不足，为重度牙周炎的治疗积累了经验。     

牙周基础治疗对2型糖尿病相关性牙周炎患者血糖控制的Meta分析

目的系统评价牙周基础治疗对2型糖尿病相关性牙周炎患者血糖控制的影响,探讨牙周基础治疗在糖尿病治疗中的具体作用。方法计算机检索Cochrane图书馆对照试验注册中心、Medline、EMbase、SIGLE、GreyNet、NTIS、中国生物医学文献数据库、中文科技期刊全文数据库、中国期刊全文数据库和万方数据库,查找有关牙周基础治疗对糖尿病血糖控制影响的研究。检索时限均为1991-2011年4月31日。均由2名评价者独立选择试验、提取资料和评估方法学质量,然后采用RevMan 5．1软件对资料进行Meta分析。纳入7个研究,共计471例受试患者。结果牙周基础治疗能明显降低2型糖尿病相关性牙周炎患者糖化血红蛋白的水平,组间差异有统计学意义（95％CI：-0．94—0．22,P=0．001）。治疗组牙周袋探诊深度低于对照组,组间差异也有统计学意义（95％CI：-2．26～0．69,P=0．0002）。结论牙周基础治疗有利于2型糖尿病相关性牙周炎患者总体血糖水平的控制。     

运用牙周特色治疗改善重度牙周炎的临床效果（附1例6年诊治随访观察报告）

牙周炎是最常见的失牙原因之一,不仅严重影响口腔健康,也是多种全身性疾病的风险因素。完善的牙周检查及系统的治疗计划是消除炎症、控制疾病进展、恢复口腔功能和美观的关键。如何尽最大可能保留存在牙周组织严重破坏的天然牙并维持其功能是口腔医生面临的挑战。文章展示了1例重度牙周炎病例的综合诊疗过程,通过完善的牙周基础治疗和恰当的手术治疗,控制了牙周炎症进展,并采用可摘局部义齿修复缺失牙,恢复口腔功能,同时定期行牙周维护治疗,随访6年,获得良好的治疗效果。基于此病例,文章探讨了重度牙周炎患牙的治疗决策,重度牙周炎诊疗中基础治疗和手术治疗的临床效果以及菌斑控制对长期维护治疗效果的作用,总结了本病例临床处理中的不足,为重度牙周炎的治疗积累了经验。     

Expression of toll-like receptors 2, 4 and 9 is increased in gingival tissue from patients with type 2 diabetes and chronic periodontitis

Rojo‐Botello NR, García‐Hernández AL, Moreno‐Fierros L. Expression of toll‐like receptors 2, 4 and 9 is increased in gingival tissue from patients with type 2 diabetes and chronic periodontitis. J Periodont Res 2012; 47: 62–73. © 2011 John Wiley & Sons A/S Background and Objective: Broad evidence indicates that diabetes both increases the risk and hastens the progression of periodontal disease. Likewise, chronic inflammation or infections seem to provoke insulin resistance and thereby contribute to the development of diabetes and its complications. Innate immune responses, which appear to be altered in individuals with diabetes, are usually mediated by the recognition of pathogens through toll‐like receptors (TLRs). The constitutive expression of some TLRs has been reported in healthy human gingival tissue. Interestingly, the expression of TLRs 2 and 4 is increased with the severity of periodontal disease. Considering that the inflammatory reaction is exacerbated in individuals with diabetes and periodontitis, we suspected that the expression of some TLRs might be increased in gingival tissue in these patients. Material and Methods: In this study, we analyzed, by immunofluorescence, the expression of TLRs 2, 3, 4 and 9 in gingival tissues from healthy individuals and from periodontal patients with or without type 2 diabetes. Results: We found that the expression levels of TLRs 2, 3, 4 and 9 were higher in all periodontal patients than in healthy individuals. The expression of some TLRs was increased in subjects with periodontitis and diabetes relative to subjects with periodontitis but without diabetes; this increase in expression was found particularly in TLR2 and TLR9 in the connective tissue and in TLR4 at the epithelial region. Conclusion: These data suggest that the expression of these TLRs 2, 3, 4 and 9 in gingival tissue is higher in individuals with diabetes because its inflammatory reaction is exacerbated. Additionally, the expression of these TLRS is positively regulated with the severity of periodontal disease.     

Bidirectional interrelationships between diabetes and periodontal diseases: an epidemiologic perspective

This review evaluates evidence for a bidirectional relationship between diabetes and periodontal diseases. A comprehensive Medline search of the post-1960 English language literature was employed to identify primary research reports of relationships between diabetes and periodontal diseases. Reports included in the review on the adverse effects of diabetes on periodontal health (DM-->PD) were restricted to those comparing periodontal health in subjects with and without diabetes. Review of adverse affects of periodontal infection on glycemic control included reports of periodontal treatment studies and follow-up observational studies in which changes in glycemic control could be assessed. Observational studies reporting DM-->PD provided consistent evidence of greater prevalence, severity, extent, or progression of at least one manifestation of periodontal diseases in the large majority of reports (supportive evidence in 44/48 total reviewed; 37/41 cross-sectional and 7/7 cohort). Additionally, there were no studies reviewed with superior design features to refute this association. Treatment studies provided direct evidence to support periodontal infection having an adverse, yet modifiable, effect on glycemic control. However, not all investigations reported an improvement in glycemic control after periodontal treatment. Additional evidence to support the effect of severe periodontitis on increased risk for poorer glycemic control comes from 2 follow-up observational studies. The evidence reviewed supports viewing the relationship between diabetes and periodontal diseases as bidirectional. Further rigorous, systematic study is warranted to establish that treating periodontal infections can be influential in contributing to glycemic control management and possibly to the reduction of the burden of complications of diabetes mellitus.     

A population-based study on the association between type 2 diabetes and periodontal disease in 12,123 middle-aged Taiwanese (KCIS No. 21)

Aim: We investigated the association between type 2 diabetes mellitus (T2DM) and periodontal disease (PD) in the context of the current periodontal aetiology model.
Material and Methods: In total, 14,747 community residents aged 35–44 years were invited to a community-based PD survey between 2003 and 2006 using the community periodontal index. Significant factors modifying the association between T2DM and PD were ascertained. We further assessed the association between T2DM and the risk for PD, within strata of significant effect modifiers, after controlling for other putative factors.
Results: The prevalence rate was 10% higher in subjects with T2DM than in those without. After controlling for significant factors, T2DM was positively associated with the risk for PD (adjusted odds ratio=1.34,95% confidence interval: 1.07–1.74). The results of interaction assessment showed that only the waist was identified as a statistically significant effect modifier for such a positive association.
Conclusions: The association between T2DM and the risk for PD among young adult was demonstrated. This finding, together with other aetiological factors, fit with the current hypothesized model of the aetiology of periodontitis. However, the effect of T2DM modified by waist measurement should be verified in future studies.     

Resolution of periodontal inflammation does not guarantee improved glycemic control in type 1 diabetic subjects

Objective: The aim of this study was to find out if periodontal therapy has any effect on glycemic control of type 1 diabetes mellitus (DM).
Subjects and Methods: The periodontal health status of 65 type 1 diabetic subjects was assessed at the baseline and 8 weeks after completion of periodontal therapy. Glycemic control was assessed on both visits by measuring the percentage of glycosylated haemoglobin (GHbA1c). The change in HbA1c (ΔHbA1c) was assessed by using both a positive or negative change 0.5% and any change in HbA1c.
Results: The mean HbA1c level (±SD) of the whole study group was 8.6% (±1.5) at the baseline and 8.5% (±1.5) after treatment. Glycemic control improved during the study period in 23 subjects (35%) and worsened in 18 subjects (28%). Approximately 78% of the bleeding sites and 87% of the sites with probing depth 4 mm presented healing. ΔHbA1c associated significantly with baseline HbA1c but not with baseline periodontal health status or periodontal healing.
Conclusion: Regardless of a significant resolution of periodontal infection, a great majority of the subjects did not present any improvement in their glycemic control.