ArticleLiterature Review

Periodontitis and chronic kidney disease: A systematic review of the association of diseases and the effect of periodontal treatment on estimated glomerular filtration rate

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Abstract

Aim: The aim of this systematic review (SR) was to evaluate the association between periodontitis and chronic kidney disease (CKD) and the effect of periodontal treatment (PT) on the estimated glomerular filtration rate (eGFR). Methods: MEDLINE, EMBASE and Cochrane Central Register of Controlled Trials (CENTRAL) databases were searched up to and including September 30, 2012 to observational (S1) and interventional (S2) studies on the association of periodontitis with CKD. Studies were considered eligible for inclusion if they reported the eGFR. Search was conducted by two independent reviewers. The methodological quality of the observational studies was assessed using the Newcastle-Ottawa Scale (NOS) adapted for this review, and the Cochrane's Collaboration risk of bias assessment tool. A random-effects odds-ratio meta-analysis was conducted to estimate the degree of association between periodontitis and CKD. Results: Search strategy identified 2456 potentially eligible articles, of which four cross-sectional, one retrospective, and three interventional studies were included. Four S1, 80.0% reported some degree of association between periodontitis and CKD. Similarly, such an outcome was supported by pooled estimates (OR: 1.65, 95% Confidence Interval: 1.35, 2.01, p < 0.00001, χ(2) = 1.70, I(2 ) = 0%). All interventional studies found positive outcomes related to treatment. Conclusion: There is quite consistent evidence to support the positive association between periodontitis and CKD, as well as the positive effect of PT on eGFR.

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... All studies were assessed utilizing the JBI Critical Appraisal Checklist for Umbrella Reviews with minor variations in appraisal ratings were observed across the included studies. Based on the JBI appraisal criteria 46 and the agreed cut-off scores between the reviewers, nine were graded as high quality, 64,67,68,[70][71][72]77,78,80 eight were assigned as moderate quality 66,69,[73][74][75][76]79,81 and one was graded as low quality. 65 (Appendix 3). ...
... The populations included in the systematic reviews covers a diverse range of geographical locations including Europe , [64][65][66]69,70,72,[79][80][81] Americas, [64][65][66]69,70,72,74,[76][77][78][79][80][81] Western Pacific, 66 Six studies did not specify the CKD definition adopted in their review. 65 ...
... The populations included in the systematic reviews covers a diverse range of geographical locations including Europe , [64][65][66]69,70,72,[79][80][81] Americas, [64][65][66]69,70,72,74,[76][77][78][79][80][81] Western Pacific, 66 Six studies did not specify the CKD definition adopted in their review. 65 ...
Article
Chronic kidney disease (CKD) and poor oral health are inter-related and their significant impact on each other is well established in the literature. Many systematic reviews and meta-analyses have demonstrated a strong relationship between CKD and periodontitis, where periodontal treatment has shown potential in improving CKD outcomes. However, the quality of the studies and heterogeneity of the results show variation. The aim of this umbrella review was to review the quality of the current systematic reviews on the relationship between CKD and oral health with an emphasis on periodontal disease and to generate clinically relevant guidelines to maintain periodontal health in patients with CKD. This umbrella review was conducted and reported in alignment with the Joanna Briggs Institute and the PRISMA 2020 guidelines. The review protocol was established prior to commencing the review and registered on JBI and PROSPERO (CRD42022335209). Search strings were established for PubMed, Embase, Web of Science, Cochrane Database of Systematic Reviews, and Dentistry & Oral Science Source up to April 2022. All systematic reviews and meta-analyses that considered the relationship between CKD and periodontitis or periodontal treatment were included. Of 371 studies identified through the systematic search, 18 systematic reviews met the inclusion criteria. Ten studies assessed the relationship between oral health status and CKD with a focus on periodontitis and CKD, five reviewed the impact of periodontal treatment on CKD outcomes, two included both relationship and effectiveness of periodontal treatment and one qualitatively reviewed oral health-related quality of life in patients with kidney failure. Findings indicate there is a bidirectional relationship between CKD and periodontal disease. In view of the heterogeneity of the existing literature on CKD and periodontal disease, specific recommendations for the management of periodontitis among patients with CKD are proposed for medical professionals, dental professionals, and aged care workers based on the evidence collated in this review.
... On the other hand, several researchers discovered no significant association between the CKD and periodontitis and suggested that further longitudinal studies be conducted to evaluate the likelihood of a link. According to prospective research conducted in the United States, there was no significant difference in the connection between periodontitis and CKD among subgroups 31 . ...
... The results of every periodontal parameter shown a good improvement needed. 5 Grubbs et al, 2015 31 L o n g i t u d i n a l analysis ...
... Periodontitis was found to have strong association to increased mortality rates in CKD patients. 3 Grubbs et al. 2011 31 Cross-sectional analysis of NHANES data ...
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Background:Several decades of research have established the relationships between systemic diseases and periodontal diseases. Chronic kidney disease (CKD) is a chronic medical condition in which the homeostatic and emunctory activity of the kidneys is progressively declines. Periodontitis is a complex, polymicrobial disease that involves both the host and the environment. Tissue destruction is primarily associated with the host’s hyperresponsiveness, resulting in the release of inflammatory markers. Aim: This paper reviewed the evidence linking CKD, inflammatory markers, and periodontal disease and the effect of periodontal therapy on inflammatory markers and kidney function as well as dental parameters. Setting and Design: The sources of data were compiledand reviewed from MEDLINE, SCOPUS and Web of Sciences from 2010 to 2021. Result and Discussion: This review identifies biologically plausible bidirectional nexus between periodontitis and CKD. Periodontitis has emerged as non-traditional risk factor of CKD and vice versa. In addition, inflammatory markers are considered to play a role in the linkages between periodontitis and CKD. Recent study, has linked an increase in the production of inflammatory markers to a poorer renal outcome in patients with CKD. Periodontal therapy is effective in lowering the inflammatory markers levels and periodontal parameters as well as halting the progression of CKD. Conclusion : Understanding these links may help in identifying high-risk individuals and providing essential care at an early stage. Bangladesh Journal of Medical Science Vol. 22 No. 02 April’23 Page : 260-271
... CKD affects 8 %-16 % of the global population, and its prevalence and incidence have constantly increased [7,14,15]. Furthermore, mortality from CKD has increased by 31.7 % in the last 10 years due to its poor prognosis, making it one of the fastest-growing causes of death [15][16][17]. Recently, studies have suggested that poor periodontal health is more prevalent and severe in adults with CKD [6,18,19]. ...
... CKD affects 8 %-16 % of the global population, and its prevalence and incidence have constantly increased [7,14,15]. Furthermore, mortality from CKD has increased by 31.7 % in the last 10 years due to its poor prognosis, making it one of the fastest-growing causes of death [15][16][17]. Recently, studies have suggested that poor periodontal health is more prevalent and severe in adults with CKD [6,18,19]. ...
... In other studies, CKD and CP have been associated with several risk factors, including impaired immunity, diabetes mellitus, smoking, impaired oral hygiene, xerostomia, and malnutrition. This may account for a link between CP and its deleterious systemic effects in CKD patients [16,17]. ...
... Previous research has observed significant benefits of periodontal therapy towards the improvement of eGFR in CKD patients [30,43]. Nevertheless, Chambrone et al. (2013) carried out a systemic review focusing on the effect of periodontal therapy on eGFR. The review concluded that there is a lack of evidence to support the hypothesis that periodontal treatment has positive effects on eGFR, considering the limited number of studies and varying methodologies. ...
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Chronic kidney disease (CKD) and chronic periodontitis (CP) contribute to the increased level of inflammatory biomarkers in the blood. This study hypothesized that successful periodontal treatment would reduce the level of inflammatory biomarkers in CKD patients. This prospective study recruited two groups of CP patients: 33 pre-dialysis CKD patients and 33 non-CKD patients. All patients underwent non-surgical periodontal therapy (NSPT). Their blood samples and periodontal parameters were taken before and after six weeks of NSPT. The serum level of high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and periodontal parameters were compared between groups. On the other hand, kidney function indicators such as serum urea and estimated glomerular filtration rate (eGFR) were only measured in CKD patients. Clinical periodontal parameters and inflammatory markers levels at baseline were significantly higher (p < 0.05) in the CKD group than in the non-CKD group and showed significant reduction (p < 0.05) after six weeks of NSPT. CKD patients demonstrated a greater periodontitis severity and higher inflammatory burden than non-CKD patients. Additionally, CKD patients with CP showed a good response to NSPT. Therefore, CKD patients’ periodontal health needs to be screened for early dental interventions and monitored accordingly.
... Patients with periodontitis have higher levels of serum inflammatory cytokines than do healthy individuals [19][20][21][22]. Recent systematic reviews and meta-analyses have reported a bidirectional relationship between CKD and periodontitis [1,[23][24][25][26][27]. Furthermore, several studies have identified periodontal disease as a novel, non-traditional risk factor for CKD [26,[28][29][30]. ...
... Recent systematic reviews and meta-analyses have reported a bidirectional relationship between CKD and periodontitis [1,[23][24][25][26][27]. Furthermore, several studies have identified periodontal disease as a novel, non-traditional risk factor for CKD [26,[28][29][30]. It has been reported that patients with CKD and periodontitis have a higher cardiovascular and all-cause mortality than those diagnosed with CKD alone [11,31,32]. ...
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Objectives To investigate the correlation between serum and gingival crevicular fluid (GCF) levels of inflammatory cytokines and the association with periodontal parameters in patients with maintenance hemodialysis (MHD) and healthy control. Materials and methods Patients who were undergoing MHD were enrolled as the MHD group. Healthy individuals who underwent oral examination were selected as the control group after matching for the MHD group. All participants underwent a full-mouth periodontal evaluation, and the levels of eight inflammatory cytokines, including IL-1β, IL-17, IL-6, IL-8, and tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase-8 (MMP-8), and C-reactive protein (CRP), in the GCF and serum were measured. Results A total of 63 MHD patients and 75 healthy persons were included. The prevalence of moderate/severe periodontitis was significantly higher in the MHD group than in the control group (88.9 vs. 66.7%, P < 0.05). The GCF levels of CRP, TNF-α, MCP-1, and MMP-8 were higher in patients in the MHD group with moderate/severe periodontitis than in the control group (P < 0.05). Serum CRP, MCP-1, TNF-α, and MMP-8 levels were positively correlated with the GCF CRP levels (P < 0.05). The GCF and serum CRP levels were positively correlated with the periodontal clinical parameters (P < 0.05). Conclusions Serum CRP, MCP-1, TNF-α, and MMP-8 may relate with the GCF CRP levels. The GCF and serum CRP levels correlated positively with the periodontal clinical parameters, including the VPI, PPD, and CAL, indicating that CRP may play an important role between periodontitis and ESRD. Clinical relevance The present study indicated that GCF and serum CRP levels correlated positively with the periodontal clinical parameters, and the CRP levels may be selected as an indicator to evaluate the severity of inflammation and the effectiveness, prognosis of periodontal treatment in ESRD patients.
... As summarized in the Proceedings of a Workshop jointly held by the European Federation of Periodontology and the American Academy of Periodontology [2], periodontal disease has been associated with diabetes [3,9,10], cardiovascular diseases (CDV) [11][12][13][14][15], adverse pregnancy outcomes [4,16,17], obesity [18,19], metabolic syndrome [20,21], chronic obstructive airways disease [22,23], cognitive impairment such as Alzheimer's [24,25], rheumatoid arthritis [26], chronic kidney diseases [27,28], psoriasis [29], depression [30], osteoporosis [31,32] and cancers [7,33]. The understanding of these associations is further complicated by the fact that several of these relationships may be bidirectional or even interrelated between systemic outcomes. ...
... Periodontitis and chronic kidney disease (CKD) present an established relationship due to the systemic inflammatory status and presence of bacteria in the bloodstream that may trigger damage to kidney endothelium and lead to CKD [27]. A systematic review and meta-analysis reported that dialysis patients who underwent PMPR presented significant decreased hs-CRP levels compared to untreated patients, whereas no significant difference was found related to IL-6 and albumin levels [75]. ...
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Periodontitis is a microbially driven host-mediated disease that leads to loss of periodontal attachment and bone. It is associated with elevation of systemic inflammatory markers and with the presence of systemic co-morbidities. Furthermore, periodontal treatment leads to a 24–48 h-long acute local and systemic inflammatory response. This systemic response might increase the burden of patients with compromised medical history and/or uncontrolled systemic diseases. The correlation between periodontitis and systemic diseases, the impact of periodontitis on the quality of life and public health, the effects of periodontal treatment on systemic health and disease, and the available methods to manage systemic inflammation after periodontal therapy are discussed. The main focus then shifts to a description of the existing evidence regarding the impact of periodontitis and periodontal treatment on systemic health and to the identification of approaches aiming to reduce the effect of periodontitis on systemic inflammation.
... It has been demonstrated that endothelial dysfunction and a decline in renal function are related to bacterial spread and inflammation. [6][7][8] Compared to healthy people, patients with periodontitis are far more likely to have chronic renal disease. On the other hand, uraemia in kidney disease patients makes them more vulnerable to infections and may result in bacterial dysbiosis, which can cause periodontitis. ...
Article
ABSTRACT INTRODUCTION: A bidirectional relationship between kidney disease and periodontitis has been proposed a link to endothelial dysfunction and decrease of renal function. Patients with periodontitis have a significantly higher risk of chronic kidney disease than do healthy individuals. Salivary creatinine and urea could be used as noninvasive markers for assessment of kidney function and diagnostics of renal failure. OBJECTIVE: To assess and correlate the salivary urea and creatinine levels among patients with and without periodontitis in diagnosing chronic kidney disease. METHODOLOGY: This case-control study was conducted among patients attending a tertiary hospital in the age group of 40–60yrs with 26 samples in each group with periodontitis and without periodontits. All participants were instructed to avoid eating or drinking for 2 hours before collection of saliva. Whole saliva was collected by spitting method. Saliva samples were stored at -20°C until laboratory analysis. Samples were defrosted at room temperature and then centrifuged at 3000 rpm for 10 min before being used for the analysis in order to remove contaminants. RESULTS: The mean values of salivary creatinine levels were 0.71mg/dl and salivary urea levels were 94.28 mg/dl among cases. The mean values of salivary creatinine level were 0.09mg/dl and salivary urea levels were 16.28 mg/dl among controls. CONCLUSION: There was a positive correlation between salivary creatinine and urea levels among Chronic Kidney Disease patients thus stating saliva can be used as a noninvasive diagnostic tool for estimating the urea & creatinine level among periodontitis patients with Chronic Kidney Disease. KEY WORDS: Salivary creatinine, Salivary urea, periodontitis, chronic kidney disease
... Studies on the association between periodontal diseases and CKD (Li et al. 2021;Ferreira et al. 2024;Yang et al. 2024) have emerged and attempted to demonstrate a bidirectional relationship between the conditions. The mechanisms potentially involved in the bidirectional association are the capability of proinflammatory cytokines to induce endothelial dysfunction and atherogenesis (Chambrone et al. 2013) and molecular mimicry of bacterial heat shock proteins secreted in response to endothelial injury, which induce atheroma formation (Fischer et al. 2009). Given such systemic effects, periodontitis is a nontraditional risk factor for CKD. ...
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To verify the prevalence of specific microorganisms of red, green, and orange microbiological complexes in periodontal pockets of chronic kidney disease (CKD) patients on hemodialysis. This systematic review was conducted according to the PRISMA statement. The search strategy included two independent reviewers who searched the PubMed, Web of Science, Scopus, Cochrane, and Lilacs databases in August 2024, using MeSH terms and keywords defined with the PICOS acronym. The studies included were cross-sectional and published from 2007-2017 in English. The risk of bias and quality of evidence were assessed with the NIH Quality Assessment Tool for Observational Cohort and Cross-sectional Studies. Quantitative analysis with proportion meta-analysis was also performed. 4,737 studies were initially selected, and five were included. The study verified the prevalence of the green complex - Aggregatibacter actinomycetemcomitans (6.69%); the orange complex - Prevotella intermedia (16.85%) and Prevotella nigrescens (37.51%); and the red complex - Treponema denticola (29.11%), Porphyromonas gingivalis (49.45%), and Tannerella forsythia (56.37%), the most predominant microorganism. In the subgingival microbiota of CKD patients on hemodialysis, the red complex showed higher rates and prevalences, and Tannerella forsythia was the most common pathogen.
... Estimated glomerular filtration rate (eGFR) was ≥60 mL/min/1.73 m 2 in 80.25% (n = 317) of participants, with 19.75% (n = 78) showing eGFR < 60 mL/min/1.73 m 2 , indicative of kidney disease. ...
Article
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C-reactive protein (CRP) and estimated glomerular filtration rate (eGFR) are key biomarkers reflecting systemic inflammation and metabolic dysfunction. This study explored systemic and oral health indicators, including CRP and eGFR, as potential factors associated with periodontitis, using a longitudinal clinical dataset comprising 23,742 records from patients identified by ICD-10 codes between 2015 and 2022. Univariate Cox analysis and Gompertz models, selected based on AIC and BIC after evaluating alternative models, were employed to assess the predictive roles of CRP and eGFR in periodontitis incidence, adjusting for oral and systemic health factors. Elevated CRP (>15 mg/L) and reduced eGFR (<60 mL/min/1.73 m2) were significant predictors of periodontitis, with hazard ratios (HR) of 1.36 [1.05–1.77] and 1.39 [1.08–1.78], respectively. Atherosclerosis (HR: 2.12 [1.11–4.06]), diseases of the hard tissues of the teeth (HR: 7.30 [5.45–9.78]), and disorders of the teeth and supporting structures (HR: 3.02 [2.05–4.43]) also demonstrated strong predictive associations. CRP and eGFR emerged as potential biomarkers for predicting periodontitis, enabling early interventions to prevent tooth loss and systemic complications. Patients with chronic kidney disease, atherosclerotic heart disease, and lipid metabolism disorders are at higher risk, emphasizing the need for integrated care addressing both systemic and oral health factors.
... Periodontitis not only leads to the destruction and loss of periodontal support tissues but is also associated with various systemic diseases such as hypertension and diabetes. A substantial body of recent research has indicated a significant correlation between periodontitis and kidney disease, with the treatment of periodontitis improving kidney function (24,25). However, current studies have primarily focused on chronic kidney disease (26), and the connection with AKI remains unclear. ...
Article
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Periodontitis is closely related to renal health, but the specific influence of Porphyromonas gingivalis (P. gingivalis), a key pathogen in periodontitis, on the development of acute kidney injury (AKI) in mice has not been fully elucidated. In our study, AKI was induced in mice through ischemia-reperfusion injury while administering oral infection with P. gingivalis. Comprehensive analyses were conducted, including 16S rRNA sequencing, liquid chromatography-mass spectrometry (LC-MS) metabolomics, and transcriptome sequencing. In vitro, the identified metabolite was used to stimulate mouse neutrophils. Subsequently, these modified neutrophils were co-cultured with mouse renal tubular epithelial cells. The results showed that oral infection with P. gingivalis significantly exacerbated AKI in mice. 16S rRNA sequencing revealed notable shifts in gut microbiota composition. LC-MS metabolomics analysis identified significant metabolic alterations, particularly the upregulation of 3-indoleacrylic acid in the serum. Transcriptome sequencing showed an increased expression of neutrophilic granule protein (Ngp), which was closely associated with 3-indoleacrylic acid, and the presence of Porphyromonas. Cellular experiments demonstrated that 3-indoleacrylic acid could activate neutrophils, leading to an elevation in NGP protein levels, a response that was associated with renal epithelial cell injury. Oral infection with P. gingivalis exacerbated AKI through the gut-kidney axis, involving gut microbiota dysbiosis, metabolic disturbances, and increased renal expression of Ngp. IMPORTANCE This study provides novel insights into the relationship between periodontal health and renal function. Porphyromonas gingivalis oral infection disrupted the balance of gut microbiota and was an important modifier determining the severity of acute kidney injury. Under the “gut-kidney axis,” P. gingivalis might cause an increase in the level of the gut microbial metabolite 3-indoleacrylic acid, interfering with kidney immunity and disrupting the maintenance of kidney epithelium.
... I(2) = 0%). They reported positive results in the estimated glomerular filtration rate (eGFR) after periodontal treatment [65]. ...
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A positive relationship has been reported between advanced periodontitis and carotid intima-media thickness (cIMT) measurement. The aim of this study was to investigate this relationship with parameters for periodontitis, such as PISA and systemic inflammation biomarkers. An observational descriptive cross-sectional study was conducted. A blood sample was collected from 75 subjects to analyze glucose, total cholesterol, HDL, LDL, and cytokine values. Increased cIMT was found in 32% of the patients with fewer teeth. Patients with periodontitis had a larger periodontal inflamed surface area (PISA) (p = 0.000) and had a 1.42-times-higher risk of having increased cIMT values compared to periodontally healthy individuals, though without a statistically significant association. Higher values in the left cIMT, IL-8, and TNF-α were found in men than in women with significant differences. In the multivariate analysis involving cytokines, age continues to be linked to increased cIMT values. INF-γ showed a trend towards a protective effect; as the IMT-M decreases, there is an increase in the expression of INF-γ, and a higher proportion of subjects with elevated INF-γ concentrations demonstrated normal IMT-C. This study did not find a statistically significant association between cIMT and periodontal disease, but the risk of having increased cIMT is 1.42-times higher for individuals with periodontitis.
... Although periodontal diseases exist in acute and chronic form, the new classification from 2017 classifies them in one group of "periodontitis" (4). As a special form is provided a periodontal disease associated with systemic diseases such as diabetes (5), cardiovascular diseases, cancer, lupus, rheumatoid arthritis, respiratory disease, and chronic renal disease (6,7). ...
Article
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Periodontal diseases involve several conditions that are defined by pathologic loss of the periodontal ligament and alveolar bone. Periodontitis is an inflammatory disease of periodontal tissue caused by a host immune response to dysbiotic microbial biofilm whose progression associated with destruction of tooth supporting tissue is promoted by host proteinases. Periradicular periodontitis is the most commonly diagnosed disease that affects the pathology of periodontal tissue in the area of the tooth root. This disease has also been described as apical periodontitis. Several experimental models of periodontal diseases have been developed in recent years. This paper provides an overview of experimentally induced animal models of periodontal disease (periodontitis and periradicular periodontitis) and the possibility of using different experimental animals to study aspects of periodontal disease, each with advantages and disadvantage.
... Tobacco use is the most important modifiable risk factor, and smoking cessation reduces the risk of periodontitis and tooth loss [82]. Moreover, over half of adults 65 years and older report taking four or more prescription drugs to manage chronic conditions, and some drugs, including those for cardiovascular diseases and diabetes, cause xerostomia, which can exacerbate periodontal issues [83,84]. ...
Article
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Oral health’s association with general health, morbidity, and mortality in older adults highlights its importance for healthy aging. Poor oral health is not an inevitable consequence of aging, and a proactive, multidisciplinary approach to early recognition and treatment of common pathologies increases the likelihood of maintaining good oral health. Some individuals may not have regular access to a dentist, and opportunities to improve oral health may be lost if health professionals fail to appreciate the importance of oral health on overall well-being and quality of life. The authors of this narrative review examined government websites, the American Dental Association Aging and Dental Health website, and the Healthy People 2030 oral objectives and identified xerostomia, edentulism, caries, periodontitis, and oral cancer as five key topics for the non-dental provider. These conditions are associated with nutritional deficiencies, poorer quality of life, increased risk of disease development and poorer outcomes for cardiovascular disease, diabetes, and other systemic conditions prevalent among older adults. It is important to note that there is a bi-directional dimension to oral health and chronic diseases, underscoring the value of a multidisciplinary approach to maintaining oral health in older adults.
... Given such systemic effects, periodontitis is considered as a non-traditional risk factor for CKD. The presence of "permanent systemic inflammation" in periodontal patients and possibility of damage to the kidney endothelium by circulating periodontal bacteria could possibly lead to increased risk of CKD (24). Indeed, a systematic review and meta-analysis by Kapellas et al (8) has shown that periodontitis patients have a 60% increased risk of CKD in comparison to healthy controls. ...
Article
Background: The association between periodontitis and systemic diseases is widely researched. Conflicting literature exists on the relationship between periodontitis and the outcomes of end-stage renal disease (ESRD) patients. We hereby reviewed evidence to examine if periodontitis and its management impact the mortality rates of ESRD patients. Material and methods: Literature was searched on the databases of PubMed, Embase, CENTRAL, Web of Science, and Scopus till 27th April 2023. All cohort studies reporting adjusted effect size of the relationship between periodontitis or its management and mortality rates of ESRD patients were included. Results: Eight studies were eligible of which six reported the association between periodontitis and mortality while two reported between periodontal treatment and mortality. Pooled analysis showed no association between the presence of periodontitis and all-cause mortality amongst ESRD patients (HR: 1.13 95% CI: 0.77, 1.65 I2=72%). Results were unchanged on sensitivity analysis. Pooled analysis of three studies showed no difference in the risk of cardiovascular mortality amongst ESRD patients with and without periodontitis (HR: 1.44 95% CI: 0.57, 3.60 I2=86%). A descriptive analysis of two studies showed that periodontal treatment could reduce the risk of mortality in ESRD patients with periodontitis. Conclusions: Limited evidence indicates that periodontitis does not impact all-cause and cardiovascular mortality in ESRD patients. Data on the role of periodontal therapy in improving outcomes is scarce. Further research is needed to generate high-quality evidence on this subject.
... A star was allotted if the study met the criteria for high quality, and the methodological quality of each study was rated based on the proportion of stars obtained. Only moderate-to high-quality papers with scores of 51% or higher were included in the meta-analysis [32]. ...
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Background: A high detection rate of diabetes among dental visitors has been reported recently. This systematic review aimed to evaluate the association between periodontitis and glycated hemoglobin (HbA1c) levels among non-diabetic individuals. Methods: The EMBASE, MEDLINE, Web of Science, Cochrane Library, PubMed, and Open GREY databases were searched, and observational studies published until 1st June 2023 were identified. A methodological quality assessment was conducted based on the original and modified versions of the Newcastle-Ottawa scale. Cohort, case-control, and cross-sectional studies that performed clinical periodontal examinations and measured HbA1c levels in non-diabetic adults were included. A meta-analysis was conducted to estimate the weighted mean difference (WMD) between individuals with and without periodontitis. Results: In total, 29 case-control and 5 cross-sectional studies were selected from 2583 potentially eligible articles. Among them, sixteen case-control and three cross-sectional studies with moderate to high quality were selected for the meta-analyses. The HbA1c levels in periodontitis patients were significantly higher than those in individuals with healthy periodontal conditions (WMD = 0.16; p < 0.001) among the non-diabetic populations. Conclusions: This study reveals a significant association between periodontitis and HbA1c levels in non-diabetic populations. Thus, HbA1c screening may be recommended to detect potential hyperglycemia in non-diabetic periodontitis patients.
... However, many researchers consider the persistent presence of a causative dental infection to be more problematic than the extraction itself [18,19], with some studies pointing to bacterial infections such as periodontitis and apical lesions as factors in the development of MRONJ [20]. The oral cavity is the front line of infection defense, and the jawbone is a special [21,22]. Inflammation lowers pH and leads to the release and activation of bone-bound BP molecules [23,24], which may well have adverse effects on the jawbone. ...
Article
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Purpose: Medication-related osteonecrosis of the jaw (MRONJ) is characterized by necrosis of the jawbone with intraoral bacterial infection and has a significant negative impact on oral health-related quality of life. Risk factors for the onset are unknown, and definitive therapeutic approaches have not yet been defined. A case-control study at a single institution in Mishima City was conducted. The purpose of this study was to examine in detail the factors that contribute to the development of MRONJ. Methods: Medical records of MRONJ patients who visited Mishima Dental Center, Nihon University School of Dentistry, during the period 2015-2021 were extracted. Counter-matched sampling design was used to select participants matched for sex, age, and smoking for this nested case-control study. The incidence factors were statistically examined by logistic regression analysis. Results: Twelve MRONJ patients were used as cases and 32 controls were matched. After adjustment for potential confounders, injectable bisphosphonates (aOR = 24.5; 95% CI = 1.05, 575.0; P < 0.05) were significantly associated with the development of MRONJ. Conclusion: High-dose bisphosphonates may be a risk factor for the development of MRONJ. Patients who use these products require careful prophylactic dental treatment against inflammatory diseases, and dentists and physicians should maintain close communication.
... The management of chronic kidney disease patients with periodontitis is medically complex and presents the dental practitioner with several challenges 20 . Among the factors which may complicate the treatment include high prevalence of anaemia, clotting deficiencies, hypertension, diabetes and renal osteodystrophy in such patients 21 . ...
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Objective: To assess the periodontal treatment needs of patients in different stages of chronic kidney disease Methodology: A Cross sectional comparative study was conducted in the department of Nephrology and Urology, Sharif Medical and Dental College, Lahore on 32 patients with chronic kidney disease in the time duration of one year. Data was collected after taking an informed consent from the patients. The demographic data along with a list of variables associated with chronic kidney disease was recorded using a structured questionnaire. Data collection was based on the following parameters: Community Periodontal Index of Treatment Needs (CPITN). Results: The highest percentage (10%) of patients who required no treatment (TN0) were stage 3 patients. Majority of the stage 5 (93.1%) patients required scaling, prophylaxis and oral hygiene instruction (TN2) followed by stage 4 (90.9%) and stage 3 (40%) respectively. None of the patients required complex treatment, scaling, prophylaxis and oral hygiene instructions (TN3) Conclusion: The highest percentage of patients with healthy periodontium were stage 3 patients. Periodontal pocket depths 4-5 mm were found to be in stage 4 patients the most followed by stage 5 and then stage 3. None of the patients had pocket depths of 6mm or more. Majority of the stage 5 patients required scaling, prophylaxis and oral hygiene instruction (TN2) followed by stage 4 and stage 3 respectively. None of the patients required complex treatment, scaling, prophylaxis and oral hygiene instructions (TN3).
... Two independent authors (D.L. and C.M.) evaluated the methodological quality and risk of bias of the included studies. For observational studies, an adapted version [18][19][20][21][22] of the Newcastle-Ottawa scale [23] was employed to evaluate the methodological quality (Supplementary table 1). The following study aspects were evaluated: 1) Selection of study groups (sample size calculation, representativeness of the patients/sites, and selection of the patients/sites), ascertainment conditions, selection of patients with similar health status, training or calibration of assessors of outcomes, prospective data collection, and use of clear inclusion/exclusion criteria 2) Comparability (comparability of patients based on study design/analysis and management of confounders) 3) Outcome (assessment of gingival thickness) 4) Statistical analysis (appropriateness/validity of statistical analysis and unit of analysis reported) ...
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Objectives To identify and report the current landmarks used for measuring gingival thickness (GT) in healthy maxillary anterior teeth. Material and methods The protocol of this Preferred Reporting Items of Systematic Reviews and Meta-Analyses (PRISMA) 2020-compliant systematic review was registered in PROSPERO. A literature search was conducted to identify articles that met the eligibility criteria published up to 2022. The methods of assessing gingival thickness and the landmarks adopted on the studies were described. Primary outcomes were identified, and the frequency of reporting in the selected articles was calculated. Additionally, risk-of-bias assessments were performed for individual articles. Results Fifty-eight articles (34 with low risk of bias and 24 with medium risk of bias) were selected. A total of 3638 individuals had their gingival thickness measured. Thirty-nine different landmarks were adopted in the studies. Fifty-six articles with 22 landmarks were included in the meta-analysis. A higher heterogeneity was found between the studies (GT ranged from 0.48 to 2.59 mm, mean GT 1.074; 95% CI: 1.024–1.104). The 3 most used landmarks were 2 mm from gingival margin (10 studies, mean GT 1.170 mm, 95% CI: 1.085–1.254), bone crest (9 studies, mean GT 1.01 mm; 95% CI: 0.937–1.083), and cemento-enamel junction (7 studies, mean GT 1.172 mm; 95% CI: 1.105, 1.239). Conclusions Within the limits of this study, a large heterogeneity in GT was found, and there was no consensus on the ideal landmark for GT measurement. Clinical relevance The landmark 2 mm from gingival margin, located at attached gingiva, can be used for GT measurement by clinical and image-based devices. This is an important step for a quantitative instead of a qualitative evaluation of phenotypes.
... Prevalence of CKD in PO patients: Conversely, kidney disease, defined as decreased glomerular filtration rate (GFR), hematuria, or albuminuria, was more frequently reported in patients with PO in different cohorts [33,34]. These associations between PO and CKD are confirmed in several systematic reviews and metanalysis [35][36][37][38][39]. In the most recent one, by Serni et al., PO was identified as a frequent CKD comorbidity, ranging from 34.35 to 93.65% in the different studies included, with a higher prevalence in advanced CKD [19]. ...
Article
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Periodontitis (PO), a chronic microbially-induced inflammation of the supporting tissues of the tooth, is linked to various systemic diseases. We analyze its bidirectional relationship to chronic kidney disease (CKD), a major health-care problem with impressive excess mortality. Overwhelming associative relationship between CKD and PO are analyzed. Major pathophysiologic mechanisms that link CKD to PO are then presented: systemic inflammation, endothelial dysfunction, and imbalance of oxidative stress characteristic of CKD have a role in PO development and might influence escape mechanisms of oral microbiota. Subclinical local and systemic inflammation induced by PO might influence in turn CKD outcomes. Homeostatic changes induced by CKD such as mineral bone disorders, acidosis, uremic milieu, or poor salivary flow are also relevant for the occurrence of PO. There is insufficient evidence to recommend a standardized diagnostic and therapeutic approach regarding association of PO to CKD.
... 45 It is evident that periodontal disease increases atherosclerosis. 24,46 The release of pro-inflammatory cytokines associated with periodontal disease results in a local and systemic inflammatory response that may result in vascular endothelial damage and promote atherosclerosis formation. 47 Periodontal pathogens have been found in atherosclerotic plaques which may increase the risk of atheroma's forming in patients with CKD. ...
Article
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End-stage renal disease (ESRD) requires renal replacement therapy (RRT), namely a renal transplant or renal dialysis or both. Dialysis corrects the electrolyte imbalance and reduces circulating urea and creatinine levels. ESRD patients may present with oral complications and disease due to impaired renal functions, associated comorbidities, or the pharmacological management thereof.To determine the prevalence of periodontal- and oral mucosal disease in ESRD patients undergoing dialysis. Recommendations will be made regarding dental treatment needs and dental management. Cross-sectional study. Fifty-three ESRD patients were evaluated for mucosal lesions and periodontal disease. Patient's age, race, gender, comorbidities, dialysis duration and medicationwere recorded. Treatment urgency was determined, and patients referred accordingly for appropriate dental treatment. Mean age of patients was 42,9 ±10,4 years with a median time on dialysis of 30 months. Majority of patients were hypertensive (94.34%). No oral mucosal lesions was found. PSR score of 3 was mostly found (36.58%). Sixty-two percent of patients had a moderate treatment urgency.A relationship between chronic kidney disease and periodontitis exists. ESRD patients should thus be enrolled into a periodontal screening and treatment program and all dental treatmen
... Previous systematic reviews have revealed an association between kidney health and generalized periodontitis in middle-aged or older adults and indicated that periodontitis might contribute to the development of CKD 8,15,22 . According to the biological hypothesis of distant pathogenic effects 23,24 , systemic inflammation is related to generalized periodontitis due to increased exposure time to microorganisms and their products in the blood circulation through persistent bacteremia. ...
Article
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This study aimed to investigate the association of localized periodontitis with proteinuria in 1281 military young adults in Taiwan. Localized periodontitis was classified as Healthy/Stage I (N = 928) or Stage II/III (N = 353). Stage 2 chronic kidney disease (CKD) was defined as an estimated glomerular filtration rate (eGFR) of 60–89 mL/min/1.73 m². Proteinuria was defined as protein levels of 2+ or 3+ on the dipstick test. Multiple logistic regression analysis with adjustments for age, sex, body mass index, remaining teeth number and other potential covariates were used to determine the association between localized Stage II/III periodontitis and dipstick proteinuria in patients with and without CKD. Localized stage II/III periodontitis was associated with a higher risk of dipstick proteinuria [odds ratio (OR) and 95% confidence interval: 1.89 (1.04–3.42)], but not with stage 2 CKD. However, the association between localized stage II/III periodontitis and dipstick proteinuria was observed only in patients with stage 2 CKD [OR: 3.80 (1.56–9.27)], while the association was null in participants without stage 2 CKD [OR: 1.02 (0.42–2.45)]. Our findings suggest that among young adults, especially those with a mildly impaired eGFR, localized periodontitis might contribute to acute or chronic kidney injury, which manifests as proteinuria.
... 26 As reflected in the current findings, previous evidence has demonstrated significantly increased odds of kidney and liver conditions in populations with periodontitis. 48,49 The risks for kidney and liver diseases in the present study were much higher than any other condition, though this value is likely influenced by the small number of studies. Other systematic reviews have quantified the odds of autoimmune diseases such as RA 50,51 and inflammatory bowel disease, 52 and inflammatory conditions such as osteoporosis. ...
Article
Introduction: The aim of this review is to examine and quantify the long-term risk of immune-mediated systemic conditions in people with periodontitis compared to people without periodontitis. Methods: Medline, EMBASE and Cochrane databases were searched up to June 2022 using keywords and MeSH headings. The 'Risk of Bias in Non-Randomised Studies of Interventions' tool was used to assess bias. Cohort studies comparing incident metabolic/autoimmune/inflammatory diseases in periodontitis to healthy controls were included. Meta-analysis and meta-regression quantified risks and showed impact of periodontitis diagnosis type and severity. Results: The search retrieved 3354 studies; 166 studies were eligible for full-text screening, and 30 studies were included for review. Twenty-seven studies were eligible for meta-analysis. The risks of diabetes, rheumatoid arthritis (RA) and osteoporosis were increased in people with periodontitis compared to without periodontitis (diabetes-relative risk [RR]: 1.22, 95% CI: 1.13-1.33; RA-RR: 1.27, 95% CI: 1.07-1.52; osteoporosis-RR: 1.40, 95% CI: 1.12-1.75). Risk of diabetes showed gradient increase by periodontitis severity (moderate-RR = 1.20, 95% CI = 1.11-1.31; severe-RR = 1.34, 95% CI = 1.10-1.63). Conclusion: People with moderate-to-severe cases of periodontitis have the highest risk of developing diabetes, while the effect of periodontal severity on risk of other immune-mediated systemic conditions requires further investigation. More homologous evidence is required to form robust conclusions regarding periodontitis-multimorbidity associations.
... Periodontitis progression can result in changes in oxidative balance, bone metabolism with the disruption of osteoblast and osteoclast activity, collapse of the teeth-supporting apparatus and, ultimately, tooth loss [21]. Moreover, periodontitis is also associated with several systemic conditions such as diabetes mellitus, lupus, cancer, rheumatoid arthritis, respiratory, cardiovascular, and renal diseases through a chronic low-level systemic inflammation [22][23][24]. ...
Article
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Açaí (Euterpe oleracea Mart.) juice is rich in phenolic compounds with high antioxidant capacity. It has been observed that the use of antioxidants may be an additional strategy to nonsurgical periodontal therapy as well as to prevent alveolar bone loss. Thus, the objective of this study was to investigate the effects of açaí supplementation on experimental periodontitis in rats. Twenty male Rattus norvegicus (Wistar) rats were assigned into control, açaí, experimental periodontitis, and experimental periodontitis with açaí supplementation groups. Periodontitis was induced by placing ligatures around the lower first molars. Animals in the açaí groups received 0.01 mL/g of clarified açaí juice for 14 days by intragastric gavage. At the end of the experimental period, blood was collected to assess the reduced glutathione (GSH), Trolox equivalent antioxidant capacity (TEAC), and lipid peroxidation (TBARS) levels. Moreover, hemimandibles were analyzed by micro-computed tomography (micro-CT) for alveolar bone loss and bone quality. Açaí supplementation increased blood total antioxidant capacity and decreased lipid peroxidation. It also reduced alveolar bone loss when compared to the experimental periodontitis group. Moreover, clarified açaí per se modulated the oxidative biochemistry and bone microstructure. Thus, açaí may be considered a viable alternative for managing periodontal oxidative stress and preventing alveolar bone loss.
... This, in turn, may lead to decreased intake of nutrients which impact the immune system. Periodontitis is associated with systemic diseases, such as diabetes mellitus [6], cardiovascular disease, respiratory disease, renal disease, obesity, osteoporosis and cancer [7,8]. ...
Article
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Background: The study aimed to estimate and compare the incidence and progression of chronic periodontitis among two generations of older Australian adults. Methods: Data were from two population-based cohort studies of Australian older adults aged 60+ years South Australian Dental Longitudinal Studies (SADLS), SADLS I (1991–1992) and SADLS II (2013–2014). American Academy of Periodontology/the U.S. Centres for Disease Control and Prevention (CDC/AAP), and the 2018 European Federation of Periodontology classification (EFP/AAP) case definitions were used to define and calculate the incidence and progression of chronic periodontitis. Multivariable Poisson regression models were used to estimate incidence risk ratios (IRRs) of periodontitis. Results: A total 567 and 201 dentate respondents had periodontal exams in SADLS I and II, respectively. The incidence rate was greater in SADLS II than in SADLS I, approximately 200 vs. 100/1000 person years, respectively. Current smokers had more than two times higher IRRs, 2.38 (1.30–4.34) and 2.30 (1.24–4.26), than their non-smoking counterparts in the previous generation under the CDC/AAP and EFP/AAP, respectively. Conclusions: The most recent generation of older adults has greater incidence and progression of periodontitis than the previous generation. Being a current tobacco smoker was a significant risk factor for both the incidence and progression of periodontitis.
... 20 In a recent study, the cross-sectional findings were extrapolated to how PD treatment would affect GFR, and showed that estimated GFR (eGFR) can be improved in CKD patients through periodontal specific therapy. 31 Finally, kidney disease patients with periodontitis have been associated with higher mortality rates. A 14-year follow up for the NHANES III data showed that CKD alone led to 1.5-to 1.7-fold increased risk for CV and allcause mortality. ...
Article
Periodontal disease has been associated with various systemic diseases including kidney disease. However, a causal relationship is yet to be established. One possible association is that periodontitis may cause an increased inflammatory response in kidney disease patients which in turn destroys endothelial vasculature. This may contribute to development of risk factors of kidney disease such as diabetic neuropathy and cardiovascular events leading the progression and mortality in kidney disease patients. The role of periodontal inflammation driving kidney disease is still under investigation. This review article highlights the role of periodontal inflammation in the development and progression of kidney disease. It is crucial that dental practitioners and nephrologists understand the association between periodontal and kidney disease. Early periodontal screening and educating patients about the importance of good oral hygiene may play an important role in prevention of progression of kidney disease.
... Importantly, periodontal disease can worsen CKD. A systemic review and meta-analysis reported an increased prevalence of CKD in patients with periodontitis (38) . Many studies have proved a positive association between the presence of chronic periodontitis and a high level of serum CRP (39,40) . ...
Article
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Background: Chronic kidney disease is a gradual loss of kidney function with diabetes and hypertension as the leading cause. Chronic kidney disease is one of these systemic diseases that can affect salivary contents. Aims: This study aimed to assess salivary immunoglobulin A, interleukin-6 and C- reactive protein in chronic kidney disease patients on hemodialysis and those on conservative treatment in comparison with control subjects. Materials and methods: Ninety subjects were included in this study divided into three groups: 30 patients with chronic kidney disease on hemodialysis for at least 6 months ago; 30 patients with chronic kidney disease on conservative treatment and 30 healthy control subjects. Secretory immunoglobulin A, interleukin-6 and C- reactive protein in saliva samples were measured by enzyme-linked immunosorbent assay ELISA. Results: No significant difference in salivary immunoglobulin A level among study groups was seen. A significant increase in salivary interleukin-6 and C- reactive protein in both chronic kidney disease patients on hemodialysis and those on conservative treatment compared to the control group. While, no significant salivary IL-6 and CRP differences were seen between both patient groups, on hemodialysis and conservative treatment. Conclusions: There was no significant difference among chronic kidney disease patients on hemodialysis, on conservative treatment and control healthy subjects regarding to salivary IgA while Salivary interleukin -6 and C- reactive protein was significantly higher in chronic kidney disease patients on hemodialysis and those on conservative treatment compared to healthy subjects.
... There is much evidence that periodontal inflammation affects renal function (Fig. 1). However, more high-quality evidence is needed for consensus [43]. ...
Article
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Purpose of Review Many clinical studies have reported an association between periodontal disease and chronic kidney disease (CKD). This review aims to update the underlying mechanism and the findings of clinical studies. Recent Findings Basic research supports that inflammation might mediate the association between CKD and periodontal disease. Clinical evidence suggests that periodontal treatment improves renal function. Poor oral health has also been reported as a predictor of mortality in patients undergoing hemodialysis. Summary Although clinical data have demonstrated a significant association between inflammation in the periodontal tissue and CKD, well-designed studies are needed for a consensus to be widely adopted. Malnutrition and systemic chronic inflammation are often interrelated in patients undergoing hemodialysis. Periodontal disease may contribute to chronic inflammation, and it is possible that a low number of teeth may be involved in impaired nutritional intake in patients undergoing hemodialysis. A novel perspective on malnutrition might be needed to manage oral health in patients with CKD, especially those undergoing dialysis, in addition to conventional factors such as bacterial infection and inflammation.
... It is now accepted that periodontitis can be an important risk factor for chronic kidney disease and kidney failure for the following reasons. 33 (a) Systemic inflammation is affected by periodontal inflammation. ...
... Periodontitis is a complex disease. Previous epidemiologic and experimental studies have shown that it may also impact several systemic diseases, whereas periodontal treatment leads to an improvement of glycaemic control in patients with type 2 diabetes [175], and metabolic syndrome [176], as well as improved renal function associated with diabetes [177]. Maternal periodontal disease also leads to an increase of preeclampsia and preterm births, as well as cardiovascular [144,145] disease, allergies, and asthma in the offspring [151,152]. ...
Article
Periodontal disease (PD) is one of the most common oral conditions affecting both youths and adults. There are some research works suggesting a high incidence of PD in pregnant women. As an inflammatory disease of bacterial origin, PD may result in the activation of the pathways affecting the course and the pregnancy outcome. The authors, based on the literature review, try to answer the PICO question: Does maternal periodontitis (exposure) influence the incidence of complications rates in pregnancy and the development of systemic diseases in childhood and adult offspring (outcome) in the humans of any race (population) compared to the offspring of mothers with healthy periodontium (comparison)? The authors try to describe the molecular pathways and mechanisms of these interdependencies. There is some evidence that maternal periodontitis may affect the pregnancy course and outcome, resulting in preeclampsia, preterm delivery, vulvovaginitis and low birth weight. It can be suggested that maternal periodontitis may affect offspring epigenome and result in some health consequences in their adult life.
... The association between CP and CKD has been studied widely since the 2000s and CP is now considered a novel, non-traditional risk factor for CKD. 8,9 Chronic periodontitis may have its share in CVD-related mortality in CKD patients. 9 However, prospective and interventional studies on this association with long follow-up periods are scarce. ...
Article
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Background. Chronic kidney disease (CKD) is associated with significant morbidity and mortality, and there are various risk factors for this disease. Although the association between CKD and periodontal disease (PD) has been reported in various cross-sectional studies, longitudinal intervention studies are scarce.
... If left without the recommended non-surgical/ surgical treatment, it may lead to tooth mobility and subsequent tooth loss [1]. Periodontal disease has been reported to be associated with several systemic disease complications, such as, cardiovascular diseases [2], rheumatoid arthritis [3], chronic kidney disease [4], and diabetes mellitus (DM) [5]. ...
Article
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Objective: Investigating osteopontin (OPN) level in gingival crevicular fluid (GCF) of patients affected by periodontitis with or without Type-2 diabetes mellitus (T2DM). The aim of this study is to explore the possibility of OPN to differentiate between periodontal health and disease. Material and Methods: A total number of 36 participants seeking periodontal treatment were recruited in this pilot study and divided into three study groups. Periodontitis [systemically healthy participants with periodontitis (probing pocket depth) PPD (probing pocket depth) ≥ 4mm], periodontitis and poorly controlled type 2 diabetes mellitus (), and control (systemically and periodontally healthy periodontium) groups. Plaque index (PI), gingival index (GI) and PPD were examined. OPN level was measured in the GCF and analysed, using Enzyme-Linked Immunosorbent assay. Results: PI and GI were significantly higher in T2DM with periodontitis compared to periodontitis and control groups. Both periodontitis and P-T2DM groups showed significant increase in the OPN levels compared to control group (p<0.001). PPD showed the only significant positive association with OPN (p<0.001) compared to other clinical parameters. The receiver operating characteristics curve analysis demonstrated that OPN had higher area under the curve value (AUC: 0.95) in periodontitis compared to P-T2DM patients (AUC: 0.86). Conclusion: In periodontitis groups, clinical parameters were equally deteriorated together with significant increase in the expression of OPN compared to control. Furthermore, GCF levels of OPN were sensitive and specific enough to discriminate between health and periodontitis even with T2DM. This could introduce OPN to be as a candidate diagnostic biomarker of periodontal disease.
... The association between periodontitis and CKD has been reported over the last decade [9,10]. Both diseases have chronic inflammatory characteristics and share some common risk factors [10]. ...
Article
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Periodontitis and chronic kidney disease are both chronic inflammatory diseases and share some common risk factors. This 3-month pilot study aimed to clarify whether non-surgical periodontal therapy is beneficial in clinical, biochemical, and microbiological conditions in patients with periodontitis and kidney failure. Kidney failure patients with moderate to severe periodontitis were recruited from two hospitals. Treatment group received non-surgical periodontal therapy, and control group received oral hygiene instruction only. Outcome assessments were conducted 1 and 3 months after treatment. Non-parametric tests were used to analyze the patient-level data. Periodontal site-level assessments were analyzed by Student t-test and paired t-test. Statistical significance was set at p-value < 0.05. A total of 11 subjects completed the study. There was no significant difference between groups in all-cause mortality, cardiovascular events, infection events, systemic parameters, and serum biomarkers. Comparing to control group, clinical periodontal parameters, gingival crevicular fluid interleukin-1β (IL-1β) level and periodontal pathogens showed significant improvement in the treatment group. Non-surgical periodontal treatment did not change systemic outcomes in kidney failure patients, but changed the local micro-environment.
... If left without the recommended non-surgical/ surgical treatment, it may lead to tooth mobility and subsequent tooth loss [1]. Periodontal disease has been reported to be associated with several systemic disease complications, such as, cardiovascular diseases [2], rheumatoid arthritis [3], chronic kidney disease [4], and diabetes mellitus (DM) [5]. ...
Article
Full-text available
Abstract Objective: Periodontitis is a multifactorial inflammatory disease usually terminated with tooth loss when untreated. Type-2 diabetes mellitus (T2DM) have shown to exacerbate periodontitis. Osteopontin, is thought to play a role to induce periodontitis-associated bone resorption. Aim was to investigate the osteopontin level in gingival crevicular fluid of patients affected by periodontitis with or without T2DM, and to explore the potential of osteopontin to differentiate between periodontal health and disease. Patients and Methods: A total number of 36 subjects seeking periodontal treatment were recruited in this pilot study. Plaque index, gingival index and probing pocket depth were examined, and the osteopontin level was measured in the GCF and analysed using Enzyme-linked immunosorbent assay. Results: Plaque index and gingival index were significantly higher in T2DM with periodontitis compared to periodontitis and control groups. Both periodontitis groups showed significant increase in the osteopontin levels (p<0.001) compared to control. probing pocket depth showed the only significant positive association with osteopontin (p<0.001) compared to other clinical parameters. The ROC curve analysis showed that osteopontin had higher AUC value (AUC: 0.95) in periodontitis compared to P-T2DM patients (AUC: 0.86). Conclusions: In both periodontitis groups, clinical parameters were equally deteriorated together with significant increase in the expression of osteopontin compared to control. Further, GCF-levels of osteopontin were sensitive and specific enough to discriminate between health and periodontitis even with T2DM. This could have an impact on osteopontin to be used as a diagnostic biomarker of periodontal disease.
Article
Background and hypothesis: It is presently unclear why there is a high prevalence of periodontal disease in individuals living with chronic kidney disease (CKD). Whilst some have argued that periodontal disease causes CKD, we hypothesised that alterations in saliva and the oral microenvironment in organisms with kidney disease may initiate periodontal disease by causing dysbiosis of the oral microbiota. Methods: Experimental kidney disease was created using adenine feeding and subtotal nephrectomy in rats, and by adenine feeding in mice. Loss of periodontal bone height was assessed using a dissecting microscope supported by micro-CT, light, confocal and electron microscopy, and immunohistochemistry. Salivary biochemistry was assessed using NMR spectroscopy. The oral microbiome was evaluated using culture-based and molecular methods, and the transmissibility of dysbiosis was assessed using co-caging and microbial transfer experiments into previously germ-free recipient mice. Results: We demonstrate that experimental kidney disease causes a reproducible reduction of alveolar bone height, without gingival inflammation or overt hyperparathyroidism but with evidence of failure of bone formation at the periodontal crest. We show that kidney disease alters the biochemical composition of saliva and induces progressive dysbiosis of the oral microbiota, with microbial samples from animals with kidney disease displaying reduced overall bacterial growth, increased alpha diversity, reduced abundance of key components of the healthy oral microbiota such as Streptococcus and Rothia, and an increase in minor taxa including those from gram-negative phyla Proteobacteria and Bacteroidetes. Co-housing diseased rats with healthy ones ameliorates the periodontal disease phenotype, whilst transfer of oral microbiota from mice with kidney disease causes periodontal disease in germ-free animals with normal kidney function. Conclusions: We advocate that periodontal disease should be regarded as a complication of kidney disease, initiated by oral dysbiosis through mechanisms independent of overt inflammation or hyperparathyroidism.
Article
Background: Patients with end-stage renal disease are at risk of dental and periodontal problems. The aim of this study was to compare the oral health index and salivary levels of calcium, phosphorus, and urea between dialysis patients and the control group. Methods: Hemodialysis patients and a control group of outpatients referring to the hospital clinics were selected for a case-control study. Socio-demographic data and the decayed, missing, and filled teeth (DMFT) index were collected using a questionnaire and dental examination by a dentist, respectively. The calcium, phosphorus, and urea levels were measured in unstimulated saliva samples. Independent t test was used to compare the mean DMFT index, calcium, phosphorus, and urea levels between the two groups. Results: A total of 50 dialysis patients and 50 control individuals were included in the study. Compared to the control group, dialysis patients had higher mean DMFT index (mean difference [MD]: 7.7, standardized mean difference [SMD]: 0.83; P<0.001), calcium level (MD: 1.8, SMD: 1.22; P<0.001), phosphorus level (MD: 18.9, SMD: 2.3; P<0.001), and urea level (42.7, 2.81; P<0.001). Conclusion: Dialysis patients with end-stage renal disease undergoing hemodialysis had worse dental and periodontal status compared to the control group. The oral and dental health status of patients with chronic kidney disease (CKD) should be regularly evaluated and monitored.
Article
BACKGROUND Many scholars have performed several clinical studies have investigated the association between chronic periodontitis (CP) and chronic kidney disease (CKD). However, there are still differences between these research results, and there is no unified conclusion. Therefore, a systematic review is required to understand this issue fully. AIM To explore the correlation between CP and CKD. METHODS Literature on the correlation between CP and CKD, as well as the clinical attachment level (CAL) and pocket probing depth (PPD) of CKD and non-CKD, were retrieved from PubMed, Embase, the Cochrane Library, and Web of Science repositories until January 2024. After the effective data were extracted, data processing and statistics were performed using Stata 12.0. RESULTS Of the 22 studies, 13 were related to CP and CKD, and 9 reported CAL and PPD in patients with CKD and healthy controls. Meta-analysis of the correlation between CP and CKD revealed that CKD probability in people with CP was 1. 54 times that of healthy individuals [relative risk = 1.54, 95% confidence interval (CI): 1.40–1.70], and CP incidence in patients with CKD was 1. 98 times that of healthy individuals [overall risk (OR) = 1.98, 95%CI: 1.53–2.57]. Meta-analysis of CAL and PPD evaluations between CKD patients and healthy individuals showed that CAL and PPD levels were higher in CKD patients [standard mean difference (SMD) of CAL = 0.65, 95%CI: 0.29–1.01; SMD of PPD = 0.33, 95%CI: 0.02–0.63]. CONCLUSION A bidirectional association exists between CP and CKD. CKD risk is increased in CP patients and vice versa. Periodontal tissue or tooth loss risks increase over time in CKD patients.
Article
Objectives The purpose of this study was to determine whether indoxyl sulfate (IS) is involved in alveolar bone deterioration and to elucidate the mechanism underlying alveolar bone loss in chronic kidney disease (CKD) patients. Materials and Methods Mice were divided into the control group, CP group (ligature‐induced periodontitis), CKD group (5/6 nephrectomy), and CKD + CP group. The concentration of IS in the gingival crevicular fluid (GCF) was determined by HPLC. The bone microarchitecture was evaluated by micro‐CT. MC3T3‐E1 cells were stimulated with IS, and changes in mitochondrial morphology and ferroptosis‐related factors were detected. RT‐PCR, western blotting, alkaline phosphatase activity assays, and alizarin red S staining were utilized to assess how IS affects osteogenic differentiation. Results Compared with that in the other groups, alveolar bone destruction in the CKD + CP group was more severe. IS accumulated in the GCF of mice with CKD. IS activated the aryl hydrocarbon receptor (AhR) in vitro, inhibited MC3T3‐E1 cell osteogenic differentiation, caused changes in mitochondrial morphology, and activated the SLC7A11/GPX4 signaling pathway. An AhR inhibitor attenuated the aforementioned changes induced by IS. Conclusions IS activated the AhR/SLC7A11/GPX4 signaling pathway, inhibited osteogenesis in MC3T3‐E1 cells, and participated in alveolar bone resorption in CKD model mice through ferroptosis.
Article
Objective To perform a systematic review with meta‐analysis to assess recent scientific evidence on the association between periodontitis and systemic parameters/conditions in individuals with chronic kidney disease (CKD). Materials and Methods The search for studies was performed in MedLine/PubMed, Scopus, Web of Science, and BIREME databases. Reference lists of selected articles were also searched. Studies with different epidemiological designs evaluating the influence of exposure to periodontitis on serum markers and mortality in individuals with CKD were eligible for inclusion. Three independent reviewers performed the article selection and data extraction. The assessment of methodological quality used the adapted Newcastle Ottawa Scale. Random effects meta‐analysis was performed to calculate association measurements and 95% confidence intervals. Results In total, 3053 records were identified in the database search, with only 25 studies meeting the eligibility criteria and, of these, 10 studies contributed data for meta‐analysis. Using a random‐effects model, periodontitis was associated with hypoalbuminemia (PR unadjusted = 2.47; 95%CI:1.43–4.26), with high levels of C‐reactive protein (PR unadjusted = 1.35; 95%CI%:1.12–1.64), death from cardiovascular disease (RR unadjusted = 2.29; 95%CI:1.67–3.15) and death from all causes (RR unadjusted = 1.73; 95%CI:1.32–2.27). Conclusions The findings of this review validated a positive association between periodontitis and serum markers and mortality data in individuals with CKD.
Article
Chronic kidney disease (CKD) is defined as persistent kidney damage, usually marked by albuminuria or a reduced glomerular filtration rate, which ultimately leads to end-stage kidney disease and a need for dialysis. CKD is a very common condition, with an estimated 13.3 million (12.9%) people affected by CKD in Japan. A potential bidirectional association between CKD and periodontal disease has been reported in recent studies. Individuals with periodontal disease exhibit endothelial dysfunction, which leads to atherosclerosis, hypertension, and CKD. Immune dysfunction and mineral bone disorder in CKD patients are suggested to be associated with development and progression of periodontal disease. Evidence of this association is accumulating through increasing numbers of well-designed cohort studies, and periodontal disease has been demonstrated to be a risk factor for CKD in older Japanese. However, only limited information about the impact of periodontal therapy on CKD patients exists. Because the prevalence of both diseases in Japan appears to be increasing, largely as a result of the aging population, further studies with Japanese participants are needed to elucidate this association.
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Objectives Although a few studies have investigated the relationship between kidney and oral function (number of remaining teeth), their results remain inconclusive. Therefore, this study aimed to investigate the relationship between kidney function and oral health in community-dwelling healthy elderlies and examine the factors associated with kidney function. Materials and Methods We used cross-sectional data from the Shimane prefecture cohort recruited by the Center for Community-Based Health Research and Education in 2019. We collected clinical data on dental status, background factors and kidney function (estimated glomerular filtration rate [eGFR], mL/min/1.73 m² and creatinine levels, mg/dL). Results The study enrolled 481 participants, whose mean age was 66.7±7.4 years, and 223 (46.4%) participants were men. Multivariate analysis revealed significant correlations between eGFR (B=0.17, P=0.04), creatinine (B=–0.54, P<0.01), and the number of remaining teeth. The number of remaining teeth was associated with creatinine and eGFR, which are indicators of kidney function. Conclusion This study suggests that preserving the teeth may prevent decline in kidney function. Dental professionals should provide instructions and professional care to reduce the risk of systemic diseases such as kidney dysfunction.
Article
Gingival bleeding is a common complaint and symptom in patients with periodontitis. In clinics, gingival bleeding is regarded as an important sign of gingival inflammation, which is also of great significance in predicting the activity of periodontitis. Existing research has indicated that periodontitis has an impact on distant sites, such as the kidney. Hematuria is the principal feature of glomerular disease, which can reflect the degree and condition of glomerular inflammation. Previous studies have revealed an association between periodontal diseases with renal diseases, so a study is necessary to discuss their representative signs of them. For the moment, there are no reports that are concerned about the correlation between gingival bleeding with hematuria. The main point of this text is to review the potential association between gingival bleeding with hematuria, reveal their underlying mechanisms, and provide instructions for the therapy of periodontitis and glomerular diseases.
Article
Background and objective: Periodontitis is immune inflammatory disease, atherosclerosis (AS) and chronic kidney disease (CKD) are two common systemic diseases. Periodontitis promotes AS and CKD, and CKD interacts with AS. The objective of this animal study was to evaluate the changes of kidney when periodontitis and atherosclerosis exist separately and the degenerative effects of periodontitis on the kidney in atherosclerotic mice. Materials and methods: A total of 40 male Apoe-/- mice were randomly divided into four groups: control (NC), periodontitis (PD), AS and AS with PD (AS + PD). AS was induced by high-fat diet feeding, and PD was induced by injection of Porphyromonas gingivalis-Lipopolysaccharide (P.g-LPS) (endotoxin suspension) into the buccal side of mouse maxillary molars. The right maxilla of mice was scanned with micro-CT to evaluate alveolar bone loss; aortic tissue was stained with HE and Oil-Red O to evaluate arterial plaque formation; serum was collected to detect the changes of blood lipids and serum renal function parameters (blood urea nitrogen [BUN], serum creatinine [Scr]); renal histopathological changes were evaluated by HE staining (glomerular and tubular damage scores), PAS staining (glomerular Mesangial matrix index) and Masson staining (percentage of renal fibrosis area); qRT-PCR and ELISA were used to evaluate the expression of renal inflammatory cytokines (tumor necrosis factor-α, Interleukin-1β, neutrophil surface marker Ly6G). Results: The amount of alveolar bone loss: PD group was significantly higher than NC group (p < .05); AS + PD group was higher than PD group, the difference was not statistically significant. Atherosclerotic plaque formation and serum lipid changes: AS group were significantly worse than NC group (p < .05), and AS + PD group were worse than AS group. The results of the corresponding qualitative and quantitative analyses of kidney tissue in experimental animals gradually deteriorated in the NC group, PD group, AS group and AS + PD group and worsened sequentially. Renal function parameters: the content of BUN in AS group was higher than that in PD group, the difference was not statistically significant; Scr in AS group was significantly higher than that in PD group (p < .05); the contents of BUN and Scr in AS + PD group were higher than those in AS group, the difference was not statistically significant. Glomerular and tubular damage scores: AS group were higher than PD group, the difference was not statistically significant; AS + PD group were significantly higher than AS group (p < .001). The ratio of glomerular mesangial matrix to glomerular area and the percentage of renal fibrosis area: AS group were significantly higher than PD group (p < .001), and AS + PD group were significantly higher than AS group (p < .001). Expression of inflammatory cytokines: AS group was higher than PD group, the difference was not statistically significant; AS + PD group was significantly higher than AS group (p < .05). Conclusion: Both PD and AS can aggravate the inflammatory stress of kidney tissue and cause the damage of kidney tissue, and the inflammatory increase and damage effect of AS is stronger; PD can promote kidney damage of atherosclerotic mice by aggravating the renal inflammation in atherosclerotic mice; renal function parameters were not completely synchronized with the changes of renal inflammation and histopathology in each group of mice; PD can promote AS, periodontal inflammation in mice with AS is more severe, and the special changes of blood lipids in mice with AS are closely related to the above results.
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Objective: This research aimed to explore the effect of periodontitis on renal tissues injury in rats and the role of Sirtuin3 (Sirt3) and its regulation of autophagy in this progression. Material and methods: Thirty Wistar rats were assigned into three groups: control, periodontitis (P), and periodontitis with gavage administration of Sirt3 activator resveratrol (P + RSV). To induce periodontitis, the wire ligature was placed around the cervical region of the rat maxillary first molar. After 8 weeks, micro-computed tomography (Micro-CT) and hematoxylin and eosin (HE) were used to evaluate the alveolar bone resorption and periodontal inflammation. Serum and urine biochemical indicators were measured to assess renal function. The pathological changes of the kidney were observed via HE and periodic acid Schiff (PAS) staining. Autophagosome was viewed by transmission electron microscopy (TEM). Real-time PCR and western blot were used to test expressions of Sirt3 and autophagy indicators in renal and periodontal tissues, including mammalian target of rapamycin (mTOR), phosphor-mTOR (p-mTOR), BECN1 (Beclin-1), and microtubule-associated protein 1 light chain 3 (LC3). Results: Alveolar bone destruction, resorption, and periodontal inflammation were observed in the P group (compared with the control group), and the above indexes were significantly improved after RSV intervention; the obvious changes in renal tissue structure in the P group were partially recovered after RSV intervention, while renal functional status was not affected (among the three groups); in addition, the levels of Sirt3 and autophagy in kidney and periodontal tissues of P group were inhibited, manifested as a decrease in the number of autophagosomes (renal tissue) and expressions of autophagy marker Beclin-1 and LC3 conversion rate and an increase in the expression of p-mTOR. After Sirt3 activation (RSV), the above indicators were significantly improved. Conclusion: Periodontitis causes renal structural damage in rats, which may be connected to the effect of Sirt3-induced autophagy.
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Several studies have demonstrated a strong relation between periodontal diseases and chronic kidney disease (CKD). The main mechanisms at the base of this link are malnutrition, vitamin dysregulation, especially of B-group vitamins and of C and D vitamins, oxidative stress, metabolic acidosis and low-grade inflammation. In particular, in hemodialysis (HD) adult patients, an impairment of nutritional status has been observed, induced not only by the HD procedures themselves, but also due to numerous CKD-related comorbidities. The alteration of nutritional assessment induces systemic manifestations that have repercussions on oral health, like oral microbiota dysbiosis, slow healing of wounds related to hypovitaminosis C, and an alteration of the supporting bone structures of the oral cavity related to metabolic acidosis and vitamin D deficiency. Low-grade inflammation has been observed to characterize periodontal diseases locally and, in a systemic manner, CKD contributes to the amplification of the pathological process, bidirectionally. Therefore, CKD and oral disease patients should be managed by a multidisciplinary professional team that can evaluate the possible co-presence of these two pathological conditions, that negatively influence each other, and set up therapeutic strategies to treat them. Once these patients have been identified, they should be included in a follow-up program, characterized by periodic checks in order to manage these pathological conditions.
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Gut dysbiosis induces ‘leaky gut,’ a condition associated with diabetes, NASH, and various auto-immune diseases. Porphyromonas gingivalis is a periodontopathic bacterium which causes periodontal tissue breakdown, and often enters the systemic blood flow. Oral administration of P. gingivalis induced gut dysbiosis in mice model, but no systemic administration of P. gingivalis has been reported thus far. In the present study, we investigated the effect of P. gingivalis-derived lipopolysaccharide (Pg-LPS) on the intestinal flora of our established mouse model. Eight-week-old C57BL/6J mice were intraperitoneally administered Pg-LPS. Three months later, DNA was extracted from stool, and RNA from the small and large intestines. After euthanizing the mice, pathological sections of the intestinal tract were prepared and stained with hematoxylin and eosin (H&E). Tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, and IL-6 expression levels were evaluated using quantitative PCR. 16S rRNA gene PCR amplicon analysis data were acquired using NGS. Microbial diversity and composition were analyzed using Quantitative Insights into Microbial Ecology 2. Furthermore, alterations in microbial function were performed by PICRUSt2. No significant inflammatory changes were observed in the H&E. No significant differences in the mRNA levels of IL-1β, IL-6, and TNF-α were observed between the groups. Pg-LPS administration decreased the abundance of Allobacterium in the gut. A predictive metagenomic analysis by PICRUSt2 and STAMP showed that 47 pathways increased and 17 pathways decreased after Pg-LPS administration. Systemic application of periodontal pathogens may cause changes in the intestinal flora which may affect the physiological functions of the intestinal tract.
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Background: Periodontal disease is a crucial oral health problem due to its high pervasiveness and correlation to general health. Several risk factors have been reported to induce periodontal disease progression. Aim: To determine the prevalence of periodontal disease and its correlation with the associated risk factors among different age groups of patients attending Umm Al-Qura University Dental Teaching Hospital. Methods: This is a retrospective study that utilizes the screening records of patients who attended the dental teaching hospital in 2018. The age, gender, periodontal condition, oral hygiene status, compliance with oral hygiene measures status, smoking status, and systemic health conditions were obtained from the patients’ screening records. Data were collected, tabulated, and analyzed using SPSS. Chi-squared and Pearson correlation tests were used to analyze the data. A p-value less than 0.05 was considered significant. Results: Of the total 4,967 attending patients, 3,158 (64%) patients presented with periodontal disease. A significant high negative correlation was found between periodontal disease and compliance with oral hygiene measures (p = 0.001; r = −0.894) and between periodontal disease and oral hygiene status (p = 0.001; r = −0.889). Furthermore, a significant positive correlationwas found between periodontal disease and smoking (p < 0.000; r = 0.689) and between periodontal disease and the systemic disease (p = 0.000; r = 0.482). Compliance with oral hygiene measures was significantly higher for females (p = 0.04), while the smoking was significantly higher for males (p = 0.001). Conclusion: The prevalence of periodontal disease among patients attending Umm Al-Qura university dental teaching hospital was 64%, and several risk factors were associated with the disease. It is necessary to educate the community about periodontal disease and its initiating and predisposing factors to decrease the risk of having the disease and to promote oral and general health.
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Because of the pressure for timely, informed decisions in public health and clinical practice and the explosion of information in the scientific literature, research results must be synthesized. Meta-analyses are increasingly used to address this problem, and they often evaluate observational studies. A workshop was held in Atlanta, Ga, in April 1997, to examine the reporting of meta-analyses of observational studies and to make recommendations to aid authors, reviewers, editors, and readers. Twenty-seven participants were selected by a steering committee, based on expertise in clinical practice, trials, statistics, epidemiology, social sciences, and biomedical editing. Deliberations of the workshop were open to other interested scientists. Funding for this activity was provided by the Centers for Disease Control and Prevention. We conducted a systematic review of the published literature on the conduct and reporting of meta-analyses in observational studies using MEDLINE, Educational Research Information Center (ERIC), PsycLIT, and the Current Index to Statistics. We also examined reference lists of the 32 studies retrieved and contacted experts in the field. Participants were assigned to small-group discussions on the subjects of bias, searching and abstracting, heterogeneity, study categorization, and statistical methods. From the material presented at the workshop, the authors developed a checklist summarizing recommendations for reporting meta-analyses of observational studies. The checklist and supporting evidence were circulated to all conference attendees and additional experts. All suggestions for revisions were addressed. The proposed checklist contains specifications for reporting of meta-analyses of observational studies in epidemiology, including background, search strategy, methods, results, discussion, and conclusion. Use of the checklist should improve the usefulness of meta-analyses for authors, reviewers, editors, readers, and decision makers. An evaluation plan is suggested and research areas are explored.
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Patients with chronic kidney disease (CKD) are at an increased risk not only for end-stage kidney disease (ESKD) but also for cardiovascular disease (CVD). In this review article, we summarize the current evidence of CKD as a high-risk condition for CVD based on reports from Japan and other countries to draw attention to the close clinical association between CKD and CVD. Several epidemiologic studies have shown that the presence of CKD and reduced renal function are independent predictors of CVD also in Japan. According to a post-hoc analysis of CASE-J, the power of CKD as a predictor of CVD is as strong as diabetes mellitus and a previous history of ischemic heart disease. CKD worsens classical risk factors including hypertension and dyslipidemia, and dyslipidemia is associated with increased thickness and stiffness of large arteries independent of major confounders. A post-hoc analysis of MEGA indicates that lipid-lowering therapy with statins reduces the risk of CVD, and that it appears to be more efficacious in patients with than without CKD. These reports from Japan and other countries suggest that CKD should be regarded as a high-risk condition comparable to diabetes mellitus, and that strict control of dyslipidemia would be beneficial in preventing CVD, at least early stages of CKD.
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The association between diabetes and periodontal diseases is well-established. Diabetes is a risk factor for periodontal disease, with diabetic patients exhibiting an increased prevalence, extent and severity of gingivitis and perio- dontitis compared to healthy adults. Several mechanisms involved in the pathogenesis of diabetes have also been associated with periodontal disease progression. It is recognized today that there is a bidirectional relationship between diabetes and periodontal disease, with recent research showing that periodontal disease may affect the metabolic control of diabetes in diabetic patients. In this review, we present the current knowledge of the interplay between periodontal diseases and diabetes through the evaluation of randomized control and longitudinal cohort studies published in the past 15 years. Current data support the conclusion that diabetic patients are at increased risk for periodontal diseases, and that patients with poorly controlled diabetes are at risk for severe periodontitis. This results in the destruction of oral connective tissue and generalized bone loss, leading ultimately to tooth loss. Although the effect of periodontal disease on glycemic control in type 1 diabetic patients is controversial, evidence does show a direct correlation between periodontal health and glycemic control in type 2 diabetic patients. Furthermore, several studies have demonstrated the beneficial effect of periodontal treatment on metabolic control of type 2 diabetic patients.
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Periodontitis is a common chronic inflammatory disease characterised by destruction of the supporting structures of the teeth (the periodontal ligament and alveolar bone). It is highly prevalent (severe periodontitis affects 10-15% of adults) and has multiple negative impacts on quality of life. Epidemiological data confirm that diabetes is a major risk factor for periodontitis; susceptibility to periodontitis is increased by approximately threefold in people with diabetes. There is a clear relationship between degree of hyperglycaemia and severity of periodontitis. The mechanisms that underpin the links between these two conditions are not completely understood, but involve aspects of immune functioning, neutrophil activity, and cytokine biology. There is emerging evidence to support the existence of a two-way relationship between diabetes and periodontitis, with diabetes increasing the risk for periodontitis, and periodontal inflammation negatively affecting glycaemic control. Incidences of macroalbuminuria and end-stage renal disease are increased twofold and threefold, respectively, in diabetic individuals who also have severe periodontitis compared to diabetic individuals without severe periodontitis. Furthermore, the risk of cardiorenal mortality (ischaemic heart disease and diabetic nephropathy combined) is three times higher in diabetic people with severe periodontitis than in diabetic people without severe periodontitis. Treatment of periodontitis is associated with HbA(1c) reductions of approximately 0.4%. Oral and periodontal health should be promoted as integral components of diabetes management.
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To determine the impact of periodontal treatment on serum levels of prohepcidin (the prohormone of hepcidin) and systemic inflammation markers, as well as correlations among these markers, in patients with chronic periodontitis and chronic kidney disease who were not undergoing dialysis. We included 56 chronic periodontitis patients, 36 with chronic kidney disease and 20 without systemic diseases and with normal renal function (control group). Chronic kidney disease was defined as suggested by the clinical practice guidelines in the National Kidney Foundation. Chronic periodontitis was defined through clinical attachment level and by probing pocket depth, according to the American Association of Periodontology. The inflammatory markers ultrasensitive C-reactive protein, interleukin-6, and prohepcidin were evaluated before and 3 months after periodontal treatment. The efficacy of periodontal treatment was confirmed by the improvement in clinical parameters of chronic periodontitis in the control and chronic kidney disease groups. Periodontal treatment resulted in significant reductions in ultrasensitive C-reactive protein, interleukin-6 and serum prohepcidin levels in both groups. Moreover, in multivariate linear regression, the reduction in prohepcidin after periodontal treatment was significantly and independently associated with interleukin-6 levels in the control group. By inducing a decline in the systemic inflammatory response and a decrease in serum prohepcidin, successful periodontal treatment may represent an important means of ameliorating the inflammatory burden seen in patients with chronic kidney disease. Trial registration: ISRCTN59866656.
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Pentraxins are classical mediators of inflammation and markers of acute-phase reactions. Pentraxin-3 (PTX3) is believed to be a true independent indicator of disease activity. It has been associated with clinical outcomes in incident chronic kidney disease (CKD) and periodontal diseases. Periodontitis is lately being considered as a risk factor for CKD. However, no data are available on elevated PTX3 in patients with CKD associated with periodontitis. Sixty subjects were divided into three groups (n = 20) based on glomerular filtration rate (GFR) and periodontal parameters: healthy (group-1), CKD (group-2), and CKD with periodontitis (group-3). Plasma samples obtained from each patient were quantified for PTX3 using Enzyme-linked Immunosorbent Assay (ELISA). Both patient groups with CKD had higher plasma PTX3 concentrations than control subjects. However, there was no significant difference between the two groups (groups 2 and 3). In all groups, plasma PTX3 correlated positively with periodontal parameters. Group 3 patients had higher concentrations of PTX3 (6.338 ng/ml) than group 2 (5.41 ng/ml) and group 1 (1.835 ng/ml). Within the limits of the present study, the difference in plasma PTX3 levels between groups 2 and 3 was not found to be statistically significant (P > 0.05). However, as PTX3 values correlated positively with periodontal parameters, this model could contribute to identifying individuals with periodontitis at high risk of CKD. Thus, periodontal disease could serve as a risk factor for developing CKD. Further large-scale studies nullifying the confounders for CKD are warranted to confirm positive results.
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David Moher and colleagues introduce PRISMA, an update of the QUOROM guidelines for reporting systematic reviews and meta-analyses
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Periodontal disease has been associated with a number of systemic diseases. A high prevalence of periodontitis among individuals with chronic kidney diseases and end-stage renal disease has been reported. However, no association between periodontal diseases and glomerulonephritis has previously been investigated. The aim of this study was to assess the severity and possible role of periodontitis in a group of patients with unknown primary glomerulonephritis. Ten patients with unknown primary glomerulonephritis, and who had a renal biopsy with stable renal function and serum creatinine <1.6 mg/dL, were recruited. Severity of the periodontal disease was clinically measured with plaque index (PI), gingival index (GI), and periodontal pocket depth (PD). The subjects received appropriate dental treatments where indicated. The patients were also put on angiotensin-converting enzyme inhibitor or angiotensin receptor blockers for controlling blood pressure and proteinuria. Six months following appropriate periodontal treatment, renal function, degree of proteinuria, and level of C-reactive protein (CRP) were measured in each individual. The median age of the patients was 30 (15.8) years. The median urine protein excretion was lower following the periodontal therapy (P=008). Prior to the dental and/or periodontal therapies, the median PI, PD, and GI were 57.5%, 4.3, and 1.1, respectively. The majority of the patients had advanced periodontal disease. In four patients, +2/+3 CRP turned negative after periodontal treatment. The present study revealed that a causative link might exist between periodontal disease and glomerulonephritis.
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The aim of this study was to assess a suggested association between periodontitis and renal insufficiency by assaying kidney disease markers. VARIABLES USED TO DIAGNOSE PERIODONTITIS WERE: (i) probing pocket depth (PPD), (ii) attachment loss (AL), (iii) bleeding on probing (BOP), (iv) plaque index (PI) and (v) extent and severity index. Blood and urine were collected from 60 apparently healthy non-smokers (men and women), consisting of a test group of 30 subjects with periodontitis (age 46±6 yrs) and a control group of 30 healthy subjects (age 43±5 yrs). Kidney function markers (urea, creatinine, uric acid and albumin contents) were measured in the serum and urine. Also, the glomerular filtration rate was estimated from creatinine clearance, from the abbreviated Modification of Diet in Renal Disease formula and from the albumin : creatinine ratio in a 24-h sample of urine. It was found that the control group had a greater mean number of teeth than the test group and that the two groups also differed in PPD, AL, BOP and PI, all these variables being higher in the test group (P=0.006). For the extent and severity index of both PPD and AL, the test group had much higher medians of both extent and severity than the control group (P=0.001). With regard to kidney function, none of the markers revealed a significant difference between the control and test groups and all measured values fell within the reference intervals. It is proposed that severe periodontitis is not associated with any alteration in kidney function.
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Chronic kidney disease (CKD) is a debilitating systemic condition. Our working hypothesis is that CKD predialysis patients with periodontitis would respond poorly to periodontal treatment owing to immunologic compromise. Twenty-one predialysis patients (group 1) and 19 individuals without clinical evidence of kidney disease (group 2) with chronic periodontitis were subjected to non-surgical periodontal treatment with no antibiotics. Clinical periodontal and systemic parameters were evaluated at baseline and 3 months after treatment. Both groups showed significant and similar post-treatment improvements in all periodontal parameters examined. Most interestingly, periodontal treatment had a statistically significant positive effect on the glomerular filtration rate of each individual (group 1, p = 0.04; group 2, p = 0.002). Our results indicate that chronic periodontitis in predialysis kidney disease patients improved similarly in patients with chronic periodontitis and no history of CKD after receiving non-surgical periodontal therapy. This study demonstrates that CKD predialysis patients show a good response to non-surgical periodontal treatment.
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Periodontal disease is associated with diabetes, heart disease, and chronic kidney disease (CKD), relationships postulated to be due in part to vascular inflammation. A bidirectional relationship between CKD and periodontal disease is plausible, though this relationship has not been previously reported. In this study, we assessed the potential for connections between CKD and periodontal disease, and mediators of these relationships using structural equation models of data from 11,211 adults ≥ 18 years of age who participated in the Third National Health and Nutrition Examination Survey. Multivariable logistic regression models were used to test the hypothesis that periodontal disease was independently associated with CKD. Given the potential that the periodontal disease and CKD relationship may be bidirectional, a two-step analytic approach was used that involved tests for mediation and structural equation models to examine more complex direct and indirect effects of periodontal disease on CKD, and vice versa. In two separate models, periodontal disease (adjusted odds ratio of 1.62), edentulism (adjusted odds ratio of 1.83), and the periodontal disease score were associated with CKD when simultaneously adjusting for 14 other factors. Altogether, three of four structural equation models support the hypothesized relationship. Thus, our analyses support a bidirectional relationship between CKD and periodontal disease, mediated by hypertension and the duration of diabetes.
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Patients with end-stage renal disease (ESRD) experience a significantly increased rate of atherosclerotic complications. Inflammation plays a central role in the pathogenesis of these complications and C-reactive protein (CRP) has been found to be predictive of all-cause and cardiovascular mortality. Many patients have elevated CRP levels without an apparent infection. Periodontal diseases in the general population have been associated with both an increased prevalence of atherosclerotic complications and an elevation in serum CRP values. This study examined the association between periodontal disease and elevated CRP in patients with ESRD on chronic dialysis. Eighty patients on chronic dialysis were included in the study. Demographic information, medical history and CRP levels were recorded. Periodontal examination was carried out by a single calibrated examiner and included gingival index (GI), bleeding on probing (BoP), probing depths (PD) and clinical attachment loss (CAL). These measurements were recorded in relation to the Ramfjord teeth. The presence in any one sextant of PD > or =4 mm or clinical loss of attachment > or =3 mm was diagnosed as periodontitis. Mean age of subjects was 50.3 +/- 9.06 years with a median time on dialysis of 24 months. 57.5% (n=46) of subjects were diagnosed as having periodontitis; of these 52.2% had CRP levels >10 mg/l. Of the 34 subjects with healthy periodontium, only 10 (29.4%) had elevated CRP levels. The serum CRP levels between these two groups were significantly different (p = 0.004). The results of the study showed significantly elevated levels of CRP in ESRD patients with periodontitis. Periodontal diseases may be an overlooked source of inflammation in ESRD patients.
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David Moher and colleagues introduce PRISMA, an update of the QUOROM guidelines for reporting systematic reviews and meta-analyses
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ACKNOWLEDGMENT: This Editors' Consensus is supported by an educational grant from Colgate-Palmolive, Inc., New York, New York, and is based on a meeting of the authors held in Boston, Massachusetts, on January 9, 2009. DISCLOSURE: Dr. Friedewald has received honoraria for speaking from Novartis, East Hanover, New Jersey. Dr. Kornman is a full-time employee and shareholder of Interleukin Genetics, Waltham, Massachusetts, which owns patents on genetic biomarkers for chronic inflammatory diseases. Dr. Genco is a consultant to Merck, Whitehouse Station, New Jersey. Dr. Ridker has received research support from AstraZeneca, Wilmington, Delaware; Novartis; Pfizer, New York, New York; Roche, Nutley, New Jersey; Sanofi-Aventis, Bridgewater, New Jersey; and Abbott Laboratories, Abbott Park, Illinois. Dr. Ridker has received non-financial research support from Amgen, Thousand Oaks, California. Dr. Ridker is a co-inventor on patents held by Brigham and Women's Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease. Dr. Ridker is a research consultant for Schering-Plough, Kenilworth, New Jersey; Sanofi-Aventis; AstraZeneca; Isis, Carlsbad, California; Novartis; and Vascular Biogenics, Tel Aviv, Israel. Dr. Van Dyke is a co-inventor on patents held by Boston University, Boston, Massachusetts, that relate to inflammation control, including consulting fees. Dr. Roberts has received honoraria for speaking from Merck, Schering-Plough, AstraZeneca, and Novartis. All other individuals in a position to control content disclosed no relevant financial relationships.
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To perform a systematic review and critical analysis of the definitions of periodontitis and the methods which have been used to identify and measure this disease. Relevant publications were identified after searching MEDLINE, EMBASE, SCISEARCH and LILACS electronic databases. Screening of titles and abstracts and data extraction was conducted independently by two reviewers. To be included in the review, studies were required to define periodontitis and to indicate how it was measured. Studies that related purely to gingivitis, and/or intervention studies, and/or studies where prevalence or severity of periodontitis was not a principal outcome were excluded. From a total of 34,72 titles and abstracts, 104 potentially relevant full text papers were identified. Of these, 15 met the criteria for inclusion in the final stage of the review. The survey revealed heterogeneity between the studies in the measurement tools used, particularly the types of probes and the sites and areas of the mouth that were assessed. There was also heterogeneity in the use of clinical attachment loss (CAL) and pocket probing depth (PPD) as criteria for periodontitis. In the 15 studies, the threshold for a diagnosis of periodontitis when CAL was the criterion ranged from 2 to > or =6 mm and when PPD was used, from 3 to > or =6 mm. This review has confirmed previous work which has suggested that epidemiological studies of periodontal diseases are complicated by the diversity of methodologies and definitions used. The studies that were reviewed utilized a minimum diagnostic threshold defining periodontitis, at a given site in terms of CAL of 2 mm and PPD of 3 mm.
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Dental plaque has been proven to initiate and promote gingival inflammation. Histologically, various stages of gingivitis may be characterized prior to progression of a lesion to periodontitis. Clinically, gingivitis is well recognized. Longitudinal studies on a patient cohort of 565 middle class Norwegian males have been performed over a 26-year period to reveal the natural history of initial periodontitis in dental-minded subjects between 16 and 34 years of age at the beginning of the study. Sites with consistent bleeding (GI=2) had 70% more attachment loss than sites that were consistently non-inflamed (GI=0). Teeth with sites that were consistently non-inflamed had a 50-year survival rate of 99.5%, while teeth with consistently inflamed gingivae yielded a 50-year survival rate of 63.4%. Based on this longitudinal study on the natural history of periodontitis in a dentally well-maintained male population it can be concluded that persistent gingivitis represents a risk factor for periodontal attachment loss and for tooth loss.
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Chronic kidney disease and its concomitant sequelae represent a major public health problem. Recent data suggest periodontal infection contributes to chronic kidney disease. This United States population-based study of 4,053 adults > or =40 years of age investigated the association between chronic kidney disease and clinical measures and serologic markers of periodontal infection. Chronic kidney disease was defined as moderate-to-severe reduction of kidney function with glomerular filtration rate of 15 to 59 ml/minute/1.73 m(2) based on stages 3 and 4 of the Kidney Disease Outcome Quality Initiative. Chronic oral inflammatory burden was measured as 1) clinical periodontal infection categorized as no periodontal disease, periodontal disease (at least one tooth with > or =4 mm loss of attachment and bleeding on probing as an indicator of inflammation), or edentulism and 2) serum immunoglobulin G antibody response to Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) and Porphyromonas gingivalis. Multiple logistic regression modeling quantified the association between chronic kidney disease and chronic inflammatory burden and other risk factors. Nine percent of the study population had chronic kidney disease, 22% had high A. actinomycetemcomitans antibody titer, 24% had high P. gingivalis antibody titer, 9% had periodontal disease, and 17% were edentulous. After simultaneously adjusting for recognized risk factors, adults with a high A. actinomycetemcomitans titer were less likely to have chronic kidney disease (adjusted odds ratio [OR(Adj)] = 0.67; 95% confidence interval [CI]: 0.46 to 0.98), and adults with edentulism were more likely to have chronic kidney disease (OR(Adj) = 1.64; 95% CI: 1.11 to 2.44). These results support considering edentulism and low serum titer to A. actinomycetemcomitans as risk indicators for chronic kidney disease.
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A systematic review may encompass both odds ratios and mean differences in continuous outcomes. A separate meta-analysis of each type of outcome results in loss of information and may be misleading. It is shown that a ln(odds ratio) can be converted to effect size by dividing by 1.81. The validity of effect size, the estimate of interest divided by the residual standard deviation, depends on comparable variation across studies. If researchers routinely report residual standard deviation, any subsequent review can combine both odds ratios and effect sizes in a single meta-analysis when this is justified. Copyright © 2000 John Wiley & Sons, Ltd.
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It is unclear whether treatment of maternal periodontal disease will reduce the risk of preterm delivery. The results of 4 randomized single-center trials suggested that periodontal treatment during pregnancy may reduce preterm births. However, a randomized, multicenter clinical trial reported no difference between treatment and control groups for mean gestational age and preterm birth. This randomized, controlled clinical trial investigated the effects of treatment of periodontal disease on the incidence of preterm birth in women receiving standard obstetric care. Between 2004 and 2007 at 3 US sites, 1806 pregnant women with periodontal disease were randomized to either a periodontal treatment arm (n = 903), consisting of scaling and root planning early in the second trimester, or a delayed treatment arm (n = 903) chat provided periodontal care only after delivery. The pregnancy and maternal periodontal status in all participants were followed to delivery and neonatal outcomes until discharge. The primary outcome was preterm birth defined as gestational age less than 37 weeks. The secondary outcome was gestational age less than 35 weeks. A total of 1760 evaluable patients were included in the final analysis. There were no differences at baseline in the treatment and control (delayed treatment) groups for any periodontal or obstetric measure. No statistically significant differences were found between the 2 groups in rates of preterm delivery or adverse events, or in major obstetric and neonatal outcomes. There were some differences among the individual study sites in effects of treatment on periodontal status. These findings demonstrate that periodontal therapy during pregnancy has no effect on rates of preterm delivery.
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The Cochrane Handbook for Systematic Reviews of Interventions (the Handbook) has undergone a substantial update, and Version 5 of the Handbook is now available online at www.cochrane-handbook.org and in RevMan 5. In addition, for the first time, the Handbook will soon be available as a printed volume, published by Wiley-Blackwell. We are anticipating release of this at the Colloquium in Freiburg. Version 5 of the Handbook describes the new methods available in RevMan 5, as well as containing extensive guidance on all aspects of Cochrane review methodology. It has a new structure, with 22 chapters divided into three parts. Part 1, relevant to all reviews, introduces Cochrane reviews, covering their planning and preparation, and their maintenance and updating, and ends with a guide to the contents of a Cochrane protocol and review. Part 2, relevant to all reviews, provides general methodological guidance on preparing reviews, covering question development, eligibility criteria, searching, collecting data, within-study bias (including completion of the Risk of Bias table), analysing data, reporting bias, presenting and interpreting results (including Summary of Findings tables). Part 3 addresses special topics that will be relevant to some, but not all, reviews, including particular considerations in addressing adverse effects, meta-analysis with non-standard study designs and using individual participant data. This part has new chapters on incorporating economic evaluations, non-randomized studies, qualitative research, patient-reported outcomes in reviews, prospective meta-analysis, reviews in health promotion and public health, and the new review type of overviews of reviews.
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The objective of this working group was to assess and make specific recommendations to improve the quality of reporting of clinical research in implant dentistry and discuss ways to reach a consensus on choice of outcomes. Discussions were informed by three systematic reviews on quality of reporting of observational studies (case series, case-control and cohort) and experimental research (randomized clinical trials). An additional systematic review provided information on choice of outcomes and analytical methods. In addition, an open survey among all workshop participants was utilized to capture a consensus view on the limits of currently used survival and success-based outcomes as well as to identify domains that need to be captured by future outcome systems. The Workshop attempted to clarify the characteristics and the value in dental implant research of different study designs. In most areas, measurable quality improvements over time were identified. The Workshop recognized important aspects that require continued attention by clinical researchers, funding agencies and peer reviewers to decrease potential bias. With regard to choice of outcomes, the limitations of currently used systems were recognized. Three broad outcome domains that need to be captured by future research were identified: (i) patient reported outcome measures, (ii) peri-implant tissue health and (iii) performance of implant supported restorations. Peri-implant tissue health can be measured by marginal bone level changes and soft tissue inflammation and can be incorporated in time to event analyses. The Workshop recommended that collaboration between clinicians and epidemiologists/clinical trials specialists should be encouraged. Aspects of design aimed at limitation of potential bias should receive attention by clinical researchers, funding agencies and journal editors. Adherence to appropriate reporting guidelines such as STROBE and CONSORT are necessary standards. Research on outcome measure domains is an area of top priority and should urgently inform a proper process leading to a consensus on outcome measures in dental implant research.
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Background: Glycaemic control is a key issue in the care of people with diabetes mellitus (DM). Some studies have suggested a bidirectional relationship between glycaemic control and periodontal disease. Objectives: To investigate the relationship between periodontal therapy and glycaemic control in people with diabetes and to identify the appropriate future strategy for this question. Search strategy: A comprehensive approach was adopted employing handsearching; searching of electronic databases including the Cochrane Oral Health Group’s Trials Register, CENTRAL, MEDLINE, EMBASE, CINAHL, ZETOC, ISI Web of Knowledge and LILACS; contact with appropriate non-English language healthcare professionals; authors and organizations. The final date for searching for studies was 24 March 2010. Selection criteria: This review studied randomized controlled trials of people with Type 1 or 2 diabetes mellitus (DM) with a diagnosis of periodontitis. Suitable interventions included mechanical periodontal therapy with or without adjunctives and oral hygiene education. Data collection and analysis: The titles and abstracts of 690 papers were examined by two review authors independently. Ultimately, seven studies were included and 19 excluded after full text scrutiny. All trials were assessed for risk of bias. Main results: Three studies had results pooled into a meta-analysis. The effect for the mean percentage difference in HbA1c for scaling/root planing and oral hygiene (+/− antibiotic therapy) versus no treatment/usual treatment after 3–4 months was −0.40% (95% confidence interval (CI) fixed effect −0.78% to −0.01%), representing a statistically significant reduction in HbA1c (P = 0.04) for scaling/root planing. One study was assessed as being at low risk of bias with the other two at moderate to high risk of bias. A subgroup analysis examined studies without adjunctive antibiotics −0.80% (one study: 95% CI −1.73% to 0.13%; P = 0.09), with adjunctive antibiotics in the test group −0.36% (one study: 95% CI −0.83% to 0.11%; P = 0.14), and with antibiotics in both test and control groups after 3/4 months −0.15% (one study: 95% CI −1.04% to 0.74%; P = 0.74). Authors’ conclusions: There is some evidence of improvement in metabolic control in people with diabetes, after treating periodontal disease. There are few studies available and individually these lacked the power to detect a significant effect. Most of the participants in the study had poorly controlled Type 2 DM with little data from randomized trials on the effects on people with Type 1 DM.
Article
The aim was to assess the quality of reporting of experimental research in implant dentistry by a critical evaluation of study design, outcome assessments and model validation. An online search was performed using the MEDLINE. Experimental studies performed in both animals and humans were included. A’stratified random sample of the included studies was extracted and used for quantitative and qualitative analyses. Modified versions of the ARRIVE guidelines were used for quality assessment. A total of 982 papers were eligible and used for quantitative analyses. A’stratified random sample of 193 publications was extracted. The dog model was the most used experimental model whereas experimental studies on humans were few. Intra-oral experimental sites dominated in human, monkey, dog and mini-pig studies. Extra oral sites dominated in rabbit, rodent and goat/sheep studies. Studies on the pathogenesis and treatment of peri-implant diseases were few. Different animal models, experimental protocols and methods of analysis have been used to address different areas of experimental research in implant dentistry. Standardized designs for investigations within this type of experimental research seem to be lacking. Furthermore, in many of these studies there were limitations in reporting on methodology and statistical methods.
Article
Early detection of decreased kidney function can help prevent the progression of kidney disease to kidney failure and cardiovascular events. Potentially significant associations between kidney function and periodontal disease have been reported in cross-sectional studies. However, no longitudinal study has been performed and no study has been performed in Japan. The aim of this longitudinal study was to investigate the effect of periodontal disease on kidney function in community-dwelling Japanese elderly. Retrospective cohort. Members of this cohort were drawn from a longitudinal interdisciplinary study of aging. Included for this analysis were 317 participants (166 men, 151 women) aged 75 years in 2003. The periodontal inflamed surface area (PISA), reflecting the amount of inflamed periodontal tissue, was calculated for each participant. Participants were classified in quartile groups according to PISA, then divided into 2 groups (highest quartile vs the other 3 groups combined). The primary outcome for the analysis was decreased kidney function, defined as a decrease in estimated glomerular filtration rate at follow-up. Multivariable logistic regression analyses were performed to predict decreased kidney function on the basis of periodontal status, risk factors for kidney disease, and other potentially relevant covariates. During the 2-year follow-up (2003-2005), 45 participants (14.2%) developed decreased kidney function. The highest PISA quartile was associated significantly with a greater cumulative incidence of decreased kidney function (OR, 2.24; 95% CI, 1.05-4.79) than the referent group (the other 3 quartiles) after adjusting for covariates. Extension of interpreting the findings to other age groups is limited. These results suggest that periodontal disease may be a risk factor for decreased kidney function in Japanese elderly.
Article
The aim of this systematic review was to evaluate whether maternal periodontal disease treatment (MPDT) can reduce the incidence of preterm birth (PB) and/or low birth weight (LBW). The Cochrane Central Register of Controlled Trials, MEDLINE and EMBASE were searched for entries up to October 2010 without restrictions regarding the language of publication. Only randomized-controlled clinical trials (RCTs) that evaluated the effect of MPDT on birth term and birth weight were included. The search was conducted by two independent reviewers and random-effects meta-analyses were conducted methodically. Thirteen RCTs provided data, but only five trials were considered to be at a low risk of bias. The results of eight studies (61.5%) showed that MPDT may reduce the incidence of PB and/or LBW. However, the results of all meta-analyses showed contrasting results for PB [RR: 0.88 (95% CI: 0.72, 1.09)], LBW [RR: 0.78 (95% CI: 0.53, 1.17)] and PB/LBW [RR: 0.52 (95% CI: 0.08, 3.31)]. The results of this review show that MPDT did not decrease the risk of PB and/or LBW; however, the influence of specific aspects that were not investigated (disease diagnosis, extension and severity and the success of MPDT) should be evaluated by future RCTs.
Article
The aims of this systematic review (SR) were to evaluate the association between maternal periodontitis and preterm birth (PB) and/or low birth weight (LBW), and the methodological quality of prospective cohort studies conducted for such a purpose. MEDLINE, EMBASE and Cochrane Central Register of Controlled Trials (CENTRAL) databases were searched up to and including October 2010 to identify prospective studies on the association of periodontitis with PB and/or LBW. Search was conducted by two independent reviewers. The methodological quality of the observational studies was assessed using a specially designed methodological tool. Random effects meta-analyses were conducted thoroughly. Search strategy identified 1680 potentially eligible articles, of which 12 prospective studies were included. One cohort study had their data reported in two articles. Of the 11 studies, 10 showed a high methodological quality and one a medium methodological quality. Nine studies (81.8%) found an association between periodontitis and PB and/or LBW. Meta-analysis showed a significant risk of preterm delivery for pregnant women with periodontitis [risk ratio (RR): 1.70 (95% confidence interval (CI): 1.03, 2.81)] and a significant risk for LBW [RR: 2.11 (95% CI: 1.05, 4.23)] or PB/LBW [RR: 3.57 (95% CI: 1.87, 6.84)], as well as a high and unexplained degree of heterogeneity between studies. Conclusion: Although this SR found a consistent association between periodontitis and PB and/or LBW, this finding should be treated with great caution until the sources of heterogeneity can be explained.
Article
We hypothesized that renal function is associated with the relationship between periodontal disease and bone metabolism. The present study evaluated the relationship of bone formation and resorption markers to periodontal disease, taking renal function into consideration, in elderly Japanese subjects. We selected 148 subjects aged 77 years. The periodontal examination included the assessment of clinical attachment level (CAL). We measured two bone formation markers (serum bone-specific alkaline phosphatase and serum osteocalcin) and two bone resorption markers (urinary deoxypyridinoline and urinary cross-linked N-telopeptide of type I collagen). Creatinine clearance per 24 h, as a measure of renal function, was also determined. The correlations between mean CAL or percentage of sites with ≥6mm CAL (6+mm CAL) and bone turnover markers, and between bone turnover markers and creatinine clearance levels, were performed by multiple linear regression analysis. There were significant negative relationships between mean CAL or 6+mm CAL and serum osteocalcin levels adjusted for gender, smoking habits and oral care habits (β=-0.25, p=0.014 and β=-0.35, p=0.001, respectively). In addition, there was a negative relationship between serum osteocalcin and creatinine clearance levels adjusted for gender and smoking habits (β=-0.45, p<0.0001). Results from the present study suggest that serum osteocalcin was significantly associated with renal function and periodontal disease. The low systemic bone metabolism, which might be caused by low renal function, is associated with periodontal disease.
Article
Recent studies suggest an overall association between chronic kidney disease (CKD) and periodontal disease, but it is unknown whether this association is similar across various subpopulations. This study was a cross-sectional analysis of 2001 to 2004 National Health and Nutrition Examination Survey data. CKD was defined as a urinary albumin-to-creatinine ratio ≥30 mg/g or estimated GFR of 15 to 59 ml/min per 1.73 m(2). Adjusted odds ratios were calculated using multivariable logistic regression with U.S. population-based weighting. These analyses included 6199 dentate adult participants (aged 21 to 75 years) with periodontal exams. The estimated prevalences of moderate/severe periodontal disease and CKD were 5.3% and 10.6%, respectively. Periodontal disease was associated with >2-fold higher risk of CKD that was moderately attenuated after adjustment for age, gender, race/ethnicity, tobacco use, hypertension, diabetes, educational attainment, poverty index ratio, and dental care use. There were no statistically significant interactions between periodontal disease and race/ethnicity, educational attainment, or poverty status. Less-than-recommended dental care use was associated with periodontal disease and CKD and was increasingly prevalent among nonwhites, lower educational attainment, and lower poverty status. The association between periodontal disease and CKD is not significantly different among subgroups. However, because nonwhites, those with a lower educational level, and the poor less frequently report use of recommended dental care, the association between periodontal disease and kidney function over time may become stronger among these groups and warrants further investigation.
Article
The relationship between periodontitis and outcomes in patients treated with long-term hemodialysis is controversial. Our previous work suggests that periodontitis is associated with malnutrition and inflammation. Here, we hypothesize that periodontitis is associated with mortality in hemodialysis patients. Prospective observational study. 253 patients undergoing hemodialysis at a single hospital-based dialysis facility. Severity of periodontal disease (mild, moderate, or severe based on oral examination of 6 teeth). All-cause and cardiovascular mortality during a 6-year follow-up after an oral health examination of index teeth. During the 6-year follow-up, 102 patients died. Death occurred in 70.6%, 41.8%, and 24.0% of patients with severe, moderate, and mild/no periodontitis, respectively. Using mild/no periodontitis as the reference group and adjustment for demographic characteristics, comorbid conditions, and selected laboratory values, HRs for all-cause mortality were 1.39 (95% CI, 0.83-2.34) and 1.83 (95% CI, 1.04-3.24) for moderate and severe periodontitis, respectively. HRs for cardiovascular mortality were not statistically significant. Single assessment of periodontal disease severity. For patients undergoing long-term hemodialysis, periodontitis is associated with increased risk of death. Clinical trials are required to determine whether treatment of periodontitis decreases mortality.
Article
The definition and classification for chronic kidney disease was proposed by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF-KDOQI) in 2002 and endorsed by the Kidney Disease: Improving Global Outcomes (KDIGO) in 2004. This framework promoted increased attention to chronic kidney disease in clinical practice, research and public health, but has also generated debate. It was the position of KDIGO and KDOQI that the definition and classification should reflect patient prognosis and that an analysis of outcomes would answer key questions underlying the debate. KDIGO initiated a collaborative meta-analysis and sponsored a Controversies Conference in October 2009 to examine the relationship of estimated glomerular filtration rate (GFR) and albuminuria to mortality and kidney outcomes. On the basis of analyses in 45 cohorts that included 1,555,332 participants from general, high-risk, and kidney disease populations, conference attendees agreed to retain the current definition for chronic kidney disease of a GFR <60 ml/min per 1.73 m(2) or a urinary albumin-to-creatinine ratio >30 mg/g, and to modify the classification by adding albuminuria stage, subdivision of stage 3, and emphasizing clinical diagnosis. Prognosis could then be assigned based on the clinical diagnosis, stage, and other key factors relevant to specific outcomes. KDIGO has now convened a workgroup to develop a global clinical practice guideline for the definition, classification, and prognosis of chronic kidney disease.
Article
To assess methods, quality and outcomes of systematic reviews (SRs) conducted to evaluate the effectiveness of root coverage (RC) procedures in the treatment of recession-type defects (RTD). MEDLINE and EMBASE were searched up to and including April 2010 to identify SRs investigating the effectiveness/efficacy of surgical interventions for the treatment of patients with RTD. Searching was conducted independently by two reviewers, and data extraction was based on the methodological criteria applied and on the effects of interventions reported by each SR. The checklist proposed by Glenny and colleagues, the Overview Quality Assessment Questionnaire and the "Assessment of Multiple systematic Reviews", instrument were used to assess the quality of SRs. Additionally, the methodological criteria applied by included reviews were compared with those proposed by the Cochrane Collaboration. Search strategy identified 716 potentially eligible articles, of which 12 papers regarding 10 SRs were included in the study. Results from different SRs showed that subepithelial connective tissue grafts associated or not to coronally advanced flaps can be used to reduce recession depth and improve the width of keratinized tissue. All quality assessment tools showed that most of the SRs were of good methodological quality, but they also highlighted key points that could be improved in future reviews. Only two SRs followed in full the guidelines proposed by the Cochrane Collaboration. All SRs agree that RC may be anticipated by different surgical procedures. However, differences in the methodological quality between reviews were quite evident, and thus making a clear indication that there is a need of standardization of the methods that will be applied by future SRs. As a result, a standardized checklist for reporting SRs was proposed by the authors.
Article
To systematically assess the factors influencing tooth loss during long-term periodontal maintenance (PM). CENTRAL, MEDLINE and EMBASE were searched up to and including September 2009. Studies limited to patients with periodontitis who underwent periodontal therapy and followed a maintenance care programme for the at least 5 years were eligible for inclusion in this review. Studies were considered for inclusion if they reported data on tooth loss during PM. The search strategy identified 527 potentially eligible articles, of which 13 retrospective case series were included in this review. The risk of bias assessment evaluated by the Newcastle-Ottawa scale showed that eight studies were considered of medium methodological quality and five of low methodological quality. Of 41,404 teeth present after active periodontal treatment, 3919 were lost during PM. The percentages of tooth loss due to periodontal reasons and of patients who did not experience tooth loss varied from 1.5% to 9.8% and 36.0% to 88.5%. Studies' individual outcomes showed that different patient-related factors (i.e. age and smoking) and tooth-related factors (tooth type and location, and the initial tooth prognosis) were associated with tooth loss during PM. The considerable heterogeneity found among studies did not allow definitive conclusions. Age, smoking and initial tooth prognosis were found to be associated with tooth loss during PM. Overall, patients must be instructed to follow periodic PM and quit smoking (smokers). Prospective cohort studies are required to confirm the possible predictors of tooth loss due to periodontal reasons. The allocation of patients into subgroups according to the type of periodontitis and smoking frequency will allow more accurate evaluations.
Article
To determine whether non-surgical periodontal treatment (PT) would exert, in subjects with generalized chronic periodontitis (GCP), some beneficial effect on renal function as indicated by surrogate measures of the glomerular filtration rate (GFR). Twenty GCP systemically healthy subjects were treated with PT. Serum samples were collected at baseline and 1 day, 7, 30, 90 and 180 days after treatment. GFR was evaluated using cystatin C, a serum marker and modification of diet in renal disease (MDRD), an equation involving creatinine, urea and albumin. Serum markers of systemic inflammation such as C-reactive protein (CRP), D-dimer, serum amyloid A (SAA) and fibrinogen were also assessed. The cystatin C level decreased significantly from baseline to the end of the trial (p<0.01). Conversely, MDRD did not vary. A significant inflammatory reaction was produced by PT in the short term. Greater increases were noted for CRP and SAA within 24 h (p<0.001 versus baseline), while D-dimer (p<0.05) and fibrinogen (p<0.01) showed mild variations. The values of inflammatory markers were normalized after 30 days. GFR, as assessed by cystatin C levels, may be positively affected by PT. Because of the exploratory nature of this trial, further research is needed to investigate this preliminary finding.
Article
To test the effects of maternal periodontal disease treatment on the incidence of preterm birth (delivery before 37 weeks of gestation). The Maternal Oral Therapy to Reduce Obstetric Risk Study was a randomized, treatment-masked, controlled clinical trial of pregnant women with periodontal disease who were receiving standard obstetric care. Participants were assigned to either a periodontal treatment arm, consisting of scaling and root planing early in the second trimester, or a delayed treatment arm that provided periodontal care after delivery. Pregnancy and maternal periodontal status were followed to delivery and neonatal outcomes until discharge. The primary outcome (gestational age less than 37 weeks) and the secondary outcome (gestational age less than 35 weeks) were analyzed using a chi test of equality of two proportions. The study randomized 1,806 patients at three performance sites and completed 1,760 evaluable patients. At baseline, there were no differences comparing the treatment and control arms for any of the periodontal or obstetric measures. The rate of preterm delivery for the treatment group was 13.1% and 11.5% for the control group (P=.316). There were no significant differences when comparing women in the treatment group with those in the control group with regard to the adverse event rate or the major obstetric and neonatal outcomes. Periodontal therapy did not reduce the incidence of preterm delivery. I.
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Acknowledgment: This Editors' Consensus is supported by an educational grant from Colgate‐Palmolive, Inc., New York, New York, and is based on a meeting of the authors held in Boston, Massachusetts, on January 9, 2009. Disclosure: Dr. Friedewald has received honoraria for speaking from Novartis, East Hanover, New Jersey. Dr. Kornman is a full‐time employee and shareholder of Interleukin Genetics, Waltham, Massachusetts, which owns patents on genetic biomarkers for chronic inflammatory diseases. Dr. Genco is a consultant to Merck, Whitehouse Station, New Jersey. Dr. Ridker has received research support from AstraZeneca, Wilmington, Delaware; Novartis; Pfizer, New York, New York; Roche, Nutley, New Jersey; Sanofi‐Aventis, Bridgewater, New Jersey; and Abbott Laboratories, Abbott Park, Illinois. Dr. Ridker has received non‐financial research support from Amgen, Thousand Oaks, California. Dr. Ridker is a co‐inventor on patents held by Brigham and Women's Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease. Dr. Ridker is a research consultant for Schering‐Plough, Kenilworth, New Jersey; Sanofi‐Aventis; AstraZeneca; Isis, Carlsbad, California; Novartis; and Vascular Biogenics, Tel Aviv, Israel. Dr. Van Dyke is a co‐inventor on patents held by Boston University, Boston, Massachusetts, that relate to inflammation control, including consulting fees. Dr. Roberts has received honoraria for speaking from Merck, Schering‐Plough, AstraZeneca, and Novartis. All other individuals in a position to control content disclosed no relevant financial relationships.
Article
An estimated 75% of the seven million Americans with moderate-to-severe chronic kidney disease are undiagnosed. Improved prediction models to identify high-risk subgroups for chronic kidney disease enhance the ability of health care providers to prevent or delay serious sequelae, including kidney failure, cardiovascular disease, and premature death. We identified 11,955 adults > or =18 years of age in the Third National Health and Nutrition Examination Survey. Chronic kidney disease was defined as an estimated glomerular filtration rate of 15 to 59 ml/minute/1.73 m(2). High-risk subgroups for chronic kidney disease were identified by estimating the individual probability using beta coefficients from the model of traditional and non-traditional risk factors. To evaluate this model, we performed standard diagnostic analyses of sensitivity, specificity, positive predictive value, and negative predictive value using 5%, 10%, 15%, and 20% probability cutoff points. The estimated probability of chronic kidney disease ranged from virtually no probability (0%) for an individual with none of the 12 risk factors to very high probability (98%) for an older, non-Hispanic white edentulous former smoker, with diabetes > or =10 years, hypertension, macroalbuminuria, high cholesterol, low high-density lipoprotein, high C-reactive protein, lower income, and who was hospitalized in the past year. Evaluation of this model using an estimated 5% probability cutoff point resulted in 86% sensitivity, 85% specificity, 18% positive predictive value, and 99% negative predictive value. This United States population-based study suggested the importance of considering multiple risk factors, including periodontal status, because this improves the identification of individuals at high risk for chronic kidney disease and may ultimately reduce its burden.
Article
A total of 104 subject were investigated and divided into 3 groups: 1. virtually healthy, without any clinical sign of periodontal inflammation; 2. periodontitis patients without internal organs affliction; 3. patients with renal pathology in which periodontitis was a concomitant disease. Biochemical investigation of the blood, oral and gingival fluids was performed. The peculiarities of periodontal involvement into renal pathology were established with lactate dehydrogenase and acid phosphatase both considerably activated in the oral and gingival fluids in groups 2 and 3. These enzymes were also activated in patients with chronic renal diseases.
Article
A method for the detection of prostaglandin E (PGE) in crevicular fluid has been developed which provides a sensitive, noninvasive technique for measurement of local concentrations of this mediator of inflammation. Assay sensitivity sufficient for the detection of 4 picograms of PGE2 was achieved by utilizing a high-affinity anti-PGE2 antibody, a solid-state second antibody and low isotope concentrations. The method permits detection of concentrations equivalent to 10(-8) M PGE2 in 1 microliter of crevicular fluid. Crevicular fluid PGE (CFPGE) concentrations were determined in samples from 12 patients with periodontal disease. Patients with periodontitis had significantly higher mean CFPGE concentrations than patients with gingivitis (179.5 +/- 51.4 pg/microliter vs 32.1 +/- 15.5 pg/microliter, mean +/- SEM). Periodontitis sites were selected on the basis of clinical and radiographic evidence of periodontal destruction. Some sites displayed low CFPGE levels, while others had CFPGE concentrations which were elevated tenfold, suggesting the presence of both inactive and active periodontal lesions. CFPGE levels greater than 100 pg/microliter were positively associated with gingival erythema and pain on probing.
Article
A systematic review may encompass both odds ratios and mean differences in continuous outcomes. A separate meta-analysis of each type of outcome results in loss of information and may be misleading. It is shown that a ln(odds ratio) can be converted to effect size by dividing by 1.81. The validity of effect size, the estimate of interest divided by the residual standard deviation, depends on comparable variation across studies. If researchers routinely report residual standard deviation, any subsequent review can combine both odds ratios and effect sizes in a single meta-analysis when this is justified.
Article
Classification systems are necessary in order to provide a framework in which to scientifically study the etiology, pathogenesis, and treatment of diseases in an orderly fashion. In addition, such systems give clinicians a way to organize the health care needs of their patients. The last time scientists and clinicians in the field of periodontology and related areas agreed upon a classification system for periodontal diseases was in 1989 at the World Workshop in Clinical Periodontics. Subsequently, a simpler classification was agreed upon at the 1st European Workshop in Periodontology. These classification systems have been widely used by clinicians and research scientists throughout the world. Unfortunately, the 1989 classification had many shortcomings, including: (1) considerable overlap in disease categories, (2) absence of a gingival disease component, (3) inappropriate emphasis on age of onset of disease and rates of progression, and (4) inadequate or unclear classification criteria. The 1993 European classification lacked the detail necessary for adequate characterization of the broad spectrum of periodontal diseases encountered in clinical practice. The need for a revised classification system for periodontal diseases was emphasized during the 1996 World Workshop in Periodontics. In 1997 the American Academy of Periodontology responded to this need and formed a committee to plan and organize an international workshop to revise the classification system for periodontal diseases. The proceedings in this volume are the result of this reclassification effort. The process involved development by the Organizing Committee of an outline for a new classification and identification of individuals to write state-of-the-science reviews for each of the items on the outline. The reviewers were encouraged to depart from the preliminary outline if there were data to support any modifications. On October 30-November 2, 1999, the International Workshop for a Classification of Periodontal Diseases and Conditions was held and a new classification was agreed upon (Figure 1). This paper summarizes how the new classification for periodontal diseases and conditions presented in this volume differs from the classification system developed at the 1989 World Workshop in Clinical Periodontics. In addition, an analysis of the rationale is provided for each of the modifications and changes.
Article
Anemia of chronic disease (ACD) is defined as the anemia occurring in chronic infections and inflammatory conditions, that is not due to marrow deficiencies or other diseases and in the presence of adequate iron stores and vitamins. The purpose of the present study was to investigate whether periodontitis patients show signs of anemia. 39 patients with severe periodontitis, 71 patients with moderate periodontitis and 42 controls, all with good general health, participated in this study. The mean age of all groups was 42 years. Several red blood cell parameters were determined from peripheral blood samples. Overall data analysis indicated that periodontitis patients have a lower hematocrit, lower numbers of erythrocytes, lower hemoglobin levels and higher erythrocyte sedimentation rates. These results were adjusted for the following possible confounders: gender, age, smoking, ethnicity and level of education. Further, more periodontitis patients (23%) than controls (7%), had hemoglobin levels below the normal reference range. The present study provides further evidence that periodontitis has systemic effects and that periodontitis may tend towards anemia. This phenomenon may be explained by a depressed erythropoiesis.