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Revista Medica de Chile Jun 2019Rheumatoid arthritis (RA) and chronic periodontitis (CP) may be related due to a bidirectional etiology. The evidence shows that CP could alter the clinical course of...
Rheumatoid arthritis (RA) and chronic periodontitis (CP) may be related due to a bidirectional etiology. The evidence shows that CP could alter the clinical course of RA. We performed a systematic search to determine if CP alters the morbidity of RA, analyzing its clinical and molecular aspects. Of 552 initial articles found, 16 were selected for a thorough review. There is a greater prevalence of CP in patients with RA. Patients with RA have significantly higher values of periodontal clinical parameters than healthy controls. Arthritis activity is significantly greater in patients who suffer from CP and decreases with nonsurgical periodontal treatment. There is a significant relationship between the severity of CP and RA activity.
Topics: Arthritis, Rheumatoid; Biomarkers; Case-Control Studies; Chronic Periodontitis; Female; Humans; Male; Risk Factors
PubMed: 31859830
DOI: 10.4067/S0034-98872019000600762 -
The ISME Journal May 2013The goals of this study were to better understand the ecology of oral subgingival communities in health and periodontitis and elucidate the relationship between...
The goals of this study were to better understand the ecology of oral subgingival communities in health and periodontitis and elucidate the relationship between inflammation and the subgingival microbiome. Accordingly, we used 454-pyrosequencing of 16S rRNA gene libraries and quantitative PCR to characterize the subgingival microbiome of 22 subjects with chronic periodontitis. Each subject was sampled at two sites with similar periodontal destruction but differing in the presence of bleeding, a clinical indicator of increased inflammation. Communities in periodontitis were also compared with those from 10 healthy individuals. In periodontitis, presence of bleeding was not associated with different α-diversity or with a distinct microbiome, however, bleeding sites showed higher total bacterial load. In contrast, communities in health and periodontitis largely differed, with higher diversity and biomass in periodontitis. Shifts in community structure from health to periodontitis resembled ecological succession, with emergence of newly dominant taxa in periodontitis without replacement of primary health-associated species. That is, periodontitis communities had higher proportions of Spirochetes, Synergistetes, Firmicutes and Chloroflexi, among other taxa, while the proportions of Actinobacteria, particularly Actinomyces, were higher in health. Total Actinomyces load, however, remained constant from health to periodontitis. Moreover, an association existed between biomass and community structure in periodontitis, with the proportion of specific taxa correlating with bacterial load. Our study provides a global-scale framework for the ecological events in subgingival communities that underline the development of periodontitis. The association, in periodontitis, between inflammation, community biomass and community structure and their role in disease progression warrant further investigation.
Topics: Actinomyces; Bacteria; Biomass; Chronic Periodontitis; Gingiva; Humans; Inflammation; Microbiota; RNA, Bacterial; RNA, Ribosomal, 16S
PubMed: 23303375
DOI: 10.1038/ismej.2012.174 -
Periodontology 2000 Feb 2016In evaluating the pathogenesis of periodontal diseases, the diagnostic potential of gingival crevicular fluid has been extensively explored during the last twenty years,... (Review)
Review
In evaluating the pathogenesis of periodontal diseases, the diagnostic potential of gingival crevicular fluid has been extensively explored during the last twenty years, from initially just confirming health and disease states to more recently investigating it as a potential prognostic tool. As host susceptibility is a critical determinant in periodontal disease pathogenesis, the inflammatory mediator levels present in gingival crevicular fluid represent relevant risk indicators for disease activity. Considerable work has been carried out to identify the many different cytokine inflammatory pathways and microbial stimuli that are associated with periodontal disease pathogenesis. Now, 'omics' approaches aim to summarize how these pathways interact and probably converge to create critical inflammatory networks. More recently, gingival crevicular fluid metabolomics appears promising as an additional diagnostic method. Biofilm structure and the host inflammatory response to the microbial challenge may induce specific inflammatory signatures. Host genetics and epigenetics may also modulate microbial colonization, adding to the multiplicity of potential causal pathways. Omics analyses of gingival crevicular fluid, measuring microbial and host interactions in association with the onset and progression of periodontal diseases, still show the potential to expand the landscape for the discovery of diagnostic, prognostic and therapeutic markers.
Topics: Biomarkers; Chronic Periodontitis; Diagnosis, Oral; Gingival Crevicular Fluid; Humans; Periodontitis
PubMed: 26662482
DOI: 10.1111/prd.12107 -
The Cochrane Database of Systematic... Jan 2018Periodontitis is a bacterially-induced, chronic inflammatory disease that destroys the connective tissues and bone that support teeth. Active periodontal treatment aims... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Periodontitis is a bacterially-induced, chronic inflammatory disease that destroys the connective tissues and bone that support teeth. Active periodontal treatment aims to reduce the inflammatory response, primarily through eradication of bacterial deposits. Following completion of treatment and arrest of inflammation, supportive periodontal therapy (SPT) is employed to reduce the probability of re-infection and progression of the disease; to maintain teeth without pain, excessive mobility or persistent infection in the long term, and to prevent related oral diseases.According to the American Academy of Periodontology, SPT should include all components of a typical dental recall examination, and importantly should also include periodontal re-evaluation and risk assessment, supragingival and subgingival removal of bacterial plaque and calculus, and re-treatment of any sites showing recurrent or persistent disease. While the first four points might be expected to form part of the routine examination appointment for periodontally healthy patients, the inclusion of thorough periodontal evaluation, risk assessment and subsequent treatment - normally including mechanical debridement of any plaque or calculus deposits - differentiates SPT from routine care.Success of SPT has been reported in a number of long-term, retrospective studies. This review aimed to assess the evidence available from randomised controlled trials (RCTs).
OBJECTIVES
To determine the effects of supportive periodontal therapy (SPT) in the maintenance of the dentition of adults treated for periodontitis.
SEARCH METHODS
Cochrane Oral Health's Information Specialist searched the following databases: Cochrane Oral Health's Trials Register (to 8 May 2017), the Cochrane Central Register of Controlled Trials (CENTRAL) (the Cochrane Library, 2017, Issue 5), MEDLINE Ovid (1946 to 8 May 2017), and Embase Ovid (1980 to 8 May 2017). The US National Institutes of Health Trials Registry (ClinicalTrials.gov) and the World Health Organization International Clinical Trials Registry Platform were searched for ongoing trials. No restrictions were placed on the language or date of publication when searching the electronic databases.
SELECTION CRITERIA
Randomised controlled trials (RCTs) evaluating SPT versus monitoring only or alternative approaches to mechanical debridement; SPT alone versus SPT with adjunctive interventions; different approaches to or providers of SPT; and different time intervals for SPT delivery.We excluded split-mouth studies where we considered there could be a risk of contamination.Participants must have completed active periodontal therapy at least six months prior to randomisation and be enrolled in an SPT programme. Trials must have had a minimum follow-up period of 12 months.
DATA COLLECTION AND ANALYSIS
Two review authors independently screened search results to identify studies for inclusion, assessed the risk of bias in included studies and extracted study data. When possible, we calculated mean differences (MDs) and 95% confidence intervals (CIs) for continuous variables. Two review authors assessed the quality of evidence for each comparison and outcome using GRADE criteria.
MAIN RESULTS
We included four trials involving 307 participants aged 31 to 85 years, who had been previously treated for moderate to severe chronic periodontitis. Three studies compared adjuncts to mechanical debridement in SPT versus debridement only. The adjuncts were local antibiotics in two studies (one at high risk of bias and one at low risk) and photodynamic therapy in one study (at unclear risk of bias). One study at high risk of bias compared provision of SPT by a specialist versus general practitioner. We did not identify any RCTs evaluating the effects of SPT versus monitoring only, or of providing SPT at different time intervals, or that compared the effects of mechanical debridement using different approaches or technologies.No included trials measured our primary outcome 'tooth loss'; however, studies evaluated signs of inflammation and potential periodontal disease progression, including bleeding on probing (BoP), clinical attachment level (CAL) and probing pocket depth (PPD).There was no evidence of a difference between SPT delivered by a specialist versus a general practitioner for BoP or PPD at 12 months (very low-quality evidence). This study did not measure CAL or adverse events.Due to heterogeneous outcome reporting, it was not possible to combine data from the two studies comparing mechanical debridement with or without the use of adjunctive local antibiotics. Both studies found no evidence of a difference between groups at 12 months (low to very low-quality evidence). There were no adverse events in either study.The use of adjunctive photodynamic therapy did not demonstrate evidence of benefit compared to mechanical debridement only (very low-quality evidence). Adverse events were not measured.The quality of the evidence is low to very low for these comparisons. Future research is likely to change the findings, therefore the results should be interpreted with caution.
AUTHORS' CONCLUSIONS
Overall, there is insufficient evidence to determine the superiority of different protocols or adjunctive strategies to improve tooth maintenance during SPT. No trials evaluated SPT versus monitoring only. The evidence available for the comparisons evaluated is of low to very low quality, and hampered by dissimilarities in outcome reporting. More trials using uniform definitions and outcomes are required to address the objectives of this review.
Topics: Adult; Aged; Aged, 80 and over; Anti-Bacterial Agents; Chronic Periodontitis; Dental Plaque; Humans; Middle Aged; Periodontal Debridement; Periodontics; Photochemotherapy; Randomized Controlled Trials as Topic; Tooth Loss
PubMed: 29291254
DOI: 10.1002/14651858.CD009376.pub2 -
Mediators of Inflammation 2019Periodontitis is characterized by a chronic inflammation produced in response to a disease-associated multispecies bacterial community in the subgingival region.... (Review)
Review
Periodontitis is characterized by a chronic inflammation produced in response to a disease-associated multispecies bacterial community in the subgingival region. Although the inflammatory processes occur locally in the oral cavity, several studies have determined that inflammatory mediators produced during periodontitis, as well as subgingival species and bacterial components, can disseminate from the oral cavity, contributing therefore, to various extraoral diseases like cancer. Interestingly, carcinogenesis associated with periodontal species has been observed in both the oral cavity and in extra oral sites. In this review, several studies were summarized showing a strong association between orodigestive cancers and poor oral health, presence of periodontitis-associated bacteria, tooth loss, and clinical signs of periodontitis. Proinflammatory pathways were also summarized. Such pathways are activated either by mono- or polymicrobial infections, resulting in an increase in the expression of proinflammatory molecules such as IL-6, IL-8, IL-1, and TNF-. In addition, it has been shown that several periodontitis-associated species induce the expression of genes related to cell proliferation, cell cycle, apoptosis, transport, and immune and inflammatory responses. Intriguingly, many of these pathways are linked to carcinogenesis. Among them, the activation of Toll-like receptors (TLRs) and antiapoptotic pathways (such as the PI3K/Akt, JAK/STAT, and MAPK pathways), the reduction of proapoptotic protein expression, the increase in cell migration and invasion, and the enhancement in metastasis are addressed. Considering that periodontitis is a polymicrobial disease, it is likely that mixed species promote carcinogenesis both in the oral cavity and in extra oral tissues and probably-as observed in periodontitis-synergistic and/or antagonistic interactions occur between microbes in the community. To date, a good amount of studies has allowed us to understand how monospecies infections activate pathways involved in tumorigenesis; however, more studies are needed to determine the combined effect of oral species in carcinogenesis.
Topics: Animals; Carcinogenesis; Chronic Periodontitis; Cytokines; Humans; Inflammation
PubMed: 31049022
DOI: 10.1155/2019/1029857 -
Frontiers in Endocrinology 2023It has been well documented that there is a two-way relationship between diabetes mellitus and periodontitis. Diabetes mellitus represents an established risk factor for... (Review)
Review
It has been well documented that there is a two-way relationship between diabetes mellitus and periodontitis. Diabetes mellitus represents an established risk factor for chronic periodontitis. Conversely, chronic periodontitis adversely modulates serum glucose levels in diabetic patients. Activated immune and inflammatory responses are noted during diabetes and periodontitis, under the modulation of similar biological mediators. These activated responses result in increased activity of certain immune-inflammatory mediators including adipokines and microRNAs in diabetic patients with periodontal disease. Notably, certain microbes in the oral cavity were identified to be involved in the occurrence of diabetes and periodontitis. In other words, these immune-inflammatory mediators and microbes may potentially serve as biomarkers for risk assessment and therapy selection in diabetes and periodontitis. In this review, we briefly provide an updated overview on different potential biomarkers, providing novel diagnostic and therapeutic insights on periodontal complications and diabetes mellitus.
Topics: Humans; Diabetes Mellitus, Type 2; Chronic Periodontitis; Risk Factors; Biomarkers; Inflammation Mediators
PubMed: 38149100
DOI: 10.3389/fendo.2023.1292596 -
Zhejiang Da Xue Xue Bao. Yi Xue Ban =... Feb 2022Chronic periodontitis is an infectious disease, which has a reciprocal relationship with a variety of systemic disorders. Parkinson's disease is a prevalent... (Review)
Review
Chronic periodontitis is an infectious disease, which has a reciprocal relationship with a variety of systemic disorders. Parkinson's disease is a prevalent neurodegenerative disease in which inflammation plays an important role for its progression. A vast number of studies suggest that there is a potential connection between chronic periodontitis and neurodegenerative diseases such as Parkinson's disease. Individuals with Parkinson's disease usually have poor periodontal health, and their oral flora composition differs from that of healthy people; at the same time, patients with chronic periodontitis have a higher risk of Parkinson's disease, which can be reduced with regular periodontal treatment. In fact, the mechanism of interaction between chronic periodontitis and Parkinson's disease is not clear. According to several studies, the clinical symptoms of Parkinson's disease prevent patients to maintain oral hygiene effectively, increasing the risk of periodontitis. Neuroinflammation mediated by microglia may be the key to the influence of chronic periodontitis on Parkinson's disease. Periodontal pathogens and inflammatory mediators may enter the brain and activate microglia in various ways, and ultimately leading to occurrence and development of Parkinson's disease. This article reviews the recent research progress on the association between chronic periodontitis and Parkinson's disease, and its potential mechanism to provide information for further research.
Topics: Chronic Periodontitis; Humans; Inflammation; Microglia; Neurodegenerative Diseases; Parkinson Disease
PubMed: 35462470
DOI: 10.3724/zdxbyxb-2021-0111 -
BMC Medicine Nov 2013The possible relationship between chronic inflammatory diseases and their co-morbidities has become an increasing focus of research. Both chronic periodontitis and... (Review)
Review
BACKGROUND
The possible relationship between chronic inflammatory diseases and their co-morbidities has become an increasing focus of research. Both chronic periodontitis and chronic obstructive pulmonary disease are neutrophilic, inflammatory conditions characterized by the loss of local connective tissue. Evidence suggests an association and perhaps a causal link between the two diseases. However, the nature of any relationship between them is unclear, but if pathophysiologically established may have wide-reaching implications for targeted treatments to improve outcomes and prognosis.
DISCUSSION
There have been a number of epidemiological studies undertaken demonstrating an independent association between chronic periodontitis and chronic obstructive pulmonary disease. However, many of them have significant limitations, and drawing firm conclusions regarding causality may be premature. Although the pathology of both these diseases is complex and involves many cell types, such as CD8 positive cells and macrophages, both conditions are predominantly characterized by neutrophilic inflammation. Increasingly, there is evidence that the two conditions are underpinned by similar pathophysiological processes, especially centered on the functions of the neutrophil. These include a disturbance in protease/anti-protease and redox state balance. The association demonstrated by epidemiological studies, as well as emerging similarities in pathogenesis at the level of the neutrophil, suggest a basis for testing the effects of treatment for one condition upon the severity of the other.
SUMMARY
Although the evidence of an independent association between chronic periodontitis and chronic obstructive pulmonary disease grows stronger, there remains a lack of definitive studies designed to establish causality and treatment effects. There is a need for future research to be focused on answering these questions.
Topics: Animals; Chronic Periodontitis; Humans; Neutrophils; Pulmonary Disease, Chronic Obstructive
PubMed: 24229090
DOI: 10.1186/1741-7015-11-241 -
Disease Markers 2016To investigate the cytokine profile as biomarkers in the gingival crevicular fluid (GCF) of chronic periodontitis (CP) patients with and without obesity, MEDLINE/PubMed,... (Comparative Study)
Comparative Study Meta-Analysis Review
To investigate the cytokine profile as biomarkers in the gingival crevicular fluid (GCF) of chronic periodontitis (CP) patients with and without obesity, MEDLINE/PubMed, EMBASE, ScienceDirect, and SCOPUS databases were combined with handsearching of articles published from 1977 up to May 2016 using relevant MeSH terms. Meta-analyses were conducted separately for each of the cytokines: resistin, adiponectin, TNF-, leptin, IL-6, IL-8, and IL-1. Forest plots were produced reporting standardized mean difference of outcomes and 95% confidence intervals. Eleven studies were included. Three studies showed comparable levels of leptin among obese and nonobese patients with CP. Four studies reported comparable levels of interleukin- (IL-) 6 and resistin whereas five studies reported comparable levels of adiponectin. Two studies reported similar levels of CRP in patients with periodontitis with and without obesity. One study showed higher levels of tumor necrosis factor-alpha in obese patients with CP. One study showed higher levels of IL-1 and IL-8 in obese patients with CP. The level of localized periodontal inflammation may have a greater influence on the GCF proinflammatory biomarker levels as compared to systemic obesity. Whether patients having chronic periodontitis with obesity have elevated proinflammatory GCF biomarkers levels compared to nonobese individuals remains debatable.
Topics: Biomarkers; Chronic Periodontitis; Cytokines; Humans; Obesity
PubMed: 27795608
DOI: 10.1155/2016/4801418 -
Clinical and Experimental Dental... Dec 2022To assess the Candida species occurrence rate and concentration in periodontal pockets in chronic periodontitis (CP) by meta-analysis. (Meta-Analysis)
Meta-Analysis Review
OBJECTIVES
To assess the Candida species occurrence rate and concentration in periodontal pockets in chronic periodontitis (CP) by meta-analysis.
MATERIALS AND METHODS
A search was performed of articles published between January 1, 2010, and October 1, 2020, in English and in Russian, in the electronic databases MEDLINE-PubMed, Google Scholar, The Cochrane Library, ClinicalTrials.gov, Research Gate, eLIBRARY, and Cyberleninka (PROSPEROCRD42021234831). The odds ratio (OR), standardized mean difference (SMD), and 95% confidence interval (CI) were calculated using Review Manager 5.4.1 to compare the risk of CP when Candida spp. were detected in the gingival sulcus or periodontal pocket and to compare Candida spp. density counts in patients with CP and periodontally healthy patients.
RESULTS
Twenty-six studies were included in the systematic review and 11 were included in the meta-analysis. The results showed that Candida spp. may increase the chance of CP development by 1.76 times (OR = 1.76; 95% CI = 1.04-2.99; Z = 2.10; p = .04; I = 61%). More Candida spp. were found in patients with CP than in periodontally healthy patients (SMD = 1.58; 95% CI = 0.15-3.02; p = .03; I = 98%). No data were found relating to the statistically significant influence of Candida glabrata, Candida krusei and Candida tropicalis on CP development.
CONCLUSION
We found that Candida albicans insignificantly increased the risk of CP development but, due to the heterogeneity of the included studies, further research is necessary to determine the exact role of Candida spp. in the development and course of the inflammatory periodontal diseases.
Topics: Humans; Chronic Periodontitis; Candida; Periodontal Pocket; Candida albicans; Gingiva
PubMed: 35903878
DOI: 10.1002/cre2.635