Aim
Statins are inhibitors of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase and are an important group of hypolipidaemic drugs, widely used in the treatment of hypercholesterolaemia and ...cardiovascular disease. Some studies have shown that statins are able to modulate inflammation and alveolar bone loss.
Methods
In order to evaluate whether statins could influence periodontal treatment, improving the clinical and radiographic parameters in chronic periodontitis, a systematic review was conducted in the databases PUBMED and BIREME, searching for articles in English and Portuguese, published between the years 2004 and 2014, using the combined keywords statin, periodontal disease, periodontitis and alveolar bone. Studies regarding the treatment of chronic periodontitis in humans, blind or double‐blind, retrospective cohort or randomized controlled trials that used statins topically or systemically were selected.
Results
Statins have important anti‐inflammatory and immune effects, reducing levels of C‐reactive protein and matrix metalloproteinases and their intermediate products, such as tumour necrosis factor‐α, and are also able to inhibit the adhesion and extravasation of leukocytes, which block the co‐stimulation of T cells. Statins reduce bone resorption by inhibiting osteoclast formation and lead to increased apoptosis of these cells. The effect of statins on bone formation is related to the increased gene expression of bone morphogenetic protein in osteoblasts.
Conclusion
Although we found biological mechanisms and clinical results that show lower alveolar bone loss and reduction of clinical signs of inflammation, further studies are needed to evaluate the clinical applicability of statins in the routine treatment of chronic periodontitis.
The aim of this article is to survey the accessible writing on the pathogenetic systems engaged with the relationship between oral malignancy and periodontitis. Gingival tissue contains multiple ...microbiota, which can induce inflammatory reactions. This reaction plays a crucial role in assessing the susceptibility of patients to periodontal diseases. The link between chronic periodontitis and the risk of malignancy through this inflammation of the affected epithelium have been studied thoroughly. Many studies have reported that, chronic periodontitis has systemic influence which has high risk of developing different types of cancers. Also, various confounding factors such as consumption of alcohol, smoking, diet, age and gender have been found to be associated with both chronic periodontitis and oral cancer. An online quest for a wide range of articles distributed was started utilizing MEDLINE/PubMed, with the keywords, for example, 'oral squamous cell carcinoma (OSCC)', 'oral microbiota,' 'microorganisms and malignancy and Porphyromonas gingivalis. This review aimed to study the current literature linking chronic periodontitis and oral cancer.
Background
There may be an association between periodontitis and cardiovascular disease (CVD); however, the evidence so far has been uncertain about whether periodontal therapy can help prevent CVD ...in people diagnosed with chronic periodontitis. This is the second update of a review originally published in 2014, and first updated in 2017. Although there is a new multidimensional staging and grading system for periodontitis, we have retained the label 'chronic periodontitis' in this version of the review since available studies are based on the previous classification system.
Objectives
To investigate the effects of periodontal therapy for primary or secondary prevention of CVD in people with chronic periodontitis.
Search methods
Cochrane Oral Health's Information Specialist searched the Cochrane Oral Health's Trials Register, CENTRAL, MEDLINE, Embase, and CINAHL, two trials registries, and the grey literature to September 2019. We placed no restrictions on the language or date of publication.
We also searched the Chinese BioMedical Literature Database, the China National Knowledge Infrastructure, the VIP database, and Sciencepaper Online to August 2019.
Selection criteria
We included randomised controlled trials (RCTs) that compared active periodontal therapy to no periodontal treatment or a different periodontal treatment. We included studies of participants with a diagnosis of chronic periodontitis, either with CVD (secondary prevention studies) or without CVD (primary prevention studies).
Data collection and analysis
Two review authors carried out the study identification, data extraction, and 'Risk of bias' assessment independently and in duplicate. They resolved any discrepancies by discussion, or with a third review author. We adopted a formal pilot‐tested data extraction form, and used the Cochrane tool to assess the risk of bias in the studies. We used GRADE criteria to assess the certainty of the evidence.
Main results
We included two RCTs in the review. One study focused on the primary prevention of CVD, and the other addressed secondary prevention. We evaluated both as being at high risk of bias. Our primary outcomes of interest were death (all‐cause and CVD‐related) and all cardiovascular events, measured at one‐year follow‐up or longer.
For primary prevention of CVD in participants with periodontitis and metabolic syndrome, one study (165 participants) provided very low‐certainty evidence. There was only one death in the study; we were unable to determine whether scaling and root planning plus amoxicillin and metronidazole could reduce incidence of all‐cause death (Peto odds ratio (OR) 7.48, 95% confidence interval (CI) 0.15 to 376.98), or all CVD‐related death (Peto OR 7.48, 95% CI 0.15 to 376.98). We could not exclude the possibility that scaling and root planning plus amoxicillin and metronidazole could increase cardiovascular events (Peto OR 7.77, 95% CI 1.07 to 56.1) compared with supragingival scaling measured at 12‐month follow‐up.
For secondary prevention of CVD, one pilot study randomised 303 participants to receive scaling and root planning plus oral hygiene instruction (periodontal treatment) or oral hygiene instruction plus a copy of radiographs and recommendation to follow‐up with a dentist (community care). As cardiovascular events had been measured for different time periods of between 6 and 25 months, and only 37 participants were available with at least one‐year follow‐up, we did not consider the data to be sufficiently robust for inclusion in this review. The study did not evaluate all‐cause death and all CVD‐related death. We are unable to draw any conclusions about the effects of periodontal therapy on secondary prevention of CVD.
Authors' conclusions
For primary prevention of cardiovascular disease (CVD) in people diagnosed with periodontitis and metabolic syndrome, very low‐certainty evidence was inconclusive about the effects of scaling and root planning plus antibiotics compared to supragingival scaling. There is no reliable evidence available regarding secondary prevention of CVD in people diagnosed with chronic periodontitis and CVD. Further trials are needed to reach conclusions about whether treatment for periodontal disease can help prevent occurrence or recurrence of CVD.
Periodontitis is a bacteria-related chronic immune-associated condition that destructs bone and connective tissues around teeth. With a high incidence rate, it is regarded as a condition that impose ...substantial health burden. About half of the variance in the severity of periodontitis is attributed to genetic factors. Long non-coding RNAs (lncRNAs) have crucial roles in the development of several disorders such as periodontitis. A number of studies have reported dysregulation of lncRNAs such as UCA1, ANRIL, FGD5-AS1, NEAT1, FAS-AS1, Linc-RAM and NKILA in gingival tissues or blood samples of patients with periodontitis in comparison with healthy subjects. Moreover, several single nucleotide polymorphisms within lncRNAs have been associated with the susceptibility to this disorder. In the current review, we discuss the most recent articles about the role of lncRNAs in the pathogenesis of periodontitis.
Periodontitis is a common infectious disease. Recent studies have indicated that the progression of periodontitis may be regulated by interactions between host immunity and periodontopathic bacteria. ...Although periodontopathic bacteria can destroy periodontal tissue, a dysfunctional host immune response triggered by the bacteria can lead to more severe and persistent destruction. Toll‐like receptors (TLRs), a type of pattern recognition receptor (PRR) that recognizes pathogens, have been implicated in host innate immune responses to periodontopathic bacteria and in the activation of adaptive immunity. TLR‐targeted drugs may hold promise to treat periodontal disease. This review summarizes recent studies on the role of TLRs in periodontitis and discusses areas needing further research. We believe TLRs may be an effective biomarker for the prevention, diagnosis, and treatment of periodontitis in the near future.
Periodontitis is an extremely prevalent disease worldwide and is driven by complex dysbiotic microbiota. Here we analyzed the transcriptional activity of the periodontal pocket microbiota from all ...domains of life as well as the human host in health and chronic periodontitis. Bacteria showed strong enrichment of 18 KEGG functional modules in chronic periodontitis, including bacterial chemotaxis, flagellar assembly, type III secretion system, type III CRISPR-Cas system, and two component system proteins. Upregulation of these functions was driven by the red-complex pathogens and candidate pathogens, e.g. Filifactor alocis, Prevotella intermedia, Fretibacterium fastidiosum and Selenomonas sputigena. Nine virulence factors were strongly up-regulated, among them the arginine deiminase arcA from Porphyromonas gingivalis and Mycoplasma arginini. Viruses and archaea accounted for about 0.1% and 0.22% of total putative mRNA reads, respectively, and a protozoan, Entamoeba gingivalis, was highly enriched in periodontitis. Fourteen human transcripts were enriched in periodontitis, including a gene for a ferric iron binding protein, indicating competition with the microbiota for iron, and genes associated with cancer, namely nucleolar phosphoprotein B23, ankyrin-repeat domain 30B-like protein and beta-enolase. The data provide evidence on the level of gene expression in vivo for the potentially severe impact of the dysbiotic microbiota on human health.
Chronic periodontitis (CP) and allergic rhinitis (AR) have attracted wide attention as global public health problems with high incidence. Recent studies have shown that circulating interleukin-27 ...(IL-27) is associated with the risk of CP and AR. The aim of this study is to analyze the causal effect between them using Mendelian randomization (MR).
Bidirectional MR analyses were performed with the use of publicly available genome-wide association study (GWAS) data. Summary data on circulating IL-27, CP, and AR published in genome-wide association studies were collected. Instrumental variables (IV) were extracted using assumptions of correlation, independence and exclusivity as criteria. Inverse variance weighting (IVW) was used as the main method, combined with weighted median method (WM) and MR-Egger and other MR Analysis methods for causal inference of exposure and outcome. Cochran's Q and MR-Egger intercept were used for sensitivity analysis.
The IVW study showed a causal effect between increased circulating IL-27 levels and increased risk of CP (OR = 1.14, 95%CI = 1.02-1.26,
= .020). Similarly, the increase of circulating IL-27 level had a causal effect on the decreased risk of AR (OR = 0.88, 95%CI = 0.80-0.97,
= .012). In addition, IVW study found that there was a causal between the increased risk of CP and circulating IL-27 level (OR = 1.05, 95%CI = 1.01-1.10,
= .016). However, there was no significant causal relationship between the risk of AR and circulating IL-27 levels (OR = 0.97, 95%CI = 0.91-1.02,
= .209). no significant heterogeneity or horizontal pleiotropy was found in sensitivity analysis.
There is a causal effect between circulating IL-27 level and CP, AR, which will help to find new ideas and methods for the diagnosis and treatment of CP and AR.
Previous studies have suggested that obesity might be associated with chronic periodontitis (CP); however, no clear conclusions have been reached so far. In this retrospective cohort study, we aimed ...to investigate the association between obesity and CP by using a large population-based dataset in Taiwan.A population-based retrospective cohort study was conducted using the Longitudinal Health Insurance Database 2010 (LHID2010) derived from the National Health Insurance Research database in Taiwan, from 2000 to 2013. Obesity and non-obesity groups were matched with sex, age, urbanization level, socioeconomic status, and the related comorbidities by using the propensity score method at a 1:2 ratio.An obese cohort (n = 4140) and a non-obese cohort (n = 8280) were included in this study, with an average age of 41.7 ± 13.8 years and 42.0 ± 14.0 years, respectively. The risk of CP for the patients with obesity was 1.12-fold compared with those without obesity (hazard ratio, 1.12; 95% confidence interval, 1.01-1.25). In the subgroup analysis according to age and sex, the hazard ratio of CP were 1.98 (95% confidence interval, 1.22-3.22) in the subgroup of age equal to or older than 65 years. The risk of CP showed no difference between obesity and non-obesity groups in both sex.This population-based cohort study demonstrated that obesity was associated with the development of CP in Taiwan.
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.
Genome-wide association studies (GWAS) of chronic periodontitis (CP) defined by clinical criteria alone have had modest success to-date. Here, we refine the CP phenotype by supplementing clinical ...data with biological intermediates of microbial burden (levels of eight periodontal pathogens) and local inflammatory response (gingival crevicular fluid IL-1β) and derive periodontal complex traits (PCTs) via principal component analysis. PCTs were carried forward to GWAS (∼2.5 million markers) to identify PCT-associated loci among 975 European American adult participants of the Dental ARIC study. We sought to validate these findings for CP in the larger ARIC cohort (n = 821 participants with severe CP, 2031-moderate CP, 1914-healthy/mild disease) and an independent German sample including 717 aggressive periodontitis cases and 4210 controls. We identified six PCTs with distinct microbial community/IL-1β structures, although with overlapping clinical presentations. PCT1 was characterized by a uniformly high pathogen load, whereas PCT3 and PCT5 were dominated by Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, respectively. We detected genome-wide significant signals for PCT1 (CLEC19A, TRA, GGTA2P, TM9SF2, IFI16, RBMS3), PCT4 (HPVC1) and PCT5 (SLC15A4, PKP2, SNRPN). Overall, the highlighted loci included genes associated with immune response and epithelial barrier function. With the exception of associations of BEGAIN with severe and UBE3D with moderate CP, no other loci were associated with CP in ARIC or aggressive periodontitis in the German sample. Although not associated with current clinically determined periodontal disease taxonomies, upon replication and mechanistic validation these candidate loci may highlight dysbiotic microbial community structures and altered inflammatory/immune responses underlying biological sub-types of CP.
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