Periodontal Microbiota Research Articles

Abstract P342: Periodontal Bacteria, Prevalent Prediabetes and Plasma Glucose Progression: The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS)

Introduction: Periodontal infections have been hypothesized as a cardiometabolic risk factor. The relationship between periodontal microbiota and early diabetes risk has not been studied. Hypothesis: We hypothesized that periodontopathic bacteria would be associated with both prevalent pre diabetes and accelerated longitudinal plasma glucose progression among diabetes-free adults. Methods: The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS) enrolled 300 diabetes-free adults (77% female) aged 20-55 years (mean=34±10). Prevalent prediabetes was defined as: i) 5.6%<HbA1C<6.5%; or ii) 99 mg/dL<fasting plasma glucose (FPG)<126 mg/dL. In 1,188 subgingival plaque samples, 11 bacterial species including Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Treponema denticola (Td), Tannerella forsythia (Tf) and Actinomyces naeslundii (An) were assessed at baseline. Modified Poisson regression evaluated prediabetes prevalence across bacterial tertiles. Risk ratios (RR), 95% confidence intervals (CI) for 3rd vs. 1st tertile are presented. Follow-up is ongoing but longitudinal FPG was available for interim analysis among the first n=100 recall-eligible participants (mean follow-up time=2±0.3 years). Mixed-effects regressions evaluated FPG time trends across baseline bacterial levels. All analyses were adjusted for cardiometabolic risk factors. Results: Prediabetes prevalence was 18% (54 of 300). RRs(95%CI) summarizing associations between bacteria and pre diabetes were as follows: Aa=2.48[1.34,4.58], p=0.004; Pg=3.41[1.78,6.58], p=0.0003; Td=1.99[0.992,4.00], p=0.052 and Tf=1.95[1.0,3.84], p=0.05; An=0.46[0.25,0.85], p=0.01. Among participants with high baseline values of Pg or Tf, FPG increased by ~2.5 mg/dl during follow-up (all p-values<0.05) while no FPG progression was observed among participants with low baseline bacterial levels. Conclusion: Periodontopathic microbiota are associated with both prevalent prediabetes and longitudinal plasma glucose increase among diabetes-free adults.

Subgingival microbiota in health compared to periodontitis and the influence of smoking.

The etiology of periodontitis has traditionally been associated to a consortium of three bacterial species—the so-called “red-complex” of periodontal disease—which has been the target for most diagnostic and therapeutic strategies. However, other species have also been found to correlate with disease severity. In addition, the influence of smoking on periodontal microbiota is poorly understood. In the current manuscript, the composition of the subgingival microbiota in healthy individuals vs. patients with chronic periodontitis has been investigated using 16S pyrosequencing and the influence of smoking on periodontal composition has been examined. Subgingival bacterial communities were sampled from 82 patients: 22 non-smoking healthy controls, 28 non-smoking periodontal patients, and 32 smoking periodontal patients. Bacterial diversity was higher in periodontal patients than in healthy subjects, which could be interpreted as the consequence of a nutritionally richer environment or a reduced immune competence. Periodontal patients showed a significantly higher prevalence/relative abundance of “established” periopathogens but also other taxa whose role is not well-established and that should be targets for future research. These include Anaeroglobus, Bulleidia, Desulfobulbus, Filifactor, Mogibacterium, Phocaeicola, Schwartzia or TM7. The microbial community of smoking-associated periodontitis is less diverse and distinct from that of non-smokers, indicating that smoking has an influence on periodontal ecology. Interestingly, the high sequencing coverage allowed the detection at low proportions of periodontal pathogens in all healthy individuals, indicating that chronic periodontitis cannot be strictly considered an infectious disease but the outcome of a polymicrobial dysbiosis, where changes in the proportions of microbial consortia trigger the inflammatory and tissue-degradation responses of the host.

Comparison of serum amyloid A protein and C-reactive protein levels as inflammatory markers in periodontitis.

The purpose of this study was to compare serum amyloid A (SAA) protein levels with high-sensitive C-reactive protein (hs-CRP) levels as markers of systemic inflammation in patients with chronic periodontitis. The association of serum titers of antibodies to periodontal microbiota and SAA/hs-CRP levels in periodontitis patients was also studied. A total of 110 individuals were included in this study. Patients were assessed for levels of hs-CRP and SAA. Nonfasting blood samples were collected from participants at the time of clinical examination. The diagnosis of adipose tissue disorders was made according to previously defined criteria. To determine SAA levels, a sandwich enzyme-linked immunosorbent assay was utilized. Paper points were transferred to a sterile tube to obtain a pool of samples for polymerase chain reaction processing and the identification of Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Tannerella forsythia. The serum level of IgG1 and IgG2 antibodies to P. gingivalis, A. actinomycetemcomitans, and T. forsythia was also determined. SAA and hs-CRP levels were higher in periodontitis patients than in controls (P<0.05). In bivariate analysis, high levels of hs-CRP (>3 mg/L) and SAA (>10 mg/L) were significantly associated with chronic periodontitis (P=0.004). The Spearman correlation analysis between acute-phase proteins showed that SAA positively correlated with hs-CRP (r=0.218, P=0.02). In the adjusted model, chronic periodontitis was associated with high levels of SAA (odds ratio [OR], 5.5; 95% confidence interval [CI], 1.6-18.2; P=0.005) and elevated hs-CRP levels (OR, 6.1, 95% CI, 1.6-23.6; P=0.008). Increased levels of serum IgG2 antibodies to P. gingivalis were associated with high levels of SAA (OR, 3.6; 95% CI, 1.4-8.5; P=0.005) and high concentrations of hs-CRP (OR, 4.3; 95% CI, 1.9-9.8; P<0.001). SAA and hs-CRP concentrations in patients with chronic periodontitis are comparably elevated. High serum titers of antibodies to P. gingivalis and the presence of periodontal disease are independently related to high SAA and hs-CRP levels.

Serum IgG antibody levels to periodontal microbiota are associated with incident Alzheimer disease.

BackgroundPeriodontitis and Alzheimer disease (AD) are associated with systemic inflammation. This research studied serum IgG to periodontal microbiota as possible predictors of incident AD.MethodsUsing a case-cohort study design, 219 subjects (110 incident AD cases and 109 controls without incident cognitive impairment at last follow-up), matched on race-ethnicity, were drawn from the Washington Heights-Inwood Columbia Aging Project (WHICAP), a cohort of longitudinally followed northern Manhattan residents aged >65 years. Mean follow-up was five years (SD 2.6). In baseline sera, serum IgG levels were determined for bacteria known to be positively or negatively associated with periodontitis (Porphyromonas gingivalis, Tannerella forsythia, Actinobacillus actinomycetemcomitans Y4, Treponema denticola, Campylobacter rectus, Eubacterium nodatum, and Actinomyces naeslundii genospecies-2). In all analyses, we used antibody threshold levels shown to correlate with presence of moderate-severe periodontitis.ResultsMean age was 72 years (SD 6.9) for controls, and 79 years (SD 4.6) for cases (p<0.001). Non-Hispanic Whites comprised 26%, non-Hispanic Blacks 27%, and Hispanics 48% of the sample. In a model adjusting for baseline age, sex, education, diabetes mellitus, hypertension, smoking, prior history of stroke, and apolipoprotein E genotype, high anti-A. naeslundii titer (>640 ng/ml, present in 10% of subjects) was associated with increased risk of AD (HR = 2.0, 95%CI: 1.1–3.8). This association was stronger after adjusting for other significant titers (HR = 3.1, 95%CI: 1.5–6.4). In this model, high anti-E. nodatum IgG (>1755 ng/ml; 19% of subjects) was associated with lower risk of AD (HR = 0.5, 95%CI: 0.2–0.9).ConclusionsSerum IgG levels to common periodontal microbiota are associated with risk for developing incident AD.

Periodontal and peri-implant microbiota in patients with healthy and inflamed periodontal and peri-implant tissues.

To compare the prevalence and levels of six bacterial pathogens within the subgingival/submucosal microbiota at teeth versus implants with various clinical conditions. Twenty-two Chinese were included. Four subgingival/submucosal sites were selected for microbiological sampling within each subject, that is, (1) healthy peri-implant tissues; (2) peri-implantitis [PPD ≥ 5mm, presence of bleeding on probing (BOP) and confirmed radiographic bone loss]; (3) healthy gingiva; and (4) periodontitis (PPD ≥4mm). Subgingival/submucosal plaque was sampled using paper points. Quantitative real-time polymerase chain reaction (q-PCR) was used to quantify six pathogens, including Porphyromonas gingivalis (P.g.), Treponema denticola (T.d.), Aggregatibacter actinomycetemcomitans (A.a.), Fusobacterium nucleatum (F.n.), Prevotella intermedia (P.i.), and Staphylococcus aureus (S.a.). Counts were log10-transformed. The most commonly detected species were S. a. and F. n., while A. a. and. P.i. had the lowest detection frequency. The detection frequencies of diseased tooth or implant sites for each of the six target species were either equal to or higher than the respective frequencies at the corresponding healthy sites. There were no statistically significant differences for any of the species or clinical sites (P>0.05, Cochran's Q test). No statistically significant differences in the bacterial loads were found among the four clinical sites; with the exception of F.nucleatum. This was more abundant in periodontitis sites (P=0.023, Friedman's 2-way anova). Both periodontal and peri-implant sites, irrespective of their health status, were revealed to harbor S.aureus cells. The log10-transformed loads of S.aureus were approximately 3.5 within each of the clinical sites (P=0.232). This was the highest of the six species analyzed. Within the same subjects, putative periodontal pathogens were common to both periodontal and peri-implant sites irrespective of health status. The prevalence and levels of P.gingivalis and F.nucleatum were significantly associated with periodontitis, but not with peri-implantitis. A.actinomycetemcomitans was associated with both disease conditions, periodontitis and peri-implantitis, but not with either gingival or mucosal health.

Periodontal disease and subgingival microbiota as contributors for rheumatoid arthritis pathogenesis: modifiable risk factors?

Since the early 1900s, the role of periodontal disease in the pathogenesis of rheumatoid arthritis has been a matter of intense research. The last decade has witnessed many advances supporting a link between periodontitis, the presence of specific bacterial species (i.e. Porphyromonas gingivalis) and their effects in immune response. This review will examine available evidence on the individuals. Epidemiological studies have stressed the commonalities shared by periodontal disease and rheumatoid arthritis. Many groups have focused their attention toward understanding the periodontal microbiota and its alterations in states of health and disease. The presence of circulating antibodies against periodontopathic bacteria and associated inflammatory response has been found in both rheumatoid arthritis (RA) patients and individuals at-risk for disease development. Most recently, the periodontal microbiota of smokers and patients with RA has been elucidated, revealing profound changes in the bacterial communities compared with those of healthy controls. This has led to several small clinical trials of progressive disease treatment as adjuvant for disease-modifying therapy in RA. Smoking and periodontal disease are emerging risk factors for the development of RA. Epidemiological, clinical, and basic research has further strengthened this association, pointing toward changes in the oral microbiota as possible contributors to systemic inflammation and arthritis.

Gingival Tissue Transcriptomes Identify Distinct Periodontitis Phenotypes

The currently recognized principal forms of periodontitis—chronic and aggressive—lack an unequivocal, pathobiology-based foundation. We explored whether gingival tissue transcriptomes can serve as the basis for an alternative classification of periodontitis. We used cross-sectional whole-genome gene expression data from 241 gingival tissue biopsies obtained from sites with periodontal pathology in 120 systemically healthy nonsmokers with periodontitis, with available data on clinical periodontal status, subgingival microbial profiles, and serum IgG antibodies to periodontal microbiota. Adjusted model-based clustering of transcriptomic data using finite mixtures generated two distinct clusters of patients that did not align with the current classification of chronic and aggressive periodontitis. Differential expression profiles primarily related to cell proliferation in cluster 1 and to lymphocyte activation and unfolded protein responses in cluster 2. Patients in the two clusters did not differ with respect to age but presented with distinct phenotypes (statistically significantly different whole-mouth clinical measures of extent/severity, subgingival microbial burden by several species, and selected serum antibody responses). Patients in cluster 2 showed more extensive/severe disease and were more often male. The findings suggest that distinct gene expression signatures in pathologic gingival tissues translate into phenotypic differences and can provide a basis for a novel classification.

Topical treatment with probiotic Lactobacillus brevis CD2 inhibits experimental periodontal inflammation and bone loss

An increasing body of evidence suggests that the use of probiotic bacteria is a promising intervention approach for the treatment of inflammatory diseases with a polymicrobial etiology. The objective of this study was to determine whether Lactobacillus brevis CD2 could inhibit periodontal inflammation and bone loss in experimental periodontitis. Periodontitis was induced by placing a silk ligature around the second maxillary molar of mice treated with L.brevis CD2 (8×10(5) CFU in 1mm(2) lyopatch) or placebo, which were placed between the gingiva and the buccal mucosa near the ligated teeth. The mice were killed after 5d and bone loss was measured morphometrically, gingival expression of proinflammatory cytokines was determined by quantitative real-time polymerase chain reaction, and CFU counts of periodontitis-associated bacteria were determined after aerobic and anaerobic culture. To determine the role of arginine deiminase released by L.brevis CD2, soluble extracts with or without formamidine (arginine deiminase inhibitor) were tested in in vitro cellular activation assays. Mice topically treated with L.brevis CD2 displayed significantly decreased bone loss and lower expression of tumor necrosis factor, and interleukin-1β, -6 and -17A as compared to placebo-treated mice. Moreover, L.brevis CD2-treated mice displayed lower counts of anaerobic bacteria but higher counts of aerobic bacteria than placebo-treated mice. In in vitro assays, the anti-inflammatory effects of soluble L.brevis CD2 extracts were heavily dependent on the presence of functional arginine deiminase, an enzyme that can inhibit nitric oxide synthesis. These data provide proof-of-concept that the probiotic L.brevis CD2 can inhibit periodontitis through modulatory effects on the host response and the periodontal microbiota.

Identification of key markers of normal and pathogenic microbiota determining health of periodontium by NGS-sequencing 16S-rDNA libraries of periodontal swabs

By using NGS-sequencing libraries of DNA from periodontal swabs with primers specific to V6 region of 16S rDNA prevalence of bacterial genera and species in periodontal microbiota of patients with aggressive periodontitis and healthy donors was analyzed. Six genera of putative periodontal protectors and eight periodontal pathogens were identified with respect to aggressive (but not chronic) periodontitis. Statistically relevant over-colonization by general Porphyromonas, Treponema, Synergistes, Tannerella, Filifactor, Ruminococcus, Parvimonas and Mycoplasma was found to be associated with the condition. From these, only three genera Porphyromonas, Treponema and Tannerella are traditionally considered as periodontal pathogens. Statistically confidential over-colonization by genus Veillonella was found in healthy patients. This genus should be considered as a relevant marker of a healthy periodontium. Genera Streptococcus, Bergeyella, Granulicatella, Kingella and Corynebacterium may be considered as putative periodontal protectors. Comparison of data of NGS-sequencing and real-time PCR demonstrated a good agreement if different PCR efficiency using independent primer pairs is taken into account.

Metagenomics: A New Realm of Uncultured Periodontal Microbes

With over 400 bacterial species the periodontal microbiota has clearly a diverse ecology and uncultivated organisms are found to be associated with the periodontal diseases. Many efforts have been made to determine why so many bacterial species cannot be cultured on conventional bacteriological media and to develop new cultural methods for their isolation. In recent years, metagenomic analysis is available, based on the direct examination of nucleic acids from samples.This review will address the new dimensions of this novel procedure which will lead to a better understanding of the role of oral microbiota in periodontal disease. DOI: http://dx.doi.org/10.3329/bjdre.v3i2.16611 Bangladesh Journal of Dental Research &amp; Education Vol.3(2) 2013: 36-40

Lessons learned and unlearned in periodontal microbiology

Periodontal diseases are initiated by bacterial species living in polymicrobial biofilms at or below the gingival margin and progress largely as a result of the inflammation elicited by specific subgingival species. In the past few decades, efforts to understand the periodontal microbiota have led to an exponential increase in information about biofilms associated with periodontal health and disease. In fact, the oral microbiota is one of the best‐characterized microbiomes that colonize the human body. Despite this increased knowledge, one has to ask if our fundamental concepts of the etiology and pathogenesis of periodontal diseases have really changed. In this article we will review how our comprehension of the structure and function of the subgingival microbiota has evolved over the years in search of lessons learned and unlearned in periodontal microbiology. More specifically, this review focuses on: (i) how the data obtained through molecular techniques have impacted our knowledge of the etiology of periodontal infections; (ii) the potential role of viruses in the etiopathogenesis of periodontal diseases; (iii) how concepts of microbial ecology have expanded our understanding of host–microbe interactions that might lead to periodontal diseases; (iv) the role of inflammation in the pathogenesis of periodontal diseases; and (v) the impact of these evolving concepts on therapeutic and preventive strategies to periodontal infections. We will conclude by reviewing how novel systems‐biology approaches promise to unravel new details of the pathogenesis of periodontal diseases and hopefully lead to a better understanding of their mechanisms.

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

To review the evidence for the molecular and cellular processes that may potentially link periodontal disease and diabetes. The pathogenic roles of cytokines and metabolic molecules (e.g. glucose, lipids) are explored and the role of periodontal bacteria is also addressed. Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered. Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review. Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small-scale clinical studies and experiments in animal models suggest that IL-1b, TNF-a, IL-6, OPG and RANKL may mediate periodontitis in diabetes. The AGE-RAGE axis is likely an important pathway of tissue destruction and impaired repair in diabetes-associated periodontitis. A role for locally activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative. There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells/tissues in vitro.

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

To review the evidence for the molecular and cellular processes that may potentially link periodontal disease and diabetes. The pathogenic roles of cytokines and metabolic molecules (e.g. glucose, lipids) are explored and the role of periodontal bacteria is also addressed. Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered. Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review. Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small-scale clinical studies and experiments in animal models suggest that IL-1β, TNF-α, IL-6, OPG and RANKL may mediate periodontitis in diabetes. The AGE-RAGE axis is likely an important pathway of tissue destruction and impaired repair in diabetes-associated periodontitis. A role for locally activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative. There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells/tissues in vitro.

High-Fat Diet Induces Periodontitis in Mice through Lipopolysaccharides (LPS) Receptor Signaling: Protective Action of Estrogens

BackgroundA fat-enriched diet favors the development of gram negative bacteria in the intestine which is linked to the occurrence of type 2 diabetes (T2D). Interestingly, some pathogenic gram negative bacteria are commonly associated with the development of periodontitis which, like T2D, is characterized by a chronic low-grade inflammation. Moreover, estrogens have been shown to regulate glucose homeostasis via an LPS receptor dependent immune-modulation. In this study, we evaluated whether diet-induced metabolic disease would favor the development of periodontitis in mice. In addition, the regulatory role of estrogens in this process was assessed.MethodsFour-week-old C57BL6/J WT and CD14 (part of the TLR-4 machinery for LPS-recognition) knock-out female mice were ovariectomised and subcutaneously implanted with pellets releasing either placebo or 17β-estradiol (E2). Mice were then fed with either a normal chow or a high-fat diet for four weeks. The development of diabetes was monitored by an intraperitoneal glucose-tolerance test and plasma insulin concentration while periodontitis was assessed by identification of pathogens, quantification of periodontal soft tissue inflammation and alveolar bone loss.ResultsThe fat-enriched diet increased the prevalence of periodontal pathogenic microbiota like Fusobacterium nucleatum and Prevotella intermedia, gingival inflammation and alveolar bone loss. E2 treatment prevented this effect and CD14 knock-out mice resisted high-fat diet-induced periodontal defects.Conclusions/SignificanceOur data show that mice fed with a diabetogenic diet developed defects and microflora of tooth supporting-tissues typically associated with periodontitis. Moreover, our results suggest a causal link between the activation of the LPS pathway on innate immunity by periodontal microbiota and HFD-induced periodontitis, a pathophysiological mechanism that could be targeted by estrogens.

Subgingival biodiversity in subjects with uncontrolled type‐2 diabetes and chronic periodontitis

There is a bidirectional relationship between periodontal disease and type-2 diabetes mellitus (DM). Inflammatory mediators may negatively affect glycemic control, and increased glucose levels and resultant glycation end-products may alter the host response against bacterial infection. However, no agreement has been reached regarding the effect of DM on periodontal subgingival microbiota. Therefore, the purpose of the present study was to compare the subgingival biodiversity in deep periodontal pockets of subjects with chronic periodontitis and either uncontrolled type-2 diabetes or no diabetes using 16S rRNA gene cloning and sequencing. Twelve subjects with uncontrolled type-2 diabetes (glycated hemoglobin > 8%) and eleven nondiabetic subjects presenting severe and generalized chronic periodontitis were selected. Subgingival biofilm from periodontal pockets > 5 mm were assessed using the 16S rRNA gene cloning and sequencing technique. Significant differences were observed in subgingival microbiota between diabetic and nondiabetic subjects. Diabetic subjects presented higher percentages of total clones of TM7, Aggregatibacter, Neisseria, Gemella, Eikenella, Selenomonas, Actinomyces, Capnocytophaga, Fusobacterium, Veillonella and Streptococcus genera, and lower percentages of Porphyromonas, Filifactor, Eubacterium, Synergistetes, Tannerella and Treponema genera than nondiabetic individuals (p < 0.05). Moreover, some phylotypes, such as Fusobacterium nucleatum, Veillonella parvula, V. dispar and Eikenella corrodens were detected significantly more often in diabetic subjects than in nondiabetic subjects (p < 0.05). Subjects with uncontrolled type-2 diabetes and chronic periodontitis presented significant dissimilarities in subgingival biodiversity compared with nondiabetic subjects.

Efecto del tratamiento periodontal sobre la microbiota subgingival en pacientes con preeclampsia

Introduction. Few studies have described subgingival microbiota in pregnant women with mild preeclampsia.Objective. Clinical periodontal and subgingival microbiota changes were identified in pregnant women with mild preeclampsia after periodontal treatment.Materials and methods. In a secondary analysis of a randomized clinical trial, 57 preeclamptic women were studied at Hospital Universitario del Valle in Cali, Colombia. Thirty one women were randomized to the periodontal intervention group (subgingival scaling and planing ultrasonic and manual) during pregnancy and 26 to the control group (supragingival prophylaxis). Periodontal clinical parameters and subgingival microbiota were characterized at the time of acceptance into the study and again atpostpartum. Eight periodontopathic bacteria and 2 herpesviruses were assessed by polymerase chain reaction. Chi-square, McNemar or Student’s t tests were used, with a significance level of p≤0.05.Results. Both groups were comparable in the clinical and microbiological variables at baseline. Periodontal treatment reduced the average pocket depth in the intervention group from 2.4±0.3 to 2.3±0.2 mm (p&lt;0.001) and in control group 2.6±0.4 to 2.44±0.4 mm, (p&lt;0.001) and bleeding index 16.4±1.5% to 7.9±0.7% in the intervention group(p&lt;0.001) and 17.1±1.8% to 10±0.9% in the control group (p=0.002). The frequency of detection of microorganisms did not differ significantly between groups.Conclusion. Scaling/root planning and supragingival prophylaxis significantly reduced the probing depth and gingival bleeding index. Periodontal treatment was not more effective than prophylaxis in reducing periodontopathic organisms or herpesvirus.

Comprehensive Periodontal Therapy: A Statement by the American Academy of Periodontology

Comprehensive Periodontal Therapy: A Statement by the American Academy of Periodontology

Diabetes mellitus and periodontitis: a tale of two common interrelated diseases

Diabetes mellitus (a group of metabolic disorders characterized by hyperglycemia) and periodontitis (a microbially induced inflammatory disorder that affects the supporting structures of teeth) are both common, chronic conditions. Multiple studies have demonstrated that diabetes mellitus (type 1 and type 2) is an established risk factor for periodontitis. Findings from mechanistic studies indicate that diabetes mellitus leads to a hyperinflammatory response to the periodontal microbiota and also impairs resolution of inflammation and repair, which leads to accelerated periodontal destruction. The cell surface receptor for advanced glycation end products and its ligands are expressed in the periodontium of individuals with diabetes mellitus and seem to mediate these processes. The association between the two diseases is bidirectional, as periodontitis has been reported to adversely affect glycemic control in patients with diabetes mellitus and to contribute to the development of diabetic complications. In addition, meta-analyses conclude that periodontal therapy in individuals with diabetes mellitus can result in a modest improvement of glycemic control. The effect of periodontal infections on diabetes mellitus is potentially explained by the resulting increase in levels of systemic proinflammatory mediators, which exacerbates insulin resistance. As our understanding of the relationship between diabetes mellitus and periodontitis deepens, increased patient awareness of the link between diabetes mellitus and oral health and collaboration among medical and dental professionals for the management of affected individuals become increasingly important.

What do ’omic technologies have to offer periodontal clinical practice in the future?

Periodontal diseases are the most common chronic inflammatory diseases of humans and a major cause of tooth loss. Inflammatory periodontitis is also a complex multifactorial disease involving many cell types, cell products and interactions. It is associated with a dysregulated inflammatory response, which fails to resolve, and which also fails to re-establish a beneficial periodontal microbiota. There is a rich history of biomarker research within the field of periodontology, but exemplary improvements in analytical platform technologies offer exciting opportunities for discovery. These include the 'omic technologies, such as genomics, transcriptomics, proteomics and metabolomics, which provide information on global scales that can match the complexity of the disease. This narrative review focuses on the recent advances made in in vivo human periodontal research by use of 'omic technologies. The Medline database was searched to identify articles currently available on 'omic technologies with regard to periodontal research. One hundred and sixty-one articles focusing on biomarkers of and 'omic advances in periodontal research were analysed for their contributions to the understanding of periodontal diseases. The data generated by the use of 'omic technologies have huge potential to inform paradigm shifts in our understanding of periodontal diseases, but data management, analysis and interpretation require a thoughtful and systematic bioinformatics approach, to ensure meaningful conclusions can be made.

Association of red complex, A. actinomycetemcomitans and non-oral bacteria with periodontal diseases

ObjectivePathogens related to systemic infections have been detected in the periodontal microbiota. The relationship amongst these pathogens, periodontal bacteria and periodontal clinical status is poorly understood. This study evaluated the association amongst red complex, A. actinomycetemcomitans (A.a) and non-oral pathogenic bacteria in subjects with good periodontal health (PH), gingivitis (G), chronic (CP) and aggressive (AP) periodontitis. MethodsSubgingival biofilm samples were obtained from 51 PH, 42 G, 219 CP and 90 AP subjects. The presence and levels of A.a, red complex (Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola), Acinetobacter baumannii, Escherichia coli, Enterococcus faecalis, Pseudomonas aeruginosa, and Staphylococcus aureus were determined by DNA probes and DNA–DNA hybridization technique. ResultsCP and AP subjects presented significantly higher prevalence and levels of A.a, red complex and A. baumannii than G and PH individuals (p<0.01), whereas S. aureus was detected in lower frequency and counts in AP as compared to the other groups (p<0.001). The predictor variables age, prevalence of red complex, and the presence of A. baumannii and P. aeruginosa were strongly associated with the frequency of sites with PD and CAL ≥5mm. Increasing age (OR 1.08), high frequency of red complex (OR 6.10), and the presence of A.a with P. aeruginosa (OR 1.90) were associated with periodontal disease (p<0.001). Subjects harbouring a high prevalence of A.a, A. baumannii, and red complex with P. aeruginosa were more likely to have AP than CP (p<0.001). ConclusionPutative periodontal pathogens and non-oral bacteria alone or in association were strongly associated with periodontitis.