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Background: A variety of systemic diseases and conditions can affect the course of periodontitis or have a negative impact on the periodontal attachment apparatus. Gingival recessions are highly prevalent and often associated with hypersensitivity, the development of caries and non‐carious cervical lesions on the exposed root surface and impaired esthetics. Occlusal forces can result in injury of teeth and periodontal attachment apparatus. Several developmental or acquired conditions associated with teeth or prostheses may predispose to diseases of the periodontium. The aim of this working group was to review and update the 1999 classification with regard to these diseases and conditions, and to develop case definitions and diagnostic considerations. Methods: Discussions were informed by four reviews on 1) periodontal manifestions of systemic diseases and conditions; 2) mucogingival conditions around natural teeth; 3) traumatic occlusal forces and occlusal trauma; and 4) dental prostheses and tooth related factors. This consensus report is based on the results of these reviews and on expert opinion of the participants. Results: Key findings included the following: 1) there are mainly rare systemic conditions (such as Papillon‐Lefevre Syndrome, leucocyte adhesion deficiency, and others) with a major effect on the course of periodontitis and more common conditions (such as diabetes mellitus) with variable effects, as well as conditions affecting the periodontal apparatus independently of dental plaque biofilm‐induced inflammation (such as neoplastic diseases); 2) diabetes‐associated periodontitis should not be regarded as a distinct diagnosis, but diabetes should be recognized as an important modifying factor and included in a clinical diagnosis of periodontitis as a descriptor; 3) likewise, tobacco smoking – now considered a dependence to nicotine and a chronic relapsing medical disorder with major adverse effects on the periodontal supporting tissues – is an important modifier to be included in a clinical diagnosis of periodontitis as a descriptor; 4) the importance of the gingival phenotype, encompassing gingival thickness and width in the context of mucogingival conditions, is recognized and a novel classification for gingival recessions is introduced; 5) there is no evidence that traumatic occlusal forces lead to periodontal attachment loss, non‐carious cervical lesions, or gingival recessions; 6) traumatic occlusal forces lead to adaptive mobility in teeth with normal support, whereas they lead to progressive mobility in teeth with reduced support, usually requiring splinting; 7) the term biologic width is replaced by supracrestal tissue attachment consisting of junctional epithelium and supracrestal connective tissue; 8) infringement of restorative margins within the supracrestal connective tissue attachment is associated with inflammation and/or loss of periodontal supporting tissue. However, it is not evident whether the negative effects on the periodontium are caused by dental plaque biofilm, trauma, toxicity of dental materials or a combination of these factors; 9) tooth anatomical factors are related to dental plaque biofilm‐induced gingival inflammation and loss of periodontal supporting tissues. Conclusion: An updated classification of the periodontal manifestations and conditions affecting the course of periodontitis and the periodontal attachment apparatus, as well as of developmental and acquired conditions, is introduced. Case definitions and diagnostic considerations are also presented. [ABSTRACT FROM AUTHOR]

Background: Periodontitis is considered to be a risk factor for preterm birth. Mechanisms have been proposed for this pathologic relation, but the exact pathologic pattern remains unclear. Therefore, the objective of the present study is to evaluate levels of four major labor triggers, prostaglandin E2 (PGE2), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, in gingival crevicular fluid (GCF) and serum samples between women with preterm birth (PTB) and full-term birth (FTB) and correlate them with periodontal parameters.Methods: PGE2, IL-1β, IL-6, and TNF-α levels were estimated using enzyme-linked immunosorbent assays in GCF and serum samples collected 24 to 48 hours after labor from 120 women (60 FTB, 60 PTB).Results: Women with PTB exhibited significantly more periodontitis, worse periodontal parameters, and increased GCF levels of IL-6 and PGE2 compared with the FTB group; there were no significant differences in serum levels of measured markers. GCF levels of IL-1β, IL-6, and PGE2 and serum levels of TNF-α and PGE2 were significantly higher in women with periodontitis compared with periodontally healthy women. Serum levels of PGE2 were positively correlated with probing depth (PD) and clinical attachment level (CAL) as well as with GCF levels of TNF-α in women with PTB.Conclusions: Women with PTB demonstrated worse periodontal parameters and significantly increased GCF levels of IL-6 and PGE2 compared with those with FTB. Based on significant correlations among serum PGE2 and PD, CAL, and GCF TNF-α in PTB, periodontitis may cause an overall increase of labor triggers and hence contribute to preterm labor onset. [ABSTRACT FROM AUTHOR]

Introduction Elucidating the microbial ecology of endodontic infections (EIs) is a necessary step in developing effective intracanal antimicrobials. The aim of the present study was to investigate the bacterial composition of symptomatic and asymptomatic primary and persistent infections in a Greek population using high-throughput sequencing methods. Methods 16S amplicon pyrosequencing of 48 root canal bacterial samples was conducted, and sequencing data were analyzed using an oral microbiome–specific and a generic (Greengenes) database. Bacterial abundance and diversity were examined by EI type (primary or persistent), and statistical analysis was performed by using non-parametric and parametric tests accounting for clustered data. Results Bacteroidetes was the most abundant phylum in both infection groups. Significant, albeit weak associations of bacterial diversity were found, as measured by UniFrac distances with infection type (analyses of similarity, R = 0.087, P = .005) and symptoms (analyses of similarity, R = 0.055, P = .047). Persistent infections were significantly enriched for Proteobacteria and Tenericutes compared with primary ones; at the genus level, significant differences were noted for 14 taxa, including increased enrichment of persistent infections for Lactobacillus , Streptococcus , and Sphingomonas . More but less abundant phyla were identified using the Greengenes database; among those, Cyanobacteria (0.018%) and Acidobacteria (0.007%) were significantly enriched among persistent infections. Persistent infections showed higher phylogenetic diversity (PD) (asymptomatic: PD = 9.2, standard error [SE] = 1.3; symptomatic: PD = 8.2, SE = 0.7) compared with primary infections (asymptomatic: PD = 5.9, SE = 0.8; symptomatic: PD = 7.4, SE = 1.0). Conclusions The present study revealed a high bacterial diversity of EI and suggests that persistent infections may have more diverse bacterial communities than primary infections. [ABSTRACT FROM AUTHOR]

Article title and bibliographic information The effect of nonsurgical periodontal therapy on hemoglobin A1c levels in persons with type 2 diabetes and chronic periodontitis: a randomized clinical trial. Engebretson SP, Hyman LG, Michalowicz BS, Schoenfeld ER, Gelato MC, Hou W, et al (16 authors). JAMA 2013;310(23):2523-32. Reviewers Wenche S. Borgnakke, Iain L. C. Chapple, Robert J. Genco, Gary Armitage, P. Mark Bartold, Francesco D'Aiuto, Paul I. Eke, William V. Giannobile, Thomas Kocher, Kenneth S. Kornman, Niklaus P. Lang, Phoebus N. Madianos, Shinya Murakami, Fusanori Nishimura, Steven Offenbacher, Philip M. Preshaw, Amin ur Rahman, Mariano Sanz, Jørgen Slots, Maurizio S. Tonetti, Thomas E. Van Dyke Purpose/Question Does non-surgical periodontal treatment reduce levels of HbA 1c in persons with type 2 diabetes and moderate to advanced chronic periodontitis? Source of funding US Government – National Institute of Dental and Craniofacial Research, National Institutes of Health: Cooperative agreements ($15.4M): 1) UO1 DE018902 (Dr. Engebretson: $11.1M) and 2) U01 DE018886 (Dr. Hyman: $4.3M) Type of study/Design Multi-center RCT. Trial Registration: clinicaltrials.gov identifier: NCT00997178 . Level of evidence Level 2: Limited-quality, patient-oriented evidence Strength of recommendation grade Not applicable [ABSTRACT FROM AUTHOR]

Abstract: Aim: To evaluate the evidence on potential biological pathways underlying the possible association between periodontal disease (PD) and adverse pregnancy outcomes (APOs). Material & Methods: Human, experimental and in vitro studies were evaluated. Results: Periodontal pathogens/byproducts may reach the placenta and spread to the foetal circulation and amniotic fluid. Their presence in the foeto‐placental compartment can stimulate a foetal immune/inflammatory response characterized by the production of IgM antibodies against the pathogens and the secretion of elevated levels of inflammatory mediators, which in turn may cause miscarriage or premature birth. Moreover, infection/inflammation may cause placental structural changes leading to pre‐eclampsia and impaired nutrient transport causing low birthweight. Foetal exposure may also result in tissue damage, increasing the risk for perinatal mortality/morbidity. Finally, the elicited systemic inflammatory response may exacerbate local inflammatory responses at the foeto‐placental unit and further increase the risk for APOs. Conclusions: Further investigation is still necessary to fully translate the findings of basic research into clinical studies and practice. Understanding the systemic virulence potential of the individual's oral microbiome and immune response may be a distinctly different issue from categorizing the nature of the challenge using clinical signs of PD. Therefore, a more personalized targeted therapy could be a more predictive answer to the current “one‐size‐fits‐all” interventions. [ABSTRACT FROM AUTHOR]

Background: It is well accepted that glycemic control in patients with diabetes mellitus (DM) is affected by systemic inflammation and oxidative stress. The effect of periodontal therapy on these systemic factors may be related to improvement on glycemic status. The aim of the present study is to assess over a period of 6 months the effect of non-surgical periodontal therapy on serum levels of high-sensitivity C-reactive protein (hsCRP), d-8-iso prostaglandin F2a (d-8-iso) as a marker of oxidative stress, and matrix metalloproteinase (MMP)-2 and MMP-9 on patients with type 2 DM. Methods: Sixty participants with type 2 DM and moderate to severe periodontal disease were randomized into intervention (IG) and control (CG) groups. IG received scaling and root planing, whereas CG received supragingival cleaning at baseline and scaling and root planing at 6 months. Participants of both groups were evaluated at baseline and 1, 3, and 6 months. Periodontal data recorded at each visit included probing depth, clinical attachment loss, bleeding on probing, and gingival index. Blood was collected at each visit for the assay of serum glycated hemoglobin Alc (Alc), hsCRP, d-8-iso, MMP-2, and MMP-9. Results: Although there was a trend to a reduction in hsCRP, d-8-iso and MMP-9 it did not reach statistical significance. MMP-2 levels remained unchanged after periodontal treatment. Conclusion: Effective non-surgical periodontal treatment of participants with type 2 DM and moderate to severe periodontal disease improved significantly Alc levels but did not result in a statistically significant improvement in hsCRP, d-8-iso, MMP-2, and MMP-9 levels. [ABSTRACT FROM AUTHOR]

Objectives: The primary aetiologic factor of periodontal disease is the bacterial biofilm. Gram-positive and Gram-negative bacteria possess a plethora of structural or secreted components that may cause direct destruction to periodontal tissues or stimulate host cells to activate a wide range of inflammatory responses. These responses are intended to eliminate the microbial challenge, but may often cause further tissue damage. Methods: This review has been divided into three parts: (a) bacterial virulence factors, which includes basic information on bacterial virulence factors, and the principle inflammatory responses that host cells elicit against these factors, (b) main receptors and signalling pathways, which includes basic information about the main receptors that interact with the bacterial virulence factors, the nature of these interactions, and the activated signalling pathways that lead to inflammatory responses, and (c) initiation of inflammation, which includes a model by which the virulence factors may interact with host cells and lead to inflammatory responses in the gingiva. Findings and Conclusions: Bacterial components/virulence factors may be involved in modulating inflammatory responses and include: lipopolysaccharides (LPS), peptidoglycans, lipotechoic acids, fimbriae, proteases, heat-shock proteins, formyl-methionyl peptides, and toxins. Potential host cell receptors involved in recognizing bacterial components and initiating signalling pathways that lead to inflammatory responses include: Toll-like receptors (TLRs), CD14, nucleotide-binding oligomerization domain proteins (Nod) and G-protein-coupled receptors, including formyl-methionyl peptide receptors and protease-activated receptors. Of the above bacterial and host molecules, evidence from experimental animal studies implicate LPS, fimbriae, proteases, TLRs, and CD14 in periodontal tissue or alveolar bone destruction. However, evidence verifying the involvement of any of the above molecules in periodontal tissue destruction in humans does not exist. [ABSTRACT FROM AUTHOR]

Objective: The purpose of this study was to determine whether microbial DNA hybridization is a useful method to study bacterial vaginosis in asymptomatic pregnant women. Study design: Vaginal specimens were collected at <26 weeks' gestation from 230 women, and analyzed for bacterial vaginosis by both Gram stain using Nugent criteria and DNA hybridization for Gardnerella vaginalis, Prevotella bivia, Bacteroides ureolyticus, and Mohiluncus curtisii. Results were analyzed using McNemar's paired test and chi-square test for trend, with significance set at P < .05. Results: By Gram stain, 60 (26.1%) of 230 were positive for bacterial vaginosis, and 134 (58.3%) were negative. By DNA hybridization, 99 (43%) were positive for at least 1 pathogen, and DNA results were significantly associated with Gram-stain results (P < .01). As the Nugent score progressed from normal to abnormal flora, the proportion with >1 pathogen detected by DNA hybridization increased significantly (P < .001). Conclusion: DNA hybridization may be a useful method to study shifts in vaginal flora during pregnancy. [ABSTRACT FROM AUTHOR]

Objective: This study was undertaken to develop a rabbit model of maternal exposure to Porphyromonas gingivalis and determine whether fetal or placental exposure occurs. Study design: Subcutaneous steel chambers were implanted in 8 New Zealand White female rabbits. On day 7 of pregnancy, 4 rabbits were inoculated through the chamber with 5 × 108 CFU/mL live P gingivalis, and 4 rabbits with broth (controls) and sacrificed at term. Polymerase chain reaction was used to detect P gingivalis in maternal and fetal liver and placenta. Fisher exact test was used to compare P gingivalis detection between groups. Results: Among exposed does, P gingivalis was detected in 33% of the maternal livers, 49% of placentas, and 34% fetal livers compared with none from controls (P < .001). Conclusion: Chronic maternal exposure to P gingivalis results in systemic dissemination, transplacental passage, and fetal exposure. This model may be useful to study placental and fetal effects of this oral pathogen and to study microbial dissemination across the placenta. [ABSTRACT FROM AUTHOR]

Background: Our objective was to describe the oral health of pregnant women, to determine oral health changes during pregnancy, and to determine factors associated with maternal periodontal health or disease. Materials and Methods: Between December 1997 and July 2001, 1,224 pregnant women at <26 weeks' gestation were enrolled in the study and oral health examinations were performed at enrollment and within 48 hours of delivery. Demographic, medical, and health behavior data were determined by chart abstraction and questionnaire. Comparisons between oral health at enrollment and delivery were made by student t test or Fisher's exact test. Ordinal logistic regression analysis was used to identify risk factors for maternal periodontal disease. Results: Among 903 women, there was a significant increase in those with health/periodontal disease absence between enrollment and delivery (P<0.001). However, we also observed a significant increase in women with four or more sites with attachment loss ≥2 mm or ≥3 mm (P <0.05. 0.001). Race, smoking, and insurance status were significantly associated with maternal periodontal disease. Black women were more likely than white women to have periodontal disease at enrollment (adj. odds ratio 2.9, 95% confidence interval 2.2 to 3.9) and delivery (adj. odds ratio 3.1, 95% confidence interval 2.2 to 4.2), and experience incident disease (adj. odds ratio 2.3, 95% confidence interval 1.6 to 3.4). Conclusions: Oral health examinations were well accepted by pregnant women. An increase in attachment loss may represent active periodontal infection accelerated by pregnancy. Further study on racial disparity in oral health among pregnant women is needed. Continued efforts to evaluate and establish appropriate definitions of oral disease in pregnancy are warranted. [ABSTRACT FROM AUTHOR]

Background: In Alabama, low birth weight (LBW) infants are about 20 times more likely to die before their first birthday compared to normal birth weight infants. While the rate of LBW has been consistently higher among African Americans compared to whites, there has been a gradual increase in LBW for both African Americans and whites over the last 15 years. In an attempt to identify modifiable risk factors for LBW, we have previously reported that a pregnant woman's poor periodontal health may be an independent risk factor for low birth weight. Methods: A predominantly African American and socio-economically homogeneous group of 443 women was followed from the second trimester of their first pregnancy. Thirty-nine LBW cases were observed at the end of follow-up. Using 17 preterm LBW cases and 63 randomly selected controls from the above cohort, the periodontal pathogen-specific maternal serum IgG levels during the second trimester of pregnancy were evaluated in relation to birth weight of the infant, while controlling for known risk factors for LBW. Results: Porphyromonas gingivalis (P.g.)-specific maternal serum IgG levels were higher in the LBW group (mean 58.05, SE = 20.00 µg/ml) compared to the normal birth weight (NBW) group (mean 13.45, SE = 3.92 µg/ml; P = 0.004). Women with higher levels of P.g.-specific IgG had higher odds of giving birth to LBW infants (odds ratio [OR] = 4,1; 95% confidence interval [CI] for odds ratio = 1.3 to 12.8). This association remained significant after controlling for smoking, age, IgG levels against other selected periodontal pathogens, and race. Conclusions: Low birth weight deliveries were associated with a higher maternal serum antibody level against P. gingivalis at mid-trimester. [ABSTRACT FROM AUTHOR]

Accumulating evidence indicates that epithelia are not merely mechanical barriers but also important elements of the innate immune system. The present study was performed to examine cytokine responses of oral epithelial cells after infection with the periodontal pathogen Porphyromonas gingivalis. The KB-cell line and primary cultures of periodontal pocket epithelium were infected with P. gingivalis for assessment of bacterial invasion by an antibiotic protection assay, and examinination of expression of interleukin-I beta, interleukin-6, interleukin-8, and tumor necrosis factor-alpha by in situ hybridization and immunohistochemistry. We observed that P. gingivalis induces a strong cytokine response, positively correlated with the adhesive/invasive potential of the infecting strain, in both KB cells and primary cultures. These findings indicate that the epithelial cells of the periodontal pocket are an integral part of the immune system, eliciting cytokine responses to a bacterial challenge. In this context, the adhesive/invasive phenotype of P. gingivalis appears to contribute to pathogenicity. [ABSTRACT FROM AUTHOR]

The present investigation explored the genotypic heterogeneity of Porphyromonas gingivalis using restriction endonuclease analysis and ribotyping of 64 P. gingivalis isolates, recovered from the periodontal pockets of 3 beagle dogs, 2 of which were reared together. The isolates originated from both healthy and periodontal disease affected sits and thereby enabled the study of bacterial genotype with respect to (i) individual host, (ii) ecological niche (site within host) and (iii) level of periodontal health. whole genomic DNA was extracted from each isolate and digested by the restriction endonuclease KpnI. Digestion fragments were separated by electrophoresis and transferred onto nylon membranes. The blots were hybridized with a digoxigenin-labeled 16S rDNA probe, and hybridization bands were detected using an anti-digoxigenin antibody conjugated with alkaline phosphatase and enhanced chemiluminescence. Fourteen genomic fingerprints and 13 ribotypes were observed among the 64 isolates. As many as 8 distinct fingerprints were detected within a single host and up to 4 fingerprints within a single periodontal pocket. The dogs reared together shared 2 common clonal types ut also exhibited clonal types unique to each dog. No clear association between clonal type and periodontal health status could be made. The results revealed an extensive intra-host genotypic heterogeneity of P. gingivalis strains in the beagle dog and indicated that ribotyping was a sensitive method for differentiating clonal types within species. [ABSTRACT FROM AUTHOR]

Background: Chronic periodontal infection is associated with an increased risk of coronary heart disease. Although the mechanism responsible for the relationship between periodontal disease and cardiovascular events is not fully understood, it is hypothesized that the chronic inflammatory burden of periodontal disease may lead to impaired functioning of the vascular endothelium. Methods: Twenty-two otherwise healthy adults with moderate to severe periodontitis who underwent complete mouth disinfection were evaluated to determine if periodontal therapy would result in improved endothelial function and a decrease in serum inflammatory markers. Subjects had measurements of periodontal disease severity, flow-mediated (endothelium-dependent), and nitroglycerin-mediated (endothelium-independent) dilation of the brachial artery, serum C-reactive protein (CRP) and interleukin 6 (IL-6), and serum total and high-density lipoprotein cholesterol levels on 2 baseline visits separated by 1 month and, again, 1 month after treatment. Results: There were no significant changes in clinical periodontal measures, flow-mediated dilation, nitroglycerin-mediated dilation, CRP, IL-6, total cholesterol, or high-density lipoprotein cholesterol between the repeated baseline measurements. Periodontal treatment, however, resulted in significant improvements in periodontal pocketing, flow-mediated dilation, and serum IL-6, as well as a trend toward reduction in serum CRP; there were no significant changes in nitroglycerin-mediated dilation or in cholesterol levels. Conclusions: These results represent proof of concept that improvement in endothelial function, as measured by flow-mediated dilation of the brachial artery, may be possible through near-elimination of chronic oral infection and suggest that the conduct of a larger controlled trial is justified. [Copyright &y& Elsevier]