Nexus between COVID-19 and periodontal disease.

Over the past several decades, studies have demonstrated the existence of bi-directional relationships between periodontal disease and systemic conditions. Periodontitis is a polymicrobial and multifactorial disease involving both host and environmental factors. Tissue destruction is primarily associated with hyperresponsiveness of the host resulting in release of inflammatory mediators. Pro-inflammatory cytokines play a major role in bacterial stimulation and tissue destruction. In addition, these cytokines are thought to underlie the associations between periodontitis and systemic conditions. Current research suggests that increased release of cytokines from host cells, referred to as the cytokine storm, is associated with disease progression in patients with coronavirus disease 2019 (COVID-19). An intersection between periodontitis and pulmonary disease is biologically plausible. Hence, we reviewed the evidence linking COVID-19, cytokines, and periodontal disease. Plaque control is essential to prevent exchange of bacteria between the mouth and the lungs, reducing the risk of lung disease. Understanding these associations may help identify individuals at high risk and deliver appropriate care at early stages.

Orally administered ovine serum immunoglobulins modulate dental plaque in cats.

The effects of orally administered ovine serum immunoglobulin on dental plaque and associated oral immunity in cats were investigated. The two treatment groups consisted of 1) cats that were fed unsupplemented kibble (control diet) and 2) cats that were fed the same kibble but coated with a freeze-dried ovine serum immunoglobulin preparation (ovine Ig) (test diet). The adult cats were randomly allocated to one of the two diets (n = 15) and received their respective kibble for a 28-day experimental period. When compared to the ovine Ig-supplemented kibble, cats consuming the unsupplemented kibble had significantly (p < 0.05) higher dental plaque scores. Cat IgA and IgG concentrations in the saliva and serum were significantly (p < 0.05) higher for cats fed the unsupplemented kibble when compared to cats receiving the ovine Ig supplement. Similarly, myeloperoxidase activity in the saliva was significantly (p < 0.05) higher for cats fed the unsupplemented kibble when compared to cats receiving the Ig-supplement. Orally administered ovine serum Ig positively influenced oral health and oral immunity in cats as evidenced by preventing an increase of dental plaque formation, salivary and serum IgA and IgG concentrations and salivary myeloperoxidase activity.

Correlation Between Oral Health and Systemic Inflammation (COHESION): A Randomized Pilot Follow-Up Trial of a Plaque-Identifying Toothpaste.

BACKGROUND: Inflammation is intimately involved in the pathogenesis of atherosclerosis and is accurately measured by high-sensitivity C-reactive protein (hs-CRP), a sensitive marker for future risk of cardiovascular disease. The Correlation between Oral Health and Systemic Inflammation (COHESION) trial was designed to test the hypothesis that PlaqueHD, a plaque-identifying toothpaste, reduces hs-CRP. METHODS: The trial was designed initially to include 132 subjects with hs-CRP between 2.0 and 10.0 mg/L but instead randomized 112 between 0.5 and 10.0, of which 103 had baseline and follow-up data and comprised the intention-to-treat sample. Of these, a prespecified subgroup analysis included 40 with baseline hs-CRP >2.0 and all hs-CRP <10. Because the distribution of hs-CRP was skewed toward higher values, to achieve normality assumptions, the significance of changes in hs-CRP between groups over time was tested on log-transformed data using a mixed effects analysis of variance. RESULTS: The intention-to-treat analysis showed no significant differences between the PlaqueHD and placebo group (P = .615). The prespecified subgroup analysis showed a significant difference between the PlaqueHD and placebo group (P = .047). Results of the analysis showed a reduction in hs-CRP at follow-up of 0.58 in the PlaqueHD and an increase of 0.55 in the placebo group. CONCLUSIONS: These findings are compatible with those of a prior pilot trial that also suggested benefits only in subjects with baseline elevations. Future trials targeting reductions of hs-CRP levels should randomize subjects with baseline hs-CRP between 2.0 and 10.0 mg/L.

Can Periodontitis Influence the Progression of Abdominal Aortic Aneurysm? A Systematic Review.

There is some evidence that periodontitis increases the risk of atherothrombosis. Abdominal aortic aneurysm (AAA) is a cardiovascular disease with specific risk factors and physiopathological mechanisms that can lead to rupture in the absence of treatment. The aim of the present systematic review was to explore the influence of periodontitis on the progression of AAAs as a specific disease. A systematic search in PubMed/MEDLINE and Embase databases was performed. Human and animal studies exploring the influence of periodontal pathogens on the progression of AAA were considered for inclusion. After systematic screening, 5 articles were included in the review. Due to the heterogeneity of the selected studies, a meta-analysis could not be performed. The descriptive analyses of the studies emphasized that periodontal pathogens or their by-products contribute to systemic and local innate immunity likely to be associated with AAA physiopathology. Periodontitis seems to play a role in the development and progression of AAA. The present systematic review suggests that the presence of periodontal bacteria in the bloodstream or in situ in the vascular lesion is a risk associated with aneurysmal disease progression.

Association between specific periodontal pathogens, Toll-like receptor-4, and nuclear factor-κB expression in placental tissues of pre-eclamptic women with periodontitis.

AIM: The aim of the present study was to determine the association between the presence of specific periodontal pathogens, Toll-like receptor-4 (TLR-4), and nuclear factor-κB (NF-κB) expression in the placental tissues of pre-eclamptic women. METHODS: Antenatal periodontal screening was performed in 25 normotensive pregnant women and 25 pre-eclamptic women. Subgingival plaque and placental tissue samples were collected from both groups and screened for the presence of Porphyromonas gingivalis (P. gingivalis), Tannerella forsythia, Aggregatibacter actinomycetemcomitans, and Prevotella intermedia (P. intermedia) using real-time polymerase chain reaction. The placental samples were also analyzed to quantify TLR-4 and NF-κB expression. RESULTS: The subgingival plaque samples of pre-eclamptic women showed significantly higher frequencies of P. intermedia. In the placental samples, P. gingivalis, P. intermedia, and the expression of TLR-4 and NF-κB were found to be at significantly higher levels compared to normotensive pregnant women. Using linear regression analysis, the expression of TLR-4 was significantly influenced by the presence of P. gingivalis (coefficient=3.176, 95% confidence interval [CI]: 367-5.986) and P. intermedia (coefficient=2.886, 95% CI: 0.77-5.696), whereas NF-κB expression was influenced only by the presence of P. intermedia (coefficient=2.220, 95% CI: 0.051-4.388) in the placental tissues of pre-eclamptic women. CONCLUSION: An association exists between P. gingivalis and P. intermedia with increased TLR-4 and NF-κB expression in the placenta of pre-eclamptic women with periodontitis.

Clinical, Immune, and Microbiome Traits of Gingivitis and Peri-implant Mucositis.

Tissues surrounding dental implants and teeth develop clinical inflammation in response to microbial stimuli. However, the literature suggests that differences exist in the microbial insult and inflammatory responses leading to gingivitis and peri-implant mucositis. In this pilot study, the authors use for the first time a systems biology approach to comprehensively evaluate clinical parameters, selected inflammatory markers, and the microbiome of subject-matched tooth and implant sites during native inflammation and in response to experimental plaque accumulation. Fifteen subjects with 2 posterior implants and corresponding contralateral teeth were examined at enrollment; at day 0, after reinstitution of gingival/mucosal health; at days 7, 14, and 21, during stent-mediated oral hygiene (OH) abstention; and at day 42, after resumption of OH. The subgingival microbiome was evaluated via 16S rRNA gene sequencing and 8 selected inflammatory markers measured in crevicular fluid. Comparison of teeth and implants via general linear models based on orthogonal polynomials showed similar responses in clinical parameters, inflammatory mediators, and proportions of individual microbial taxa during OH abstention. Implants, however, accumulated less plaque and underwent more heterogeneous shifts in microbiome structure. A multilevel, within-group, sparse partial least squares analysis of covariation of microbial, inflammatory, and clinical parameters throughout all study visits found inflammation around teeth and implants positively correlated with IL-1 alpha and IL-1 beta and with the proportions of Selenomonas, Prevotella, and 5 species-level phylotypes. Gingivitis, however, showed a stronger positive correlation with lactoferrin and IL-1ra and a stronger negative correlation with Rothia. Peri-implant mucositis, on the contrary, correlated positively with certain microbial taxa not associated with gingivitis by a previous study or the current one. In summary, differences existed between implants and tooth sites in microbiome evolution during OH abstention and in the correlation of specific inflammatory mediators and microbial taxa with clinical inflammation. Common biological features, however, were also identified for gingivitis and mucositis.

Risk factors that may modify the innate and adaptive immune responses in periodontal diseases.

Plaque-induced periodontal diseases occur in response to the accumulation of dental plaque. Disease manifestation and progression is determined by the nature of the immune response to the bacterial complexes in plaque. In general, predisposing factors for these periodontal diseases can be defined as those factors which retain or hinder the removal of plaque and, depending upon the nature of the immune response to this plaque, the disease will either remain stable and not progress or it may progress and result in chronic periodontitis. In contrast, modifying factors can be defined as those factors that alter the nature or course of the inflammatory lesion. These factors do not cause the disease but rather modify the chronic inflammatory response, which, in turn, is determined by the nature of the innate and adaptive immune responses and the local cytokine and inflammatory mediator networks. Chronic inflammation is characterized by vascular, cellular and repair responses within the tissues. This paper will focus on how common modifying factors, such as smoking, stress, hormonal changes, diabetes, metabolic syndrome and HIV/AIDS, influence each of these responses, together with treatment implications. As treatment planning in periodontics requires an understanding of the etiology and pathogenesis of the disease, it is important for all modifying factors to be taken into account. For some of these, such as smoking, stress and diabetic control, supportive health behavior advice within the dental setting should be an integral component for overall patient management.

Subgingival Plaque in Periodontal Health Antagonizes at Toll-Like Receptor 4 and Inhibits E-Selectin Expression on Endothelial Cells.

The ability of the subgingival microbial community to induce an inappropriate inflammatory response ultimately results in the destruction of bone and gingival tissue. In this study, subgingival plaque samples from both healthy and diseased sites in the same individual were obtained from adults with chronic periodontitis and screened for their ability to either activate Toll-like receptor 2 (TLR2) or TLR4 and to antagonize TLR4-specific activation by agonist, Fusobacterium nucleatum LPS. Subgingival plaque from diseased sites strongly activated TLR4, whereas matched plaque samples obtained from healthy sites were significantly more variable, with some samples displaying strong TLR4 antagonism, while others were strong TLR4 agonists when combined with F. nucleatum LPS. Similar results were observed when TLR4 dependent E-selectin expression by endothelial cells was determined. These results are the first to demonstrate TLR4 antagonism from human plaque samples and demonstrate that healthy but not diseased sites display a wide variation in TLR4 agonist and antagonist behavior. The results have identified a novel characteristic of clinically healthy sites and warrant further study on the contribution of TLR4 antagonism in the progression of a healthy periodontal site to a diseased one.

Pep19 drives epitope spreading in periodontitis and periodontitis-associated autoimmune diseases.

BACKGROUND AND OBJECTIVE: Epitope spreading is one of valid mechanisms operating in immunopathological processes of infection-induced autoimmune diseases. We hypothesized that the peptide 19 from Porphyromonas gingivalis heat shock protein (HSP) 60 (Pep19) may be the dominant epitope from which epitope-specific immune response to subdominant epitopes may diversify sequentially into autoimmune responses directed at human neoepitopes in P. gingivalis-induced periodontitis and autoimmune diseases. However, the exact feature and mechanism on how Pep19 may drive epitope spreading into human autoantigens in chronic periodontitis or P. gingivalis-induced experimental periodontitis has not been clarified. The present study was performed with the following specific aims: (i) to delineate retrospectively the features of epitope spreading by human cross-sectional analysis; (ii) to demonstrate prospectively the epitope spreading into new antigenic determinants in an ordered, predictable and sequential manner in experimental periodontitis; and (iii) to clarify the mechanism on how immunization with Pep19 may mobilize helper T cells or elicit B-cell responses to human autoantigens and neoantigen. MATERIAL AND METHODS: The study was devised for two independent investigations - a cross-sectional analysis on clinical subjects and a prospective analysis on experimental periodontitis - each being subdivided further into two additional independent observations. Cross-sectional dot immunoblot pattern against a panel of peptides of P. gingivalis HSP60 and human HSP60 was performed among age-dependent healthy subjects and between healthy subjects, patients with chronic periodontitis and patients with autoimmune disease, to identify epitope spreading. A peptide-specific T-cell line was established for phenotype analysis and for proliferation assay to an array of identical peptides. An identical prospective analysis was performed in P. gingivalis-induced experimental periodontitis or in Pep19-immunized mice. Cross-reactivity of anti-Pep19 monoclonal antibody was also investigated. RESULTS: A dominant immune response exclusively to Pep19 prevailed in healthy human subjects (before the age of 40) and mice that persisted in chronic periodontitis and autoimmune diseases without being replaced further by subsequent subdominant epitopes. A sequential epitope spreading provoked by Pep19 to subdominant autoantigen peptide 19 from human HSP60 (Hu19) in most healthy human subjects and mice, and to autoantigen peptide 9 from human HSP60 (Hu9) and neoantigen oxidized low-density lipoprotein (ox-LDL) in P. gingivalis-induced chronic periodontitis and autoimmune diseases could be demonstrated in a reproducible and predictable manner. T-cell proliferative activity to multiple autoantigens Hu19, Hu9 and ox-LDL, and cross-reactivity of anti-Pep19 monoclonal antibody to these epitopes may be proposed as cellular and molecular mechanisms responsible for the phenomenon. Moreover, the predictive value of Pep19 for Hu9 increased remarkably in the disease group when compared with that of the healthy group. CONCLUSION: Taken together, epitope spreading to Hu19, Hu9 and ox-LDL provoked by Pep19 could be proposed as a solid phenomenon observed in P. gingivalis-induced chronic periodontitis and infection-induced autoimmune diseases in a reproducible and predictable manner. T-cell proliferative activity to these peptides and cross-reactivity of anti-Pep19 antibodies to multiple human autoantigens could be proposed as cellular and molecular mechanisms responsible for this phenomenon.

T cells, teeth and tissue destruction - what do T cells do in periodontal disease?

The microbial plaque biofilm resides adjacent to the tissue-destructive inflammatory infiltrate in periodontitis. Although not sufficient, this biofilm is necessary for this inflammatory response. Patients with periodontitis generate antibodies specific for bacteria in the biofilm - although the role of these antibodies is not clear, there is, undoubtedly, an adaptive immune response in periodontitis. T lymphocytes are central to adaptive immunity, and provide help for B cells to generate specific antibodies. T-cell receptor recognition of peptide antigen in the context of major histocompatibility complex can result in T-cell activation. The activation and differentiation of the T-cell can take many forms, and hence numerous types of T cells have been described. The role of adaptive immune responses, and the T-cell component thereof, in periodontitis remains relatively poorly defined. This review aims to broadly summarize findings about T cells and their role in periodontitis, focusing primarily on studies of human disease with a short discussion of some animal studies.

TLR4, NOD1 and NOD2 mediate immune recognition of putative newly identified periodontal pathogens.

Periodontitis is a polymicrobial inflammatory disease that results from the interaction between the oral microbiota and the host immunity. Although the innate immune response is important for disease initiation and progression, the innate immune receptors that recognize both classical and putative periodontal pathogens that elicit an immune response have not been elucidated. By using the Human Oral Microbe Identification Microarray (HOMIM), we identified multiple predominant oral bacterial species in human plaque biofilm that strongly associate with severe periodontitis. Ten of the identified species were evaluated in greater depth, six being classical pathogens and four putative novel pathogens. Using human peripheral blood monocytes (HPBM) and murine bone-marrow-derived macrophages (BMDM) from wild-type (WT) and Toll-like receptor (TLR)-specific and MyD88 knockouts (KOs), we demonstrated that heat-killed Campylobacter concisus, Campylobacter rectus, Selenomonas infelix, Porphyromonas endodontalis, Porphyromonas gingivalis, and Tannerella forsythia mediate high immunostimulatory activity. Campylobacter concisus, C. rectus, and S. infelix exhibited robust TLR4 stimulatory activity. Studies using mesothelial cells from WT and NOD1-specific KOs and NOD2-expressing human embryonic kidney cells demonstrated that Eubacterium saphenum, Eubacterium nodatum and Filifactor alocis exhibit robust NOD1 stimulatory activity, and that Porphyromonas endodontalis and Parvimonas micra have the highest NOD2 stimulatory activity. These studies allowed us to provide important evidence on newly identified putative pathogens in periodontal disease pathogenesis showing that these bacteria exhibit different immunostimulatory activity via TLR4, NOD1, and NOD2 (Clinicaltrials.gov NCT01154855).

GM-CSF and uPA are required for Porphyromonas gingivalis-induced alveolar bone loss in a mouse periodontitis model.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) and urokinase-type plasminogen activator (uPA) can contribute to the progression of chronic inflammatory diseases with possible involvement of macrophages. In this study, we investigated the role of both GM-CSF and uPA in Porphyromonas gingivalis-induced experimental periodontitis using GM-CSF-/- and uPA-/- mice. Intra-oral inoculation of wild-type (WT) C57BL/6 mice with P. gingivalis resulted in establishment of the pathogen in plaque and a significant increase in alveolar bone resorption. The infected mice also exhibited a CD11b(+) CD86(+) macrophage infiltrate into the gingival tissue, as well as P. gingivalis-specific pro-inflammatory cytokine and predominantly IgG2b antibody responses. In comparison, intra-oral inoculation of P. gingivalis did not induce bone resorption and there was significantly less P. gingivalis recovered from plaque in GM-CSF-/- and uPA-/- mice. Furthermore, P. gingivalis did not induce a macrophage gingival infiltrate or activate isolated peritoneal macrophages from the gene-deficient mice. Pro-inflammatory P. gingivalis-specific T-cell cytokine responses and serum interferon-gamma (IFN-γ) and IgG2b concentrations were significantly lower in GM-CSF-/- mice. In uPA-/- mice, T-cell responses were lower but serum IFN-γ and IgG2b levels were comparable with WT mice levels. These results suggest that GM-CSF and uPA are both involved in the progression of experimental periodontitis, possibly via a macrophage-dependent mechanism(s).

Smoking decreases structural and functional resilience in the subgingival ecosystem.

AIMS: Dysbiotic microbial communities underlie the aetiology of several oral diseases, especially in smokers. The ability of an ecosystem to rebound from the dysbiotic state and re-establish a health-compatible community, a characteristic known as resilience, plays an important role in susceptibility to future disease. The present investigation was undertaken to examine the effects of smoking on colonization dynamics and resilience in marginal and subgingival biofilms. MATERIALS AND METHODS: Marginal and subgingival plaque and gingival crevicular fluid samples were collected from 25 current and 25 never smokers with pre-existing gingivitis at baseline, following resolution, after 1, 2 4, 7, 14 and 21 days of undisturbed plaque formation and following resolution. 16S cloning and sequencing was used for bacterial identification and multiplexed bead-based flow cytometry was used to quantify the levels of 27 immune mediators. RESULTS: Smokers demonstrated an early pathogenic colonization that led to sustained pathogen enrichment with periodontal and respiratory pathogens, eliciting a florid immune response. Smokers also demonstrated greater abundance of pathogenic species, poor compositional correlation between marginal and subgingival ecosystems, and significantly greater pro-inflammatory responses following resolution of the second episode of disease. CONCLUSIONS: The ability of the subgingival microbiome to "reset" itself following episodes of disease is decreased in smokers, thereby lowering the resilience of the ecosystem and decreasing its resistance to future disease.

A clinical guide to periodontology: pathology of periodontal disease.

An appreciation of dental plaque and the host response provides an essential basis from which to understand the disease process and treatment rationale. This information will help the reader to understand not only the way that plaque may have an impact on oral tissues but also why regular effective cleaning may improve periodontal health and why some individuals appear to have a greater susceptibility to periodontitis than others, either intrinsically or in relation to various systemic factors.

Periodontitis as a risk factor of atherosclerosis.

Over the last two decades, the amount of evidence corroborating an association between dental plaque bacteria and coronary diseases that develop as a result of atherosclerosis has increased. These findings have brought a new aspect to the etiology of the disease. There are several mechanisms by which dental plaque bacteria may initiate or worsen atherosclerotic processes: activation of innate immunity, bacteremia related to dental treatment, and direct involvement of mediators activated by dental plaque and involvement of cytokines and heat shock proteins from dental plaque bacteria. There are common predisposing factors which influence both periodontitis and atherosclerosis. Both diseases can be initiated in early childhood, although the first symptoms may not appear until adulthood. The formation of lipid stripes has been reported in 10-year-old children and the increased prevalence of obesity in children and adolescents is a risk factor contributing to lipid stripes development. Endothelium damage caused by the formation of lipid stripes in early childhood may lead to bacteria penetrating into blood circulation after oral cavity procedures for children as well as for patients with aggressive and chronic periodontitis.

Bis-enoxacin blocks rat alveolar bone resorption from experimental periodontitis.

Periodontal diseases are multifactorial, caused by polymicrobial subgingival pathogens, including Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. Chronic periodontal infection results in inflammation, destruction of connective tissues, periodontal ligament, and alveolar bone resorption, and ultimately tooth loss. Enoxacin and a bisphosphonate derivative of enoxacin (bis-enoxacin) inhibit osteoclast formation and bone resorption and also contain antibiotic properties. Our study proposes that enoxacin and/or bis-enoxacin may be useful in reducing alveolar bone resorption and possibly bacterial colonization. Rats were infected with 10(9) cells of polymicrobial inoculum consisting of P. gingivalis, T. denticola, and T. forsythia, as an oral lavage every other week for twelve weeks. Daily subcutaneous injections of enoxacin (5 mg/kg/day), bis-enoxacin (5, 25 mg/kg/day), alendronate (1, 10 mg/kg/day), or doxycycline (5 mg/day) were administered after 6 weeks of polymicrobial infection. Periodontal disease parameters, including bacterial colonization/infection, immune response, inflammation, alveolar bone resorption, and systemic spread, were assessed post-euthanasia. All three periodontal pathogens colonized the rat oral cavity during polymicrobial infection. Polymicrobial infection induced an increase in total alveolar bone resorption, intrabony defects, and gingival inflammation. Treatment with bis-enoxacin significantly decreased alveolar bone resorption more effectively than either alendronate or doxycycline. Histologic examination revealed that treatment with bis-enoxacin and enoxacin reduced gingival inflammation and decreased apical migration of junctional epithelium. These data support the hypothesis that bis-enoxacin and enoxacin may be useful for the treatment of periodontal disease.

Immunological and microbiological findings after the application of two periodontal surgical techniques: a randomized, controlled clinical trial.

AIM: To examine microbiological and immunological alterations following two periodontal surgical techniques, over a 6-month period. MATERIALS AND METHODS: A total of 30 chronic periodontitis patients participated in the present randomized controlled clinical trial and were randomized in two groups. Modified Widman flap (MWF) was applied in the control group and apically positioned flap (APF), without intervention to the bone, in the experimental group. Gingival crevicular fluid samples and subgingival plaque samples from the operated sites were collected at baseline, 6th, 12th and 24th post-operative week. RESULTS: No major differences were noticed in immunological and microbiological profile of patients receiving either modified MWF or APF, for a period of 6 months. CONCLUSIONS: The choice of the periodontal surgical procedure does not seem to affect the immunological and the microbiological profile of patients with chronic periodontitis.

Manual versus sonic-powered toothbrushing for plaque reduction in patients with dental implants: an explanatory randomised controlled trial.

PURPOSE: The aim of the present study was to investigate plaque levels following sonic-powered and manual toothbrushing in subjects with dental implants. MATERIALS AND METHODS: This study included 36 male and 47 female partially edentulous patients (age range 45-78 years, mean age 59.8 years) that were randomly assigned to one of two treatment groups: the sonic toothbrush group (n = 42; Philips Sonicare FlexCare® toothbrush) or the manual toothbrush group (n = 41; Oral-B P40®). Clinical, microbiological and immunological examinations were performed blinded at baseline and after 3, 6, 9 and 12 months. Microbiological analyses were performed by real-time polymerase chain reaction. Immunological analyses (prostaglandin E2) were performed by chromatography-electrospray spectrometry. RESULTS: The plaque index difference between baseline and 12 months at implants showed no significant difference between sonic or manual toothbrushing in a two-sided Mann-Whitney test (W = 773.5, P = 0.426, 95% CI -0.64 to 0.20). At the end of the study, there were no significant changes in plaque index, bleeding on probing, gingival index, pocket probing depth, gingival recession, clinical attachment level or the microbiological and immunological outcomes at implants or teeth in either group. CONCLUSIONS: This study uncovered no significant difference between sonic and manual toothbrushing for plaque reduction at implants and teeth. Both toothbrushes maintain healthy peri-implant soft tissue.

Influence of periodontal disease, Porphyromonas gingivalis and cigarette smoking on systemic anti-citrullinated peptide antibody titres.

BACKGROUND: Anti-citrullinated protein antibody (ACPA) responses may precede clinical onset of rheumatoid arthritis. Porphyromonas gingivalis peptidylarginine deiminase can citrullinate proteins possibly inducing autoimmunity in susceptible individuals. AIM: To determine whether periodontitis, carriage of P. gingivalis, smoking and periodontal therapy influence ACPA titres. METHODS: Serum and plaque samples were collected from 39 periodontitis patients before and after non-surgical periodontal treatment, and from 36 healthy subjects. Carriage of P. gingivalis was determined by PCR of plaque DNA. ACPA was determined by anti-cyclic citrullinated peptide (CCP) enzyme-linked immunosorbent assay (ELISA). Anti-P. gingivalis titres were determined by ELISA. RESULTS: Untreated periodontitis patients had higher anti-CCP antibody titres than healthy controls [three patients (8%) greater than manufacturer suggested assay diagnostic threshold (5 Assay Units/AU) versus none (0%); mean ± SEM: 1.37 ± 0.23 versus 0.40 ± 0.10 AU, p < 0.0001]. Periodontitis patients who smoked demonstrated lower anti-P. gingivalis (15956 ± 4385 versus 2512 ± 1290 Units/ml, p < 0.05), but similar anti-CCP than non-smoking periodontitis patients (smokers: 1.31 ± 0.35; non-smokers: 1.41 ± 0.32 AU). Healthy smokers demonstrated elevated anti-CCP titres (0.75 ± 0.19 AU), at levels between healthy non-smokers (0.15 ± 0.05 AU) and non-smoker periodontitis patients. Six months after periodontal treatment, there were significant reductions in anti-CCP (non-smokers p < 0.05) and anti-P. gingivalis (all participants p < 0.01). CONCLUSION: In subjects with periodontitis, P. gingivalis infection may be responsible for inducing autoimmune responses that characterize rheumatoid arthritis.

Obesity, diabetes and periodontitis--a triangular relationship?

The global rise of obesity, both adult and childhood, has been paralleled by a rise in type 2 diabetes, a trend predicted to continue for at least the next two decades. The combined effect will create a burden of direct and co-morbidities that will strain the physical and financial resources of all countries. While it is accepted that both type 1 and type 2 diabetes are major risk factors for the development and progression of periodontal disease, there is growing evidence that obesity is both an indirect risk factor because it affects glycaemic control and a direct risk factor because secretion of pro-inflammatory agents by adipose tissue modifies the periodontal reaction to the plaque biofilm. Recent research suggests that periodontitis may adversely affect glycaemic control, which can be improved by periodontal treatment with reduced risk of diabetic co-morbidity, thereby creating a two-way relationship. Furthermore it appears possible that periodontitis may stimulate inflammatory change in adipose tissue, creating a triangular self-generating cycle of morbidity linking obesity, diabetes and periodontal disease. Dentists should recognise these interlinked risk factors and consider including an assessment of glycaemic control and adiposity, possibly by waist-to-hip ratio, when periodontitis is diagnosed and in collaboration with medical practitioners provide treatment to help reduce the development of systemic disease.