Periodontopathic bacterial adhesion to different restorative materials used to elevate proximal subgingival margins.

This study compared the periodontopathic bacterial adhesion to four restorative materials used for deep margin elevation at 2, 24, and 48-h after incubation. Discs were produced from four restorative materials: resin modified glass ionomer, glass hybrid, flowable bulk fill resin composite, and bioactive ionic resin. Root dentin was used as control. Specimens were coated with saliva and used to culture a biofilm comprised of three strains of periodontopathic bacteria; Porphyromonas gingivalis, Prevotella intermedia, and Aggregatibacter actinomycetemcomitans. Bacterial adherence was assessed by colony count assay, crystal violet staining, and visualized using confocal laser scanning microscopy. Data were analyzed by two-way ANOVA followed by Tukey's post hoc tests. The adhesion values for the control specimens were significantly higher than for other materials, while those for the flowable bulk fill were significantly lower than for any other material within all evaluation assays. The 2-h incubation period showed the lowest adhesion values regardless of the group. The 48-h adhesion values were higher than the 24-h results in all groups except the flowable bulk fill. Microscopic imaging partially supported the findings of the measurements. In terms of periodontopathic bacterial adhesion, the tested flowable bulk fill may be preferable for subgingival use over other tested materials.

Concise evaluation and therapeutic guidelines for severe periodontitis: A public health perspective.

The main goal of periodontology is to prevent and arrest gingivitis and periodontitis to avoid tooth loss and focal infection of periodontal origin. Periodontal scaling or flap surgery of moderate-to-severe periodontitis have shortcomings, most likely because removal of herpesviruses and bacterial pathogens in deep periodontal lesions and the adjacent inflamed gingiva requires systemic antimicrobial treatment (or gingivectomy). Valacyclovir (1000 mg twice daily on day 1, and 500 mg twice daily on day 2 and on day 3) is a potent anti-herpesvirus agent. Antibiotic combinations against bacterial pathogens include amoxicillin-metronidazole (250 mg of each, thrice daily for 4 days; for systemically healthy adults) and ciprofloxacin-metronidazole (500 mg of each, twice daily for 4 days; for immunosuppressed individuals and patients exposed to contaminated water and poor sanitation). Supportive antiseptic treatment may consist of 0.1%-0.2% sodium hypochlorite (regular household bleach) as cooling spray in ultrasonic scalers, flosser fluid in oral irrigators, and mouthrinse in patient self-care. The anti-infective treatment described here helps control cases of severe periodontitis and constitutes an exceedingly inexpensive alternative to conventional (mechanical) periodontal therapy.

Periodontal disease-related nonalcoholic fatty liver disease and nonalcoholic steatohepatitis: An emerging concept of oral-liver axis.

Periodontal disease, a chronic inflammatory disease of the periodontal tissues, is not only a major cause of tooth loss, but it is also known to exacerbate/be associated with various metabolic disorders, such as obesity, diabetes, dyslipidemia, and cardiovascular disease. Recently, growing evidence has suggested that periodontal disease has adverse effects on the pathophysiology of liver disease. In particular, nonalcoholic fatty liver disease, a hepatic manifestation of metabolic syndrome, has been associated with periodontal disease. Nonalcoholic fatty liver disease is characterized by hepatic fat deposition in the absence of a habitual drinking history, viral infections, or autoimmune diseases. A subset of nonalcoholic fatty liver diseases can develop into more severe and progressive forms, namely nonalcoholic steatohepatitis. The latter can lead to cirrhosis and hepatocellular carcinoma, which are end-stage liver diseases. Extensive research has provided plausible mechanisms to explain how periodontal disease can negatively affect nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, namely via hematogenous or enteral routes. During periodontitis, the liver is under constant exposure to various pathogenic factors that diffuse systemically from the oral cavity, such as bacteria and their by-products, inflammatory cytokines, and reactive oxygen species, and these can be involved in disease promotion of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Also, gut microbiome dysbiosis induced by enteral translocation of periodontopathic bacteria may impair gut wall barrier function and promote the transfer of hepatotoxins and enterobacteria to the liver through the enterohepatic circulation. Moreover, in a population with metabolic syndrome, the interaction between periodontitis and systemic conditions related to insulin resistance further strengthens the association with nonalcoholic fatty liver disease. However, most of the pathologic links between periodontitis and nonalcoholic fatty liver disease in humans are provided by epidemiologic observational studies, with the causal relationship not yet being established. Several systematic and meta-analysis studies also show conflicting results. In addition, the effect of periodontal treatment on nonalcoholic fatty liver disease has hardly been studied. Despite these limitations, the global burden of periodontal disease combined with the recent nonalcoholic fatty liver disease epidemic has important clinical and public health implications. Emerging evidence suggests an association between periodontal disease and liver diseases, and thus we propose the term periodontal disease-related nonalcoholic fatty liver disease or periodontal disease-related nonalcoholic steatohepatitis. Continued efforts in this area will pave the way for new diagnostic and therapeutic approaches based on a periodontologic viewpoint to address this life-threatening liver disease.

Primer on etiology and treatment of progressive/severe periodontitis: A systemic health perspective.

Periodontology is an infectious disease-based discipline. The etiopathology of progressive/severe periodontitis includes active herpesviruses, specific bacterial pathogens, and proinflammatory cytokines. Herpesviruses and periodontopathic bacteria may interact synergistically to produce periodontal breakdown, and periodontal herpesviruses may contribute to systemic diseases. The infectious agents of severe periodontitis reside in deep pockets, furcation lesions, and inflamed gingiva, sites inaccessible by conventional (purely mechanical) surgical or nonsurgical therapy but accessible by systemic antibiotic treatment. This brief overview presents an effective anti-infective treatment of severe periodontitis, which includes systemic chemotherapy/antibiotics against herpesviruses (valacyclovir [acyclovir]) and bacterial pathogens (amoxicillin + metronidazole or ciprofloxacin + metronidazole) plus common antiseptics (povidone-iodine and sodium hypochlorite) and select ultrasonic scaling. The proposed treatment can cause a marked reduction or elimination of major periodontal pathogens, is acceptably safe, and can be carried out in minimal time with minimal cost.

How Does Epstein-Barr Virus Contribute to Chronic Periodontitis?

Chronic periodontitis is spreading worldwide and mutually interacts with systemic diseases like diabetes mellitus. Although periodontopathic bacteria are inevitable pathogens in their onset and progression, many cases are not ascribable to the virulence of these bacteria because the effect of plaque control is limited. In contrast, Epstein-Barr virus (EBV) in the periodontium has been correlated with chronic periodontitis and has recently been considered as a promising pathogenic candidate for this disease. However, several important questions have yet to be addressed. For instance, although EBV latently infects more than 90% of individuals over the world, why do patients with chronic periodontitis exclusively harbor progeny EBV in the oral cavity? In addition, how does latently infected or reactivated EBV in the periodontium relate to the onset or progression of chronic periodontitis? Finally, is periodontitis incurable because EBV is the pathogen for chronic periodontitis? In this review, we attempt to answer these questions by reporting the current understanding of molecular relations and mechanisms between periodontopathic bacteria and EBV reactivation in the context of how this relationship may pertain to the etiology of chronic periodontitis.

Establishment of potent and specific synthetic substrate for dipeptidyl-peptidase 7.

Bacterial dipeptidyl-peptidase (DPP) 7 liberates a dipeptide with a preference for aliphatic and aromatic penultimate residues from the N-terminus. Although synthetic substrates are useful for activity measurements, those currently used are problematic, because they are more efficiently degraded by DPP5. We here aimed to develop a potent and specific substrate and found that the kcat/Km value for Phe-Met-methylcoumaryl-7-amide (MCA) (41.40 ±â€¯0.83 µM-1 s-1) was highest compared to Met-Leu-, Leu-Leu-, and Phe-Leu-MCA (1.06-3.77 µM-1 s-1). Its hydrolyzing activity was abrogated in a Porphyromonas gingivalis dpp7-knockout strain. Conclusively, we propose Phe-Met-MCA as an ideal synthetic substrate for DPP7.

Response of epithelial cells infected by Treponema denticola.

OBJECTIVE: In the gingival crevice, the interaction between epithelial cells and periodontopathic bacteria is important for the development of periodontitis. Treponema denticola is a major pathogen of chronic periodontitis and possesses several virulence factors, such as major surface protein (Msp) and prolyl-phenylalanine-specific protease (dentilisin). Here, we investigated the behaviours of epithelial cells infected with T. denticola by measuring the expression of interleukin (IL)-1ß, IL-6, ß defensin 2 (BD-2) and heat-shock protein 70 (HSP70). METHODS: Epithelial cells were infected with T. denticola wild-type strain, Msp-deficient mutant or dentilisin-deficient mutant, and the expression levels of the above targets were analysed by polymerase chain reaction. RESULTS: Infection with T. denticola wild-type strain and mutants induced the production of IL-6 and HSP70. The level of BD-2 induced by T. denticola wild-type strain at 24 hr was significantly higher than that of the dentilisin-deficient mutant. The level of IL-1ß mRNA in the wild-type strain and dentilisin-deficient mutant was slightly lower than that in the uninfected control. CONCLUSION: These results suggest that the levels of BD-2 were affected by Msp and dentilisin. This effect may contribute to the disruption of the response of epithelial cells to eradicate T. denticola.

Regulation of the NLRP3 inflammasome in Porphyromonas gingivalis-accelerated periodontal disease.

OBJECTIVE: Porphyromonas gingivalis is involved in the pathogenesis of chronic inflammatory periodontal disease. Recent studies have suggested that the NLRP3 inflammasome plays an important role in the development of chronic inflammation. We investigated a possible association between the inflammasome in gingival inflammation and bone loss induced by P. gingivalis infection using NLRP3-deficient mice. METHODS: Wild-type and NLRP3-deficient mice were injected orally with P. gingivalis. We assessed alveolar bone loss, expression of pro-interleukin (IL)-1ß, pro-IL-18, receptor activator of nuclear factor kappa-B ligand (RANKL), and osteoprotegerin (OPG) in gingival tissue, as well as IL-1ß, IL-18, and IL-6 production and caspase-1 activity in peritoneal macrophages. RESULTS: Porphyromonas gingivalis challenge significantly increased alveolar bone loss; gingival gene expression of pro-IL-1ß, pro-IL-18, and RANKL; production of IL-1ß, IL-18, and IL-6; and caspase-1 activity in peritoneal macrophages of wild-type mice, but did not affect NLRP3-deficient mice. Meanwhile, OPG mRNA expression in gingival tissue and peritoneal IL-6 production were significantly higher in NLRP3-knockout mice. CONCLUSIONS: Porphyromonas gingivalis activated innate immune cells via the NLRP3 inflammasome. These results suggest that the NLRP3 inflammasome, followed by a response from the IL-1 family, is critical in periodontal disease induced by wild-type P. gingivalis challenge via sustained inflammation.

Influence of a triclosan toothpaste on periodontopathic bacteria and periodontitis progression in cardiovascular patients: a randomized controlled trial.

BACKGROUND AND OBJECTIVE: Triclosan/copolymer toothpaste is effective in controlling plaque and gingivitis and in slowing the progression of periodontitis. This study describes its influence on microbiological and clinical outcomes, over a 5-year period, in patients with established cardiovascular disease (CVD). MATERIAL AND METHODS: Four-hundred and thirty-eight patients were recruited from the Cardiovascular Unit at The Prince Charles Hospital, Brisbane, Australia, and randomized to triclosan or placebo groups. Six sites per tooth were examined annually for probing pocket depth and loss of attachment. These outcomes were analysed, using generalized linear modelling, in 381 patients who had measurements from consecutive examinations. Concurrent load of the periodontal pathogens Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum, Tannerella forsythia and Porphyromonas gingivalis was determined, using quantitative real-time PCR, in 437 patients with baseline plaque samples. Group comparisons were expressed as geometric means. The chi-square test was used to test for differences between the two groups of patients with regard to the proportion of patients with different numbers of bacterial species. RESULTS: There was no difference in general health or periodontal status between the groups at baseline. There was a significant reduction in the number of interproximal sites showing loss of attachment between examinations, by 21% on average (p < 0.01), in the triclosan group compared with the placebo group. The prevalence of patients with F. nucleatum and A. actinomycetemcomitans was high and remained relatively constant throughout the 5 years of the study. In contrast, the prevalence of T. forsythia and P. gingivalis showed more variability; however, there was no significant difference between the groups, at any time point, in the prevalence of any organism. A significant difference in the geometric means for P. gingivalis (p = 0.01) was seen at years 1 and 4, and for F. nucleatum (p = 0.01) and in the total bacterial load (p = 0.03) at year 2; however, these differences were not statistically significant following a Bonferroni correction for multiple comparisons. There was no difference between the groups in the geometric means for each organism at year 5. CONCLUSION: Within the limitations of the study, these data suggest that the use of triclosan/copolymer toothpaste significantly slowed the progression of periodontitis in patients with CVD but that it had little influence on key subgingival periodontopathic bacteria in these patients over the 5 years of the study.

The role of Toll-like receptors in 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.

Porphyromonas Gingivalis Elevated High-Mobility Group Box 1 Levels After Myocardial Infarction in Mice.

High mobility group box 1 (HMGB1) is a nuclear protein released from necrotic cells, inducing inflammatory responses. Epidemiological studies suggested a possible association between periodontitis and cardiovascular diseases (CVDs). Due to tissue damage and necrosis of cardiac cells following myocardial infarction (MI), HMGB1 is released, activating an inflammatory reaction. However, it remains unclear whether periodontitis is also involved in myocardial damage. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis (P.g.) after MI in mice.C57BL/6J wild type mice in post-MI were inoculated with P.g. in the infected group (P.g.-inoculated MI group) and with phosphate buffer saline (PBS) in the control group (PBS-injected MI group). Plasma samples and twelve tissue samples from mice hearts after MI were obtained. We determined the expression of HMGB1 by ELISA and immunohistochemistry.The level of HMGB1 protein in the P.g.-inoculated MI group was significantly higher than in the PBS-injected MI group on day 5, but not on day 14. Immunohistochemistry analysis revealed that HMGB1 was mainly expressed in cardiomyocytes, immune cells, and vascular endothelial cells in the PBS-injected MI group, while HMGB1 was seen broadly in degenerated cardiomyocytes, extracellular fields, immune cells, and vascular endothelial cells in the P.g.-inoculated MI group. A significant increase in the number of HMGB1 positive cells was observed in the P.g.-inoculated MI group compared to the PBS-injected MI group.Infection with P.g. after MI enhanced myocardial HMGB1 expression. There is a possible relationship between periodontitis and post-infarction myocardial inflammation through HMGB-1.

Point-of-care detection of Tannerella forsythia using an antigen-antibody assisted dielectrophoretic impedance measurement method.

UNLABELLED: The importance of periodontal treatment planning based on diagnosis with clinical detection of periodontal pathogens has been well recognized. However, reliable detection and quantification methods that can be conveniently used at chair-side have yet to be developed. This study aimed to evaluate the clinical use of a novel apparatus which uses an antigen-antibody reaction assisted dielectrophoretic impedance measurement (AA-DEPIM) for the detection of a prominent periodontal pathogen, Tannerella forsythia. A total of 15 patients with a clinical diagnosis of chronic periodontitis, three periodontally healthy volunteers and two with gingivitis were subjected to clinical and microbiological examinations. Saliva samples were analyzed for the presence of T. forsythia using AA-DEPIM, PCR-Invader and real-time PCR methods. The measurement values for total bacteria and T. forsythia using the prototype AA-DEPIM apparatus were significantly greater in periodontitis group than those in healthy/gingivitis group. Using the AA-DEPIM apparatus with tentative cut-off values, T. forsythia was detected for 14 (12 with periodontitis and 2 either healthy or with gingivitis) out of 20 individuals. The measurement for the detection of T. forsythia by the AA-DEPIM method showed a significant positive correlation with the detection by PCR-Invader (r = 0.541, p = 0.01) and the real-time PCR method (r = 0.834, p = 0.01). When the PCR-Invader method was used as a reference, the sensitivity and specificity of the AA-DEPIM method were 76.5% and 100%, respectively. The results suggested that the AA-DEPIM method has potential to be used for clinically evaluating salivary presence of T. forsythia at chair-side. TRIAL REGISTRATION: UMIN Clinical Trials Registry (UMIN-CTR) UMIN000012181.

Effects of ozone nano-bubble water on periodontopathic bacteria and oral cells - in vitro studies.

The aims of the present study were to evaluate the bactericidal activity of a new antiseptic agent, ozone nano-bubble water (NBW3), against periodontopathogenic bacteria and to assess the cytotoxicity of NBW3 against human oral cells. The bactericidal activities of NBW3 against representative periodontopathogenic bacteria, Porphyromonas gingivalis (P. gingivalis) and Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) were evaluated using in vitro time-kill assays. The cytotoxicity of NBW3 was evaluated using three-dimensional human buccal and gingival tissue models. The numbers of colony forming units (CFUs)/mL of P. gingivalis and A. actinomycetemcomitans exposed to NBW3 dropped to below the lower limit of detection (<10 CFUs mL-1) after only 0.5 min of exposure. There were only minor decreases in the viability of oral tissue cells after 24 h of exposure to NBW3. These results suggest that NBW3 possesses potent bactericidal activity against representative periodontopathogenic bacteria and is not cytotoxic to cells of human oral tissues. The use of NBW3 as an adjunct to periodontal therapy would be promising.

Effects of Oleanolic Acid Derived from Wine Pomace on Periodontopathic Bacterial Growth in Healthy Individuals: A Randomized Placebo-Controlled Study.

Periodontal disease is caused by oral pathogenic bacteria and is associated with systemic disease and frailty. Therefore, its prevention is crucial in extending healthy life expectancy. This study aimed to evaluate the effect of orally administered oleanolic acid, extracted from wine pomace, on periodontopathic bacterial growth in healthy individuals. In this randomized, placebo-controlled, double-blind, parallel-group comparison study, 84 healthy adults were assigned to a placebo (n = 29), low-dose (n = 29, 9 mg oleanolic acid), or high-dose (n = 26, 27 mg oleanolic acid) groups. The number of oral bacteria in their saliva, collected before and 5 h after administration, was determined using the polymerase chain reaction-invader technique. The proportion of periodontopathic bacteria among the total oral bacteria in the saliva was calculated. Oleanolic acid significantly decreased the proportion of Porphyromonas gingivalis among the total oral bacteria in a dose-dependent manner (p = 0.005 (low-dose) and p = 0.003 (high-dose) vs. placebo, Williams' test). Moreover, high-dose oleanolic acid decreased the proportion of Tannerella forsythia (p = 0.064 vs. placebo, Williams' test). Periodontopathic bacteria are closely associated with the development and progression of periodontal disease; thus, the continuous daily intake of oleanolic acid derived from pomace may be helpful in maintaining a healthy oral microbiome by controlling the proportion of periodontopathic bacteria.

Quantification of key periodontal pathogens in insulin-dependent type 2 diabetic and non-diabetic patients with generalized chronic periodontitis.

Periodontitis is a common problem in patients with diabetes mellitus (DM), however, differences in the putative periodontal pathogens in subjects with DM compared to non-DM subjects are still inconclusive. The red complex, which includes Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, encompasses the most important pathogens in adult periodontal disease. The aim of the present study was to compare cell numbers of P. gingivalis, T. denticola, T. forsythia and Aggregatibacter actinomycetemcomitans in gingival sulcus of healthy, gingivitis and periodontitis sites of non-diabetes mellitus (NDM), controlled and poorly controlled insulin-dependent DM (CDM and PDM) patients with generalized chronic periodontitis. Subgingival plaque samples were collected from 19 CDM, 19 PDM and 19 NDM patients. Taqman real time-PCR was used to determine bacterial cell number. At subject level, the quantity of red complex bacteria was significantly higher in PDM than those of NDM and positively correlated with HbA1c. At site level (total 342 sites), cell numbers of T. denticola and T. forsythia in healthy sites of CDM and PDM were significantly higher than those of NDM. In gingivitis sites, the numbers of P. gingivalis in CDM and PDM and T. forsythia in PDM were significantly higher than those of NDM while in periodontitis sites, higher quantity of P. gingivalis in PDM was observed. Our study indicated that poor glycemic control is associated with increasing cell numbers of red complex bacteria in subgingival biofilm.

Periodontitis and periodontopathic bacteria as risk factors for rheumatoid arthritis: A review of the last 10 years.

Rheumatoid arthritis (RA) is characterized by chronic inflammatory destruction of joint tissue and is caused by an abnormal autoimmune response triggered by interactions between genetics, environmental factors, and epigenetic and posttranslational modifications. RA has been suggested to be interrelated with periodontitis, a serious form or stage of chronic inflammatory periodontal disease associated with periodontopathic bacterial infections, genetic predisposition, environmental factors, and epigenetic influences. Over the last decade, a number of animal and clinical studies have been conducted to assess whether or not periodontitis and associated periodontopathic bacteria constitute risk factors for RA. The present review introduces recent accumulating evidence to support the associations of periodontitis and periodontopathic bacteria with the risk of RA or the outcome of RA pharmacological treatment with disease-modifying antirheumatic drugs. In addition, the results from intervention studies have suggested an improvement in RA clinical parameters after nonsurgical periodontal treatment. Furthermore, the potential causal mechanisms underlying the link between periodontitis and periodontopathic bacteria and RA are summarized.

Oral-gut axis as a novel biological mechanism linking periodontal disease and systemic diseases: A review.

Substantial evidence suggests that periodontal disease increases the risk of developing and progressing extraoral manifestations such as diabetes, atherosclerosis, rheumatoid arthritis, and inflammatory bowel disease. The most probable causative mechanism behind this is the influx of bacteria and/or bacterial products (endotoxin) and inflammatory cytokines into the systemic circulation originating from inflamed periodontal tissues. However, recent studies have revealed that oral bacteria, especially periodontopathic bacteria, play a role in inducing dysbiosis of the gut microbiota resulting induction of gut dysbiosis-related pathology associated with systemic diseases. Conversely, the disruption of gut microbiota has been shown to have a negative impact on the pathogenesis of periodontal disease. Based on our study findings and the available literature, this review presents an overview of the relationship between periodontal disease and systemic health, highlighting the mouth-gut connection.

Xylitol-Containing Chewing Gum Reduces Cariogenic and Periodontopathic Bacteria in Dental Plaque-Microbiome Investigation.

Background: Dental caries and periodontal disease remain the most prevalent oral health problems in the world. Chewing xylitol gum may help reduce the risk of caries and periodontitis for dental health benefits. However, little evidence has shown healthy food estimation by sequencing 16S rDNA in oral microbial communities. This study investigated the clinical effect of xylitol chewing gum on dental plaque accumulation and microbiota composition using the PacBio full-length sequencing platform in 24 young adults (N = 24). The participants were randomly assigned to xylitol chewing gum and control (no chewing gum) groups. Participants in the chewing gum group chewed ten pieces of gum (a total of 6.2 g xylitol/day). Dental plaque from all teeth was collected for weighing, measuring the pH value, and analysis of microbial communities at the beginning (baseline, M0) and end of the 2-week (effect, M1) study period. Results: The results suggested a 20% reduction in dental plaque accumulation (p < 0.05) among participants chewing xylitol gum for 2 weeks, and the relative abundance of Firmicutes (a type of pathogenic bacteria associated with caries) decreased by 10.26% (p < 0.05) and that of Bacteroidetes and Actinobacteria (two types of pathogenic bacteria associated with periodontitis) decreased by 6.32% (p < 0.001) and 1.66% (p < 0.05), respectively. Moreover, the relative abundance of Fusobacteria was increased by 9.24% (p < 0.001), which has been proven to have a higher proportion in dental plaque of healthy adults. However, the dental plaque pH value stayed in a healthy range for the two groups. Conclusion: In conclusion, chewing xylitol gum would benefit cariogenic and periodontal bacterial reduction in the oral cavity, which could help to prevent the diseases related to these bacteria.

Relationship between the prevalence of oral human papillomavirus DNA and periodontal disease (Review).

Human papillomavirus (HPV) is a small DNA virus that infects the basal keratinocytes of squamous epithelium in the skin, and in the oral and genital mucosa. Smoking and sexual behavior have been recognized as significant risk factors for oral HPV infection. In the present review, the findings of recent studies of oral HPV infection in relation to periodontitis are discussed, as well as periodontopathic bacteria and periodontal herpes virus. Previous research suggests that HPV localizes to the inflammatory periodontal tissue. Inflammatory periodontal pockets may thus act as a reservoir for HPV. The interactions between HPV and periodontopathic bacteria remain unclear, but it is hypothesized that oral HPV infection may be related to a characteristic oral microbiome. Smoking is associated with HPV and periodontitis, as smoking induces destruction of periodontal tissue and suppresses the host defense, allowing HPV to infect periodontal tissue. Carcinogenic HPV and periodontitis may lead to the development of oral cavity cancer. However, oral HPV E6/E7 expression (transcriptionally active HPV) has not yet been fully investigated in patients with periodontitis. Collectively, the evidence suggests that oral HPV prevalence may be associated with periodontitis. The effect of clinical factors (age, sex, smoking, immunosuppressive condition and vaccination) on oral HPV DNA prevalence should be considered when clarifying the relationship between oral HPV and periodontitis. Additionally, the sampling method should be carefully chosen to directly detect HPV DNA in periodontal tissues.

Synergistic antibacterial activity of herbal extracts with antibiotics on bacteria responsible for periodontitis.

INTRODUCTION: Development of bacterial resistance and antimicrobial side-effect has shifted the focus of research toward Ethnopharmacology. A biologically active compound derived from the plants may increase the effectiveness of antibiotic when used in combination. The present study aims to determine the synergistic antibacterial effect of ethanolic extracts of Punica granatum (pericarp), Commiphora molmol, Azadirachta indica (bark) in combination with amoxicillin, metronidazole, tetracycline, and azithromycin on periodontopathic bacteria: Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola and Aggregatibacter actinomycetemcomitans. METHODOLOGY: Periodontopathic bacterial strains were isolated from the plaque sample that was collected from periodontitis patients and grown under favorable conditions. Susceptibility of bacteria to the antibiotics and extracts was determined by disc diffusion method by measuring the diameter of the inhibition zones. Minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of plant extracts were evaluated against each bacterium. Synergistic effect of plant extract in combination with antibiotics was tested against each bacterium by measuring the diameter of zone of inhibition (ZOI). RESULTS: Findings revealed that all plant extracts exhibited an inhibitory effects on the proliferation and growth of periodontopathic bacteria. The maximum antibacterial effect was exhibited by C. molmol on P. gingivalis (ZOI = 20 ± 0.55 mm, MIC = 0.53 ± 0.24 mg/mL and MBC = 5.21 ± 1.81 mg/mL) (p < 0.05), meanwhile, no antibacterial activity was exhibited by P. granatum on T. forsythia. Synergistic antibacterial effect was recorded when plant extracts were used in combination with antibiotics. The best synergism was exhibited by P. granatum with amoxicillin against A. actinomycetemcomitans (24 ± 1.00 mm) (p < 0.05). CONCLUSIONS: The synergistic test showed significant antibacterial activity when plant extracts were combined with antibiotics against all the experimented bacteria.