Etiology Of Chronic Periodontitis Research Articles

Evaluation of serum mineral micronutrients (Zn, Cu, Fe, Mg) and their correlation with clinical parameters (gingival index, probing pocket depth, clinical attachment loss) in chronic periodontitis patients

Background: Nutrition especially micro-mineral nutrients plays a major role in the etiology of chronic periodontitis. Serum levels of micro-mineral nutrients can be used as markers for the incidence of periodontitis and may also be used as indicators for dietary supplementation. Aims and Objectives: The aim of the study was to estimate the serum levels of Zn, Cu, Fe, and Mg of chronic periodontitis patients and normal healthy controls., to measure the clinical parameters (gingival index, probing pocket depth [PPD], and clinical attachment loss) in chronic periodontitis patients and normal healthy controls., to compare the levels of serum Zn, Cu, Fe, and Mg levels of chronic periodontitis patients and healthy controls and to correlate the levels of serum micronutrients with clinical parameters (gingival index, PPD, and clinical attachment loss) in chronic periodontitis patients and healthy controls. Materials and Methods: A total of 110 subjects, 55 subjects with chronic periodontitis and 55 healthy control subjects in the age group 35–65 years were selected for the study. Serum micronutrient levels of Cu, Fe, Zn, Mg, and the clinical parameters were measured. Results: Serum concentrations of Cu and Fe showed statistically significant increase and serum Zn and Mg showed a significant decrease in peridontitis patients as compared to normal healthy controls. Copper and Fe showed a significant positive correlation and Zn and Mg showed a significant negative correlation with clinical parameters (gingival index, PPD, and clinical attachment loss). Conclusion: The present study supports and extends the view that the assessment of serum mineral micronutrient can serve as possible biomarkers or indicators for an inflammatory condition like chronic periodontitis.

Inhibitory activity of jackfruit (Atrocarpus heterophyllus Lam.) leaf extract on the growth of Porphyromonas gingivalis bacteria

Background: Periodontitis is an inflammation that affects the periodontal tissue, causing pocket formation, loss of attachment, and tooth mobility. Periodontitis caused by a complex interaction between the body's immune response and microorganisms in dental plaque. One of the main agents in the etiology of chronic periodontitis is Porphyromonas gingivalis. Jackfruit (Atrocarpus heterophyllus Lam.) leaf contains active compounds such as saponin, flavonoid, and tannin. Objective: This study is aimed to determine the inhibition of jackfruit leaf extract (Atrocarpus heterophyllus Lam.) on the growth of Porphyromonas gingivalis bacteria. Method: This research is an in vitro laboratory experiment. Jackfruit leaf extraction was carried out by maceration method with 70% ethanol solvent, then diluted serially by dilution to obtain various concentrations. Concentrations used include 100%; 50%; 25%; 12.5%; 6.25%; 3.125%; 1.56%; and 0.78%. Inhibition test against Porphyromonas gingivalis bacteria was carried out by spectrophotometric method and colony count. Result: Jackfruit leaf extract with a concentration of 12.5%; 25%; 50%; and 100% can kill Porphyromonas gingivalis bacterial colonies resulting in 0 colonies. A concentration of 6.25% inhibited the growth of bacteria by 91.77%. The results of statistical tests obtained a significance value of 0.001 (P <0.05). Conclusion: Jackfruit leaf extract (Atrocarpus heterophyllus Lam.) has an inhibitory effect on the growth of Porphyromonas gingivalis bacteria with MIC values ​​at a concentration of 6.25% and MBC at a concentration of 12.5%.

To evaluate the serum cortisol, salivary cortisol, and serum interleukin-1 B level in patients of chronic periodontitis with smoking and stress and without smoking and stress.

The role of cognitive, social and biological factors in the etiology of chronic periodontitis has been reported.The aim of this study was to evaluate the salivary cortisol level and interleukin-1 B level in patients of Chronic periodontitis in smokers and stress and nonsmokers without stress.The design of study randomized, prospective, double-blinded, and prospective study.The total sample size was comprised of 600 subjects between the ages of 20 and 50 years. The sample size was divided into 300 males and 300 females. Out of 600 subjects, 200 subjects comprised of subjects with chronic periodontitis with positive depression level with a history of smoking (Group I), 200 subjects comprised of subjects with chronic periodontitis without depression and without smoking (Group II), and 200 subjects who were taken as the control group comprised of healthy subjects without chronic periodontitis, without depression level, and no smoking history (Group III). Salivary cortisol levels were determined by enzyme-linked immunosorbent assay (ELISA).The result showed that there was a positive correlation between morning and evening salivary cortisol level in all the groups with correlation coefficient. There was significant higher value of salivary cortisol in Group I patients when compared with Group II and Group III. However, when the comparison of salivary cortisol levels was done between the Group II and Control group, the result showed nonsignificant P value.It is suggested that stress is positively correlated with the salivary cortisol levels in smokers and nonsmokers.

Filifactor alocis and its role in the etiology of chronic periodontitis

The review is devoted to the analysis of modern ideas about the role of bacteria Filifactor alocis in the etiology of chronic periodontitis. The study of these bacteria, discovered in 1985, is complicated by the difficulty of their detection with cultural methods. According to modern researches, the bacteria F.alocis with good reason can be included in the red complex of periodontal pathogens as the most important pathogens of chronic periodontitis. F.alocis is a synergist of such a key pathogen Porphyromonas gingivalis, as well as a frequent satellite of Fusobacterium nucleatum and, somewhat less frequently, Aggregatibacter actinomycetemcomitans. F.alocis is practically not found in healthy people (except for smokers), with a high frequency accompanies the aggressive course of periodontal disease, and also recorded in endodontitis. Due to the ability to participate in the metabolism of arginine, expressed protease activity, a wide range of virulence factors, F.alocis not only colonizes the periodontal tissues, but also significantly affects the formation of the community of periodontal microorganisms (including viruses), contributing to their invasion of epithelial tissues. F. alocis has a number of unique properties, including resistance to oxidative stress conditions in the home defeat, induction of apoptosis of epithelial cells, extracellular matrix degradation of periodontal tissues, activation of proinflammatory cytokines formulation in sites of its presence, suppression of protective reactions of neutrophilic granulocytes, inhibition of the process of complement activation.

Opportunistic Pathogen Porphyromonas gingivalis Modulates Danger Signal ATP-Mediated Antibacterial NOX2 Pathways in Primary Epithelial Cells.

Porphyromonas gingivalis, a major opportunistic pathogen in the etiology of chronic periodontitis, successfully survives in human gingival epithelial cells (GECs). P. gingivalis abrogates the effects of a host danger molecule, extracellular ATP (eATP)/P2X7 signaling, such as the generation of reactive oxygen species (ROS) via the mitochondria and NADPH oxidases (NOX) from primary GECs. However, antimicrobial functions of ROS production are thoroughly investigated in myeloid-lineage immune cells and have not been well-understood in epithelial cells. Therefore, this study characterizes antibacterial NOX2 generated ROS and host downstream effects in P. gingivalis infected human primary GECs. We examined the expression of NOX isoforms in the GECs and demonstrate eATP stimulation increased the mRNA expression of NOX2 (p < 0.05). Specific peptide inhibition of NOX2 significantly reduced eATP-mediated ROS as detected by DCFDA probe. The results also showed P. gingivalis infection can temporally modulate NOX2 pathway by reorganizing the localization and activation of cytosolic molecules (p47phox, p67phox, and Rac1) during 24 h of infection. Investigation into downstream biocidal factors of NOX2 revealed an eATP-induced increase in hypochlorous acid (HOCl) in GECs detected by R19-S fluorescent probe, which is significantly reduced by a myeloperoxidase (MPO) inhibitor. MPO activity of the host cells was assayed and found to be positively affected by eATP treatment and/or infection. However, P. gingivalis significantly reduced the MPO product, bactericidal HOCl, in early times of infection upon eATP stimulation. Analysis of the intracellular levels of a major host-antioxidant, glutathione during early infection revealed a substantial decrease (p < 0.05) in reduced glutathione indicative of scavenging of HOCl by P. gingivalis infection and eATP treatment. Examination of the mRNA expression of key enzymes in the glutathione synthesis pathway displayed a marked increase (p < 0.05) in glutamate cysteine ligase (GCL) subunits GCLc and GCLm, glutathione synthetase, and glutathione reductase during the infection. These suggest P. gingivalis modulates the danger signal eATP-induced NOX2 signaling and also induces host glutathione synthesis to likely avoid HOCl mediated clearance. Thus, we characterize for the first time in epithelial cells, an eATP/NOX2-ROS-antibacterial pathway and demonstrate P. gingivalis can circumvent this important antimicrobial defense system potentially for successful persistence in human epithelial tissues.

Effect of cigarette smoking on subgingival bacteria in healthy subjects and patients with chronic periodontitis

BackgroundCigarette smoking is known to increase the risk of periodontal destruction and developing chronic periodontitis (CP). It is also reported to affect the subgingival bacterial profile among CP patients. However, studies on the effect of smoking on the bacterial profile among healthy subjects are still limited. Therefore, the aim of this study was to investigate the impact of smoking on the subgingival bacterial profile in both healthy adults and CP patients.MethodsSubgingival plaque samples were collected from CP patients (30 nonsmokers and 9 smokers) and healthy subjects (37 non-smokers and 18 smokers). Genomic DNA was extracted and 25 bacterial species were detected using PCR of 16S rRNA. Comparing smokers to non-smokers from each group was conducted using chi2 and binary logistic regression analysis.ResultsAfter correcting for confounding factors, the odds of having Slackia exigua, Selenomonas sputigena and Campylobacter rectus was higher among healthy smokers (ORadj = 10.1, 6.62 and 5.62 respectively). While for CP group, the highest odds were observed for Treponema amylovorum, Treponema medium, Slackia exigua and Treponema vincentii (ORadj = 20.7, 7.97, 6.37 and 5.37 respectively) and the increase in Treponema amylovorum was statistically significant (p = 0.05).ConclusionSmoking affects the subgingival bacterial profile in healthy individuals and is responsible for the depletion of beneficial bacteria and the increase in periodontopathogenic bacteria. In the CP patient group, our study suggests that subgingival bacteria (particularly Treponema species) make a more substantial contribution in the etiology of CP among non-smokers. Further studies using a larger sample set and more sensitive and quantitative techniques (such as real -time PCR) are needed to enhance our understanding of the exact effect of smoking on subgingival biofilm.

Association of three putative periodontal pathogens with chronic periodontitis in Brazilian subjects

ABSTRACTObjective The aim of this study was to evaluate the association of Porphyromonas endodontalis, Filifactor alocis and Dialister pneumosintes with the occurrence of periodontitis.Material and Methods Thirty subjects with chronic periodontitis (ChP) and 10 with periodontal health (PH) were included in the study. Nine subgingival biofilm samples were collected as follows: i) PH group - from the mesial/buccal aspect of each tooth in two randomly chosen contralateral quadrants; ii) ChP group - from three sites in each of the following probing depth (PD) categories: shallow (≤3 mm), moderate (4-6 mm) and deep (≥7 mm). Checkerboard DNA-DNA hybridization was used to analyze the samples.Results We found the three species evaluated in a higher percentage of sites and at higher levels in the group with ChP than in the PH group (p<0.05, Mann-Whitney test). We also observed these differences when the samples from sites with PD≤4 mm or ≥5 mm of subjects with ChP were compared with those from subjects with PH (p<0.05, Mann-Whitney test). In addition, the prevalence and levels of D. pneumosintes, and especially of F. alocis were very low in healthy subjects (0.12x105 and 0.01x105, respectively).Conclusion F. alocis and D. pneumosintes might be associated with the etiology of ChP, and their role in the onset and progression of this infection should be further investigated. The role of P. endodontalis was less evident, since this species was found in relatively high levels and prevalence in the PH group.

Role of Porphyromonas gingivalis in rheumatoid arthritis and inflammatory spondyloarthropathies

The most recent studies confirm the link between rheumatoid arthritis (RA) and periodontal disease. RA patients have higher prevalence of chronic periodontitis and periodontal disease is often more severe in these patients. Both RA and PD show similar pathophysiological mechanisms and risk factors. Autoimmunity to citrullinated peptides is the primary element in the pathogenesis of RA, not found in other diseases. Porphyromonas gingivalis, the major periodontal pathogen associated with the etiology of chronic periodontitis, is the only bacterium currently known to produce the enzyme peptidylarginine deiminase (PAD) allowing protein citrullination. This bacterium likely fulfils a significant role in the pathogenesis of RA due to its capacity for citrullination of its own protein and host peptides, which may result in a loss of immune tolerance. A few epidemiological studies also indicate the potential link between spondyloarthropathies and periodontal disease.

Increased Interleukin-18 in the Gingival Tissues Evokes Chronic Periodontitis after Bacterial Infection

Periodontal disease is a chronic inflammatory disease that results in the breakdown of the tooth-supporting tissues, and can ultimately lead to resorption of the alveolar bone. Recently, several studies have shown a close relationship between increased interleukin-18 (IL-18) levels and the pathogenesis of chronic periodontitis, a major cause of tooth loss. However, it has yet to be shown whether chronic periodontitis results from or causes an increase in IL-18 after bacterial infection. In the present study, we investigated how IL-18 overexpression relates to periodontal disease using IL-18 transgenic (Tg) mice. IL-18Tg and wild-type mice were inoculated intraorally with Porphyromonas (P.) gingivalis, which has been implicated in the etiology of chronic periodontitis. Seventy days after P. gingivalis infection, alveolar bone loss and gingival cytokine levels were assessed using histo-morphological analysis and enzyme-linked immuno-absorbent assay, respectively. Periodontal bone loss was evoked in IL-18Tg mice, but not in wild-type mice. Interestingly, levels of bone-resorptive cytokines, including IL-1α, IL-1β, tumor necrosis factor-α, and IL-6, were unchanged in the gingival tissues of IL-18Tg mice infected with P. gingivalis, although levels of interferon γ (a proinflammatory T-helper 1 cytokine) decreased. RT-PCR analysis showed elevated expression of mRNAs for receptor activator of nuclear factor kappa-B ligand (a key stimulator of osteoclast development and activation) and CD40 ligand (a marker of T cell activation) in the gingiva of IL-18Tg mice infected with P. gingivalis. We conclude that increased IL-18 in the gingival tissues evokes chronic periodontitis after bacterial infection, presumably via a T cell-mediated pathway.

Porphyromonas gingivalis Strain Diversity

Porphyromonas gingivalis is implicated in the etiology of chronic periodontitis. Genotyping studies suggest that genetic variability exists among P. gingivalis strains; however, the extent of variability remains unclear and regions of variability remain largely unidentified. To assess P. gingivalis strain diversity, we previously used heteroduplex analysis of the ribosomal operon intergenic spacer region (ISR) to type strains in clinical samples and identified 22 heteroduplex types. Additionally, we used ISR sequence analysis to determine the relatedness of P. gingivalis strains to one another and demonstrated a link between ISR sequence phylogeny and the disease-associated phenotype of the strains. In the current study, heteroduplex analysis of the ISR was used to determine the worldwide genetic variability and distribution of P. gingivalis, and microarray-based comparative genomic hybridization (CGH) analysis was used to more comprehensively examine the variability of major heteroduplex type strains by using the entire genome. Heteroduplex analysis of clinical samples from geographically diverse populations identified 6 predominant geographically widespread heteroduplex types (prevalence, > or = 5%) and 14 rare heteroduplex types (prevalence, <2%) which are found in one or a few locations. CGH analysis of the genomes of seven clinically prevalent heteroduplex type strains identified 133 genes from strain W83 that were divergent in at least one of the other strains. The relatedness of the strains to one another determined on the basis of genome content (microarray) analysis was highly similar to their relatedness determined on the basis of ISR sequence analysis, and a striking correlation between the genome contents and disease-associated phenotypes of the strains was observed.

Prevalence of Porphyromonas gingivalis and Bacteroides forsythus in Chronic Periodontitis by Multiplex PCR

The present research decided to study prevalence of Porphyromonas gingivalis and Bacteroides forsythus in chronic periodontitis patient by use of Multiplex PCR. The subgingival plaque samples from 61 patients suffering from chronic periodontitis with probing depth PD > or = 6 and 40 healthy controls were collected by sterile curette. In this study we used two species-specific Forward primers in combination with a single Reverse primer. These primers target variable and conserved region of 16S rRNA gene, respectively. The study included 61 patients (34 women, 27 men; 24-69 years of age; mean 43) and 40 periodontally healthy controls (22 Women, 18 men, 21-69 years in age; mean 41.35%). Porphyromonas gingivalis was detected in 51 samples (83.61%) and 16 samples (40%) of chronic periodontitis patients and healthy subjects, respectively and Bacteroides forsythus was detected in 32 samples (52.50%) of chronic periodontitis patients and was not detected in any sample from healthy persons. We set up Multiplex PCR in order to detect P. gingivalis and B. forsythus simultaneously. The present data suggest that P. gingivalis is a more important cofactor in etiology of chronic periodontitis. Further studies are needed to determine spectrum of pathogenicity of the disease and effective management of diagnosis and treatment in order to decrease the risk of periodontic complicates such as systemic infection.

Construction of a sIgA-enhancing anti- Porphyromonas gingivalis FimA vaccine and nasal immunization in mice

Porphyromonas gingivalis is implicated in the etiology of chronic periodontitis. Fimbriae are one of several critical surface virulence factors of P. gingivalis. Interleukin 15 (IL-15) is a critical important cytokine for the differentiation of B-1 cells into IgA-inducing cells in mucosal tissues and the proliferation of B cells. The present study constructed a co-expression plasmid pIRES-fimA:IL-15 encoding fimbrinllin (FimA), a subunit of fimbriae and IL-15 as a sIgA-enhancing anti- P. gingivalis FimA vaccine. The plasmid pIRES-fimA:IL-15 was transfected to CHO cells. The expressions of FimA and IL-15 in CHO cells were verified by Western blot and ELISA. Mice were immunized with pIRES-fimA:IL-15 via nasal or intramucusal route. The results showed that nasal immunization was capable of promoting Ag-specific immune responses in the oral region as well as systemic immunity. When immunized via nasal route, IL-15 expressed by the plasmid enhanced FimA-specific sIgA antibody response. In conclusion, a co-expression plasmid pIRES-fimA:IL-15 has been constructed, and when immunized via nasal route, antigen-specific sIgA antibody response could be modulated positively in immunized mice.