A randomized controlled trial to evaluate the effectiveness of a novel mouth rinse in patients with gingivitis.

BACKGROUND: This single-center, randomized controlled trial aimed to determine the effectiveness of a novel, biofilm-disrupting, mouth rinse that combines Cetylpyridinium chloride (CPC) and essential oils in preventing re-accumulation of supragingival plaque and supragingival microbiome in patients with gingivitis after dental prophylaxis. METHODS: One hundred eighteen participants were randomly assigned in a 1:1 ratio to receive twice-daily test mouth rinse (59) or carrier rinse control (59) for 12 weeks after dental prophylaxis. RESULTS: In a per-protocol analysis that included patients who completed the intervention, the treatment group (39) had significantly lower supragingival plaque scores at 6 and 12 weeks compared to the control group (41; p = 0.022). Both groups showed similar improvement in gingivitis score, but neither group had improvement in bleeding score or probing depth. Thirty-eight (29%) patients did not complete the study due to loss of follow-up (17) or early discontinuation of the assigned intervention (21). Microbiome sequencing showed that the treatment rinse significantly depleted abundant and prevalent members of the supragingival plaque microbiome consortium. CONCLUSIONS: Among patients with gingivitis, the novel mouth rinse significantly reduced re-accumulation of supragingival plaque following dental prophylaxis by depleting supragingival plaque microbiome. However, long-term adherence to the rinse may be limited by adverse effects ( ClinicalTrials.gov number, NCT03154021).

Subgingival microbiome of deep and shallow periodontal sites in patients with rheumatoid arthritis: a pilot study.

BACKGROUND: Subgingival microbiome in disease-associated subgingival sites is known to be dysbiotic and significantly altered. In patients with rheumatoid arthritis (RA), the extent of dysbiosis in disease- and health-associated subgingival sites is not clear. METHODS: 8 RA and 10 non-RA subjects were recruited for this pilot study. All subjects received full oral examination and underwent collection of subgingival plaque samples from both shallow (periodontal health-associated, probing depth ≤ 3mm) and deep subgingival sites (periodontal disease-associated, probing depth ≥ 4 mm). RA subjects also had rheumatological evaluation. Plaque community profiles were analyzed using 16 S rRNA sequencing. RESULTS: The phylogenetic diversity of microbial communities in both RA and non-RA controls was significantly higher in deep subgingival sites compared to shallow sites (p = 0.022), and the overall subgingival microbiome clustered primarily according to probing depth (i.e. shallow versus deep sites), and not separated by RA status. While a large number of differentially abundant taxa and gene functions was observed between deep and shallow sites as expected in non-RA controls, we found very few differentially abundant taxa and gene functions between deep and shallow sites in RA subjects. In addition, compared to non-RA controls, the UniFrac distances between deep and shallow sites in RA subjects were smaller, suggesting increased similarity between deep and shallow subgingival microbiome in RA. Streptococcus parasanguinis and Actinomyces meyeri were overabundant in RA subjects, while Gemella morbillorum, Kingella denitrificans, Prevotella melaninogenica and Leptotrichia spp. were more abundant in non-RA subjects. CONCLUSIONS: The aggregate subgingival microbiome was not significantly different between individuals with and without rheumatoid arthritis. Although the differences in the overall subgingival microbiome was driven primarily by probing depth, in contrast to the substantial microbiome differences typically seen between deep and shallow sites in non-RA patients, the microbiome of deep and shallow sites in RA patients were more similar to each other. These results suggest that factors associated with RA may modulate the ecology of subgingival microbiome and its relationship to periodontal disease, the basis of which remains unknown but warrants further investigation.

The Importance of Being an Antagonist as Well as Persistent.

The current work by Jain et al. (S. Jain, A. M. Chang, M. Singh, J. S. McLean, et al., J Bacteriol 201:e00683-18, 2019, https://doi.org/10.1128/JB.00683-18) reports the cloning of the lipid A deacylase gene of Porphyromonas gingivalis and the phenotypic characterization of the enzyme. Attempts to clone the gene and thus provide proof of the existence of this enzyme had gone on for 2 decades. The enzyme is central to the bacterium's ability to modify and tailor the structure of its lipid A, changing a lipid A that is a moderate Toll-like receptor 4 (TLR4) agonist to an antagonist or silencer and thereby potentially changing the course of infection.

Porphyromonas gingivalis strain-dependent inhibition of uterine spiral artery remodeling in the pregnant rat.

Porphyromonas gingivalis (Pg) is an important periodontal pathogen that is also implicated in pregnancy complications involving defective deep placentation (DDP). We hypothesized that Pg invasion of the placental bed promotes DDP. Pregnant rats were intravenously inoculated with sterile vehicle, Pg strain W83, or A7436 at gestation day (GD) 14 (acute cohort). Nonpregnant rats received repeated oral inoculations for 3 months before breeding (chronic cohort). Tissues and/or sera were collected at GD18 for analysis. Pg infection status was determined by seroconversion (chronic cohort) and by presence of Pg antigen in utero-placental tissues processed for histology and morphometric assessment of spiral artery remodeling. Mesometrial tissues from seropositive dams were analyzed for expression of interleukin 1ß, 6, and 10, TNF, TGF-ß, follistatin-related protein 3, and inhibin beta A chain since these genes regulate extravillous trophoblast invasion. The in situ distribution of W83 and A7436 antigen in utero-placental tissues was similar in both cohorts. In the acute cohort, mesometrial stromal necrosis was more common with W83, but arteritis was more common with A7436 infection (P < 0.05). Increased vascular necrosis was seen in mesometrium of chronically infected groups (P < 0.05). Only A7436-infected animals had increased fetal deaths, reduced spiral artery remodeling, reduced inhibin beta A expression, and an increased proportion of FSLT3 positive extravillous trophoblasts within spiral arteries. While infection with both Pg strains produced varying pathology of the deep placental bed, only infection with strain A7436 resulted in impaired spiral artery remodeling.

Matrix Metalloproteinase Response of Dendritic Cell, Gingival Epithelial Keratinocyte, and T-Cell Transwell Co-Cultures Treated with Porphyromonas gingivalis Hemagglutinin-B.

Matrix metalloproteinases (MMPs) are enzymes involved in periodontal tissue destruction. Hemagglutinin B (HagB) from the periodontal pathogen Porphyromonas gingivalis induces an elevated MMP response in dendritic cells, but responses from cultures of single-cell types do not reflect the local tissue environment. The objective of this study was to measure HagB-induced MMP responses in a transwell co-culture system containing dendritic cells, gingival epithelial (GE) keratinocytes, and CD4+ T-cells. Transwell co-cultures were assembled and treated with or without HagB. Immunoassays were used to determine production of MMP1, MMP7, MMP9, and MMP12 in response to HagB up to 64 h. Control responses were subtracted from HagB-induced responses. A two-way fixed effect ANOVA was fit to log-transformed concentrations and pairwise group comparisons were conducted (p < 0.05). At 64 h, dendritic cells produced elevated MMP1 and MMP9 responses, which were attenuated in the 3-cell co-culture (p < 0.05). There were also significant differences in MMP7 and MMP12 production between single-cell cultures and co-cultures. These results support the need to use multiple cell types in culture models to evaluate a more representative response to proinflammatory agonists. This three-cell transwell co-culture model may help us better understand the inflammatory process in periodontal disease and test novel therapeutic approaches.

The collagen binding protein Cnm contributes to oral colonization and cariogenicity of Streptococcus mutans OMZ175.

Streptococcus mutans is the etiological agent of dental caries and one of the many bacterial species implicated in infective endocarditis. The expression of the collagen-binding protein Cnm by S. mutans has been associated with extraoral infections, but its relevance for dental caries has only been theorized to date. Due to the collagenous composition of dentinal and root tissues, we hypothesized that Cnm may facilitate the colonization of these surfaces, thereby enhancing the pathogenic potential of S. mutans in advancing carious lesions. As shown for extraoral endothelial cell lines, Cnm mediates the invasion of oral keratinocytes and fibroblasts by S. mutans. In this study, we show that in the Cnm(+) native strain, OMZ175, Cnm mediates stringent adhesion to dentinal and root tissues as well as collagen-coated surfaces and promotes both cariogenicity and carriage in vivo. In vitro, ex vivo, and in vivo experiments revealed that while Cnm is not universally required for S. mutans cariogenicity, it contributes to (i) the invasion of the oral epithelium, (ii) enhanced binding on collagenous surfaces, (iii) implantation of oral biofilms, and (IV) the severity of caries due to a native Cnm(+) isolate. Taken together, our findings reveal that Cnm is a colonization factor that contributes to the pathogenicity of certain S. mutans strains in their native habitat, the oral cavity.

Development of a novel ex vivo porcine skin explant model for the assessment of mature bacterial biofilms.

Bacterial biofilms have been proposed to be a major factor contributing to the failure of chronic wounds to heal because of their increased tolerance to antimicrobial agents and the prolonged inflammation they cause. Phenotypic characteristics of bacterial biofilms vary depending on the substratum to which they attach, the nutritional environment, and the microorganisms within the biofilm community. To develop an ex vivo biofilm model that more closely mimics biofilms in chronic skin wounds, we developed an optimal procedure to grow mature biofilms on a central partial-thickness wound in 12-mm porcine skin explants. Chlorine gas produced optimal sterilization of explants while preserving histological properties of the epidermis and dermis. Pseudomonas aeruginosa and Staphylococcus aureus developed mature biofilms after 3 days that had dramatically increased tolerance to gentamicin and oxacillin (∼100× and 8,000× minimal inhibitory concentration, respectively) and to sodium hypochlorite (0.6% active chlorine). Scanning electron microscopy and confocal microscopy verified extensive exopolymeric biofilm structures on the explants. Despite a significant delay, a ΔlasI quorum-sensing mutant of P. aeruginosa developed biofilm as antibiotic-tolerant as wild-type after 3 days. This ex vivo model simulates growth of biofilms on skin wounds and provides an accurate model to assess effects of antimicrobial agents on mature biofilms.

Periodontal bacterial invasion and infection: contribution to atherosclerotic pathology.

OBJECTIVE: The objective of this review was to perform a systematic evaluation of the literature reporting current scientific evidence for periodontal bacteria as contributors to atherosclerosis. METHODS: Literature from epidemiological, clinical and experimental studies concerning periodontal bacteria and atherosclerosis were reviewed. Gathered data were categorized into seven "proofs" of evidence that periodontal bacteria: 1) disseminate from the oral cavity and reach systemic vascular tissues; 2) can be found in the affected tissues; 3) live within the affected site; 4) invade affected cell types in vitro; 5) induce atherosclerosis in animal models of disease; 6) non-invasive mutants of periodontal bacteria cause significantly reduced pathology in vitro and in vivo; and 7) periodontal isolates from human atheromas can cause disease in animal models of infection. RESULTS: Substantial evidence for proofs 1 to 6 was found. However, proof 7 has not yet been fulfilled. CONCLUSIONS: Despite the lack of evidence that periodontal bacteria obtained from human atheromas can cause atherosclerosis in animal models of infection, attainment of proofs 1 to 6 provides support that periodontal pathogens can contribute to atherosclerosis.

Both the unique and repeat regions of the Porphyromonas gingivalis hemagglutin A are involved in adhesion and invasion of host cells.

Porphyromonas gingivalis is one of the major etiologic agents of adult periodontitis and has been associated with cardiovascular diseases. It expresses multiple hemagglutinins that are significant virulence factors and play an important role in bacterial attachment and invasion of host cells. The objective of this study was to determine the impact of P. gingivalis hemagglutinin A (HagA) on the attachment to and invasion of human coronary artery endothelial cells (HCAEC) and gingival epithelial cells (GEC). Bacterial strains expressing the HagA protein (or subunits), including Escherichia coli carrying plasmid pEKS5, E. coli carrying plasmid ST2, and Salmonella enterica serovar Typhimurium with plasmid pNM1.1 were used in this study. The strains were tested for their ability to attach to and invade HCAEC and GEC using antibiotic protection assays. In addition, the unique 5' N-terminal non-repeated segment of HagA was purified in recombinant form and a monoclonal antibody was created against the polypeptide. The monoclonal antibody against the unique portion of HagA was tested for inhibitory activity in these assays. The attachment of both E. coli strains expressing HagA fragment to host cells was significantly increased compared to their respective controls. However, they did not invade GEC or HCAEC. Interestingly, HagA expression in the Salmonella strain increased both adherence to and invasion of HCAEC, which may be due to the presence of the entire hagA ORF. A monoclonal antibody against the unique 5' N-terminal portion of HagA reduced invasion. Further experiments are needed to determine the role of the unique and the repeat segments of P. gingivalis HagA.

Fusobacterium is enriched in oral cancer and promotes induction of programmed death-ligand 1 (PD-L1).

Recently, increased number of studies have demonstrated a relationship between the oral microbiome and development of head and neck cancer, however, there are few studies to investigate the role of oral bacteria in the context of the tumor microenvironment in a single head and neck subsite. Here, paired tumor and adjacent normal tissues from thirty-seven oral tongue squamous cell carcinoma (SCC) patients were subjected to 16S rRNA gene sequencing and whole exome sequencing (WES), in addition to RNA sequencing for tumor samples. We observed that Fusobacterium was significantly enriched in oral tongue cancer and that Rothia and Streptococcus were enriched in adjacent normal tissues. A decrease in alpha diversity was found in tumor when compared to adjacent normal tissues. While increased Fusobacterium in tumor samples was not associated with changes in immune cell infiltration, it was associated with increased PD-L1 mRNA expression. Therefore, we examined the effects of Fusobacterium on PD-L1 expression in head and neck SCC cell lines. We demonstrated that infection with Fusobacterium species can increase both PD-L1 mRNA and surface PD-L1 protein expression on head and neck cancer cell lines. The correlation between Fusobacterium and PD-L1 expression in oral tongue SCC, in conjunction with the ability of the bacterium to induce PD-L1 expression in vitro suggests a potential role for Fusobacterium on modulation of the tumor immune microenvironment in head and neck cancer.

A Novel Regulation of K-antigen Capsule Synthesis in Porphyromonas gingivalis Is Driven by the Response Regulator PG0720-Directed Antisense RNA.

The periodontal pathogen Porphyromonas gingivalis strain W83 displays at least three different surface glycans, specifically two types of lipopolysaccharides (O-LPS and A-LPS) and K-antigen capsule. Despite the importance of K-antigen capsule to the virulence of P. gingivalis, little is known as to how expression of genes involved in the synthesis of this surface glycan is regulated. The genes required for K-antigen capsule synthesis are located in a locus that encodes a number of transcripts, including an operon (PG0104 to PG0121, generating ~19.4-kb transcript) which contains a non-coding 77-bp inverted repeat (77 bpIR) region near the 5'-end. Previously, we identified a 550-nucleotide antisense RNA molecule (designated asSuGR for antisense Surface Glycan Regulator) encoded within the 77-bpIR element that influences the synthesis of surface glycans. In this study, we demonstrate that the DNA-binding response regulator PG0720 can bind the promoter region of asSuGR and activate expression of asSuGR, indicating that PG0720 may indirectly influence transcript levels of the K-antigen capsule operon expressed from the sense strand. The data show that deletion of the PG0720 gene confers a defect in the presentation of surface polysaccharides compared with the parent strain and quantitative RT-PCR (qPCR) analysis determined that the overall expression of genes involved in K-antigen capsule synthesis were down-regulated in the PG0720 mutant. Furthermore, the defects of the PG0720 deletion mutant were restored by complementation. Importantly, the PG0720 deletion mutant showed reduced virulence. Altogether, our data show that the response regulator PG0720 regulates expression of asSuGR, a trans-acting antisense RNA molecule involved in modulating the production of surface polysaccharides in P. gingivalis strain W83. The data provide further evidence that surface glycans are key virulence determinants and significantly advances our understanding of the molecular mechanisms controlling the synthesis of P. gingivalis K-antigen capsule, a key virulence determinant.

Fusobacteria modulate oral carcinogenesis and promote cancer progression.

Background: Evidence suggest periodontal bacterial infection can contribute to oral cancer initiation and progression. Aim: To investigate the effects of periodontal bacteria on oral cancer cell behavior using a cell-based system and a mouse carcinogenesis model. Methods: Oral cancer cell lines were polyinfected with four periodontal bacteria. Cytokine levels and relative changes in oncogene mRNA expression were determined post-infection. Oral tumours in mice induced by 4-nitroquinoline-1-oxide (4NQO) were compared with and without administrating periodontal bacteria. Results: Polyinfected oral cancer cells had upregulated MMP1, MMP9, and IL-8. The expression of cell survival markers MYC, JAK1, and STAT3 and epithelial-mesenchymal transition markers ZEB1 and TGF-ß were also significantly elevated. Monoinfections showed F. nucleatum alone had comparable or greater effects than the four bacteria together. Fusobacterial culture supernatant, primarily LPS, was sufficient to induce IL-8 secretion, demonstrating that direct contact of live Fusobacteria with cancer cells might not be required to exert changes in cancer cell behaviour. In the 4NQO-induced oral tumour model, mice infected with bacteria developed significantly larger and more numerous lesions compared to those not infected. Conclusion: This study demonstrated that Fusobacteria could potentially enhance cancer cell invasiveness, survival, and EMT when presented in the oral tumour microenvironment. Abbreviations: 4NQO, 4-nitroquinoline-1-oxide; ELISA, enzyme-linked immunosorbent assay; EMT, epithelial-mesenchymal transition; IL-8, interleukin-8; JAK1, Janus kinase 1; LPS, lipopolysaccharide; MMP, matrix metalloproteinase; OSCCs, oral squamous cell carcinomas; PK, proteinase K; PMB, Polymyxin B; qRT-PCR, quantitative real-time polymerase chain reaction; STAT3, signal transducer and activator of transcription 3; TGF-ß, transforming growth factor beta; ZEB1, zinc finger E-Box binding homeobox 1.

A Uniquely Altered Oral Microbiome Composition Was Observed in Pregnant Rats With Porphyromonas gingivalis Induced Periodontal Disease.

Porphyromonas gingivalis is an anaerobic bacterium commonly found in the oral cavity and associated with the development of periodontal disease. P. gingivalis has also been linked to several systemic vascular and inflammatory diseases including poor pregnancy outcomes. Little is known about the changes in the oral flora during pregnancy in connection to P. gingivalis infection. This pilot study aims to explore changes in the oral microbiome due to P. gingivalis inoculation and pregnancy in an in vivo rat model of periodontal disease. A metagenomic sequencing analysis targeting seven of the 16S rRNA gene variable regions was performed for oral samples collected at the following time points: baseline control (week 0), P. gingivalis inoculated (week 11), P. gingivalis inoculated and pregnant rat at necropsy (week 16). A second set of animals were also sampled to generate a sham-inoculated (week 11) control group. We found that the rat oral microbiome profiles were more similar to that of the human oral cavity compared to previous reports targeting one or two 16S variable regions. Overall, there appears to be a relatively stable core microbiome in the oral cavity. As expected, P. gingivalis induced periodontal disease resulted in oral microbiome dysbiosis. During pregnancy, some aspects of the oral microbiome shifted toward a more baseline-like profile. However, population analyses in terms of dissimilarity measures and especially metagenomic based predictions of select characteristics such as cell morphology, oxygen requirement, and major metabolite synthesis showed that pregnancy did not restore the composition of the oral microbiome. Rather, a uniquely altered oral microbiome composition was observed in pregnant rats with pre-established periodontal disease.

Dataset on the chemokine and cytokine responses of multi-cell cultures treated with Porphyromonas gingivalis hemagglutinin B.

Chemokines and cytokines produced in gingival tissues exposed to microorganisms and microbial products in dental plaque lead to local inflammation and tissue damage seen in periodontal disease. Bates et al. 2018 [1] reported that Porphyromonas gingivalis hemagglutinin B (HagB)-induced matrix metalloproteinase (MMP) responses of single cell cultures containing dendritic cells, gingival epithelial (GE) keratinocytes, or T cells were significantly different from the MMP responses of these same cells grown in multi-cell cultures. Here we report the concentrations (pg/ml) of HagB-induced IL1α, IL6, IL8, IL12(p40), GM-CSF, MIP1α, MIP1ß, RANTES, TNFα, and VEGF produced by dendritic cells, GE keratinocytes, or T cells in single cell cultures, two-cell cultures, or three-cell cultures.

Human alpha- and beta-defensins bind to immobilized adhesins from Porphyromonas gingivalis.

Human neutrophil peptide alpha-defensins (HNPs) and human beta-defensins (HBDs) are small well-characterized peptides with broad antimicrobial activities and a diversity of innate immune functions. Although the interactions of defensins with bacteria and their membranes have been well characterized, the interactions of defensins with bacterial adhesins have not. Here we determine if HNPs and HBDs bind to the immobilized adhesins of Porphyromonas gingivalis strain 381, recombinant hemagglutinin B (rHagB) and recombinant fimbrillin A (rFimA), by surface plasmon resonance spectroscopy. Association of HNPs and HBDs with rHagB or rFimA was dose dependent and defensin specific. HBD3, HNP-2, and HNP-1 bound more readily to immobilized rHagB than HBD2 and HBD1 did. HNP-2, HNP-1, and HBD3 bound more readily to immobilized rFimA than HBD1 and HBD2 did. Binding of defensins to adhesins may serve to prevent microbial adherence to tissues, attenuate proinflammatory cytokine responses, and facilitate delivery of bound antigen to antigen-presenting cells with defensin receptors.

Porphyromonas gingivalis and the autophagic pathway: an innate immune interaction?

Autophagy is a mechanism used to maintain several intracellular functions essential to eukaryotic cells. Recently, a role for autophagy in innate and adaptive immunity has also been established including the elimination of invading bacteria. Although some intracellular pathogens are killed by autophagy, several others subvert autophagy to the pathogen's benefit for survival and replication. Porphyromonas gingivalis, an important periodontal pathogen, has been shown to stimulate autophagy in endothelial cells and to use the autophagic pathway to its advantage. In human coronary artery endothelial cells (HCAEC), P. gingivalis localizes within autophagosomes. After intracellular uptake, P. gingivalis transits from early autophagosomes to late autophagosomes and prevents the formation of autolysosomes, either by delaying the autophagosome-lysosome fusion or by redirecting the normal autophagic trafficking. In addition, P. gingivalis was also found to stimulate autophagy in human aortic endothelial cells (HAEC) since co-localization of LC3-II, an autophagosome marker, with P. gingivalis was observed. The trafficking of P. gingivalis into the autophagic pathway appears to be dependent upon the host cell type. Survival of P. gingivalis through the subversion of the host autophagic pathway can be considered a bacterial strategy to evade the innate immune system and persist in the host.

Colonization of maternal and fetal tissues by Porphyromonas gingivalis is strain-dependent in a rodent animal model.

OBJECTIVE: The objective of this study was to develop a rodent model of Porphyromonas gingivalis infection during pregnancy. STUDY DESIGN: Sprague Dawley rats were infected intravenously with 10(5), 10(7), or 10(9) CFU per dam of P gingivalis strain W83, ATCC 33277, or A7436 at gestational day 14 and necropsied at gestational day 18. Maternal organs were cultured to assess the spread of the infection. Six fetal units (placenta, amniotic fluid, membranes, and fetus) per dam were cultured; additional fetal units were examined by histopathology. Polymerase chain reaction was performed on placentas. RESULTS: Colonization rates were dependent on the strain of P gingivalis used and the infection dose. At an infection dose of 10(9) CFU/dam, P gingivalis W83, ATCC 33277, or A7436 was detected in 33%, 83%, or 100% of placentas, respectively. Epithelial hyperplasia, cellular necrosis, and inflammatory infiltrate were observed in infected placental tissues. CONCLUSION: This study demonstrated that P gingivalis can invade both maternal and fetal tissues, resulting in chorioamnionitis and placentitis.

Deletion of a conserved transcript PG_RS02100 expressed during logarithmic growth in Porphyromonas gingivalis results in hyperpigmentation and increased tolerance to oxidative stress.

The oral obligate anaerobe Porphyromonas gingivalis possesses a small conserved transcript PG_RS02100 of unknown function we previously identified using small RNA-seq analysis as expressed during logarithmic growth. In this study, we sought to determine if PG_RS02100 plays a role in P. gingivalis growth or stress response. We show that a PG_RS02100 deletion mutant's (W83Δ514) ability to grow under anaerobic conditions was no different than wildtype (W83), but it was better able to survive hydrogen peroxide exposure when cultured under heme limiting growth conditions, and was more aerotolerant when plated on enriched whole blood agar and exposed to atmospheric oxygen. Together, these results indicate that PG_RS02100 plays a role in surviving oxidative stress in actively growing P. gingivalis and that P. gingivalis' response to exogenous hydrogen peroxide stress is linked to heme availability. Relative qRT-PCR expression analysis of oxyR, trx-1, tpx, sodB, ahpC, dinF, cydB, and frd, in W83Δ514 and W83 in response to 1 h exogenous dioxygen or hydrogen peroxide exposure, when cultured with varying heme availability, support our phenotypic evidence that W83Δ514 has a more highly primed defense system against exogenous peroxide, dioxygen, and heme generated ROS. Interestingly, W83Δ514 turned black faster than W83 when cultured on whole blood agar, suggesting it was able to accumulate heme more rapidly. The mechanism of increased heme acquisition observed in W83Δ514 is not yet known. However, it is clear that PG_RS02100 is involved in modulating the P. gingivalis cell surface in a manner related to survival, particularly against oxidative stress.

Porphyromonas gingivalis and adverse pregnancy outcome.

Porphyromonas gingivalis is a Gram-negative, anaerobic bacterium considered to be an important pathogen of periodontal disease that is also implicated in adverse pregnancy outcome (APO). Until recently, our understanding of the role of P. gingivalis in APO has been limited and sometimes contradictory. The purpose of this review is to provide an overview of past and current research on P. gingivalis that addresses some of the controversies concerning the role of this organism in the pathogenesis of APO.