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Background We report the first protocol for a multicenter, randomized comparison study to compare the efficacies of periodontal scaling and root-planing treatment against that of tooth-brushing treatment for nonalcoholic fatty liver disease (NAFLD) (PERION: PERIOdontal treatment for NAFLD). Nonalcoholic steatohepatitis (NASH) is an advanced form of NAFLD, which can progress to cirrhosis and hepatocellular carcinoma. Increased endotoxemia is associated with the progression of NAFLD. Periodontal bacteria possess endotoxins; Porphyromonas gingivalis is well-known as a major pathogenic bacterium in periodontitis, and serum antibody levels for P. gingivalis are high in patients with periodontitis. Several reports have indicated that P. gingivalis is related to NAFLD. This study aims to investigate the effect of periodontal treatment for liver damage, P. gingivalis infection, and endotoxemia on patients with NAFLD. Methods We will include adult patients (20–85 years old) with NAFLD, alanine aminotransferase (ALT) ≥ 40 IU/L, and equivalent steatosis grade ≥ 1 (target sample size, n  = 40 patients; planned number of patients with outcome data, n  = 32). Participants will be randomly assigned to one of two groups: a scaling and root-planing group or tooth-brushing as the usual group. The primary outcome will be the change in ALT levels from baseline to 12 weeks; the key secondary outcome will be the change in the serum immunoglobulin G (IgG) antibody titer for P. gingivalis at 12 weeks. Discussion This study should determine whether periodontal treatment decreases liver damage, P. gingivalis infection, and endotoxemia in patients with NAFLD. Trial registration University Hospital Medical Information Network (UMIN) Clinical Trials Registry, ID: UMIN000022079 .

Atherosclerotic vascular disease (ASVD) is a chronic process, with a progressive course over many years, but it can cause acute clinical events, including acute coronary syndromes (ACS), myocardial infarction (MI) and stroke. In addition to a series of typical risk factors for atherosclerosis, like hyperlipidemia, hypertension, smoking and obesity, emerging evidence suggests that atherosclerosis is a chronic inflammatory disease, suggesting that chronic infection plays an important role in the development of atherosclerosis. Toll-like receptors (TLRs) are the most characteristic members of pattern recognition receptors (PRRs), which play an important role in innate immune mechanism. TLRs play different roles in different stages of infection of atherosclerosis-related pathogens such as Chlamydia pneumoniae ( C. pneumoniae ) , periodontal pathogens including Porphyromonas gingivalis ( P. gingivalis ) , Helicobacter pylori ( H. pylori ) and human immunodeficiency virus (HIV). Overall, activation of TLR2 and 4 seems to have a profound impact on infection-related atherosclerosis. This article reviews the role of TLRs in the process of atherosclerosis after C. pneumoniae and other infections and the current status of treatment, with a view to providing a new direction and potential therapeutic targets for the study of ASVD.

Abstract Porphyromonas gingivalis is a Gram-negative oral anaerobe that is involved in the pathogenesis of periodontitis, an inflammatory disease that destroys the tissues supporting the tooth, eventually leading to tooth loss. Porphyromonas gingivalis has can locally invade periodontal tissues and evade the host defence mechanisms. In doing so, it utilizes a panel of virulence factors that cause deregulation of the innate immune and inflammatory responses. The present review discusses the invasive and evasive strategies of P. gingivalis and the role of its major virulence factors in these, namely lipopolysaccharide, capsule, gingipains and fimbriae. Moreover, the role of P. gingivalis as a ‘keystone’ biofilm species in orchestrating a host response, is highlighted.

Porphyromonas gingivalis ( P. gingivalis ) is a gram-negative, black-pigmented, anaerobic pathogen known for its biofilm formation and its central role in periodontal disease. More recently, P. gingivalis has been implicated in various systemic conditions, including atherosclerosis, Alzheimer’s disease, and certain types of cancer, such as pancreatic and oral cancer. This bacterium employs several mechanisms to evade environmental stress, thereby contributing to its pathogenicity. The viable but non-culturable (VBNC) state is characterized by bacteria that remain viable but have reduced metabolic activity and are unable to form colonies on conventional culture media. To induce the VBNC state in P. gingivalis , we subjected the bacterium to oxidative stress using H 2 O 2 and subsequently resuscitated it from this state with sodium pyruvate. We utilized viability staining, confocal microscopy, and flow cytometry (FC) to count live and dead bacteria, confirming the presence of significant numbers of viable P. gingivalis cells both before and after stress induction. Despite being viable, the stressed P. gingivalis failed to form colonies on blood agar plates after seven days of incubation, indicating it had entered the VBNC state. We were then able to resuscitate the VBNC P. gingivalis by adding sodium pyruvate, and the growth of the resuscitated bacteria on plates was comparable to that of control P. gingivalis . Investigation into the invasiveness of P. gingivalis in the VBNC state was conducted using human coronary artery endothelial cells (HCAECs). P. gingivalis in the VBNC state demonstrated the ability to invade and based on live/dead staining, showed that a substantial proportion of the VBNC P. gingivalis remained viable within the host cells for extended periods. In this study, we explore the VBNC survival strategy previously described in many aerobic bacteria but not previously reported in anaerobes such as P. gingivalis . The objectives of this study are to verify the VBNC state in P. gingivalis, determine whether this state can be reversed and assess the extent to which it impacts the ability of P. gingivalis to invade host cells. Understanding the VBNC and resuscitation states will be instrumental in guiding the development of more effective therapies for periodontitis and other diseases associated with P. gingivalis infection.

Abstract Iron and heme are crucial for pathogenic bacteria living in the human host but are not available in free form due to their binding by iron- and heme-sequestering proteins. Porphyromonas gingivalis causes dysbiosis in the oral microbiome and is considered a keystone pathogen in the onset and progression of periodontal diseases. Its ability to infect and multiply in host cells and its presence in distant tissues and fluids highlights its pathogenic versatility and explains the relationship between periodontal diseases and systemic or neurodegenerative diseases. Porphyromonas gingivalis has evolved specialized mechanisms that allow it to thrive in the host under adverse nutrient-limited conditions. This review presents the updated summary of the mechanisms of iron and heme acquisition by P. gingivalis, with a central role played by gingipains and the unique Hmu system. The potential role of other iron and heme acquisition systems, such as Hus and Iht, indicates the importance of the partially conserved heme biosynthesis pathway, involving homologs of the HemN, HemG, and HemH proteins. In light of increasing antibiotic resistance, difficulties with diagnosis, and drug administration, targeting the mechanisms of heme and iron acquisition of P. gingivalis represents a promising target for developing diagnostic tests, preventive or therapeutic strategies. This review presents the heme and iron acquisition mechanisms of periodontopathogen Porphyromonas gingivalis, highlighting the roles of gingipains, the Hmu, Hus, and Iht systems, and a partially conserved heme biosynthesis pathway.

Porhyromonas gingivalis , a causative bacterium of periodontitis, is implicated in the etiology of rheumatoid arthritis (RA), mainly because of expressing peptidyl arginine deiminase (PAD) that generates RA-related autoantigens. However, compared with other periodontopathic bacteria, the precise role of P . gingivalis in RA is largely unknown. We found that orally administered P . gingivalis changed the gut microbiome with concomitant elevation of serum endotoxin and inflammatory markers, and impairment of the gut barrier function. Based on findings showing a relationship between gut microbiota and RA, we investigated whether the change of gut microbiota induced by P . gingivalis and Prevotella intermedia , another periodontopathic bacterium without PAD, is associated with collagen-induced arthritis (CIA). DBA/1J mice were orally administered with or without bacteria followed by induction of CIA. P . gingivalis , but not P . intermedia , administration significantly aggravated arthritis with increased interleukin-17 levels in sera and culture supernatants, increased Th17 cell proportions among mesenteric lymphocytes, and a significant change in the gut microbiome. However, P . gingivalis administration did not elevate the level of anti-citrullinated protein antibody. These results suggest a unique role of P . gingivalis in the link between periodontitis and RA by affecting the gut immune system and the gut microbiota composition.

Porphyromonas gingivalis is a causative agent in the onset and progression of periodontal disease. This study aims to investigate the effects of quercetin, a natural plant product, on P. gingivalis virulence properties including gingipain, haemagglutinin and biofilm formation. Antimicrobial effects and morphological changes of quercetin on P. gingivalis were detected. The effects of quercetin on gingipains activities and hemolytic, hemagglutination activities were evaluated using chromogenic peptides and sheep erythrocytes. The biofilm biomass and metabolism with different concentrations of quercetin were assessed by the crystal violet and MTT assay. The structures and thickness of the biofilms were observed by confocal laser scanning microscopy. Bacterial cell surface properties including cell surface hydrophobicity and aggregation were also evaluated. The mRNA expression of virulence and iron/heme utilization was assessed using real time-PCR. Quercetin exhibited antimicrobial effects and damaged the cell structure. Quercetin can inhibit gingipains, hemolytic, hemagglutination activities and biofilm formation at sub-MIC concentrations. Molecular docking analysis further indicated that quercetin can interact with gingipains. The biofilm became sparser and thinner after quercetin treatment. Quercetin also modulate cell surface hydrophobicity and aggregation. Expression of the genes tested was down-regulated in the presence of quercetin. In conclusion, our study demonstrated that quercetin inhibited various virulence factors of P. gingivalis .

Protein secretion systems are vital for prokaryotic life, as they enable bacteria to acquire nutrients, communicate with other species, defend against biological and chemical agents, and facilitate disease through the delivery of virulence factors. In this review, we will focus on the recently discovered type IX secretion system (T9SS), a complex translocon found only in some species of the phylum. T9SS plays two roles, depending on the lifestyle of the bacteria. It provides either a means of movement (called gliding motility) for peace-loving environmental bacteria or a weapon for pathogens. The best-studied members of these two groups are , a commensal microorganism often found in water and soil, and , a human oral pathogen that is a major causative agent of periodontitis. In and some other periodontopathogens, T9SS translocates proteins, especially virulence factors, across the outer membrane (OM). Proteins destined for secretion bear a conserved C-terminal domain (CTD) that directs the cargo to the OM translocon. At least 18 proteins are involved in this still enigmatic process, with some engaged in the post-translational modification of T9SS cargo proteins. Upon translocation across the OM, the CTD is removed by a protease with sortase-like activity and an anionic LPS is attached to the newly formed C-terminus. As a result, a cargo protein could be secreted into the extracellular milieu or covalently attached to the bacterial surface. T9SS is regulated by a two-component system; however, the precise environmental signal that triggers it has not been identified. Exploring unknown systems contributing to bacterial virulence is exciting, as it may eventually lead to new therapeutic strategies. During the past decade, the major components of T9SS were identified, as well as hints suggesting the possible mechanism of action. In addition, the list of characterized cargo proteins is constantly growing. The actual structure of the translocon, situated in the OM of bacteria, remains the least explored area; however, new technical approaches and increasing scientific attention have resulted in a growing body of data. Therefore, we present a compact up-to-date review of this topic.

Porphyromonas gingivalis is a Gram-negative oral anaerobe that is involved in the pathogenesis of periodontitis and is a member of more than 500 bacterial species that live in the oral cavity. This anaerobic bacterium is a natural member of the oral microbiome, yet it can become highly destructive (termed pathobiont) and proliferate to high cell numbers in periodontal lesions: this is attributed to its arsenal of specialized virulence factors. The purpose of this review is to provide an overview of one of the main periodontal pathogens—Porphyromonas gingivalis. This bacterium, along with Treponema denticola and Tannerella forsythia, constitute the “red complex,” a prototype polybacterial pathogenic consortium in periodontitis. This review outlines Porphyromonas gingivalis structure, its metabolism, its ability to colonize the epithelial cells, and its influence upon the host immunity.

Periodontitis is caused by Gram-negative bacteria. Porphyromonas gingivalis, a major Gram-negative periodontal pathogen, produces virulence factors such as gingipains, lipopolysaccharide (LPS), and lipoproteins, which contribute to tissue destruction. Ozone ultrafine bubble water (OUFBW) has been studied for its antimicrobial effects against various bacteria and toxin protein inactivation. This present study aimed to explore the effects of OUFBW on P. gingivalis and its virulence factors. OUFBW was generated and applied to P. gingivalis to assess bactericidal activity. OUFBW effects on morphological changes in P. gingivalis and its membrane vesicles (MVs) were analyzed using transmission electron microscopy. Gingipain activities in OUFBW-treated P. gingivalis culture supernatant was tested using fluorogenic substrates and endogenous substrates, E-cadherin and IL-6. Degradation of OUFBW-treated gingipains was analyzed by silver staining and western blotting. Effects of OUFBW on P. gingivalis lipoproteins and LPS were evaluated using HEK-Blue cells expressing Toll-like receptor 2 (TLR2) and TLR4, respectively. Cytotoxicity of OUFBW on human gingival cells was analyzed using an MTT assay. OUFBW disrupted the inner membrane of P. gingivalis , leading to elimination of the bacterium and reduction of MVs. OUFBW also decreased gingipain activities and inhibited gingipain-induced degradation of E-cadherin and IL-6 due to gingipain breakdown. Additionally, OUFBW suppressed lipoprotein-induced TLR2 activation but had no effect on LPS-mediated TLR4 signaling. OUFBW showed low cytotoxicity in human gingival cells. Our findings indicate that OUFBW can sterilize P. gingivalis and inactivate gingipains and lipoproteins. These results suggest that OUFBW would be used to disinfect periodontal treatment instruments.