Porphyromonas gingivalis, a periodontal pathogen, enhances myocardial vulnerability, thereby promoting post-infarct cardiac rupture.

There is a strong association between periodontal disease (PD) and atherosclerosis. However, it remains unknown whether PD is also involved in myocardial damage. We hypothesized that infection with periodontal pathogens could cause an adverse outcome after myocardial infarction (MI). C57BL/6J mice were inoculated with Porphyromonas gingivalis (P.g.), a major periodontal pathogen, or injected with phosphate-buffered saline (PBS) into a subcutaneously-implanted steelcoil chamber before and after coronary artery ligation. A significant increase in mortality, due to cardiac rupture, was observed in the P.g.-inoculated MI mice. Ultrastructural examinations revealed that P.g. invaded the ischemic myocardium of the P.g.-inoculated MI mice. The expression of p18 Bax, an active form of pro-apoptotic Bax protein, markedly increased in the P.g.-inoculated MI hearts. In vitro experiments demonstrated that gingipain, a protease uniquely secreted from P.g., cleaved wild type Bax at Arg34, as evidenced by the observation that the cleavage of Bax by gingipain was completely abolished by the Arg34Ala mutation in Bax. Treatment with immunoglobulin Y against gingipain significantly decreased the mortality of the P.g.-inoculated MI mice caused by cardiac rupture. Furthermore, inoculation of P.g. also resulted in an increase of MMP-9 activity in the post-MI myocardium by enhancing oxidative stress, possibly through impairing the selective autophagy-mediated clearance of damaged mitochondria. In conclusion, infection with P.g. during MI plays a detrimental role in the healing process of the infarcted myocardium by invasion of P.g. into the myocardium, thereby promoting apoptosis and the MMP-9 activity of the myocardium, which, in turn, causes cardiac rupture.

Influence of surface pre-reacted glass-ionomer (S-PRG) filler eluate on collagen morphology, remineralization, and ultimate tensile strength of demineralized dentin.

OBJECTIVE: To evaluate the effect of ions released from surface pre-reacted glass-ionomer (S-PRG) filler on collagen morphology, remineralization, and ultimate tensile strength (UTS) of demineralized dentin. MATERIALS AND METHODS: Bovine incisor root dentins were demineralized with EDTA and divided into three treatment groups: 1) water (control); 2) S-PRG filler eluate; 3) 125 ppm sodium fluoride (NaF). After a 3-min treatment, the specimens were stored in simulated body fluid (SBF) for 3 months. Collagen morphology and remineralization were assessed using transmission electron microscopy (TEM), scanning electron microscopy (SEM), and Fourier-transform infrared spectroscopy (FTIR). Additionally, ultimate tensile strength (UTS) was measured. RESULTS: TEM and SEM demonstrated that S-PRG induced more effective remineralization compared to NaF, while the control group exhibited faint mineral deposition with collagen degradation. S-PRG displayed the most homogenous mineral deposition in collagen fibrils, along with closure of interfibrillar spaces. Extensive mineral precipitation was observed within dentinal tubules in the S-PRG group. In addition, S-PRG filler eluate demonstrated significantly higher phosphate-to-amide ratio and UTS compared to NaF and control groups (p < 0.05). CONCLUSIONS: Ion released from S-PRG filler positively influenced collagen morphology, remineralization, and ultimate tensile strength of demineralized dentin. CLINICAL SIGNIFICANCE: S-PRG filler enhances remineralization and improve the biomechanics of demineralized dentin.

The effect of antimicrobial photodynamic therapy using yellow-green LED and rose bengal on Porphyromonas gingivalis.

INTRODUCTION: This study aimed to investigate the effects of a new antimicrobial photodynamic therapy (aPDT) system using yellow-green light-emitting diode (YGL) and rose bengal (RB) on Porphyromonas gingivalis (Pg) in vitro. MATERIALS AND METHODS: Pg suspension mixed with RB was irradiated with YGL (565 nm) or blue light-emitting diode (BL, 470 nm) at 428 mW/cm2 in comparison with chlorhexidine (CHG) treatment. The cells were cultured anaerobically on agar plates, and the number of colony-forming units (CFU) was determined. The treated suspension was anaerobically incubated, and the cell density (OD600nm) was monitored for 24 h. Also, the viability of treated human gingival fibroblast (HGF-1) was measured using WST-8 assay. Pg morphology was observed with a scanning electron microscope. The RNA integrity number of aPDT-treated Pg was determined and gene expressions were evaluated by quantitative real-time polymerase chain reaction. RESULTS: RB + YGL (aPDT) demonstrated a significantly higher reduction of CFU, compared to RB + BL (aPDT) and CHG, furthermore the OD value rapidly decreased. Morphological changes of Pg with RB + YGL were more severe than with CHG. Although RB + YGL reduced HGF-1 viability, aPDT's impact was significantly lower than CHG's. With RB + YGL treatment, RIN values decreased; furthermore, gene expressions associated with DNA replication and cell division were remarkably decreased after 12 h. CONCLUSION: The results of this study demonstrated that a novel aPDT system using RB + YGL may have potential as a new technical modality for bacterial elimination in periodontal therapy.