Effects of D-arginine on <i>Porphyromonas gingivalis</i> biofilm

Abstract

Porphyromonas gingivalis (P. gingivalis) is one of the major pathogenic bacteria of periodontitis or peri-implantitis. P. gingivalis tends to attach to the implant's neck with the formation of biofilm, leading to peri-implantitis. d-arginine has been shown to have a potential antimicrobial role. In this study, P. gingivalis was cultured in Brain Heart Infusion broth together with d-arginine. After 3 days (inhibition) or 6 days (dissociation), these were characterized using crystal violet (CV) staining for the biofilm, extracellular polysaccharide (EPS) production from the biofilm, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay for biofilm activation. Furthermore, the P. gingivalis biofilm was observed by scanning electron microscopy (SEM). d-arginine effectively reduced biomass accumulation and promoted dissociation at concentrations of ≥50 mM and 100 mM, respectively. Through CV staining, d-arginine concentrations of EPS production from the biofilm for inhibition and dissociation effects was ≥50 mM and 100 mM, respectively. In addition, d-arginine affected biofilm activation for the corresponding concentrations: ≥60 mM for inhibition and ≥90 mM for dispersal. Under SEM observation, d-arginine changed the P. gingivalis biofilm structure in relatively high concentrations for inhibition or dissociation, respectively. The authors concluded that d-arginine could inhibit the formation of P. gingivalis biofilm and promote the dissociation of P. gingivalis biofilm.

Synergistic effects of D-arginine, D-methionine and D-histidine on the inhibition and eradication of Porphyromonas gingivalis biofilm

“…Owing to the high molecular weight and viscosity of polysaccharides, the scattered polysaccharides still adhered to remaining bio lm or the bottom of plate. Therefore, the EPS content of RM/MH/RMH might be more than 0 group, consistent with our previous research 16 . In summary, there are multiple factors in uencing the content of EPS matrix, hence, it is not an appropriate index to measure the effects of D-AAs on P. gingivalis bio lm.…”

“…We previously reported that D-arginine and D-valine were effective in inhibiting P. gingivalis bio lm formation and promoting the disassembly of mature P. gingivalis bio lm respectively 15,16 . Considering that different D-AAs might be involved in different metabolic forms of bacteria, we speculated that combined application of D-AAs would present synergistic effects on bio lm.…”

“…Afterwards, several D-AAs were found effective in inhibiting bio lm formation of classic pathogenic bacteria [12][13][14] . Our previous research revealed that Darginine, D-valine, and several other D-AAs had the abilities of both inhibiting P. gingivalis bio lm formation and triggering the disassembly of mature P. gingivalis bio lm 15,16 . Considering the cytotoxic effects of D-AAs at certain concentrations 17 , D-AAs should be used biocompatibly to combat bio lm and nding an ideal strategy to avoid the cytotoxicity of D-AAs is urgent.…”

Trace Element-Augmented Titanium Implant With Targeted Angiogenesis and Enhanced Osseointegration in Osteoporotic Rats

“…The antibacterial abilities were measured and turned out almost the same on the four Zn-doped groups, namely, Zn@TiO 2 , 1SrZn@TiO 2 , 2SrZn@TiO 2 , and 3SrZn@TiO 2 . P. gingivalis is one of the major pathogenic bacteria of periimplantitis ( Li et al, 2020 ). The bacterial Live/Dead staining of P. gingivalis on titanium surfaces was also conducted ( Figure 5C ).…”

Targeting Biofilms Therapy: Current Research Strategies and Development Hurdles

“…D-arginine (D-Arg) also can work well on bacterial biofilms. It shows that D-Arg can inhibit and dissociate EPS from biofilms when its concentration exceeds 50 mM and 100 mM, respectively, and can change the P. gingivalis biofilm structure at relatively high concentrations [ 181 ]. In addition to Arg, L-methionine (L-Met) has also been identified as a promising adjuvant to treating P. aeruginosa biofilms, which can trigger biofilm disassembly, increasing sensitivity towards ciprofloxacin in a mouse model of chronic pneumonia, and enhancing survival of infected mice [ 182 ].…”