Immunization against Porphyromonas gingivalis for Prevention of Experimentally Induced Periodontitis in Rats

Abstract

Aim: Periodontitis is an inflammatory disease causing destruction of tooth-supporting structures. It is often caused by gram-negative microorganisms such as Porphyromonas gingivalis (P. gingivalis ). Common treatments for periodontitis are often nonspecific and include mechanical plaque removal and surgery. This study aimed to assess the amount of bone loss and antibody titer against P. gingivalis in rats. Materials and methods: This in vitro experimental study was conducted on 66 Surrey rats free of black pigmented pathogens, which were randomly divided into six groups of 11. Groups I and II were vaccinated with formalin-killed whole-cell (FKWC) P. gingivalis with incomplete Freund's adjuvant as the vaccine carrier, and groups III and IV were vaccinated with incomplete Freund's adjuvant and PG buffer. Groups V and VI were considered as positive and negative controls, respectively. Three weeks later, they were vaccinated with a booster dose. At 28 days, groups I, III, and V were inoculated with viable P. gingivalis (ATCC 33277) four times at 48-hour intervals for induction of periodontitis. One week after booster dose administration and two weeks after oral inoculation of bacteria, serum and saliva samples were obtained for assessment of antibody titer. Ten weeks after final bacterial inoculation, the serum and saliva samples were obtained to assess antibody titer, and subgingival plaque samples were obtained from the maxillary second molar site to assess the bacterial count. The rats were then sacrificed to assess bone loss. Results: Serum and saliva antibody titers in groups I and II were significantly different from those in other groups one week after booster dose and two and 10 weeks after oral inoculation of bacteria (p < 0.001). In terms of bone loss and bacterial count in the subgingival plaque, group I was not significantly different from the negative control group and groups II, IV, and VI (p > 0.99), but had a significant difference with the positive control (group V) and group III (p < 0.001). Conclusion:This study showed successful immunization against P. gingivalis , which increased serum IgG and saliva IgA titers, limited the colonization of P. gingivalis in subgingival plaque, and restricted the alveolar bone loss.

Proteomic Profiling Reveals Cytotoxic Mechanisms of Action and Adaptive Mechanisms of Resistance in Porphyromonas gingivalis: Treatment with Juglans regia and Melaleuca alternifolia

“…Furthermore, P. gingivalis initiates the production of several virulence factors, such as proteases (gingipains), assisting in breaking down of the host immune proteins such as IL-1 CD 14; lipopolysaccharides, cell surface lipopolysaccharides which help to resist the host complement system; and short-chain fatty acids which promote and induce host cells to undergo apoptosis. 26 As such, antibacterial and cytotoxic mechanisms affecting multiple metabolic pathways and proteins would lead to abated pathogenesis and virulence factors, whereas adaptive and resistive responses would lead to augmented pathogenesis and virulence factors.…”

“…It catalyzes fatty acid biosynthesis by an irreversible reaction forming malonyl-CoA by carboxylation of acetyl-CoA, 57 and lipid biosynthesis is important for the pathogenesis of P. gingivalis and virulency. 26 Furthermore, the primary mode of action of moiramide B antibiotics is targeting acetyl coenzyme A carboxylases. Therefore, the downregulation of acetyl coenzyme A on treatment with JR and MA suggests that these extracts can inhibit the first essential step in lipid biosynthesis, affecting cellular activity and growth by modulating the protein expression of this essential enzyme.…”

“…Identifying the proteomic profile of microbes treated with natural agents compared to the untreated control helps to identify their mode of action, regulated proteins, active genes, and transcriptional regulatory mechanisms during treatment, which may facilitate the design of new drugs to preclude antimicrobial resistance. Furthermore, P. gingivalis initiates the production of several virulence factors, such as proteases (gingipains), assisting in breaking down of the host immune proteins such as IL-1 CD 14; lipopolysaccharides, cell surface lipopolysaccharides which help to resist the host complement system; and short-chain fatty acids which promote and induce host cells to undergo apoptosis . As such, antibacterial and cytotoxic mechanisms affecting multiple metabolic pathways and proteins would lead to abated pathogenesis and virulence factors, whereas adaptive and resistive responses would lead to augmented pathogenesis and virulence factors.…”

“…Acetyl coenzyme A (acetyl-CoA) carboxylase in bacteria is a multisubunit heterohexamer enzyme essential for bacterial growth and development. It catalyzes fatty acid biosynthesis by an irreversible reaction forming malonyl-CoA by carboxylation of acetyl-CoA, and lipid biosynthesis is important for the pathogenesis of P. gingivalis and virulency . Furthermore, the primary mode of action of moiramide B antibiotics is targeting acetyl coenzyme A carboxylases.…”

Green synthesis of silver nanoparticles and evaluation of their effects on the Porphyromonas gingivalis bacterial biofilm formation

“…Among the known pathogens, Porphyromonas gingivalis is recognized as a crucial contributor to chronic periodontitis in humans. This bacterium has a bacillus-shaped, asaccharolytic, immobile, gram-negative, anaerobic nature, and belongs to the black-pigmented family (Torkzaban et al, 2017(Torkzaban et al, , 2019. In medicine and dentistry, metal nanoparticles have gained attention due to their antibacterial properties (Hashemi et al, 2019;Song & Ge, 2019).…”