Immunization, Periodontitis, Porphyromonas gingivalis, Rats,Bone loss
Citation Information :
Torkzaban P, Hedayatipanah M, Zamani A, Yousefimashouf R, Faradmal J. Immunization against Porphyromonas gingivalis for Prevention of Experimentally Induced Periodontitis in Rats. World J Dent 2019; 10 (3):170-176.
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.
Lindhe J, Lang NP. Clinical periodontology and implant dentistry, 6th ed, Wiley Blackwell, 2015.
Han X, Lin X, et al. Porphyromonas gingivalis infection-associated periodontal bone resorption is dependent on receptor activator of NF-kappaB ligand. Infect Immun 2013;81(5):1502–1509. DOI: 10.1128/IAI.00043-13.
Rajapakse PS, O'Brien-Simpson NM, et al. Immunization with the RgpA-Kgp proteinase-adhesin complexes of Porphyromonas gingivalis protects against periodontal bone loss in the rat periodontitis model. Infect Immun 2002;70(5):2480–2486. DOI: 10.1128/IAI.70.5.2480-2486.2002.
Han X, LaRosa KB, et al. DNA-based adaptive immunity protect host from infection-associated periodontal bone resorption via recognition of Porphyromonas gingivalis virulence component. Vaccine 2014;32(2):297–303. DOI: 10.1016/j.vaccine.2013.09.004.
O'Brien-Simpson NM, Paolini RA, et al. RgpA-Kgp peptide-based immunogens provide protection against Porphyromonas gingivalis challenge in a murine lesion model. Infect Immun 2000;68(7):4055–4063. DOI: 10.1128/IAI.68.7.4055-4063.2000.
O'Brien-Simpson NM, Pathirana RD, et al. An immune response directed to proteinase and adhesin functional epitopes protects against Porphyromonas gingivalis-induced periodontal bone loss. J Immunol 2005;175(6):3980–3989. DOI: 10.4049/jimmunol.175.6.3980.
O'Brien-Simpson NM, Pathirana RD, et al. Porphyromonas gingivalis RgpA-Kgp proteinase-adhesin complexes penetrate gingival tissue and induce proinflammatory cytokines or apoptosis in a concentration-dependent manner. Infect Immun 2009;77(3):1246–1261. DOI: 10.1128/IAI.01038-08.
Pathirana RD, O'Brien-Simpson NM, et al. Host immune responses to Porphyromonas gingivalis antigens. Periodontol 2000;52(1):218–237. DOI: 10.1111/j.1600-0757.2009.00330.x.
Wilensky A, Polak D, et al. The role of RgpA in the pathogenicity of Porphyromonas gingivalis in the murine periodontitis model. J Clin Periodontol 2013;40(10):924–932. DOI: 10.1111/jcpe.12139.
Condorelli F, Scalia G, et al. Isolation of Porphyromonas gingivalis and detection of immunoglobulin A specific to fimbrial antigen in gingival crevicular fluid. J Clin Microbiol 1998;36(8):2322–2325.
Pathirana RD, O'Brien-Simpson NM, et al. The role of the RgpA-Kgp proteinase-adhesin complexes in the adherence of Porphyromonas gingivalis to fibroblasts. Microbiology 2008;154(Pt 10):2904–2911. DOI: 10.1099/mic.0.2008/019943-0.
Sharma A, Honma K, et al. Oral immunization with recombinant Streptococcus gordonii expressing porphyromonas gingivalis FimA domains. Infect Immun 2001;69(5):2928–2934. DOI: 10.1128/IAI.69.5.2928-2934.2001.
Marchesan JT, Morelli T, et al. Divergence of the systemic immune response following oral infection with distinct strains of Porphyromonas gingivalis. Mol Oral Microbiol 2012;27(6):483–495. DOI: 10.1111/omi.12001.
Tam V, O'Brien-Simpson NM, et al. Characterization of T cell responses to the RgpA-Kgp proteinase-adhesin complexes of Porphyromonas gingivalis in BALB/c mice. J Immunol 2008;181(6):4150–4158. DOI: 10.4049/jimmunol.181.6.4150.
Bender P, Burgin WB, et al. Serum antibody levels against Porphyromonas gingivalis in patients with and without rheumatoid arthritis—a systematic review and meta-analysis. Clin Oral Investig 2017;21(1):33–42. DOI: 10.1007/s00784-016-1938-5.