BACKGROUND AND OBJECTIVE: Inflammatory immune reactions that occur in response to periodontopathogens are thought to protect the host against infection, but may trigger periodontal destruction. However, the molecular and genetic mechanisms underlying host susceptibility to periodontal infection and to periodontitis development have still not been established in detail. MATERIAL AND METHODS: In this study, we examined the mechanisms that modulate the outcome of Aggregatibacter (Actinobacillus) actinomycetemcomitans-induced periodontal disease in mice mouse strains selected for maximal (AIRmax) or minimal (AIRmin) inflammatory reactions. RESULTS: Our results showed that AIRmax mice developed a more severe periodontitis than AIRmin mice in response to A. actinomycetemcomitans infection, and this periodontitis was characterized by increased alveolar bone loss and inflammatory cell migration to periodontal tissues. In addition, enzyme-linked immunosorbent assays demonstrated that the levels of the cytokines interleukin-1beta, tumor necrosis factor-alpha and interleukin-17 were higher in AIRmax mice, as were the levels of matrix metalloproteinase (MMP)-2, MMP-13 and receptor activator of nuclear factor-kappaB ligand (RANKL) mRNA levels. However, the more intense inflammatory immune reaction raised by the AIRmax strain, in spite of the higher levels of antimicrobial mediators myeloperoxidase and inducible nitric oxide synthase, did not enhance the protective immunity to A. actinomycetemcomitans infection, because both AIRmax and AIRmin strains presented similar bacterial loads in periodontal tissues. In addition, the AIRmax strain presented a trend towards higher levels of serum C-reactive protein during the course of disease. CONCLUSION: Our results demonstrate that the intensity of the inflammatory immune reaction is associated with the severity of experimental periodontitis, but not with the control of A. actinomycetemcomitans periodontal infection, suggesting that the occurrence of hyperinflammatory genotypes may not be an evolutionary advantage in the complex host-pathogen interaction observed in periodontal diseases.
BACKGROUND AND OBJECTIVE: Inflammatory immune reactions that occur in response to periodontopathogens are thought to protect the host against infection, but may trigger periodontal destruction. However, the molecular and genetic mechanisms underlying host susceptibility to periodontal infection and to periodontitis development have still not been established in detail. MATERIAL AND METHODS: In this study, we examined the mechanisms that modulate the outcome of Aggregatibacter (Actinobacillus) actinomycetemcomitans-induced periodontal disease in micemouse strains selected for maximal (AIRmax) or minimal (AIRmin) inflammatory reactions. RESULTS: Our results showed that AIRmax mice developed a more severe periodontitis than AIRmin mice in response to A. actinomycetemcomitans infection, and this periodontitis was characterized by increased alveolar bone loss and inflammatory cell migration to periodontal tissues. In addition, enzyme-linked immunosorbent assays demonstrated that the levels of the cytokines interleukin-1beta, tumor necrosis factor-alpha and interleukin-17 were higher in AIRmax mice, as were the levels of matrix metalloproteinase (MMP)-2, MMP-13 and receptor activator of nuclear factor-kappaB ligand (RANKL) mRNA levels. However, the more intense inflammatory immune reaction raised by the AIRmax strain, in spite of the higher levels of antimicrobial mediators myeloperoxidase and inducible nitric oxide synthase, did not enhance the protective immunity to A. actinomycetemcomitans infection, because both AIRmax and AIRmin strains presented similar bacterial loads in periodontal tissues. In addition, the AIRmax strain presented a trend towards higher levels of serum C-reactive protein during the course of disease. CONCLUSION: Our results demonstrate that the intensity of the inflammatory immune reaction is associated with the severity of experimental periodontitis, but not with the control of A. actinomycetemcomitans periodontal infection, suggesting that the occurrence of hyperinflammatory genotypes may not be an evolutionary advantage in the complex host-pathogen interaction observed in periodontal diseases.
Authors: Ana Claudia Araujo-Pires; Andreia Espindola Vieira; Carolina Favaro Francisconi; Claudia Cristina Biguetti; Andrew Glowacki; Sayuri Yoshizawa; Ana Paula Campanelli; Ana Paula Favaro Trombone; Charles S Sfeir; Steven R Little; Gustavo Pompermaier Garlet Journal: J Bone Miner Res Date: 2015-03 Impact factor: 6.741
Authors: Marcelo O Freire; Parish P Sedghizadeh; Christoph Schaudinn; Amita Gorur; Jennifer S Downey; Jeong-Ho Choi; Weizhen Chen; Joong-Ki Kook; Casey Chen; Steven D Goodman; Homayoun H Zadeh Journal: J Periodontol Date: 2011-01-11 Impact factor: 6.993
Authors: S Mahabady; N Tjokro; S Aharonian; H H Zadeh; C Chen; H Allayee; P P Sedghizadeh Journal: Mol Oral Microbiol Date: 2017-06-27 Impact factor: 3.563
Authors: Tatiane Canhamero; Brandon Reines; Luciana C Peters; Andrea Borrego; Patricia S Carneiro; Layra L Albuquerque; Wafa H Cabrera; Orlando G Ribeiro; Jose R Jensen; Nancy Starobinas; Olga M Ibañez; Marcelo De Franco Journal: Inflammation Date: 2011-10 Impact factor: 4.092
Authors: M O Freire; A Devaraj; A Young; J B Navarro; J S Downey; C Chen; L O Bakaletz; H H Zadeh; S D Goodman Journal: Mol Oral Microbiol Date: 2016-04-05 Impact factor: 3.563