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. Author manuscript; available in PMC: 2009 Mar 2.
Published in final edited form as: J Clin Periodontol. 2008 Feb;35(2):89–105. doi: 10.1111/j.1600-051X.2007.01172.x

Table 3. Hypotheses Tested in the Oral Gavage Model.

References
Genetic basis for host susceptibility or resistance to periodontal disease
Different genetic mouse strains display differential susceptibility to P. gingivalis-induced periodontal bone loss. (Baker, 2005)
Il1b, Tnf, and Stat6 are associated with susceptibility, whereas Il15 and Selp with resistance to P. gingivalis-induced periodontal bone loss (Hart, et al., 2004)
Role of specific cytokines or antimicrobial molecules in periodontal disease
Increased susceptibility of IL-10 knockout mice to P. gingivalis-induced periodontal bone loss (Sasaki H, et al., 2000)
IL-17-receptor-knockout mice display increased susceptibility to P. gingivalis-induced periodontal bone loss (Yu, et al., 2007)
Inducible nitric oxide synthase (iNOS)- knockout mice exhibit increased periodontal bone loss in response to P. gingivalis infection (Alayan, et al., 2006)
Identification of potential virulence factors
Wild-type P. gingivalis, but not a FimA-deficient mutant, induces periodontal bone loss and accelerates atherosclerosis. (Gibson, et al., 2004)
Diminished induction of periodontal bone loss by P. gingivalis mutant expressing FimA fimbriae lacking the FimCDE accessory components. (Wang, et al., 2007)
Diminished induction of periodontal bone loss by P. gingivalis mutants lacking expression of Kgp and/or RgpB. (Pathirana, et al., 2007)
Diminished induction of periodontal bone loss by T. forsythia mutant lacking BspA adhesin. (Rai, et al., 2005)
Immune evasion through exploitation of innate receptors
TLR2 deficiency attenuates P. gingivalis-induced periodontal bone loss. (Burns, et al., 2006)
Blockade of complement receptor-3 inhibits P. gingivalis-induced periodontal bone loss. (Hajishengallis, et al., 2007)
Periodontal disease connection with systemic diseases
Oral infection with P. gingivalis accelerates atherosclerosis. (Gibson, et al., 2004)
(Lalla, et al., 2003)
P. gingivalis-induced periodontal bone loss is enhanced in diabetes. (Lalla, et al., 1998)
Blockade of RAGE (receptor for advanced glycation end products) suppresses periodontal bone loss in diabetic mice. (Lalla, et al., 2000)
Proof-of-principle immunization studies to identify candidate vaccine antigens
Systemic immunization using RgpA and Kgp gingipain peptides protects against P. gingivalis-induced periodontal bone loss (O’Brien-Simpson, et al., 2005)
Systemic immunization using intact RgpA protects against P. gingivalis-induced periodontal bone loss. (Gibson & Genco, 2001)
Oral immunization with FimA-expressing S. gordonii vector protects against P. gingivalis-induced periodontal bone loss. (Sharma, et al., 2001)
Potential and Future Uses of This Model
To determine the role of pattern-recognition receptors in protection or susceptibility to periodontitis using genetically modified mice.
To determine the impact of aging in periodontal disease susceptibility using young and aged mice.
To investigate the protective potential of specific antagonists of disease-promoting mechanisms (e.g., destructive inflammation, bacterial evasion of immunity).
To investigate the role of specific bacterial genes in interbacterial co-adherece and biofilm formation.