IADR Abstract Archives
Periodontal Symptoms During IBD: An Innovative HLA-B27 Rat Model
Objectives: An increased risk of periodontitis (PD) is reported in patients affected with inflammatory bowel disease (IBD). The underlying biological mechanisms which explain this epidemiological association have not yet been elucidated. The HLA-B27 transgenic rat presents spontaneous severe colitis and extra-intestinal manifestations similar to clinical symptoms in IBD-affected patients. This study describes the occurrence and natural progression of the periodontal disease correlated to the digestive status in this animal model.
Methods: Six weeks old rats (n=14 HLAB-27+ and n=16 Wild Type rats) were included. Periodontal symptoms (clinical inflammation index) and digestive status (consistency of feces and presence of blood) were monitored twice a week. Rats were sacrified at 3 time points (6, 12 and 18 weeks; n=10 per time point), alveolar bone loss (micro-CT) and the inflammatory markers in the blood, gums and colon were determined by RT-qPCR, LUMINEX and ELISA. The data was analyzed using a Mann-Whitney test (α=0.05).
Results: At 18 weeks, HLA-B27 rats presented a spontaneous severe colitis resulting in diarrhea (p〈0.0001), an increased gingival index (p〈0.0001) and an accelerated alveolar bone loss (p〈0.05) comparing to the WT rats. An over-expression of pro-inflammatory cytokine mRNAs was found in the colon (IL-6, IL-1β, IL-17, TNFα), the gum (IL-17, TNF, RANKL/OPG, MMP8/TIMP2, LCN2) (p〈0.005), and the blood (IL-1β, IL-17) (p〈0.05) of HLA-B27+ rats (vs WT rats).
Conclusions: These results support that the HLA-B27 transgenic rats develop simultaneously a severe colitis associated with the spontaneous progression of a periodontal inflammatory condition similar to IBD and PD in humans. Thus, this innovative model could help to better understand the physio-pathological mechanisms linking PD to IBD and to develop new therapeutic approaches toward both IBD and PD. Mechanistic studies to investigate how the periodontal and intestinal conditions could influence each other are ongoing.
Methods: Six weeks old rats (n=14 HLAB-27+ and n=16 Wild Type rats) were included. Periodontal symptoms (clinical inflammation index) and digestive status (consistency of feces and presence of blood) were monitored twice a week. Rats were sacrified at 3 time points (6, 12 and 18 weeks; n=10 per time point), alveolar bone loss (micro-CT) and the inflammatory markers in the blood, gums and colon were determined by RT-qPCR, LUMINEX and ELISA. The data was analyzed using a Mann-Whitney test (α=0.05).
Results: At 18 weeks, HLA-B27 rats presented a spontaneous severe colitis resulting in diarrhea (p〈0.0001), an increased gingival index (p〈0.0001) and an accelerated alveolar bone loss (p〈0.05) comparing to the WT rats. An over-expression of pro-inflammatory cytokine mRNAs was found in the colon (IL-6, IL-1β, IL-17, TNFα), the gum (IL-17, TNF, RANKL/OPG, MMP8/TIMP2, LCN2) (p〈0.005), and the blood (IL-1β, IL-17) (p〈0.05) of HLA-B27+ rats (vs WT rats).
Conclusions: These results support that the HLA-B27 transgenic rats develop simultaneously a severe colitis associated with the spontaneous progression of a periodontal inflammatory condition similar to IBD and PD in humans. Thus, this innovative model could help to better understand the physio-pathological mechanisms linking PD to IBD and to develop new therapeutic approaches toward both IBD and PD. Mechanistic studies to investigate how the periodontal and intestinal conditions could influence each other are ongoing.