Investigation Of The Pathogenesis Of Inflammatory Bowel Disease Associated With Osteoarthritis In Mice

Inflammatory bowel disease(IBD) mainly includes Crohn’s disease(CD) and ulcerative colitis(UC), chronic relapsing inflammatory conditions that involve the mucosa, submucosa, and muscles in large and small bowels. There are varieties of clinical manifestations of the inflammatory bowel disease,including gastrointestinal and general symptoms, and complex extra-intestinal manifestations. Many studies have shown that osteoarthritis(OA) is the highest incidence of the extra-intestinal manifestations in IBD patients. Also,there is inflammatory response in the process of OA development. Based on the information above, we investigated the relationship between the development of OA and intestinal inflammation in a mouse model of OA.Results from this investigation will provide novel insights into the pathogenesis of the inflammatory bowel disease associated with OA. A spontaneous mouse model of OA, type XI collagen-haploid sufficiency(Col11a1+/- or chondrodysplasia, cho) in mice, was used in this study. The phenotype of the disease in this model mimics the characteristics of human OA. After breeding, we obtained 40 pups. All of the pups were genotyped.We received 17 cho/+ mice and 23 +/+ mice. Sixteen mice were randomly selected from the 40 pups for experiments including 4 males and 4 females cho/+ mice as the experimental group and 4 males and 4 females +/+ mice as the control group. Two time points were also selected in this study. The null hypothesis, which is no significant relationship between OA and the onset and development of IBD, was applied in this investigation. The intestine of mice at the ages of 3 and 9 months old was collected and evaluated according toDisease Activity Index. After fixation, paraffin embedding, tissue section and HE staining, the tissues were assessed for pathological analysesbased on Colonic Mucosa Damage Index. We observed that there were no significant differences between the cho/+ group and wild-type littermates clinically and histopathologically at both time points.The results demonstrated that OA was not related to the onset of intestinal inflammation in mice and IBD was not exacerbated at the development of OA in mice.