Location is important: differentiation between ileal and colonic Crohn's disease.

Crohn's disease can affect any part of the gastrointestinal tract; however, current European and national guidelines worldwide do not differentiate between small-intestinal and colonic Crohn's disease for medical treatment. Data from the past decade provide evidence that ileal Crohn's disease is distinct from colonic Crohn's disease in several intestinal layers. Remarkably, colonic Crohn's disease shows an overlap with regard to disease behaviour with ulcerative colitis, underlining the fact that there is more to inflammatory bowel disease than just Crohn's disease and ulcerative colitis, and that subtypes, possibly defined by location and shared pathophysiology, are also important. This Review provides a structured overview of the differentiation between ileal and colonic Crohn's disease using data in the context of epidemiology, genetics, macroscopic differences such as creeping fat and histological findings, as well as differences in regard to the intestinal barrier including gut microbiota, mucus layer, epithelial cells and infiltrating immune cell populations. We also discuss the translation of these basic findings to the clinic, emphasizing the important role of treatment decisions. Thus, this Review provides a conceptual outlook on a new mechanism-driven classification of Crohn's disease.

Occurrence of spontaneous periodontal disease in the SAMP1/YitFc murine model of Crohn disease.

BACKGROUND: Oral involvement is often associated with inflammatory bowel disease (IBD). Recent evidence suggests a high incidence of periodontal disease in patients with Crohn disease (CD). To the best of the authors' knowledge, no animal model of IBD that displays associated periodontal disease was reported previously. The aim of this study is to investigate the occurrence and progression of periodontal disease in SAMP1/YitFc (SAMP) mice that spontaneously develop a CD-like ileitis. In addition, the temporal correlation between the onset and progression of periodontal disease and the onset of ileitis in SAMP mice was studied. METHODS: At different time points, SAMP and parental AKR/J (AKR) control mice were sacrificed, and mandibles were prepared for stereomicroscopy and histology. Terminal ilea were collected for histologic assessment of inflammation score. Periodontal status, i.e., alveolar bone loss (ABL) and alveolar bone crest, was examined by stereomicroscopy and histomorphometry, respectively. RESULTS: ABL increased in both strains with age. SAMP mice showed greater ABL compared with AKR mice by 12 weeks of age, with maximal differences observed at 27 weeks of age. AKR control mice did not show the same severity of periodontal disease. Interestingly, a strong positive correlation was found between ileitis severity and ABL in SAMP mice, independent of age. CONCLUSIONS: The present results demonstrate the occurrence of periodontal disease in a mouse model of progressive CD-like ileitis. In addition, the severity of periodontitis strongly correlated with the severity of ileitis, independent of age, suggesting that common pathogenic mechanisms, such as abnormal immune response and dysbiosis, may be shared between these two phenotypes.

Evaluation of the Crohn's Disease Activity Index (CDAI) and the Dutch Index for severity and activity of Crohn's disease. An analysis of the data from the European Cooperative Crohn's Disease Study.

In the European Cooperative Crohn's Disease Study a general documentation of clinical and laboratory data was made at the entry into the study in 452 patients. These patients were in different states of their disease from quiescent to very active. In all patients the Crohn's Disease Activity Index of Best (CDAI) and the Dutch Index of van Hees was calculated. Three gastroenterologists did a global clinical rating and a separate laboratory rating without knowledge of the indices. The ratings were then correlated with the indices in the individual patients. The clinical rating correlated well with the CDAI (r = 0.88) and less with the Dutch Index (r = 0.672). On the other hand the laboratory rating showed a better correlation with the Dutch Index (r = 0.742) than with the CDAI (r = 0.573). This demonstrates that the CDAI preferably is an estimate of the clinical severity of the disease and not of the activity of inflammation. Vice versa the Dutch Index is mainly reflecting the activity of the inflammatory process.