Transmural inflammation and submucosal fibrosis are important hallmarks of Crohn’s disease (CD) (1). Intestinal fibrosis concerns extracellular matrix accumulation and mesenchymal cell expansion (2,3). In this process, inflammation is the main activator of mesenchymal cells and an essential factor to initiate
fibrogenesis. Still, once fibrosis is established, it may be selfpropagating (3,4). In the setting of CD, patients with inflammatory lesions are considered medical therapy-responsive, while those with more fibrotic lesions will eventually need surgery (4). Hence, despite all the available therapies targeting inflammation, intestinal fibrosis remains difficult to treat and pre vent (3,4).
Strictures are subdivided in fibrotic, inflammatory, and mixed forms (5). Pure fibrotic or inflammatory strictures are rare, with both components presenting overlapped histopathology (3,6–10). In CD, transmural intestinal inflammation can be assessed by cross-sectional imaging (2,11–16). On the other hand, fibrosis cannot be measured by this technique nor through biomarkers (16,17). Endoscopy or biopsy-based histology (2,11) is not feasible as tissue remodeling occurs mostly in deeper layers (18). Thus, the extent and severity of fibrosis must
be evaluated by histopathological analysis of intestinal resection specimens, resorting to several histopathological scoring systems (19,20).
The main objective of our work was to characterize and quantify inflammation and fibrosis, in ileal CD resection specimens, according to a CD transmural histopathological scoring system. We also aimed to correlate inflammation and fibrosis profiles with progressive disease.info:eu-repo/semantics/publishedVersio
