Endoscopic management of intestinal strictures in Crohn’s disease: Current status and future perspectives

Figure 1 Schematic illustration of the multifactorial pathogenesis of fibrostenotic Crohn’s disease, highlighting immune, mesenchymal, microbial, and mesenteric fat contributions leading to extracellular matrix deposition. Th: T lymphocyte helper cells; IL: Interleukin; IFN-γ: Interferon gamma; TNF-α: Tumor necrosis factor alpha; Wnt: Wingless/Integrated signaling pathway; mTOR: Mammalian target of rapamycin; EMT: Epithelial to mesenchymal transition; EndoMT: Endothelial to mesenchymal transition; ECM: Extracellular matrix; AIEC: Adherent-invasive Escherichia coli; MMP-1: Matrix metalloproteinase 1; TIMP: Tissue inhibitors of metalloproteinase; miR: MicroRNA.

Figure 2 Overview of endoscopic treatment modalities for Crohn’s disease strictures, including indications, technical aspects, advantages, and limitations of endoscopic balloon dilation, endoscopic stricturotomy, and stenting. CD: Crohn’s disease; EBD: Endoscopic balloon dilation; ESt: Endoscopic stricturotomy; RCT: Randomized controlled trial.

Figure 3 Proposed multidisciplinary management algorithm for Crohn’s disease-associated intestinal strictures integrating medical, endoscopic, and surgical options based on stricture characteristics and patient factors. CD: Crohn’s disease; MRE: Magnetic resonance enterography; CTE: Computed tomography enterography; IUS: Intestinal ultrasonography; Rx: Treatment; TNF: Tumor necrosis factor; UST: Ustekinumab; VDZ: Vedolizumab; EBD: Endoscopic balloon dilation; CRE TTS: Controlled radial expansion through-the-scope; ESt: Endoscopic stricturotomy; FCSEMS: Fully covered self-expandable metal stents; ESTx: Endoscopic strictureplasty; LAMS: Lumen apposing metal stents; MDT: Multidisciplinary team.