ECCO 2026,Stockholm, Sweden

Patients with long-standing Inflammatory Bowel Disease (IBD), particularly Ulcerative colitis and colonic Crohn's disease, are at increased risk of developing Colorectal dysplasia, a precursor to Colorectal cancer. Histologically, dysplasia in IBD is broadly categorised into conventional dysplasia and non-conventional dysplasia, each with distinct morphological characteristics and clinical implications.

Conventional dysplasia is the most common type encountered in IBD surveillance biopsies. It resembles the dysplasia seen in sporadic colorectal adenomas and is classified as low-grade or high-grade dysplasia based on architectural and cytological abnormalities. Histologic features include elongated hyperchromatic nuclei, loss of nuclear polarity, increased mitotic activity, glandular crowding, and epithelial stratification. Conventional dysplasia may present endoscopically as visible lesions or be detected incidentally on random biopsies during surveillance colonoscopy.

In contrast, non-conventional dysplasia encompasses several less common histological patterns that differ from the classical adenoma-like morphology. These include serrated dysplasia, hypermucinous dysplasia, crypt cell dysplasia, goblet cell–deficient dysplasia, and sessile serrated–like lesions. These variants may have subtle or atypical microscopic features, making them more difficult to recognise and potentially leading to underdiagnosis.

Recent studies have highlighted that certain forms of non-conventional dysplasia may carry a higher risk of progression to advanced neoplasia compared with conventional dysplasia. Therefore, accurate histological recognition is crucial for appropriate clinical management.

In clinical practice, detection of dysplasia typically prompts close surveillance, endoscopic resection of visible lesions, or surgical management in selected cases. Increasing use of advanced endoscopic techniques, such as chromoendoscopy, has improved the detection of dysplastic lesions in IBD patients undergoing surveillance.

Overall, awareness of both conventional and non-conventional dysplasia patterns is essential for pathologists and clinicians to ensure early detection and effective prevention of colorectal cancer in patients with IBD.

Artificial Intelligence (AI) is rapidly transforming the diagnosis, monitoring, and management of Inflammatory Bowel Disease (IBD), including Crohn's disease and Ulcerative colitis. With the growing availability of large clinical datasets, imaging libraries, and digital pathology platforms, AI tools are increasingly being integrated into routine IBD care.

One of the most promising applications of AI is in endoscopy. AI-assisted systems can automatically detect mucosal abnormalities, quantify disease severity, and identify subtle inflammatory changes during colonoscopy. These tools help improve diagnostic accuracy and reduce interobserver variability among endoscopists. AI algorithms are also being developed to assist in the detection of dysplasia during surveillance colonoscopy, which is critical for cancer prevention in long-standing IBD.

AI is also advancing the field of digital pathology. Machine learning models can analyze histological slides to quantify inflammatory activity, identify dysplasia, and standardize histological scoring systems. This may improve reproducibility and reduce variability in histopathological assessment.

Another important application is in predictive analytics. AI models can integrate clinical data, biomarkers, imaging findings, and genetic information to predict disease course, treatment response, and risk of complications. Such tools may help clinicians personalize therapy and select the most appropriate treatment strategy for individual patients.

AI is further being used to analyze radiological imaging and intestinal ultrasound, assisting in automated assessment of bowel wall thickness, inflammation, and complications.

Despite its promise, challenges remain, including the need for high-quality datasets, validation across diverse populations, and integration into clinical workflows. Nevertheless, AI is clearly entering a new phase in IBD care, offering opportunities to enhance diagnostic precision, improve treatment decisions, and support personalized medicine in the management of IBD.

Strictures are a common complication of Crohn's disease, resulting from chronic, transmural inflammation of the intestinal wall that leads to progressive fibrosis and luminal narrowing. Histologically, Crohn’s strictures reflect a complex interplay between ongoing inflammation, tissue remodelling, and fibrogenesis.

In the early stages, strictures often demonstrate active inflammatory changes, including dense infiltration of lymphocytes, plasma cells, and macrophages within the mucosa and submucosa. Neutrophilic activity may be present in areas of acute inflammation, along with mucosal ulceration and crypt distortion. As the disease progresses, transmural inflammation extends through the entire bowel wall, involving the muscularis propria and serosa.

A hallmark of Crohn’s strictures is the development of fibrosis, characterised by excessive deposition of extracellular matrix proteins such as collagen. This process is driven by activation of fibroblasts and myofibroblasts, stimulated by pro-fibrotic cytokines including transforming growth factor-β (TGF-β). Histologically, this leads to submucosal fibrosis, thickening of the muscularis propria, and hypertrophy of smooth muscle layers, contributing to progressive luminal narrowing.

Additional pathological features include neural hyperplasia, lymphoid aggregates, and mesenteric fat wrapping (“creeping fat”), reflecting chronic immune activation and structural remodelling. Over time, strictures may evolve into predominantly fibrotic lesions with minimal active inflammation.

Clinically, differentiating inflammatory versus fibrotic strictures is important because inflammatory strictures may respond to medical therapy, whereas fibrotic strictures often require endoscopic dilation or surgical intervention.

Understanding the pathological mechanisms underlying Crohn’s strictures is crucial for developing anti-fibrotic therapeutic strategies, an area of growing research interest aimed at preventing long-term structural damage in Crohn’s disease.

In vivo histology refers to advanced endoscopic techniques that allow real-time microscopic visualisation of the intestinal mucosa during endoscopy, enabling assessment of cellular and vascular structures without the need for immediate tissue biopsy. This concept is increasingly relevant in the management of Inflammatory Bowel Disease (IBD), particularly Ulcerative colitis and colonic Crohn's disease, where accurate evaluation of mucosal inflammation and dysplasia is essential.

Several advanced imaging modalities enable in vivo histology. Confocal Laser Endomicroscopy (CLE) provides high-resolution images of the mucosa at nearly cellular magnification after administration of fluorescent contrast agents. CLE allows visualisation of crypt architecture, epithelial integrity, and inflammatory cell infiltration, helping identify microscopic inflammation and early neoplastic changes.

Another technique, Endocytoscopy, offers ultra-high magnification imaging that can directly visualise cellular details such as nuclei and goblet cells. This technique can help differentiate inflammatory changes from dysplasia during endoscopic examination.

In vivo histology has several clinical applications in IBD, including the detection of microscopic inflammation, the evaluation of mucosal healing, and the identification of dysplasia during surveillance colonoscopy. It may also reduce the need for multiple random biopsies by enabling targeted sampling of suspicious areas.

However, there are limitations. These techniques require specialised equipment, additional training, and may increase procedure time. Interpretation can also be operator-dependent, and standardised diagnostic criteria are still evolving.

Overall, in vivo histology represents a promising advancement in endoscopic imaging, bringing endoscopy closer to “optical biopsy.” As technology and expertise improve, it may play an increasing role in precision diagnosis and surveillance in IBD management.

Histopathological assessment has become an increasingly important endpoint in Inflammatory Bowel Disease (IBD), particularly in Ulcerative colitis, where histologic remission is now recognised as a predictor of improved clinical outcomes, including lower relapse rates and reduced risk of hospitalisation or surgery. (The Belgian Society of Pathology)

Over the last decade, several standardised histological scoring systems have been developed to quantify microscopic inflammation. The three most widely used and validated indices are the Geboes Score, Robarts Histopathology Index (RHI), and Nancy Index (NI). These scoring systems evaluate features such as chronic inflammatory infiltrate, neutrophilic activity, epithelial damage, and ulceration to assess the degree of mucosal inflammation. (Wjgnet)

The Nancy Index is a relatively simple scoring system based on three histological components—chronic inflammation, acute inflammation, and ulceration—graded from 0 to 4, making it easier to apply in routine practice. (PMC) In contrast, the Robarts Histopathology Index provides a broader quantitative assessment of histologic activity and may offer greater sensitivity to changes during treatment. (SRS Journal)

Recent comparative studies have demonstrated that the Geboes Score, RHI, and Nancy Index all show good reliability and responsiveness to changes in disease activity, although the Geboes Score and RHI may perform slightly better in detecting treatment-related improvement in clinical trials. (OUP Academic)

Despite these advances, challenges remain. Routine clinical adoption is limited by interobserver variability, complexity of scoring systems, and lack of universal reporting standards. (SRS Journal) Additionally, standardised histologic scoring in Crohn's disease remains difficult because of the patchy and transmural nature of the disease. (MDPI)

Future directions include simplified scoring systems, integration with endoscopic and biomarker endpoints, and the use of digital pathology and artificial intelligence to improve reproducibility. These developments are expected to further establish histologic remission as a key therapeutic target in modern IBD management.

Diagnosing Inflammatory Bowel Disease (IBD) in children can be particularly challenging due to the overlap of symptoms with several other gastrointestinal and systemic conditions. Pediatric patients with suspected Crohn's disease or Ulcerative colitis may present with nonspecific symptoms such as chronic diarrhoea, abdominal pain, weight loss, fatigue, and growth failure. These features can also be seen in infections, food intolerances, functional gastrointestinal disorders, or other inflammatory conditions, making early diagnosis difficult.

An additional complexity in pediatric patients is the variation in disease presentation. Children often show extraintestinal manifestations such as delayed puberty, anaemia, or poor linear growth before classic gastrointestinal symptoms appear. These atypical presentations may delay recognition of underlying IBD.

Accurate diagnosis requires a comprehensive and multidisciplinary approach. Initial evaluation typically includes laboratory markers of inflammation, stool tests to exclude infections, and imaging studies. Ileocolonoscopy with biopsy remains the cornerstone of diagnosis, allowing direct visualisation of mucosal inflammation and histological confirmation. In addition, cross-sectional imaging such as Magnetic Resonance Enterography is valuable for assessing small bowel involvement and complications.

Another challenge is distinguishing IBD from other conditions, such as infectious enterocolitis, celiac disease, intestinal tuberculosis, or primary immunodeficiency disorders, which may present with similar clinical and histological features.

Because of these complexities, optimal care requires collaboration among pediatric gastroenterologists, radiologists, pathologists, nutritionists, and paediatricians. Early recognition and accurate diagnosis are crucial to initiate appropriate therapy, prevent growth impairment, and improve long-term outcomes in pediatric IBD patients.

Patients with Inflammatory Bowel Disease (IBD), including Ulcerative colitis and Crohn's disease, are at increased risk of superinfections due to chronic intestinal inflammation, mucosal barrier disruption, and the frequent use of immunosuppressive therapies. These infections can mimic disease flares and significantly influence disease course and treatment decisions.

One of the most important superinfections in IBD is Clostridioides difficile infection, which can occur even in the absence of prior antibiotic exposure. It often presents with worsening diarrhoea, abdominal pain, and systemic symptoms, and should always be considered when patients experience an acute flare. Early testing and prompt treatment are essential to prevent complications.

Another significant pathogen is Cytomegalovirus colitis, particularly in patients with severe or steroid-refractory ulcerative colitis. CMV infection can exacerbate mucosal inflammation and lead to poor response to conventional therapies. Diagnosis typically requires endoscopic biopsy with histology or PCR-based detection.

Other infections that may complicate IBD include bacterial enteric infections (such as Salmonella or Campylobacter), parasitic infections, and opportunistic pathogens associated with immunosuppressive therapy. These infections may present with symptoms similar to active IBD, making differentiation challenging.

Accurate diagnosis requires a combination of stool studies, endoscopic evaluation, and histological examination. Identifying superinfection is crucial because management differs from standard IBD flare treatment and may require antimicrobial or antiviral therapy.

In summary, clinicians should maintain a high index of suspicion for superinfections in patients with worsening symptoms of IBD, especially those receiving corticosteroids, immunomodulators, or biologic therapies. Early recognition and appropriate treatment are key to improving patient outcomes and avoiding unnecessary escalation of immunosuppressive therapy.

Pouchitis is an inflammatory condition affecting the ileal pouch created after Ileal pouch–anal anastomosis (IPAA), most commonly performed for patients with Ulcerative colitis. Histological examination of pouch biopsies provides important insights into the underlying inflammatory processes and helps differentiate pouchitis from other pouch disorders.

On microscopic evaluation, acute pouchitis is characterised by neutrophilic infiltration of the lamina propria and epithelium, often with cryptitis and crypt abscess formation. Surface epithelial damage, mucosal oedema, and ulceration may also be present. In contrast, chronic pouchitis demonstrates architectural distortion of crypts, villous atrophy, increased lymphoplasmacytic infiltration, and basal plasmacytosis, reflecting persistent mucosal injury.

Advanced histological studies have shown alterations in mucosal immune responses, including increased infiltration of T lymphocytes, macrophages, and dendritic cells. Upregulation of pro-inflammatory cytokines such as tumour necrosis factor (TNF), interleukin-1β, and interleukin-6 contributes to sustained inflammation. Changes in epithelial barrier function and dysbiosis of the pouch microbiota also play significant roles in disease pathogenesis.

In some patients, histology may reveal features suggestive of Crohn's disease–like pouch complications, including granulomas, deep fissuring ulcers, or transmural inflammation. These findings raise the possibility of Crohn’s disease of the pouch rather than simple pouchitis.

Advanced diagnostic approaches, including immunohistochemistry and molecular profiling, are increasingly being explored to better characterise inflammatory pathways and differentiate various pouch-related disorders. Such insights may help guide targeted therapeutic strategies in patients with refractory pouchitis.

Terminal ileitis refers to inflammation of the terminal ileum, and histological examination plays a critical role in differentiating underlying etiologies. In the context of Crohn's disease, the characteristic histologic features include focal, patchy transmural inflammation, often with discontinuous involvement of the intestinal wall. The mucosa may demonstrate architectural distortion of crypts, focal cryptitis, and crypt abscesses, accompanied by infiltration of lymphocytes and plasma cells in the lamina propria.

A key diagnostic feature is the presence of non-caseating granulomas, although these are identified in only a subset of cases. Additional findings include lymphoid aggregates, mucosal ulceration, and fissuring ulcers extending deep into the bowel wall. Chronic disease may also show submucosal fibrosis, muscular hypertrophy, and neural hyperplasia, reflecting long-standing inflammation and tissue remodeling.

Infectious causes of terminal ileitis may show different histological patterns. For example, intestinal tuberculosis often demonstrates caseating granulomas with central necrosis, whereas bacterial infections may show acute neutrophilic infiltration with mucosal erosions.

Advanced histological techniques, including immunohistochemistry and molecular assays, can further characterize immune cell populations and inflammatory pathways involved in ileal inflammation. These approaches help distinguish Crohn’s disease from other causes of terminal ileitis and contribute to a more precise understanding of disease pathogenesis.

Patients with Inflammatory Bowel Disease (IBD), including Ulcerative colitis and Crohn's disease, have an increased risk of certain malignancies, primarily due to chronic intestinal inflammation, disease duration, and long-term immunosuppressive therapy. The most well-recognised cancer associated with IBD is Colorectal cancer, particularly in patients with extensive colitis and long-standing disease.

The risk of colorectal cancer generally increases after 8–10 years of disease duration, especially in individuals with pancolitis, persistent inflammation, or a family history of colorectal cancer. Patients with concomitant Primary sclerosing cholangitis have an even higher risk and require more intensive surveillance. Regular endoscopic surveillance with targeted biopsies or chromoendoscopy is therefore recommended to detect dysplasia at an early stage.

Apart from colorectal cancer, patients with IBD may also have an increased risk of small bowel adenocarcinoma, lymphoma, and certain skin cancers. Some of these risks are influenced by the use of immunosuppressive therapies such as thiopurines or biologic agents. For example, long-term thiopurine therapy has been associated with an increased risk of lymphoma and non-melanoma skin cancers, although the absolute risk remains relatively low.

Despite these concerns, modern IBD management aims to balance the potential risks of therapy with the benefits of adequate disease control. Persistent uncontrolled inflammation itself is a major driver of carcinogenesis. Therefore, effective treatment strategies that achieve mucosal healing may ultimately reduce cancer risk.

Preventive strategies include regular colonoscopic surveillance, careful selection and monitoring of immunosuppressive therapies, sun protection, dermatologic screening, and vaccination programs. Risk stratification based on disease extent, duration, and individual patient factors helps guide surveillance intervals.

In summary, malignancy remains an important long-term complication of IBD, but with appropriate surveillance and modern therapeutic approaches, early detection and risk reduction are increasingly achievable in routine clinical practice.