Thioketal-linked glycol chitosan nanosystem for targeted and sustained drug delivery of mesalazine in inflammatory bowel disease.

This paper reports a rare case of congenital hairy polyp arising from the posterior edge of the nasal septum in a child. The patient presented with poor ventilation in the right nasal cavity since birth, which gradually progressed to bilateral nasal obstruction with purulent rhinorrhea and nasal malodor. Over the years, the patient underwent multiple MRI examinations at several hospitals, which consistently suggested"posterior nasal mass: meningoencephalocele teratoma ". In June 2024, the patient underwent "endoscopic transoral-nasal combined plasma resection of the nasal septal mass" under general anesthesia in our department. Postoperative pathology confirmed the diagnosis of hairy polyp. The patient was discharged on the second postoperative day and has been followed up for more than 3 months. The patients clinical symptoms have resolved, and the surgical outcome is satisfactory. Re-examination by nasal endoscopy shows good healing of the nasal septal mucosa, with no posterior choanal or nasopharyngeal stenosis and no tumor recurrence.

Bomidin prevents inflammatory responses in macrophages by inhibiting toll-like receptor 4/nuclear factor-κB activation and blocking metabolic reprogramming to alleviate periodontal inflammation.

An antioxidant metal-organic framework with functional coatings for oral anti-TNF-α antibody delivery in inflammatory bowel disease treatment.

Chrysophanein of Rhubarb rescues ILC3-Derived IL-22 by blocking CCDC25/ILK/HIF-1α for mucosal healing in ulcerative colitis mice.

Chitosan-sodium tripolyphosphate-zinc nanogel for synergistic hydrogen and ion release to eradicate Helicobacter pylori and promote gastric mucosal healing.

This investigation was conducted to determine the potential of Punica granatum as a protective treatment for ulcerative colitis and for nephroprotection. The aqueous extract of Punica granatum peel (APPE) was subjected to phytochemical examination by qualitative and quantitative techniques. Sulfasalazine at a dose of 600 mg/kg and APPE at doses of 200 and 400 mg/kg were orally administrated to male Wistar rats during 21 days. On day 17, the rats were transrectally given acetic acid to induce ulcerative colitis. A comparative analysis was conducted using a positive control group with colitis and a negative control group without colitis. Colon macroscopic damage, ulcer index, oxidative stress markers, histological investigation, and anti-inflammatory factors were evaluated. Nephroprotective activity was investigated in an animal model of sulfasalazine-induced kidney damage. The phytochemical analysis of APPE revealed the presence of various bioactive compounds, and the HPLC-UV profile of APPE revealed an important content of polyphenolic compounds, such as resveratrol (552.17 μg/ml), chlorogenic acid (376.15 μg/ml), and 3,4-dihydroxybenzoic acid (329.00 μg/ml). The results obtained show that APPE exhibited activity against ulcerative colitis by significantly modulating antioxidant defense mechanisms, namely superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), in the colon tissues of APPE-treated groups in comparison with the positive group. The histopathological assessment showed a notable decrease in microscopic damage in groups receiving sulfasalazine and APPE at 400 mg/kg, which facilitated mucosal healing and reduced inflammatory cell infiltration. The examination of the kidneys revealed histopathological changes confirmed by tubulointerstitial necrosis. Nevertheless, the biochemical parameters were substantially improved in rats pre-treated with graded oral doses of the extract in a dose-related manner. The extract provided the most effective nephroprotection at 400 mg/kg/day. It would be interesting to conduct further tests in the use of APPE extracts as a pre-treatment for ulcerative colitis and nephropathy.

Treat-to-target optimization of biologic therapy is effective on endoscopic and histologic outcomes in a real-life cohort of ulcerative colitis-the TACTIC-UC study.

Research Progress on Exclusive Enteral Nutrition Combined with Biologics in the Treatment of Adult Crohn's Disease.

Background: Dolichandrone falcata, traditionally used for gastrointestinal disorders, has demonstrated antiulcer activity, but the underlying protective mechanisms remain unclear. This study evaluated the methanolic extract of D. falcata for gastroprotective, antioxidant, and anti-inflammatory activities using ethanol- and pylorus-ligation–induced ulcer models in rats. Methodology: Wistar rats were divided into control, standard, and treatment groups. Ulcers were induced by ethanol or pyloric ligation. The extract (100, 200, and 400 mg/kg) and omeprazole (20 mg/kg) were administered orally. Ulcer index, gastric parameters, oxidative stress markers [malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT)], and inflammatory cytokines [TNF-α, IL-6] were assessed, supported by histopathological examination. Results and Discussion: The extract produced a dose-dependent reduction in the ulcer index in both models, with 76.6% protection at 400 mg/kg, comparable to omeprazole (79.7%). Histology revealed marked restoration of the gastric mucosa with minimal necrosis. MDA levels decreased significantly, while GSH, SOD, and CAT levels were elevated toward normal. TNF-α and IL-6 were markedly suppressed, indicating a reduction in oxidative and inflammatory injury. Conclusion: D. falcata extract demonstrated potent gastroprotective effects through antioxidative, anti-inflammatory, and mucosal-healing mechanisms. This is the first biochemical and cytokine-based validation of its traditional use, suggesting strong potential for developing D. falcata as a plant-derived therapeutic for ulcer management.

BackgroundEndoscopic evaluation remains the gold standard for assessing Crohn’s disease (CD) activity and mucosal healing (MH), but it is invasive, expensive and time consuming. Therefore, there is an urgent need for a non-invasive quantitative alternative method.AimTo develop a topological radiomics-based multi-task deep learning model for simultaneous prediction of MH status and endoscopic activity scores in CD.MethodsA total of 81 CD patients were stratified into training (n=60) and validation (n=21) groups at a 7:3 ratio. Topological radiomic features were extracted from multiphase CT enterography. A multi-task model was trained to predict MH (classification) and SES-CD (regression), integrating feature selection and SHAP-based interpretability.ResultsThree discriminative topological features were identified across arterial and portal phases. For MH prediction, the multi-task model achieved an AUC of 0.938 for training set and 0.875 for validation set. For SES-CD prediction, it showed lower MSE and MAE, with higher R2 and C-index than the single-phase models.ConclusionThe multi-task topological radiomics framework enables accurate, non-invasive assessment of mucosal healing and endoscopic activity in CD, offering a clinically interpretable approach with strong translational potential. Future studies with larger cohorts are warranted to further validate its robustness.

HighlightsWhat are the main findings?FAK activation accelerates ischemic ulcer healing, in part by enhancing angiogenesis.FAK activation during an initial injury reduces susceptibility to recurrent NSAID-induced intestinal injury.What are the implications of the main findings?FAK activation may represent a novel therapeutic avenue for gastrointestinal injury.FAK activation may be especially valuable for patients requiring long-term NSAID therapy.Background: Gastrointestinal (GI) mucosal injury is a frequent complication of long-term nonsteroidal anti-inflammatory drug (NSAID) use. Effective mucosal healing requires coordinated epithelial migration, proliferation, and angiogenesis, which may be influenced by focal adhesion kinase (FAK). This study aimed to determine whether our newly developed FAK activators promote intestinal mucosal healing by enhancing angiogenesis and whether FAK activation increases resistance to reinjury. Methods: Ischemic jejunal ulcers were induced in C57BL/6 mice. After 24 h, mice received intraperitoneal injections of the FAK activator ZINC40099027 (ZN27, 900 µg/kg every 6 h) or vehicle for 2, 4, or 14 days. Ulcer areas were quantified, and liver and kidney function were assessed. Ulcer and adjacent tissues were analyzed by immunofluorescence staining for angiogenesis and proliferation markers. In vitro, human umbilical vein endothelial cells (HUVECs) were treated with ZN27 to evaluate proliferation, migration, angiogenesis, and intracellular signaling. In a reinjury model, male C57BL/6J mice received continuous infusion of the FAK activator M64HCl (25 mg/kg/day) or vehicle for 7 days, with a single subcutaneous injection of indomethacin (10 mg/kg) on day 1 to induce GI injury. Fourteen days after the first dose of indomethacin, the mice received a second indomethacin challenge, and one day later, total ulcer areas in the pyloric opening and small intestine were quantified. Results: Ulcer areas were significantly smaller in ZN27-treated mice compared with vehicle-treated controls at 3 and 5 days, accompanied by increased expression of angiogenesis and proliferation markers. In vitro, ZN27 enhanced HUVEC migration via FAK activation in an ERK1/2-dependent manner and increased the number of angiogenic sprouts. In the reinjury model, treatment with M64HCl during the initial indomethacin-induced injury resulted in significantly smaller ulcer areas in both the pyloric opening and small intestine after the second indomethacin challenge compared with controls. Conclusions: FAK activation accelerates ischemic ulcer healing, in part by enhancing angiogenesis. Moreover, FAK activation during an initial injury reduces susceptibility to recurrent NSAID-induced intestinal injury, perhaps because it promotes initial higher-quality ulcer repair.

Ulcerative colitis (UC) exhibits a heterogeneous clinical course, complicating prognostication and therapeutic decision making. Current tools inadequately predict progression or identify patients most likely to benefit from biologic therapies. We aimed to develop a machine learning model for risk stratification and evaluate its utility in optimizing biologic therapy outcomes. In this multicenter retrospective study, we analyzed 481 UC patients as the training cohort and 131 external validation patients. Disease progression-defined as treatment escalation, UC-related hospitalization, or surgery-served as the primary endpoint. Four models (Cox regression, logistic regression, random forest, XGBoost) were developed to predict progression risk. Biologic-treated patients (n = 235) were stratified into risk groups using the optimal model, with outcomes including mucosal healing, relapse, and acute severe UC assessed. The random forest model demonstrated superior performance, achieving an area under the curve of 0.959 in training set and 0.759 in validation set. High-risk biologic-treated patients (n = 172) exhibited lower mucosal healing rates (33.7% vs 55.2%; P = .049) and higher hazards of clinical relapse (hazard ratio [HR], 3.35; P = .003), hospitalization (HR, 2.03; P = .014), and acute severe UC (HR, 2.70; P = .030) compared with low-risk patients (n = 63). No differences in serological remission, surgery, or biologic switching were observed. Our random forest model enables precise risk stratification in UC, distinguishing patients with divergent responses to biologics. Low-risk patients derive significant benefit from timely biologics, while high-risk subgroups may require intensified strategies. This framework advances personalized UC management, though prospective validation is warranted.

Medication-related osteonecrosis of the jaw (MRONJ) is a severe adverse event triggered by antiresorptive and/or anti-angiogenic agents, characterized by bone destruction, sequestrum formation, and refractory mucosal defects. Effective mucosal healing can be a critical factor for MRONJ prevention and treatment. While endoplasmic reticulum stress (ER stress) has been implicated in tissue repair, its role in MRONJ-associated mucosal healing impairment remains undefined. This study investigated the effects of the anti-angiogenic drug sunitinib on oral mucosal healing and its underlying mechanisms. A mouse model of palatal mucosal defects was established, RNA-seq, transmission electron microscopy, and morphological analyses were used to assess how sunitinib affects ER function during mucosal repair. Using human oral keratinocytes (HOKs), we further elucidated the subcellular mechanisms through which sunitinib influences cell proliferation, migration, cell cycle progression, tight junctions, and apoptosis via techniques such as qPCR, Western blotting, immunofluorescence, and flow cytometry. Our findings demonstrated that sunitinib might induce significant alterations in the morphology of the ER and mitochondria. Both in vivo and in vitro experiments revealed that sunitinib persistently activates the GRP78 (BIP)/PERK/ATF4/CHOP axis in HOKs. This sustained ER stress can inhibit keratinocytes migration and proliferation, disrupt tight junctions, and trigger the intrinsic mitochondrial apoptotic pathway, ultimately leading to impaired oral mucosal healing and barrier dysfunction. Critically, pharmacological inhibition of ER stress was shown to restore keratinocytes’ function and promote effective mucosal healing. These results indicated that targeting sunitinib-induced persistent ER stress might represent a promising therapeutic strategy to prevent and treat oral mucosal toxicity associated with this drug.

Inflammatory bowel diseases (IBD), comprising Crohn's disease and ulcerative colitis, are chronic, inflammatory, immune mediated, relapsing-remitting conditions of the gastrointestinal tract with multidimensional and often negative effects on patients' quality of life. The global burden of IBD is increasing and is forecast to affect 1% of the population in early industrialized nations over the next 10 years. Advances in our understanding of the causes and pathogenesis of IBD in the past three decades have translated into new treatments that modulate the immune inflammatory cascade. Modern goals of treatment are clinical remission through assessment of patient reported outcomes and deep remission defined as mucosal healing on colonoscopy or imaging. Achieving both clinical and deep remission affords patients a better long term prognosis and quality of life. This review summarizes the latest evidence on IBD diagnosis, staging, and prognosis, with a detailed focus on current treatments.

Ulcers, injuries, and various oral surgical treatments frequently cause damage to the oral mucosa. Current oral wound dressings face critical limitations of short protection time due to their weak wet adhesion capability. To address this issue, we developed a Janus bilayer oral wound dressing (P-N/QCS) with dual functional components. ‌The oral cavity-facing surface of the P-N/QCS film demonstrates effective resistance to salivary erosion, while its opposing surface facilitates integration with biological tissues upon absorption of interfacial fluids or blood. This enables immediate adhesion through physical bonding, subsequently reinforced by molecular entanglement and covalent crosslinking. In vitro tests verified that our dressing exhibited significantly superior wet adhesive strength (53.3 ± 3.7kPa). The protective duration of P-N/QCS exceeded the commercial product Oral Aid by 521.7% (12 ± 0.5h vs. 2.3 ± 0.3h). Additionally, the Janus dressings showed potent hemostatic capability and excellent antibacterial activity. In the model of rat oral ulcer, the adhesive dressings accelerate the healing of the ulcer by suppressing inflammation and promoting epithelialization. In summary, the Janus bilayer oral wound dressing demonstrates promising clinical potential for oral mucosal repair.

Familial aggregation of inflammatory bowel disease (IBD) has been observed, but data from the Middle East, particularly Egypt, remain limited. This study investigated clinical differences, treatment responses, and predictors of response in familial and sporadic IBD patients. This case‒control study was conducted on ninety IBD patients (30 familial, 60 sporadic). Clinical history, inflammatory markers, endoscopic findings, and treatment outcomes were analysed over a one-year period. Predictors of response and mucosal healing were assessed via logistic regression. Mucosal healing was achieved in a greater percentage of patients in the familial group (73.3%) compared to those in the sporadic group (55%), but the difference did not reach statistical significance (P = 0.093). The percentages of patients with mucosal healing, clinical response, clinical remission and normalization of C-reactive protein (CRP) levels at one year were significantly greater in ulcerative patients in the familial group [17 (85%), 18 (90%), 18 (90%) and 18 (90%), respectively] than in ulcerative patients in the sporadic group [21 (53.8%), 19 (48.7%), 19 (48.7%) and 20 (51.3%), respectively], with p values of 0.018, 0.002, 0.002 and 0.003, respectively. However, there was no statistically significant difference between Crohn's disease patients of both groups regarding the outcome of the studied patients. A lower platelet count (≤ 324 × 10³/µL) and faecal calprotectin concentration (≤ 679µg/g) were significant predictors of mucosal healing in familial cases (P = 0.012, P = 0.008, respectively). Familial IBD patients may present with a more severe initial inflammatory response but have better long-term treatment outcomes. These findings suggest that genetic and environmental influences play a role in IBD, highlighting the need for region-specific studies.

Ulcerative colitis represents a chronic inflammatory bowel disease with limited therapeutic options due to inadequate efficacy and adverse effects of current treatments. This study investigated the therapeutic potential of Beaucarnea recurvata leaf extract (BRLE) against ulcerative colitis using integrated computational and experimental approaches to address the need for safer, multi-targeted interventions. Phytochemical profiling was performed using UPLC-ESI-MS/MS analysis. Network pharmacology and molecular docking predicted therapeutic targets and mechanisms. In vivo validation employed an acetic acid-induced ulcerative colitis rat model with BRLE treatment at 100, 200, and 400 mg/kg doses, evaluating clinical parameters, histopathology, oxidative stress markers, inflammatory cytokines, and protein expression. UPLC-ESI-MS/MS revealed diverse bioactive compounds including steroidal saponins, triterpenes, and flavonoids. Network pharmacology identified 24 hub targets, and molecular docking revealed strong binding affinities (−6.5 to −9.1 kcal/mol) between BRLE compounds and inflammatory proteins including EGFR, SRC, STAT3, and AKT1. BRLE at 200 mg/kg significantly improved disease activity, restored glutathione levels, reduced malondialdehyde, normalized IL-10 and TNF-α levels, downregulated EGFR, SRC, STAT3, and AKT1 expression, and enhanced mucosal healing with reduced inflammatory infiltration. BRLE demonstrates significant anti-inflammatory, antioxidant, and tissue-protection effects through multi-target mechanisms, representing a promising therapeutic intervention for ulcerative colitis treatment. Further studies in chronic models, pharmacokinetic assessments, and clinical trials are needed to support its translation into therapeutic use.

This article aims to elucidate the potential role of a comprehensive tooth extraction procedure in preventing mdication-related osteonecrosis of the jaw (MRONJ) through a prospective cohort study. By systematically assessing clinical outcomes following this procedure, the study seeks to provide evidence regarding its effectiveness in MRONJ prevention, thereby contributing to improved clinical guidelines and patient care related to dental extractions in at-risk populations. Patients using anti-resorptive agents (ARAs) who required extraction of at least one tooth were included in the study. Patients' medical history, medication history, and intraoral dental conditions were documented, and CBCT scans were performed. Following a standardized treatment protocol, patients received professional oral cleaning and antibiotics preoperatively. During surgery, minimally invasive extraction and concentrated growth factor (CGF) filling were performed with meticulous suturing whenever possible. Postoperatively, mouthwash was used within one month. Follow-up visits were scheduled at 10, 30, and 90 days to monitor and analyze MRONJ incidence and surgical outcomes. A total of 101 patients were included in the study, with 20 receiving oral ARAs for osteoporosis, 57 receiving intravenous ARAs for osteoporosis, 13 undergoing combination therapy for osteoporosis, and 11 using ARAs for malignancy. Zoledronic acid and denosumab were the most commonly used drugs. Increased bone density was observed on preoperative CBCT in 26 patients, and on postoperative CBCT at 90 days in 31 patients. In total, 248 teeth were extracted, mostly due to severe defects; periapical periodontitis and periodontitis were also major reasons for extraction. Most patients could not achieve complete and tight suturing. All patients remained free of MRONJ during the 90‑day postoperative period, with complete mucosal healing in every case. This prospective cohort study provides evidence that implementing an effective and rational treatment protocol during tooth extractions significantly benefits high-risk MRONJ patients. Adherence to such protocols minimizes the risk of postoperative infection, fosters improved healing of extraction sites, and maximizes the prevention of MRONJ. Not applicable.

To evaluate whether Er: YAG surgery and Nd: YAG-based low-level laser therapy (LLLT), combined with medical collagen, improve early postoperative outcomes after extraction of impacted mandibular third molars.Adults undergoing surgical removal of mesioangular or horizontal impacted mandibular third molars were randomized equally (1:1:1:1) to blank control (BCG), collagen only (COL), lasers only (LAS), or collagen plus lasers (COL + LAS). Primary endpoints were pain (VAS; spontaneous and swallowing; POD1/3/7), swelling (POD1/3/7), trismus (POD1/3/7), and early mucosal healing (POD3/7). Secondary endpoints were bleeding (30min post-extraction only), cutaneous induration/ecchymosis (POD7), alveolar osteitis (POD3/7), and local cytokines (IL-1β, IL-6, TNF-α; POD3/7).In 120 patients, COL + LAS was superior: less pain, swelling, and trismus at POD1/3 and higher early mucosal-healing rates at POD3/7 than BCG, COL, or LAS; by POD7, between-group differences in pain, swelling, and trismus were minimal. All active arms reduced 30-min bleeding versus BCG. At POD7, cutaneous induration was lowest with COL + LAS (ecchymosis not significant). Cytokines declined overall; IL-1β and TNF-α were lowest with COL + LAS at POD3/7, whereas IL-6 decreased similarly across active arms.Er: YAG surgery plus Nd: YAG-based LLLT with medical collagen improved short-term recovery after impacted mandibular third-molar surgery.