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Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

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Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
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Inflammatory Bowel Disease I: Ulcerative Colitis01:27

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Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
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Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
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Peptic Ulcer Disease II: Pathophysiology01:28

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Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
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Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide...
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Updated: Sep 11, 2025

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
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Ulcerative Colitis Aggravates Periodontitis via Inducing Myelopoiesis.

Xinyi Kuang1,2, Xiaoyue Jia1,3, Xian Peng1

  • 1State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

Inflammatory Bowel Diseases
|August 12, 2025
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Summary

Ulcerative colitis (UC) exacerbates periodontitis by increasing gut permeability and altering gut microbiota, leading to myeloid cell dysfunction and periodontal bone loss. Berberine treatment and understanding trained immunity are key to managing this oral-intestinal link.

Keywords:
HSPCsneutrophils extracellular trapsperiodontitistrained immunityulcerative colitis

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Area of Science:

  • Oral and gastrointestinal health
  • Immunology
  • Microbiome research

Background:

  • Periodontitis and inflammatory bowel disease (IBD), particularly ulcerative colitis (UC), share known interconnections.
  • Patients with UC exhibit higher rates and severity of periodontitis, but the mechanisms remain unclear.

Purpose of the Study:

  • To elucidate the mechanisms by which UC exacerbates periodontal inflammation and bone destruction.
  • To investigate the role of gut barrier integrity, microbial dysbiosis, and immune cell differentiation in UC-related periodontitis.

Main Methods:

  • Utilized murine models of DSS-induced colitis (DIC) and ligature-induced periodontitis (LIP).
  • Investigated berberine's effect on DIC/LIP and LIP following DIC remission.
  • Analyzed gut barrier function, microbiota, serum markers (LPS, IL-1), hematopoietic stem and progenitor cells (HSPCs), and neutrophil extracellular traps (NETs).

Main Results:

  • DIC mice showed disrupted gut barriers, dysbiosis, elevated LPS and IL-1, and aggravated periodontal bone resorption with NETs.
  • UC promoted HSPC myelopoiesis via myeloid differentiation pathways.
  • Berberine treatment reduced colitis, corrected myeloid skewing, and alleviated periodontal damage.
  • Periodontitis after UC remission still showed bone loss and myeloid skewing, suggesting trained immunity.

Conclusions:

  • Increased gut permeability and dysbiosis in UC elevate LPS and IL-1, causing myeloid skewing of HSPCs with immune memory.
  • Inflammatory myeloid cells contribute to NETs accumulation and periodontal destruction in UC-related periodontitis.