L22 Gastrointestinal diseases

Gastrointestinal Diseases

Course Information¹

• Institution: The University of Western Australia | Oral Health Centre of Western Australia
• Presenter: Bobby Joseph, Associate Professor

Lecture Focus

This lecture focuses on the intersection of gastroenterology and dentistry, specifically how systemic GI conditions manifest in the oral cavity.

• Year: 2026

Learning Objectives

Clinical Competencies and Knowledge²

• Develop a sound knowledge of the oral manifestations of gastrointestinal (GI) diseases.
• Understand the necessary modifications required in the treatment plan for patients presenting with these conditions.
• Gain comprehensive knowledge of the investigations and common laboratory tests available to assess the status of gastrointestinal diseases.
• Gain familiarity with investigations and lab tests used to assess disease status
• Understand the oral features associated with common GI diseases

Oral Manifestations of Gastrointestinal Tract Diseases

General Characteristics³

• Oral lesions may occur in several gastrointestinal tract (GIT) diseases.

• Primary oral lesions: In a few cases, these resemble the lesions found in the lower gut.

• Secondary lesions: In almost all cases, these may be due to malabsorption and surgical resection of the gut

  • Secondary lesions are often caused by deficiencies in iron, B12, or folic acid resulting from gut issues.

• Fatty meals are also a significant predisposing factor for reflux.

Gastro-Oesophageal Reflux Disorder

Pathophysiology and Predisposing Factors

Gastro-oesophageal Reflux in Healthy Individuals⁴

• This term describes the backflow of acid from the stomach into the oesophagus.

Gastro-oesophageal Reflux Disorder (GORD)⁵

• Characterized by increased frequency and duration of reflux.
• Damage is caused to the oesophageal mucosa by the regurgitation of gastric contents.

Predisposing Factors⁶

Gastrointestinal Disorders

• High acidity of gastric contents
• Impaired gastro-oesophageal motility

Extra-Gastrointestinal Conditions

• Obesity
• Large meals
• Smoking
• Excessive alcohol consumption

Clinical Features and Complications

Clinical Symptoms⁷

• Heartburn
• Uncomfortable burning sensation behind the sternum after a meal
• Acid taste
• Epigastric pain
• Dysphagia
• Chronic cough

Complications

• Stricture
• Ulceration
• Iron deficiency anaemia
• Reflux oesophagitis
• Epithelial metaplasia (Barrett’s oesophagus)

Dental Aspects and Erosion

Dental Erosion and GORD⁸

• Gastric contents with a pH as low as 1 cause dental erosion.
• Erosion is typically seen on the palatal aspects of upper anterior teeth and premolars.
• The gastric acid is strong enough to erode enamel, which is the hardest substance in the human body.
• The condition is exacerbated if salivation is impaired.

Clinical Assessment⁹

• Patients presenting with palatal dental erosion should be assessed for GORD.
• Dentists may be the first to identify GORD based on clinical signs like thin enamel and exposed dentin.
• Affected teeth are often highly sensitive to temperature and touch.

Management and Drug Therapy

Diagnosis and Lifestyle Management¹⁰

• Diagnosis: Confirmed by oesophageal pH monitoring.
• Symptom Relief:
  • Losing weight
  • Raising the head of the bed at night
  • Frequent small meals with antacids
    • Regular exercise is also recommended as part of lifestyle management.

Pharmacological Therapy

• H₂ blockers:
  • Cimetidine
  • Ranitidine
• Proton-pump inhibitors:
  • Omeprazole
  • Lansoprazole

H2 Blockers (Histamine H2 Receptor Antagonists)¹¹

• Histamine stimulates parietal cells to release acid.
• H2 blockers stop parietal cells from responding to histamine, thereby reducing acid production.
• Examples: Cimetidine, ranitidine.

Proton Pump Inhibitors

• Reduce the amount of acid made by the stomach.
• Block a chemical system known as hydrogen-potassium adenosine triphosphatase.
• Examples: Omeprazole, lansoprazole.

Barrett Oesophagus

Characteristics of Barrett Oesophagus¹²

• A premalignant condition where normal squamous epithelium is replaced by metaplastic columnar epithelium.
• Occurs as a consequence of chronic gastro-oesophageal reflux.
• It is a common but often under-diagnosed entity, frequently found incidentally during endoscopy.

Pseudomembranous Colitis

Etiology and Clostridium Difficile

Pseudomembranous Colitis (Antibiotic Associated Colitis)¹³

• Inflammation of the colon associated with the overgrowth of Clostridium difficile.
• Overgrowth is related to recent antibiotic use.
• Pathogenesis involves the production of enzymes and toxins A and B.
  • Toxins A and B specifically damage the gut lining.

Clostridium Difficile Profile¹⁴

• Gram-positive, spore-forming anaerobic rod found in soil, sand, and faeces.
• Spores are implicated in the spread of infection.
• Colonizes 2-3% of asymptomatic adults and up to 50% of the elderly.

Clinical Presentation and Risk Factors

Clinical Presentation¹⁵

• Symptoms usually begin after a few days of antibiotic therapy or up to several weeks after finishing the course.
• Abdominal cramps, pain, or tenderness.
• Presence of pus or mucus in the stool.
• Watery diarrhea (5 to 10 times per day) or bloody stools.

Risk Factors for Pseudomembranous Colitis¹⁶

• Frail elderly patients.
• Patients staying in hospitals or nursing homes.
• Patients on tube feeding.
• HIV patients.
• Increased inhalation of spores (e.g., in farm environments).
• Rarely affects infants or children.

Diagnosis and Complications

Diagnostic Procedures¹⁷

• Stool cytotoxin test (high sensitivity).
• Immunoassay for C. difficile toxin in the stool.
• Colonoscopy.
• Plain X-rays and CT scanning may be helpful.

Complications of Colitis¹⁸

• Low levels of potassium
• Dehydration
• Metabolic acidosis
• Hypotension
• Peritonitis
• Toxic megacolon: Swelling of the colon where it is incapable of expelling gas and stool, potentially causing the colon to rupture.

Management and Dental Considerations

Management Protocols¹⁹

Mild Pseudomembranous Colitis

• Discontinue use of the causative antibiotics.

Severe Pseudomembranous Colitis

• Discontinue use of the causative antibiotics.
• Prescribe antibiotics to eradicate C. difficile:
  • Metronidazole 400mg every 8 hours.
  • Vancomycin 125mg every 6 hours.

Metronidazole Considerations

Metronidazole can cause a metallic taste and is strictly contraindicated with alcohol consumption or in patients with liver damage.

• Surgical resection may be required in extreme cases.
• Relapse occurs in 5-20% of cases.

Dental Considerations²⁰

• Maintain knowledge of antibiotics that predispose elderly, debilitated, or previously affected patients to PC.
• PC following short-term use of Clindamycin has not been reported when used for AHA prophylactic regimens.
• No elective treatment should be performed until the resolution of PC.
• Monitor for oral candidiasis following PC therapy.

Coeliac Disease

Overview of Coeliac Disease²¹

• Also known as gluten-sensitive enteropathy.
• ==Also known as Gluten-Induced Enteropathy==
• ==A permanent intolerance to gliadin (found in wheat, rye, and barley)==
• Not uncommon; frequently associated with the Celtic ethnic group.
• May not be recognized if symptoms are not severe.
• A genetically determined hypersensitivity to gluten that affects the jejunum.

Clinical Features and Oral Manifestations

Clinical Features²²

• Patients may appear healthy despite the disease.
• Manifestations of malabsorption are common.
• Diarrhoea, weight loss, and weakness.
• Increased risk of osteoporosis, infertility, and malignancy
• Approximately 3% of patients with aphthae (mouth ulcers) have underlying coeliac disease.
  • Ulcers are typically well-circumscribed and painful

Oral Manifestations²³

• Recurrent Aphthous Stomatitis (RAS) / Ulcers
• Angular stomatitis
• Glossitis
  • Presents as a "bald" tongue due to atrophy of papillae from hematinic deficiencies
• Dental hypoplasia
  • Includes enamel defects and pitting

Diagnosis and Management

• Specialist referral is necessary for definitive diagnosis.
• Haematological and gastrointestinal investigations are indicated.
• Testing for antibodies to gluten, reticulin, endomysin, and transglutaminase.
• Small bowel biopsy is required for confirmation.
• Management includes a strict gluten-free diet.
  • Diet is curative for most, though some may still require topical corticosteroids or chlorhexidine mouthwash for persistent ulcers
• Deficiencies in Iron (Fe), folate, and Vitamin B₁₂ should be rectified.

Orofacial Granulomatosis and Crohn Disease

Orofacial Granulomatosis Syndrome

Definition and Characteristics²⁴

• Describes a clinical syndrome presenting with swelling of the face, lips, and oral tissues.
• Histological evidence shows non-caseating granulomatous inflammation.
• Note: Caseating granulomas are characteristic of tuberculosis.

Diagnostic Classification²⁵

• OFG is regarded as a provisional diagnosis rather than a final disease entity.
• The condition includes:
  1. Localised disorders affecting the mouth and face.
  2. Oral manifestations of systemic diseases:
     • Sarcoidosis
     • Crohn’s disease
     • Melkersson-Rosenthal syndrome
     • Cheilitis granulomatosa

Aetiology and Associations²⁶

• The cause remains unclear; suggested causes include allergy, infection, and heredity.
• Intolerance to certain foods, flavourings, or toothpaste constituents.
• Dietary preservatives: cinnamaldehyde, cocoa, benzoates.
• Occasionally associated with dental materials.

Crohn Disease Clinical Features

Crohn Disease Overview²⁷

• A chronic inflammatory idiopathic granulomatous disorder.
• Affects mainly the small intestine (ileum), but can affect any part of the GIT, including the mouth.
• 10% of patients with Crohn’s disease of the bowel have oral lesions.
• Oral lesions can occur in the absence of GIT involvement, presenting similarly to OFG.

Systemic Clinical Features²⁸

• Mucosal inflammation with ulceration and fistulae formation.
• Lymph node hyperplasia leading to obstructive oedema.
• Abdominal pain and diarrhoea, often with the passage of blood and mucus.
• Extra-GI involvement: Can affect the skin, joints, liver, and bone marrow.
• Anaemia and weight loss.

Shared Orofacial Features

Common Orofacial Presentations of Chron’s disease and OFG²⁹

• Swelling of the lip
• Lip fissures
  • Deep cuts specifically in the midline of the lip.
• Angular cheilitis
• Cobblestoning of the mucosa
  • Edematous, hyperplastic thickening of the buccal or labial mucosa.
• Full-width gingivitis
  • Persistent redness and swelling of the attached gingiva.
• Ulcers
• Mucosal tags
  • Polypoid-like lesions or deep folds that can mimic denture-induced irritation.

Diagnosis and Management of Crohn Disease

Diagnostic Investigations³⁰

• Thorough investigation including screening for underlying systemic conditions.
• Oral biopsy.
• Haematological, GIT, and biochemical investigations (specifically to rule out sarcoidosis).
• Patch testing.
• Consultation with a gastroenterologist.

Biopsy Technique

A deep biopsy is required because granulomas are often located deep within the muscle; superficial biopsies may result in a false negative.

Management Strategies³¹

• Oral Ulcers: Treated with topical or intralesional corticosteroids, and antiseptic or analgesic mouthwashes.
• Systemic Treatment: Short courses of systemic steroids (e.g., budesonide, which has fewer side effects).
• Medication: Mesasalazine (aminosalicylates
• Biologicals and Immunosuppressants: Use of anti-TNF alpha antibodies such as Infliximab and Adalimumab.).
• Referral: Mandatory referral to a gastroenterologist.

Sarcoidosis

Systemic and Orofacial Features

Sarcoidosis Overview³²

• A multi-system granulomatous disorder of unclear aetiology.
• Frequently affects young adult females, particularly those of Afro-Caribbean descent.
• Granulomas form in the lungs, lymph nodes, salivary glands, and mouth.
• Characterized by non-caseating granulomas in the lungs and lymph nodes.
• Key features include bilateral hilar lymphadenopathy and erythema nodosum.

Orofacial Features of Sarcoidosis³³

• Heerfordt’s Syndrome: Characterized by salivary and lacrimal gland swelling, facial palsy, and uveitis.
• Xerostomia (dry mouth).
• Mucosal nodules.
  • Commonly found on the palate.
• Gingival swelling.
• Labial swelling.

Management and Referral Criteria

Diagnostic Management³⁴

• Biopsy of labial salivary glands.
• Serum angiotensin-converting enzyme (SACE) levels are typically raised.
• Positive gallium scan of lacrimal and salivary glands.
• Chest radiography to check for enlarged hilar lymph nodes.

Referral Criteria

• Suspected malignancy in the neck, including lymphoma.
• Suspected metastatic disease in the neck.
• Unexplained lymphadenopathy.

Melkersson-Rosenthal Syndrome

Clinical Triad³⁵

• Lip or facial swelling
  • Often presents as recurrent swelling (Orofacial Granulomatosis).
• Fissured tongue
• Lower motor neurone facial palsy

Ulcerative Colitis

Clinical Features and Complications

Ulcerative Colitis Overview³⁶

• An uncommon inflammatory disease mainly affecting adults.
• Non-infectious inflammation limited to the colorectal mucosa, extending proximally from the anal margin.
• Characterized by ulcers and polyps in the colon.
• Associated with a risk of malignant change.
• Symptoms include persistent diarrhoea, passage of blood and mucus, iron deficiency anaemia, and weight loss.

Complications and Oral Manifestations³⁷

• Systemic Complications: Widespread ulceration of the colon, haemorrhage, perforation, and malignancy.
• Oral Manifestations: Severe aphthae and candida infections
  • Oral features are less common than in Crohn's disease.
• Secondary Effects: Oral lesions may be secondary to nutritional deficiencies resulting from malabsorption.

Management of Ulcerative Colitis

• Specialist referral is necessary.
• Diagnostic tests: Biopsy, Full Blood Count (FBC), and sigmoidoscopy.
• Treatment of secondary deficiencies using haematinics.
• Pharmacological treatment: Topical steroids (pessaries or enemas) and systemic sulfasalazine.
• Additional pharmacological management includes aminosalicylates and immunosuppressants.

Pyostomatitis Vegetans

Clinical Presentation³⁸

• A rare disorder where bowel symptoms typically precede oral involvement by months or years.
• Characterized by pustular lesions on the oral mucosa and gingiva.
• Vegetative outgrowths on inflamed, erythematous mucosa may also be present.
• Pustular lesions rupture to form erosions and “snail track” ulceration.

Management

• Topical steroids are often successful.
• Management of the associated Inflammatory Bowel Disease (IBD) typically leads to improvement of oral lesions.
• Systemic management of the underlying colitis is often the primary driver for resolving oral symptoms.

Diagnostic Significance³⁹

• Pyostomatitis vegetans serves as an important oral marker for inflammatory bowel disease.

Clinical Action

Because this condition is a highly specific marker for IBD, its presence often necessitates an immediate referral for GI investigation.

Gastrointestinal Polyposis Syndromes

Gardner Syndrome

Clinical Features of Gardner Syndrome⁴⁰

• Multiple osteomas of the jaws.
  • Visible on X-rays as radio-opacities
  • Considered benign bone tumors
• Epidermal or sebaceous cysts of the skin.
• Multiple fibrous tumours.
• Polyposis coli: Characterized by a marked tendency to undergo malignant change.

Peutz-Jeghers Syndrome

Etiology and Systemic Features⁴¹

• An autosomal dominant inherited disorder.
• Caused by a germline mutation in the liver kinase B1 (LKB1) tumour suppressor gene.
• Associated with an increased cancer risk in adult life.
• Hamartomatous polyps develop early in life.
• Complications include abdominal pain, bleeding, anaemia, and acute intestinal obstruction.

Clinical Manifestations⁴²

• Brown to blue-black macules (pigmentation) around the mouth, nose, and eyes.
  • Pigmentation also commonly affects the oral mucosa
• Polyps primarily in the small intestine, though rare cases occur outside the GIT.
• Polyps may undergo intussusception or malignant changes.

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