```markdown THE UNIVERSITY OF WESTERN AUSTRALIA | Oral Health Centre of Western Australia Gastrointestinal diseases Bobby Joseph Associate Professor 2026 ``` #### Course Information - **Institution:** The University of Western Australia | Oral Health Centre of Western Australia - **Presenter:** Bobby Joseph, Associate Professor - **Year:** 2026 # Learning objectives - To have a sound knowledge of the oral manifestations of GI diseases and the modifications required in the treatment plan for patients with these diseases. - To have a good knowledge on the investigations and common lab tests available to assess the status of these diseases. #### Clinical Competencies and Knowledge - 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. # Oral lesions and GIT diseases - Oral lesions may occur in several gastrointestinal tract diseases - In a few, these are **primary oral lesions** resembling those of the lower gut - In almost all, **secondary lesions** may be due to malabsorption and surgical resection of the gut #### General Characteristics - 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. Gastro-oesophageal reflux (healthy individuals) - Term used to describe a backflow of acid from the stomach into the oesophagus  #### Gastro-oesophageal Reflux in Healthy Individuals - This term describes the backflow of acid from the stomach into the oesophagus. A labeled anatomical diagram showing the human upper digestive system, highlighting the esophagus, lower esophageal sphincter, and stomach. The diagram illustrates the location of these organs in relation to the body, with labels pointing to each structure. Gastro-oesophageal reflux disorder (GORD) - Increased frequency and duration of reflux - Damage caused to oesophageal mucosa by regurgitation of gastric contents #### Gastro-oesophageal Reflux Disorder (GORD) - Characterized by increased frequency and duration of reflux. - Damage is caused to the oesophageal mucosa by the regurgitation of gastric contents. ```markdown GORD (predisposing factors) GI disorders - High acidity of gastric contents - Impaired gastro-oesophageal motility Extra-GI conditions - Obesity - Large meals - Smoking - Excessive alcohol consumption ```  #### Predisposing Factors **Gastrointestinal Disorders** - High acidity of gastric contents - Impaired gastro-oesophageal motility **Extra-Gastrointestinal Conditions** - Obesity - Large meals - Smoking - Excessive alcohol consumption The image displays a structured list of predisposing factors for GORD (gastroesophageal reflux disease), categorized into GI disorders and extra-GI conditions. Under GI disorders, it lists high acidity of gastric contents and impaired gastro-oesophageal motility. Under extra-GI conditions, it includes obesity, large meals, smoking, and excessive alcohol consumption. The text is presented in a clean, hierarchical format with bullet points and subheadings. ```markdown GORD: clinical features **Symptoms** - 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) ```    #### Clinical Symptoms - 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) The title 'GORD: clinical features' is prominently displayed at the top of the page, indicating the main topic of the slide. This heading introduces the content that follows, which includes a list of symptoms and complications related to GORD. A bulleted list under the heading 'Symptoms' details various clinical manifestations of GORD, including heartburn, uncomfortable burning sensation behind the sternum after a meal, acid taste, epigastric pain, dysphagia, and chronic cough. A bulleted list under the heading 'Complications' outlines potential adverse outcomes of GORD, such as stricture, ulceration, iron deficiency anaemia, reflux oesophagitis, and epithelial metaplasia (Barrett's oesophagus). # GORD: Dental aspects - Gastric contents pH as low as 1 cause dental erosion - Seen on the palatal aspects of upper anterior teeth and premolars - Worse if impaired salivation <img src="https://i.imgur.com/3XZQZ5l.png" alt="Dental erosion caused by GORD, showing lesions on upper anterior teeth and premolars">   #### Dental Erosion and GORD - 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 condition is exacerbated if salivation is impaired. A clinical photograph showing dental erosion on the palatal aspects of upper anterior teeth, with a blue arrow highlighting the affected area. The image illustrates the impact of gastric contents with low pH on dental structures, consistent with GORD-related damage. A close-up clinical photograph depicting dental erosion on the palatal surfaces of upper premolars, with a blue arrow indicating the lesion. This image supports the text's explanation of GORD-induced dental damage, particularly in areas with reduced salivation. ```markdown GORD - Patients presenting with palatal dental erosion should be assessed for GORD ```  #### Clinical Assessment - Patients presenting with palatal dental erosion should be assessed for GORD. A close-up photo of a patient's mouth showing palatal dental erosion, with visible damage to the teeth and surrounding tissue, illustrating the condition that should be assessed for GORD. ```markdown GORD: management **Diagnosis:** Confirmed by oesophageal pH monitoring **Symptoms relieved:** - Losing weight - Raising the head of bed at night - Frequent small meals with antacids **Drugs** **H₂ blockers** - cimetidine - ranitidine **Proton-pump inhibitors** - omeprazole - lansoprazole 10 ```  #### Diagnosis and Lifestyle Management - **Diagnosis**: Confirmed by oesophageal pH monitoring. - **Symptom Relief**: - Losing weight - Raising the head of the bed at night - Frequent small meals with antacids #### Pharmacological Therapy - **H₂ blockers**: - Cimetidine - Ranitidine - **Proton-pump inhibitors**: - Omeprazole - Lansoprazole A structured list detailing the management of GORD, including diagnosis confirmed by oesophageal pH monitoring, symptoms relieved such as losing weight, raising the head of bed at night, and frequent small meals with antacids, and a categorized list of drugs including H₂ blockers (cimetidine, ranitidine) and proton-pump inhibitors (omeprazole, lansoprazole). # Drug therapy: GORD ## H2 Blockers (histamine H2 receptor antagonist) - Histamine stimulates parietal cells to release acid - H2 blockers stop parietal cells from responding to histamine - Reduces acid production - Examples: cimitidine, ranitidine ## Proton pump inhibitors - Reduce the amount of acid made by stomach - Block a chemical system: hydrogen-potassium adenosine triphosphatase - Examples: omeprazole, lansoprazole #### H2 Blockers (Histamine H2 Receptor Antagonists) - 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’s oesophagus - Premalignant condition - Normal squamous epithelium replaced by metaplastic columnar epithelium - Consequence of chronic gastro-oesophageal reflux - Common, under diagnosed entity - Incidental finding at endoscopy  #### Characteristics of Barrett Oesophagus - 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. Endoscopic image showing Barrett's oesophagus, characterized by a reddish, columnar epithelium replacing the normal pale squamous epithelium in the lower oesophagus. The image illustrates the appearance of the affected tissue during endoscopy, consistent with the described premalignant condition. Pseudomembranous colitis (antibiotic associated colitis) - Inflammation of the colon associated with overgrowth of Clostridium difficile - Overgrowth of C.difficile related to recent antibiotic use - Production of enzymes and toxins A and B #### Pseudomembranous Colitis (Antibiotic Associated Colitis) - 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. ```markdown # Pseudomembranous colitis ## Clostridium difficile - Gram+, spore-forming anaerobic rod, seen in the soil, sand and faeces - Spores formed are implicated in spread of infection - Colonizes 2-3% of asymptomatic adult and up to 50% of the elderly ``` #### Clostridium Difficile Profile - 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. ```markdown # Pseudomembranous colitis - Symptoms usually begin after a few days of antibiotic therapy or as long as several weeks after finishing taking the antibiotic - Abdominal cramps, pain or tenderness - Pus or mucous in stool - Watery diarrhea (5 to 10 times per day) or even bloody ``` #### Clinical Presentation - 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 (PC) - Frail elderly patients - Patients staying in the hospitals or a nursing home - Patients on tube feeding - HIV patients - Increased inhalation of spores (e.g. in farms) - Rarely affecting infants or children #### Risk Factors for Pseudomembranous Colitis - 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. ```markdown # Diagnosis (PC) - Stool cytotoxin test which has high sensitivity - Immunoassay for C.difficile toxin in the stool - Colonoscopy - Plain X-rays and CT scanning may be helpful ``` #### Diagnostic Procedures - Stool cytotoxin test (high sensitivity). - Immunoassay for *C. difficile* toxin in the stool. - Colonoscopy. - Plain X-rays and CT scanning may be helpful. # Complications - Low levels of potassium - Dehydration - Metabolic acidosis - Hypotension - Peritonitis - Toxic megacolon: swelling of the colon, incapable of expelling gas and stool, cause colon to rupture #### Complications of Colitis - 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. ```markdown | Pseudomembranous colitis Management | |---| | **Mild PC** | | Discontinue use of antibiotics | | **Severe PC** | | • Discontinue use of antibiotics | | • Prescribe antibiotics to eradicate C. difficile | | Surgical resection | | Metronidazole 400mg 8hrly | | Vancomycin 125 mg 6hrly | | 5-20 % Relapse | ```  #### Management Protocols **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. - Surgical resection may be required in extreme cases. - Relapse occurs in 5-20% of cases. A flowchart titled "Pseudomembranous colitis Management" that outlines treatment pathways for mild and severe cases. For mild PC, it recommends discontinuing antibiotics. For severe PC, it suggests discontinuing antibiotics, prescribing antibiotics to eradicate C. difficile, and considering surgical resection. The diagram also lists specific antibiotics (metronidazole and vancomycin) and notes a 5-20% relapse rate. # Dental consideration - Have a good knowledge of frequently used antibiotics that predisposes to PC in elderly, debilitated and those with previous history of PC - PC following short-term use of Clindamycin has not been reported after use of AHA prophylactic regimen - No elective treatment until resolution of PC - Oral candidiasis following PC therapy #### Dental Considerations - 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 (gluten-sensitive enteropathy) - Not uncommon - Ethnic group: Celts - Not recognised if not severe - Genetically determined hypersensitivity to gluten - Affects the jejunum #### Overview of Coeliac Disease - Also known as gluten-sensitive enteropathy. - 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. # Coeliac disease: clinical features - Patients may appear healthy - Manifestations of malabsorption - 3% of patients with aphthae have coeliac disease - Diarrhoea, weight loss, weakness #### Clinical Features - Patients may appear healthy despite the disease. - Manifestations of malabsorption are common. - Diarrhoea, weight loss, and weakness. - Approximately 3% of patients with aphthae (mouth ulcers) have underlying coeliac disease. ```html <table> <tr> <td> <img src="https://i.imgur.com/1.png" alt="Ulcers (RAS)"/> </td> <td> <img src="https://i.imgur.com/2.png" alt="Angular stomatitis"/> </td> </tr> <tr> <td> <img src="https://i.imgur.com/3.png" alt="Glossitis"/> </td> <td> <img src="https://i.imgur.com/4.png" alt="Dental hypoplasia"/> </td> </tr> </table> ```     #### Oral Manifestations - Recurrent Aphthous Stomatitis (RAS) / Ulcers - Angular stomatitis - Glossitis - Dental hypoplasia A close-up photograph showing oral ulcers (RAS) on the inner cheek, characterized by small, white, circular lesions on a red, inflamed mucosal surface. A photograph of angular stomatitis, showing a red, inflamed lesion at the corner of the mouth with a black arrow pointing to the affected area. A photograph of glossitis, displaying a smooth, red, and swollen tongue with a loss of papillae, indicating inflammation. A photograph of dental hypoplasia, showing teeth with yellowish, irregular enamel defects and structural abnormalities. # Management: coeliac disease - Specialist referral is necessary - Haematological and gastrointestinal investigations indicated - Antibodies to gluten, reticulin, endomysin, transglutaminase - Small bowel biopsy required - Gluten free diet - Fe, folate, Vit B₁₂ def. should be rectified #### 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. - Deficiencies in Iron (Fe), folate, and Vitamin B₁₂ should be rectified. Orofacial granulomatosis (OFG) Describes a clinical syndrome presenting with swelling of face, lips, oral tissues in association with histological evidence of non-caeseating granulomatous inflammation Caeseating granuoma: tuberculosis   #### Definition and Characteristics - 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. Microscopic image showing non-caseating granulomatous inflammation with pink and blue staining, illustrating the histological evidence associated with orofacial granulomatosis (OFG). Microscopic image depicting a caseating granuloma with central necrosis and surrounding inflammatory cells, characteristic of tuberculosis, contrasting with non-caseating granulomas. ```markdown # Orofacial granulomatosis **Not a disease entity** Regarded as a provisional diagnosis Condition includes: 1. Localised disorders affecting mouth and face 2. Oral manifestations of systemic disease 2a. Sarcoidosis 2b. Crohn’s disease 2c. Melkersson-Rosenthal syndrome 2d. Cheilitis granulomatosa ```  #### Diagnostic Classification - 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 A structured table detailing the condition 'Orofacial granulomatosis,' which is described as not a disease entity but a provisional diagnosis. The table lists the components of the condition, including localized disorders affecting the mouth and face, and oral manifestations of systemic diseases such as sarcoidosis, Crohn's disease, Melkersson-Rosenthal syndrome, and cheilitis granulomatosa. # OFG: aetiology & other associations - Cause unclear - Allergy, infection and heredity-suggested causes - Intolerance to certain foods, flavourings, constituents of toothpastes - Preservatives in the diet: cinnamaldehyde, cocoa, benzoates - Occasionally dental materials #### Aetiology and Associations - 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. ```markdown # Crohn’s disease - Chronic inflammatory idiopathic granulomatous disorder - Affects mainly small intestine (ileum), can affect any part of GIT including mouth - 10% of patients with Crohn’s disease of the bowel have oral lesions - Oral lesions can be seen in the absence of GIT involvement, same as those seen in OFG ``` #### Crohn Disease Overview - 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. Crohn’s disease: clinical features - Mucosal inflammation with ulceration & fistulae formation - Lymph node hyperplasia: obstructive oedema - Abdominal pain, diarrhoea and with passage of blood & mucus - Anaemia, weight loss  #### Systemic Clinical Features - 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. - Anaemia and weight loss. A circular endoscopic image showing mucosal inflammation with ulceration and fistulae formation in Crohn's disease, displaying a reddish, inflamed intestinal lining with visible ulcerated areas and possible fistulae. # Orofacial features: Crohn’s disease & OFG Swelling of lip Lip fissures Angular cheilitis Cobblestoning of mucosa Full-width gingivitis Ulcer Mucosal tag  #### Common Orofacial Presentations - Swelling of the lip - Lip fissures - Angular cheilitis - Cobblestoning of the mucosa - Full-width gingivitis - Ulcers - Mucosal tags This figure displays a collage of seven clinical photographs illustrating orofacial features associated with Crohn's disease and orofacial granulomatosis (OFG). The images show various manifestations including swelling of the lip, lip fissures, angular cheilitis, full-width gingivitis, cobblestoning of the mucosa, an ulcer, and a mucosal tag, each labeled for identification. **Diagnosis: crohn's disease** - Thorough investigation including underlying systemic conditions - Oral biopsy - Haematological, GIT & biochemical investigations (to rule out sarcoidosis) - Patch testing - Consultation with the gastroenterologist #### Diagnostic Investigations - 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. # Management: Crohn's Disease - Oral ulcers: topical or intralesional corticosteroids, antiseptic & analgesic mouthwash - Short courses of systemic steroids (budesonide: less side effects) - Mesasalazine (aminosalicylates) - Refer to gastroenterologist #### Management Strategies - **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). - **Referral**: Mandatory referral to a gastroenterologist. ```markdown # Sarcoidosis - Multi-system granulomatous disorder of unclear aetiology - Affects young adult females, especially Afro-Caribbeans - Granulomas form in lungs, lymph nodes, salivary glands, mouth - Causes bilateral hilar lymphadenopathy - Erythema nodosum ``` #### Sarcoidosis Overview - 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. - Key features include bilateral hilar lymphadenopathy and erythema nodosum. **Orofacial features: sarcoidosis** - Heerfordt’s syndrome - (salivary and lacrimal glands swelling, facial palsy, uveitis) - Xerostomia - Mucosal nodules - Gingival swelling - Labial swelling   #### Orofacial Features of Sarcoidosis - **Heerfordt’s Syndrome**: Characterized by salivary and lacrimal gland swelling, facial palsy, and uveitis. - Xerostomia (dry mouth). - Mucosal nodules. - Gingival swelling. - Labial swelling. A close-up photograph of the oral cavity showing mucosal nodules on the palate, with arrows pointing to the affected areas. This image illustrates the orofacial features of sarcoidosis, specifically mucosal nodules, as listed in the surrounding text. A close-up photograph of the lower lip and gingival region, highlighting labial swelling and gingival swelling. The image visually supports the text listing these features as part of the orofacial manifestations of sarcoidosis. # Management: sarcoidosis - Biopsy of labial salivary gland - Serum angiotensin-converting enzyme raised - Positive gallium scan of lacrimal and salivary glands - Chest radiography (for enlarged hilar lymph nodes) ## Patients to refer: - Suspected malignancy in neck, including lymphoma - Suspected metastatic disease in neck - Unexplained lymphadenopathy #### Diagnostic Management - 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 Lip or facial swelling Fissured tongue Lower motor neurone facial palsy    #### Clinical Triad - Lip or facial swelling - Fissured tongue - Lower motor neurone facial palsy A close-up photo of a person's lips showing significant swelling, illustrating the symptom of lip or facial swelling associated with Melkersson-Rosenthal syndrome. A photo of a fissured tongue, showing deep grooves and a reddish appearance, corresponding to the symptom of fissured tongue in Melkersson-Rosenthal syndrome. A photo of a person with a facial asymmetry, demonstrating lower motor neurone facial palsy, a symptom of Melkersson-Rosenthal syndrome. # Ulcerative colitis - Uncommon inflammatory disease, mainly affects adults - Ulcers and polyps in the colon - May undergo malignant change - Persistent diarrhoea - Passage of blood & mucous - Iron deficiency anaemia - Weight loss #### Ulcerative Colitis Overview - An uncommon inflammatory disease mainly affecting adults. - 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. ```markdown # Ulcerative colitis - Widespread ulceration of the colon - Complicated by- haemorrhage, perforation, malignancy - Oral lesions-severe aphthae, candida also seen - Secondary to nutritional deficiency resulting from malabsorption ```  #### Complications and Oral Manifestations - **Systemic Complications**: Widespread ulceration of the colon, haemorrhage, perforation, and malignancy. - **Oral Manifestations**: Severe aphthae and candida infections. - **Secondary Effects**: Oral lesions may be secondary to nutritional deficiencies resulting from malabsorption. A close-up photo of an oral cavity showing severe aphthous ulcers on the tongue and inner cheek, illustrating oral lesions associated with ulcerative colitis. The image highlights the characteristic appearance of these painful sores, which are a common complication of the disease. # Management - Specialist referral is necessary - Biopsy, FBC - Sigmoidoscopy - Haematinics needed to treat secondary deficiency - Topical steroids (pessarries or enemas), systemic sulfasalazine #### 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. # Pyostomatitis vegetans - Rare disorder - Bowel symptoms precede oral involvement by several months or years - Pustular lesions on the oral mucosa & gingiva - Pustular lesions rupture-lead to erosions & ulceration-snail track ulceration - Topical steroids successful - Management of associated IBD-improvement of oral lesions  #### Clinical Presentation - A rare disorder where bowel symptoms typically precede oral involvement by months or years. - Characterized by pustular lesions on the oral mucosa and gingiva. - 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. Two clinical photographs showing oral lesions in pyostomatitis vegetans. The top image displays pustular lesions on the gingiva and oral mucosa with erythematous, inflamed tissue. The bottom image shows more extensive involvement with erosions and ulceration, consistent with snail track ulceration, affecting the lower gingiva and surrounding mucosa. Pyostomatitis vegetans is an important oral marker for inflammatory bowel disease   #### Diagnostic Significance - Pyostomatitis vegetans serves as an important oral marker for inflammatory bowel disease. A close-up photo showing the oral cavity with inflamed, red, and ulcerated tissue on the inner cheek and gums, consistent with pyostomatitis vegetans, a condition associated with inflammatory bowel disease. A photo of the tongue and surrounding oral mucosa displaying a large, raised, and irregularly textured lesion with a reddish, granular appearance, indicative of pyostomatitis vegetans. ```markdown Gardner’s syndrome - Multiple osteomas of jaws - Epidermal/sebaceous cysts of skin - Multiple fibrous tumours - Polyposis coli (marked tendency to undergo malignant change) ```    #### Clinical Features of Gardner Syndrome - Multiple osteomas of the jaws. - Epidermal or sebaceous cysts of the skin. - Multiple fibrous tumours. - **Polyposis coli**: Characterized by a marked tendency to undergo malignant change. X-ray image showing multiple osteomas of the jaws, indicated by a black arrow pointing to a dense, calcified lesion in the mandible. X-ray image of a hand showing multiple fibrous tumors, indicated by a white arrow pointing to a radiolucent lesion in the forearm. Microscopic image of a colon specimen showing polyposis coli, indicated by a black arrow pointing to numerous polyps lining the intestinal wall. # Peutz-Jeghers syndrome - Autosomal dominant inherited disorder - Caused by germline mutation in the liver kinase B1 (LKB1) tumour suppressor gene - Increased cancer risk in adult life - Hamartomatous polyps develop early in life - Cause complications: abdominal pain, bleeding, anaemia, acute intestinal obstruction #### Etiology and Systemic Features - 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. ```markdown Peutz-Jeghers syndrome - Brown to blue-black macules around the mouth, nose, eyes - Polyps in the small intestine, rare cases outside GIT - May undergo intussusception or malignant changes ```   #### Clinical Manifestations - Brown to blue-black macules (pigmentation) around the mouth, nose, and eyes. - Polyps primarily in the small intestine, though rare cases occur outside the GIT. - Polyps may undergo intussusception or malignant changes. Close-up photograph showing brown to blue-black macules around the mouth, illustrating a key feature of Peutz-Jeghers syndrome as described in the text. Endoscopic image showing a polyp in the small intestine, visually representing the intestinal polyps associated with Peutz-Jeghers syndrome. [^1]: Original PDF page 1: [[L22 Gastrointestinal Diseases.pdf#page=1|L22 Gastrointestinal Diseases, p.1]] [^2]: Original PDF page 2: [[L22 Gastrointestinal Diseases.pdf#page=2|L22 Gastrointestinal Diseases, p.2]] [^3]: Original PDF page 3: [[L22 Gastrointestinal Diseases.pdf#page=3|L22 Gastrointestinal Diseases, p.3]] [^4]: Original PDF page 4: [[L22 Gastrointestinal Diseases.pdf#page=4|L22 Gastrointestinal Diseases, p.4]] [^5]: Original PDF page 5: [[L22 Gastrointestinal Diseases.pdf#page=5|L22 Gastrointestinal Diseases, p.5]] [^6]: Original PDF page 6: [[L22 Gastrointestinal Diseases.pdf#page=6|L22 Gastrointestinal Diseases, p.6]] [^7]: Original PDF page 7: [[L22 Gastrointestinal Diseases.pdf#page=7|L22 Gastrointestinal Diseases, p.7]] [^8]: Original PDF page 8: [[L22 Gastrointestinal Diseases.pdf#page=8|L22 Gastrointestinal Diseases, p.8]] [^9]: Original PDF page 9: [[L22 Gastrointestinal Diseases.pdf#page=9|L22 Gastrointestinal Diseases, p.9]] [^10]: Original PDF page 10: [[L22 Gastrointestinal Diseases.pdf#page=10|L22 Gastrointestinal Diseases, p.10]] [^11]: Original PDF page 11: [[L22 Gastrointestinal Diseases.pdf#page=11|L22 Gastrointestinal Diseases, p.11]] [^12]: Original PDF page 12: [[L22 Gastrointestinal Diseases.pdf#page=12|L22 Gastrointestinal Diseases, p.12]] [^13]: Original PDF page 13: [[L22 Gastrointestinal Diseases.pdf#page=13|L22 Gastrointestinal Diseases, p.13]] [^14]: Original PDF page 14: [[L22 Gastrointestinal Diseases.pdf#page=14|L22 Gastrointestinal Diseases, p.14]] [^15]: Original PDF page 15: [[L22 Gastrointestinal Diseases.pdf#page=15|L22 Gastrointestinal Diseases, p.15]] [^16]: Original PDF page 16: [[L22 Gastrointestinal Diseases.pdf#page=16|L22 Gastrointestinal Diseases, p.16]] [^17]: Original PDF page 17: [[L22 Gastrointestinal Diseases.pdf#page=17|L22 Gastrointestinal Diseases, p.17]] [^18]: Original PDF page 18: [[L22 Gastrointestinal Diseases.pdf#page=18|L22 Gastrointestinal Diseases, p.18]] [^19]: Original PDF page 19: [[L22 Gastrointestinal Diseases.pdf#page=19|L22 Gastrointestinal Diseases, p.19]] [^20]: Original PDF page 20: [[L22 Gastrointestinal Diseases.pdf#page=20|L22 Gastrointestinal Diseases, p.20]] [^21]: Original PDF page 21: [[L22 Gastrointestinal Diseases.pdf#page=21|L22 Gastrointestinal Diseases, p.21]] [^22]: Original PDF page 22: [[L22 Gastrointestinal Diseases.pdf#page=22|L22 Gastrointestinal Diseases, p.22]] [^23]: Original PDF page 23: [[L22 Gastrointestinal Diseases.pdf#page=23|L22 Gastrointestinal Diseases, p.23]] [^24]: Original PDF page 24: [[L22 Gastrointestinal Diseases.pdf#page=24|L22 Gastrointestinal Diseases, p.24]] [^25]: Original PDF page 25: [[L22 Gastrointestinal Diseases.pdf#page=25|L22 Gastrointestinal Diseases, p.25]] [^26]: Original PDF page 26: [[L22 Gastrointestinal Diseases.pdf#page=26|L22 Gastrointestinal Diseases, p.26]] [^27]: Original PDF page 27: [[L22 Gastrointestinal Diseases.pdf#page=27|L22 Gastrointestinal Diseases, p.27]] [^28]: Original PDF page 28: [[L22 Gastrointestinal Diseases.pdf#page=28|L22 Gastrointestinal Diseases, p.28]] [^29]: Original PDF page 29: [[L22 Gastrointestinal Diseases.pdf#page=29|L22 Gastrointestinal Diseases, p.29]] [^30]: Original PDF page 30: [[L22 Gastrointestinal Diseases.pdf#page=30|L22 Gastrointestinal Diseases, p.30]] [^31]: Original PDF page 31: [[L22 Gastrointestinal Diseases.pdf#page=31|L22 Gastrointestinal Diseases, p.31]] [^32]: Original PDF page 32: [[L22 Gastrointestinal Diseases.pdf#page=32|L22 Gastrointestinal Diseases, p.32]] [^33]: Original PDF page 33: [[L22 Gastrointestinal Diseases.pdf#page=33|L22 Gastrointestinal Diseases, p.33]] [^34]: Original PDF page 34: [[L22 Gastrointestinal Diseases.pdf#page=34|L22 Gastrointestinal Diseases, p.34]] [^35]: Original PDF page 35: [[L22 Gastrointestinal Diseases.pdf#page=35|L22 Gastrointestinal Diseases, p.35]] [^36]: Original PDF page 36: [[L22 Gastrointestinal Diseases.pdf#page=36|L22 Gastrointestinal Diseases, p.36]] [^37]: Original PDF page 37: [[L22 Gastrointestinal Diseases.pdf#page=37|L22 Gastrointestinal Diseases, p.37]] [^38]: Original PDF page 38: [[L22 Gastrointestinal Diseases.pdf#page=38|L22 Gastrointestinal Diseases, p.38]] [^39]: Original PDF page 39: [[L22 Gastrointestinal Diseases.pdf#page=39|L22 Gastrointestinal Diseases, p.39]] [^40]: Original PDF page 40: [[L22 Gastrointestinal Diseases.pdf#page=40|L22 Gastrointestinal Diseases, p.40]] [^41]: Original PDF page 41: [[L22 Gastrointestinal Diseases.pdf#page=41|L22 Gastrointestinal Diseases, p.41]] [^42]: Original PDF page 42: [[L22 Gastrointestinal Diseases.pdf#page=42|L22 Gastrointestinal Diseases, p.42]] [^43]: Original PDF page 43: [[L22 Gastrointestinal Diseases.pdf#page=43|L22 Gastrointestinal Diseases, p.43]] [^44]: Original PDF page 44: [[L22 Gastrointestinal Diseases.pdf#page=44|L22 Gastrointestinal Diseases, p.44]]