Git Disorders for Dentists PDF

# Git Disorders for Dentists **Dr. Mohamed Abdelaziz MD PhD MRCPUK** Assistant Professor of Internal Medicine and Gastroenterology Beirut Arab University ## Contents - Gastroesophageal Reflux Disease (GERD) - Peptic Ulcer - Malabsorption (Celiac Disease) - Inflammatory Bowel Disease (IBD) (Crohn'...

# Git Disorders for Dentists **Dr. Mohamed Abdelaziz MD PhD MRCPUK** Assistant Professor of Internal Medicine and Gastroenterology Beirut Arab University ## Contents - Gastroesophageal Reflux Disease (GERD) - Peptic Ulcer - Malabsorption (Celiac Disease) - Inflammatory Bowel Disease (IBD) (Crohn's- Ulcerative Colitis) ## Gastro-Esophageal Reflux Disease (GERD) - Healthy individuals experience GERD after a meal, which is due to relaxation of the esophageal sphincter. - Patients with GERD experience increased frequency and duration of reflux, and the esophageal mucosa is damaged by regurgitation of gastric contents. - GERD symptoms include reflux esophagitis, ulceration, stricture, or epithelial metaplasia (Barrett's esophagus). ## Clinical Features of GERD - Heartburn - Epigastric pain and regurgitation - "Silent refluxers" have no symptoms - Dental erosion, particularly of the palatal aspects of the teeth - Patients who consume antacid preparations regularly may have a high sugar content, which could predispose them to cavities - Orofacial manifestations of iron deficiency ## Treatment of GERD - Simple antacids or covering agents - H2 receptor blockers (cimetidine) that inhibit gastric acid secretion. - Proton-pump inhibitors (omeprazole) that inhibit acid production. - Surgery is rarely indicated. (Periodic Dilation) ## Gastroesophageal Reflux Disease Diagram A diagram depicting a healthy esophagus and stomach, compared to one with GERD. The healthy esophagus is closed at the sphincter, while the GERD esophagus is open, allowing food to reflux. ## Dental Erosion and GERD A picture of a mouth, showing the palatal surfaces of the teeth. Text reads, "Patients presenting with palatal dental erosion should be assessed for GERD." ## Bulimia vs. GERD Two pictures are presented, side-by-side: - The First shows the teeth of someone with bulimia. - The second shows the teeth of someone with GERD. The text below the images reads, "Bulimia", "GERD." ## Peptic Ulcer Disease A diagram depicting the esophagus, duodenum and stomach. The stomach is lined in red, demonstrating ulcers throughout. Text reads, "Mucosa", "Submucosa", "Peptic Ulcer Disease," "Muscle," and "ulcer". ## Peptic Ulcer - Peptic ulcer disease occurs in the duodenum, stomach, or the lower esophagus due to reflux of gastric contents. - Peptic ulcer is rarely found in the small intestine. ## Pathophysiology A diagram showing the "defensive" and "aggressive" factors in peptic ulcer disease: - Defensive Factors: - Bicarbonate - Mucus Layer - Prostaglandins - Mucosal Blood Flow - Epithelial Renewal - Aggressive Factors: - Helicobacter Pylori - NSAIDS - Pepsins - Bile Acids - Smoking and Alcohol ## Pathophysiology Explanation - Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. - Mucosal injury and peptic ulcer disease occur when the balance between aggressive factors and defense mechanisms is disrupted. - Aggressive factors such as NSAIDS, H pylori infection, alcohol, bile salts, acid, and pepsin alter the mucosal defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury. ## Etiology/Risk Factors - **Lifestyle:** - Smoking - Acidic drinks - Medications - **H Pylori Infection:** - 90% of sufferers have this bacterium - Passed from person to person (fecal-oral or oral-oral route) - **Age:** - Duodenal 30-40 - Gastric over 50 - **Gender:** - Duodenal are increasing in older women - **Genetic Factors** - More likely if a family member has a history of peptic ulcers - **Other Factors:** - Stress can make symptoms worse, but is not a cause of peptic ulcer ## Types - Gastric Peptic Ulcer - Duodenal Peptic Ulcer ## Gastric and Duodenal Ulcers A diagram showing the stomach, with the greater curvature, lesser curvature, cardia, fundus, body, antrum, pyloric sphincter, duodenal ulcer, and gastric ulcer labeled. ## Duodenal vs. Gastric Ulcers | Feature | Duodenal Ulcer | Gastric Ulcer | | -------- | ---------------------------------------- | ---------------------------------------------- | | Age | Any age, especially 30-40 | Middle age 50-60 | | Sex | More in males | More in females | | Occupation | Stress job, e.g. manager | Same | | Pain | Epigastric, discomfort | Epigastric, can radiate to back | | Onset | 2-3 hours after eating & midnight | Immediately after eating | | Agg. by | Hunger | Eating | | Relieved by | Eating | Lying down or vomiting | | Duration | 1-2 months | Few weeks | | Vomiting | Uncommon | Common (to relieve pressure) | | Appetite | Good | Patient is afraid to eat | | Diet | Good, eat to relieve the pain | Avoid fried food | | Weight | No weight loss | Weight loss | | Hematemesis | 40% | 60% | | Melena | 60% | 40% | ## Investigation - Stool examination for fecal occult blood. - Complete blood count (CBC) for decrease in blood cells. ## Diagnostic Tests - **Esophagogastrodeodenoscopy (EGD):** - Endoscopic Procedure that can: - Visualize ulcer crater - Obtain tissue biopsy for R/O cancer and diagnose H Pylori - **Upper Gastrointestinal Series (UGI):** - Barium swallow - X-ray showing structures of the upper GI tract - **Urea Breath Testing** - Used to detect H Pylori - The client drinks a carbon-enriched urea solution - Exhaled carbon dioxide is then measured ## "Alarming Symptoms" - Endoscopy is required for all patients with the following "alarming symptoms:" - Dysphagia - Weight loss - Vomiting - Anorexia - Hematemesis or Melena ## Complication of Peptic Ulcers - **Hemorrhage:** - Blood vessels are damaged when the ulcer erodes into the muscles of the stomach or duodenal wall. - Coffee-ground vomitus or occult blood in tarry stools are signs of hemorrhage. - **Perforation:** - The ulcer erodes through the entire wall. - Bacteria and partially digested food spill into the peritoneum, causing peritonitis. - **Narrowing and Obstruction (Pyloric):** - Swelling and scarring can cause obstruction of food leaving the stomach. - This results in repeated vomiting. ## Management of Peptic Ulcers - Life style modification - Hyposecretory drug therapy - H Pylori eradication therapy - Surgery ## Life Style Modifications - Discontinue NSAIDs - Smoking cessation - Alcohol cessation - Stress reduction ## Hyposecretory Drugs - **Proton Pump Inhibitors:** - Suppress acid production - Prilosec, Prevacid - **H2 Receptor Antagonists:** - Block histamine-stimulated gastric secretions - Zantac, Pepcid, Axid - **Antacids:** - Neutralizes acid and prevents formation of pepsin - Maalox, Mylanta - Administered 2 hours after meals and before sleep - **Prostaglandin Analogs:** - Reduce gastric acid and enhances mucosal resistance to injury - Cytotec - **Mucosal Barrier Fortifiers:** - Forms protective coat - Carafate/Sucralfate - Cytoprotective ## H Pylori Eradication Therapy - **Triple Therapy:** - Proton pump inhibitor - Two Antibiotics: - Metronidazole + Clarithromycin - Clarithromycin + Amoxicillin ## Malabsorption Syndrome - Malabsorption syndrome is defined as a state arising from abnormality in absorption of food nutrients across the gastrointestinal tract (GIT). - Impairment can involve a single or multiple nutrients, depending on the abnormality. - This can lead to malnutrition and a variety of anemias. ## Malabsorption - Malabsorption constitutes the pathological interference of the normal physiological sequence of the body, such as: - Digestion (intraluminal process) - Absorption (mucosal process) - Transport (postmucosal events) of nutrients ## Causes of Malabsorption - Intestinal malabsorption can be due to: - Digestive failure caused by enzyme deficiencies - Structural defects - Mucosal abnormality - Infective agents - Systemic diseases affecting the GIT ## Digestive Failure - **Pancreatic Insufficiencies:** - Cystic fibrosis - Chronic pancreatitis - Carcinoma of pancreas - **Bile Salt Insufficiency:** - Obstructive jaundice - Bacterial overgrowth ## Structural Defects - Inflammatory bowel disease, specifically Crohn's disease - Gastrectomy and gastro-jejunostomy - Fistulae, diverticulae, and strictures - Infiltrative conditions such as amyloidosis, lymphoma - Short bowel syndrome - Eosinophilic gastroenteropathy ## Mucosal Abnormality - Celiac disease ## Enzyme Deficiencies - Lactase deficiency, resulting in lactose intolerance - Disaccharidase deficiency - Enteropeptidase deficiency ## Infective Agents - Whipple's disease - Intestinal tuberculosis - Tropical sprue - Parasites such as *Giardia lamblia* ## Systemic Diseases - Hypothyroidism and hyperthyroidism - Diabetes mellitus - Hyperparathyroidism and hypoparathyroidism - Carcinoid syndrome - Malnutrition ## Symptoms of Malabsorption - **Extraintestinal** - **Intraintestinal** - Diarrhea, often steatorrhea is the most common sign and is due to impaired water, carbohydrate, and electrolyte absorption. - Other symptoms include: - Weight loss - Growth retardation - Swelling or edema - Anemia - Muscle cramps and bleeding tendencies ## Celiac Disease - Celiac disease is defined as a permanent intolerance to gliadin, the protein component of wheat. It has a genetic component. - Celiac disease is defined as a lifelong inflammatory condition of the gastrointestinal tract that affects the small intestines. - Malabsorption is caused by morphological abnormalities in the small intestinal mucosa. - Celiac disease is reversible. - In adult celiac disease, diarrhea, weight loss, and weakness are the classic signs and symptoms. - "Celiac Sprue" - Sprue comes from the Dutch word for aphthous ## Incidence of Celiac Disease - The incidence of biopsy-proven celiac disease in the UK is 1 in 2000. - Using markers, such as anti-endomysial antibodies, the actual incidence approaches 1:300. - About 5-10% of patients with celiac disease have an affected first-degree relative. - About 5-10% of people with Type I diabetes will also have celiac disease. - Dermatitis herpetiformis is the classical non-gastrointestinal manifestation of celiac disease. - Hematinic deficiencies in iron and folate are likely to be present in celiac disease patients due to malabsorption. ## Diagnosis of Celiac Disease - **Blood Tests:** Full blood count, hematinic assays, IgA anti-gliadin, IgA antireticulin, and endomysial autoantibodies. - **Biopsy:** Increased lymphocytic infiltration; crypt hyperplasia occurs before villous atrophy and crypt hyperplasia. - Patients with positive blood tests, but a normal biopsy, are defined as having celiac disease. ## Management of Celiac Disease - Gluten-Free diet - Iron and folate supplements ## Oral Manifestations of Celiac Disease - Recurrent aphthous stomatitis with celiac disease is less than 5% based on recent studies. - Angular cheilitis. - Dental enamel defects (hypoplasia), typically on the permanent lower incisors, indicate that celiac disease has been present for at least the first two years of life. This may have gone unnoticed because it may not be accompanied by symptoms. - It can cause: - Oral ulceration (RAS) - Glossitis - Angular cheilitis - Enamel hypoplasia ## Inflammatory Bowel Disease (IBD) - Inflammatory bowel disease (IBD) is a general classification of inflammatory processes affecting the large and small intestines. - It includes: - Crohn's disease - Ulcerative colitis ## Introduction to IBD - Ulcerative colitis is more prevalent than Crohn's disease. - The incidence of IBD is 3.9-10 new cases per 100,000 people. - It shows three peak prevalence rates: - 20 to 24 years - 40 to 44 years - 60 to 64 years - IBD most commonly affects Caucasians and Jews. ## Pathogenesis of IBD - IBD is considered to be idiopathic. - It is increasingly believed to be the result of an interaction between environmental and genetic factors. ## Pathogenesis Diagram of IBD A diagram representing the interaction of genetics and environmental triggers that cause IBD. It shows: - A disrupted protective mucous layer - A dendritic cell presenting an antigen - A dendritic cell sampling luminal bacteria - Infiltrating lymphocytes - Proinflammatory cytokines, such as Tumor Necrosis Factor-alpha (TNF-alpha) and interleukins - Inappropriate and sustained recruitment of inflammatory T-cells - Increased adhesion molecules - Vascular permeability ## Ulcerative Colitis - Ulcerative colitis is a form of colitis characterized by ulcers or open sores that specifically attack the large intestine. - Ulcerative colitis is marked by rectal bleeding and diarrhea. ## Crohn's Disease - Crohn's disease is another type of IBD that may affect any part of the gastrointestinal tract from the mouth to the anus. - The term "Crohn's syndrome" or "regional enteritis" are used to describe this condition. - Crohn's disease can be non-perforating or perforating (aggressive). - This condition most commonly affects middle-aged women between the ages of 20-39 years. ## Clinical Features of Crohn's Disease A diagram showing a seated person with the following features: - Primary sclerosing cholangitis - Right iliac fossa mass/pain - Skin rash (pyoderma, erythema nodosum) - Diarrhea, blood, mucus - Apthous ulcers - Anemia, uveitis, fevers, sweats, and jaundice - Abdominal pain - Arthritis/arthralgia - Weight loss ## Oral Manifestations of Crohn's Disease - Oral manifestations of Crohn's disease can be categorized as: - Specific - Non-specific - Complications of malabsorption caused by the bowel inflammation - Side effects or complications of the medications prescribed to treat the bowel disease ## Specific Manifestations of Crohn's Disease - **Crohn's Disease:** Orofacial Crohn's disease - **Ulcerative Colitis:** Pyostomatitis vegetans ## Non-Specific Manifestations of Crohn's Disease - **Crohn's Disease:** - Angular cheilitis - Apthous ulcers/Aphthous stomatitis - Dry mouth - Halitosis - **Ulcerative Colitis** - Apthous ulcers/Aphthous stomatitis. - Glossitis - Cheilitis - Halitosis ## Complications of Malabsorption Caused by IBD - **Folic Acid Deficiency:** - Red and painful tongue (acute) - Shiny and smooth tongue (chronic) - Glossitis and cheilitis - **Vitamin A Deficiency:** - Hyperkeratosis of the oral mucosa - **Vitamin B12 Deficiency:** - Beefy red tongue - Mouth ulcers - **Vitamin K Deficiency:** - Gum bleeding - **Vitamin C Deficiency:** - Ulceration of gums and mucosa ## Side Effects of Therapeutic Drugs | Drug | Side Effects | | -------------- | ----------------------------------------------------------------------------------------------- | | Budesonide | Glossitis, dry mouth | | Cyclosporine | Gum hyperplasia | | Ciprofloxacin | Oral candidiasis, angioedema, Stevens-Johnson syndrome, epidermal necrolysis | | Loperamide | Dry mouth, Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (SJS/TEN), angioedema | | Metronidazole | Unpleasant metallic taste, furry tongue, glossitis, stomatitis, candidiasis, dry mouth | | Prednisolone | Oral candidiasis (thrush) | | Sulfasalazine | Altered taste, stomatitis, oral candidiasis | ## Oral Manifestations of Ulcerative Colitis A collage of mouth pictures showing various oral effects of ulcerative colitis. The text below the images reads "Oral manifestation of Ulcerative colitis." ## Pyostomatitis Vegetans - Pyostomatitis vegetans is characterized by a large number of broad-based, tiny abscesses developing in areas of intense erythema. - It most commonly affects the gingiva and hard palate. - The tongue is least commonly affected. - Histologically, it is characterized by: - Hyperplastic stratified squamous epithelium - Intraepithelial or sub-epithelial micro abscesses ## Diagnosis and Treatment of Pyostomatitis Vegetans - **Diagnosis:** Biopsy of perilesional tissue with histopathological and immunostaining examinations. - **Treatment:** - Topical corticosteroids such as clobetasol and flucinolone - Treatment of the underlying disease - Some patients report benefit from zinc supplementation: - Greater than 1 year: 10mg once daily - Less than 1 year: 5mg once daily - Antibiotic therapy is usually not helpful because the lesions are often refractory. ## Recurrent Aphthous Ulcer - Recurrent aphthous ulcers appear in two forms: minor apthae and multiple apthae. - **Multiple Apthae** are characterized by: - Small ulcers (2-4mm or 1 cm wide) - Round or ovoid ulcers - A circumscribed margin, with erythematous haloes with yellow or grey floors. ## Management of Recurrent Aphthous Ulcers - Topical, intra-lesional, systemic corticosteroids - Topical and systemic analgesics such as 2% lidocaine gel orabase - Thalidomide: An immune-modulating and angiogenesis inhibiting drug. It is effective for refractory cases at 300 mg daily. - Colchicines: 0.6mg three times daily for 2 weeks - Pentoxyphylline (TRENTAL 400mg): Used when topical steroids do not work. ## Therapeutic Doses | Category | Drug | Therapeutic Dose | | --------------- | -------------------------- | -------------------------------------------------------------------------------------- | | Antimicrobials | Chlorhexidine | 0.2% mouth rinse or 1% gel | | | Tetracycline | 5% Tetracycline used as mouthwash | | | Penicillin-G | 50 mg penicillin-G four times a day for 4 days | | Steroid | Flucinonide | 0.05% gel applied 2-4 times daily until healing; or 0.1% gel applied 2-4 times daily until healing | | | Triamcinolone acetonide | 1-2 mg/kg/day | | | Prednisolone | 1-2 mg/kg/day | | Immunomodulators | Thalidomide | 300 mg daily | | | Pentoxyphylline | 400 mg three times daily for 1 month | | | Colchicine | 0.6 mg three times daily for 2 weeks | | Others | Dapsone | 400 mg three times daily | | | Diphenhydramine with viscous lidocaine | 12.5 mg/ml with 2% lidocaine in a 1:1 ratio - 5-10 ml, swish and spit. | ## Glossitis and Cheilitis - **Glossitis:** Inflammation with depilation of the dorsal surface of the tongue. - **Cheilitis:** Inflammation of the lips. ## Oral Manifestations of Crohn's Disease A collage of pictures showing various oral manifestations of Crohn's disease ## Orofacial Crohn's Disease - Signs of orofacial Crohn's disease include: - Mucogingivitis - Deep linear ulcers in the vestibule - Hyperplastic margins - Rolled edge - Presence of non-caseating granulomas - Mucosal tags - Cobblestone appearance of the cheek lining ## Angular Cheilitis and Crohn's Disease - Angular cheilitis is defined as erythema and/or fissuring of the angle of the mouth. - It is secondary to nutritional deficiencies following malabsorption, or concomitant infections. ## Management of Oral Lesions - **Treatment of Underlying Pathology** - **Maintenance of Proper Hygiene** - **Topical Antifungal medication:** - Clotrimazole (0.1%) - Amphotericin B - Ketoconazole - **Topical Corticosteroids:** Help with inflammation. ## Management of IBD - A detailed history, physical examination, gastrointestinal radiography, and endoscopy are recommended. ## Medical Management of IBD - **First Line Drug:** - Sulfasalazine: Initiate and maintain remission. Take 500 mg three to four times per day. - **Corticosteroid:** - **Initiation Dose:** 40-60 mg prednisolone oral daily (Emsolone 5, 10, 20, 40 mg tablet) - **Maintenance Dose:** 10-20 mg prednisolone oral daily - **Second Line Drugs:** - **Antibiotic agents** - **Immunosuppressive drugs:** - Azathioprine (Azoran) 50 mg 1.5 to 2.5 mg/kg body weight. ## Surgical Management of IBD - Proctocolectomy combined with ileostomy is used to manage 15-20% of cases. ## Supportive Therapy for IBD - Bed rest, dietary manipulation, and nutritional supplementation are used to support patients with IBD. ## Management of Oral Lesions - Chlorhexidine gluconate 0.2% is used as a swish and expectorate. - Moderate-potency topical steroids, such as 0.01% fluocinolone FLUCORT-H ointment, or ultra-potency preparations (eg. clobetasol 0.05% LOBATE cream), can be applied topically four times a day. - Do not exceed two continuous weeks of topical steroids. - If the lesions are disseminated, dexamethasone 0.5 mg/5 ml (DEXONA) is used as a rinse for 1 minute, four times a day, and expectorated. ## Dental Evaluation of Patients with IBD - Evaluate the diagnosis of the type of IBD. - Determine the severity of disease and its current control. - Determine what medications are being used, paying special attention to past steroid therapy. - Determine the history of surgical therapy. ## Treatment Planning Modifications for Patients with IBD - Schedule appointments during remission. - Minimize stress by shortening appointments and utilizing adjunctive sedation techniques. - Evaluate hypothalamic/pituitary/adrenal cortical function to ascertain the patient's ability to tolerate extensive dental procedures. ## Dental Management for Patients with IBD - Frequent preventive and routine dental care is recommended to prevent destruction of hard and soft tissue. - If the patient is on corticosteroid therapy, obtaining blood pressure and blood glucose measurement prior to dental treatment is highly recommended. - Routine dental treatment, such as oral prophylaxis and simple restorations, can be carried out as normal. - Delayed wound healing, an increased risk of infection, and suppression of respiration are concerns. ## Dental Management for Patients on Long-Term Steroid Therapy | Dental Surgical Procedure | Current Systemic Steroid Use | | --------------------------- | ------------------------------------------------------------------------------------------ | | Routine dental procedure | No supplementation required | | Minor oral surgery lasting < 1 hour | Consider supplementation with 25 mg hydrocortisone equivalent before the procedure | | Oral surgery with or without GA lasting > 1 hour | 50-100 mg hydrocortisone equivalent on the day of surgery | | Major Oral surgery done under GA lasting > 1 hour with significant blood loss | Usual daily dose plus 50 mg hydrocortisone equivalent intravenously every 8 hours after the initial dose up to 72 hours | ## Dental Management for Patients with a History of Immunosuppressive Agents - For patients currently taking immunosuppressive agents, liver function testing is recommended. - Complete blood studies, including hemoglobin, hematocrit, red cell count, prothrombin time, and partial thromboplastin time are required. ## Dental Management for Patients on Any Medication - The use of topical steroids should be minimized. If they are used, they should be short-term and monitored carefully for signs of mucosal atrophy and systemic absorption. - NSAIDs should be avoided. - Avoid antibiotics that could aggravate diarrhea, such as amoxicillin-clavulanate (AMOXICLAB) and clindamycin.