1. GIT disorders Prof. Elsanousi M Taher BDS, M.Sc., FFDRCSI E-mail: sanosident@yahoo.com

2. At the end of this topic you should be able to: –Identify the clinical features of the common GIT disorders that have dental or oral significance –Be familiar with the general management of such conditions –Recognize the oral and dental manifestations of this diseases –Know what to treat and what to refer of oral complains related to such diseases

5. Signs and symptoms Dysphagia Dysphagia Dyspepsia or Heartburn: Dyspepsia or Heartburn: –also known as upset stomach or indigestion, refers to a condition of impaired digestion. –It is characterized by chronic or recurrent pain in the upper abdomen –It can be functional dyspepsia ( non-ulcer dyspepsia) or ulcer or erosion related pain as in: – DU, GU, Gastritis and Duodenitis

6. Pain: Pain: –Odynophagia : pain with swallowing –Epigastric pain –Abdominal cramps –It may presented as chest pain !! Bleeding: Bleeding: –Hematemesis: Fresh blood Fresh blood Ground –coffee Ground –coffee –Melena: Fresh Fresh Occult Occult Nausea Nausea

7. Signs and symptoms Vomiting: Vomiting: the forceful expulsion of gastric contents through a relaxed esophageal sphincter and open mouth the forceful expulsion of gastric contents through a relaxed esophageal sphincter and open mouth Diarrhoea: watery or bloody Diarrhoea: watery or bloody –Acute: infections, food poisoning, drugs –Chronic: IBDs, chronic infections

8. Constipation Constipation –perception of abnormal bowel movements that may include straining, hard stools, decreased frequency, and a feeling of incomplete evacuation –It can be caused by: Systemic Systemic Structural Structural Medications Medications Idiopathic Idiopathic

9. Weight loss: Weight loss: –involuntary decrease in body weight of at least 5% is a problem that requires clinical evaluation Regurgitation : Regurgitation : –acid regurgitation –sudden, spontaneous reflux of small volumes of bitter tasting acidic material into the mouth (Mouth brash)

10. Jaundice Jaundice Finger clubbing Finger clubbing Ascites Ascites Other signs of liver diseases Other signs of liver diseases Others Others

11. Ascites Ascites may be a sign of chronic liver disease and other GIT disorders Ascites may be a sign of chronic liver disease and other GIT disorders

12. Finger clubbing Q: In what condition you might see clubbing of the fingers? Q: In what condition you might see clubbing of the fingers?

13. Dysphagia

14. –The esophagus is about 25 mm musclar tube (cervical, thoracic, abdominal) –Its basic function is to transport swallowed material from the pharynx into the stomach –Retrograde flow of gastric contents into the esophagus is prevented by the lower esophageal sphincter (LES) –Entry of air into the esophagus is prevented by the upper esophageal sphincter (UES)

15. Dysphagia Swallowing is a complex activity involving a coordinated action of lips, tongue, soft palate, pharynx, larynx and oesophagus which are innervated by VII, IX, X and XII nerves

16. Dysphagia is a subjective difficulty in swallowing Dysphagia is a subjective difficulty in swallowing Unless it is associated with sore throat or oropharyngeal ulceration it is a serious symptom Unless it is associated with sore throat or oropharyngeal ulceration it is a serious symptom It may be: It may be: Total: for solid and liquid and usually indicate a neuralgic cause Selective: for solid as in tumors or benign stricture Intermittent: spasm of crico-laryngeal muscles

17. Etiology Dysphagia could be of: –acute onset as in stroke –slowly developed as in tumour and motor neuron disease

18. The site of the cause may be: 1.In the lumen of oesophagus (foreign body) 2.In the wall of oesophagus (tumour or disorder in motility) 3.Pressure from outside (mass or tumour)

19. Causes of dysphagia: –Structural diseases: –Functional causes: –Functional causes:

20. Structural diseases: Oral causes: Oral causes: Oral painful and ulcerative conditions Oral painful and ulcerative conditions Infections: tonsillitis, pericoronitis and Ludwig's angina Infections: tonsillitis, pericoronitis and Ludwig's angina Xerostomia & oral submucous fibrosis Xerostomia & oral submucous fibrosis Oral malignancies Oral malignancies Esophageal causes: Esophageal causes: Foreign bodies Foreign bodies Mechanical obstruction or stricture Mechanical obstruction or stricture Ulceration Ulceration Diverticula: outpouching of a hollow (or a fluid-filled) structure in the body Diverticula: outpouching of a hollow (or a fluid-filled) structure in the body Surgery Surgery Tumor e.g. Carcinoma Tumor e.g. Carcinoma Plumer-Venson syndrome Plumer-Venson syndrome Scleroderma Scleroderma External pressure from enlarged lymph node External pressure from enlarged lymph node

21. Diverticulum

22. Strictures caused by Caustic Ingestion

24. Neurological causes: Difficulty in initiating swallowing associated with choking, nasal regurgitation, drooling of saliva and dysartheria Difficulty in initiating swallowing associated with choking, nasal regurgitation, drooling of saliva and dysartheria Bulbar (lesion or condition that affect IX, X, XI or XII due to lower motor neuron Lesion “ subnuclear “) and pseudobulbar palsy (arise from UMN lesion “supranuclear Or cortico- bulbar “) Bulbar (lesion or condition that affect IX, X, XI or XII due to lower motor neuron Lesion “ subnuclear “) and pseudobulbar palsy (arise from UMN lesion “supranuclear Or cortico- bulbar “) Myasthenia gravis Myasthenia gravis Esophageal spasm Esophageal spasm

25. Neurological causes –Stroke – present in up to 47% –Poliomyelitis –Parkinson’s Disease –Multiple Sclerosis –Muscular Dystrophy –Myasthenia Gravis

26. Systemic structural causes: o Systemic Sclerosis o Systemic Lupus Erythematosis o Dermatomyosits o Mixed Connective Tissue Disease o Mucosal Pemphigoid, o Epidermolysis Bulosa o Sjogren’s Syndrome (xerostomia) o Aging: –Dysphagia is present in 2% > 65 –Poor dentition –Loss of tongue connective tissue –Increased pharyngeal transit time

27. Functional causes: Achalasia of the cardia (failure of the lower oesophageal sphincter to relax) Achalasia of the cardia (failure of the lower oesophageal sphincter to relax) Globus hystericus (psychogenic) and not necessary related to swallowing as there is a sense of a lump in the throat at all times Globus hystericus (psychogenic) and not necessary related to swallowing as there is a sense of a lump in the throat at all times

28. Diagnosis of Dysphagia –History and clinical examination –Endoscopy: used for detection of the lesion, biopsy and dilatation –Barium swallow x-ray –FBC –ENT consultation if suspected pharyngeal cause –Chest x-ray

29. Dysphagia A barium swallow showing an esophageal web (arrow) in a patient with the Plummer-Vinson syndrome A barium swallow showing an esophageal web (arrow) in a patient with the Plummer-Vinson syndrome

30. Barium meal Normal Abnormal

31. Dysphagia esophageal stricture shown by barium meal follow through

32. Dysphagia Oesophageal carcinoma Oesophageal carcinoma

33. Treatment of dysphagia –According to cause –The dentist can manage the oral causes –For non-oral causes refer to medical or surgical specialist

34. Halitosis

35. Halitosis is a term applied oral malodour and to foul, offensive bad breath. is a term applied oral malodour and to foul, offensive bad breath. Others like friends and family members are more aware of halitosis than the individual himself except in case of psychogenic causes Others like friends and family members are more aware of halitosis than the individual himself except in case of psychogenic causes

36. The true prevalence of halitosis is unknown, the available evidence suggests that halitosis is common and can affect people of all ages. The true prevalence of halitosis is unknown, the available evidence suggests that halitosis is common and can affect people of all ages. Most studies have reported that about 20% to 40% of the population have halitosis, although some have reported the figure to be as high as 50%. Most studies have reported that about 20% to 40% of the population have halitosis, although some have reported the figure to be as high as 50%.

37. Causes of halitosis: –bad oral hygiene, carious and periodontal diseases (volatile sulphur containing compounds) Periodontal infections (especially Periodontal infections (especially necrotizing gingivitis necrotizing gingivitis periodontitis periodontitis Pericoronitis Pericoronitis Other types of oral infections Other types of oral infections Infected extraction sockets Infected extraction sockets Ulcers. Ulcers. –Certain foods –Xerostomia

38. –tonsillitis, pharyngitis and sinusitis –lung abscess and bronchiectasis –diabetes (sweet and acetone smell) as in keto -acidosis

39. –Uraemia (ammonia) due to excretion of urea through salivary glands, poor oral hygiene and dry mouth –Liver cirrhosis (fishy smell): foeter hepaticum –Esophageal reflux & hiatus hernia –Alcohol consumption

40. –Certain types of food and smoking –Psychogenic: Real clinical dilemma Real clinical dilemma No clinical evidence No clinical evidence delusion or monosymptomatic hypochondriasis (self-oral malodour; halitophobia) delusion or monosymptomatic hypochondriasis (self-oral malodour; halitophobia)

41. Many of these patients will adopt behaviour to minimize their perceived problem, such as: Many of these patients will adopt behaviour to minimize their perceived problem, such as: Covering the mouth when talking; Covering the mouth when talking; Avoiding or keeping a distance from other people; Avoiding or keeping a distance from other people; Avoiding social situations; Avoiding social situations; Using chewing gum, mints, Using chewing gum, mints, mouthwashes or sprays designed to reduce malodour; mouthwashes or sprays designed to reduce malodour;

42. Such psychogenic patients unfortunately fail to recognize their own psychological condition, never doubt they have oral malodour and thus are often reluctant to visit a psychology specialist. Such psychogenic patients unfortunately fail to recognize their own psychological condition, never doubt they have oral malodour and thus are often reluctant to visit a psychology specialist.

43. Management of halitosis: According to the cause According to the cause Rule out and treat dental and oral causes Rule out and treat dental and oral causes Mouth washes and fresheners can only mask halitosis Mouth washes and fresheners can only mask halitosis

44. –Treat any identifiable cause (this may need antimicrobials). –Avoid odiferous foods such as onions, garlic, spices and durian. –Avoid habits that may worsen breath odour, such as: –Alcohol; –Tobacco. –Eat a good breakfast, and take regular meals including fresh fruit: –Brush your teeth after meals.

45. Keep oral hygiene regular and good: Keep oral hygiene regular and good: Oral Prophylaxis; Oral Prophylaxis; Tooth brushing and Flossing; Tooth brushing and Flossing; Rinse at least twice daily with chlorhexidine (eg Chlorohex, Corsodyl, Eludril), triclosan (Total), essential oils (Listerine), cetylpyridinium (MacLeans), chlorine dioxide (Retardex) or other mouthwashes; Rinse at least twice daily with chlorhexidine (eg Chlorohex, Corsodyl, Eludril), triclosan (Total), essential oils (Listerine), cetylpyridinium (MacLeans), chlorine dioxide (Retardex) or other mouthwashes; Brush your tongue before going to bed: use a tongue scraper if that helps. Brush your tongue before going to bed: use a tongue scraper if that helps. Keep your mouth as moist as possible by using: Keep your mouth as moist as possible by using: –Sugar-free chewing gums (eg Orbit, EnDeKay); –Use proprietary ‘fresh breath’ preparations eg Dentyl pH. If you have dentures, leave them out at night and in hypochlorite (eg Dentural) or chlorhexidine. If you have dentures, leave them out at night and in hypochlorite (eg Dentural) or chlorhexidine.

46. Refer patients to specialist if: –Suspected systemic disease; –Suspected malignancy; –Patients with imagined halitosis.

47. Gastric acid reflux –Gastroesophageal reflux disease (GERD) is a condition in which the stomach contents leak backwards from the stomach into the esophagus. –This can irritate the esophagus and cause esopagitis, heartburn and other symptoms.

49. Gastric acid reflux Predisposing factors: Predisposing factors: –Hiatus hernia –Pregnancy and increased intra-abdominal pressure –Obesity and weight –Smoking –Medications –Dietary factors –it may be habitual as in bulimia nervosa

50. Medications that cause gastric reflux –Beta-blockers for high blood pressure or heart disease –Bronchodilators for asthma –Calcium channel blockers for high blood pressure –Dopamine-active drugs for Parkinson disease Parkinson diseaseParkinson disease –Progestin for abnormal menstrual bleeding or birth control –Sedatives for insomnia or anxiety –Tricyclic antidepressants

51. Consequences of reflux oesophagitis Ulceration Ulceration Stricture Stricture Glandular metaplasia (Barrett’s oesophagus) Glandular metaplasia (Barrett’s oesophagus) Carcinoma Carcinoma

52. Oral manifestations: –erythema and oral ulceration –non-carious tooth surface loss specially in the palatal surface of upper incisors

53. Esophageal Reflux Palatal Surface Erosion of the of upper incisor teeth

54. Peptic ulcers Classified into: –Gastric ulcers –Duodenal

55. –DU are 4 times as common as gastric ulcers and tend to affect young men –Cause is unknown but it is believed to be due to imbalance in acid production and defensive factors such as mucous production, bicarbonate secretion and mucosal resistance –Generally peptic ulcers may be caused by: deregulation of acid production deregulation of acid production Interference with mucosal integrity Interference with mucosal integrity Disruption of mucosal barrier Disruption of mucosal barrier

56. –The integrity of the mucosa is dependent upon the endogenous prostaglandin which promote bicarbonate secretion, maintain mucosal blood flow and are released during epithelial repair –Acid secretion in gastric ulcer is normal or less than normal

57. Predisposing factors of peptic ulcers Infection (Helicobacter pylori): colonization occur in 95% of duodenal ulcers and 70% of gastric ulcer Infection (Helicobacter pylori): colonization occur in 95% of duodenal ulcers and 70% of gastric ulcer –Eradicating H pylori decreases the relapse rate of DU Steroids and NSAID Steroids and NSAID Genetic predisposition (Hereditary): blood group “O” are more susceptible (duodenal) Genetic predisposition (Hereditary): blood group “O” are more susceptible (duodenal) Stress Stress

58. Predisposing factors of peptic ulcers Smoking Smoking Alcohol Alcohol Zolllinger-Ellison syndrome: ( severe peptic ulceration, gastric acid hypersecretion, tumour of non  - Cells of Islets of pancreas (gastrinoma) or hyperplasia) Zolllinger-Ellison syndrome: ( severe peptic ulceration, gastric acid hypersecretion, tumour of non  - Cells of Islets of pancreas (gastrinoma) or hyperplasia)

59. Clinical features: –may be asymptomatic, mild discomfort or severe abdominal pain –epigastric pain: hunger pain relieved by antacids & vomiting –associated with meal time: just before meal (dudenal ulcer) or after meal (gastric ulcer) –Bleeding –signs of anemia –signs of perforation or pyloric stenosis (vomiting)

60. FeaturesGastric ulcerDuodenal ulcer IncidenceLess common 4 times common than GU M:F ratio 6:13:1 Age incidenceTypically elderly, after the age of 50 years Young adults & represent 80-85% of peptic ulcers at this group CauseCaused by changes in mucosal surfaces More commonly associated with H. pylori Gastric secretion Associated with achlorohydria or hyposecretion Gastric hypersecretion Malignant tendency Malignant tendency is higher Rarely become malignant Nature of painPain is related to meals and relieved by antacids but may be asymptomatic The pain typically occurs before meals and worse at night and relived by eating or drinking milk 80% relapse within 1 year of healing

61. Complication of peptic ulcers: –Perforations –Gastric outlet obstruction –Bleeding –80% of duodenal ulcers relapse within 1 year of healing

62. Epigastric pain is common symptom of peptic ulcer

63. PEPTIC ULCERS Can not be diagnosed by history and examination only PEPTIC ULCERS Can not be diagnosed by history and examination onlyInvestigations: –Endoscopy –Barium meal swallow –Biopsy –FBC –Investigate for helicobacter pylori status: – Breath test – Histological biopsy – Serology

64. Duodenal Ulcer

65. Hiatus hernia

66. –Hiatus hernia or hiatal hernia is the protrusion (or herniation) of the upper part of the stomach into the chest cavity through a tear or weakness in the diaphragm. –Occurs in 30% of population over 50 years –Often asymptomatic –May cause heartburn and regurgitation

68. Hiatus Hernia

69. Management of peptic ulcers

70. Medical management: life style modification: stop smoking, alcohol, change food habits and avoid NSAID life style modification: stop smoking, alcohol, change food habits and avoid NSAID H 2 receptor blockers: cimetidine, ranitidine … etc. H 2 receptor blockers: cimetidine, ranitidine … etc. proton pump blockers: Omeprazole proton pump blockers: Omeprazole antibiotics: for eradication of H. Pylori (amoxicillin or metronidazole) antibiotics: for eradication of H. Pylori (amoxicillin or metronidazole) antacids: Ca carbonate, Mg hydroxide & aluminum hydroxide antacids: Ca carbonate, Mg hydroxide & aluminum hydroxide sedatives sedatives surface coating agents: e.g. bismuth surface coating agents: e.g. bismuth anticholinergic drugs: less commonly used nowadays anticholinergic drugs: less commonly used nowadays

71. Surgical management of peptic ulcers

72. Oral manifestations and consideration: –signs of iron def. anemia –adopt stress reduced protocol in dental treatment –avoid using steroids and aspirin and other NSAID –deficiency of IF in post gastrectomy syndrome –antacids may decrease the absorption of certain antibiotics by 75-85% (specially tetracycline and erythromycin ) so these drugs should be given at least 2 hours before or after taking antacids –omeprazole is rare cause of stomatitis

73. Coeliac disease (Gluten sensitive enteropathy) Coeliac disease (Gluten sensitive enteropathy)

74. –Characterized by mucosal atrophy of small intestine, particularly jejunum and respond well to withdraw of gluten from diet –Associated with dermatitis herpetiformis

75. Etiology: –α- gliadin in the gluten containing food (wheat, rye, barely and oat)cause immunologically mediated damage in genetically susceptible individuals and cause atrophy of the villi –Incidence is 1:2500

76. Clinical features in childhood: –Steatorrhoea: is the presence of excess fat in feces. Stools may also float due to excess lipid, and can be especially foul-smelling. feces –Abdominal pain –Weight loss and fatigue –The sign and symptoms are associated with iron and folate deficiency –Hypocalcemia and compensatory hyperparathroidism –Poor growth & short stature

77. Clinical features in adults –The symptoms are less severe –Diarrhea, weight loss, anemia, osteomalacia –Some times associated with dermatitis herpetiformis

78. Investigations: –FBC –serum iron, serum and red cell folate, TIBC –low serum calcium –jejunal biopsy (fibre -optic endoscopy) –gluten challenge: challenge with some gluten-containing food in one meal a day over 2–6 weeks before repeating the investigations challenge with some gluten-containing food in one meal a day over 2–6 weeks before repeating the investigations –immunological tests: IgA antiendomysial antibodies can detect Coeliac disease with a sensitivity and specificity of 90% and 99% IgA antiendomysial antibodies can detect Coeliac disease with a sensitivity and specificity of 90% and 99%sensitivityspecificitysensitivityspecificity α- gliadin antibodies α- gliadin antibodies

79. Celiac disease Normal villi of small intestine increase surface area available for absorption of nutrients Normal villi of small intestine increase surface area available for absorption of nutrients

80. Atrophy of the villi and lymphocytic infiltration of the submucosal layer Atrophy of the villi and lymphocytic infiltration of the submucosal layer

81. Celiac disease Note the atrophy of the villi of small intestine Note the atrophy of the villi of small intestine

82. Treatment: –Life long gluten free diet –Some patients with aphthous ulcers respond to gluten free diet although they don’t have any intestinal lesions but they show high level of antigliadin antibodies

83. Oral manifestations: Aphthous ulcers (5% of patients with ROU may have intestinal disease) Aphthous ulcers (5% of patients with ROU may have intestinal disease) Enamel hypoplasia (in children) Enamel hypoplasia (in children) Glossitis, BMS and angular cheilitis Glossitis, BMS and angular cheilitis Dermatitis herpetiformis Dermatitis herpetiformis Uncommon skin disease associated with coeliac disease like DH may have oral manifestations Uncommon skin disease associated with coeliac disease like DH may have oral manifestations Common in middle aged males Common in middle aged males

84. Dermatitis herpetiformis Itchy vesiculo-papular lesion on extensor surface of the arm with pigmented area on healing Itchy vesiculo-papular lesion on extensor surface of the arm with pigmented area on healing The cause is unknown. However, dermatitis herpetiformis is frequently linked to gluten sensitivity in the small bowel. The cause is unknown. However, dermatitis herpetiformis is frequently linked to gluten sensitivity in the small bowel. The itching is so sever that may force the patient to commit suicide The itching is so sever that may force the patient to commit suicide Biopsy show granular deposits of IgA, C3 & fibrin along the BMZ Biopsy show granular deposits of IgA, C3 & fibrin along the BMZ

85. Dermatitis herpetiformis

87. Oral lesion may be erythematous, vesicular or ulcerative lesions Oral lesion may be erythematous, vesicular or ulcerative lesions May respond to gluten free diet and dapson May respond to gluten free diet and dapson

88. Linear Ig A disease is an acquired, autoimmune blistering disease that may present with a clinical pattern of vesicles indistinguishable from dermatitis herpetiformis, or with vesicles and bullae in a bullous pemphigoid-like appearance is an acquired, autoimmune blistering disease that may present with a clinical pattern of vesicles indistinguishable from dermatitis herpetiformis, or with vesicles and bullae in a bullous pemphigoid-like appearance

89. Linear Ig A disease

90. Inflammatory bowel diseases

91. Inflammatory bowel disease (IBD) Crohn’s disease Crohn’s disease Ulcerative colitis Ulcerative colitis

92. –Inflammatory bowel disease (IBD) involves chronic inflammation of all or part of the digestive tract. –IBD primarily includes ulcerative colitis and Crohn's disease. –Both usually involve severe diarrhea, pain, fatigue and weight loss. IBD can be debilitating and sometimes leads to life-threatening complications.

93. Severe colitis noted during colonoscopy in a patient with inflammatory bowel disease. The mucosa is grossly denuded, with active bleeding noted. The patient had her colon resected very shortly after this view was obtained.

94. Crohn’s disease

96. –Crohn's disease is an IBD that cause inflammation of the lining of the digestive tract. –Chronic granulomatous inflammatory bowl disease that may affect any part of GIT discontinuously (mouth to anus) –In Crohn's disease, inflammation often spreads deep into affected tissues. –Unlike ulcerative colitis it is characterised by skip lesions –Terminal ileum and proximal colon are commonly affected –Young adults are more commonly affected (20-40)

97. Etiology: –Exact cause is unknown but viral, bacterial and food allergy has been incriminated ?? –Genetic predisposition –Interaction between genetic and environmental factors

98. Pathogenesis IBD GenesEnvironment

99. Clinical features: –depend on severity of the disease and site of involvement –may be asymptomatic with signs of malabsorption –abdominal pain that may mimic appendicitis –weight loss –finger clubbing –finger clubbing

100. –abdominal mass (right iliac fossa mass) –per-anal area may show fistula, fissures and sinuses –fever, malaise, uveitis, iritritis and erythema nodosum –The disease progress with relapses and remissions

101. Crohn’s Disease: Anatomic Distribution Small bowel alone (33%) Colon alone (20%) Ileocolic (45%) LeastMost Freq of involvement

102. The great majority of cases (70-85%) of Crohn’s colitis have small bowel involvement and relative sparing of the rectum The great majority of cases (70-85%) of Crohn’s colitis have small bowel involvement and relative sparing of the rectum in IBD major perianal lesions are a feature exclusively of Crohn’s disease. in IBD major perianal lesions are a feature exclusively of Crohn’s disease. In CD There is relatively normal intervening mucosa and segmental rather than diffuse or continuous distribution, and asymmetric involvement of different parts of the wall within given segments of bowel. In CD There is relatively normal intervening mucosa and segmental rather than diffuse or continuous distribution, and asymmetric involvement of different parts of the wall within given segments of bowel. Fistulization into surrounding tissues and organs occurs only in Crohn’s disease as opposed to ulcerative colitis. Fistulization into surrounding tissues and organs occurs only in Crohn’s disease as opposed to ulcerative colitis.

103. DISTINGUISHING FEATURES OF CROHN’S DISEASE

104. Crohn's Disease Colonoscopy view Colonoscopy view

105. Crohn's Disease Colonoscopy view

106. Crohn's Disease barium follow-through of small intestine showing ulceration of transverse colon

107. Crohn's Disease

108. (conjunctivitis & iritis) (conjunctivitis & iritis)

109. D. D: Sarcoidosis Sarcoidosis Ofg Ofg Tb Tb Angio-edema Angio-edema Others Others

110. Investigations: –FBC, serum iron, red cell folate, ESR –Acute phase proteins (c-reactive proteins) –Barium enema and barium swallow & follow through –Colonoscopy and sigmoidscopy –Small bowel barium enema –Biopsy (rectal): Crohn disease is characterized on pathology by non-caseating granulomas but these are not always found on bowel biopsy. Crohn disease is characterized on pathology by non-caseating granulomas but these are not always found on bowel biopsy.

111. Treatment: depend on case severity –Oral steroids: prednisolone –Azathioprine: as steroid sparing agents –Cyclosporine –Sulphasalazine –Surgery: indicated in Symptoms persist despite treatment Symptoms persist despite treatment Intestinal obstruction Intestinal obstruction Local complications: fistulae, abscess, perforation Local complications: fistulae, abscess, perforation

112. Complications of IBD: –Severe life threatening inflammation of colon due to dilatation of the colon and pass of bacterial toxins into portal circulation –Perforation of small intestine or colon –GIT obstruction –Life threatening Bleeding and anemia –Fissures and fistulae of perianal diseases –Ca of bowel –Severe malabsorption

113. Ulcerative colitis Ulcerative colitis is an inflammatory bowel disease that causes long-lasting inflammation and ulcers in the innermost lining of your large intestine (colon) and rectum.

114. Ulcerative colitis –Usually affect large bowel starting at the rectum and proceed proximally (no skip lesions) (no skip lesions) –First attack usually followed by remissions and relapses –Rectal bleeding and bloody diarrhea and mucous discharge –Little constitutional symptoms (fever, lethargy and abdominal discomfort)

115. –Characterized by protracted course that extends over years –Remitting and relapsing course –Both diseases are very similar clinically and it may be very difficult to differentiate between them –The crucial difference is that UC involve only colon while CD can involve any part of GIT

116. Complications of IBD –Longstanding case are at increased risk of developing colon cancer –Severe IBD may cause an acute abdomen termed “toxic megacolon” which may need surgical management

117. Ulcerative colitis

118. Ulcerative Colitis - Ulcerations

119. Treatment: Treatment: –Rectal steroids –Salphasalazine –Oral steroids –Surgery

120. Emergency Surgery Toxic megacolon Toxic megacolon Perforation Perforation Massive haemorrhage Massive haemorrhage Failure of a severe attack to resolve Failure of a severe attack to resolve

122. Any questions? Thank you

123. Oral mucosa manifestations of inflammatory bowel disease The changes of the face and oral mucosa associated with inflammatory bowel disease can be divided into four main categories: The changes of the face and oral mucosa associated with inflammatory bowel disease can be divided into four main categories: 1. Specific, meaning these occur only in association with the bowel disease and/or show characteristic histology of that condition. 2. non-specific, meaning these occur more commonly with the bowel disease than in the general population, but also do occur without bowel disease, and the pathology is not diagnostic for the bowel disease. 3. Complications of malabsorption caused by the bowel inflammation resulting in deficiencies in vitamins and minerals. 4. Side effects or complications of medications prescribed to treat the bowel disease.

124. –The first three of these categories may be useful in directing the doctor to the bowel problem and making the specific diagnosis.

125. Oral Signs of Crohn's disease –The oral mucosa is commonly affected in Crohn's disease with up to one third of patients reported to have oral changes, and even higher in children. –In some studies, the oral changes preceded the diagnosis of Crohn's disease in 60%. Of cases –Specific oral mucosal changes: orofacial Crohn's disease (oral Crohn’s) orofacial Crohn's disease (oral Crohn’s)

126. Oral Signs of Crohn's disease Angular cheilitis Angular cheilitis Angular cheilitis Angular cheilitis Aphthous ulcers/aphthous stomatitis – has been reported to affect up to 20-30% of patients with Crohn's disease Aphthous ulcers/aphthous stomatitis – has been reported to affect up to 20-30% of patients with Crohn's disease Aphthous ulcers/aphthous stomatitis Aphthous ulcers/aphthous stomatitis Redness and scaling around the lips Redness and scaling around the lips Pyostomatitis vegetans – very rare in Crohn's disease Pyostomatitis vegetans – very rare in Crohn's disease Pyostomatitis vegetans Pyostomatitis vegetans Recurrent vomiting and regurgitation can cause oral soreness and teeth erosion Recurrent vomiting and regurgitation can cause oral soreness and teeth erosion

127. Oral Signs of Crohn's disease –Angular cheilitis: –Aphthous stomatitis: has been reported to affect up to 20-30% of patients with Crohn's disease has been reported to affect up to 20-30% of patients with Crohn's disease –Redness and scaling of the lips –Pyomyositis vegetans: very rare in Crohn's disease –Recurrent vomiting and regurgitation can cause oral soreness and teeth erosion

128. Nonspecific changes in the mouth and surrounding facial skin associated with Crohn's disease: Nonspecific changes in the mouth and surrounding facial skin associated with Crohn's disease: –Aphthous type ulcers –Diffuse swelling of gingiva, cheek, lips –“cobble stone” mucosal swellings of buccal mucosa with deep fissures in between –Indurated fissured lip –Angular cheilitis –Pyostomatitis vegetans –Taste disturbances

129. “cobble stone” mucosal swellings of buccal mucosa

130. Crohn's Disease Lip swelling and central fissure of the lip Lip swelling and central fissure of the lip Q: what is the differential diagnosis of this swollen lip ? Q: what is the differential diagnosis of this swollen lip ?

131. Crohn's Disease Oral Crohn’s presented as Swollen lip

132. Orofacial granulomatosis OFG: –Is a term given to lesions in the orofacial area that have similar histopathological appearances to Crohn’s disease without detectable systemic Crohn’s disease at the time of diagnosis –Systemic Crohn's may appear later –OFG may be a allergic reactions to food stuff or preservatives like cinnamaldehyde and benzoate or certain medications –Oral lesions are the same as in CD –Management of OFG: Exclusion of the offending substances Exclusion of the offending substances Clofazimine, dapsone, thalidomide Clofazimine, dapsone, thalidomide Steroid and systemic and intralesional Steroid and systemic and intralesional

133. Melkersson-Rosenthal syndrome: –Facial swelling –Facial palsy –And fissured tongue –Such patients may have incomplete or asymptomatic CD or may develop the disease later

135. Crohn's Disease Aphthous ulcer of the lip

136. What is the D.D of this ulcer ? What is the D.D of this ulcer ?

137. Crohn's Disease Mucosal tags in buccal mucosa

138. Crohn's Disease Cobble stone appearance in buccal mucosa Cobble stone appearance in buccal mucosa

139. Mucosal changes have been reported in some patients with ulcerative colitis – Oral manifestations of UC are rare –Specific orofacial changes of ulcerative colitis pystomatitis (very characteristic) –Nonspecific changes of the mouth and surrounding skin associated with ulcerative colitis: Minor and major aphthous stomatitis Minor and major aphthous stomatitis Glossitis Glossitis Cheiltis Cheiltis Since uveitis, skin lesion and mouth ulcers are present in UC, it should be differentiated from Behcet disease Since uveitis, skin lesion and mouth ulcers are present in UC, it should be differentiated from Behcet disease Dental Management may be complicated by disease or its treatments Dental Management may be complicated by disease or its treatments

140. Pyostomatitis vegetans Pyostomatitis vegetans (PV) is a rare condition characterized by pustules that affect the oral mucosa. It is a highly specific marker for inflammatory bowel disease (UC in particular) and its correct recognition may lead to the diagnosis of ulcerative colitis or Crohn’s disease. Thus, a presumptive diagnosis of PV should suggest a complete gastrointestinal investigation

141. –PV pathogenesis is as yet unknown, although immunological and microbial factors have been suggested as possible –Pyostomatitis vegetans is characterized by erythematous, thickened oral mucosa with multiple pustules and superficial erosions. –A peripheral eosinophilia has been observed in most cases reported. What this might indicate? –Treatment of PV focuses on control of the underlying disease

142. Any questions, suggestions or comments? Thank you