This document provides an overview of several gastrointestinal diseases and their potential oral manifestations. It discusses celiac disease, inflammatory bowel diseases like Crohn's disease and ulcerative colitis, orofacial granulomatosis, pyostomatitis vegetans and gangrenosum, and gastroesophageal reflux disease. For each condition, it describes the defining gastrointestinal symptoms and pathology, as well as common oral signs such as recurrent aphthous stomatitis, angular cheilitis, cobblestoning, and dental enamel defects. The document emphasizes that oral examination can help identify underlying bowel diseases, and management involves treating both the oral and gastrointestinal components of each condition.

1. ORAL MANIFESTATIONS OF GASTROINTESTINAL
DISEASES
DR. HADI MUNIB
ORAL AND MAXILLOFACIAL SURGERY RESIDENT

2. OUTLINE
 Celiac Diseases
 Inflammatory Bowel Disease
 Orofacial Granulomatosis
 Ulcerative Colitis
 Pyostomatitis Vegetans
 Pyostomatitis Gangrenosum
 Gastro- Esophageal Reflux Disease
 References

3. CELIAC DISEASES
 Permanent intolerance to gliadin; the protein component of wheat. “Genetic”
 Lifelong inflammatory condition of the gastrointestinal tract that affects the small intestine
 Malabsorption due to morphological abnormalities in the small intestinal mucosa.
 Reversible.
 In adult coeliac disease, diarrhea, weight loss, and weakness are the classic signs and
symptoms.
 “Celiac Sprue” Sprue: Dutch for Aphthous

4. CELIAC DISEASE
 The incidence of biopsy-proven coeliac disease in the UK is 1 in 2000,
 The incidence using markers as anti-endomysial antibodies actually approaches 1:300.
 Approximately 5–10% of patients with coeliac disease have an affected first-degree relative.
 Approximately 5–10% of people with Type I diabetes will also have coeliac disease.
 Dermatitis herpetiformis is the classical non-gastrointestinal manifestation of coeliac disease.
 Hematinic Deficiencies in Iron and Folate are likely to be present in Celiac Disease patients due to
malabsorption

5. DIAGNOSIS OF CELIAC DISEASE
 Blood Tests; Full Blood Count and Hematinic assays, IgA anti-gliadin, IgA antireticulin, and IgA
endomysial autoantibodies.
 Biopsy; Increased lymphocytic infiltration; Crypt hyperplasia occurs next then Villous Atrophy; Due to
Crypt Hyperplasia
 Patients with positive blood tests but the biopsy is essentially normal are defined as having latent
coeliac disease.

6. MANAGEMENT OF CELIAC DISEASES
 Gluten- Free Diet
 Iron and Folate Supplements

7. ORAL MANIFESTATIONS OF CELIAC DISEASES
 Recurrent Aphthous Stomatitis with coeliac disease in recent studies indicate it to be less than 5%.
 Angular Cheilitis.
 Dental enamel defects (hypoplasia) on the permanent teeth particularly lower incisors; indicates that
the celiac disease has been present at least in the first 2 years of life even though it might have been
clinically silent.

8. INFLAMMATORY BOWEL DISEASE
 Lifelong conditions resulting from aberrant inflammation of the mucosal lining of the gastrointestinal
tract.
 The two main categories are:
 Crohn's disease, which may affect the gut anywhere
 Ulcerative colitis, which is predominantly within the colon.
 Oral involvement has been recognized in patients suffering from both Crohn's disease and to a lesser
extent, ulcerative colitis.
 Oral lesions may precede or accompany gastrointestinal disease and can be the only site of involvement.

9. CROHN’S DISEASE
 Was described as “Regional Ileitis”.
 Mucosal inflammation and ulceration, obstructive edema [Lymph Node Hyperplasia] and the production
of granulomatous lesions.
 The clinical progression of the disease is very variable with inactive phases.

10. AGGRESSIVE STAGES OF CROHN’S DISEASE
 Abdominal pain
 Diarrhea
 Malaise
 The production of fistulae.
 Arthropathies
 Skin granulomas

11. TREATMENT OF CROHN’S DISEASE
 The aetiology of the disease is not known.
 Treatment is medical; using steroids, azathioprine (and other immunosuppressive agents) or amino-
salicylates
 Dietary treatment strategies; favored in children.
 Replacement therapy to correct malabsorption.
 Surgery.

12. OROFACIAL GRANULOMATOSIS
 The term ‘orofacial granulomatosis’ (OFG) was introduced to encompass these disorders and to describe
a clinical syndrome presenting with swelling of the face, lips, or oral tissues with histological evidence of
noncaseating granulomatous inflammation.
 Oral Crohn's disease
 Oral sarcoid
 Melkersson–Rosenthal syndrome
 Mieschener's Cheilitis granulomatosa (granulomatous Cheilitis).

13. CLINICAL FEATURES OF OFG AND CROHN’S
 The most common feature is: Orofacial swelling, particularly involving the lips
 Painless, firm ‘rubbery’ consistency; and can involve both lips with varying severities.
 The floor of the mouth, periorbital and chin regions can be occasionally involved.
 The buccal mucosa is thickened and folded, characteristic ‘COBBLESTONE’ appearance.
 Lip fissures and Angular Cheilitis.
 History of recurrent or persistent swelling of the submandibular lymph nodes. There may also be
persistent erythema and scaling of the perioral tissues. Mucosal tags may be present, particularly in the
retromolar regions.

14. CLINICAL FEATURES OF OFG AND CROHN’S
 RAS and NON-RAS ulcers
 Persistent linear ulcers occur in the buccal and labial sulci at the base of hyperplastic tissue, can be painful,
particularly when eating.
 The gingivae may appear hyperplastic and edematous and usually has a “full thickness pattern” – GM to
Non-Keratin.

15. ORAL MANIFESTATIONS

18. HISTOLOGY OF OFG
 Noncaseating and epithelioid granulomas, with or without multinucleated giant cells, are seen in
90% of the cases.
 Granulomas are not always present and their absence does not exclude the clinical diagnosis of
OFG.

19. OFG AS A PREDICTOR TO CROHN’S?
 The interrelationship between oral Crohn's disease and OFG is a matter for debate.
 In one study, 10% of 60 OFG patients had definite evidence of Crohn's disease affecting the intestine.
 Another study demonstrated asymptomatic intestinal involvement in 37% who presented solely with
features of OFG.
 The prevalence of asymptomatic intestinal disease in patients with OFG has been reported as between
10 and 50% in various series.

20. AETIOLOGY OF OROFACIAL GRANULOMATOSIS
 The aetiology of OFG unrelated to systemic disease remains unclear.
 Allergy, Infections, and hereditary causes have all been implicated, together with infectious agents such as
Saccharomyces cerevisiae, Mycobacterium Para-tuberculosis , and ‘Campylobacter-like’ bacteria.
 Clinical atopy is more prevalent in OFG.
 It remains unknown whether sensitivity to food additives is the primary factor for some patients with OFG or a
secondary aggravating factor to an underlying process.

21. DIAGNOSIS OF OROFACIAL GRANULOMATOSIS
 Hematological investigations
 Biochemical investigations, including inflammatory markers
 Estimation of the serum Angiotensin Converting Enzyme (ACE)
 Chest X-Ray
 Biopsy [deeper beyond the superficial tissue].
 Esophago-Gastro-Duodenoscopy
 Ileo-Colonoscopy
 Small bowel radiographs

22. MANAGEMENT OF OROFACIAL GRANULOMATOSIS
 Treatment of OFG is unsatisfactory and response to drug-therapy is disappointing.
 Lip-swelling can cause considerable embarrassment.
 Short courses of systemic steroids can be effective at reducing the swelling
 Long-term systemic steroids are contraindicated, particularly in children.
 Intralesional steroids.
 A large number of systemic drugs have been tried with mixed success [Azathioprine, Clofazimine,
Hydroxychloroquine, Danazol, cyclosporine, sulazosulfapyridine, thalidomide, and antimicrobials ]
 Topical steroids and antiseptic and analgesic mouthwashes for managing the oral ulceration.
 Angular Cheilitis and lip fissures frequently become secondarily infected can be improved by the
application of an antifungal cream

23. ULCERATIVE COLITIS
 Young adult life
 Inflammatory changes in the colonic mucosa and submucosa lead to widespread ulceration.
 May be complicated by hemorrhage, perforation, and, occasionally malignancy.
 Pain, diarrhea, and generalized abdominal discomfort are the predominant symptoms.
 ‘Diseases of civilization’.
 The treatment of ulcerative colitis is by the use of sulfasalazine and steroids, used either locally or
systemically.
 Surgery may be necessary if medical treatment fails.
 Ulcerative colitis only affects the large bowel.

25. PYOSTOMATITIS VEGETANS
 Rare oral Disorder and a highly specific marker for IBD.
 The bowel symptoms often precede oral involvement by several months or years.
 Male: Female ratio = 3:1 and affects all ages.
 It is the oral equivalent of pyoderma vegetans.

26. PYOSTOMATITIS VEGETANS
 Miliary abscesses and pustular lesions affecting the oral mucosa and gingiva
 Gingivae become thickened, erythematous, and may exhibit vegetations or ‘cobblestoning’.
 ‘Snail-track’ ulcers.
 The oral lesions predominantly affect the labial, buccal mucosa and the labial gingiva can
affect the hard and soft palate, vestibule, and tonsillar region.
 The histological features are often characteristic, although not pathognomonic, showing
intraepithelial and sub-epithelial microabscesses containing large numbers of eosinophils.

27. TREATMENT OF PYOSTOMATITIS VEGETANS
 Topical steroid therapy has been successful for the treatment.
 Systemic treatment, with or without azathioprine or sulfamethoxypyridazine is required.
 Management of the associated IBD may also result in improvement of the oral lesions.
 It has been suggested that all patients should be investigated for bowel disease.

28. SNAIL- TRACK ULCERS

31. PYOSTOMATITIS GANGRENOSUM
 Other forms of stomatitis have been reportedly associated with IBD and
include irregular, deep, foul-smelling ulcers of varying size, with rolled
margins and a greyish, fibrinous base.

32. GASTRO- ESOPHAGEAL REFLUX DISEASE (GERD)
 Healthy individuals experience GERD after a meal and this is due to the relaxation of the lower
esophageal sphincter.
 In patients with GERD, there is increased frequency and duration of reflux and the esophageal
mucosa is damaged by regurgitation of gastric contents.
 Reflux esophagitis, ulceration, stricture, or epithelial metaplasia (Barrett's oesophagus).

33. CLINICAL FEATURES OF GERD
 Heart-burn
 Epigastric pain and regurgitation.
 The ‘silent refluxers’ have no symptoms.
 Dental erosion particularly of the palatal aspects of the teeth.
 Patients who regularly chew antacid preparations may have a high sugar content that can
predispose to caries.
 Orofacial manifestations of iron deficiency.

34. 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]

36. PATIENTS PRESENTING WITH PALATAL DENTAL EROSION SHOULD BE
ASSESSED FOR GERD.

39. REFERENCES
 Chapter 12: Gastrointestinal Diseases

40. THANK YOU