This document discusses the oral manifestations of various gastrointestinal diseases. It covers conditions like peptic ulcer disease, inflammatory bowel diseases, celiac disease, and GERD. Common oral signs include glossitis, oral ulcers, angular cheilitis, and tooth erosion. Glossitis can be seen in conditions that cause nutritional deficiencies like celiac disease. Oral complications of medications used to treat gastrointestinal diseases are also reviewed, such as fungal infections from antibiotics or dry mouth from antacids. Dentists need to be aware of gastrointestinal conditions and how they may present orally.

1. Oral Manifestation of
Gastro-intestinal
Disease
drg. Pudji Handayani, Sp.PM
Department of Oral Medicine
Dentistry, Faculty of Medicine Universitas Sriwijaya

2. Gastro-intestinal Disease
• peptic ulcer disease
• inflammatory bowel disease
• Celiac Disease
• Gastroesophageal Reflux Disease (GERD)
dentist:
aware of the patient’s condition
monitor for symptoms indicative of initial disease or relapse
aware of drugs that interact with gastrointestinal medications.
https://www.cancer.gov/publications/dictionaries/cancer-terms/def/gastrointestinal-tract

3. Gastrointerstinal Diseases
• most common conditions associated with the development of an
atrophy of the tongue's mucosa related to a nutritional aetiology.
• Ex. Celiac disease (CD)  poor nutrition absorbtion

4. Peptic Ulcer Disease
• a well-defined break in the gastrointestinal  results from chronic
acid/pepsin secretions and the destructive effects of and host
response to Helicobacter pylori.
• develop in regions of the gastrointestinal tract that are proximal to
acid/pepsin secretions (Figure 12-1).

5. Pathophysiology and Complications

6. Signs and Symptoms
• most develop epigastric pain that is longstanding (several hours) and sharply localized  “burning”
or “gnawing” but may be “illdefined” or “aching.”
• The discomfort of a duodenal ulcer manifests most commonly on an empty stomach, usually 90
minutes to 3 hours after eating, and frequently awakens the patient in the middle of the night.
• Ingestion of food, milk, or antacids provides rapid relief in most cases.
• In contrast, patients with gastric ulcers, however, are unpredictable in their response to food and
may develop abdominal pain from eating.
• Symptoms associated with peptic ulceration tend to be episodic and recurrent.
• Epigastric tenderness often accompanies the condition.
• Protracted vomiting a few hours after a meal is a sign of gastric outlet (pyloric) obstruction.
• Melena (bloody stools) or black tarry stools indicate blood loss due to gastrointestinal hemorrhage.

7. Laboratory Findings
A peptic ulcer is diagnosed primarily by fiber
optic endoscopy and laboratory tests for
H. pylori.
• Endoscopy affords the opportunity for
visualization, access for biopsy, and
therapeutic procedures if bleeding is
present.
• Serology and/or H. pylori stool antigen
tests are less commonly used.
• urea breath tests (UBTs): measure
indirectly the presence of H. pylori before
treatment and its eradication after
treatment.

8. MEDICAL MANAGEMENT
• antisecretory drugs are administered (Table 12-1).
• If the patient is infected with H. pylori, inhibitors of gastric acid secretion and antimicrobial agents
are recommended.

10. Oral Complications and Manifestations
• systemic antibiotics for peptic ulcer disease  fungal overgrowth
(candidiasis) in the oral cavity: median rhomboid glossitis, in this
patient population (Figure 12-4)  antifungal agents.
Rationale for Treatment
• To re establish a normal balance of oral flora and to improve oral
hygiene. Medication should be continued for 48 hours after clinical
signs have disappeared, to prevent immediate recurrence.
Topical Antifungal Agents.
Rx. Nystatin (Mycostatin, Nilstat) oral suspension 100,000 units/mL
Disp: 60 mL
Sig: Take 2 to 5 mL 4 times a day. Rinse for 2 minutes, and swallow.
*Nystatin suspension has a high sugar content; therefore, good oral
hygiene should be reinforced

11. Erosion of the enamel
• result of persistent regurgitation of gastric juices into
the mouth when pyloric stenosis occurs (Figure 12-5).
• history of reflux indicates that the patient must be
evaluated by a physician.
Medications for the treatment of peptic ulcer disease 
produce oral manifestations:
• Proton Pump Inhibitor (PPIs) can alter taste
perception.
• Cimetidine and ranitidine may have a toxic effect on
bone marrow; infrequently  anemia, agranulocytosis,
or thrombocytopenia.
• Mucosal ulcerations may be a sign of agranulocytosis
• anemia may present as mucosal pallor and
thrombocytopenia as gingival bleeding or petechiae.
• Xerostomia has been associated with the use of
famotidine and anticholinergic drugs, such as
propantheline (Pro-Banthine).
• A chronic dry mouth renders the patient susceptible to
bacterial infection (caries and periodontal disease) and
fungal disease (candidiasis).
• Erythema multiforme is associated with the use of
cimetidine, ranitidine, and lansoprazole.

12. Oral Ulceration in Inflammatory
Bowel Disease (IBD)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4851452/pdf/0140046.pdf

13. Overview
• IBD: chronic inflammatory disorders of the digestive tract  mainly
by Crohn’s disease (CD) and ulcerative colitis (UC).
• main oral manifestations of IBD:
• cobblestoning of the oral mucosa.
• labial swellings with vertical fissures
• pyostomatitis vegetans
• angular cheilitis
• perioral erythema
• and glossitis.

14. https://www.cdc.gov/ibd/what-is-IBD.htm

15. Crohn’s disease (CD)
• Oral manifestation: 8% to 10% of patients  specific or unspecific.
• Specific manifestations: rare, sometimes precede gastrointestinal lesions, which may evolve with
time  include:
• cobblestoned oral mucosa
• granular gingival swelling of hyperplastic aspect
• labial swelling accompanied by vertical fissures
• deep and linear ulcers associated with hyperplastic mucosa folds on the vestibule fold.
• Nonspecific oral lesions:
• recurrent aphthous stomatitis (RAS)
• pyostomatitis vegetans
• angular cheilitis
• persistent submandibular lymphadenopathy
• decreased saliva production
• Halitosis
• caries, gingivitis, candidiasis, odynophagia, dysphagia, increased intrinsic salivary glands, perioral erythema,
recurrent oral abscesses, glossitis, pale mucosa, lichen planus, and metallic dysgeusia.

16. Cobblestoned oral mucosa
doi:10.3121/cmr.2015.1307

17. Ulcerative colitis (UC)
• Oral manifestations:
• aphthous ulcers or superficial hemorrhagic ulcers
• angular cheilitis
• less frequent  similar to the unspecific expression of CD.
• Pyostomatitis vegetans: the only condition that is more prevalent in UC
patients, compared to individuals with CD.

19. Pyostomatitis vegetans
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5296587/

20. Gastroesophageal Reflux Disease (GERD)
• Acid reflux into the esophagus  heartburn is a burning sensation in
the chest, radiating toward the mouth.
• Heartburn is also often associated with a sour taste in the back of the
mouth with or without regurgitation of the refluxate.
• a common cause of non-cardiac chest pain.
• Extraesophageal symptoms are more likely due to reflux into the
larynx  throat clearing and hoarseness.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6140167/

21. Tooth erosion (corrosion)
https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/j.1440-1746.2011.06945.x

24. Glossitis

25. Definition
• absence of filiform or fungiform papillae on the dorsal surface of the
tongue.
• ordinary texture and appearance of the dorsal tongue: papillary
protrusion  soft and smooth aspect.
• Associated factors:
• Local: congenital or developmental affections, infections, neoplasia; or they
may be idiopathic.
• Systemic: associated to metabolic disorders, blood dyscrasias and
immunological diseases, also be correlated with protein deficiency and a
hypocaloric diet; as well as deficiency of iron, vitamin B12, folic acid (B9)
riboflavin (vit B2), and niacin (vit B3).

29. Glossitis Related to Nutritional
Deficiencies
• mechanisms involving cellular oxygenation and/or the iron
concentration in tongue's cells have been associated to glossitis due
to nutritional deficiencies.
• Deficiency of each one of the nutrients  direct or an indirect
mechanism: poor diet, malabsorption, excessive consumption.

32. Celiac Disease

34. Celiac disease
• autoimmune intolerance to gliadin, a protein contained in gluten.
• mucosa of the small intestine  development of histological lesions
characterized by villous atrophy, crypt hyperplasia, damage to the surface
epithelium, an increased number of lymphocytes and other inflammatory
cells in the lamina propria  poor absorption of nutrients: deficiency of
vitamin B12, folic acid and iron.
• Tongue lesions: to celiac diseases  indirect symptoms.
• Pastore and Lo Muzio: the importance of the recognition of glossitis to
obtain the diagnosis of a celiac disease  “the single most important step
in diagnosing celiac disease is to first consider the disorder by recognizing
its myriad clinical features”  glossitis: been described as the only clinical
sign leading to suspect the diagnosis of celiac disease.

35. Alcohol abuse
• Alcoholic tongue atrophy, two possible explanations:
• Malnutrition: characterises alcohol abusers  contradiction is due to an alteration in
hepatic enzyme levels  patients can show symptoms or signs of vitamin B12
deficiency even if its levels are normal.
• direct chemical damage to the tongue mucosa.
• Direct damage of tongue tissues:
• epithelial atrophy  on the lingual dorsum, with an increase in basal cells size and
also a decrease in superficial cells.
• role of alcohol as co-carcinogen  Alcohol consumption determined a reduction of
epithelial thickness associated to increased cellular proliferation in the basal layer.
• Alcohol determined a cytotoxic effect: atrophy of the oral mucosa followed by an
hyper-regeneration  associated with an increased susceptibility to carcinogenic
substances.

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