Dental management of patients with gastrointestinal conditions

1. DENTAL MANAGEMENTS OF
PATIENTS WITH
GASTROINTESTINAL DISEASE
DR OYETOLA ELIJAH O

2. GASTROINTESTINAL TRACT

3. • The digestive tract is a long muscular tube
that move food and accumulated secretions
from the mouth to the anus
• Gastrointestinal diseases refers to disease
conditions affecting gastrointestinal/digestive
tract from the mouth/pharyn- anus.

4. • The GIT has a contiguous relationship with the
mouth, being the posterior extension,
sometimes some refers to GIT as extending
from the mouth to the anus
• Oral health care professionals (especially oral
medicine) are expected to be able to
recognize, diagnose, and treat oral conditions
associated with GIT disorders

5. DISEASES OF UPPER DIGESTIVE TRACT
Gastrointestinal reflux disease
• The incidence is increasing especially in
developed world, up to 10% of the population
experience heartburn daily
• During gastroesophageal reflux, gastric content
passively move from the stomach into the
oesophagus
• Heartburn is the cardinal symptom, defined as a
sensation of burning or heat that spread upwards
from the epigastrium to the neck

6. • Resultant injury are ulceration, pharyngitis, stricture,
and dysplasia
• Other symptoms are chest pain, dysphagia,
odynophagia, laryngitis, chronic cough, hoarseness of
voice
• Barret esophagitis variant of GERD in which normal
squamous epithelium is replaced by columnar
epithelium, increased incidence of adenocarcinoma
• The basic pathology is the relaxation of lower
esophageal sphincter

7. aetiology
• Physiological/normal- in case of burp,
relaxation of lower esophageal sphincter to
relief pressure in the stomach
• Sclerodermas
• Surgery
• Drugs e.g anticholinergics, cardiac
vasoconstrictors, nicotine,
• oetrogen-progesteron combination(OCP),
pregnancy, also decrease the sphincter

8. • The summary of events going on through the digestive
system is the hydrolysis of large non absorbable
molecules into smaller absorbable molecules through
secreted enzymes, the remaining unabsorbed food are
excreted via the anus.
• Dentists should also be able to give dental treatments
to patients with GIT disorders bearing in mind:
– The precautions to accommodate their underlying
systemic disease
– Drug interactions
– Effect of concurrent therapy on their dental treatment

9. • Treated with proton pump inhibitor:
omeprazole
• Promotility drugs, encourage clearance of acid
from osophagus: Cisapride.
• surgery

10. Oral manifestations and Tx
• Dysgesia
– Promotility drugs
• Dentine sensitivity
– restorative
• dental erosion
• Pulpitis
• Epithelia atrophy
– treated by sodium bicarbonate rinse
– Prevent infection

11. • Erethema
– treated by sodium bicarbonate rinse
• Ulceration
– treated by sodium bicarbonate rinse
– Prevent infection
– Vit c

12. Dental management of GIT px
• Fluoride therapy
• Avoid intravascular infiltration
– Patients on cimetidine may experience toxic reaction to
lidocaine(or other amide LA) if injected intravascularly.
• Treatment of fungi disease
– Lidocaine reduce absorption of ketoconazole
• Planning GA session
– Stricture ma interfere with intubation in GA
• Erythema and atrophy can be treated by sodium
bicarbonate rinse

13. Hiatal Hernia
• The esophagus passes through the
diaphragmatic hiatus and into the stomach
just inferior to the diaphragm.
• The hiatus causes an anatomic narrowing of
the opening into the stomach and thus helps
prevent reflux of stomach contents into the
esophagus.

14. • Some patients have a weakened or enlarged
hiatus, perhaps due to hereditary factors. It may
also may be caused by obesity, exercising (eg,
weight lifting), or chronic straining when passing
stools.
• When a weakened or enlarged hiatus occurs, a
portion of the stomach herniates into the chest
cavity through this enlarged hole, resulting in a
hiatal hernia
• Hiatal hernia occurs in 20-60% cases

15. Hiatal Hernia

16. • Defects present at birth may correct
themselves
• Antiacids help relief symptoms
• H2 receptor help antagonists are effective in
inhibiting the action of histamine on parieta
cells

17. • If treated with xerogenic drugs, there may be
dry mouth
• Carious lesion is not uncommon
• Influx into the oral cavity ma cause same
lesion as in GERD

18. Peptic ulcer
• Peptic ulcer=GU+DU, duodenal ulcer more common
• A common benign ulceration of the epithelia ,inning of
the stomach
• About 6% of dental px has peptic ulcer
• Gastric results from altered mucosa defenses whereas
duodenal ulcers are associated with increased acid
production
• At both sides, H pylori play some role as a complex is
being formed between host defense system, the
presence of elevated acid, pepsin level and H.pylori

19. • Anaemia from GI bleeding present as pale
mucosa
• Signs of regurgitation on teeth
• Vascular malformations on the lips have been
reported
• H.pylori has been reported in dental plaque
indicate this might be the origin of the
bacteria

20. • Avoid lengthy dental procedure
• Minimize stress
• Avoid prescribing drug that causes ulceration NSAIDS
• Because many antacids contain calcium, magnesium,
and aluminum salts that bind antibiotics such as
erythromycin and tetracycline, the dentist should be
aware that administration of one of these drugs within
an hour of antacid therapy may decrease the
absorption of the antibiotic by 75 to 85%.
• Consequently, antibiotics should be taken 2 hours
before or 2 hours after ingestion of antacids

21. • Exogenous steroid administration is likely to
exacerbate the ulcer because of the increased
production of acid caused by the steroid and
should be avoided
• Also note that anticholinergic are xerogenic
• Manage appropriately e.g artificial saliva

22. INFLAMMATORY BOWEL DISEASE
• Inflammatory process involving small and
large intestine
• IBD=CD+UC
• Ulcerative colitis involved the mucosa and sub
mucosa of colon. Hallmark is rectal bleeding
and diarrhea
• Chrohn’s disease a regional enteritis, involves
all the layers of the gut

23. • Chrohn’s disease causes intense inflammation of
digestive tract
• Common symptoms are abdominal pain, severe
diarrhea, fatigue, weight loss and malnutrition.
• Risk factors are
– Age <30 years
– Family history
– Smoking
– NSAID use
– Ethnicity : Eastern European (Ashkenazi) Jewish descent,
the incidence of Crohn's disease is increasing among Black
people who live in North America and the United Kingdom.

24. Oral signs
• Aphthous ulceration
• Pyostomititis vegetants
– Purulent inflammation of the mouth, xtrised by deep
tissue proliferation that undergo suppuration and
then suppuration. Lesion disappear after colectomy.
Believed to be due to the effects of circulating
immune complexes
• Chronic stomatitis
• Cobble stone appearance of the mucosa
• Gingivitis
• Persistent lip swelling

25. Oral ulcer

26. • Large numbers of broad
based tiny abscesses
developing in areas of
intense erythema

27. Pyostomititis vegetants Ulcerative colitis

28. Cobble stones appearance
Cobble stone appearance
:where polygonal cells bulge
out from the mucosal surface
to a varying degree

29. • A cobblestone appearance is an uncommon
finding, where polygonal cells bulge out from the
mucosal surface to a varying degree
• It supposedly reflects lymphoid nodular
hyperplasia of the immune system responding to
stimulating factors such as acid reflux, postnasal
drainage, breathing in dry air, or more likely
allergies, as in our case
• Its presence ma suggestive of allergic rhinitis and
should prompt physicians to perform an
allergologic assessment.

30. • Lichenoid mucosa reaction
• Granulomatous inflammation of minor
salivary glands
• Candidiasis
• Angular cheilitis
• Hairy leucoplakia
• Other sign of malabsorption

31. Lichenoid drug reaction

32. Dental management
• Px is prone to infection because of the
immunosuppression
• Prophylactic antibiotic
• Invasive dental treatment should be avoided as
much as practically possible
• Hematologic investigation before dental tx is
necessary since they are prone to bleeding(vit k
absorption) and anemia
• Before prescribing drugs metabolized by the liver,
check the reports of the liver function cell

33. Liver cirrhosis
• Cirrhosis is neither a single process nor a
single disease; rather, it is the end result of a
variety of conditions that produce chronic
inflammatory change and liver cell injury. The
progressive scarring leads to abnormal fibrosis
and nodular regeneration
• The liver is firm/hard on palpation. The
progressive scarring causes fibrosis and
nodular generation

34. Oral findings
• Associated with vitamin deff-
 angular cheilitis,
 pale mucosa,
 glossitis
• Yellow pigmentation
• Salivary gland dysfunction secondary to
Sjogren syndrome associated with biliary
cirrhosis

35. GASTROINTESTINAL SYNDROMES
Eating disorders: Anorexia and Bulimia nervosa
• Anorexia involves individuals who intentionally
starve themselves when they are already
underweight. Those who suffer from anorexia are
unable to perceive their physical appearance
accurately.
• They may successfully diet for a short time, but
they often again lose the ability to restrict food
intake, often as a result of some emotional
trauma.

36. • Bulimia nervosa consume large amounts of
food during “binge” episodes in which they
feel out of control of their eating.
• Bulimic individuals are also not as successful
in dieting as are those with anorexia.
• Both are psychyatric disease with oral
manifestations

37. ORAL ASPECT
• Erosion on lingual surface of maxillary teeth
• Acids from chronic vomiting are the cause
• Examination of the patient’s fingernails may
disclose abnormalities related to the use of
fingers to initiate purging
• Parotid enlargement may develop as a sequel of
starvation.
• Rarely does one observe soft-tissue changes of
the oral mucosa because of trauma from gastric
acids.

38. Plummer-Vinson Sydrome
• Plummer-Vinson syndrome, originally described
as “hysterical dysphagia,” is noted primarily in
women in the fourth and fifth decades of life.
• The hallmark of this disorder is dysphagia
resulting from esophageal stricture, causing many
patients to have a fear of choking.
• Patients may present with a lemon-tinted pallor
and with dryness of the skin, spoon-shaped
fingernails, koilonychia, and splenomegaly.

39. Oral aspects
• The oral manifestations are the result of an
iron deficiency anemia.
• Other oral findings include:
– atrophic glossitis with erythema or fissuring,
– angular cheilitis,
– thinning of the vermilion borders of the lips,
– leukoplakia of the tongue.
• Inspection of the oral mucous membranes
will disclose atrophy and hyperkeratinization

40. • Thorough oral, pharyngeal, and
esophageal examinations are mandatory
to ensure that carcinoma is not present.
• Artificial saliva may reduce the sensation
(and thereby, the fear) of choking

41. Peutz-Jeghers syndrome
• Peutz-Jeghers syndrome is characterized
by multiple intestinal polyps throughout the
gastrointestinal tract but primarily in the
small intestine.
• Malignancies in the gastrointestinal tract
and elsewhere in the body have been
reported in approximately 10% of patients
with this syndrome.

42. • Pigmentation (present from birth) of the
face, lips, and oral cavity is a hall- mark of
this syndrome.
• 58
• Interestingly, the facial pigmentation fades
later in life although the intraoral mucosal
pigmentation persists.
• No specific oral treatment is necessary.

43. Cowden’s syndrome
• Cowden’s syndrome (multiple hamartoma and
neoplasia syndrome) is an autosomal dominant
disease characterized chiefly by
trichilemmomas, gastrointestinal polyps, breast
and thyroid neoplasms, and oral abnormalities.
• Cowden’s syndrome is considered to be a
cutaneous marker of internal malignancies.
• Check the other class notes for Gardner’s
synfdrome

44. CLASS DISCUSSION
• Discuss oral signs that may suggest
comprehensive gastrointestinal examination
and investigation.

45. • THANKS FOR YOUR ATTENTION