Transcript GIT sdisorders - WordPress.com

GIT disorders
Prof. Elsanousi M Taher
BDS, M.Sc., FFDRCSI
E-mail: [email protected]
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
Signs and symptoms

Dysphagia

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

Pain:
–
–
–
–

Odynophagia: pain with swallowing
Epigastric pain
Abdominal cramps
It may presented as chest pain !!
Bleeding:
– Hematemesis:


Fresh blood
Ground –coffee
– Melena:



Fresh
Occult
Nausea
Signs and symptoms

Vomiting:


the forceful expulsion of gastric contents through
a relaxed esophageal sphincter and open mouth
Diarrhoea: watery or bloody
– Acute: infections, food poisoning, drugs
– Chronic: IBDs, chronic infections

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
 Structural
 Medications
 Idiopathic



Weight loss:
– involuntary decrease in body weight of at
least 5% is a problem that requires clinical
evaluation
Regurgitation:
– acid regurgitation
– sudden, spontaneous reflux of small
volumes of bitter tasting acidic material
into the mouth (Mouth brash)

Jaundice

Finger clubbing

Ascites

Other signs of liver diseases

Others
Ascites

Ascites may be a
sign of chronic
liver disease and
other GIT
disorders
Finger clubbing

Q: In what
condition you
might see clubbing
of the fingers?
Dysphagia
– 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
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



Dysphagia is a subjective difficulty in
swallowing
Unless it is associated with sore throat or
oropharyngeal ulceration it is a serious
symptom
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
Etiology
Dysphagia could be of:
– acute onset as in stroke
– slowly developed as in tumour and motor
neuron disease
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)
Causes of dysphagia:
–
Structural diseases:
–
Functional causes:
Structural diseases:
 Oral causes:





Oral painful and ulcerative conditions
Infections: tonsillitis, pericoronitis and Ludwig's angina
Xerostomia & oral submucous fibrosis
Oral malignancies
Esophageal causes:









Foreign bodies
Mechanical obstruction or stricture
Ulceration
Diverticula: outpouching of a hollow (or a fluid-filled) structure
in the body
Surgery
Tumor e.g. Carcinoma
Plumer-Venson syndrome
Scleroderma
External pressure from enlarged lymph node
Diverticulum
Strictures caused by Caustic
Ingestion
Neurological causes:

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 corticobulbar “)
 Myasthenia gravis
 Esophageal spasm

Neurological causes
– Stroke – present in up to 47%
– Poliomyelitis
– Parkinson’s Disease
– Multiple Sclerosis
– Muscular Dystrophy
– Myasthenia Gravis
Systemic structural causes:
o
o
o
o
o
o
o
o
Systemic Sclerosis
Systemic Lupus Erythematosis
Dermatomyosits
Mixed Connective Tissue Disease
Mucosal Pemphigoid,
Epidermolysis Bulosa
Sjogren’s Syndrome (xerostomia)
Aging:
–
–
–
–
Dysphagia is present in 2% > 65
Poor dentition
Loss of tongue connective tissue
Increased pharyngeal transit time
Functional causes:


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
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
Dysphagia

A barium swallow
showing an esophageal
web (arrow) in a
patient with the
Plummer-Vinson
syndrome
Barium meal
Normal
Abnormal
Dysphagia
esophageal stricture
shown by barium meal
follow through
Dysphagia

Oesophageal carcinoma
Treatment of dysphagia
– According to cause
– The dentist can manage the oral
causes
– For non-oral causes refer to medical
or surgical specialist
Halitosis
Halitosis


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


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%.
Causes of halitosis:
– bad oral hygiene, carious and periodontal
diseases (volatile sulphur containing
compounds)
Periodontal infections (especially
 necrotizing gingivitis
 periodontitis
 Pericoronitis
 Other types of oral infections
 Infected extraction sockets
 Ulcers.

– Certain foods
– Xerostomia
– tonsillitis, pharyngitis and sinusitis
– lung abscess and bronchiectasis
– diabetes (sweet and acetone smell) as
in keto -acidosis
– 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
– Certain types of food and smoking
– Psychogenic:
 Real clinical dilemma
 No clinical evidence
 delusion or monosymptomatic hypochondriasis
(self-oral malodour; halitophobia)

Many of these patients will adopt
behaviour to minimize their perceived
problem, such as:
Covering the mouth when talking;
 Avoiding or keeping a distance from other people;
 Avoiding social situations;
 Using chewing gum, mints,
 mouthwashes or sprays designed to reduce
malodour;


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.
Management of halitosis:



According to the cause
Rule out and treat dental and oral
causes
Mouth washes and fresheners can only
mask halitosis
– 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.

Keep oral hygiene regular and good:
Oral Prophylaxis;
 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;
 Brush your tongue before going to bed: use a tongue
scraper if that helps.
 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.
Refer patients to specialist if:
– Suspected systemic disease;
– Suspected malignancy;
– Patients with imagined halitosis.
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.
Gastric acid reflux
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
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
– Progestin for abnormal menstrual bleeding or
birth control
– Sedatives for insomnia or anxiety
– Tricyclic antidepressants
Consequences of reflux
oesophagitis




Ulceration
Stricture
Glandular
metaplasia
(Barrett’s
oesophagus)
Carcinoma
Oral manifestations:
– erythema and oral ulceration
– non-carious tooth surface loss specially in
the palatal surface of upper incisors
Esophageal Reflux
Palatal Surface Erosion
of the of upper incisor
teeth
Peptic ulcers
Classified into:
– Gastric ulcers
– Duodenal
– 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
 Interference with mucosal integrity
 Disruption of mucosal barrier

– 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
Predisposing factors of peptic ulcers

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
Genetic predisposition (Hereditary): blood
group “O” are more susceptible (duodenal)
Stress
Predisposing factors of peptic ulcers

Smoking

Alcohol

Zolllinger-Ellison syndrome: ( severe peptic
ulceration, gastric acid hypersecretion,
tumour of non - Cells of Islets of pancreas
(gastrinoma) or hyperplasia)
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)
Features
Incidence
M:F ratio
Gastric ulcer
Less common
6:1
Duodenal ulcer
4 times common than GU
3:1
Age incidence
Typically elderly, after
the age of 50 years
Young adults & represent
80-85% of peptic ulcers at
this group
Cause
Caused 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 pain
Pain is related to meals
The pain typically occurs
and relieved by antacids before meals and worse at
but may be asymptomatic night and relived by eating
or drinking milk
80% relapse within 1 year of healing
Complication of peptic ulcers:
– Perforations
– Gastric outlet obstruction
– Bleeding
– 80% of duodenal ulcers relapse within 1
year of healing
Epigastric pain is common symptom
of peptic ulcer
PEPTIC ULCERS Can not be diagnosed by
history and examination only
Investigations:

– Endoscopy
– Barium meal swallow
– Biopsy
– FBC
– Investigate for helicobacter pylori status:
–
Breath test
–
Histological biopsy
–
Serology
Duodenal Ulcer
Hiatus hernia
– 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
Hiatus Hernia
Management of peptic ulcers
Medical management:

life style modification: stop smoking, alcohol, change
food habits and avoid NSAID

H receptor blockers: cimetidine, ranitidine … etc.

proton pump blockers: Omeprazole

antibiotics: for eradication of H. Pylori (amoxicillin or
2
metronidazole)

antacids: Ca carbonate, Mg hydroxide & aluminum
hydroxide

sedatives

surface coating agents: e.g. bismuth

anticholinergic drugs: less commonly used nowadays
Surgical management of peptic
ulcers
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
Coeliac disease (Gluten sensitive
enteropathy)
– Characterized by mucosal atrophy of small
intestine, particularly jejunum and respond
well to withdraw of gluten from diet
– Associated with dermatitis herpetiformis
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
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.
– 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
Clinical features in adults
– The symptoms are less severe
– Diarrhea, weight loss, anemia, osteomalacia
– Some times associated with dermatitis
herpetiformis
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
– immunological tests:


IgA antiendomysial antibodies can detect Coeliac
disease with a sensitivity and specificity of 90% and
99%
α- gliadin antibodies
Celiac disease

Normal villi of small
intestine increase
surface area available
for absorption of
nutrients

Atrophy of the
villi and
lymphocytic
infiltration of the
submucosal layer
Celiac disease

Note the atrophy
of the villi of small
intestine
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
Oral manifestations:
 Aphthous
ulcers (5% of patients with
ROU may have intestinal disease)
 Enamel
hypoplasia (in children)
 Glossitis,
BMS and angular cheilitis
 Dermatitis
herpetiformis
 Uncommon
skin disease associated with
coeliac disease like DH may have oral
manifestations
Dermatitis herpetiformis

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 itching is so sever that may force the
patient to commit suicide

Biopsy show granular deposits of IgA, C3 &
fibrin along the BMZ
Dermatitis herpetiformis
Dermatitis herpetiformis

Oral lesion may be erythematous,
vesicular or ulcerative lesions

May respond to gluten free diet and
dapson
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
Linear Ig A disease
Inflammatory bowel diseases
Inflammatory bowel disease
(IBD)

Crohn’s disease

Ulcerative colitis
– 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.
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.
Crohn’s disease
– 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)
Etiology:
– Exact cause is unknown but viral, bacterial and
food allergy has been incriminated ??
– Genetic predisposition
– Interaction between genetic and environmental
factors
Pathogenesis
IBD
Genes
Environment
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
– 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
Crohn’s Disease: Anatomic Distribution
Small bowel
alone
(33%)
Ileocolic
(45%)
Freq of involvement
Most
Least
Colon alone
(20%)
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 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.

DISTINGUISHING
FEATURES OF CROHN’S
DISEASE
Crohn's Disease

Colonoscopy view
Crohn's Disease
Colonoscopy view
Crohn's Disease
barium follow-through of
small intestine showing
ulceration of
transverse colon
Crohn's Disease
Crohn's Disease

(conjunctivitis &
iritis)
D. D:

Sarcoidosis

Ofg

Tb

Angio-edema

Others
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.
Treatment: depend on case severity
– Oral steroids: prednisolone
– Azathioprine: as steroid sparing agents
– Cyclosporine
– Sulphasalazine
– Surgery: indicated in

Symptoms persist despite treatment

Intestinal obstruction

Local complications: fistulae, abscess,
perforation
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
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.
Ulcerative colitis
– Usually affect large bowel starting at the
rectum and proceed proximally
(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)
– 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
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
Ulcerative colitis
Ulcerative Colitis - Ulcerations

Treatment:
– Rectal steroids
– Salphasalazine
– Oral steroids
– Surgery
Emergency Surgery




Toxic megacolon
Perforation
Massive haemorrhage
Failure of a severe attack to resolve
Any questions?
Thank you
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:
1.
2.
3.
4.
Specific, meaning these occur only in association with the
bowel disease and/or show characteristic histology of that
condition.
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.
Complications of malabsorption caused by the bowel
inflammation resulting in deficiencies in vitamins and minerals.
Side effects or complications of medications prescribed to
treat the bowel disease.
– The first three of these categories
may be useful in directing the doctor
to the bowel problem and making the
specific diagnosis.
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)
Oral Signs of Crohn's disease


Angular cheilitis
Aphthous ulcers/aphthous stomatitis – has been
reported to affect up to 20-30% of patients with
Crohn's disease

Redness and scaling around the lips

Pyostomatitis vegetans – very rare in Crohn's disease

Recurrent vomiting and regurgitation can cause oral
soreness and teeth erosion
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
– 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


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
“cobble stone” mucosal swellings of
buccal mucosa
Crohn's Disease


Lip swelling and
central fissure of
the lip
Q: what is the
differential
diagnosis of this
swollen lip ?
Crohn's Disease
Oral Crohn’s
presented as
Swollen lip
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
 Clofazimine, dapsone, thalidomide
 Steroid and systemic and intralesional

Melkersson-Rosenthal syndrome:
–
–
–
–
Facial swelling
Facial palsy
And fissured tongue
Such patients may have incomplete or
asymptomatic CD or may develop the disease
later
Crohn's Disease
Aphthous ulcer of the lip
Aphthous ulcer of the lip

What is the D.D of this
ulcer ?
Crohn's Disease
Mucosal tags in buccal mucosa
Crohn's Disease

Cobble stone
appearance in
buccal mucosa
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
• Glossitis
• Cheiltis
•
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
•
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
– 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
Any questions, suggestions or
comments?
Thank you