Download Oral ulcerations

Oral ulcerations
Prof. Elsanousi M Taher
BDS, MSc., FFDRCSI
Email: [email protected]
“ an ulcer is break in the continuity or loss
of integrity of skin or mucous membrane”
“ an erosion is superficial and partial loss
of epithelium”
Classifications of oral ulcers
On etiology:
 Traumatic
 Infective
 Neoplastic
 Dermatological
 Hematological
 Nutritional
 Immunological
 Cytotoxic drug related
Classifications of oral ulcers
On initial presentation:
 Primary ulcer: arise “du novo”:
 Trauma
 Dematoses
 Neoplastic
 Secondary ulcer: Preceded by vesicle or bullae:
 Viral infections
 Some dermatoses
 Angina bullosa hemorrhgica
Traumatic ulcers

Mechanical:
–

Of acute nature
Physical: e.g. radiation
Traumatic ulcers

Chemical:
–
Aspirin burn after sloughing
–
Phenol (carbolic acid) used as a disinfectant
–
Silver nitrate that used as cauterizing agent
–
Trichloroacetic acid used as a stringent for
gingival retraction
–
Excessive use of mouth wash
Traumatic ulcers
Traumatic ulcer may mimic neoplastic
ulcer
 Traumatic ulcer due to use of tooth
paste containing formaldehyde
Management of traumatic ulcers:
– Treat the cause
– Symptomatic treatment
– Should heal within a week other wise rethink
!!
– May need biopsy
Infective ulcers
 Bacterial:
 Viral:
 Fungal:
Tuberculous ulcer
Neoplastic ulcers
Features:
– painless at early stages
– single
– long duration
– indurated
– rolled and everted edge
– may be associated with palpable lymph node
Neoplastic ulcers
The neoplastic ulcers may be seen in:
 SCC
 BCC
 Melanoma
 Salivary gland tumor
 Lymphoma
Dermatological ulcers:
 LP
 LE
 DH
 Linear IgA disease
Linear IgA disease
 Variant of DH but not associated
with Gluten
 Non specific oral ulcers
 Skin lesions
 Diagnosed by linear deposition of IgA along
the BMZ in DIF sections
Linear IgA disease
Treatment:

Dapsone

Steroids

Sulfones
Nutritional ulcers
 See anemia
Cytotoxic drugs related ulcers
 The drug cause:
 suppression of the immune system
 depression of bone marrow
 some other drugs may also cause anemia like
phenytoin
Recurrent aphthous ulceration or
stomatitis
 The most common type of non traumatic
ulcers of the mouth
 Affects 15-20% of the population
 May start in childhood but usually on teens
and early twenties
 Affect both sexes
 RAU may be associated with systemic
disease like:
–
–
–
–
GIT
Behçet disease
HIV
Cyclic neutropenia
Etiology Of RAS
 Unknown but may be associated or related
to:
– Hereditary and genetic predisposition:
 Seen in children of affected parents
 familial tendencies (1/3 of patients)
 Associated with certain HLA groups
– Traumatic: precipitating factor and not a
causative
– Hormonal:
 occurs at premenstrual days
 improved during pregnancy
Etiology Of RAS
 GIT disorders: celiac and Crohn’s
diseases other malnutrition conditions
 Psychosomatic:
 H/O stress
 affect stressful professional people
 students during exams
Etiology Of RAS
 Hypersensitivity:
– some times it is associated with atopy & food
allergy
 Microbial:
 Hypersensitivity reactions to S. sanguis & L. forms
 Cross reactions of oral mucosa with S. sanguis
 Viral etiology ( adenoviruses)
Etiology Of RAS
 Nutritional:
– Iron, folate, vit. B12 deficiency were
found in 5-10 % of patients
– Association with celiac disease, DC & UC
Etiology Of RAS
 Immunological:
– Evidences are conflicting and not consistent
–
It may be delayed type hypersensitivity reaction
– It may be immuncomplex reactions (vasculitis of local type)
– It may be due to inherent imbalance of the immune
regulation that results in disturbance in the ratio between
T4 & T8
Etiology Of RAS
 “ From different studies, even though some
of the evidence has been conflicting, it
appears likely that aphthous ulceration
results from focal immune dysfunction in
which T lymphocytes play a significant role.
The nature of the initiating stimulus remains
a mystery. The causative agents could be
endogenous ( autoimmune) antigen or
exogenous (hyperimmune) antigen, or it could
be non specific factor such as trauma in
which a chemical mediators may be involved
Clinically three stages of the ulcers may be
seen:


II- Pre-ulcerative stage: prodromal symptoms
o
Lasts for 18-72 hrs
o
Paraesthesia
o
Red macule
II- Ulcerative stage:
o
Gray round to oval white primary ulcers surrounded by
erythematous hallo

III- Resolution stage:
o
Less pain
o
Epithelial regeneration
 Aphthous ulcers are primary ulcers
 on clinical bases they are classified
into:
 minor type (80%): less than 1 cm & heal
without scar, are round, shallow that persist for
10-14 days
 major type (10%): more than 1 cm, lip & soft
palate, patient is rarely ulcer free, heal with
scar, interfere with eating and speech
 herpetiform (10%) type: recurrent crops of
dozens of ulcers that coalesce together, may
resond to 2% tetracycline moutwash
Compare between the size of
major & minor aphthous ulcers
D.D :
 Recurrent herpes
 CMV infection in immunocompromised patient
 Behçet syndrome
 MMP
 Pemphigus
 Trauma
 Rule out systemic disease: CD, celiac disease
 Major aphthous ulcer
that mimic SCC
Investigations: of aphthous ulcers
 The diagnosis of aphthous ulceration is
dependent mainly on proper history & clinical
examination
 It is necessary therefore to enquire about
 eye, genital, gastrointestinal or skin lesions and
 fever;
 some investigations is to be carried out to
rule out any systemic cause/s.
 This is especially important if it appears
suddenly on middle aged and above
 These investigations may include:
 CBC
 Serum
 TIBC
 Serum
 Serum
 Serum
iron
ferritin
B12
folate
 Investigate for celiac or CD if
appropriate
Management of RAU
1. Explain to the patient the nature of
the disease
2. Current treatment aimed at controlling
rather than curing
3. Treatment modalities may include:
A. Mouth rinses:
A. 0.2% chlorhexidine gluconate
B. benzydamine hydrochloride
B. Topical steroids:
Steroid
Dosage
Medium potency:
Betamethasone phosphate tablets
(Betnesol)
0.5 mg ; use as
mouth wash
High potency:
Beclometasone
(Beclomethasonedipropionate spray)
1 puff (200 mg) to
C. Antimicrobial: tetracycline
mouthwash
D. Topical LA preparations
E. Immunomodulators:
a)
b)
c)
d)
Lavmisol
Cholchicine
Dapsone
Thalidomide
F. Systemic steroids:
Management of RAU
4. Local preparations of cyclosporine
5. Soft laser in refractory major aphthae
Management of RAU
6. Treat the systemic disease and
restore deficiency if present:
 Thiamine (vit. B12)
 Pyridoxine (B6)
 Iron supplements
Behçet syndrome
 It is serious disease because the eye &
CNS involvement are quite serious
 Etiology:
 unknown but it is associated with HLA B-51
 immune dysfunction
 viral etiology & vasculitis
Behçet syndrome
Major criteria for diagnosis of Behçet
syndrome include:
 RAS
 Genital ulcers
 Ocular lesions
 CNS lesions
 Skin lesions
Behçet syndrome
Minor criteria for diagnosis of Behçet
syndrome include:
 Arthralgia
 Superficial or deep migratory thrombophlebitis
 Inflammatory bowel disease
 Lung disease (pneumonitis)
 Renal disease: hematuria and Proteinurea
Diagnostic criteria (as suggested by the
5th international conference on Behçet
disease 1990)
1) Oral ulcerations:
–
–
–
aphthous like
not explained otherwise
persisted for at least 3 times over the last year
2) Any two of the following:
– Genital area: recurrent genital ulceration
– Eye lesions: retinal vasculitis/ ant. or posterior
uveitis and optic neuritis ( eye and CNS are quite
serious)

Inflammation of the eye, which can involve the front of
the eye (uvea) causing uveitis, or the back of the eye
(retina) causing retinitis, can lead to blindness. Symptoms
of eye inflammation include pain, blurred vision, tearing,
redness, and pain when looking at bright lights. It is very
important for patients to have this sensitive area
monitored by an eye specialist (ophthalmologist).
– Skin: erythema nodosum or acniform lesion &
positive pathergy test result
Behçet syndrome
3)
C.T disease, Reiter’s disease, inflammatory bowel disease must
be excluded before making diagnosis of Behçet disease
4) Other features considered to be useful in confirming the
diagnosis of Behçet disease:
– CNS features: similar to MS
– Other features:





Deep venous thrombosis
Subcutaneous thrombophlebitis
Epididmitis
Arthritis
GIT ulcerations & aneurysmal formations
Eye lesions in Behçet disease
Erythema modosum
Behçet syndrome
 D.D:
– Reiter’s syndrome
– Sweet syndrome: oral ulcers,
conjunctivitis, episcleritis and inflamed
tender skin papules or nodules
– CT disease
– inflammatory bowel disease
Investigations:
– CBC: leukocytosis, eosinophillia
– Raised ESR, raised CRP and acute phase
protiens
– CNS investigations
– GIT to exclude inflammatory bowel disease
 Behçet syndrome has POOR PROGNOSIS
Treatment:
 Topical steroids
 Colchicine 0.6 mg bd ( inhibit the
effect of leukocyte migration)
– Get the approval of FDA in 2009
– it is mainly used for gout
 Systemic steroids
 Steroid sparing agents:
o Azathioprine
o Cyclosporine
o Cyclophosphomide
o Interferon-
 Management of eye lesions
Reiter's syndrome
Etiology:
 unknown but probably post infection
(GUTI)
 associated with HLA-B27
Features of Reiter's syndrome:
 young males
 fever, malaise & weight loss
 migratory polyarthritis
 conjunctivitis & uveitis
 urethral discharge (sterile, non gonococcal
urethritis)
 keratoderma blenorrhagica
 circinate balanitis
 aphthous like ulcers
 geographic tongue like lesions
 Features of Reiter's
syndrome:
 young males
 fever, malaise & weight
loss
 migratory polyarthritis
 conjunctivitis & uveitis
 urethral discharge
(sterile, non gonococcal
urethritis)
 keratoderma blenorrhagica
 circinate balanitis
 aphthous like ulcers
 geographic tongue like
lesions
• Keratoderma blennorrhagica (or keratoderma blennorrhagicum) are skin
lesions commonly found on the palms and soles but which may spread
to the scrotum, scalp and trunk also, and which resemble psoriasis.
• Keratoderma blennorrhagica is commonly seen as an additional feature
of Reiter's syndrome in almost 15% of male patients.
• The appearance is usually of a vesico-pustular waxy lesion with a
yellow brown colour.
These lesions may join together to form larger crusty plaques with
desquamating edges.
D.D:
– Behçet syndrome
– GIT inflammatory conditions
– Psoriasis : keratotic scaly lesions,
arthritis, geographic tongue like lesions(
clinically & histopathologically)
Treatment:
 no specific treatment
 NSAID
 antibiotics
An approach to diagnosing oral ulcers
 Oral ulceration is probably the commonest oral
mucosal disease seen; it may also be the most
serious
 It is important, therefore, to have an approach to
the management of oral ulcers firmly established in
your mind
 is the ulcer single or multiple?
 is it persistent or recurrent?
 is it primary type or preceded by blister?
An approach to diagnosing oral ulcers
 Where is the site and distribution?
 Is the size enlarging?
 Onset?
 Duration and chronicity? >3 weeks after cause
removal do biopsy
 Pain and bleeding?
 Aggravating and relieving factors?
 Any associated phenomenon
Examination and describing an ulcer
should include
– Size
– Site (anatomical locations)
– Shape
– Base
– Edge
– Induration
Examination and describing an
ulcer should include
– Discharge
– fixation
– Is it painful?
– Lymph drainage
– General condition of the patient
D.D of ulcers: depends on etiology:
consider (TINNDVIM):
 T traumatic
 I infective
 N neoplastic
 N nutritional
 D degenerative
 V vascular

I immunological

M metabolic
GDP have to refer Patients with oral ulcers
into OM specialist in:
– Patients with ulceration unresponsive to topical
therapy;
– Suspected Malignancy;
– HIV-related ulceration;
– Syphilis;
– TB;
– Drug-related ulceration;
– Systemic disease;
– Mucocutaneous disorders.