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2- Patients with rrecurring oral

ulcer
1-Recurrent Aphthous stomatitis
A-Minor form
B-Major form
C-Herpetiform
2- Behcet’s disease
3- Recurrent herpes simplex virus infection
A-Recurrent intraoral herpes
B-Recurrent herpes labialis
Aphthous ulcers
Definition:- Painful, single or multiple recurring
ulceration, commonly affect the non keratinized oral
mucosa
Prevalence:- the most common lesions of the mouth after
caries and periodontal diseases

Types

Minor form 80%


Major form 10%
Herpetiform 10%
Age:- childhood and teenagers. Sex:- Females more than males.
Site:- more in non keratinized mucosa and rare on keratinized mucosa
Minor Aphthous ulceration

prodromal
features 24 hours Erythematous Necrosis of
tingling and macule or the covering
burning epithelium
papules
sensation

Healing in
10-14 days by
epithelization
from the Aphthous Sloughing of
margin with Ulceration the necrotic
epithelium
no scar
Minor Aphthous ulcers
Chief complain Rate of recurrence
Frequent: every month
First:- very painful
or every few months.
due to tissue
destruction. Infrequent:- once or
twice every year or
Later on:- 4-6 days, several years.
discomfort due to
decreased tissue In some persons:- there
destruction and the is no ulcer free period.
i.e. development of new
ulcer had reached its
ulcers during the healing
maximum size.
of the previous ones.
Major Aphthous ulceration
prodromal features (periadenitis mucosa necrotica recurrence)
fever, headach,
maliase and Erythematous Necrosis of
regional macule or the covering
lymphadenopathy
papules epithelium

Healing after few


months with scar
due to destruction
of the deep tissues.
A cobblestone
appearance due to
Aphthous Sloughing of
continuous recurrence Ulceration the necrotic
and multiple scaring epithelium
Major Aphthous ulcers (periadenitis mucosa necrotica recurrence)
Chief complain Rate of recurrence
@ Interference with The lesions may last for
mobility of tongue few months, with
and uvula. tendency to form
elevated margin for the
@ Difficulty in eating ulcer.
and swallowing. This
So; it may be mistaken
due to:-
as a malignant ulcer.
• deep destruction.
N.B. several minor ulcers may coalesce
• slow healing. to form larger ulcer more than 1cm but
in this case isn't considered to be MAU
•Scar formation.
Minor aphthous ulcers Major aphthous ulcers
Number 1-6 solitary or multiple

Sites Common on non any where especially soft


keratinized mucosa palate & tonsillar areas
Rare on keratinized
Shape Rounded (lip and cheek) Irregular
oval(vestibules)
Size less than 1 cm larger than 1 cm

Scar formation healing without scarring leave scars formation

lymph nodes No lymph nodes lymph nodes enlargement


enlargement
Depth shallow Deeper in C.T, minor
salivary glands, facial
muscles
Margins Slightly raised, regular and Raised due to edema, shiny
erythematous and erythematous
Floor Covered by grayish or Covered by gray slough
yellowish white fibrinous
exudate
Base Non indurated Indurated
Herpetiform Aphthous Ulceration
The least common variant of RAS. Not preceded by vesicles as HS
Number Multiple (dozen)

Size Tiny pinhead sized (1 – 2mm) may coalesce forming larger ulcer.

Chief Complaint Extremely painful, interfere with eating and speaking

Site Non keratinized mucosa,


Tongue (lateral margin and tip)
Floor of the mouth.

healing Quicker than MAU and MiAU, without scar

duration The whole cycle takes 3 -4 days with the development of new crops,
the whole cycling pattern takes 2 weeks.

Recurrence Rate Frequent:- development of new set of ulcers that overlaps the
previous group.
Spontaneous remission:- occurs after 5 years.
Histopathological features
• Preulcerative stage:- T4 lymphocytes
accumulates in submucosa and around
blood vessels.
• Ulcerative stage:-
@ T8 begin to dominate.
@ Extravasation of RBCs and neutrophils.
@ Mast cells and macrophages are present
in the ulcer base.
Etiology
• Although the primary cause is unknown RAU may
be attributed to:-
1- Hereditary 2- Immunological factors:-
Factors:- A- Cell mediated cytotoxic reaction; these
reactions are against oral epithelial cells.
• Occur more
Mediated by neutrophils, natural killer
frequently in cells and T-cytotoxic cells.
related persons.
B- Alteration of Ts/Th cells ratio.
•Frequent
association with C- Local immune complex reaction:-
MHC class II. antigen +antibody deposited around blood
vessels and activate the complement.
3- Aphthous ulcer may be 4- Recurrence
associated with : precipitated by:-
A- Hematological deficiencies,
A- Trauma.
deficient folate, Vit.B12,
zinc, iron and deficiency in B- Hormonal changes;
circulating neutrophils. decreasing oestrogen and
B- GIT diseases:- ulcerative increasing progesterone.
colitis and Crohn’s disease. During menstruation,
C- Allergic factors:- atopy, drug ulcers fall during
and food allergy. pregnancy and
exacerbated during
D- Behcet’s disease.
menopause.
E- AIDs.
C- Emotional factors:-
F- FAPA syndrome in children increased incidence
less than 5 years during examination
Treatment of RAU
1- RAU secondary to systemic disease:-
As:- @ Chronic inflammatory bowel diseases.
@ Cyclic neutropenia.
@ Behcet’s disease.
@ FAPA syndrome.
@ Aids.
@ Iron and Folate deficiency.
Treatment of the underlying systemic disease.
Treatment of RAU
2- RAU unrelated to systemic disease:-
The treatment is directed toward controlling
rather than curing of the lesion.
First step;- is patient education regarding
the:-
@ Nature of the disease.
@ Clinical course of the disease.
@ Recurrence.
@ Aim of the drug prescribed.
Treatment of RAU
2- RAU unrelated to systemic disease:-
Second step;- active treatment of the ulcers
A- Corticosteroids:-
2- Short course 3- Intralesional
1- Topical steroids:- injection of
systemic steroids steroid:- ulcer
Used for 2 months (for MAU):- 20- resistant to healing
(for MAU) used as 40mg predisone for 5-7 days.
mouth bath or 1.5hrs after arising
10-20mg injectable
aerosol. as single dose for 5 - triamcinolone
7 days reduced to acetonide diluted to
With antifungal drug 0.5-1ml with 2%
10-20mg over the
one week out of every next few days lidocain, used 2-
4 weeks 3times/week
1) Topical corticosteroids
Start with weak preparations
hydrocortisone hemisuccinate lozenges 2.5 mg q.d.s.
0.1% triamcinolone ointment in
orabase q.d.s
0.1% - 0.2% triamcinolone
acetonide mouth wash

Mouth rinse, prepared by the pharmacist from injectable triamcinolone


acetonide and distilled water. The patient is advised to use 5ml as mouth rinse
q.d.s.
this provides:-
* ease of use
* wide spread
*effective application compared with cream or ointments or lozenges.
4- betamethasone 0.1 mg lozenges q.d.s.
5- Betamethasone valerate
aerosol

effective in mild cases


All topical corticosteroids should be applied four times per day
after meal time and at bed time and to take nothing by mouth for
at least one hour after application of the drug
2) systemic corticosteroids
short course of systemic
steroid to supplement the
topical steroid specially in
case of ulceration.
High dose (20 - 40 mg) of
prednisone given as a single
dose daily 1.5 hour after
arising for 5 – 7 consecutive
days, followed by 10 – 20 mg
1.5 hours after arising every
other morning for additional 2
weeks.
3- intralesional steroid
injection:-
Used in resistant ulcers.
2-3 injections weekly
starts 5-7 days after topical
or systemic steroid
therapy.
10 – 20 mg of injectable
triamcinolone acetonide
diluted to 0.5 – 1 ml with
lidocaine 2% because
steroid injection is very
painful.
Treatment of RAU
2- RAU unrelated to systemic disease:-
Second step;- active treatment of the ulcers
B- Tetracycline mouth bath:- C- the dentist should avoid
Tetracycline + nystatin Using silver nitrate, phenol and
(Mysteclin capsules) other caustics in treatment of
aphthous ulcer, this will relief pain
or Tetracycline +
but it delay healing and enhance
amphotericin (Mysteclin healing with scar.
syrup); dissolved in 5ml of
water/3minutes/t.d.s better to D- the patient should avoid
be followed by topical steroids. Consuming irritating
The best line for treatment of substances , it causes pain
herpetiform AU
Summary of treatment of RAU
A- Mild to moderate cases:- B- Severe cases:-
1- Analgesic before eating to 1- Chloretetracycline mouth
releif pain, lidocain gel, or bath followed by potent
benzydamine hydrochloride as topical steroid after eating and
mouth bath. at bed time.
D- the patient should avoid
2- Ora base (sodium carboxy 2- Systemic corticosteroid.
methyl cellulose), topical
steroids, chlortetracycline 3- Intra-lesional injection of
mouth bath/after eating and bed steroids.
time. 4- Dapsone may be tried in
3- Short course of non-steroidal Major AU.
anti-inflammatory drug as adjunct.
iii-Dapsone:-
(Malaria, pneumocystis
carinii and leprosy)
Used in severe bullous –
erosive lesions.
Control T lymphocyte
mediated process.
Modulates the release of
inflammatory chemotactic
factors from mast cells or
neutrophils.
Treatment
1- Treatment of under lying systemic diseases
2- Corticosteroids:
a- Systemic b- Topical
3 -Tetracycline mouth bath.
4-Dentist should avoid irritating substances as
phenol.
5-Patient should avoid citrus fruits & spiced
food.

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