Professional Documents
Culture Documents
Oral ulceration
Announcement:
From now on the oral medicine lecture will be at 12:30 and the radio lecture
at 1:30.
Let’s start:
Our lecture today is about ulceration this is just to remind you how an oral
ulcer looks like, I found that there is a problem for some students to diagnose
or identify the oral ulcer.
In oral ulcers there must be brake in the integrity of epithelium, yellowish or
pale color of the mucosa, erosion, abrasion is not enough to call it ulcer,
Fordyce’s granules, perulis in the gingiva might have yellow color but they are
not ulcers, again erosion, abrasions in the buccal mucosa this is not an ulcer it
is just abrasion or erosions. In ulcers as we said there must be complete
removal of epithelium, complete sloughing of epithelium exposing the
connective tissue, this is an example of an ulcer, you found that there is a step
between the ulcer and the normal mucosa.
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Diagnosis of oral ulcers:
In the oral cavity several lesions might look the same making it difficult to
diagnose; so to be able to differentiate between the different lesions we relay
as always on:
1- HISTORY:
• Recurrence: You need to know if this is the first time the patient is having
the ulcer, if it is recurrent or not, if there is certain pattern in this
recurrence like every month or several weeks or three to four times per
year so this should be mentioned.
• The age of onset: when this ulcer started (very long time ago, since
childhood or adult age, or its very late onset)
• The distribution of ulcers: where it is located; is it in the movable part of
the oral mucosa or the attached one, the keratinized or the non‐
keratinized, all these will help us to know different types or diagnosis of
the recurrent oral ulcers.
• Family history: the presence of family history will also help in the
diagnosis.
• Pattern of ulcers: if it has certain appearance like irregular or round
shape, the size of this ulcer, all these should be asked during taking the
history.
• Associated systemic and oral signs/symptoms:
For example if there is fever accompanying the presence of the ulcers, or
the patient is not feeling well or having malaise during these episodes of
ulcers, if there is any other symptoms associated with these ulcers
particularly, we ask the patient about GI problems, skin lesions or genital
ulcers. All these should be asked if the ulcers are associated with oral
lesions like for example if they started as vesicle then rupture forming an
ulcer.
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2- EXAMINATION:
• Fever/malaise: You need to check if the patient is feverish, if he is
not feeling well.
• Ulcers: you need to check for the ulcer, if it is well defined, single or
multiple ulcers joined together.
• Scaring: you can notice if there is a region of scaring, particularly for
patients with major aphthous ulcers, or for sever traumatic ulcer,
sometimes it heals with scaring. You can see during examination like
swallowing in the tongue or the soft palate showing the site of the
scar.
• Other intraoral changes(vesicles or striations):
Presence of oral striations accompanied with the ulcer, or vesicles at
the site where these ulcers are around the oral cavity, in the buccal
mucosa, tongue or the hard palate.
3-SPECIAL INVESTIGATIONS:
Sometimes history and examination are enough to get in to a
diagnosis, other times I need to do certain investigations like blood
testing or other to get to a definitive diagnosis of the recurrent
ulcers.
• Blood testing: is very useful for diagnosis of oral ulcers because
several conditions like anemia and decrease in the white blood cells
can be presented as oral ulcers. So we usually do CBC (complete
blood count), serum/red cell foliate, serum B12, and serum ferritin
and erythrocyte sedimentation rate (ESR) if we are expecting the
presence of either infection or immune mediated disorder.
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• Anti‐ gliadin and anti‐ endomysial auto antibodies:
We use this particular test for testing immunoglobulin in case of
celiac disease, so if we are suspecting celiac disease like the
presence of diarrhea or other GI problems we might do this test,
usually we send the patient for internist or GI specialist to do the
testing and endoscopy to examine if the patient is having a celiac
disease.
• Biopsy: Finally we might have to do a biopsy to confirm our
diagnosis particularly for long standing lesions.
We know now how the oral ulcers looks like, we know that it might be
single or multiple, it might appear once or it might be recurrent, the
recurrent could have certain pattern, there might be family history, so we
know all the things we need to look for while examining and taking history
from the patient.
Now what are the options I have, what I need to have in my mind while
examining the patient?
1‐ Traumatic ulcer:
The first thing that comes to our mind is traumatic ulcer as it is the most
common cause for the ulcers.
2‐ Microbial infection:
Like Syphilis can be presented as ulcer, TB particularly in the tongue can
appear as long standing ulcer, herpes it might appear like ulcer, so we
have different diagnosis.
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3‐ Recurrent aphthous stomatitis (RAS)
4‐ Mucocutanous disease
5‐ Systemic disorders
6‐Drug therapy: as a side effect of taking certain drugs.
Now my task would be how I can suggest one of these diagnoses to be most
likely is the diagnosis of the ulcer.
We will talk about each of them particularly traumatic and RAS, we will talk
about them in details in this lecture, other causes will be discussed when
we talk about GI or blood disorders, and we will know how we can make
the most likely diagnosis.
1- TRAUMATIC ULCER:
History:
Usually the patient report mechanical, thermal or chemical injury, I
noticed in the clinic that students don’t rely on the history, when they see
an ulcer the first thing that comes to their mind is squamous cell
carcinoma, and if the patient is smoker it will become a definitive
diagnosis, and they forget completely that taking history will solve almost
like 85% of the problem.
Patient came to the clinic and during the routine examination they found
ulcer in the floor of the mouth and it was in the healthy stages start to re‐
epithelilized again, the first thing that comes to the students mind was
squamous cell carcinoma, speckled leukoplakia but they forget
completely to ask the patient do you have any trauma in this site, and it
was burning in the floor of the mouth due to hot tea, so you need to ask
the patient if there is any mechanical or chemical trauma like aspirin
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burns or any material they put in tooth to relief its pain like zanjabeel its
irritant and might cause ulcers in the oral mucosa, so in the history we
can identify traumatic ulcer.
Examination:
it’s painful and sore and the borders could be irregular, it depends on
how the trauma took place and it would coincide to the cause of trauma,
for example I wouldn’t think of trauma happening like in the gingiva or
the alveolar ride it’s not very common site for trauma unless the patient
report how the trauma took place.
But for example the tongue, buccal mucosa are very common sites for
trauma & we need to match if the cause of trauma is really coinciding
with the site of the ulcer, for example, here (pic) there is an ulcer in the
lateral border of the tongue & it coincides with this over erupted tooth,
so the provisional diagnosis most likely will be traumatic ulcer.
Q: in the picture it doesn’t appear that the over erupted tooth is the
cause??
A: here while you are examining you ask the patient to protrude his
tongue & you see the ulcer, you expect that this outstanding tooth
is the cause of the ulcer, when the patient relaxes, puts his tongue
back; it comes next to the tooth.
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Management:
1‐ Remove underlying cause, like sharp edges or broken tooth.
2‐ Prevent secondary infection by giving chlorhexidine mouthwash.
3‐ Review patient after 10 days, the ulcer should be either healed or very
close to the healing state; if there is no improvement at all for traumatic
ulcer it’s very necessary to take a biopsy to know what is it.
FACTITIOUS ULCER is again traumatic ulcer but the patient is causing
this trauma to himself like self injury, or harming himself usually the
patient give vague history you can’t rely on his history, contradicting
facts while taking the history and of course he denied doing any harm or
traumatizing himself, usually you see it is a solitary ulcer and it is
accessible site of the patient, most of the time it’s the gingiva, the
tongue, buccal mucosa or labial mucosa and the management of course
is like any ulcer it should be managed by chlorhexidine mouth wash and
if the patient comes back with ulcer he need to be followed up by a
psychiatric.
‐It’s the most common oral mucosa disorder.
‐ Its acute and extremely painful, it is size don’t indicates how painful it
is.
‐ Usually it involves the non keratinized oral mucosal site; it is the major
point to differentiate the recurrent aphthous stomatitis ulcer from
herpes ulcers. We agreed that herpes ulcers usually appears in the
keratinized sites particularly the hard palate and the gingiva, but RAS will
never appear at these sites, usually in the mobile parts, buccal mucosa,
tongue, floor of the mouth, soft palate it may interfere with eating,
drinking or swallowing, particularly the lesions or the ulcers in the
tongue they are extremely painful and they will alter the patient speech
and eating.
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‐ They are classified according to their size in to minor, major and
herpetiform and according to weather they cause scar or not.
‐Taking history again is very important, it is recurrent, usually it affect
young age group even children might be affected with recurrent oral
ulcers, but the peak incidence of RAS is among teenagers.
Again three forms of the lesions (major, minor or herpetiform) and there
is no associated systemic signs or symptoms, this is the major point in
diagnosis recurrent ulcers, when you give a diagnosis of RAS in other
word you are saying that you excluding any hematic deficiencies, GI
problems any underlying or related mucocutanous disorders, the only
thing the patient is having is recurrent oral ulcers, so we don’t reach the
diagnosis of RAS until we exclude all other possibilities.
‐In examination these are the 3 forms that you can see in the oral cavity.
The minor are the most common, the size is less than 1cm in diameter you can
see here the yellowish base of the ulcer and the erythematous margins and of
course it heals without scaring.
The major type is the most problematic, it can occur again anywhere but most
of the cases took place in the soft palate, oropharynx which makes it very
painful for the patient; it last for more than 14 days or may be longer, and it
heals with scaring. So you might notice the scars in the soft palate you find the
uvula a bit deviated due to scaring, if there was an ulcer in the soft palate.
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The herpetiform is the least common type of ulcer it’s called herpetiform, it
has nothing to do with the herpes simplex virus but because of the appearance
of small ulcers, it was named herpetiform ulcers, it appear in huge numbers,
and some of them come together and form one big ulcer, it is different than
the minor ulcer, you see this has irregular shape or irregular borders because it
is composed of several or many ulcers all together. It appears in the lip, tip of
the tongue; these are the commonest site for herpetiform ulcers.
Etiology:
Its idiopathic we diagnose it by excluding any other systemic causes or
haematic deficiencies.
The etiology of this disease is not yet known but we know it’s one of the
complex diseases, we mean by complex that the cause is not well identified
and it has many or several factors causing the disease;
1‐ genetic factor: several pleomorphism or mutations in the cytokine,
interleukin 1 , 10, TNF all these cytokines mutations is more common in RAS
patients than the others, this might explain the more active immune
reactions or hyper activated immune system.
2‐hormonal: could be another cause and it might explain why during
puberty the recurrent ulcers increase, pregnancy and menstruation might
also affect the recurrence rate of oral ulcers.
3‐ Hyper sensitivity: for example hyper sensitivity for food might induce
recurrent ulcers.
4‐ Microbial: like viral or bacterial infections might acts as trigger not a
cause for the disease.
5‐ Stress, smoking cessation
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All these factors might contribute to recurrent aphthous stomatitis, so
the problem in RAS patients that they have a hyperactive immune system
that can be provoked by any minor trauma which in normal individuals
does not cause any problems.
Again in herpes disease the ulcers are formed because of the disease, this
is only in research like for example they found the viral load in affected
individuals with RAS is higher than the normal individuals, but there is no
direct relationship between the virus or ulcers, all what they do is to act
as a trigger stimulating the excited immune system to initiate this lesion.
You should know the difference between auto immune and immune
mediated;
In auto immune disease there is antibodies against a particular tissues
causing the disease, while in immune mediated there is no antibodies
specific to it, for example the oral mucosa there is no specific
immunoglobulin or antibodies but there is a deregulation in the immune
system like hyper active T cells causing the immune reaction, increase the
production of cytokines as a consequence to any minor trauma, stress or
minor stimulation might provoke this immune reaction.
So it is not an auto immune disease but it is an immune mediated.
Pre ulcerative ulcerative
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Histologically: it’s divided into three stages: pre ulcerative, ulcerative and
healing phase.
This is the pre ulcerative stage , you can see the epithelium is intact, there
is no brake in the epithelium but we can see the huge number of
lymphocytes aggregates in the CT and initiating an inflammatory reaction,
this is what we mean by immune mediated there is exaggerated immune
response.
This is the ulcerative stage where there is brake in the epithelium
exposing the CT, notice the huge number again in the T cells.
We agreed that RAS is idiopathic not related to any other condition, but
there are different lesions or conditions that might be presented with
ulcer in the oral cavity, they are very similar to RAS and clinically we can’t
distinguish between these ulcers, they exactly look like RAS, but the
problem that they are related systemic cause for example:
1‐ Nutrition deficiency like anemia, decrease in vit B12, and decrease in
foliate or iron all of these might induce recurrent oral ulcers, they might
be recurrent in nature and clinically they will look exactly like recurrent
aphthous stomatitis either as minor, major or herpetiform.
2‐GI disease like celiac or crohn disease we will take about them later in a
separate lecture about GI problems, so if you suspect any GI problem like
diarrhea or sensitivity to certain type of food we have to refer the patient
to GI specialist to confirm the diagnosis.
3‐Cyclic neutropenia which is common in children that have a periodic
time where the neutrophil number goes down, during this stage they
have eruptions of the ulcers, fever, malaise, they are not feeling well and
then they will go back to normal. Its repeated like every 3 to 4 weeks, so
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if there is pattern of ulcer in a young child every month this child is having
recurrent ulcers episode, and is associated with fever, or may be the
mother will describe it as if the child is having a common cold, so we must
suspect cyclic neutropenia and we need to refer the patient to internist
for follow up.
5‐Systemic conditions like MAGIC (mouth and genital ulcer with inflamed
cartilage) or PEAPA (periodic fever, aphthous ulcer, pharyngitis and
cervical adenitis), so if there is any association of RAS with other lesions
the patient should be referred to a specialist to diagnose the condition.
‐NSAID (Aspirin is not NSAID as the Dr said), Ibuprofen declevicerate
sodium (As I heard)
‐necorandil which is potassium channel activator used for angina again
this drug might induce RAS.
‐methotrexate is immune modulator and used as a part of chemotherapy
all these medicating might induce RAS.
If during history we suspect GI problems or the patient is having any of
these drugs, any other accompanied symptoms we can’t diagnose it as
RAS, the diagnosis will be confirmed by the specialist.
A student asked but I couldn’t hear the question but this is the answer
Hyper active immune response, we know that immune response is very
important to protect the body against pathogens but when the immune
system become hyperactive it start damaging the self cells like in auto
immune disease, the difference between the auto immune and immune
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deregulation is in auto immune there is antibodies specific for example to
kidney tissues causing glomerulonephritis but in immune deregulation
there is exaggerated immune response most of the cases its cellular
immune response and it is generalized.
Another question that I couldn’t hear, but this is what the doctor said:
HIV? You mean it should be in the HIV infection, any way there is
deregulation in the immune response we agree that CD4 T‐cells are
suppressed but it is presented by aphthous ulcers, it is the most common
feature in Aids pts to have RAS like lesions and usually they are persistent,
probably because of the deregulation in the immune system.
Management of RAS:
First of all we need to confirm our diagnosis that it is RAS not associated
with any other condition, when the patient come to our clinic we usually
do blood testing particularly ferritin, B12, Iron, serum and red blood cell
foliate we check these first to exclude any blood disorders or hematic
deficiency that might cause the ulcer, then if it is normal and we are not
suspecting any systemic condition at this case we start our treatment.
The therapy depends on how sever are the symptoms, and if the patient
is managing or getting well in spite of these symptoms, also how
frequent the ulcers are and the location of these ulcers.
Treatment options:
1‐ Not providing any treatment for the pt if the attacks are very
infrequent and they are like minor not causing great problem or if the
patient is getting used to it, you know that the pain threshold is different
between people so some people can manage with the minor ulcers and
it’s not causing any problem for them.
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2‐ Prevention of possible causes or treatment of possible causes like for
example sensitivity to sodium lauryl sulfate (SLS) that is present in the
tooth paste we might ask the patient to change the tooth paste, having
which is free from the SLS to remove any irritants, good oral hygiene, ill
fitting prosthesis should be repaired because all these will cause minor
trauma which might initiate an inflammatory reaction and then aphthous
ulcers.
3‐If prevention doesn’t improve the condition of the patient, topical or
systemic therapy could be used and referral if there is a sever condition
that can’t be managed in the clinic.
One main point is usually the patients scared when they have recurrent
ulcers particularly the major type of ulcer, and you need to assure them
that this condition is benign not going to develop into something serious
like cancer, it is not an indication for cancer.
We had a female patient like 40 years old she is been moving and going
to several doctors, Internist, general practitioners and specialists for her
recurrent oral ulcer and I don’t know whether they knew the diagnosis or
they could not confirm that diagnosis but they never talked to her about
it and she thought that she is not improving, because it’s getting worse
and its probably cancer and it is spreading. When we talked to the
patient we did the blood testing and everything was normal. The only
complaint for her was the recurrent oral ulcers. we reassured her that it
is common disease and it’s not going to get worse and all our treatment
will be just how to manage during the presence of these ulcers and there
is no treatment to prevent them from coming back and if they come back
this doesn’t mean that its bad signal or its going to develop into
something serious.
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So reassurance is a major part of your treatment, sometimes the patient
come to the clinic not because he is in severe pain, it may be because he
is very worried so you need to reassure him that it is not serious and
your treatment will be just to reduce his pain or make him able to adapt
in the presence of oral ulcers.
Topical therapy:
1‐ Mainly Chlorhexidine month wash.
2‐ Analgesics they are useful for patients who complain from severe
pain like lignocane rinses, particularly before eating Benzydamine
hydrochloride.
3‐ Covering agents like orabases or aloclaire you remember that we
said they provide a layer over the ulcer.
4‐ Corticosteroids either hydrocortisone succinate 2.5 mg dissolved
in water and the patient use it as a rinse 4 times daily, its good
particularly for the lesion in the soft palate where it is difficult to get
using the orabases.
Tiramcinolone acetonide again we use it in treating ulcers but
usually patients don’t like it because it’s very sticky, your advice
would be for the patient to get benefit from this drug is to use a
gauze and apply the paste on the gauze and put it directly in to the
ulcer and leave it for 15 min on the ulcer to have its action, then the
patient can remove the gauze and stop eating or drinking for about
half an hour to keep the effect of steroids in the mouth, he has to
use this 4 times daily, and the most important one is just before
going to sleep because it will have the effect all the night, it is very
good medication particularly if there is one or two ulcers.
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Steroids have tow effects:
1. 1‐ Anti‐inflammatory action modifies progress of ulcer at all stages
2. Blocking effect of T lymphocyte – epithelial cell interaction in pre‐
ulcerative stage
So it has the ability to block the accumulation of t lymphocytes in the CT,
and to have this effect the medication (steroids) should be applied in the
pre ulcerative stage before these lymphocytes aggregate, if we take it
after aggregation it will have only the anti inflammatory effect, so your
advice to the patient is to use this medication as soon as the symptoms
start, usually it starts as tingling sensation and then it will progress in to
ulcer which will increase in size.
So the patient should get used on how to use the steroid medication, he
should have the oral rinse ready with him whenever he start feeling the
tingling sensation he should take the medication immediately to avoid
the enlargement of the ulcer.
5‐ Antibiotics:
Tetracycline / chlortetracycline (250mg cap in 100ml water), and it is used
as a rinse, it very good for herpetiform type of ulcers; it improves greatly
using this type of antibiotics.
In topical medications you need to be aware that medications effective
only when they are at the ulcer site so the patient need to have the
medication as longer as possible and gets applied as we said after meals
and bed time.
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Systemic therapy:
1‐prednisolone: there is something called burst therapy, we use it to
treat oral ulcer (5‐20mg once in morning for 5 days).
You know steroids should be given once in the morning to mimic the
peak of the steroids naturally produced in the body so we give this 20mg
steroids prednisolone tablets once in the morning for 4‐5 days in this
case it doesn’t need any tapering not like the steroids when it’s taken for
a long duration.
2‐ immonomodulators which we don’t use or relay on in the oral
medicine because they need follow up like azathioprine, colchicines,
thalidomide which was removed from the pharmacies because of its
teratogenic effect, now it’s back but it should not be given for any female
in the pregnancy age, and also it affects the peripheral nerves so the
patient should be tested for the conductivity of the peripheral nerve
every 3 months, so these immune modulators we don’t prescribe them,
they are left for the medical doctors who can observe and they are used
on dealing with these drugs and knowing its side effects.
So we talked in details about RAS, now Professor Hulusi Behçet the
Turkish dermatologist who was the first one to describe condition of oral
aphthous ulcer, genital ulcers and uveitis.
‐The aphthous ulcers are exactly the same as RAS could be minor, major
or herpetifprm type.
‐Eye lesions may be conjunctivitis, hypopyon uveitis can you notice here
the yellow color this is the pus, the white blood cells accumulating here
so this is hypopyon uveitis very specific for pehget disease.
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There is no particular test to enable us to diagnose pehget disease, in the
oral medicine books they are dealing with it as very rare disease while
it’s not in our countries as we will mention later.
And diagnosing this condition as we said there is no certain test like
serology test that you can identify the disease, so they relayed on certain
criteria which was approved by the international group for pehget
disease in the 1990, it says to diagnose pehget disease the patient must
have a recurrent aphthous oral ulcers 3 times in a year period and any of
these two either recurrent genital ulcers or eye lesions, skin lesions or
positive pathergy test.
A. Gül
1995 A. Gül
1995
Pathergy test is they insert a needle in the skin, in normal individuals it
should not have any effect because it is sterile but in these patients it
induce a reaction showing a pustule, here the reason why because the
immune reaction again is like recurrent aphthous ulcer is deteriorated
hyperactive immune system, so any cuts or wounds in the body of the
patient might provoke a sever immune reaction.
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As we said its very common particularly in our region here turkey, Jordan
and again in Japan its all the way in this region where the disease spread
it said to be started in the far east and spread to the middle east (turkey)
through the ancient silk road trips, particularly because they inhabited in
this regions, got married so it spread like their genes, while in other
areas like in UK, USA its considered as one of the rare diseases.
I think the main problem is there is a genetic susceptibility for the
disease and its spread during these trips.
Prevalence on UK is very rare as we said while in turkey 80‐370 per
100000 was affected and you can see there is family history there are
some families having this disease in Jordan.
Treatment it is Multidisciplinary approach, the pahget patients are not
followed up by a dentist or oral medicine specialist, he must be followed
up by group of specialist, in UK there used to be a pahget clinic where a
dermatologist, primatologist and oral medicine specialist all of them see
the patient.
So usually primatologist follow up these patients, he have the
consultations of the eye doctors or oral medicine to control the eye and
oral lesions, treatment is a systemic therapy, the problem with pahget
disease that it starts during the 20‐30s start like storm very sever acute
symptoms, eye, oral , skin and genital lesions all come together, the
patient might start having oral ulcers for couple of years then all other
symptoms start to appear it will last for couple of years then these
symptoms start to fade.
We need to manage the patient during this time so that he get out of this
storm with the least cost mainly the eye lesions that cause blindness so
usually these patients should be followed up routinely by the eye and
primatologist doctors, ophthalmologist and dermatologist and they are
mainly on different types of medications, the response to medications
differ from one patient to another, corticosteroids are the main
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treatment and other medications are added like colchicines, thalidomide,
azathioprin any of them can be added to control the exaggerated immune
response, after a couple of years it might last for 10‐15 years then these
symptoms starts to fade, and the patients will have only RAS, in this case
the systemic medications are withdrawn and the patient is managed only
on topical steroids for RAS until the condition is improved.
Other causes of RAS will be discussed under other topics.
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ﻟﻤﺎ ﺗﺎآﻞ ﻣﺎ ﺑﺘﺠﻮع وﻟﻤﺎ ﺗﻨﺎم ﻣﺎ ﺑﺘﻨﻌﺲ.2
اﻻﻧﺴﺎن زي اﻟﺒﻨﻲ ﺁدام إذا ﺗﻮﻓﻰ ﻣﺎت.3
وﺑﺘﻤﻨﻰ ﺗﻜﻮن هﺎﻟﻨﺼﺎﺋﺢ دﻟﻴﻠﻜﻢ ﺑﺎﻟﺤﻴﺎة وﺑﻘﺺ اﻳﺪي إذا ﻓﻬﻤﺘﻮ ﺷﻲ ﻣﻦ ﺧﺮاﺑﻴﻄﻲ ﺑﺲ أهﻢ ﺷﻲ اﻟﻨﻴﺔ وﺣﺐ اﻟﻮﻃﻦ
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Big thank for my sweet sister Dandoooon for her help.
Just wanna say hi to my wonderful friends:
Domdom, Jojo, Jumjoma, 3`adoosh, Nour, Nesreen( thnx any way), Ferma, Dana,
Dina, Maram, 3beer,Zain, Mays, Made7a, Do3a2 5alayleh and all the Malaysian
girls, Nour (3ene, hedayo, 2yman, nadya, nadya) 3ean zobayda and all the dof3a.
Your Colleague:
Arwa A. Makhlouf
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