ﺑﺴﻢ ﷲ اﻟﺮﺣﻤﻦ اﻟﺮﺣﻴﻢ 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. 2 | P a g e
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. • Size and number. • Lymph nodes: you need to examine the lymph nodes to see if there is lymphadenopathy associated with the presence of the recurrent ulcers. 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. 3 | P a g e
• 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.
List of differential diagnoses: 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. 4 | P a g e
3‐ Recurrent aphthous stomatitis (RAS) 4‐ Mucocutanous disease 5‐ Systemic disorders 6‐Drug therapy: as a side effect of taking certain drugs. 7‐ Squamous cell carcinoma: the end of my differential diagnoses list. 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 5 | P a g e
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. 6 | P a g e
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.
Recurrent aphthous stomatitis RAS: ‐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. 7 | P a g e
‐ 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.
Minor major herpetiform 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. 8 | P a g e
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 9 | P a g e
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.
RAS like lesions: 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 11 | P a g e
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. 4‐HIV associated aphthous stomatits we mentioned before that in Aids patients when the CD 4 T‐cells dropped below 200 cells, the main feature may appear is RAS and usually it’s very sever. 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. 6‐Drug induced aphthus stomatitis ‐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 12 | P a g e
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. 14 | P a g e
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. 17 | P a g e
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 19 | P a g e
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. ﺗﻤﺖ ﺑﺤﻤﺪ اﷲ ("_") اﺣﻢ اﺣﻢ ﺑﻌﺮف إﻧﻪ ﻧﺺ اﻟﺪﻓﻌﺔ ﺑﺪهﺎ ﺗﺨﻨﻘﻨﻲ واﻟﻨﺺ اﻟﺘﺎﻧﻲ ﺑﺪهﻢ ﻳﻤﻮﺗﻮﻧﻲ وﻓﻲ رواﻳﺔ أﺧﺮى ﻳﻄﺨﻮﻧﻲ ﻋﺸﺎن اﺗﺄﺧﺮت ( ﺑﺲ ﻟِـ اﻟﻐﻴﺎب أﺳﺒﺎب وﻣﺘﻞ ﻣﺎ ﺑﻴﻘﻮل اﻟﻤﺜﻞ اﻟﺼﻴﻨﻲ )إذا ﻋﺮف اﻟﺴﺒﺐ ﺑﻄﻞ اﻟﻌﺠﺐ.. اﻟﻤﺤﺎﺿﺮة آﺘﻴﺮ ( وﺗﺮﺟﻤﺘﻪ ﺑِـ اﻟﻌﺮﺑﻲ )ﺗﺸﻦ ﺗﺸﺎن ﺗﺸﻲ آﻞ ﻣﺎ أﺷﺘﻐﻞ ﺑﻮاﺣﺪ ﺑﻴﺨﺮب ) أو اﻳﺪي اﻟﻔﺎﻳﺮوس.. infection اﻟﻈﺎهﺮ إﻧﻪ اﻟﻼﺑﺘﻮﺑﺎت ﺻﺎﺑﻬﺎ.. ﺑِـ اﺧﺘﺼﺎر ( اﷲ أﻋﻠﻢ .. اﷲ ﻳﺨﻠﻴﻨﺎ أﻻء ﻋﻤﺎﻳﺮة اﻟﻠﻲ أﻧﻘﺬﺗﻨﺎ ﺑﺂﺧﺮ ﻟﺤﻈﺔ وأﻋﻄﺘﻨﺎ ﻻب ﺗﻮب ﺳﻠﻴﻢ : اﻟﻌﺒﺮة اﻟﻤﺴﺘﺨﻠﺼﺔ ﻓﺎﻧﻮس100 اﻟﻤﻨﺤﻮس ﻣﻨﺤﻮس وﻟﻮ ﺿﻮوا ﻟﻪ.1 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 ("_") 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 20 | P a g e