OM Sheet #6 By Khaled Rashaydeh

View previous topic View next topic Go down

OM Sheet #6 By Khaled Rashaydeh

Post by Sura on 31/10/2012, 1:58 am

avatar
Sura

عدد المساهمات : 484
النشاط : 2
تاريخ التسجيل : 2010-09-29

Back to top Go down

Re: OM Sheet #6 By Khaled Rashaydeh

Post by Shadi Jarrar on 15/11/2012, 6:46 pm

Oral white & red lesions
*Fordyce’s granules :

-it’s normal anatomic variation ,it’s sebaceous glands without hair follicles.

-etiology :developmental anomaly.

-whitish yellowish raised papules . the most common sites on buccal mucosa & it become prominent during puberty . increase in number & size with age .but eventually it goes away.

-80% of population are affected , mostly 1-2 on buccal mucosa or upper lip , but some people have hundreds of fordyce’s granules ,so they afraid from that & go to doctor to take biopsy , imagine that !!!!!!!!!

-upper lip more than lower lip

-buccal mucosa around the papillae

-diagnosis :clinical ,no biopsy .

-treatment : - eventually they go away with age.

-there is medicaments for esthetic reasons only like when they are on the borders of upper or lower lips , there is Tretinoin gel or cream which more favorable ,preferable to be in combination with alpha hydroxyacid agent.

-other treatment options : 1- Trichleroacetic acid (TCA) chemical peel ( دهون)

2- CO2 laser or electro desiccation

3- pulse dye laser but it’s expensive

4-surgical diathermy

But the most perfect one on dr’s opinion is Tretinoin gel.



*Leukoedema :

-anatomic variation usually in children (3-5 years of age) but noticed during adolescence .

-it’s developmental anomaly ,opalescent thin whitish layer that covers the buccal mucosa bilaterally on (right & left ) & it’s intracellular oedema thickened epithelium , so as a result of thickened epithelium it’s developmental not pathological ,& may it give wrinkled surface & the most important about the leukoedema that when you make stretching for buccal mucosa outwards it will disappear & that’s how we diagnose it .

-diagnosis :clinically

-leukoedema have ill-defined border & it’s mingled with mucosa ,while leukolplakia have sharply defined borders & that how we differentiate between leukoedema & leukoplakia.

-treatment :-no treatment -does not change with age

-may be affected by smoking , because more pronounced , & may become less pronounced when stop smoking.



*White sponge naevus :

-rare, the most important about it that it’s inherited lesion , so that several members of family are affected , so that help us in diagnosis, so it’s developmental anomaly but it’s inherited

-clinically :it affects more the buccal mucosa bilaterally & may be on the floor of the mouth & usually it’s well-demarcated not like leukoedema , thick corticated wrinkled whitish lesion & it’s adherent ( we can not remove it ), & if it’s stretched it’s does not go away , so this is inherited & there is nothing to do with it .

-diagnosis : clinically diagnosed & from family history .but if we are not sure , it may be leukoplakia but leukoplakia is more whitish while the white sponge naevus is grayish white & the two are well-demarcated .

-white sponge naevus widely spread & diffuse while leukoplakia more discrete .

-painless asymptomatic but it’s appearance not esthetic .

-treatment : assurance (no treatment for it )

-incision biopsy if we are not sure if it leukoplakia or not.



*Linea alba buccalis :

-it’s a frictional keratosis , linear white line that extended from the corners of the mouth back to the retromolar area opposite to the occlusal plane of the teeth.

-frictional keratosis due to sucking trauma especially in who have fatty cheeks or very stressful people , it’s benign lesion .

-it’s just in dentate people

-assurance (no treatment )

-clinically diagnosed .



*Lip & cheek biting :

-mild chronic biting , chewing, sucking of the mucosa or lip (labial mucosa ) or buccal mucosa anteriorly .

-mostly lower lip & commissural areas intaorally.

-actually it’s stress related habits affect more the females , so it’s self-inflected injury . Newly they talk about genetic background (genetics about stress not lesion )

-we see erosions (no ulcers) , so macerated area of mucosa & also have redness , may it give burning sensations in severe cases & swelling & tenderness & ragged borders (mucosa مقطعة من chewing or sucking )

-clinically diagnosed .

-the most important thing to warn the patient that it’s habit & he must stop the habit but in severe cases we can make splint or dental guard on upper teeth & also in severe cases we can refer the patient for psychological analysis.

-chlorahexidine or hexitidine , if there is burning & to prevent inflammation ( hexitidine more preferable although it’s effect less than chlorahexidine but it does not stain the teeth black)

-example of chlorahexidine (hexana ( اردني), corsodyl (اجنبي )

Hexetidine (hexedene (اردني) , oraldene (اجنبي )









*Leukoplakia :

-the most important one in oral white lesions

-potentially malignant lesion (can convert to malignancy )

-WHO definition “it’s a clinical term (any lesion that can’t be rubbed off & can’t be identified clinically or pathologically as any other disease.

-3% of population in the world are affected

-affected people age (40-70 years old )

-etiology : -most important one is tobacco use (smoked or chewed )

-sharp edges of a teeth ( chronic irritation makes hyperkeratosis ) ,HPV (human papilloma virus ), Candida albicans , alcohol consumption

-bloodroot (الشمندر)(sanguinaria )is also associated with leukoplakia.

-most common sites (buccal mucosa ,floor of the mouth , tongue ), & may be on mandibular alveolar ridge more than maxillary alveolar ridge.

- (3-33% ) of leukoplakia cases turns into squamus cell carcinoma in period of 10 years < so leukoplakia must be treated & followed up.

-types of leukoplakia depends on clinical appearance , it varies from thin , raised whitish black to papillary ,indurated or warty

-clinically we divide it to high & low risk , but from it’s clinical appearance & it’s site , I can know if it’s high potentially or low potentially malignant lesion .

1- homogenous leukoplakia (low risk malignancy ) : uniformaly white patch ,well-demaracted ,discrete (not all buccal mucosa )

2- homogenous leukoplakia (high risk malignancy ).

Slide # 22 of oral white & red lesions slides

“homogenous leukoplakia ,but this is tongue anatomy the lesion is not indurated or papillary , so notice how it’s whitish in color & well-demarcated & this lesion is low risk bcz of site .

While in slide #23 : (sublingual keratosis ) is homogenous leukoplakia but it’s high risk .why ? bcz of site )

-sublingual keratosis affect floor of the mouth or ventral surface of the tongue bilaterally & it’s homogenous , & it’s high risk bcz they think there is stasis in these regions , so there is lesion & oncogenic microorganisms that enter & makes the lesion at high risk.

-Question by student : what’s the meaning of homogenous ?

It’s not papillary , not warty,not indurated , not thick ,it’s uniform lesion & it’s a whole piece (قطعة واحدة متساوية) , but most important about it that it’s well-demarcated.

-tobacco use & alcohol consumption are the main factors.

Slide # 24 : this homogenous ( sublingual keratosis ) but it’s dead .

Slide # 25 (proliferative verucous leukoplakis ), mostly affect elderly women , why ? unknown , it affects more the mandibular alveolar ridge than the maxillary alveolar ridge , & it progress by spreading laterally , & it becomes high risk lesion converted to either verrucous (or papillary )carcinoma (مثل رأس الزهرة (القرنبيط)) or speckled leukoplakia ( means it means white & red lesion together )

-Diagnosis : biopsy , from where I take it --à if there is thick & thin areas we always take it from the thick part bcz squamous cell carcinoma will be presented clinically as thick whitish black , so when we take a biopsy we take it from the thick , the papillary or warty areas bcz it’s more dangerous than the homogenous flat one.

Note: usually homogenous is always low risk except in sublingual keratosis what determines it’s low or high risk is the site.

-slide # 28 this is commissural area ( a triangular area ) , there is a lesion (white blacks & intermingled & between them there is red fossae )àspeckled leukoplakia.

- risk ( from low to high ) :

White lesion-àspeckled lesion -à red lesion

-speckled leukoplakia not just high risk lesion bcz it comes from verrucous leukoplakia but also it usually it’s infected with Candida albicans , so routinely when I take biopsy from any leukoplakia ( ask for gram stain to show if there is candidal hyphae invading superfacial layers or not .why it’s important ? bcz any mucosa invaded by candida albicans is more susceptible to transform into malignancy (candida albicans (oncogenic organism ))

So any white lesion ask for gram stain , bcz any invasion of hyphae makes the lesion more dangerous of candida albicans

If homogenous lesion without candida àlow risk

If homogenous lesion + candida albicansà high risk despite of clinical appearance

- Candidal leukoplakia it is more in smokers , but also we can see it in non-smokers due to vitamins deficiencies for example.

- In Europe bcz they can’t smoke tobacco they chew it < so they put tobacco in mucobuccal fold , so there will be lesion called smokless tobacco leukoplakia ( slide # 29 ), discrete asymptomatic well-defined rarely associated with malignancy (very low risk lesion ) , but we have to take biopsy to be sure , & it’s surface may be shown as wrinkled

-Diagnosis : - clinical appearance

- smoking & alcohol consumption

- serum levels of vitamins A,B12 , C & folic acid that might be low especially when smoking not a factor , bcz sometimes if give a vitamin A for example for patient who have deficiency there will be resolution in lesion

-incisional biopsy to know if there is neoplastic or dysplastic changes in the leukoplakia & when I take it , I take it from the most susceptible like the more thick , the indurated , verrucous or papillary areas , or if there are red & white lesions I take it from the red one

-sometimes there is large lesion & homogenous & I don’t know from where I want to take biopsy , there is mouth wash called salagone (not found in Jordan )(toluidine blue ), so the stained areas is the areas that have transformation of cells , so areas have dysplastic changes or malignancy it will stained deeply & then I take biopsy from these areas .

- newer than toluidine blue is oral brush biopsy ( device in lab ,& in clinic there is spinning brush that allows the pathologist to take cells and put on slides & send it to the lab to show abnormal cells ( not found in Jordan )

-the most important & newest one is VELscope ( screening device to detect early oral cancer & uses bright blue light , visualize the areas that might have malignant changes or atypia or dysplasia or carcinoma in situ (malignant in epithelium not entered into connective tissue yet )or invading carcinoma.

-Treatment:- smoking cessation, over 50% of patients have resolution in leukoplakia after stopping smoking but must be no dysplastic changes to resolution to happen.

-in smokeless patients who have vitamins deficiencies especially vitamin A (note: deficiency in vitamin A makes whitening in oral mucosa ), so the resolution happened after giving vitamin especially if the patient non-smoker & there is no dysplastic changes .

-if it candidal leukoplakia ( after we check it by gram or PAS stain )& there is superficial hyphae (not invading ) , but if invaded epithelial layers it becomes oncogenic or carcinogenic , so patient with lesions have invading superficial layers , so we not give them topical nystatin ( not effective ) but we give them systemic antifungal

-azole derivative (fluconazole (trade name : diflucan ) à100 mg *2 per day for one week then 100 mg per day for two weeks & then follow up < if there is no dysplastic changes there will be resolution by using antifungals .

-surgically excision if there is dysplastic changes or atypia , but if large area excised we might need a graft.

-cryotherapy and laser ablation (not preferable . why ?bcz we burn tissue & we can not examine it histologically )

-any patient have leukoplakia with or without dysplastic changes it’s preferable in dr’s opinion to follow up every 3 or 6 months.



*Erythroplakia :

- very dangerous type

- rare, affects the eldery more than 65 years old

-presented as asymptomic isolated flat red lesions or red black

-most common sites :tongue , floor of the mouth , soft palate.

-cause : could be associated with smoking & alcohol consumption.

- 90% malignancy change over 10 years period

-usually isolated red lesion but sometimes could be associated with leukoplakia or speckled leukoplakia

-slide # 35 : white area on left (leukoplakia ) ,red & white area in middle (speckled leukoplakia ), red area on soft palate (erythroplakia )

So if the patient comes to you presented with isolated well defined flat red lesion , it’s so dangerous , ask for incisional biopsy , & if there is malignancy or dysplasia àexcisional biopsy then graft .

- The problem in leukoplakia & erythroplakia in malignant or dysplastic areas that excised that it may return back so follow up is so important.



*Nicotinic stomatitis :

-also called (smoker’s palate )

-white black that affect hard palate & part of soft palate , presented initially as redding & progresses into white lesion with swelling of the minor salivary glands & diluted orifices.

So the area appear as thick layer of hyperkeratosis with red spots (swollen minor salivary glands )

-cause : pipe & reverse cigarette smoking (chemical & heat irritation )& it’s more dangerous than normal smoking .(mostly in india & asia )

- if a patient with denture & he has pipe or reverse smoking habit he will not affected by that lesion.

-affect more the males at age of 45 years old & above.

- the lesion considered bengin except if the habit of reverse smoking & there is combination of chemicals & heat so it may be potentially malignant lesion

-slide# 39 : patient with reverse smoking & have squamous cell carcinoma & usually when squamous cell carcinoma happened in smoker’s palate it will not happen within the lesion but on perpheries.

Diagnosis :clinically

-if there is reverse smoking & you afraid of malignancy (punch biopsy )(انبوبة صغيرة مثل في الجلدية , بتعمل كشط وبيطلع قطعة صغيرة وما بيحطو stetches )

& we use it here bcz we can’t do incisional biopsy bcz the mucosa is very tight

-Treatment :- smoking cessation & if there is no malignancy or dysplastic changes there will be resolution in the lesion within one-two weeks



*Oral submucous fibrosis :

-affect more the indian , the asians & it’s chronic debilitating disease of oral cavity.

-most common cause is areca nut chewing which is the main component of betel quid.

-excessive intake of red chillies (or even green ones ) , may be also chronic anemia >

-clinically : -the mucosa become less resilient (collagen degeneration & fiber deposition ) & when the patient comes he complaining from difficulty in swallowoing & eating & they come in moderate or advanced cases.

- in early stages the mucosa is leathery while in advanced stages it us very stiff.

-it’s inflammation progressive fibrosis until it becomes so stiff & hard & rigid so the patient can not open his mouth (trismus ) , & this is a potentially malignant lesion

Diagnosis :early stage & I know he uses betel quid < & if there is still resiliency , if he stops habit there will be resolution but most patients come with moderate & severe stages & this irreversible & it’s important to take biopsy to diagnose it & exclude dysplastic changes

-Treatment :-avoid the etiology (chewing reca nut )

-antioxidants (A ,C , E ) & also B –complex & iron supplement especially in anemic patient .

- other antioxidants that prevent transformation of lesion to cancer like lycopene found in tomatto ( & nowadays can come in pellets) , that removes free radicules & reduce the precentage of cancers in general

-antioxidants in market ( the most important one ) (reservartrol ) especially after age of 40 (if possible one pellet per day ) it’s taken from black grape

-alpha lipoic acid (very good antioxidants ) & also lycopene

-in moderate cases I have to inject cortisone in the affected area (intralesional corticosteroid injection once per week until the lesion go away.

But if it advanced I need to refresh the blood circulation in this area by vasoactive agent medicaitions like (pentoxifyiline )& if there is limitation in mouth opening I can make excisional removal of the lesion.







Oral Medicine lect # 6

Tuesday 23/10/2011

Dr.Samer burqan

Done by : khaled rashydah
avatar
Shadi Jarrar
مشرف عام

عدد المساهمات : 997
النشاط : 12
تاريخ التسجيل : 2009-08-28
العمر : 27
الموقع : Amman-Jordan

http://jude.my-rpg.com

Back to top Go down

View previous topic View next topic Back to top

- Similar topics

 
Permissions in this forum:
You cannot reply to topics in this forum