Oral Epithelial Tumours

1. Oral Epithelial Tumours • It’s very important to know if the origion of the lesion is epithelial tissue or connective tissue • Lesions of epithelial origin have some features like : localized hyperplasia, change in color (more whitish than the surrounded tissue) & change in texture • Ulceration, change in site & lymphadenopathy  all indicate malignancy

2. Papillomas are mainly of 3 types .. • Regular papillomas • Common warts • Venereal warts (sexually transmitted disease (STD)) • These 3 types are associated with human papilloma virus (HPV) with different subgroups • The 1st type (regular papilloma) is not contagious, but the last 2 types (common warts & venereal warts) are contagious. • Common warts are contagious  this mean it can affect multiple sites (fingers , intraoral) and especially in children (the lesion is spreading by autoinoculation which means the lesion is spreading in the same person but from site to site) , but if we notice it in older patients there is something inherit in that person make him susceptible for that type of papilloma (like some sort of autoimmune problem or HIV)

3. However papillomas are typically in adults , typically solitary (could be multiple but they are all in the mouth , and you can’t see them on extremities or other sites outside of the oral cavity) • Venereal wart on the other hand are sexually transmitted disease, so there is special patients that have special habits and belong to special societies and its distribution is very related to the clinical signs and symptoms

4. If you look to the histo path we have common things .. • Thick epithilium • Basal cell layer hyperplasia • Acanthosis • Koliocytes • These 4 features are found in all types , but there is something special about common warts which is the cupping effect (base is coming from a certain center and making some sort of concavity like a base of a cup) , usually it doesn’t need treatment unless it is esthetically unpleasant or if it affects the function. • Venereal need a special treatment and habit consultation • Koliocytes ( have a big nucleus, hallo around the nucleus, thin irregular cytoplasm ) and they are very easy to be detected

5. Squamous papilloma

6. Verruca vulgaris(common wart)

7. Condyloma acuminatum(venereal wart)

8. Focal epithelial hyperplasia (Heck’s disease) • It’s also a human papilloma virus related disease , however this is seen in subset of people (native Indians), so its diagnosis is easier, also it’s multiple and it’s not localized , they occur in early age, they regress on their own (don’t need any treatment), later on in life they go away on their own, they are not very obvious, you don’t really want to worry about the management of this hereditary disease • They are associated with Koilocytes, thick epithelium, and related to HPV

9. Melanocytic naevi • Healthy, completley normal melanocytes that are producing melanin and they don’t really grow unless something bad is happening, so they are multiple, occur in adults, and they are superficial, they have 3 subtypes : (junctional , compound , intramucosal ), cause pigmentation for the gingiva and they are localized, they need no treatment • Lesion at skin is very common however intraorally they are not that common • There are many reasons that cause pigmentation for the gingiva and the oral mucossa like : ratial pigmentation, some drugs, smoking , addrenal disease & caushin disease ) • Melanocytic naevi or amalgam tattoo  amalgam tattoo is darker and its location is near the restoration

11. Blue naevi • In comaprison to melanocytic naevi it’s deeper , spindle shape melanocytes with typical melanin inside • They are more deeper so they are more bluish rather than more brownish

12. Malignant melanoma • Change in color, change in site, change in size, change in surface texture (ulcers), lymphadenopathy, matastasis, aggressive • The biggest risk to get melanoma is the sun exposure • Very malignant disease • Mainly it’s for extra oral sites but sometimes intraorally • Divided into : superficial spreading and nodular , they are different in prognosis • Intra oral melanomas are a big concern because the site is very important in prognosis ( which mean the same size of tumor if it is in the skin it is different from that which is intra cranial or in mandible or in maxilla ) • The major treatment is surgery , so if it’s in the maxilla which is very related to the components of the skull ( like temporal fossa , intracranial spaces , base of skull and foramina) unlike the mandible which can be removed from the skull , so it’s very dangerous to leave the lesion if it’s in the maxilla • Location , size , lymph node involvement  these are very important in prognosis

13. Melanomas in general are bad diseases • Kaposi sarcoma is a malignant vascular tumor which is misdiagnosed with melanomas  can be distingished by taking history (for example if the patient is HIV positive .. For sure it’s kaposi) • There is another type of melanoma which is : Amelanomatic melanoma (they don’t produce melanin) , in this type you have to make histochemistry test to detect the cell receptors

14. Oral melanoma

15. Sublingual varices • Dilated sublingual veins • They are not always sublingual we can see them at the lower lip

16. Squamous cell carcinoma • We have intraoral site and extraoral site • One of the common extra oral site is the lower lip , and it’s associated with sun exposure. • Note (diseases related to sun exposure: melanoma & sqamous cell carcinoma of the lip) • Squamous cell carcinoma of the lip has a relatively good prognosis, it’s much nicer from a differentiation point of view, there is no lymph nodes involvement and there is no metastasis

17. Intra oral sqamous cell carcinoma • - The worst prognosis • The most common site is the lateral border of the toungh , floor of the mouth and retromolar pad area . • It’s like a “ u “ shape in the lower part of the mouth • Logically every carcinogens and smoking product and environmental product dissolve in saliva then pools in the floor of the mouth , so this situation expose these locations to high concentration of carcinogens , s they have high potential to go bad .

18. -The first thing to do is taking history , if your patient come and told you he smokes package for 20 year it’s a sign . - Any male his age more than 40 year should have proper follow up.- Tobacco is a bad thing smoking or storing in the mouth , in American western movies we see cowboys showing tobacco and do reverse smoking , in India and Pakistan the put spices and store them in their mouth for a long time like algat القات . -If we add risk factors the issue problem increase expetatially meaning that if your patient is( male + >40 year + smoker + drinker ) her we should to be carful.

19. Premalignant lesion • ( condition ) • systemic Disease in the mouth expose the mouth for precancerous and lesions in the mouth have premalignant potential .- like erosion liken empanels disease >>> bilaterally on the mucosa and have striation more whitish and more of lukoplakia , the erosive type have the potential to be malignant ,More in females • Having a male > 40 year and smoker and drinker and has syphilis they add up risk factors so taking history is so important . • The erosive type has the potential to go malignant . • Premalignant lesion • is Lukoplakia and erythroplakia

20. Squamous cell carcinoma Cancer does not start like this so if we do our job as the way we should we can make prognosis less

21. Squamous cell carcinoma and erythroplakia is also Squamous cell carcinoma , so Squamous cell carcinoma of the head or neck , the prognosis and the treatment depends on : 1- size (C) . 2- lymph node ( N) . 3- metastasis ( M ) The system for the classification and staging of head and neck carcinoma is CNM Lateral border of the tongh and floor of the mouth is not that site of entry to see all the details so we have to look for it by gauze visually then palpation it’ surveillance which is our job.

22. Guidelines : • If we have ulcer and broken teeth , the first thing to think about is trauma , so we restore the tooth and play smart we distribute the filling ,( because if we said that we want to restore the tooth and follow up it wont work with our patient ) then we see the patient after 2 or 3 weeks , if we treat the tooth that we thought its because the trauma but the ulcer persistence it need biopsy • a persistence ulcer for more than 2 weeks need biopsy specially if it in the dangerous zone which are :1- lateral border of the tonugh .2- floor of the mouth .3- retro molar pad area . • The presence of lymphatic , vascular, prenural invasion , metastasis and bony invasion is major terminitic prognosis .

23. - Erythroplakia is More serious than lukoplakia , in lukoplakia when it non- homogenous its more serious than very smooth we should remember the risk factor for any lesion depend on size , color and texture . - Histopath is very important in diagnosis beside the staging

24. normal epithelium , the epithelium in sub mucosa so we have invasion ., however we have basement membrane on top of it we have densely stained basal layer , and some sort of spinosum , then keratin cells so they look like normal this is good this is well differentiated . • In the center they are blushed , irregular their is keratin it is moderately differentiated . • Then we have cells , this is does not resemble any thing we know ( kidney shape , mitotic figures ) the only way to know if they are epithelium is location and stain it is poorly differentiated.

25. Moderately differentiated Well – differentiated Poorly differentiated

26. Better variant is hasolkin carcinoma : ( we will take it later on don’t worry about it ) • - Male > 60 year tobacco in sulcus PIV . • Much better prognosis , invasion is easy to handle • Does not metastasis , very little lymphatic invasion .

27. The advancing front is the moment the tumor meets the connective tissue , it has a blunt sharp and unless we know its submucosa we think that it’s a normal epithelium . • The cells are like a unite connected with each other like a unit coherent group , not haphazard in between its much better prognosigly , that’s go for seqamous cell carcinoma under the microscope they are like a unit which give us better prognosis .

28. Basal cell carcinoma because of sun exposure : • - They are skin disease they don’t have intra oral site , any thing on skin is clear helps in diagnosis we treat it by surgery . • So the lesions that are because of sun exposure : 1- Basal cell carcinoma . • 2- sequamous cell carcinoma : one piece but the stage the histopath , location and differentiation might differ so it has multiple treatment like chemotherapy or surgery or radiation , we might start by surgery and continue by radiation , or if the lesion is big and the surgeon think its not resictable we start by radio then continue by surgery and chemotherapy so it doesn't have a strict sequence in treatment , sometimes we don’t have anything to do so we try to change the life style ( cancer mean survival , so if we had a patient survive for 10 years it’s a good thing) . • 3-melanoma

29. Typical basal cell carcinoma - Basal cell aggregation of basaloid like cells look like basaloid have basement membrane still working in groups and in coherent manner so the prognosis is better

30. Done By : Rand Al-Kilani Alaa Yousef Good Luck