Oral pathology sheet # 13 - Ibraheem Al3omari

View previous topic View next topic Go down

Oral pathology sheet # 13 - Ibraheem Al3omari

Post by Shadi Jarrar on 12/8/2011, 4:45 pm

بسم الله الرحمن الرحيم


This lecture will be about epithelium Cancers, prognosis, premalignant legion and risk factors
First will speak about risk factors :
*tobacco use in general regardless the form (like cigar or chowing …. Etc.) is the major cause for the oral cancer
*relative risk for smoker to have a cancer depends on the dose ( like how many cigarette he/she smoke per day)
*heavy smokers have 20 times more risk for having an oral cancer than the non-smokers
*high tar ( ge6ran) content in the cigarette the more carcinogenic the cigarette
*the form that tobacco being served increase or decrease the risk of cancer (like having a cigarette without a filter is more carcinogenic)
*the risk of having a cancer for smokers will return to normal (the risk level for non-smokers) after 10 years from stopping smoking (but it's only for cancer not for the rest diseases)
* Even using dry tobacco (in some countries they put it in bags like tea bags in the buccal or labial vestibule instead of burning it) and chewing it will cause oral cancer specially in the area where they put it, in some countries the put other things with tobacco and chew it all day long specially in India and Pakistan they call it "Paan chew" (that’s way 40% of malignant tumors that affect the body is oral cancers, most common cancer) and all the component of the "Paan chew" is carcinogen but tobacco is major one .

2- alcohols
*second most important disposing factor for oral cancer
*the risk depends on the:
1- quantity: dose
3- quality :if it has poor quality , home made it may have other carcinogen in it or it alcohol is the solvent for carcinogenic materials (like tobacco) and make it more absorbable for oral cavity

* it also cause nutritional deficiency which will decrease the immunity and increase the risk for cancer
* to calculate the risk of having a cancer for smoker and alcohol drinker , you have to multiply the risk factor for smoking by the risk factor for alcohol drinking ( which is 5 folds for heavy drinker ) you will have the risk factor for who is smoking and drinking ( the doctor said it is 50 folds but I think it is 100 = 5*20)
* they thought that tertiary syphilis makes oral cancer(In the dorsum of the tongue ) but recently they discovered that the drug that they used was the reason for the oral cancer
*candida >> leukoplakia >> dysplasia >> cancer in the oral cavity
4-viruses :
1-human papilloma virus(specially 16 and 18) causes cervical cancer so it's accused to cause oral cancer (because it is found in the oral cavity )
2- herpes simplex, herpes simplex and HIV they is no prof for causing oral cancer (but HIV cause immunosuppression so it causes cancer by this way not by itself)

people with immunosuppression they have increased risk for oral cancer specially lip caner

6- nutrition problems
*patient with sever iron defeasance anemia they have increased risk for oral cancer or pharyngeal caner (
Plummer–Vinson syndrome)
*good intake of fruit(specially vitamins A,C and D) and vegetables help in prevention of oral cancer

7- oral hygiene
there is no clear answer for the relation between the oral hygiene and oral cancer … but they say if the patient have bad oral hygiene then s/he will be more carless life style and probably s/he will be a smoker and drinker
8-chronic trauma and irritant (like from a denture)
help in causing oral cancer but not carcinogen by itself … that means if there is another predisposing factor like smoking chronic trauma will help the tobacco effect to cause cancer , but if the patient do not smoke and there is chronic trauma >>> no cancer will happen
9-occupational :

the place they work in could help in causing oral cancer (like cotton wool dust )

lip cancer is the most common cancer in the perioral region and the most important predisposing factor is sun-bite so it's more common :
1-on the lower lip
2- in male
3- people who work in the sun for long hours
4- in light skin people more than dark people (becuz melanin protect them )
start as premalignant legion and it's called "solar keratosis " (crusted lesion sometimes with whitish areas, and contain dysplasia ) then it will become an oral cancer
Premalignant lesion: are not necessary to prosed an oral cancer but there is signs and lesion like leukoplakia (unknown cause, reddish or whitish lesion) chronic hyperplastic or atrophy
*atrophy in the long run could cause cancer: (all of the next cause atrophy)
1-syphilis cause atrophy for epithelium and by that increase the risk for the smoker and alcohol drinker
2- solar keratosis
3-Submucous Fibrosis ( discussed next year )
Plummer–Vinson syndrome-5
6-Lichen Planus(low risk for cancer 1-2%)
Prognosis(the survival rate of the patient):
Tumor is an uncontrolled proliferation of cells … and any mutation in this prosses there is genes that monitor and control it
mutation may be in the repair gens (tumor suppression like P53 ) or in the gens that stimulate proliferation (tumor oncogene like RAS , T5 ) >>> that mutation will cause cancer.
Early detection is the most prognostic factor and the survival rates will be higher >> so we have to know how the cancer look in the early stages (early lesion)
1- look innocent whitish or reddish lesion , appeared with unknown reason , and chronic
2- it could be small or fissure but chronic
Now signs of malignancy:
3- Chronic (ulcers that don’t heal in couple of weeks
4- destruction for the surrounding tissue (like bone resorption)
5- Associated lymphadenopathy (enlarged lymphnode ), without known cause (not from infection) and painless lymphnodes >>> enlarged lymphnodes doesn't mean necessarily there is metastasis .. How?? by the reaction between the ulcer and the lymphnode but not from the metastasis >> but if there is metastasis then the survival rate will decrease by 50% so it's really important to diagnose it before metastasis because u will increase the patient survival rate

late lesion it looks more like cancer
thick deep ulcers, raised margins, undermined ,fungating mass (like fungus ) and surface is crusted , bleeding , necrotic or Distorted

if you see this presentation it is cancer and you must make a biopsy
Histologically :
Invasion to underling lamina propria and tissue
the epithelium is proliferated and invaded the underling tissue after destruction the tissues goes to the lymphnodes, blood vessels and metastasis to other places
The most important prognosis factor for the pathologist is the patterns of invasion:
1-every cell alone (gives BAD prognosis) >> it means more mutation and it's more deferent from the surface epithelium >> and that it is worse
2-move as one mass (gives GOOD prognosis) >> it means less mutation and it's less deferent from the surface epithelium(well differentiation : there is keratin , there is layers "basal, spinosam, granulose, surface") >> and that it is better
3- something in between
They will invade all the surrounding tissue: lymphatic, blood vessels , around nerves (easier to invade it's surrounding tissue) , bone ( examples: metastasis from gingiva goes to the bone from the crest of the alveolar ridge , or making resorption and enter >> inside the bone they go in the spaces >> so some times in a radiograph it looks small so it's just the resorption to enter but actually it's worse than it's look because they are in the spaces )
The prognosis for the survival rate depends on :
1-the time of diagnosis (the early the better prognosis)
2- the age (the older the worse because they have other diseases usually)
3-males have worse prognosis (because they don’t care for their health, so it's diagnosed in a late stage )
4- The site of the cancer ( the easier and accessible the tumor the easier the earlier the diagnosis and easier the treatment) >>> exp.
5- Differentiation and the pattern of invasion (as we said before the more differentiated the better prognosis)
6-size of the tumor (the bigger the worse ) and the stage of oral cancer ( the stage of a cancer is a description (usually numbers I to IV with IV having more progression) of the extent the cancer has spread. The stage often takes into account the size of a tumor, how deeply it has penetrated, whether it has invaded adjacent organs, how many lymph nodes it has metastasized to (if any), and whether it has spread to distant organs)wiki. >> by dr. stage T1 = 2cm in size >> so better prognosis
Some types of epi. Cancers

#verrucous carcinoma >> a type of squamous cell carcinoma related to chewing tobacco habit (like paan) , more in males(they use it more than females ), over 60 years(becuz it need time), and buccal sulcus and adjacent area or labial vestibule (where they but the tobacco ) it's deferent from squamous cell carcinoma by the white finger like projection (papillary projection ), slowly growing , and grow laterally more than to the underneath tissue ( widely distributed )
Heavily keratinized (so appear white clinically )
Well defined border >>so Invade as one mass
Spread laterally
Blunt rete process, and the epithelium in them is well differentiated (still look like the surface epithelium )
Underneath it there is tense inflammatory cells infiltrate
Basil cell carcinoma:
Don’t affect oral cavity (related to hair follicles) , but our role is to tell the patient if we see it , becuz people they think it's normal and they leave , but it's very destructive (but don’t metastasis) and it may affect the area near the vermilion zone(most upper lip) , and we could think it's from the oral cavity but it's not(but it's from the skin nearby)
Appears at the beginnings as a papule >>enlargement >> center ulceration (rodent ulcer)
Typical basil cell carcinoma (basiloid epithelium shaped)
Invasive locally but don’t metastasis to far places
developmental lesion , and it's a collection of melanocyte (hamartomas of melanocyte) in the skin and could be in the oral mucosa(but rare)
Appears at young age and it's common on the skin (anyone may have about 20 of them)
oral Nevi(naevi) in adults , rare ,slightly elevated and mostly in the hard palate and buccal mucosa
Types in the oral cavity depends on the place of the Melanocyte (all appears the same clinically but the deference is histologically ):
1- Junctional epithelium ( in the basil region )
2- compound ( between epithelium and lamina propria)
3-Intramucosal (underlying lamina propria) "most common intramucosal"
4.blue naevus (dark blue dome shaped papule)"second most common" heavily pigmented spindle shaped melanocyte …deep in the lamina propria (it looks deep blue not black "like the res types" becuze it is deep in the lamina propria )
Rare development to melanoma
Now u have to understand something that every naevus starts as junctional >>then it migrate to the junction between epithelium (compound )>> then it migrate to the lamina propria (intermucosal) that’s why it's the most common (becuz all the naevus ends at that stage)
Malignant melanoma
Related to sun exposed areas … but it may appear in the oral cavity
The most important prognostic factor is its depth >> the more the depth the worse the prognosis
Types(on the way that it speads) :

· Superficial spreading type:

_ More common, pears brown or black and irregular (it's bigger and darker than naevi, and the border is irregular)

_ Radial growth(naevi don’t grow) & then vertical growth (at first it spreads laterally then in the end stages , and the prognosis of it depends on the vertical spread >> the more vertical spread the worse the prognosis)

· Nodular type: ( less common)

_ Red, brown or black nodules(elevated), commonly ulcerated

_little or no lateral growth but it grow in depth (so poor prognosis)

· Oral melanoma

_ poor prognosis

_Variable color, it may be macular(bog3ah) or nodular(elevated) with or without ulceration
_most common in males , area : posterior alveolar ridge of the maxilla and hard palate

_in early stage: pigmented, asymptomatic >> in late stage: more malignant signs (destruction , mobility of teeth ,ulceration and necrosis ) >> then spread to lymph nodes and deferent areas "metastasis"


Melanocyte well pigmented , sometimes we need special stains to assure that they are melanocyte becuz they may be not well differentiated

Shadi Jarrar
مشرف عام

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


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