Download sheet#12,Dr Faleh,Raghad Alawnah

4/8/2014
sheet#12
Raghad Alawneh
Squamous cell carcinoma
Epidemiology:
Most common malignant tumor in the oral cavity more than 90% in different areas
Incidence:
Different incidence in different areas:
High incidence in India 30-40%
Low incidence in UK & USA <4%
Globally: 4th commonest cancer in men and 6th in women
Age:
98% of the patients > 40 years
Linear increased in incidence with increasing age.
Gender distribution:
Intraoral: more in males but nowadays the incidence in women start increase (because women start smoking)
… 3:2>>M: F
Lip: more in males (8:1 >> M: F)
Site:
Overall: lower lip (the most common)
Intra-orally: tongue & buccal mucosa
U-shaped area: (floor of the mouth, ventral surface of the tongue, lateral border of the tongue, lingual gingival
in the mandible) .20% from surface area of oral cavity but 70% of cancer in the U-shaped area because of
pooling of carcinogenic agents.
Rare in hard palate and mid dorsum of the tongue
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4/8/2014
sheet#12
Raghad Alawneh
Etiology:
There are multiple sources but the tobacco is the most incriminated factor in the etiology of oral sqaumous
cell carcinoma
Tobacco contains a lot of carcinogenic material:
Polycyclic aromatic hydrocarbon:
-nitrosamines
-N-nitrosonornictines
Regardless of the form (cigarette, pipe, chewing…) >> it’s carcinogenic lead to oral SCC
Relative risk:
1-dose: more dose >> high RR of oral cancer
Heavy smokers are 20 fold greater risks than non-smokers
2- Tar
3- Tobacco /curing method (Bidi smoker)
Method:
1-reversed smoking (especially in females): by putting the burned part of cigarette in the mouth so the heat
and carcinogenic agents affect the palate mainly. It’s the most method that cause palate cancer which is the
rare type of oral cancer
If you stop smoking, after 10 years the relative risk will become the same as non-smokers
2- Smokeless tobacco: snuff; snuff-dipping, sachets, chewing.
In chewing tobacco, where you put the tobacco the oral cancer happen. So the oral cancer occurs in the buccal
vestibule not the tongue and lateral border…
Tobacco cause many complications other than oral cancer (lung cancer, arteriosclerosis, staining,
hypertension, infertility, lymphoma, ulcer …)
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4/8/2014
sheet#12
Raghad Alawneh
Betel quid (pan) chewing:
Compositions: betel leaves (A) with slaked lime (B) areca nut (C) and tobacco (D).
This type of chewing used constantly with different ages in India that’s why the percentage of cancer in India
high up to 40%
Alcohol:
-Second cause of oral cancer
-Relative risk: dose; duration, quality
-When the dose (high) , long duration , poor quality >> more carcinogenic by-product >> oral cancer
-In the west: the percentage of oral cancer high because of smoking and alcohol at the same time.
-Mechanism of alcohol to cause oral cancer: 1-alcohol works as solvents for other carcinogenic by-product 2alcohol lead to nutritional deficiencies (liver diseases)
-If the alcohol associated with smoking the risk increases.
Heavy drinkers have a 5-fold greater risk and those who drink alcohol and smoke have 50-fold greater risk.
There are other etiological factor for lip cancer especially in the vermilion border of lower lip :
Actinic radiation:
-UV
-relative risk:
1-light-skinned more than black people (they have melanin that protects them from UV)
2-Males more than females (they expose to the sun more)
3-Outdoor (frequently expose to the sun)
-Solar keratosis: potential malignant lesions in the lower lip appear as atrophy white region.
Q: is there any association of X-radiation with oral cancer??
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Raghad Alawneh
Infections:
-Syphilis (at the dorsum of the tongue) nowadays it’s rare to cause oral cancer because of using antibiotics
-Candida
-Viruses: HSV, EBV, HIV, HPV (16, 18)>> the most common virus cause
Immunosuppression:
Immunity protects us from mutations since it suppressed the proliferation of mutation cells so decrease the
risk of cancer. So people who have HIV >> they have high risk of SCC and lymphoma.
Nutritional deficiencies:
-People who have severe iron-deficiency (Plummer-Vinson syndrome) more prone to oral cancer and
pharyngeal cancer
-Eating fresh fruit and vegetables (contain vitamins A, C & E) protect us from oral cancer
Dental factors: (poor oral hygiene, restoration …) it’s unproven
Occupation: textile workers; cotton and wool dust.
The previous factors more probably are promoting factors for the developmental of oral cancer not
initiated factors that cause mutations.
Potentially malignant disorders:
Leukoplakia & erythroplekia, chronic hyperplastic candidosi >>>more prone to oral cancer
Epithelial atrophy: the thickness of epithelium becomes thin so any carcinogenic agents will enter the basal
lesion where the proliferation occur and cause mutation then cancer.
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Development of oral cancer as other cancers there are genes control the proliferation called tumor-suppressor
gene: p53. And there are genes encourage the proliferation called oncongenes: C-myc, ras, erb B1.
If any mutation happens in the tumor-suppressor genes >> the patient becomes more prone to cancer.
Clinical presentations:
We have to know the clinical presentation of oral cancer well. We have to help in early diagnosis of oral
cancer.
Early lesions: difficult to diagnose the oral cancer at early stages. But the lesions appear:
1-small red lesions
2-benign looking whitish lesions
3-small ulcers, nodules
Signs of malignancy:
1-chronicity:
Imagine there’s red lesion in oral cavity if this lesion is:
a-Benign, ulcer or trauma >> within short period the heeling occur
b-Oral cancer >> no heeling occur & it will persist for prolonged period
2-induration: hard when palpated
3-fixation:
Imagine there’s lesion on the labial mucosa if this lesion is:
a-When move it by something it will move
b-Malignant: it won’t
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4-bone resorption: if the lesion on the alveolar bone and you take radiograph finding bone resorption then
you have to think about oral cancer.
5-lymph adinopathy
Late lesions: can be differentiated easily
Appear as large deep necrotic space with elevated margins also contains the signs of malignancy (fixation,
indurations’ …). May find fungating mass on the surface, also may necrosis or bleeding happen.
Notes:
If the lesion near the tongue & the fixation happens then the mobility of the tongue reduced.
Early lesion: at the beginning the oral cancer >>> painless. But at late stages: there’s pain and if it’s near the
alveolar bone it may enter the alveolar bone and affect the inferior alveolar nerve causing parasthesia
especially in lower lip and can occur in the tongue.
Histological:
It originated from the cyst epithelium. Cancer start when the cyst epithelium invade the underlying tissue
toward lamina propria, muscles, bone… (invade the basement membrane) >>it’s the early finding of oral
cancer.
The features of oral cancer:
1-invasion
2-metastasis: at late stage it may invade the lymphatic vessels going to the lymph nodes (submandibular and
cervical) or blood vessels going to brain, lung, bone …
There’s pattern of invasion: large island, Small Island or even individual cells …
When the cells are far from each other, the prognosis will be worse.
If the pattern of invasion was individual cells then they will invade to the lymphatic & blood vessels easily. So
the pattern of invasion associated with prognosis.
Metastasis depends on pattern of invasion.
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Also prognosis depends on the differentiation mean when the invasion of epithelium similar to the cyst
epithelium, the prognosis will be better.
When the pattern of invasion is large lesion and notice this lesion still do its normal function which is the
keratin formation >> that’s mean no a lot of mutation so the prognosis is better.
Well-differentiated >>> well-prognosis
If the invading cell becomes less tendency to form keratin and there’s pleomorphisms (variation in size and
shape of nuclei & cells), hyperchromatism (dark nuclei), high mitotic activities >> moderately differentiated >>
not good prognosis as well-differentiated
If the tumor cells not similar to sqaumous cells, not perform its normal function (keratin formation), high
pleomorphisms, high hyperchromatism & very high abnormal mitotic activity>> poor differentiated
(anaplastic) >> the worst prognosis
After invasion, it spreads to:
1-lymphatic vessels >> submandibular and central lymph nodes
2-blood vessel >> lung, liver, brain…
3-invasion of bone and perineural invasion
(inside the mandible bone >> the cells proliferate to the maxilla space so when we took a radiograph you think
its size is small but actually it’s larger because at periphery the cells proliferates inside the maxilla bone)
4-metastatic spread: high metastatic, worse prognosis, the survival rate decrease
Prognosis: depend on many factors
1-delay treatment
2-increased age
3-male more than female
4-site of oral cancer
At lip: can diagnosis easily. But at the posterior lesion of the tongue >> delayed diagnosis >> bad prognosis. So
the management for the hidden areas is difficult.
5-anaplastic (differentiation)
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6-TNM stage (the most important factor)
T: size of the tumor
N: nearby LNs that are involved
M: metastasis
Verrucous carcinoma:
-Variant of well-differentiated sqaumous cell carcinoma
-In males >60 years
-Appear in the mandibular buccal sulcus and adjacent areas.
-This type of carcinoma spread in areas where people chewing tobacco and snuff-dipping.
Slowly growing, white, exophytic, papillary projection, diffusely distributed.
-Diffuse laterally so better diagnosis comparing to SCC.
Histological:
-closely packed papillary masses
-heavy keratinized at the surface that’s why it becomes whitish.
-lower border well defined so well diagnosis since it’s diffuse laterally.
-blunt rete process
-intense CICI
-the epithelium is well-differentiated (well-diagnosis)
Basal cell carcinoma:
Rare in the oral cavity but can appear in the upper vermillion zone (mainly in the upper face)
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Clinically:
-Appear as papule that enlarged then ulceration occur called Rodent ulcer but later on it causes destruction
for the lesion.
-BCC rarely occur in the oral cavity but it can affect the skin adjacent to the vermillion zone & spread at the lip
in the vermillion zone affecting the oral cavity.
Histological: proliferation of besoloid epithelium.
Prognosis: invades but rarely metastasizes. It spreads at the lesion itself but not to LNs, blood vessels, bone …
so it causes local destruction if not managed.
Melanocytic nevi: ‫شامات‬
-Common in developmental lesions of skin (mainly in head & neck) and mucosa (in oral cavity)
-It’s focal collection (nests) of normal rounded melanocyts.
-More in childhood and adolescence.
-About 20-30 nevi per person.
-Oral nevi rare: mainly adult patients slightly raised or elevated pigmented lesions, most commonly in hard
palate and buccal mucosa.
Types of nevi (whether in skin or oral cavity):
1-junctional: the nevus cells are located along the junction of the basal epithelium.
2-Compound: mixture of basal epithelium & inside the lamina propria.
3-intramucosal: just on the lamina propria.
-different stages of same lesion
-nevi can developed from junctional >> compound >> intramucosal
-malignant change exceedingly rare
Blue-nevus: (4th type)
Appear in the oral cavity >> dark-blue, dome-shaped papule or flat macule.
Second most common after intramucosal
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Most common in hard palate
Heavily pigmented spindle melanocyts, deep.
Malignant melanoma (skin-tumor)
Can occur in the mucus membranes including the oral cavity
1-superfecial spreading:
-
Spread laterally.
The prognosis is better than nodular.
Most common, appear brown-black, irregular macule then become elevated lesion & may occur
ulceration.
2-nodular: Spread vertically.
Oral melanoma:
-In the oral cavity the most common type posterior maxillary alveolar ridge and hard palate.
(Upper jaw > lower jaw)
-Variable color (brown-black)
-At the beginning: flat >> macules >> nodularity >> elevated lesion >> +/- ulceration
-More common in men (40-60 years)
-Asymptomatic at early stages
-Later rapid growth with destruction (cheek, lip, bone …) >> low prognosis
-It’s malignant proliferation of melanocyts.
Histological: Intensely pigmented brown, spindle cells “melanocyts”
GOOD LUCK
DONE BY: RAGHAD ALAWNEH
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