bedah oral cancer

8/11/2019 bedah oral cancer

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ORAL CAVITY CANCER


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Oral cavity cancer is cancer originating from bothepithelial mucosa or salivary glands in the walls of

the oral cavity and organs in the mouth. Oral cavitycancer is more prevalent in males than females witha ratio of 3/2 - 2/1. It mostly occurs in the ageabove 40 years (70%) and it spread all over the

world. The highest incidence are in France andIndia, while the lowest is in Japan.

The etiology of oral cavity cancer is exposure tocarcinogens, which are widely found in cigarettes or

tobacco. High risk of oral cavity cancer gets there inthe smoker, nginang / fringe, alcohol, dental caries,poor oral hygiene


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Goal

1. To know the definition of carcinoma of the oral cavity2. Can explain the pathophysiology of carcinoma of the

oral cavity

3. To determine the risk factors for oral squamous

4. To find a variety of carcinomas of the oral cavity

5. To determine the clinical symptoms of oral carcinoma

6. To find out how to diagnose carcinoma of the oralcavity

7. To determine the treatment of carcinoma of the oralcavity


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Oral Cavity Carcinoma

A. Definition

Oral cavity cancer is cancer originating from bothepithelial mucosa or salivary glands in the walls of theoral cavity and organs in the mouth

The boundaries of the oral cavity is: Front : the edge of the upper lip vermilion and lower lip

Above: the hard palate and molle

Lateral: right and left buccal

Bottom: floor of the mouth and tongue Rear: left and right anterior arch pharyngeus and uvula,

left and right arch glossopalatinus, the lateral edge of thetongue, the tongue circumvallate papillae


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B. Pathophysiology

DNA is a chemical in every cell of the body that will form the gene,showed that the cells in the body to function properly. Some geneshave instructions for controlling when cells grow and divide. Genes

that stimulate cell division are called oncogenes. Genes that slowdown cell division or cause cells to die at the right time are calledtumor suppressor genes.

When tobacco and alcohol damage the cells that line the mouthand throat, the cells should grow more rapidly to repair this damage.In this case there is an opportunity to make a mistake when copying a

gene so that DNA into cancer cells. Many of the chemicals found intobacco can damage DNA directly. This damage can lead to oncogenesand tumor suppressor genes were damaged, DNA changes thatactivate oncogenes or deactivate tumor gensupresor produceabnormal cells to form tumors.

With the additional damage, Human Papilloma Virus infection,

causing the cells to make 2 protein, the E6 and E7. This protein killsseveral genes that keep cell growth under control, so that the cellgrowth becomes uncontrolled and become cancerous. HPV DNA wasfound in the tumor cells, especially in cells of patients with non-smokers who drank little or no alcohol consumption alcohol. HPV isestimated to be the likely cause of cancer


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C. Risk factor

Smoke

Consumption of alcohol

Infection of Human Papilloma Virus (HPV)

Sex

Age Ultraviolet (UV)

Malnutrition

Weak Immune System

Genetic


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D. Clinical diagnosis Anamnesis.

Patient complaints, grievances previous dental, generalmedical history past and present, lifestyle habits, familyhistory, socioeconomic status and occupation. While doinganamnesis physician can also see the state of the patient oralextras, such as lip and facial asymmetry.

Clinical examination

1. Change the color, whether oral mucosal abnormal color,such as white, red or black.

2. Consistency, whether hard tissue, chewy, soft, fIuktuan ornodular.

3. Contour, whether mucosal surface rough, ulceration,

asymmetry or swelling.4. Temperature.

5. Function, whether the patient can open the mouthperfectly.

6. Lymphnode cervical


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Characteristic

Generally, early stage oral cancer does not cause

symptoms, less than 2 cm in diameter, mostly red with or

without white components, slick, smooth and showed minimalelevation. Often beginning of malignancy characterized by the

presence of ulcers. If there are ulcers that do not heal within 2

weeks, then the situation can already be suspected as early in

the process of malignancy.

Other signs of malignancy include ulcers process painless

ulcer, rolled edge, higher than the surrounding area and

induration (harder), can essentially bumps and peeling.

Growth carcinoma ulcer forms are referred to as growth

endofitik. Besides oral carcinoma is also seen as a growtheksofitik (superficial lesions) that can be shaped or papillary

cauliflower, bleeds easily. Eksofitik lesions are more easily

recognized its existence and has a better prognosis.


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E. Histopathology classification

Type of histology

The majority ( 90%) cancers originate from the mucosa ofthe oral cavity in the form of epidermoid carcinoma orsquamous cell carcinoma with well differentiation, but can alsomoderate, bad or anaplastic. When the pathological picture

showed a rhabdomyosarcoma, fibrosarcoma, malignant ormalignant tumors fibrohistiocytoma other soft tissue, shouldbe carefully examined whether the tumor was actually amalignant tumor of the oral cavity (C00-C06) or a malignanttumor of the soft tissues of the cheek, skin or bone invasionheld into the oral cavity.

NO HISTOLOGY TYPE ICD.M

1 Squamous cell carc. 5070/3

2 Adenocarcinoma 8140/3

3 Adenoid cyst.carc 8200/3

4 Ameloblastic carc 9270/2

5 Adenolymphoma 8561/3

6 Mal. mixed tumor 8940/3

7 Pleomorphic carc 8941/3

8 Melanoma maligna 8720/3

9 Lymphoma maligna 9590/3-9711/3


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Degree of Differentiation Standard Pathology Reports

To report on the results of the pathological examination ofthe specimen operations include:

1. Histologic type of tumor2. The degree of differentiation (grade)

3. Examination to determine the stage of pathologicalTNM (pTNM)

T = primary tumor Size of tumor The invasion into the blood

vessels / lymph

Operating radicalism

N = regional nodes number KGB found

Level KGB positive

The number of positivenodes

Invasion of the tumor outkapsel KGB

The extra-nodal metastases

M = distant metastasis

Degree of Diffeentiation

GRADE KETERANGAN

G1 Differensiasi baik

G2 Differensiasi sedang

G3 Differensiasi jelek

G4 Tanpa differensiasi = anaplastik


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F. Clinical stadium classification

Determining the stage of cancer of the oral cavity is recommended using TNM

system of UICC, 2002. Treatment depends on the stage of therapy. Instead of staging to

delineate the severity of cancer can also be widely used extension of disease.

ST T N M TNM KETERANGAN

0 TIS N0 M0 T0 Tidak ditemukan tumor

TIS Tumor in situ

I T1 N0 M0 T1 2 cm

T2 >2 cm - 4 cm

II T2 N0 M0 T3 > 4 cm

T4a

T4b

Bibir :infiltrasi tulang, n.alveolaris inferior, dasar mulut, kulitRongga mulut : infiltrasi tulang, otot lidah (ekstrinsik /deep), sinus maksilaris,

kulit

Infiltrasi masticator space, pterygoid plates, dasar tengkorak, a.karotis interna

III T3 N0 M0

T1 N1 M0 N0 Tidak terdapat metastase regional

T2 N1 M0 N1 KGB Ipsilateral singel, 3 cm

T3 N1 M0 N2a KGB Ipsilateral singel, >3 - 6 cm

N2b KGB Ipsilateral multipel, < 6 cm

IVA T4

Tiap

T

N0,N

1

N2

M0

M0

N2c KGB Bilateral /kontralateral, < 6 cm

N3 KGB > 6 cm

IVB Tiap

T

N3 M0

IVC Tiap

T

Tiap

N

M1 M0 Tidak ditemukan metastase jauh

M1 Metastase jauh


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G. DIAGNOSTIC PROCEDURE

Clinical examination

anamnesa

Anamnesa kwesioner by the patient or family.1) Complaints

2) Course

3) the etiology and risk factors

4) What treatment has been given

5) How do the results of treatment6) How long delays

physical examination

general status

General examination from head to toe

Determine:a. Appearance

b. General condition

c. Distant metastases

the local

inspection


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bimanual palpation

Abnormalities in the oral cavity checked by inspection and palpationwith the help spatel tongue and illumination using a flashlight or headlamp. The entire oral cavity seen, from the lips to the posteriororopharynx. Palpability of lesions of the oral cavity is done by inserting

one or two fingers into the mouth. To determine which lesions areperformed by touching bimanuil. One or two fingers left or right hand isinserted into the cavity of the mouth and the fingers of his other handfingered lesions outside the mouth.

For the inspection of the tongue and oropharynx can the tip of thetongue that has been wrapped with a 2x2 inch gauze is held with the

examiner's left hand and pulled out the mouth and directed right and leftto see the surface of the dorsal, ventral and lateral tongue, floor of themouth and oropharynx. Inspections can be better when using the help ofa mirror examiner.

Determine where the primary tumor site, how it would look, howmuch in cm, how much infiltration, how operabilitasnya.

regional status

Palpation is there any enlargement of cervical lymph nodesipsilateral and contralateral neck. If there is enlargement specify thelocation, number, size (the largest), and mobility.


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Radiography Examination a. X-plain

X-mandibular photo AP, lateral, Eisler, panoramic, occlusal,mandibular gingiva done on the tumor or tumors attached to the

mandible Lateral head X-photo, Waters, occlusal, gingival done on the

tumor, maxillary or maxillary tumor attached to

X-Hap photo done on the hard palate tumor

X-thorax photo, for the presence of pulmonary metastases

B. Imaging (made only on indication)

Liver ultrasound to look at the liver metastases CT-scan or MRI to assess tumor extension vast lokoregional

A bone scan, if suspected metastasis to bone

LaboratoryRoutine laboratory examinations, such as blood, urine,

SGOT / SGPT, alkaline phosphatase, BUN / creatinine, albumin,globulin, serum electrolytes, physiological hemostasis, toassess the general condition and preparation of the operation.


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Pathology examination All patients with oral cancer or suspected cancer of the oral cavity

should be carefully examined pathologically.

Specimens taken from tumor biopsies

Fine-needle biopsy (FNA) for cytological examination can beperformed on the primary tumor or metastatic cervical lymph nodes.

excision biopsy : when small tumors, excision of 1 cm or less extensiveexcision is undertaken as definitive surgery (1 cm from the edge of thetumor)

Biopsy cakot incision or biopsy (punch biopsy) using alligator forceps:

if the tumor is large or inoperable What should be examined is in preparation histopathologic type,

differentiation and extensive invasion of the tumor.

large tumors predicted operabel:

A biopsy should be performed under general anesthesia and can bedone at the same time bimanuil exploration to determine the extent oftumor infiltration (staging)

the expected large inoperable tumor:

A biopsy is done with local anesthetic block in normal tissue aroundthe tumor. (Anesthetic infiltration of the tumor should not be done toprevent the spread of cancer cells).


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H. DIAGNOSIS upheld

primary diagnosis

macroscopic description of the cancer disease itself,which is a clinical diagnosis

Diagnosis of complications

Other disease that is caused by cancer

Secondary Diagnosis

Another disease that has nothing to do with cancer

suffered, but it may affect treatment or prognosenya.

diagnosis pathology

A microscopic picture of the cancer


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I. TREATMENT PROCEDURESOral cavity cancer treatment should be multidisciplinary involving several specialist

areas, namely : Oncologic Surgeon

Plastic & Reconstructive Surgeon

Radiation oncologist Medical oncologist

Dentists

Rehabilitation specialists

Some things to consider in the treatment of oral cancer is the eradication of thetumor, restoring the function of the oral cavity, as well as the cosmetic aspect orappearance of the patient. Some factors to consider in determining the kinds of therapyare:

Age of the patient

The general state of the patient

Facilities available

Ability doctor

The choice of the patient.

For small lesions (T1 and T2), surgery or radiotherapy alone can provide a high curerate, with a note that radiotherapy alone on T2 gives a higher recurrence rate than surgery.

For T3 and T4, the combination of surgery and radiotherapy treatment gives the bestresults. Giving neo-adjuvant radiotherapy and or chemotherapy prior to surgery may begiven to the cavity cancer locally advanced (T3, T4).

Radiotherapy can be given as interstitial or external tumors eksofitik with small sizewill be more successful than endofitik tumors with large size. The role of chemotherapy inthe treatment of oral cancer is still not much in the research phase of chemotherapy is onlyused as neo-adjuvant pre-operative or post-operative adjuvant for sterilization possibility ofmicro-metastasis .


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ST T.N.M. OPERASI RADIOTERAPI KHEMOTERAPI

I T1.N0.M0 Eksisi radikal atau Kuratif, 50-70 Gy Tidak dianjurkan

II T2.N0.M0 Eksisi radikal atau Kuratif, 50-70 Gy Tidak dianjurkan

III T3.N0.M0

T1,2,3.N1.M0

Eksisi radikal dan Post op. 30-40 Gy (dan) CT

IVA T4N0,1.M0

Tiap T.N2.M0

Eksisi radikal dan Post.op 30-40 Gy

IVB Tiap T.N3.M0

-operabel

-inoperabel

Eksisi radikal

-

dan

Post.op 30-40 Gy

Paliatif, 50-70 Gy (dan)

CT

IVC TiapT.tiapN.M1 Paliatif Paliatif Paliatif

Residif local Operasi untukresidif post RT

RT untuk residifpost op

dan CT

Metastase Tidak dianjurkan Tidak dianjurkan CT


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carcinoma of the lip T1: wide excision or radiotherapy

T2: wide excision. When the commissure, radiotherapy will provide relief to the function andbetter cosmetic

T3, 4: wide excision + + deseksi suprahioid postoperative radiotherapy

Carcinoma of the mouth T1: wide excision or radiotherapy

T2: not attached periosteum wide excision, wide excision periosteum Sticking withmarginal mandibulektomi

T3, 4: wide excision with marginal mandibulektomi dissection supraomohioid + +postoperative radiotherapy

carcinoma of tongue T1, 2: wide excision or radiotherapy

T3, 4: wide excision + + deseksi supraomohioid postoperative radiotherapy

carcinoma of the buccal T1, 2: wide excision. When the commissure oris, radiotherapy provide relief to the function

and better cosmetic

T3, 4: wide excision + + deseksi supraomohioid surgical radioterapipasca

carcinoma ginggiva T1, 2: wide excision with marginal mandibulektomi

T3: wide excision with marginal mandibulektomi dissection supraomohioid + + postoperativeradiotherapy

T4 (infiltration of bone / tooth extraction after tumor): wide excision with segmentalmandibulektomi dissection supraomohioid + + postoperative radiotherapy


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carcinoma of the palate T1: wide excision to periost

T2: wide excision to the underlying bone

T3: wide excision to the underlying bone dissection supraomohioid + +postoperative radiotherapy

T4 (bone infiltration): Maksilektomi infrastructural partial / total lesiondepends extensive dissection supraomohiod + + postoperative radiotherapy.

Retromolar trigone carcinoma T1, 2: wide excision with marginal mandibulektomi

T3: wide excision with marginal mandibulektomi dissection supraomohioid + +

postoperative radiotherapy T4 (bone infiltration): Wide excision with segmental mandibulektomi

dissection supraomohioid + + postoperative radiotherapy

For carcinoma of the oral cavity T3 and T4, N0 handling do deseksi selectiveneck or postoperative regional radiotherapy. While N1 obtained at each T todo deseksi radical neck. Where possible, wide excision of the primary tumorand neck deseksi should be done en-block.

Giving regional radiotherapy after surgery depends on the results ofpathological lymph node metastases (the number of positive lymph nodemetastasis, lymph node capsule penetration / extra lymph nodes).


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1. Curative TherapyCurative treatment for cancer of the oral cavity is given in oral cavitycancer stage I, II, and III.

a. The main therapy

Primary therapy for stage I and II is that surgery or radiotherapy,each of which has advantages and disadvantages of each. Whereas forstage III and IV are still operabel is a combination of surgery andpostoperative radiotherapy .

In curative therapy should be considered: According to proper procedure, because if one of the results are not to be

curative. Function mouth to speak, eat, drink, swallow, breathe, stay well.

Cosmetic quite acceptable

Operation

Indication of operation: Case operabel

Age is relatively young The general state of good

There is no co-morbidity of severe


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The basic principle of operation of oral cancer are: The opening should be large enough to be able to see the entire tumor with extension

The basic principle of operation of oral cancer are:

Exploration of tumor: to determine the extent of tumor extension

Wide excision of tumor

The tumor does not invade the bone, 1-2 cm wide excision of tumor beyond Invaded bones, wide excision with resection of the invaded bone

regional nodes dissection (RND = Radical Neck Disection or modification), if there areregional nodes metastasis. Enblok dissection is done with the primary tumor wheneverpossible.

Determine radicalism durante operation of edge incision surgery with frozencut checks. If you do not create a radical new line of larger incision to free thetumor.

Reconstruction of defects that occur. radiotherapy

indications of radiotherapy

The case of inoperable

T1, 2 specific place (see above)

Cancer of the tongue

Age is relatively old

Reject operation There is a severe co-morbidities

Radiotherapy can be given by:

Teletherapy wear: ortovoltase, Cobalt 60, Linec dose of 5000-7000 rads.

Brachytherapy: a booster with intratumoral implantation of radium needles Irridium 192or 226 at a dose of 2000-3000 rads.

b Additional Therapy


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b. Additional Therapy

Radiotherapy

Additional radiotherapy is given in the case of the main therapy surgery. post-surgical radiotherapy

Given on T3 and T4a after surgery, the case can not be done radical excision, radikalitasnyadoubtful, or the operating field contamination by cancer cells.

pre-surgical radiotherapyPre-surgical radiotherapy is given in cases operabilitasnya doubt or inoperable.

Operation

Operations Carried out in cases of therapy after primary radiotherapy orradiotherapy to operabel residif arising after radiotherapy.

Chemotherapy

Chemotherapy given in the case of the operating field contamination bycancer cells, cancer stage III or IV or raised residif after surgery and or radiotherapy.

c. Therapy Complications

Therapeutic Complications of disease

In general, stage I to II disease has been no Complications, but Complicationscan occur due to therapy.

Treatment depends on the Complications that exist, for example (Sunarto, 2003) - Pain: analgesics

Infection: antibiotic

Anemia: haematinics

Therapeutic Complications of therapy Complications of surgery: by type of complication

Complications of radiotherapy: by type of complication

Complications of chemotherapy: by type of complication


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c. Therapy Complications

Therapeutic Complications of disease

In general, stage I to II disease has been no Complications, butComplications can occur due to therapy.

Treatment depends on the Complications that exist, for example(Sunarto, 2003)

- Pain: analgesics


Anemia: haematinics

Therapeutic Complications of therapy Complications of surgery: by type of complication

Complications of radiotherapy: by type of complication

Complications of chemotherapy: by type of complication

d. assisted therapy

Can be given proper nutrition, vitamins, etc. ..e. secondary therapy

If there is a secondary disease therapy was given According to thetype of illness.


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2. Palliative Therapy

Palliative therapy is to improve the quality of life of patients and reducethe grievances especially to people who are no longer curable. Palliativetherapy given to patients with oral cavity cancer :

Stage IV has demonstrated distant metastases There are severe co-morbidities with a short life expectancy

Curative treatment fails

Very advanced age

Complaints need palliation include: Loko regional

ulcers in the mouth / throat Pain

It is difficult to eat, drink, swallow

Oral smell

Anorexia

oro-cutaneous fistula

Systemic: Pain

Shortness of breath

It is difficult to talk

Cough-cough

The agency took care

A weak


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1) The Main Therapya) Without distant metastases: Radiotherapy dose

5000-7000 rads.

If you need to combine the operationsb) There are distant metastases: Chemotherapy

Chemotherapy can be used include:

epidermoid carcinoma:

Drugs that can be used: Cisplatin, Methotrexate,Bleomycin, Cyclophosphamide, Adryamycin, withnumbers 20 -40% remission. For example:

a single drug: Methotrexate 30 mg/m2 2x a week

Drug combinations:

V = vincristine: 1.5 mg/m2 hlB = Bleomycin: 12 mg/m2 hl + 12 hours ==> repeatedevery2-3 weeks

M = Methotrexate: 20 mg/m2 h3, 8


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adeno carcinoma:

Drugs that can be used include: Flourouracil,Mithomycin-C, Ciplatin, Adyamycin, the remission rate 20 30%.

For example: single drug: Flourouracil

Dose starters: 500 mg/m2

Maintenance dose: 20 mg/m2 every 1-2 weeks

Drug combinations:

F = Flourouracil: 500 mg/m2, hl, 8,14,28

A = Adryamycin: 50 mg/m2, hl, 21 ==> repeated every

M = Mithomycin-C: 10 mg/m2, h1 6 weeks

2) Additional Therapy

If necessary: Surgery, chemotherapy, or radiotherapy


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3) Treatment of complications Pain: analgesics according to the "step ladder WHO

Shortness of breath: tracheostomy

Difficult to dine: gastrostomy


Halitosis: mouthwash

Etc..

4) Therapeutic aid Good Nutrition

vitamin

5) Secondary Therapy

If there is a secondary disease, treatment according todisease concerned.


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Tongue Carcinoma

Tongue is the sense of taste has a role as an importantfunction of taste in the mouth, and the benefits of allowingone to choose according to his favorite food, and by the needfor certain nutrients physiologically, generally tongue has atleast four functions of primary taste sour, salty, sweet, and

bitter.Nearly 80% of tongue cancer is the 2/3 anterior tongue

(usually on the lateral edge and under the tongue) and insmall amounts in the posterior tongue. Symptoms depend onthe location in patients with cancer. When located at the 2/3

anterior tongue, the main complaint is the emergence of amass that often feels no pain. When you arise in the 1/3posterior, the cancer is not always known to the patient andthe pain experienced is usually associated with throat pain.


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Mechanism of carcinoma of the mouth and tongue: Leukoplakia

Leukoplakia is pramaligna abnormalities in the oral cavity witha picture of hyperkeratosis. The occurrence of these disorders areaffected by chronic stimulation, such as use of tobacco, betel nut,alcohol, or a prosthesis that does not fit. Leukoplakia seen as whitepatches are slightly thickened and usually do not cause complaints.Leukoplakia is often found in the gums, buccal mucosa and tongue,generally the adult males (Sjamsuhidayat, 2007).

The lesion was not painful but sensitive when touched orexposed to spicy foods. If left unchecked, a small part of it will turnout to be malignant in time can not be determined, sometimes fordecades. If a lesion is suspected as leukoplakia, it is necessary toscrape smear cytological examination. When the results ofcytological examination showed grade I s / d III, repeated

cytological examination the next 3 months while eliminating thefactors that cause leukoplakia. When the results of cytologicalexamination showed class IV-V, need to do a biopsy withhistopathological examination to determine whether malignantchange.


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Erythroplakia

Erythroplakia appears as reddish spots demarcated,soft and thickened. Usually found in men aged 65-74

years, and is often associated with smoking.Erythroplakia generally located bottom mouth, tongueand soft palate. Sometimes erythroplakia located on theedge of leukoplakia.

Microscopic erythroplakia can be severe dysplasia,

carcinoma in situ, or invasive squamous cell carcinomain 90% of patients.

Eksisional biopsy needs to be done to find a picturehitopatologisnya. Wide excision performed if the resultsof histopathologic examination showed malignancy.

Erythroplakia often recur, and therefore needs to bemonitored for a long time.


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LIP CARCINOMA

The cause of squamous cell carcinoma that is not known. The cause issuspected carcinogens and related materials predisposisi.4 factors of oralcancer incidence associated with age may reflect a buildup, genetic changesand the length of exposure to initiators and promoters (such as chemical,physical irritants, viruses, and hormonal influences), and cellular aging declinedue to aging immunologic. Predisposing factors that can lead to the

development of oral cancer include tobacco, alcohol, and other supportingfactors such as chronic illness.

KSS molecular pathogenesis reflects the accumulation of genetic changesthat occur over a period of many years. These changes occur in genes thatencode proteins that control the cell cycle, the safety cell, cell motility andangiogenesis dental, nutritional deficiencies, fungal, viral, and environmentalfactors.

Lip cancer is always associated with people who have outside activitiessuch as fishing and farming. Sunlight may be involved in cancer Datogeneselips. Generally more common in the lower lip finger on upper lip.


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At the beginning of growth, the lesions may be small module or ulcer that doesnot heal. Detection of tumors in this situation provides an opportunity to find an earlycarcinoma. Lesions that can further shape papillari, ulcerative or infiltrative. Typepapilomatous can be initiated from a thickened epithelium and most of these remainon the epithelial superficial. Ulcerative lesions and infiltrative initiated from epithelial

thickening but subsequently experienced a deeper infiltration. The most importantsign is the induration are obtained on the outskirts of the ulcer. Each geneticmutations provide a selective growth advantage, allowing clonal expansion of mutantcells with increased potential for malignancy.

Carcinogenesis is a genetic process that leads to changes in cell morphology andbehavior. The main genes involved in SCC include the proto-oncogenes and tumorsuppressor genes (tumor suppresor genes / TSGs). Another factor that played a role in

the progression of the disease include loss of alleles on the other chromosome ratio,mutations in proto-oncogenes and TSG, or epigenetic changes such as DNAmethylation or histonin acetylated. Cytokine growth factors, angiogenesis, celladhesion molecules, immune function and homeostatic regulation in normal cells thatsurround also play a role. formation of squamous cell carcinoma is malignant duemenyirih composition, menyirih frequency, duration menyirih, and use all night.

Clinical features of squamous cell carcinoma at an early stage often show no

obvious symptoms. No complaints and no pain. Generally the form of leukoplakia,erythroplakia or at an advanced stage of erosion and can be shaped in the formeksofitik papules and nodules, which can be either or endofitik ulcer, erosions,fissures.

At the beginning of growth is the most common ulcer. Cancer of the lip has avaried clinical picture of cancer eksofitik large ulcerations that the above process untila mild swelling of the edge of the vermilion, or crusty lesions that are not suspicious.


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BSIA MOUTH CANCER

Cancer of the floor of the mouth is usually associatedwith the use of alcohol and tobacco. At the initial stagemay not cause symptoms. When lesions develop patientwill complain of a lump in the mouth or feeling

uncomfortable.Clinically the most common form of ulceration are

lesions with a raised edge and hardened located near thelingual frenulum. The other form is a thickening of

mucosal redness, nodules that do not hurt or be derivedfrom the leukoplakia. In the advanced stages of cancercan occur eksofitik or infiltrative growth.


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CHEEK MUCOSA CANCER

In developing countries, cancer of the cheek mucosaassociated with the habit of chewing a mixture of arecanut, betel leaf, lime and tobacco. Susur is in contact withthe left and right cheek mucosa for several hours.

At first the lesions do not cause symptoms, seen as anerythematous area, a small ulceration, induration and redareas are sometimes associated with the type of nodularleukoplakia. With the increasing size of the tumor, trauma

will be targeted at chew, so tend to become ulcerated andinfiltrative.


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CANCER IN GINGGIVA

Cancer of the gingiva usually come from areas wherethe quid of tobacco were placed on the people who havethis habit. The area involved is usually more frequent inmandibular gingiva than maxillary gingiva.

Early lesions appear as Ulger indolent, smallgranulomas or as nodules. Overview lesions appearsimilar to lesions produced by trauma or chronicinflammatory hyperplasia. Lesions were more in the formof growth or growth eksofitik infiltrating deeper. Growth

eksofitik like cauliflower, bleeds easily. Infiltrative growthusually grows invasive mandibular bone and causedesdruktif.


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CANCER IN PALATE

In areas where people have the habit of smokingcigarettes in reverse, on the palate cancer is cancer of the oralcavity are common of all oral cancers. Changes that occur inthe oral mucosa associated with cigarette smoking in reverseis the ulceration, erosions, nodules and spotting areas.

Describing a microinvasive carcinoma to describe an earlylesion in the form of a small, oval or round reddish color, thesmooth erosion areas surrounding hyperkeratotic lesionsusually occur in the glandular zone of the hard palate andasymptomatic. If you are getting pressure to bleed.

Most of palate cancer is eksofitik growth and extensivegrounds with bernodul surface. If the lesion is growing willprobably fill the entire palate. Cancer of the palate can lead toperforation of the palate and extends to the nasal cavity.


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