CANCEROUS LESION IN ORAL

Drg Rina Kartika Sari SpPM

DEPARTEMEN ILMU PENYAKIT MULUT

FKG UNISSULA
SASARAN BELAJAR

• Memahami diagnosis, etiopatogenesis, dan

perawatan lesi cancer

SUB POKOK BAHASANRAN BELAJAR

• Oral Melanoma
• Kaposi Sarkoma
• Adenokarsinoma
• Limfangioma
 ORAL
MELANOMA
 DEFINITION
• Melanoma is the malignant neoplasm of melanocytic
origin that arises from a benign melanocytic lesion or
de novo from Melanocytes within otherwise normal
skin or mucosa.
• Amelanotic malignant melanoma was defined as a
tumor composed of nonpigmented melanocytes
• Neoplasm of epidermal melanocytes  tumor that
lacks pigmentation clinically and has melanin
pigmentation histopathologically is also included in
this category
EPIDEMIOLOGY

●
Third most common cancer of skin but they may
Prevalence ●
develop at any site where melanocytes is present.
Oral melanoma 0.2 to 8% of all melanomas

Rare below 30yo. Range 40-70 yo. ±55yo

Age&Sex
●

●
More common in men

●
Oral palate and the maxillary gingiva
●
Head&Neck mucosa  conjunctiva,upper
respiratory tract and the oral cavity.
 PHASE OF GROWTH
RADIAL GROWTH PHASE
•  initial phase of growth of the tumor.
• During this period, which may last many years, the
neoplastic process is confined to the epidermis.
• In the early stages  the radial growth phase tends to
predominate in lentigo-maligna melanoma, superficial
spreading melanoma and acral lentiginous melanoma.
• In these lesions, the malignant melanocytes tend to
spread horizontally through basal layer of the epidermis
VERTICAL GROWTH PHASE
• begins when neoplastic cells populate the underlying
dermis. With nodular melanoma, the radial growth
phase is very short or nonexistent and the vertical
growth predominates.
TYPE OF MELANOMA
CLINICAL FEATURES
• Pigmented nodular type
• Nonpigmented nodular
type
• Pigmented macular type
• Pigmented mixed type
• Nonpigmented mixed type
CLINICOPATHOLOGIC (SKIN)
• Superficial spreading
melanoma
• Nodular melanoma
• Lentigo-maligna
melanoma
• Acral lentiginous
melanoma
CLINICAL FEATURES
• Superficial spreading melanoma—it develops over several
years into a sharply outlined, slightly elevated pigmented
patch. The lesion presents as a tan, brown, black or admixed
lesion on sun-exposed skin, especially in blacks. The most
common sites of origin are the intercapsular area of males
and the back of the legs of females.
• Nodular melanoma—clinically, it appears as darkly pigmented
elevations on skin or mucous membrane. Nodular melanoma
is usually a deeply pigmented exophytic lesion, although
sometimes the melanoma cells are so poorly differentiated
that they no longer can produce melanin, resulting in a
nonpigmented amelanotic melanoma. This form of Melanoma
is invasive in nature from the start and Metastasizes early. It
has relatively poor prognosis.
• Lentigo-maligna melanoma—clinically, it appears as a
flat, irregularly pigmented patch with an ill-defined
margin. The appearance of nodularity with a lentigo-
maligna signals the onset of the invasive or vertical
growth phase.
• Acral lentiginous melanoma—it begins as a darkly
pigmented, irregularly marginated macule which later
develops a nodular invasive growth phase
• begins as a brown to black
macule with irregular borders.
The macule extends laterally and
a lobulated exophytic mass
develops once the vertical
growth is initiated.
• Ulceration may develop early
but many lesions are dark,
lobulated, exophytic masses
without ulceration at the time of
diagnosis
• pain is not a common feature
except in ulcerated lesions and
most lesions are relatively soft on
palpation.
• Site—in most cases, only the soft tissues are affected.
• Both primary and secondary malignant melanoma
rarely involve the bone of the jaws.
• Moth eaten appearance—some melanomas in the jaws,
may present radiographic appearances which are almost
indistinguishable from osteomyelitis and patients have
even been treated for this condition, until with the
passage of time the error becomes apparent. Underlying
or adjacent bone may show radiographic evidence of
irregular or “moth-eaten” destruction.
 DIFFERENTIAL DIAGNOSIS

• Oral melanotic macule  Asymmetry

(because its uncontrolled growth pattern),
Borders irregularity (often with notching),
Color variation (which varies from shades of
brown to black, white, red and blue,
depending upon amount and depth of
melanin pigmentation) and Diameter often
greater than 0.5 cm.
• Melanotic neuroectodermal tumor of infancy—occurs in
infants.
• Ecchymotic patch—it disappears within few days.
• Melanoplakia—it is firm and occurs in infancy or puberty
without change.
• Intramucosal compound or blue nevus—same as oral
melanotic macule.
• Pigmented fibroma—histopathological diagnosis should
be done.
 MANAGEMENT

• Surgical excision— cutaneous malignant melanoma is surgical excision.

Although regional lymph node dissection is indicated when nodes are
involved; prophylactic lymph node dissection is very controversial.
• Radiotherapy— mainly on patients unable to surgical or as an adjuvant to
surgery.
• Preoperative chemotherapy—preoperative chemotherapy to reduce the size
of the melanoma and improve surgical management. The first line
chemotherapeutic agent is dimethyltriazeno, imidazole carboxamide solely
or in combination with vincristine or dactinomycin. Other
immunotherapeutic drugs that are occasionally used include interferon and
cimetidine which when used together are believed to activate killer T-cells
and inhibit suppressor T-cells resulting in the reduction of the size of the
melanoma.
• Intralesional injection—Intralesional injection of interferon and Polyvalent
melanoma antigen vaccine.
Multiple idiopathic hemorrhagic sarcoma of Kaposi’s,
Angioreticuloendothelioma.

KAPOSI’S SARKOMA
DEFINITION

• Kaposi’s sarcoma is an unusual and uncommon disease of

blood vessels which occasionally manifests in the oral Cavity
• Classical (sporadic) Kaposi’s sarcoma was describedby
Moritz Kaposi in 1872 in central Europe among elderly
persons of Mediterranean or Jewish origin as a multiple
pigmented sarcoma of the skin.
• Kaposi’s is most accurately described as a multifocal
angioproliferative neoplasm that primarily involves the skin
in non-HIV infected person.
• KS is a neoplasm now most commonly a manifestation of
infection with the human immunodeficiency virus (HIV),
that frequently affects the oral cavity.
• causal relationship between the immune deficiency and the
appearance of this neoplasm.
• Pathogens or factors suspected to be associated with KS include
human herpes virus type 6, cytomegalovirus, human
immunodeficiency virus, mycoplasm penetons, sex hormones and
nitrate inhalants.
• may present as cutaneous, oral or visceral lesion either
independently or synchronously.
• The frequency is higher in homosexual and bisexual male than in
other risk group for HIV infection.
• There is also an increased incidence of Kaposi’s sarcoma among
transplant patients, which can resolve after immunosuppression
drug therapy
 A
Ia
●

Cl E
●
Late ●
iatrogen
Adult benig ic
●
Man n immuno
●
Italian, suppres
nodul
Jewish
or
salvic a ar
type n
sionasso
ciated
KS most
often
tr
●
An

●
ancest
ry
Multip
ss
aggre
ssive
d
occurs
in
recipien
t’s organ
o
le type
g
transpla
bluish ●
A nts.

ic e related
●
purple florid to the
macul form loss of
es and
plaque
●
A cellular
immunit e
m
uniqu y, which
s on
the e occurs

skin of
the
lymp
hade
as a
result of
immuno
ni
lower
extre
mities
nopat
hic
type
ic suppres
sive
drug
c
• oral mucosa are identical in appearance with cutaneous
nodules.
• Any oral site but most frequently in attached mucosa of
the palate, gingiva and dorsum of tongue.
• red to purple nodules and macule with mucosal
ulceration in some of the more mature cases.
• pain, dysphagia, difficulty with mastication, bleeding,
and may be cosmetically displeasing.
• Progression from the flat to the nodular form, associated
with increasing grades of immunocompression
• does not blanch with pressure.
• Early lesion may similar to ecchymosis or hemangioma.
DIFFERENTIAL DIAGNOSIS

• Hemangioma—it blanches on pressure.

• Purpura—it is presented as multiple papules on the
soft palate.
• Nevi—it is not so aggressive lesion.
• Melanoma—it is not multicentric process.
MANAGEMENT
RADIATION
• for skin lesions in the classic
form.
• Radiotherapy for oral KS is
most often fractionated to
result in a dose of 25 to 30
Gy over 1 week.
SURGICAL
• Surgical is difficult because of
the multiplicity of lesions.
• The carbon dioxide or argon
laser can be very effective in
the surgical treatment or
palliation of KS involving the
upper aerodigestive tract.
MANAGEMENT
SYSTEMIC CHEMOTHERAPY
• If KS progresses at multiple
sites, systemic chemotherapy
• alternating weekly vinblastine
and vincristine.
• Other effective agents:
doxorubicin in low doses,
bleomycin and methotrexate.
• Etoposide has also been used.
• Recombinant interferon
alpha2A and alpha2b
efficacious agents
INTRALESIONAL INJECTION
• the intralesional use of
vinblastine, in doses varying
from 0.01 to 0.04mg (multiple
intralesional injections),  an
effective alternative treatment
for small KS lesion of the
mouth.
• repeated every 2-4 weeks until
the remission.
Combination therapy for AIDS related Kaposi’s sarcoma
• (AIDS associated) KS : single agents, combined chemotherapy,
or zidovudine with interferon—alpha and radiotherapy have
been tried.
• CD4 T-lymphocyte > 500 cells/mI excision, cryotherapy, or
even sclerotherapy, to which they rapidly respond.
• CD4 level , 200 cells/mI  systemic chemotherapy and
antiretroviral treatment is advisable;
• Intermediate CD4 counts interferon with zidovudine.
• Prognosis is variable, depending on the form of disease and
the patient’s immune status.
ADENOKARSINOMA
DEFINITION

• It is a malignant epithelial tumor showing tubules or

papillary glandular formation.
• All adenocarcinoma are highly malignant and
metastasize to regional lymph nodes and general
viscera.
• Adenocarcinomas of the salivary glands are rare but
aggressive tumors
CLINICAL FEATURES

• > 40 years of age. Men= women.

• ½ parotid glands, the minor salivary
glands,particularly the palate, lip and tongue are the
next most commonly affected sites.
• Clinical presentation  enlarging mass.
• 25% of patients will complain of pain or facial
weakness
HPA FEATURES

• Low-grade
adenocarcinoma
formation of many
ductal structures.
• Mitotic fi gures are rare
• High power view showing
nuclear atypia
TREATMENT

• Complete local excision

• In the parotid  facial nerve sacrifice.
• In the minor salivary glands, a portion of the maxilla
or mandible may have to be resected with the tumor.
• Postoperative radiation therapy does seem to be of
some benefit.
• Lymph node metastasis is not uncommon and in
patients with palpable neck disease neck dissection is
warranted. Local recurrence rates vary in as high as
51%.
MUCOEPIDERMOID CARCINOMA
• Umumnya melibatkan kelenjar ludah mayor, yaitu
kelenjar ludah parotis.
• Sebagian kecil dapat timbul dari kelenjar ludah
minor, dan yang paling sering melibatkan kelenjar
ludah minor di palatum
• jenis terbanyak dari keganasan kelenjar saliva yang
diakibatkan oleh radiasi
 EPIDEMIOLOGI

Dekade 30-40

75% bengkak asimptomatis

13% sakit
Sebagian kecil paralisis nervus facialis
GAMBARAN KLINIS

• berasal dari sel epithelial interlobar dan intralobar

duktus saliva.
• Tidak berkapsul, dan metastasis kelenjar limfe
ditemukan sebanyak 30-40 %.
• Penentuan derajat keganasan berdasarkan
histopatologi terdiri atas derajat rendah,menengah,
dan tinggi
• Benjolan kemerahan
• lunak
• Secara mikroskopis  low
grade,intermediate grade
dan high grade.
• Gambaran mikroskopis
menunjukan campuran sel
skuamous, sel kelenjar
penghasil mucus, dan sel
epitel tipe intermediate.
Ketiga sel ini berasal dari
sel duktus yang berpotensi
mengalami metaplasia.
• Tipe low grade  masa yang kenyal dan yang
mengandung solid proliferasi sel tumor, pembentukan
struktur seperti duktus, dan adanya cystic space yang
terdiri dari sel epidermoid (sel skuamous) dan sel
intermediate, sel-sel sekresi kelenjar mukus.
• Tipe intermediate ditandai dengan masa tumor yang
lebih solid sebagian besar epidermoid dan sel
intermediate dengan sedikit memproduksi kelenjar
mukus.
• Tipe poorly differential ditandai dengan populasi sel-sel
pleomorfik dan tidak terlihat sel-sel berdiferensiasi
PERAWATAN

• Perawatan karsinoma epidermoid adalah eksisi

seluruh jaringan tumor.
• Prognosis baik  well differentiated/ low grade,
tetapi dapat bermetastasis, 90% bertahan hidup
sampai 5 tahun
• Poorly differentiated/high grade, prognosis menjadi
buruk, dan kemampuan bertahan hidup 5 tahun
menjadi rendah (sekitar 20-40%)
ADENOCARCINOMA
DEFINISI

• Adenocarcinoma /kanker kelenjar ludah adalah tumor

ganas dari jaringan yang memproduksi air liur
• salah satu dari lima jenis utama kanker di daerah kepala
dan leher
• Sering dijumpai menyerang kelenjar parotis
• Jarang pada usia 40 tahun, kejadian pada usia-usia lanjut
• Lebih banyak menyerang laki-laki daripada perempuan
• Etiologi belum diketahui secara pasti.
• Pencegahan  diet dengan lebih banyak
mengkonsumsi sayuran dan buah-buahan yang banyak
mengandung vitamin C .
• Diduga berhubungan dengan agen karsinogenik seperti
radiasi
• sinar ultraviolet, immunosupresi, dan banyak ditemukan
pada penderita yang terserang virus Eipsten Barr .
• Eropa  pekerja pabrik karet dan pabrik nikel.
• Agen karsinogenik  mutasi gen.
GAMBARAN KLINIS

• sebagian besar bersifat asimtomatik,tumbuh lambat,

dan berbentuk massa soliter.
• Rasa sakit /nyeri episodik mengindikasikan adanya
peradangan atau obstruksi daripada akibat
keganasan itu sendiri
• dapat bermetastasis ke kelenjar limfe regional, paru,
liver, maupun pada tulang.
• Metastasis berkembang menurut gambaran
histologis. Metastasis jarang terjadi pada low-grade,
namun pada highgrade mencapai 30%-46% dari
kasus
1.ADENOID CYSTIC CARCINOMA

• dahulu dikenal dengan istilah cylindroma,

• tumor ganas yang berasal dari kelenjar ludah yang
tumbuhnya lambat, cenderung local invasive, dan
kambuhan setelah operasi.
• Usia 40 dan 60 tahun
• potensial ganas derajat tinggi.
• 3 % parotis, 15 % submandibular, dan
30 % kelenjar saliva minor.
• Sebagian asimptomatik, sebagian besar
terfiksasi pada struktur di atas atau di
bawahnya.
• perjalanan penyakit yang panjang
ditandai oleh kekambuhan lokal yang
sering, dan kekambuhan dapat terjadi
setelah 15 tahun.
• angka harapan hidup tinggi hingga lima
tahun, angka harapan hidup sepuluh
tahun ditemukan kurang dari 20%
• gambaran/pola bervariasi.
• Sel-sel tumor berukuran kecil, sitoplasma
jelas, dan tumbuh dalam suatu massa yang
padat atau berupa kelompok kecil,
kelompok sel yang beruntai atau
membentuk suatu kolum-kolum.
• Di dalam kelompoknya, sel-sel tumor saling
berhubungan membentuk suatu rongga
kistik menghasilkan suatu kelompok tumor
yang solid, tubulus, atau cribiform
• Sel-sel tumor menghasilkan membran
basalis yang homogen menyerupai
bentuk silindris.
• cenderung infiltrasi ke spasia perineural
sehingga seringkali menimbulkan rasa sakit
2. ACINIC CELL CARCINOMA

• tumor ganas kelenjar ludah parotis yang jarang

terjadi  10%
• Laki2 muda 20-30 tahun
• Berkapsul  proliferasi membentuk massa bulat
• Tanda patologik khas adalah adanya amiloid
• Asal sel  komponen serosa asinar dan sel duktus
intercalated
• Histologi berisi sel – sel asinar yang seragam
dengan nukleus kecil berada di sentral dengan
sitoplasma yang basofilik dan padat mirip sel – sel
sekretorius (asinar) dari kelenjar ludah normal.
• Dapat bermetastasis ke limfonodi regional
• Terapi  eksisi bedah + radiasi