ORAL MEDICINE

( I. Penyakit Mulut )
Definition : Oral mucosal disease
Oral mucosa : - gingiva
- buccal/labial mucosa
- tongue
- palate

Gingiva : part of teeth

supporting tissue, attach to
the teeth and alveolar bone
Teeth supporting tissue
consist of :

1. Gingiva

2. Periodontal membrane
3. Cement
4. Alveolar proc.

Gingiva
Sign of healthy gingiva:
a. pink colour
b. attach to the teeth & alveolar
bone
c. does not bleed easily
d. no edema
e. no exudate
f. gingiva sulcus < 2 mm

Gingival Enlargement
( K 06.1 ICD WHO )

1. Hypertrophy or inflamatory
enlargement ( increase in the
size of the cellular elements )
2. Hyperplasi or fibrotic
enlargement ( increase in the
number of the cellular elements )

Causes of the Gingival

Enlargement
1.Local Inflammatory and
traumatic factors
a. Poor oral hygiene and
accumu
lation of calculus
b. Malposed teeth
c. Incorrect toothbrush habits

 d.Occlusal interferences
e. Irritation from ill-fitting prosthetic
or orthodontic appliances
f. Mouth breathing

2. Systemic predisposing
factors
A. Endocrine
a. Puberty
b. Menstruation, pregnancy,
contraseption medication
c. Diabetes
d. Hypothyroidism & pituitary
dysfunction

B. Nutritional
a. Scurvy
b. Nutritional deficiencies
C. Blood dyscrasias
a. Leukemias
b. Polycethemia vera
D. Drugs (dilantin & barbiturat )
E. Idiophatics : diffuse
fibromatosis

HYPERTROPHY GINGIVA
-Hypertrophy is more commonly than
hyperplasia
- begins at an area of poor oral hygiene
mechanical irritation, food impaction
- first the interproximal gingiva then
spread to----- intire labial / buccal
- edema, bright red or purplish red color,
tendency to hemorrhage

TREATMENT
1. Establish excellent oral
hygiene
2. Eliminate the local
predisposing f
3. Eliminate the systemic
predispo sing causes
4. Proper home care

HYPERPLASI G.E
- normal pink color
- firm, hard and fibrous in
concystency
- does not bleed readily
- are associated with dilantin, rarely
the
barbiturates
- long standing gingival
hypertrophy

diffuse fibromatosis ----change of

profile and face appearance interfe
the speech , difficulty in chewing fo
--- idiophatic
TREATMENT
- stop administration of dilantin
- gingivectomy
, gingivoplasty

FUSO SPIROCHAETAL
INFECTION
A. Acute Necrotizing Ulcerative
Gingivostomatitis = Vincents stomatitis = Trench mouth
The precise etiology is not known, it is
believed to be a polymicrobial infection
Vincent identified Borrelia vincentii ( a
spirochaeta) and Bacillus vincentii
(fusiform)
Fusobacterium necrophrom, prevotella
intermedia, treponema species

Predisposing factors
1. Local factors
a. erupting or malposed teeth,
perico ronal infection
b. faulty restoration, ill-fitting
prosthetic ---- food impaction
c. poor oral hygiene
d. local circulatory and nutritional
disturbances of marginal gingiva

2. Systemic factors
a. malnutrition
vit. C and Bc deficiencies, vit A
b. disease of the blood forming
tissues
----- leukemia, anemia

c. gastrointestinal and
endocrine

disturbances
d. stressful situation and
extreme

fatigue

Sign and symptom

Onset is sudden
severe burning
pain
hypersalivation
metallic taste spon
-tanous bleeding of
the gingiva tissue
bad odor
teeth are sensitive
to pressure

 punch out ulceration developing

most on the
interdental papil
and margin
gingiva
yellowish gray
membrane

Ulceration may on the cheek,

lips, tongue, palate and

pharyngeal areas ----- alveolar
proc--- sequestration

TREATMENT
1. Control of bacteri : topical or systemic
antibiotic (penicillin , metronidazole)
2. Elimination of the local & systemic
predisposing factors
3. Educationing the correct OH habits
4. Surgical manipulation is contra indicated

B. Noma
Is a rapidly spreading and frequently
fatal gangraen of the mucocutaneous
orifices such as the lips, nostrils,
external auditory canal or genital
Noma of the oral cavity (the most
frequent site) is called cancrum oris
---- begins on the mucosa surface
A rare disease

- commonly in malnourish children,

adult and the aged
- transmissible
Predisposing factors
a. systemic : - malnutrition

- circulatory
inadequate
b. local
: - poor oral hygiene

- chronic irritation

- trauma

Cancrum Oris in Children

Premature infant
or malnourish
children
foul, putrid odor
extensive necrotic
area of the cheek
mucosa--sequestration of
alveolar bone
exfoliation of the
t.

 Perforation of
the effected
cheeks and lips,
hipersalivation
Treatment
antibiotics
systemic in high
dose
improvement in
nutrition & gen.
resist.

Cancrum oris in adults and the

aged
oral surgery on patient with ANUG
Develops in illness patients
Treatment = in children

ULCERATIVE , VESICULAR
and BULLOUS LESIONS
( K 12 ICD WHO )
Ulceration is the most frequently
Signs & symptoms of diseases
ranging from the most benign
traumatic of mastication, to the most
rapidly fatal form of malignancy
careful attention ! ! !

- history
- onset, recurrences,
frequency,
severity
- chronic progressive
process????
- evaluation of lymp nodes
- laboratory
- biopsy

1. Primary Acute Herpetic

Gingivostomatitis
Etiologi : herpes simplex virus (HSV)
prevalence is not known, increase in
crowded environment
a prodrome 24 hours or more prior to
the appearance of oral lesion with
malaise, headache , adenopathy,
gastrointestinal upset and fever
pain in food intake

 Mucosal vesicle &

ulceration appear
in the mouth on
the 2nd or 3rd
day, on the lips ,
cheeks, tongue,
palate, floor of
the mouth,
gingivae.

 General Gingivitis,lack of necrosis

Vesicles rupture & form crateriform
ulceration, extremely painful,
surrounded by bright inflammatory
red areolae

Treatment :
- supportive
- mouth rinse
- acyclovir ( if
needed)

2. Recurrent Herpes Labialis .

Etiologi : herpes simplex virus
a prodome of 12-24 hours marked by

hyperesthesi and burning sensation

of the forming lesion of the lip
local edema & erythema of the lip are
initial clinical change ----- 8-24 hours
vesicle appears, clear, friable,
odourless fluid, ruptures easily ----ulceration with irregular

 The base is serohae

-morrhagic---coagulates form an
adherent clot. The
lesion disappear in
7-10 days
recurrences interval
2-12 months

Treatment
supportive ( vit
C & Bc )
Lip lesion
maybe minimize
with acyclovir
cream 5%
applied in the
prodrome

3. Recurrent Aphthous
Ulceration / stomatitis
Characterized by the reccurent
appearances of painful ulcers on the
oral mucosa membr.
A prodome of 1-24 hours, sensation
of burning & tingling in the effected
mucosa
Initial change : appearance of small
erythematous macules crateriform
ulcers, extremely painful
difficulty in eating & speaking

Etiology of RAS
- is not intirely clear
- a minor degree of immunological
dysregulation underlies aphthae
- praedisposing factors :
* genetic
* deficiency : Fe, folic acid.
* stress
* trauma from biting, dental appliances
* allergies to food
* endocrine factors : menstrual c ,
contra- ceptive pill
- immunological features

 The labial &

buccal mucosa
are the most
common site. The
tongue, floor of
the mouth, palate
and gingiva are
less frequent.
3 form of RAS
:mayor, minor ,
herpetic

 Minor aphthous ulcers (80%) are less

than 5 mm in diameter, heal in 7-14
days (self limiting)
Mayor aphth. are larger , heal slowly
over weeks or months with scarring
Herpetic form ulcers are multiple
pinpoint ulcers, heal within about a
month

Treatment :
corticosteroid :
locally
systemically
mouth rinse
eliminate
etiology factors

4. Herpes Zoster
Etiologi reactivation of
varicella zoster virus
( produces varicella
zoster )
Following resolution,
the virus lies dormant
in the dorsal root
ganglia until
reactivation along

Predisposing
factors
- overwork,
fatique
- stress
- malnutrition
- chronic disease
(leukemia, cancer,
hiv)
- radiasi

Sign & Symptom

An itching sensation and a stabbing
burning, constant or intermittent
pain
unilateral, along the distribution of
a sensory nerve trunk
involvement the 2nd & 3rd of the
5th nerve ----result both dermal
and oral manifestation
vesicle formation surrounded by
erythematous base ---- ulcers

Treatment
Supportive
acyclovir (if needed)
though the lesion dissapear ---neuralgia may persist weeks or
months

5. Erythema Multiforme
Dermatosis characterized by great
variation in the form, size,
distribution and appearance of the
lesion
80-90% mouth involvement
etiologi ??? Herpes virus ?
Occurs in infant, children, young
adult

Sign & Symptom

Onset is sudden,
fever, sore throat,
joint pain, acute
ill ---- skin &
mucosal eruption.
Initial lesion is
vesicular or
bullous, found on
the lips,cheeck,
palate, tongue

 lesions are irregular, reddish,

raised areas of
varying size
bloody, crusted le
-sion on the
vermi -llion
border of the lips,
edem.

 Ulcerated moist mucosa

the tongue is extremely painful,
identation marking , lymphadenopathy
Syndromes :

-Steven Johnson : EM
+conjunctivitis

- Behcet : dermal,oral, conjunct.

genital

- Reiter : dermal, acute arthritic

 D.D: - stomatitis medicamentosa

- recurrent aphthous stomatitis

TREATMENT
- corticosteroid
- antimicrobial agent topically or
parenteral
- mouthwash
- vit Bc & C

WHITE LESIONS
Devided into 2 main groups :

A. not associated with

hyperkeratosis

B. associated with hyperkeratosis

A. Not associated with hyperkeratosis

a. -traumatic lesions of the lips &

cheeks

-thermal burns ----- foods

-medicaments ------ aspirin

b. Moniliasis
-the common form is thrush
-etiology : Monilia ( candida)
Predisposing factors :

1. Marked change in the oral flora

- administration of AB

- excessive use of antibacterial

mouth wash

- xerostomia

2. Chronic local iritation

- denture
- heavy smoking
3. Corticosteroid
- topical , sistemic
4. Radiation to head & neck
5. Age :
- infancy, old age
6 Hospitalization
7. Systemic diseases :
- diabetes, leukemia, lymphomas, HIV

The lesion of thrush in infants

( premature, malnourish )
-white or bluishwhite adherent
patch on the oral
mucosa
-non painful
Remove with
difficulty, leaving
a raw, painful,
bleeding surface

The lesions of candidiasis in

adult
-inflamation,
erythema, painful
eroded areas
Diagnosis : made
by microscopis
examination -----scraping

Treatment :
nystatin drop / susp
3-5x/day 1-2 weeks

B. White lesions associated with

Hyperkeratosis
1. LICHEN PLANUS

- an immunologically mediated
mucocutaneous disorder

- can affect stratified squamous

epithelia the skin, oral mucosa , genitalia

- frequent occurrence on the oral

mucosa

precede skin eruption

- stress has been widely held to be an

important aetiological factor

- maybe group into :

a.Non erosive form

slightly raised, diffusely
outline,bluish-white areas which
have
linear, reticular configuration

- typically bilateral
-on the buccal mucosa (mostly), the
pa late ,tongue, floor of the mouth,
gingiva, vermillion portion of lower lip
Diagnosis is clinical supported by
biopsy
Treatment :
- Topical vit A

b. Erosive form ( Bullous )

-more frequently
-pain, interference when eating
-cheek mucosa, tongue, attched
gingiva, palate

-pre-maglinant potential
Treatment : - anaesthetic
- mouthwash

- steroid - topical

- systemic

2. LEUKOPLAKIA
- is used as a clinical descriptive term
- potentially precancerous
- the most serious lesion in the oral
mucosa
Etiology :

- multiple etiologic factors, local &

systemic

1. Systemic
a. Possible constitutional
characteristic

b. Possible nutritional factors :

1. Vit. A hyponutrition
2. Vit Bc complex hyponutrition
c. Possible endocrine factors
d. Possible relation to systemic
disease:
syphilis

2. Local (chronic irritation)

a. Trauma

-sharp edges of teeth

-iritation malposed teeth,
prosthetic
appliances
b. Chemical and thermal
c. Bacterial : - poor O.H
- periodontal disease

Sign and symptom

Lesion may vary
from a small to
an extensive
hyperkeratotic
of large area
Lack of painful
symptoms, if the
lesion becomes
eroded--- painful
--- maglinancy
The yellowishwhite area with

loss of flexibility,
well defined
Find on the cheek
mucosa, tongue
(lack of papillae)
floor of the mouth,
palate, dentulous
ridge
Smoker patch: a
white plaque on
the vermellion
border of lip

Treatment
biopsy ---- non dyskeratotic lesions:

-eliminate all traumatic microbial &

other sources of iritation

-vit Bc & C

-vit A

-should be followed
------ hyperkeratosis with dyskeratosis

-maglinant ------- surgical

TONGUE
( K 14 ICD Disease of tongue )
4 main types of papillae :
1. Circumvallate papillae

- 8 - 12 in number

- posterior dorsum of the tongue

- do not participate in atrophic

tongue change

- a large propotion of the taste buds

2. The foliate papillae

- along the lateral margin of posterior

part

- do not participate in atrophic

changes

- some taste perception

3. The fungiform papillae

- entire dorsal surface
- more near the tip & lateral margin

- can participate in atrophic change

- contain most of the taste buds
4. The filliform papillae
- most numerous papillae of the
tongue
- distributed over the dorsal surface
- atrophic changes are indicator of
disturbances in intracellular
oxidation process

Lesion of the tongue

1.
2.
3.
4.
5.
6.
7.

Developmental anomalies
Benign migratory glossitis (BMG)
Black Hairy tongue
Glossodynia & glossopyrosis
Changes in tongue coating
Identation marking
Traumatic injuries

1.Developmental anomalies
1. Ankyloglossia

- a shortened

lingual
frenulum
- cause of
speech

impairment
- if severe -----
surgical

2. Bifid tongue
- incomplete
fusion of
lateral halves
- rare
- clinical
curiosity

3. Scrotal tongue
- commonest
deve- lopment
anomalies
- the length,
depth and
number is
increased
- inflammation
occurs in the
fissure

4. Median Rhom
-boid Glossitis
( K 14.2 )
- a rhomboid or
diamondshaped non
papillated area
found in the
midline, smooth
- red

5. Macroglossia
- true : creatinism
mongolism

- may arise from

limphangiomatou
s&
hemangiomatous
process
- radiationsurgery

2.Benign Migratory
Glossitis (BMG)
( K 14.1 )
= Geographic tongue
etiologi : unknown
occurs in children and young adult
stress ?, heriditary ?,creatinase ?
Usually multiple, wide variation
from patient to patient, from day
to day in the same patient

 Irregular outline,
nonindurated
pink to red
macular spot
margin are well
defined, slightly
raised, yellow
no treatment,
self limiting

3.Black Hairy Tongue =

Lingua Nigra
( K 14.3 )

growth of a blck
pigment
producing fungus
True BHT : elonga
tion of filiform p.
&
Pseudo BHT : dis coloration from
fruits, candy,
drugs

4. GlossopyrosisGlossodynia
( K 14.6 )
A painful or burning tongue
an early or a nonspecific manifestation
of systemic disorder
may be local causation or psychogenic
divided into 2 groups :
1. Associated with clinical change
2. Without clinical change

1. Associated with clinical change

Less than 25%
local or systemic caucation or
combination
local irritation : tongue habits, allergy
prosthetic/orthodontic appliances
systemic disordes : vit Bc deficiency

uncontrolled
diabetes

anemia

General change in color & papillary

atrophy ----- systemic factors
-pernicious

anaemia
: tip & lateral margins have bright,
red color , painful
-Vit Bc def. : exten
sive generalized
atrophy, raw red
or purplish-red
color

 -uncontrolled
diabetes : red
color, burning
-Fe def. :
general
atrophy of
papillary
coating,
burning

2. Without observable clinical

change
- larger group, between 4th - 7th
decade
- predominantly postmenopausal
women
- insomnia
- psychologic stress

5. Changes in tongue coating

The filliform & fungiform papillae
with food debris, desquamated
epithelial cells, bacteri and saliva
comprise the coating tongue
The amount of tongue coating varies
in different individuals and during
different period of the day.

1. Atrophy in tongue coating

atrophy of the filliform and fungiform
papillae
deficiency of oxidase enzym systems
iron deficiency, nutritional dificiency

2. Increase in tongue coating

local or general condition

 Febrile illness, soft or liquid diet,

poor O.H, deminished salivary
flow due to fever and general
body dehidration.
Result halitosis

6. Identation Marking
Along the margin of the tongue
associated with systemic diseases
any inflamatory process-----enlargement of the tongue
macroglossia
vit. Bc hyponutrition, uncontrolled
diabetes, myxedema

7. Traumatic Injuries
A frequent site of injury
accident, epilectic seizures,
injuries in dental treatment

Disease of the salivary

glands
( K 11 )
Mayor glands : sublingual,
submandibular, parotis
Minor glands : oral mucosa
Saliva for lubrication of tissue,
adequate chewing and for swollowing
Normal salivary flow ------ mechanical
cleansing
saliva has general bacteriostatic
properties

 Contains bacteriolytic enzymes

Grouping of salivary glands
disorder
1. Developmental defect ----absence of one or more pairs of
salivary glands
2. Functional disorders

A. Increased secretion -----sialorrhea

- physiologic in infancy &
childhood particularly during
eruption of the dentation
- acute form of stomatitis :
ANUG, primary herpetic G.
- effect of drugs stimulate para
sympathetic nervous system

B. Decreased salivary
secretion =

asialorrhea = xerostomia

physiologic in the aged

psychic stimuli ------ depressive
dehydration states
drug that depress parasymphatetic
activity
- irradiation of the head & neck

3. Obstruction of salivary flow

A. calculus
B. collaps of ducts
--------------- mucocele, ranula

4. Acute pyogenic infection

a post operative complication .

5. Asymptomatic enlargement of the

parotid or submandibular salivary
glands
Associated with malnutrition or
alcoholism
barbiturate addiction

6. Specific infection process of the

salivary glands

viral infection : epidemic parotitis

bacterial infection : tuberculosis

Halitosis
bad breath / odor
a symptom, not a disease
a social handicap, especially who work in
close contact with the public
local and systemic factors
slightly sweetish odor is normal depending
on
- time of the day
- salivary flow

- microbial population of the mouth

- physiologic process
Divided by 5 groups :
1. In relation with non pathologic local
factors
- decreasing of salivary flow
- denture
2. In relation with pathologic local
factors
-- poor O.H


- dental caries

- periodontal disease

- infection

- cancrum oris

- neoplasma
3. In relation with non
pathologic systemic factors

- age

- food

4. In relation with pathologic

systemic
factors
- diabetes, renal failure, hepar failure
lung abscess, gastrointestinal
disturbances
- neuropsychiatri, etc
5. Drugs

Allergy
- similar to cutaneous allergy, except that
the mucous has mucous glands for
lubrication & protection, and no hair
follicles
The oral lesion resulting from the
absorption of drugs ----- stomatitis
medicamentosa. Resulting from contact
-------- stomatitis venenata

1. Stomatitis medicamentosa
Lesion are produced by
certain of drugs
due absorption via the
gastrointestinal tract ,
respiratory tract or skin
occur in any area of the
body
the lesions are multiple,
amorphous, eroded or
fungoid appearance
vary from marked
erythema to vesicle, an
erosive , an ulcerative or
gangraen lesion

2. Stomatitis Venenata = Contact

Allergi Stomatitis
contact of the causative agent with
the tissues
include two different processes :
a. stomatitis due to physical agents
or
irritants
b. stomatitis due to sensitizing
substances
the symptoms are local

 In the early stages : red color and

smooth wax-like appearance
in mild reaction : small shallow
ulcerations
in severe reactions : actual necrosis of
the mucosal tissues
the lesion develop soon after contact
with the causative agent

Treatment
a. elimination of the causative agents
b. local symptomatic care :

- anti allergy

- anaesthetic troche

Oral Manifestation of
Systemic Disease
1. Leukemia
A. Acute Leukemia

- adenopathy

- gingival enlargement with or

without area of necrosis

- ulceration of the cheeck, tonsils,

 bleeding from
the gingiva
after tooth
extraction
severe
odontalgia
mobility of the
teeth

Treatment
- maintaining good OH
- relieving pain
- minimizing irritation of the
necrotic lesion
- parentral antibiotic to minimize
the development of the
ulceronecrotic mucosal lesion
- extraction, oral biopsies, deep
scalling are contra indicated

B. Chronic Leukemia

-adenopathy
gingival hiperplasi
ulceration
petechie and
echymosis

Treatment
= Acute Leukemia

2. Diabetes
-75% of uncontrolled adult diabetics -----periodontal disease
-gingiva is a deep red color, edema,
slightly enlarged
- a generalized painful suppuration of the
marginal gingiva and interdental papillae
-the teeth are sensitive to percussion
-recurrent periodontal abscess

 - extensive loss of supporting

tissues ------ loosening of the teeth
- rapid deposition of calculus
- xerostomia
- enlargement and hyperaemi of
the fungi form papillae
glossopyrosis & glossodynia

 -musculature of the
tongue is flabby
-indentation marking
-increase incidence of
caries
-severe odontalgia
without caries
-candidiasis
-oral surgical procedures
including curettage are
contra indicated

Dental surgery in the diabetic

require a consideration of :
a. prevent an elevation in
blood sugar
b. choice of anaesthetic
c. prevent postoperative
complication

3. Syphilis
A. Acute Syphilis
a. Prenatal Syphilis = Congenital S. =
Heredity S.

- the first 16 weeks of pregnancy the

fetus is protected

- after 16 weeks becomes vulnerable

to
infection ----- occur after 6 months

Oral aspects of congenital syphilis :

1. postrhagadic scarring about
the
mouth
2. the changes in the teeth ---Hutchinsons teeth, mulberry
molar
3. dentofacial abnormalities :
open bite

b. Acquired Syphilis
1. Chancre of orofacial

- the oral cavity is the most

frequent site
of extra genital

- the genital chancres are painless ,

brown- crusted indurated lesion

- the oral chancres are slightly

painful
, covered with greyish-white film

 The location are

on the lips,
tongue,
cheek, soft
palate, gingiva.
Many lesios were
not contacted
through sexual,
but by kissing,
dental instr.

2. Syphilitic mucous patch

The most infectious lesion
moderately painful
grayish-white lesion , slightly raised,
surrounded by an erythematous base
common site : tongue, lips, vermillion
border

B. Chronic
Syphilis
1. Syphilitic gummata

-most frequently on the

palate, tongue
-also salivary glands and
jaw bone
-early stage : ulcerated,
purple in color----- ----necrosis ----- destruction
of the bone ----------perforation of the palate

2. Paresis and Tabes dorsalis

-Paresis : involvement of cerebral

tissue

Tabes dorsalis : involvement of

posterior root ganglia ----neurosyphilis
-trigeminal neuralgia , loss of taste
-necrosis alveolar proc. ,
parasthesis in the lips, tongue,
cheek--extraction
without
anaesth.

AIDS
Oral manifestation of HIV
infection :

- gingivitis

- periodontitis
marginalis

- proc. Alv
destruction- ----sequester

- stomatitis , ANUG,
- Kandidiasis

- Leukoplakia

- Ca Kaposi

Leukoplakia

Stomatitis

Deteksi Dini Kanker

Rongga Mulut
Pendahuluan
-kanker rongga mulut cenderung
meningkat
-di AS > 30.000 penderita kanker
mulut & faring / th., menyebabkan
8000 kematian/th.
-data R.S dr. Sutomo, 1976-1983 ada
201 kasus kanker mulut dari 12.128
kasus kanker ( 1,7% )

Etiologi
Belum jelas, beberapa faktor dikaitkan :
-zat karsinogen : tembakau, alkohol
dll.
-sinar matahari ---- kanker bibir
-infeksi : sifilis, kandidiasis, virus
-kelainan mukosa mulut : leukoplakia,

lichen planus
-genetik
-defisiensi nutrisi
- faktor lokal: OH jelek. Iritasi kronik

Gambaran klinis
-sering dimulai dari lesi
prakanker
(precancerous lesion)
-tidak semua lesi prakanker jadi
kanker
-tidak semua kanker berasal
dari lesi pra kanker

WHO membagi prakanker menjadi

2:
a. Lesi prakanker (precancerous lesion)
ialah perub. morfologi jaringan ----kanker
mudah terjadi dibanding normal :
leukoplakia, erytroplakia
b. Keadaan prakanker
ialah keadaan umum dimana kondisi
resiko untuk dapat terjadi kanker >
normal ,
contoh : sifilis, lichen planus

Bentuk Awal Kanker Mulut

1. Lesi kemerahan ( eritroplakia )

-adalah daerah/bercak sangat merah,

berbatas tegas, secara klinis/patologis
bukan kelompok kelainan/penyakit ,
warna merah krn atropi epitel &
inflamasi

-permukaan halus (beludru), kadang

ada
bercak putih diatasnya

 Permukaan rata
atau sedikit diba
-wah permukaan
warna merah tak
selalu
eritroplakia ,
dpt trauma fisik,
ki- mia atau
inflamasi

 Apabila
penyebab tidak
diketahui atau
lesi merah dlm
1 bulan tidak
sembuh ----curiga
erytroplakia

2. Lesi Putih (leukoplakia)

-lesi putih dalam mulut

dapat karena bermacam

sebab a.l iritasi setempat,
lichen planus, leukoplakia
dll.
-kanker mulut bentuk lesi
putih, insidennya kecil
-lesi putih dengan ulcerasi
/celah-celah atau
dengan lesi merah segera
biopsi

3. Ulkus
Tidak khas bentuk
kanker , dapat
ulkus stomatitis
aftosa, ulkus
dekubitis dll.
-penting riwayat
peny.:
sakit/tidak,
sembuh/tidak,
kambuh/tidak

 Iritasi/trauma
krn karies,
tambalan atau
protesa yang
tajam

4. Lesi Eksofilik
dpt krn reaksi
jar. berlebihan
krn iri -tasi --contoh hiperplasi
krn gigi palsu.
Iritasi
dihilangkan---- tidak sembuh
---biopsi