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
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 fibrimato sis

-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
HYPERTROPHY GINGIVA
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 interfered
the speech , difficulty in chewing food
--- idiophatic

TREATMENT

- stop administration of dilantin
- gingivectomy
, gingivoplasty
FUSO SPIROCHAETAL
INFECTION
A. Acute Necrotizing Ulcerative
Gingivostomatitis = Vincents sto-
matitis = 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 ulcerat-
ion developing
most on the
interdental papil
and margin gingiva
yellowish gray mbr
ulceration may on
the cheek, lips, tongue, palate and
pharyng --eal areas ----- alveolar
proc--- sequestration



TREATMENT
1. Control of bacteri : topical or sistemic
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 b.
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
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 environtment
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 Gingivi -
tis,lack of necrosis
Vesicles rupture &
form crateriform
ulceration,
extremely painful,
surrounded by
bright inflam -
matory 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, odourless fluid,
ruptures easily ----- ulceration with
irregular, friable
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
aciclovir cream
5% aplplied in the
prodrome
3. Recurrent Aphthous Ulceration
/ stomatitis
Characterized by the reccurent
appearances of painful ulcers on the oral
mucosa membr.
A prodome 0f 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
Aetiology 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
Mayor aphth. are larger , heal slowly
over weeks or months with scarring
Herpeticform ulcers are multiple
pinpoint ulcers, heal within about a
month
Treatment :
corticosteroid :
locally
systemically
mouth rinse
4. Herpes Zoster
Etiologi : varicella virus
recurrent disease of
skin and nerves
predisposing factors :
- overwork
- fatigue
- malnutrition
- chronic disease
.
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
Sign & Symptom
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 ????
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 irregu-
lar, 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
The lesion of thrush in infants (
premature, malnourish )
-white or bluish-
white 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 /
suspension
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 : topikal 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
- sistemic
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 yellowish-
white 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
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. Developmental anomalies
2. Benign migratory glossitis (BMG)
3. Black Hairy tongue
4. Glossodynia & glossopyrosis
5. Chanhes in tngue coating
6. Identation marking
7. 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
- a rhomboid or
diamond-shaped
non papillated
area found in the
midline, smooth
- red
5. Macroglossia
- true : creatinism
mongolism
- may arise from
limphangiomatous
&
hemangiomatous
process
- radiation-surgery
2.Benign Migratory Glossitis
(BMG)
= Geographic tongue
etiologi : unknown
occurs in children and young adult
stress ??? , heriditary ?????
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
growth of a blck
pigment producing
fungus
True BHT : elonga
tion of filiform p. &
Pseudo BHT : dis -
coloration from
fruits, candy,
drugs
4. Glossopyrosis-Glossodynia
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 mar-
gins have bright,
red color , painful
-Vit Bc def. : exten
sive generalized
atrophy, raw red or
purplish-red color
-uncontrolled
dia -betes : 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
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, pri -
mary 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
a. viral infection : epidemic parotitis
b. 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
- angina pectoris


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 medica- mentosa.
Resulting from contact ---- stoma- titis
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. Leukemia Akut
- 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
O.H

-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 tajam
Gambaran klinis
-sering dimulai dari lesi prakanker
(precancerous lesion)
-tidak semua lesi prakanker jadi kanker
-tidak semua kanker berasal dari lesi pra
k.
-WHO membagi status prakanker jadi 2:
a. Lesi prakanker (precancerous lesion)

ialah perub. morfologi jaringan -----
kanker
mudah terjadi dibanding normal :
leukopla-
kia, 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 macam 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/tdk
pernah
kambuh/tidak
Iritasi/trauma krn
karies, tambalan
atau protesa yang
tajam
4. Lesi Eksofilik
dpt krn reaksi jar.
berlebihan krn iri -
tasi --- contoh
hiper
plasi krn gigi
palsu.
Iritasi dihilangkan--
--- tidak sembuh ---
biopsi