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.
Anatomi Gigi
 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
Gingivitis
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
consistency
 - 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 = Vincent’s 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
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sequestr
ation of alveolar
bone exfoliation of
the teeth
 Perforation of the
effected cheeks
and lips,
hipersalivation
 halitosis, fever,
malaise, and
regional
lymphadenopathy
are common
Treatment
 antibiotics systemic
in high dose
 improvement in
nutrition
 Local wound care
Cancrum oris in adults and the aged
 oralsurgery 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 * stress
* deficiency : Fe, folic acid.
* trauma from biting, dental appliances
* allergies to food
* endocrine fc : menstrual c, contraceptive 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
 corticosteroid
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
 Hypersensitivity reaction
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
Cheek biting
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 , systemic
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 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 / 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
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 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
 -malignant ----- 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. Developmental anomalies
 2. Benign migratory glossitis (BMG)
 3. Black Hairy tongue
 4. Glossodynia & glossopyrosis
 5. Changes in tongue 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
development
anomalies
 - the length, depth
and number is
increased
 - inflammation
occurs in the
fissure
4. Median Rhom -
boid Glossitis
( K 14.2 )
 - 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
 Macroglossia

True Pseudo

Generalised Localised

Congenital Congenital
Inflammatory Inflammatory
Traumatic Traumatic
Metabolic Neoplastic
 Metabolic

Congenital
Traumatic Traumatic

Neoplastic
Congenital
2.Benign Migratory Glossitis
(BMG)
( K 14.1 ) = Geographic tongue
 etiologi : unknown
 idiopathic disorder characterized by the
loss of filiform papillae
 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
 Irregularoutline,
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 black
pigment producing
fungus
 True BHT : elonga
tion of filiform p.
 Pseudo BHT : dis -
coloration from
fruits, candy, drugs
4. Glossopyrosis-Glossodynia
( 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 caution or combination
 local irritation : tongue habits, allergy
prosthetic/orthodontic appliances
 systemic disorders : 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
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
 Febrileillness, 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
 - gum and periodontal disease
 - infection
 - cancrum oris
 - neoplasma/oral cancer
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, respiratory and sinus
conditions
- neuropsychiatri, etc
5. Medications
- antihistamines, antipsychotics,
antispasmodics, antidepressants 
xerostomia
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 cheek, 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 ----
Hutchinson’s 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
lesions 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 : HIV INFECTION
3 phases :
a. primary infection
b. prolonged (10 years) period of clinical
latency
c. clinically apparent disease

Lab test :
CD4 count
HIV viral load
Neutrophil count
Oral manifestations of
HIV infection :
 - gingivitis
 - periodontitis marg
 - proc. Alv destruction
 sequester
 - stomatitis , ANUG,
 - Kandidiasis
 - Leukoplakia Sarkoma Kaposi
 - Ca Kaposi
 Stomatitis
Leukoplakia
Marginal periodontitis
Kaposi’s sarcoma

Necrotizing Stomatitis

ANUG
 GASTROINTESTINAL DISEASES
Crohn’s Disease
= unknown etiology, an inflammatory,
fissuring, fistulae of the small intestine,
colon  thickening narrowing of the lumen
= the gastrointestinal signs and symptoms :
cramping, pain, nausea, and diarrhea.
= swelling of lips, angular cheilitis,
hyperplastic rigid buccal mucosa, linier
ulcerations in the buccal vestibule, fissuring
lower lip, apthous ulcers, gingivitis
Oral Manifestations

fissuring lower lip hyperplastic buccal mucosa

angular cheilitis apthous ulcers

 Tx : palliative rinses/ointment/topical
steroid
(dexamethasone elixir 0.5mg/5mL
rinse/gargle, 1minute, 4xdaily)
GI Tract Disease : Crohn’n disease,
Ulcerative Colitis, Inflammatory Bowel
Disease

linier ulcerations in the buccal vestibule

Deteksi Dini Kanker Rongga
Mulut
Pendahuluan
 -kanker rongga mulut cenderung meningkat
 -di AS > 35.000 penderita kanker mulut &
faring / th., menyebabkan 8000
kematian/th.
 -data R.S dr. Sutomo, 1987-1992, 994 ca
mulut dari 2193 kasus tumor rongga mulut (
45,3% )
 Depkes 1998 : ca mulut 4,6 orang/100rb
penduduk
Pentingnya Deteksi Dini :
 Makin dini terdeteksi, makin baik
prognosisnya
 Komplikasi akibat pengobatan
keganasan ini makin kecil
 Metastase ke bagian lain juga makin
kecil
 ↓ morbiditas dan mortalitas
 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, eritroplakia
 - genetik ; ↓imunologik ; polusi lingk
 - defisiensi nutrisi ; obat-obatan
 - 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
risiko untuk dapat terjadi kanker >
normal
contoh : sifilis, lupus eritematosus
 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,
kimia 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 dg ulcerasi
/celah-celah atau
dg 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
GEJALA OBYEKTIF
1. Indurasi
2. Ulserasi
3. Eksofilik
4. Peninggian permukaan
5. Fiksasi
6. Gigi goyang tanpa sebab
7. Lidah  fungsi bicara dan menelan↓
8. Pembesaran kel.sub mandibula
 Lesi khronis

Ulkus tunggal
Indurasi+
Tanda Trauma lokal
keganasan +
Risiko+ Hilang penyebab Hilang penyebab
Lesi hilang Lesi tetap >2mg

KSS Ulkus dekubitus biopsi

KSS

Skema Manajemen Lesi Prakanker Berupa Ulkus

 Leukoplakia

Iritan + Iritan -

Hilangkan iritan
Biopsi

Respons + Respons -
Displasia - Displasia +

Observasi Tx kanker

Skema Manajemen Lesi Prakanker Berupa Leukoplakia

SELAMAT
BELAJAR