P rogram P endidikan S pesialis D okter G igi

D epartemen Ilmu P enyakit M ulut FKGUI

Yuniardini S Wimardhani
2008
LE S I PU TIH
 HE R E D ITAR Y WHITE LE S IO N
 R E AC TIVE /INFLAM M ATO R Y WHITE
LE S IO N
 D evelopmental white lesion
 G ingival and palatal cyst of newborn and
adult
 M iscellaneous lesions
H E R E DITAR Y WH ITE
LE S ION
 Unclear etiology M icroscopically:
 Normal variation  Thickening epith 
parakeratos is
Features:  E dema intracellular at
 B ilateral, buccal s tratum spinos um
mucosa
 Faint, white, diffus e, Treatment:
filmy appearance,  No treatment
foldedwrinkling
mucosa
 #scrapped off,
fade/disappear on
strecthing
 Asymptomatic, no
malignant change
 R are autosomal disorder
 >affect non-cornified epith
 Identified at birth, > intense
at puberty
 R elated with K4 and K13
gene dis turbances
Features
 White lesion, elevated,
irregular fis sures plaque
 Buccal mucosa
 D ysphagia if es ophagus
involved
 D D / with leukoplakia,
plaque type candidiasis
M icroscopically:
 Obvious intracelullar
edema of >>stratum
spinosum
 P yknotic nuclei
 No/mild infiltration of
inflammation cells
M anagement:
No treatment
 Benign condt’n
 Antibiotic in several
studies no cons is tent
res ults
 = Witkop’s disease M icroscopically:
 R are autosomal  P arakeratinis ed
dominant disorder  S tratum s pinos um
Features: thickening with
 Thick, corrugated, dys keratotic features
asymptomatic white
spongy plaque of M anagement:
buccal&labial mucosa O ral les ion: no treatment
 D etected at 1 st year of O ccular les ion 
life, >>intense until opthalmologis t
teens
 B ulbar conjuctiva
lesion
 O ccular irritation,
photophobia, blindness
 R are X -linked G enodermatosis
 O ral changes  erythro/leukoplakia
 D ysthropic nails, hyperpigmentation of
skin (face, neck, chest)
 Haematologic changes
 C arcinoma in early adulthood
R E A C T I V E /I N FL A M M A T O R Y
WH ITE LE S ION
Linea alba, frictional keratosis, cheek
chewing, chemical injuries of oral mucosa,
actinic keratosis, smokeless tobacco
induced keratosis, nicotine stomatitis,
sanguinaria induced leukoplakia
 a white horizontal M anagement:
streak on the buccal,  No treatment
occlus al plane  M ay disappear
 associated with spontaneously
pressure, frictional
irritation, s ucking
trauma
 > in < overjet
 a white plaque, rough
surface,related to
mechanical irritation
usually resolve on
elimination of the irritant
(rough or maladjusted
dentures,sharp cusps
and edges of broken
teeth)
 D D / leukoplakia
M icroscopically:
 Hyperkeratosis
 Achantosis
M anagement:
 E limination of irritant
 Biopsy for 2 weeks non
healing lesion after agent
removal
 chronic irritation sucking,
nibbling, or chewing 
thickened, scarred, and
paler mucosa
 stress or in psychological
situations  habitual
cheek biting
 Lateral tongueD D /
O HL
 D D /WS N, burns,
candidias is
M icroscopically:
 hyperparakeratosis
and acanthosis
 shaggy and ragged
keratin w/ adherent
bacterial
M anangement:
 a plas tic occlusal
night guard
 Lab invest ? O HL
 Transient non-  aspirin, silver nitrate,
keratotic white formocresol, sodium
lesions a result of hypochlorite,
chemical injuries paraformaldehyde,
caus tic when dental cavity
retained in the mouth varnis hes,
for long periods acidetching materials,
and hydrogen
peroxide.
 premalignant M icroscopically:
epithelial lesion  Atrophic epithelium
 long-term s un  Lamina propria:
expos ure elas tosis/basophilic
 Biops ies les ions homogenous
repeatedly ulcerate, amorphous alteration
crust over, with of the collagen
thickened white area.  D ysplastic features
 P eople w/outdoor
occupations , and/or
fair complexions
 white mucos al les ion  Biops y atypical
in the area of les ion: ulceration,
tobacco contact erythroplakia, intense
 found in habitual whiteness, or a
users of s mokeles s verrucoid or papillary
tobacco.  M alignant
 Anterior mandibular trans formation >4x
– posterior for chronic smokeless
 C essationnormal tobacco users.
mucos al 1-2weeks
 >1m.obiopsy
 =stomatitis nicotina Features :
palati, smoker’s  Numerous
palate papules ,punctate red
 specific white les ion centers (inflamed,
on hard and metaplastically minor
softpalate of heavy salivary gland ducts)
cigarette, pipe, and resolve 2 weeks of
cigar s mokers. ces sation
 areas expos ed to  Biops y persistent
concentrated amount les ion> 1 month of
of hot smoke ces sation
 Not malignant
 S anguinaria extract,  Inducing dysplastic
a mixture of keratosis
benzophenanthridine  Avoid!
alkaloids (from  No regression in
bloodroot plant some Viadent-
S anguinaria induced leukoplakias
canadens is ), us ed in  months after the
oral rinses and ces sation of Viadent
toothpaste s ince use.
1982. (e.g Viadent)
D E VE LO P M E NTAL WHITE
LE S IO N
 C ystic ectopic lymphoid tiss ue (oral
lymphoepithelial cyst)
 >pos terior lateral border of the tongue (lingual
tonsil) and Waldeyer’s ring.( tonsillar tissue
:lingual, pharyngeal, palatine tonsils)
 reddis h yellow or white submucos al dome-
shaped nodules.
 D iagnosed:clinical features.
 large enough to require a biopsy soft palate
irritation and itchingremoval
 multiple sessile dome shaped lesions 2 to
3 mm, chalk white, maxillary anterior
alveolar ridge just lingual to the crest.
 posterior region of the jaw on the crest of
the ridge occlusal to the crowns of the
molar teeth
 seen in newborn or very young infants
and disappear shortly after birth; originate
from remnants of the dental lamina.
 =erythema migrans, benign migratory glossitis,
erythema areata migrans , stomatitis areata
migrans
 common benign condition dorsal surface
tongue
 Association with ps oria s is
 Both conditions feature annular lesions of the
tongue with slightly depressed atrophic centers
(devoid of filiform papillae) and raised white
borders
 clinical term=abnormal coating
dorsal surface c/desquamation of cells
that make up the secondary filiform
papillabuildup of keratinhighly
elongated hairs
 black colour :tobacco (heavy smoking)
and psychotropic agents, broad-spectrum
antibiotics (penicillin and the use of
systemic steroids).
 slowly progressive chronic fibrotic disease
of the oral cavity and oropharynx, w/
fibroelastic change and inflammation of
the mucosaprogressive inability to open
the mouth, swallow, or speak
 Very resistant to treatment
 be a premalignant condition
 oral cancer developed in 7.6% of patients
malignant transformation rate was 4 to
13%