1. WHITE
LESIONS
Prepared by:
Dr. Rea Corpuz

2. White Lesions
 lesions of the oral mucosa,
which are white results
from a
 thickened layer of keratin
 epithelial hyperplasia
 intracellular epithelial
edema
 reduced vascularity of subjacent connective

3. White Lesions
 white or yellow lesions
may also be due to fibrous
exudate covering an:
 ulcer
 submucosal deposit
 surface debris
 fungal colonies

4. White Lesions
 (1) Leukoedema
 (2) Leukoplakia
 (3) Lichen Planus
 (4) Candidiasis
 (5) White Sponge Nevus
 (6) Nicotine Stomatitis

5. White Lesions
 (7) Geographic Tongue
 (8) Hairy Tongue
 (9) Dental Lamina Cyst
 (10) Fordyce’s Disease
 (11) Perleche

6. (1) Leukoedema
 generalized opacification
of buccal mucosa that is
regarded as a variation
of normal
 can be identified in majority
of population

7. (1) Leukoedema
 Etiology & Pathogenesis
 to date, cause has not
been established
 smoking
 chewing tobacco none
 alcoholo ingestion are
 bacterial infection proven
 salivary condition cause
 electrochemical interactions
have been implicated

8. (1) Leukoedema
 Clinical Features
 usual discovered as
incidental finding
 asymptomatic
 symmetrically distributed
in buccal mucosa

9. (1) Leukoedema
 Clinical Features
 appear as gray-white,
diffuse, filmy or milky
surface
 more exaggerated cases,
whitish cast with surface
textural changes
• wrinkling
• or corrugations

10. (1) Leukoedema
 Clinical Features
 with stretching of buccal
mucosa, opaque changes
dissipate
 more apparent in non-whites,
especially African-American

11. (1) Leukoedema
 Treatment
 NO treatment is necessary
 since there is no malignant
potential
 if there is any doubt about
diagnosis, a biopsy can
be performed

12. (2) Leukoplakia
 also known as Leukokeratosis;
Erythroplakia
 Leuko= white
 Plakia = patch
 defined by World Health Organization
(WHO) as a white patch or plaque
that cannot be characterized
clinically or pathologically as
any other disease

13. (2) Leukoplakia
Leukoplakia
 clinical term indicating a
white patch or plaque of
oral mucosa
 cannot be rubbed off
 cannot be characterized clinically
as any other disease
 biopsy is mandatory to
establish a definitive diagnosis

14. (2) Leukoplakia
 Mild or Thin Leukoplakia
 Homogenous or
Thick Leukoplakia
 Granular or Nodular
Leukoplakia
 Verrucous or Verruciform
Leukoplakia

15. (2) Leukoplakia
 Proliferative Verrucous
Leukoplakia (PVL)
 Erythroleukoplakia or
Speckled Leukoplakia

16. (2) Leukoplakia

17. (2) Leukoplakia
 Mild or Thin Leukoplakia
 seldom shows dysplasia
on biopsy
 may disappear or continue
unchanged

18. (2) Leukoplakia
 Homogenous or Thick Leukoplakia
 for tobacco smokers who do
not reduce their habit
 2/3 of such lesions slowly
extend laterally, become
thicker + acquire distinctly
white appearance

19. (2) Leukoplakia
 Homogenous or Thick Leukoplakia
 affected mucosa may become
leathery to palpation
 fissures may deepen
 become more numerous
 most thick, smooth lesions
remain indefinitely at this
stage

20. (2) Leukoplakia
 Homogenous or Thick Leukoplakia
 some, perhaps as many
as 1/3, regress or disappear

21. (2) Leukoplakia
 Granular or Nodular Leukoplakia
 few become even more
severe
 develop increased surface
irregularities

22. (2) Leukoplakia
 Verrucous or Verruciform
Leukoplakia
 lesions that demonstrate
sharp or blunt projections

23. (2) Leukoplakia
 Proliferative Verrucous
Leukoplakia (PVL)
 high risk form of
leukoplakia
 development of multiple
keratotic plaques
 with roughened
surface projections

24. (2) Leukoplakia
 Proliferative Verrucous
Leukoplakia (PVL)
 tend to slowly spread
 involve additional oral
mucosal sites
 gingiva is frequently involved
 although other sites may be
affected as well

25. (2) Leukoplakia
 Proliferative Verrucous
Leukoplakia (PVL)
 as lesions progress, there
may go through a stage
indistinguishable
 transform into full-fledged
squamous cell carcinoma
(usually within 8 years of
initial PVL diagnosis)

26. (2) Leukoplakia
 Proliferative Verrucous
Leukoplakia (PVL)
 lesions rarely regress
despite therapy
 strong female predilection
 minimal association with
tobacco use

27. (2) Leukoplakia
 Erythroplakia
 leukoplakia may become
dysplastic
 even invasive, with no change
in its clinical appearance
 however, some lesions eventually
demonstrate scattered patches
of redness called erythroplakia

28. (2) Leukoplakia
 Erythroleukoplakia or
Speckled Leukoplakia
 such areas usually represent
sites in which epithelial
cells are so immature
or atrophic that they can no
longer produce keratin

29. (2) Leukoplakia
 Erythroleukoplakia or
Speckled Leukoplakia
 intermixed red-and-white
lesion
 pattern of leukoplakia
that frequently reveals
advanced dysplasia on
biopsy

30. (2) Leukoplakia
 Etiology & Prognosis
 many cases are etiologically
related to use of tobacco
in smoked or smokeless
forms and may regress
after discontinuation
of tobacco use

31. (2) Leukoplakia
 Etiology & Prognosis
 other factors, such as
• alcohol abuse may have
• trauma a role in
• C. albicans infection etiology

32. (2) Leukoplakia
 Etiology & Prognosis
 nutritional factors have
been cited as important,
especially iron deficiency
anemia

33. (2) Leukoplakia
 Clinical Features
 associated with middle-aged
+ older population
 vast majority of cases occur
after age of 40 years

34. (2) Leukoplakia
 Site of Occurence
 Vestibule
 Buccal
 Palate
 Alveolar Ridge
 Lip
 Tongue
 Floor

35. (2) Leukoplakia
 leukoplakia of lips + tongue
also exhibits relative high
percentage of dysplastic or
neoplastic change

36. (2) Leukoplakia
 Treatment & Prognosis
 absence of dysplastic or
atypical epithelial changes
• periodic examinations +
rebiopsy of new suspicious
areas are recommended

37. (2) Leukoplakia
 Treatment & Prognosis
 if diagnosis as moderate to
severe dysplasia
• excision is obligatory
 for large lesions, grafting
procedures may be necessary after
surgery
 may recur after complete removal

38. (3) Lichen Planus
 chronic mucocutaneous
disease of unknown cause
 relatively common
 typically presents as bilateral
white lesions
 occasionally with associated
ulcers

39. (3) Lichen Planus
 Pathogenesis
 although cause is unknown
 generally considered to be
a immunologically mediated
process
 resembles hypersensitivity
reaction

40. (3) Lichen Planus
 Clinical Features
 disease of middle age
 affects men + women in
nearly equal numbers
 children rarely affected

41. (3) Lichen Planus
 Clinical Features
 Types:
• Reticular
• Erosive (ulcerative)
• Plaque
• Papular
• Erythematous (atrophic)

42. (3) Lichen Planus
 Clinical Features
 Reticular Form
• most common type
• numerous interlacing white
keratotic lines or striae
(Wickham’s striae)
 produces anular or lacy
pattern

43. (3) Lichen Planus
 Clinical Features
 Reticular Form
• buccal mucosa is the site
most commonly involved
• may also be noted on:
 tongue
 gingiva – less common
 lips

44. (3) Lichen Planus
 Clinical Features
 Plaque Form
• resembles leukoplakia
• but has multifocal distribution
• range from slightly elevated
to smooth and flat

45. (3) Lichen Planus
 Clinical Features
 Plaque Form
• primary sites are
 dorsum of tongue
 buccal mucosa

46. (3) Lichen Planus
 Clinical Features
 Erythematous Form
• red patches
• with very fine white
striae
• attached gingiva commonly
involved

47. (3) Lichen Planus
 Clinical Features
 Erythematous Form
• patchy distribution often
in four quadrants
• patient may complain of
 burning
 sensitivity
 generalized discomfort

48. (3) Lichen Planus
 Clinical Features
 Erosive Form
• central area of lesion is
ulcerated
• fibrinous plaque or
pseudomembrane covers
ulcer
• changing patterns of involvement
from week to week

49. (3) Lichen Planus
 Treatment
 although it cannot be
generally cured
 some drugs can provide
satisfactory control
 corticosteroids are the single
most useful group of drugs
in the management of lichen
planus

50. (3) Lichen Planus
 Treatment
 corticosteroid
• ability to modulate
inflammation + immune
response

51. (3) Lichen Planus
 Treatment
 topical application +
local injection of steroids
have been used successfully
in controlling but not
curing this disease

52. (4) Candidiasis
 common oppurtunistic
oral mycotic infection
 develops in the presence of
one of several predisposing
factors
• immunodeficiency
• endocrine disturbances
• hypoparathyroidism
• diabetes mellitus
• poor oral hygiene
• xerostomia

53. (4) Candidiasis
 caused by Candida albicans
 infection with this organism
is usually superficial, affecting
the outer aspects of involved
oral mucosa or skin

54. (4) Candidiasis
 in severely debilitated +
immunocompromised patients
such as patients with AIDS
 infection may extend into
alimentary tract (candidal
esophagitis
 bronchopulmonary tract
 and other organ system

55. (4) Candidiasis
 Clinical Features
 most common form is
acute pseudomembranous
also known, as thrush
• young infants + elderly
are commonly affected

56. (4) Candidiasis
 Clinical Features
 oral lesion of acute
candidiasis (thrush)
• white
• soft plaques that sometime
grow centrifugally + merge
• wiping plaques with gauze
sponge leaves a painful,
eroded, eryhtematous or
ulcerated surface

57. (4) Candidiasis
 Clinical Features
 Chronic Erythematous
Candidiasis
• commonly seen on
geriatric individuals
• who wear complete
maxillary denture

58. (4) Candidiasis
 Clinical Features
 Chronic Erythematous
Candidiasis
• distinct predilection for
palatal mucosa as
compared with mandibular
alveolar arch

59. (4) Candidiasis
 Clinical Features
 Chronic Erythematous
Candidiasis
• chronic low-grade
resulting from poor
prosthesis fit
• failure to remove
appliance at night

60. (4) Candidiasis
 Clinical Features
 Chronic Erythematous
Candidiasis
• bright red
• relative little
keratinization

61. (4) Candidiasis
 Clinical Features
 Hyperplastic Candidiasis
• may involve dorsum of
tongue
• pattern referred to as
median rhomboid
glossitis

62. (4) Candidiasis
 Clinical Features
 Hyperplastic Candidiasis
• usually asymptomatic
• usually discovered on
routine oral
examination

63. (4) Candidiasis
 Clinical Features
 Hyperplastic Candidiasis
• found anterior to
circumvallate
papillae
• oval or rhomboid
outline

64. (4) Candidiasis
 Clinical Features
 Hyperplastic Candidiasis
• may have smooth,
nodular or fissured
surface
• range in color from
white to more red

65. (4) Candidiasis
 Clinical Features
 Mucocutaneous Candidiasis
• long standing
• persistent candidiasis of
 oral mucosa
 skin
 vaginal mucosa

66. (4) Candidiasis
 Clinical Features
 Mucocutaneous Candidiasis
• often resistant to treatment
• begins as a pseudomembranous
type of candidiasis
• soon followed by nail +
cutaneous involvement

67. (4) Candidiasis
 Treatment
 majority of infections may
be simply treated with
topical applications of
nystatin suspension
• nystatin cream or
ointment often effective
when applied directly to
denture-bearing surface itself

68. (4) Candidiasis
 Treatment
 topical applications of either
nystatin or clotrimazole
should be continued for at
least 1 week beyond
disappearance of clinical
manifestations of disease

69. (4) Candidiasis
 Treatment
 Hyperplastic Candidiasis
• topical + systemic antifungal
agents may not be effective
at completely removing
lesions
 surgical management
may be necessary

70. (4) Candidiasis
 Treatment
 Chronic Mucocutaneous
Candidiasis associated
with immunosuppression
• topical agents may not
be effective

71. (4) Candidiasis
 Treatment
 Chronic Mucocutaneous
Candidiasis associated
with immunosuppression
• systemic administration
of medications:
 Ketoconazole
 Fluconazole
 Itraconazole

72. (5) White Sponge Nevus
 autosomal-dominant condition
 due to point mutations for
genes coding for keratin 4
and/or 13.
 affects oral mucosa bilaterally
 NO treatment is required

73. (5) White Sponge Nevus
 Clinical Features
• asymptomatic
• folded white lesions
• may affect several mucosal
sites
• lesions tend to be thickened
+ spongy consitency

74. (5) White Sponge Nevus
 Clinical Features
• presentation intraorally
is almost always bilateral
+ symmetric
• usually appears early in
life, typically before
puberty

75. (5) White Sponge Nevus
 Clinical Features
• usually observed in buccal
mucosa
• tongue + vestibular mucosa
may be involved

76. (5) White Sponge Nevus
 Treatment
• NO treatment necessary
since it is asymptomatic
+ benign

77. (6) Nicotine Stomatitis
 common tobacco-related
form of keratosis
 typically associated with pipe
+ cigar smoking
 with positive correlation
between intensity of smoking
+ severity of condition

78. (6) Nicotine Stomatitis
 combination of tobacco
carcinogens + heat is markedly
intensified in reverse smoking
(lit end positioned inside the
mouth)
 adding a significant risk for
malignant conversion

79. (6) Nicotine Stomatitis
 Clinical Features
 palatal mucosa initially
responds with an erythematous
change follwed by
keratinization

80. (6) Nicotine Stomatitis
 Clinical Features
 subsequent to opacification
or keratinization of palate
• red dots surrounded by
white keratotic rings
appear
 dot represent inflammation
of salivary gland excretory
duct

81. (6) Nicotine Stomatitis
 Treatment
 condition rarely evolves into
malignancy
 except in individuals who
reverse smoke
 discontinuation of tobacco
habit

82. (7) Geographic Tongue
 also known as erythema migrans,
benign migratory glossitis
 prevalent among whites +
blacks
 strongly associated with fissure
tongue
 inversely associated with cigarette
smoking

83. (7) Geographic Tongue
 emotional stress may enhance
the process

84. (7) Geographic Tongue
 Clinical Features
 affects women slightly more
than men
 children occasionally may
be affected
 characterized initially by
presence of atrophic patches
surrounded by elevated
keratotic margins

85. (7) Geographic Tongue
 Clinical Features
 desquamated areas appear
red + may be slightly
tender
 followed over a period of
days or weeks, pattern
changes
 appearing to move across
dorsum of tongue

86. (7) Geographic Tongue
 Clinical Features
 most patients are asymptomatic
 occasionally patients complain
of irritation or tenderness
 especially in relation to
consumption of spicy foods
+ alcoholic beverages

87. (7) Geographic Tongue
 Clinical Features
 lesions periodically disappear
 recur for no apparent reason

88. (7) Geographic Tongue
 Treatment
 NO treatment is required
because of self-limiting +
usually asymptomatic nature
of this condition

89. (7) Geographic Tongue
 Treatment
 when symptoms occur,
• topical steroids especially
ones containing antifungal
agent
 helpful in reducing symptoms

90. (7) Geographic Tongue
 Treatment
 mouth clean using mouthrinse
composed of sodium
bicarbonate in water
 reassure patients that condition
is totally benign

91. (8) Hairy Tongue
 clinical term referring to a
condition of filiform papillae
overgrowth on dorsal surface
of tongue
 there are numerous initiating
or predisposing factors for
hairy tongue

92. (8) Hairy Tongue
 broad spectrum antibiotics
such as penicillin + systemic
cortiocosteroids are often
identified in clinical
history of patients with
this condition

93. (8) Hairy Tongue
 oxygenating mouthrinses
containing:
 hydrogen peroxide
 sodium perborate
 carbamide peroxide
 have been cited as
possible etiologic agents

94. (8) Hairy Tongue
 Clinical Features
 clinical alteration translates
to hyperplasia of filiform
papillae; result is
• thick serves to trap
• matted surface bacteria, fungi,
foreign materials

95. (8) Hairy Tongue
 Clinical Features
 extensive elongation of
papillae occurs,
• gagging may be
• tickiling sensation felt

96. (8) Hairy Tongue
 Clinical Features
 color may range from white
to tan to deep brown
depending on:
• diet
• oral hygiene
• composition of bacteria
inhabiting papillary surface

97. (8) Hairy Tongue
 Treatment
 brush/scrape tongue with
baking soda
 maintain good oral hygiene
 emphasize to patients that
this process is entirely benign

98. (8) Hairy Tongue
 Treatment
 self-limiting
 tongue should return to
normal after institution
of physical debridement
+ proper oral hygiene

99. (9) Dental Lamina Cyst
 also known as Gingival Cyst of
New Born or Bohn’s nodules
 appear as multiple nodules
along alveolar ridge in neonates

100. (9) Dental Lamina Cyst
 similar epithelial inclusion
cysts may occur along midline
of palate (palatine cyst of
new born or Epstein’s pearls)
 developmental origin
 derived from epithelium
 included in fusion line
between palatal shelves +
nasal processes
 no treatment; resolve spontaneously

101. (9) Dental Lamina Cyst
 Treatment
 not necessary because nearly
all spontaneously rupture
before patient is 3 months
of age

102. (10) Fordyce’s Granules
 represents ectopic sebaceous
glands or sebaceous
choristomas
 normal tissue in abnormal
location
 regarded as developmental
 considered a variation of normal

103. (10) Fordyce’s Granules
 multiple
 often seen in aggregates
 sites of predilection include
• buccal mucosa
• vermillion of upper lip

104. (10) Fordyce’s Granules
 lesions generally are symmetrical
distributed
 tend to become obvious after
puberty
 maximal expression occurring
between 20-30 years of age

105. (10) Fordyce’s Granules
 lesions are asymptomatic
 discovered during routine
oral examination

106. (10) Fordyce’s Granules
 Treatment
 No treatment is indicated
• glands are normal in
character
• do not cause any untoward
effects

107. (11) Perleche
 also known as Angular
Cheilitis
 inflammation + atrophy
of skin of folds at angles
of mouth

108. (11) Perleche
 may be due to:
 excessive lip licking
 thumb sucking
 sagging of facial skin
in edentulous or elderly
persons

109. (11) Perleche
 may be due to:
 prolonged contact with
saliva results in
maceration
 with possible secondary
infection by Candida
or staphylococci

110. (11) Perleche
 Clinical Features
 skin at angles of mouth
has erythematous fissures
 often with exudate + crust
 further licking to moisten
inflamed area exacerbates
the problem

111. (11) Perleche
 Treatment
 applying antimicrobial
creams
 followed by low-potency
steroid creams until
symptoms resolve
 protective lip balm may help
prevent recurrence

112. References:
 Books
 Cawson, R.A: Cawson’s Essentials of Oral
Oral Pathology and Oral Medicine,
8th Edition
• (page 165-167 )
 Neville, et. al: Oral and Maxillofacial Pathology
3rd Edition
• (pages 388- 397; 590-592; 819-820)
Regezi, et. al: Oral Pathology: Clinical Pathologic
Correlations, 5th Edition
• (pages 73-105; 241-242; 296-299; 394)