The presentation explain white lesions in oral cavity and the classification the demonstrate the etiology, histopathology, diagnosis and treatment for each one.

1. White lesions in oral cavity

2. Prof .Dr.Amal M. El Deeb
PROF.OF ORAL PATHOLOGY
FACULTY OF DENTISTRY,UMM AL
QURRA UNIVERSITY,MAKKA,SA

3. White lesions in oral cavity
Def.
lesions appear as white patches in oral
cavity.
Causes of white lesions:-
1-Increase in thickness of one or more of
epithelial layers.
2-Abnormal character of keratin.
3-Abnormal permeability of epithelium.

4. Classification:-
A) Keratotic White lesions:-
1.Focal (frictional) keratosis.
2.White sponge nevus.
3.Lichen planus.
4.Hairy leukoplakia.
5.Leukoplakia.
6.Candidal leukoplakia.
7.Discoid lupus erythromatosis.
B) Non keratotic white lesions:-
1.Leukodema.
2.Candidiasis.
3.Mucosal burns.

6. 1) Focal (frictional) keratosis:-
Etiology:-
1-chronic rubbing of friction against an oral
mucosa.
2-It represents a protective action against
low grade, long term trauma as
habitual lip or cheek biting.

7. Clinically:-
Age: 5-6 decades.
Sex: male>female.
Site: mandibular mucosa, cheek,
palate, floor of the mouth,
maxillary mucosa, tongue,
buccal mucosa along occlusal
line, edentulous ridges.
Shape: focal keratosis clinically
show outlined white patches,
not indurated ,have no red
margin, painless.

8. Histopathology
1-hyperkeratosis or
hyperparakeratosis.
2-thickening of granular cell
layer.
3-acanthosis but the
individual cells are
normal.
4-a few chronic
inflammatory cells in
adjacent connective
tissue.

9. Diagnosis:-
1. Careful history taking.
2. Careful examination.
3. Biopsy must be taken if no exact cause
is known.
Treatment:-
Removal of the cause, the lesion may
disappear in 2-3 weeks.

10. White sponge nevus
(familial white folded gingivostomatitis)
Etiology:-
It is a hereditary disease.
Site:-
Cheek mucosa along occlusal line bilaterally,
ventral surface of tongue, floor of mouth,
esophagus, rectum, vagina,larynx.

11. Shape:-
The mucosa appears
thickened, folded,
corrugated (velvety), with
a spongy texture and a
peculiar white opalescent
hue.
It is bilateral and
symmetrical

12. Histopathology:-
1- The epithelium is irregular,
thickened, showing both
hyperparakeratosis and
acanthosis.
2-The superficial epithelial cells fail
to take any stain (washed out
appearance).
3-These vaculated cells may show
pyknotic nuclei
4-The connective tissue show a mild
inflammatory cell infiltration.
5-Intra-cellular and inter-cellular
odema.

13. D.D.
1-hereditary bengin epithelial dyskeratosis.
2-Lichen planus (hypertrophic type).
3-Cheek biting.
4-Leukodema.
Treatment:-
No specific treatment.
Topical tetracycline.

14. Lichen Planus:-
Def:-
It is a chronic inflammatory disease, not
infectious.
It is one of the most common
dermatological disease to manifest itself in
oral cavity, in which oral lesions precede
the skin lesions.

15. Its importance relates to:-
1- its degree of frequency of occurrence.
2- its occasional similarity to other mucosal
diseases.
3- its occasional painful nature.
4- its possible connection to malignancy.

16. Etiology:-
Unknown, it may be:-
1)emotional stress, over work, trauma,
infection, malnutrition.
2)Psychosomatic in origin.
3)Auto-immune disease:
* the epithelial cells are the primary the
target cells.
* The mechanism of basal cell damage is
related to cell mediated immune process
involving Langerhans cells, T-lymphocytes,
Macrophages.

17. Stimulus activate langerhans cells,
macrophages Interleukin 1
attract T-
lymphocytes &
stimulate them to
produce Interleukin 2

18. Interleukin 2 T-cell proliferation.
T-cell activation.
Activated lymphocytes
toxic for basal cells.
Secrete Gamma
interferon
Gamma interferon induce keratinocytes to express
HLA-DR class 2 histocompatibility antigen.
Lymphocytes normally express HLA-DR.
Linkage of these HLA-DR occur which result in
inappropriate epithelial antigenic information
passed to lymphocytes.
So, self antigen may be recognized as foreign, by
host T-lymphocytes resulting in auto immune
response.

19. Clinically:-
Age: middle age, rare in children.
Sex: male=female.
Site:-
1) skin lesions: any where, bilateral, symmetrical
on flexor surface of wrist, inner aspect of
thighs, trunk, nails, vulvar mucosa.
2) Oral lesions: gingiva, cheek, lips, tongue,
palate.

20. Oral lesions:-
Lichen planus has patterns in oral cavity:-
1- Reticular lichen planus.
2- Hypertrophic lichen planus.
3- Atrophic lichen planus.
4- Erosive lichen planus.
5- Bullous lichen planus.

21. Reticular Lichen planus:-
The most common type.
Site: posterior buccal
mucosa bilaterally, lips,
palate, gingiva.
Shape: radiating white,
velvety, thread like
papules in a linear,
annular or retiform
arrangement.
A tiny white elevated dots
is present at the
intersection of white lines
known as (striae of
wickham).

22. Erosive Lichen Planus:-
Site: posterior- inferior
aspect of buccal mucosa
adjacent to mandibular
molar teeth.
Shape: atrophic,
erythematous areas with
central ulceration, the
periphery of atrophic
regions is bordered by
fine, white radiating
striae.

23. Atrophic Lichen planus:-
Site: attached gingiva.
Shape: smooth red,
poorly defined
atrophic zones, at its
margins there are
whitish keratotic
striae radiating
peripherally and
blending into
surrounding mucosa.

24. Hypertrophic lichen planus:-
Site: dorsum of tongue
and buccal mucosa.
Shape: well
circumscribed white
lesions (plaque like)
which range from
slightly elevated and
smooth to slightly
irregular.

25. Histopathology:-
1-Hyperorthokeratosis or hyperparakeratosis.
2-Variable degree of acanthosis.
3- Destruction of basal cell layer of epithelium
(hydropic degeneration) with vacuolization of
basal cell layer.
4- Rete process may be absent, hyperplastic or
saw-toothed shape.
5- tearing between epithelium and C.T.
6-presence of colloid (civatte, hyaline, cytoid
bodies) as discrete eosinophilic ovoid bodies at
basal cell layer.

26. Lichen planus

27. Atrophic Lichen Planus
Erosive Lichen Planus

28. D.D.
1- candidiasis.
2-leukoplakia.
3-squamous cell carcinoma.
4-drug eruption.
5-discoid lupus erythromatosis.
N.B. Grinspan`s syndrome:-
Lichen planus.
Diabetes mellitus.
Vascular hypertension.

29. Treatment:-
No specific systemic or local therapy.
Corticosteroids (topical, intralesional ,systemic).
Antifungal therapy.
Retinoids.

30. Prognosis:-
It is a benign lesion , it was not considered
a premalignant condition But a large
number of cases of epidermoid carcinoma
developing in oral lesions of lichen planus.
The majority of cases of cancer have
occurred in erosive and atrophic types .

31. Hairy leukoplakia:-
Def.:-
It is an unusual white lesion with a hairy appearance or
corrugated surface that occurred on the lateral border or
dorsum of tongue.
Etiology:-
1-In male homosexuals.
2-An opportunistic infection relates to Epstein-Barr virus.
3-It is related to AIDS patients.
N.B. Viral particles are present and replicated within the epithelial
cells of tongue. Human papilloma virus present in co-existence
with EBV.

32. Clinically:-
Site: lateral surface of
tongue, dorsum of
tongue, floor of mouth,
palate.
Shape: unilateral or bilateral
surface which is folded or
corrugated or papillary(
hairy).
No associated symptoms
unless it is superimposed
by candidal infection.

33. Histopathology:-
1-Epithelial hyperplasia.
2-Marked hyperparakeratosis.
3- Formation of keratotic surface
irregularities and ridges.
4-Spinous cell layers show
koilocytosis.
5-Alterationas of nuclear chromatin in
form of viral inclusions.
6-Candidal albicans hyphae extend
into superficial epithelial layers.
7- No inflammatory cell infiltration in
C.T.

34. Diagnosis:-
1) Immunohistochemical staining technique
using anti-viral antibodies.
2) Ultrastructural study using electron
microscope.
3) Southern blot hybridization procedure .

35. D.D.
1-idiopathic leukoplakia.
2-leukoplakia associated with tobacoo use.
3-lichen planus.
4-chronic hyperplastic candidiasis.
5-frictional keratosis.
6-keratotic reaction associated with
electrochemical interactions.

36. Treatment:-
Acyclovir
Topical corticosteroids.

38. Candidiasis (Moniliasis)
Def.
This is a term that encompasses a group of mucosal and
cutaneous conditions with a common etiological agent
from the Candida genus of fungi.
Etiology:-
The causative organism is Candida Albicans.
The predisposing factors are:-
1-topical corticosteroids.
2-malabsorption , malnutrition.
3-poor oral hygiene.
4-xerostomia.
5-systemic antibiotic therapy.
6-Cancer chemotherapy.
7- AIDS.

39. Classification of Oral Candidiasis:-
A) Acute Candidiasis:
1-pseudomembranous (Thrush).
2-atrophic (antibiotic sore mouth).
B) Chronic Candidiasis:
1-atrophic (denture sore mouth & angular chelitis)
2-hypertrophic (candidal leukoplakia &median
rhomboid glossitis & chronic multifocal
candidiasis).
C) Mucocutanous forms:
1-localized.
2-familial.
3-syndrome-associated.

40. Thrush

41. Laboratory findings:-
1-remaval of a portion of
the candidal plaque.
2-It is smeared on a
microscopic slide,
macerated with 20%
potassium hydroxide.
3-Then examination for
typical hyphae.
4-Culture identification and
quantification of
organisms may be
performed with a variety
of media as blood agar or
cornmeal agar.

42. Histopathology:-
Histological section is stained with
periodic acid Schiff reagent PAS
will show presence of yeast cells
and hyphae in the superficial
and deeper layers of involved
epithelium give bright magenta
color.
Histological features include:-
1-hyperparakeratosis.
2- chronic inflammatory cell
infiltration in CT
3-collections of neutrophils (micro-
abscess) in parakeratin layer.
4-The candidal hyphae embedded
in parakeratin layer.

43. D.D.
1-slough associated with chemical burns.
2-traumatic ulcerations.
3-mucous patches of syphilis.
4-white keratotic lesions.
Treatment:-
1) Nystatin.
2)Imidazole agents.
3)Triazole agents.

44. Leukodema:-
Def.
It is an abnormality of the buccal mucosa of
unknown cause.
It may be considered as variation of the normal rather
than a disease.
Etiology:-
Causative factors as: smoking, alcohol, bacterial infection.

45. Site: buccal mucosa,
labial mucosa, floor of
the mouth.
Shape: bilateral,
symmetrical filmy
opalescence mucosa
become grayish white
in late stage with
corrugated surface.
Race: blacks > whites.

46. Histopathology:-
1-The epithelium is acanthotic, parakeratotic.
2-The enlarged cells in the superficial part of
stratum spinosum appear vacuolated because
they contain glycogen.
3-The rete ridges are broad and enlarged.

47. Diagnosis:-
1-gentle stroking with a gauze pad will not remove
it ( not rub off )
2-With stretching of buccal mucosa, the opaque
changes will dissipate.
D.D.
1-leukoplakia.
2-white sponge nevus.
3-response to chronic cheek biting.
Treatment:-
No treatment is necessary.

48. Mucosal burns:-
Chemical Burns:-
Topical applications of
chemicals as aspirin
tablets which is used in
self medication and held
locally against a painful
tooth and allowed to
dissolve slowly.
Thermal Burns:-
Common in hard palatal
mucosa caused by hot,
sticky food.

50. Premalignant lesion:-
It is a benign , morphologically altered
tissue that has a greater than normal risk
of malignant transformation.
Ex. 1-leukoplakia.
2-erythroplakia.
3-sublingual keratosis.
4-candidal leukoplakia.
5-stomatitis nicotina.

51. Premalignant condition:-
It is a disease or patient habit that doesn`t
necessarily alter the clinical appearance of local
tissue but is associated with a greater than
normal risk of precancerous lesion or cancer
development in that tissue.
Ex. 1-Oral sub mucous fibrosis.
2-Paterson-Kelly syndrome.
3-lichen planus.
4-Discoid lupus erythematosis.

52. Leukoplakia:-
Def.
It is a white patch or plaque that cannot be characterized
clinically or pathologically as any other disease.
It is a clinical term.
Etiology:-
Exact etiology is unknown ,it may be:-
1-tobacco.
2-alcohol.
3-ultraviolet radiation.
4-trauma.
5-nutritional deficencies.
6-micro-organisms (treponema pallidum , candida albicans ,
human papilloma virus ).

53. Clinically:-
Age: middle age 4-6 decades.
Sex: male > female.
Site: Tongue, floor of mouth, buccal mucosa,
palate, lower lip, retro molar sites.
Shapes:-
1-mild ( thin ) leukoplakia.
2-Homogenous (thick) leukoplakia.
3-Granular or nodular leukoplakia.
4-Verrucous leukoplakia.
5-Proliferative verrucous leukoplakia.
6- Erythroleukoplakia or speckled leukoplakia.

54. Leukoplakia

55. Proliferative verrucous leukoplakia

56. Speckled Leukoplakia

57. Histopathology:-
It varies as follow:-
1-Hyperkeratosis: thickened keratin layer of
surface epithelium either hyperparakeratosis or
hyperorthokeratosis.
2-Acanthosis: thickened spinous layer.
3-Surface hyperkeratosis but show atrophy or
thinning of surface epithelium.

58. 4- epithelial dysplasia:-
It is a term to sum up various disturbances of epithelial
growth as:-
1-drop-shaped epithelial ridges.
2-basal layer hyperplasia.
3-loss of basal cell polarity.
4-loss of normal stratification.
5-cellular pleomorphism.
6-nucleal pleomorphism and hyperchromatism.
7-increased nuclear/cytoplasm ratio.
8-loss of intercellular adherence.
9-individual cell keratinization.
10-incrased normal and abnormal mitosis in shape, site,
number.

59. Epithelial dysplasia

60. Epithelial dysplasia is classified according to the
severity as follow:-
Mild: when alterations limited to basal and
parabasal layers.
Moderate: when alterations involve from basal
layer to midportion of spinous layer.
Severe: when alterations involve from basal layer
to a level above midpoint of epithelium.

61. Carcinoma in situ:-
Def.
Dysplastic epithelial cells that extend from
basal layer to surface of mucosa (Top-to-
Bottom) changes.
It is called (intra-epithelial carcinoma).

62. D.D.
1-frictional keratosis.
2-galvanic keratosis.
3-verrucous hyperplasia.
4-lichen planus.
5-leukodema.
6-white sponge nevus.

63. Treatment:-
1-Identification of the etiological factor
discontinuation.
2-If no dysplastic changes are found, periodic
and careful follow-up is needed every 6
months.
3-Removal of dysplastic changes : surgically,
cryosurgery, electrodessication.
4- In case of extensive lesions, grafting is needed.

64. Candidal Leukoplakia:-
Age: adult
Histopathology:-
1-mitotic activity is 4 times higher than that of
idiopathic leukoplakia.
2-heavly infiltration of surface epithelium with hyphae
of Candida.
3-chronic inflammatory cells are more numerous.
Treatment: antifungal therapy may improve the
condition.

65. Nicotinic Stomatitis:-
Def.
It is the most frequently leukoplakic lesion
of the palate.
Etiology:-
1-pipe and cigar smoking.
2-long term use of extremely hot beverges.
3-reverse smoking.

66. Clinically:-
Age: more than 45 years.
Sex: male > female.
Site: palatal mucosa.
Shape:-
Erythematous patches over time
increase in keratinization
,opacification. Red dots are
seen in posterior portion of
hard palate.
These dots are surrounded by
white keratotic ring , these
dots represent inflammation of
ductal elements of underlying
minor salivary gland.

67. Histopathology:-
1-epithelial hyperplasia.
2-acanthosis.
3-hyperkeratinization.
4-chronic inflammatory cell
infiltration of sub epithelial
connective tissue.
5-minor salivary gland show
moderate degrees of
inflammation.
6-excretory ducts show
squamous metaplasia.

68. Treatment:-
1-Stop smoking.
2-It is a completely reversible habit, the
palate return to normal within 1-2 weeks
of smoking cessation.

69. Erythroplakia:-
Def.
It is a clinical term represents a red patch that
can't be clinically or pathologically diagnosed as
any other condition.
Etiology:-
Unknown, Some etiological factors as : tobacco,
alcohol ,nutritional defects, chronic irritation.
N.B. Erythroplakia is less common but more
dangerous than leukoplakia.

70. Clinically:-
Age: 50-70 years.
Sex: male > female.
Site: floor of mouth,
retro molar area ,
tongue, soft palate.
Shape:-
1-homogenous: red
patch ,velvety ,well
demarcated, soft
macule or papule.
2-spkeled: associated
with focal white area.

71. Histopathology:-
90% of cases show
severe dysplasia.
50% of cases show
invasive squamous
cell carcinoma.
40% of cases show
carcinoma in situ.

72. D.D.
1-atrophic candidiasis.
2-macular form of Kaposi sarcoma.
3-vascular malformation.
4-contact allergic reaction.
5-psoriasis.

73. Treatment:-
1-careful examination.
2-biopsy taking is necessary.
3-surgical excision is necessary.
4-post operative histopathological
examination is necessary.

75. Oral submucous fibrosis
Def.
It is a chronic , progressive, scarring high
precancerous condition of oral mucosa.
Etiology:-
1-chronic chewing of areca and betel nut.
2-general nutritional deficiency.
3-hypersensitivity to various dietary constituents
as spicy.

76. Clinically:-
Race: North America, Pakistanis.
Age: wide range, 20-40 years.
Site: buccal mucosa, retro molar area, soft
palate may extend into pharynx, esophagus.
Shape: White yellowish lesion, the oral mucosa
loses its resilience and elasticity, the process
progresses from lamina propria to underlying
musculature.

77. Histopathology:-
1-hyperkeratosis with epithelial atrophy.
2-variable degrees of dysplastic changes.
3-superficial portions of lamina propria are poorly
vascularized and hyalinized.
4-submucosal deposition of extremely dense and
a vascular collagenous C.T. with variable
numbers of chronic inflammatory.

78. D.D.
1-radiating related sub epithelial fibrosis.
2-mucosal scarring secondary to thermal or
chemical burn.
Treatment:-
1-stop the habit.
2-stretching exercises.
3-introlesional injection of corticosteroids.
4-surgical excision of fibrous bands and sub
mucosal placement of placental grafts.

79. Paterson-Kelly syndrome.
(Plummer-Vinson Syndrome):-
It Includes:-
1-glossitis.
2-hystrical dysphagia.
3-hypochromic microcytic anemia.
Etiology:-
1-micro-organisms:Candida Albicans, Staph.
2-xerostomia.
3-nutritional deficiencies.
4-anamias.
5-mechanical trauma.
6-neurologic abnormalities.

80. Clinically:-
Age: middle age 40-50 years.
Sex: female.
Site: soft palate, buccal mucosa.
Symptoms: pain, burning sensation, altered taste
and xerostomia.
Shape: lemon-tinted pallor skin, angular cheilosis,
smooth glazy painful tongue .koilonchia.

81. Histopathology:-
1-atrophy of the epithelium.
2-complete absence of rete process.
3-hyalinization of lamina propria.
4-narrowing of blood vessels.
Treatment:
1-replacement nutritional therapy.
2-identification of the cause and treat it.
3-high protein diet.

83. Nevus
Def.
It is a congenital or developmental malformation of skin
and mucosa leads to pigmented lesion composed of
nevus cells.
Nevus cell:-
Origin : melanoblasts originates from neural crest cells in
dorsal region of embryo and migrates to skin and
mucous membrane along the course of peripheral
nerves.
Shape:
*Oval, round or polygonal.
*Tend to make nests ( Theques).
*Produce melanin in superficial areas of lesion.

84. Clinically:-
Age: childhood.
Sex: female > male.
Race: whites > blackes.
Site:-
In skin : in any site most common above waist.
Intra-orally: palate, buccal mucosa, labial mucosa,
gingiva, alveolar mucosa, vermilion.
Colour: range from tan to black depending on the
amount of melanin produced and the depth of
the lesion.

86. Histopathology:-
It is characterized by a benign unencapsulated
proliferation of nevus cells which has a
characteristic feature is that the superficial
nevus cells tend to be organized into round
aggregates (Theques).
There are 3 types:-
1-junctional nevus.
2-compound nevus.
3-intradermal nevus.

87. 1- junctional nevus:-
Theques of vevus cells are found only along the basal cell
layer of epithelium, especially at tips of rete ridges.
It presents at junctional zone between epithelium and
C.T.

88. 2-Compound nevus:-
Groups of nevus cells proliferate to drop off into
underlying dermis or lamina propria.
Nevus cells present both along junctional area and
within underlying C.T.

89. 3-Intradermal (intramucosal) nevus:-
Nevus cells are found only within underlying C.T.

90. Oral Nevi:-
* The most common type is intramucosal
nevus.
* The lesion may or may not show some
degree of melanin pigmentation.

91. Malignant transformation of nevus
(dysplastic nevus):-
Clinically:-
1-varies pigmentation.
2-irregular margins.
3-distorted surface architecture.
Histopathology:-
1-disorded proliferation of nevus cells at dermal-
epidermal junction.
2-nuclear atypia as nuclear pleomorphism,
hyperchromatism.

92. Blue nevus:-
Def.
It is a benign proliferation of dermal
melanocytes usually deep within
subepithelial connective tissue.
Types:-
1-common blue nevus.
2-cellular blue nevus.

93. 1-Common blue nevus:-
Site: dorsa of hands, feet, palate.
Age: children.
Sex: female.
Shape: macular lesion, blue or black.
Size: < 1cm.
Histopathology:-
It is composed of collection of elongated,
slender melanocytes with branching
dendritic extensions located within dermis.
These cells align themselves parallel to
surface.

94. 2-Cellular blue nevus:-
Site: buttock region.
Age: 2-4 decades.
Size: > 2cm.
Shape: slow-growing blue-black papule or
nodule.
Histopathology:-
Wellcircumscribed ,highly cellular
aggregation of plump,melanin producing
spindle cells within dermis or submucosa ,
more typical pigmented dendritic spindle
cells are seen at the periphery of the
lesion.

95. D.D.
1-Kaposi sarcoma.
2-Haemangioma.
3-Early melanoma.
Treatment:-
Conservative surgical excision.