This document classifies and describes various oral white lesions. It discusses hereditary lesions such as leukoedema and white sponge nevus. Reactive lesions including frictional keratosis and nicotine stomatitis are covered. Preneoplastic lesions like actinic cheilitis and idiopathic leukoplakia are summarized. Other white lesions such as geographic tongue and lichen planus are also described. Non-epithelial lesions including candidiasis and Fordyce's granules are briefly outlined. Definitions of histopathological features and guidelines for differential diagnosis are provided.

1. Oral White
lesions
Aiman A. Ali, DDS, PhD.

2. Classification of oral white
lesions
Hereditary
Reactive
Preneoplastic
Other white lesions
Non-epithelial
White-yellow lesions
Aiman A. Ali, DDS, PhD.

3. Oral White Lesions

Hereditary:
Leukoedema
 White sponge nevus.
 Hereditary benign intraepithelial dyskeratosis.


Follicular keratosis.
Aiman A. Ali, DDS, PhD.

4. Oral white lesions

Reactive:
Frictional hyperkeratosis.
 WL associated with smokeless tobacco
 Nicotine stomatitis.
 Hairy leukoplakia
 Hairy tongue
 Dentifrice-associated slough

Aiman A. Ali, DDS, PhD.

5. Oral white lesions
Preneoplastic
 Actinic
cheilitis
 Idiopathic leukoplakia
Aiman A. Ali, DDS, PhD.

6. Oral white lesions

Others:



Geographic tongue
Lichen planus
Lupus erythematosus
Aiman A. Ali, DDS, PhD.

7. Non-epithelial white-yellow lesions
Candidiasis
 Mucosal burns
 Submucous fibrosis
 Fordyce’s granules
 Ectopic lymphoid tissue
 Gingival cyst
 Parulis
 Lipoma

Aiman A. Ali, DDS, PhD.

8. Definitions
 Acanthosis
Aiman A. Ali, DDS, PhD.

9. Definitions
 Hyperorthokeratosis
Aiman A. Ali, DDS, PhD.

10. Definitions
 Hyperparakeratosis
& epithelial dysplasia
Aiman A. Ali, DDS, PhD.

11. Definitions
 Intercellular
& Intracellular edema
Aiman A. Ali, DDS, PhD.

12. Definitions
 Atrophic
epithelium
Aiman A. Ali, DDS, PhD.

13. Dyskeratosis
US
EU
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14. Why we see these
lesions clinically as
white ?
Aiman A. Ali, DDS, PhD.

15. Aiman A. Ali, DDS, PhD.

16. Increase amount of
collagen fibers
Aiman A. Ali, DDS, PhD.

17. Leukoedema
Etiology: Unknown
Clinically: Symmetrical, gray-white or
milky buccal mucosa, dissipate
with stretching
Histopathologically: Acanthosis,
parakeratosis and intracellular
edema.
No treatment is necessary
Aiman A. Ali, DDS, PhD.

18. White sponge nevus
Etiology: hereditary
Clinically: asymptomatic, symmetrical,
folded and spongy white lesion
usually
appears early in life.
Histopathologically: severe acanthosis,
parakeratosis, characteristic perinuclear
eosinophilic condensation
of prickle cell
cytoplasm.
No treatment is necessary
Aiman A. Ali, DDS, PhD.

19. Hereditary benign intraepithelial
dyskeratosis [Witkop’s disease]
Etiology: hereditary
Clinically: Oral WL with conjunctivitis
appear in the 1st year and increase with
age. Occur anywhere of the oral mucosa.
Blindness were reported in some cases.
Histopathologically: Epithelial hyperplasia,
intracellular edema, and dyskeratotic
elements in the superficial half of the
epithelium.
No treatment is necessary
Aiman A. Ali, DDS, PhD.

20. Hereditary benign intraepithelial
dyskeratosis [Witkop’s disease]

21. Follicular keratosis
[Darier’s disease]
Etiology: hereditary
Clinically: occur between 6 and 20 years. In 13% of cases it affects the
oral cavity. Skin lesions are small symmetrical papules over
the face, and trunk which become greasy due to keratin
production; fingernail changes. Keratinized mucosa is favored
oral sites where it appears as small whitish papules which may
extend to the oropharynx.
Aiman A. Ali, DDS, PhD.

22. Follicular keratosis
[Darier’s disease]
Histopathologically: - proliferation of the basal layer.
- formation of suprabasal clefts containing
acantholytic cells.
- corps nods, which are dyskeratotic cells.
Treatment : administration of vitamin A
Aiman A. Ali, DDS, PhD.

23. Frictional hyperkeratosis
Etiology: chronic friction
Clinically: adjacent to the etiologic factor
(cheek and lip mucosa, lateral borders
the tongue, alveolar ridges).
Histopathologically: Hyperkeratosis,
acanthosis and mild II.
Treatment remove the cause.
Aiman A. Ali, DDS, PhD.
of

25. WL associated with smokeless
tobacco
Etiology: mechanical/chemical irritation
induced by smokeless tobacco
Clinically: asymptomatic lesion localized in
the area where tobacco is placed,
lesion
appears granular, wrinkled or
folded,
less often erythroleukoplakic.
Histopathologically: parakeratosis, mild II
superficial intracellular edema. ED may
develop in long-time users.
Treatment remove the cause, biopsy in
persistent lesions.
Aiman A. Ali, DDS, PhD.

26. Aiman A. Ali, DDS, PhD.

27. Nicotine stomatitis
Etiology: Pipe and cigar or reverse smoking
Clinically: palatal white plaques with red
dots, which represent inflammation of the
salivary gland duct.
Histopathologically: epithelial hyperplasia
and hyperkeratosis, inflammatory
changes of the minor salivary glands,
squamous metaplasia of the ducts.
Treatment is remove the cause
Aiman A. Ali, DDS, PhD.

28. Hairy leukoplakia
Etiology: - HIV, EBV, medically induced
suppression, corticosteroids, few
cases in
healthy persons.
Clinically: papillary or filiform white plaque,
the vast majority occur bilaterally on
the borders of the tongue.
Histopathologically: acanthosis, parakeratosis
edematous S. cells, nuclear viral
inclusion in the upper layers.
Treatment no specific treatment, antiviral
drugs may improve the case.
Aiman A. Ali, DDS, PhD.

29. Hairy tongue
Predisposing factors: use of antibiotics,
systemic corticosteroids, mouth rinse,
intense smoking, and radiotherapy.
Clinically: elongation of the papillae, the
color vary from white to deep brown or
black depending on diet and other factors.
Histopathologically: elongated filiform
papillae, surface contamination,
subjacent inflammation.
Treatment remove the cause, brushing the
tongue with sodium bicarbonate and water
Aiman A. Ali, DDS, PhD.

30. Dentifrice-associated slough
Etiology: chemical burn due to the use of
different brands of toothpaste
Clinically: painless superficial whitish slough
of the buccal mucosa.
Treatment change the toothpaste
Aiman A. Ali, DDS, PhD.

31. Actinic cheilitis
Etiology: Ultraviolet light waves (2900-3200 nm)
Clinically: atrophic silvery gray glossy, fissured
lesion commonly affect the lower lip, in
some
cases erosion or ulceration can be seen.
Histopathologically: atrophic and hyperkeratotic
epithelium, elastin replacement of collagen fibers
and telangiectasia.
Treatment: use of lip protectors (sunscreen agents),
biopsy is mandated in aggressive cases. In
cases with atypical changes vermilionectomy
in combination with cryosurgery or chemotherapy
Aiman A. Ali, DDS, PhD.

32. Idiopathic leukoplakia
Definition: white patch that cannot be
rubbed off and cannot be characterized
clinically as any other disease.
Risk factors: Tobacco, alcohol, nutrition,
unknown.
Clinical features: - Age and sex
- Site
- Clinical type
Aiman A. Ali, DDS, PhD.

33. Aiman A. Ali, DDS, PhD.

34. Aiman A. Ali, DDS, PhD.

35. Idiopathic leukoplakia
 Histopathologically:
Non-dysplastic
 Dysplastic

 Epithelial
dysplasia:
Drop shaped rete ridges
 Basal cell crowding
 Increased mitotic figures
 Nuclear pleomorphism & hyperchromatism
 Individual cell keratinization
 Cellular pleomorphism
 Altered nuclear-cytoplasm ratio

Aiman A. Ali, DDS, PhD.

37. Idiopathic leukoplakia
Treatment:
- conservative: remove the cause,
vitamins A & E.
- Surgery: resection, Laser.
Prognosis and classification .
Aiman A. Ali, DDS, PhD.

39. Geographic tongue
Etiology: unknown
Clinically: asymptomatic red desquamated
and white keratotic areas, this map
change within few days.
Histopathologically: red area: atrophic
filiform papillae, white area: HK
and acanthosis.
No treatment is necessary
Aiman A. Ali, DDS, PhD.

40. Lichen planus
Etiology: Chronic, inflammatory, mucocutaneous, immunologically mediated
process
Clinically: - age and sex,
- types
Histopathologically: according to the type,
dense band of inflammatory cell
infiltration (T8 lymphocytes),
liquefaction degeneration of basal cells,
saw teeth rete ridges, hyperkeratosis,
atrophic epithelium or fibrotic yellow
pseudomembranous
Treatment & prognosis: SAID, vit.A
Aiman A. Ali, DDS, PhD.

42. Aiman A. Ali, DDS, PhD.

43. Lupus erythematosus
Etiology: connective tissue, autoimmune, mucocutaneous disease. Systemic and Discoid.
Clinically: DLE: Disk-shaped erythematous plaques
common on the face and scalp, lip and oral
cavity. SLE: involve multiple organs,
erythematous rash of butterfly distribution,
fever malaise loss of weight.
Histopathologically: E atrophy, HK, BC destruction,
subepithelial and perivascular II, dilatation
of BV. IgG, IgA, IgM & C3 along the BM.
Treatment is topical or systemic corticosteroids.
Aiman A. Ali, DDS, PhD.

44. Candidiasis
Etiology: mainly C. albicans,
predisposing factors:
- Immunodeficiency
- Endocrine disturbances:
- Diabetes mellitus
- Pregnancy
- Hypo pitutirism & parathyroidism
- Corticosteroid therapy
- Long-term antibiotic therapy
- Malignancies and their therapy
- Xerostomia and bad oral hygiene
Aiman A. Ali, DDS, PhD.

45. Candidiasis
Clinical features:
- Acute:
- Thrush
- Erythematous
- Chronic:
- Erythematous
- Hyperplastic
- Mucocutaneous:
- Localized
- Familial
- Syndrome associated
Aiman A. Ali, DDS, PhD.

46. Candidiasis
Histopathological features: fungal hyphae
(PAS) penetrating the upper layers of the
epithelium, Neutrophilic infiltration of the
epithelium, and epithelial hyperplasia.
Treatment: antifungal, nystatin,
muconazole, clotrimazole, fluconazole
and ketokonazole.
Aiman A. Ali, DDS, PhD.

47. Mucosal burns
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48. Submucous fibrosis
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49. Fordyce’s granules
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50. Ectopic lymphoid tissue
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51. Gingival cyst
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52. Parulis
Gingival abscess, puss or fistula.
Aiman A. Ali, DDS, PhD.

53. Lipoma
Tumor of adipose tissue
Aiman A. Ali, DDS, PhD.

54. Main Points for Differential
Diagnosis
 Keratotic
or non-keratotic
 Symmetrical or asymmetrical
 Biopsy and microbiology
Aiman A. Ali, DDS, PhD.