3. INTRODUCTION
• White lesions of the oral cavity are not
uncommonly encountered during clinical
practice. Many of them are harmless and do not
require any treatment other than reassurance
from the side of the clinician.
• But still a small minority roughly 4% are
potentially dangerous if left unattended
4. INTRODUCTION
• Identifying and recognizing a premalignant
lesion or a frank malignancy in the early stages
will go a long way in averting the development
of a malignancy and will provide an excellent
prognosis with minimal disfiguration and
functional handicaps.
5. DEFINITIONS
• Pathologies that increase the thickness of the
oral epithelium will cause it to appear white.
• It appears white due to an increased distance
between the vascular bed and the surface
epithelium.
• The white appearance may be due to the
thickness of the keratin layer- hyperkeratosis
6. • Or a thickess of the spinous cell layer-
acanthosis
• Or due to fluid within the epithelium –
leukoedema
• Or due to a reduced vascularity in the
underlying lamina propria.
• Surface ulcerations which are covered by
fibrin also appear white.
7. CLASSIFICATION
A. Inflammatory/ Reactive
B. Dysplastic/neoplastic
C. Oral manifestations of common dematologic
disease (eg Lichen planus)
D. Oral manifestations of systemic disease
E. Developmental/Hereditary.
10. Hereditary White Lesions.
Leukoedema
• Not a true pathology but a variation of a
normal condition. Predominant in black
children, teenagers and adults.
• Affects the buccal mucosa bilaterally, rarely
seen on the labial mucosa, soft palate and the
floor of the mouth
11. • Presents as a faint white diffuse area with filmy appearance.
• Numerous surface folds results in wrinkling of the oral mucosa.
• Lesion tends to fade as the mucosa is stretched but it cannot be
wiped off.
• Persistent low grade
irritation thought to
be a risk factor.
• It’s a benign condition,
No treatment is
required.
12. White Sponge Nevus
WSN is rare, an autosomal dominant lesion
with high penetrance and variable expressivity.
Affects the mucosa of the mouth and the nose,
oesophagus, genitalia and rectum less
frequently.
Hereditary White Lesions.
13. • The lesions appears at birth or in early
childhood and presents as asymptomatic,
symmetrical, white corrugated or velvety
diffuse plaques on the buccal mucosa
bilaterally.
14. • Condition doesn’t present with any symptoms
has no risk of malignant change.
• Biopsy essential for definitive diagnosis.
• No treatment is essentially required.
15. Hereditary Benign Intraepithelial Dyskeratosis (HBID) or
Witkop’s disease
• Autosomal dominant condition that present with oral and
bilateral limbal conjuctival plaques
• Predominant among Whites, Native Americans and African
Americans.
• Oral lesions are similar to those of WSN and manifest in the
first year of life.
• The major aspect of HBID is the involvement of the bulbar
conjuctiva where thick gelatinous foamy and opaque
plaques form adjacent to the cornea.
Hereditary White Lesions.
16. • The oral lesions show thick corrugated white
plaques on the buccal and labial mucosa.
• Ocular involvement may lead to blindness.
• No treatment required for the oral lesions, refer
the eye lesions to the ophthalmologist.
17. Dyskeratosis Congenita (DC)
(Zinsser-Cole-Engman syndrome)
A very rare disorder.
3 patterns of inheritance- X-linked recessive,
autosomal dominant, and autosomal recessive.
The most common mode of inheritance is the X-
linked recessive form which affects mainly males
Caused by mutation of the DKC1 gene at the
Xq28 site.
Hereditary White Lesions.
18. • The oral lesions start before the age of 10 years as
bullae on the tongue and buccal mucosa and are
followed by erosions and later turning to squamous
cell carcinoma.
• Classic triad- nail dystrophy, reticulate skin
pigmentation over the trunk and neck, and white
plaques typically in the oral cavity
• The oral lesions are managed symptomatically and
periodic recall to check for malignant
transformation.
20. Pachyonychia Congenita:
• Pachyonychia congenita is an autosomal dominant
condition .
• Tubular configuration of the nails due to accumulation of
keratinaceous material in the nail beds.
• Thick, callous-like thickenings and hyperhidrosis are
noted in the palms and soles.
• Oral lesions are seen only in type I pachyonychia
congenita in the form of thickened white plaques on the
dorsum and lateral margins of the tongue.
• Oral lesions do not require treatment.
Hereditary White Lesions.
21. Reactive and Inflammatory White Lesions
Frictional Keratosis:
• Frictional keratosis refers to a white lesion with a
rough surface and is related to an identifiable
source of mechanical irritation and is reversible
on elimination of the irritant.
• This lesion is frequently associated with rough
dentures or sharp cusps. On removal of the
offending agent, the lesion should resolve within
2 weeks. Biopsies should be performed on lesions
that do not heal to rule out a dysplastic lesion.
23. Cheek chewing/Morsicatio Buccarum.
• White lesions of buccal mucosa which may result
from repeated chewing, sucking or biting of the
cheek.
• The lesions are thickened, shredded white area that
may be intermixed with areas of erythema and
ulceration which are often found bilaterally on the
anterior buccal mucosa along the plane of occlusion.
• The tongue may be simultaneously affected by the
same process.
• Females and those above 35 years are usually
affected.
• No treatment is usually indicated, a plastic nightguard
may be needed as a habit breaker.
Reactive and Inflammatory White Lesions
24. Linea Alba(White Line)
• A horizontal streak on the buccal mucosa at the
level of the occlusal plane.
• It extends from the commissure to the
posterior teeth.
• Caused by pressure, frictional irritation,
• Bilateral and may be pronounced in some
individuals, especially those with reduced
overjet of the posterior teeth.
• Scalloped and restricted to dentulous areas.
• No treatment needed.
Reactive and Inflammatory White Lesions
26. Chemical burns of the oral mucosa
• Chemical injuries due to caustic agents, such
as aspirin, formocresol, hydrogen peroxide and
sodium hypochlorite can cause white lesion.
• These are due to formation of a superficial
pseudomembrane composed of a necrotic
surface and an inflammatory exudate.
• The lesions are usually located on the
mucobuccal fold area and gingiva.
Reactive and Inflammatory White Lesions
27. • With short exposure, the affected mucosa
exhibits a white, wrinkled appearance.
• Long term contact can cause necrosis and
sloughing of mucosa.
• Most superficial burns heal within 2 weeks,
methyl cellulose may provide relief. While
deep burns required debridement followed by
antibiotic coverage.
• Extensive damage by corrosive agents will
require surgery.
29. Actinic Keratosis (Cheilitis)
• A premalignant epithelial lesion that is directly
related to long-term sun exposure areas of the
skin and the vermillion border of the lower lip.
• On the lip, it appears as a white plaque, oval to
linear in shape, usually measuring < 1 cm in
size. The surface may be crusted and rough to
the touch.
Reactive and Inflammatory White Lesions
30. • Biopsies should be performed on lesions that
repeatedly ulcerate, crust over, or show a
thickened white area.
• Treatment options include surgery, CO2 laser
therapy and chemotherapeutic agents such as
topical 5-fluorouracil have been used with
some success.
• About 10% of these lesions will undergo
malignant transformation
32. • Nicotine Stomatitis:
• Nicotine stomatitis refers to a white lesion that
develops on the palate in heavy cigarette, pipe and
cigar smokers in response to heat of tobacco
smoke.
• The palatal mucosa becomes diffusely gray or
white. Numerous elevated white papules with red
centers representing inflamed ductal orifices are
noted.
• The condition is reversible, usually within 1to 2
weeks of smoking cessation.
Reactive and Inflammatory White Lesions
34. • Oral Lichen Planus:
• Oral lichen planus is an immunologically
mediated mucocutaneous disease, in which T
lymphocytes accumulate beneath the epithelium.
• Women are more commonly affected.
• It is characterized by keratotic plaques (white
lichen) and or erythematous/ulcerative (red
lichen) oral lesions with or without skin
involvement
Immunologic white lesions.
35. • Lichen Planus:
• The most common reticular form consists of interlacing
white lines called Wickham's striae, seen usually on the
posterior buccal mucosa bilaterally.
• Other intraoral sites involved include tongue, gingiva
and palate. On the dorsum of the tongue the lesion
appear as keratotic white plaques with atrophy of the
papillae.
• Lesions show remissions and exacerbations associated
with periods of stress.
Immunologic white lesions.
36. Clinical features
• Types include
a. Reticular (numerous interlacing white keratotic lines
(Wickham’s striae). Affects the buccal mucosa and tends
to be bilateral and symmetrical and may affect the
tongue.
b. Plaque form. Resembles leukoplakia but has a
muiltifocal distribution. Dorsum of the tongue and
buccal mucosa primarily affected.
Reticular form
37. Clinical features
• Types include
c.Papular type. Present in the intial phase of the
disease, shows as small white dots.
d. Atrophic (erythematous). Red pathces with very fine
white striae, may be present with the erosive or
reticular type. Affects the attached gingiva.
Papular type.
38. e. Erosive form (ulcerative). Ulceration with
fine keratotic striae.
f. Bullous. Short lived bullae followed by a
painful ulcer. Reticulated and striated areas
seen.
Erosive form
39. • Treatment- Topical & systemic steroids plus
antifungal therapy, systemic and topical Vit A,
photodynamic therapy.
• Risk of malignant transformation necessitates
follow up.
• OLP tends to follow a chronic course and it is
more resistant to treatment than skin lesions
40. • Lichenoid Reaction:
• Lichenoid reaction has lesions clinically and
histologically similar to lichen planus, but is
associated with administration of a drug or
contact with metal. The lesions resolve when
the drug or other factors are eliminated.
Immunologic white lesions.
41. • Candidiasis:
• Candidiasis is the most common oral fungal infection
caused by candida albicans. The pseudomembranous
and hyperplastic type of candidiasis present as white
lesions of the oral cavity.
• Pseudomembranous candidiasis has white plaques
resembling curdled milk. Scraping the white lesion
can remove the plaques.
Infectious white lesions.
42. • Candidiasis:
• The hyperplastic candidiasis or candidal leukoplakia
presents as non-scrapable white patch usually located
on the anterior buccal mucosa.
• The diagnosis is confirmed by the presence of
candidal hyphae in the lesions. There is resolution of
the lesion after antifungal therapy.
Infectious white lesions.
43. • Mucous Patches in Secondary Syphilis:
• The lesions of secondary syphilis in oral cavity
are characterized by multiple painless grayish-
white plaques overlying an ulcerated necrotic
surface.
• The lesions occur on the tongue, gingiva, palate
and buccal mucosa.
• The associated systemic features include fever,
sore throat, malaise and headache. The lesions are
highly infective, but resolve within few weeks.
Infectious white lesions.
44. • Mucous Patches in Secondary Syphilis:
Infectious white lesions.
45. • Oral Hairy Leukoplakia (OHL):
• OHL is a corrugated white lesion seen commonly in
severe immunodeficient patient and is caused by
Epstein Barr virus (EBV).
• The most common disease associated with oral hairy
leukoplakia is HIV infection (25% of adults with HIV
infection & up to 80% in AIDS).
• OHL clinically presents as white vertical streaks or
thickened, furrowed white areas on the lateral or ventral
surfaces of the tongue.
Infectious white lesions.
46. • Oral Hairy Leukoplakia (OHL):
• The definitive diagnosis is made by demonstration of EBV
within the lesion using in situ hybridization, PCR,
Southern blot or electron microscopy.
No treatment is indicated. The condition usually
disappears when antiviral medications are used in the
treatment of the HIV infection
Topical application of podophyllin resin or tretinoin has
led to short-term resolution of the lesions, but relapse is
often seen.
Infectious white lesions.
48. • Uremic Stomatitis: Uremic stomatitis is a
complication of renal failure.
• The onset is abrupt, with white plaques present
predominantly on the buccal mucosa, tongue
and floor of the mouth. The clinician may
detect an odor of ammonia or urine on the
patient's breath.
Systemic disease.
49. • Leukoplakia:
• Leukoplakia is defined as “white patch or
plaque that cannot be characterized clinically
or pathologically as any other disease”. The
term is strictly clinical. The habit of tobacco is
closely associated with leukoplakia
development. Leukoplakia is divided into two
clinical types, homogeneous and non-
homogeneous types.
Potentially malignant white lesions.
50. • Leukoplakia:
• Homogeneous lesions are slightly elevated
grayish white non-scrapable plaques, which
may appear fissured or wrinkled. On palpation,
these lesions may feel leathery to “dry, or
cracked mud-like.”
Potentially malignant white lesions.
51. • Leukoplakia:
• Non-homogeneous varieties include
• a) Speckled: mixed white and red lesions, but
retaining predominantly white color .
• b) Nodular: small polypoid outgrowths. Higher
malignant transformation rate.
• c) Verrucous: corrugated surface appearance
• d) Proliferative verrucous leukoplakia (PVL):
multiple keratotic plaques with roughened surface
projections.
Potentially malignant white lesions.
52. • Leukoplakia:
• Leukoplakia is a potentially malignant disorder
with a malignant transformation rate ranging
from 4% to 47%. HPV-16 may be associated
with an increased risk of malignant
transformation.
• Habit cessation is recommended along with
clinical evaluation for every 6 months.
Potentially malignant white lesions.
53. • Human papillomavirus (HPV), particularly
subtypes HPV-16 and HPV-18
• HPV-16 may be associated with an increased
risk of malignant transformation.
Leukoplakia: Leukoplakia:
54. • NEOPLASTIC:
• Oral Squamous Cell Carcinoma (OSCC):
OSCC can present clinically as a white patch
resembling leukoplakia. In such cases biopsy
is mandatory to know if the dysplastic features
are limited to the epithelium or if true invasion
into the underlying connective tissue has
occurred.
55. CONCLUSION:
• White lesions of the oral cavity can range from
genetic disorders like white spongy nevus to
neoplastic lesions like Oral squamous cell
carcinoma.
• Proper diagnosis is important because the
corresponding treatment varies. A careful
observant eye and sensible judgement can add
to the diagnostic skills of the clinician and are
considered important for proper patient care.
57. REFERENCES
• Isaac van der waal, oral lichen planus and oral lichenoid
lesions; a critical appraisal with emphasis on the diagnostic
aspects, med oral patol oral cir bucal. 2009 jul 1;14 (7):E3104.
• Speight pm: update on oral epithelial dysplasia and progress to
cancer; head and neck pathol (2007) vol. 1 no.1 p 61-66.
• White lesions of the oral cavity - diagnostic appraisal &
management strategies * joshy v.R ** hari.S * reader, dept of
oral pathology, yenepoya dental college, yenepoya university,
mangalore – 575 018.
• White lesions of oral mucosa - a diagnostic dilemma journal of
dental sciences & oral rehabilitation
Editor's Notes
Unlike LP that tends to be more prevalent on stretching.
Histology shows acanthosis with oedema in the stratum spinosum.
There is also hyperkeratosis with irregular rete ridges
Increased mitoses, dyskeratosis, connective tissue atypia, and surface keratinization typical of cancerous lesions are not evident
No treatment is required.
Other intra oral site like ventral tongue, labial mucosa, soft palate, floor of the mouth and extra oral sites like nasal, pharyngeal
and anogenital mucosa may also be involved.
Histology shows epithelial thickening, parakeratosis and perinuclear condensation of the epithelium and vacuolation of the suprabasal layer of keratinocytes.
Histologic features are characteristic with the presence of many dyskeratotic cells.
The DKC gene encodes the amino acid sequence for dyskerin, a multifunctional protein involved in RNA biosynthesis, ribosomal subunit assembly, and centromere or microtubule binding.
Deficiencies in dyskerin are therefore likely to affect tissues with a high cell turnover, such as the bone marrow and skin.
Histologically,, presence of multiple nucleoli in the epithelial cells of the granular layer as a manifestation of dyskeratosis) can be seen in electron microscopic studies
reticulate skin pigmentation over the trunk and neck
but the quality of life is affected due to nail loss and
continuous removal of excess keratin on the soles and palms
Stress is a common predisposing factor.
Histology shows acanthosis and hyperkeratosis.
The palatal mucosa becomes diffusely gray or white. Numerous elevated white papules with red centers representing inflamed ductal orifices are noted.
Histology features the following
Hyperkeratosis
Apoptotic basal cells and basal zone vacuolation
T-lympocytes recruitment.
Saw tooth rete ridges in long standing lesions
are characterized by multiple painless grayish-white plaques overlying an ulcerated necrotic surface.
white vertical streaks or thickened, furrowed white areas on the lateral or ventral surfaces of the tongue.
Human papillomavirus (HPV), particularly subtypes HPV-16 and HPV-18