This document discusses various types of red and white lesions that can occur in the oral mucosa. It describes hereditary lesions including leukodema, white sponge nevus, and hereditary benign intraepithelial dyskeratosis. It also covers reactive/inflammatory lesions such as frictional keratosis. Infectious lesions covered include oral hairy leukoplakia caused by Epstein-Barr virus and various forms of oral candidiasis. Idiopathic "true" leukoplakia and erythroplakia are also discussed. Treatment options are provided for many of the conditions.

1. Red and white lesions of the
oral mucosa

2. .Hereditary white lesions
 Leukodema
 White sponge nevus
 Hereditary benign intraepithelial
dyskeratosis
 Darrier’s disease

3. Reactive/inflammatory white
lesions





Frictional (Traumatic) keratosis
Chemical injuries of the oral mucosa
Actinic keratosis (cheilitis)
Smokeless tobacco-induced keratosis
Nicotine stomatitis

4. Infectious white lesions and white
:and red lesions



Oral hairy leukoplakia
Candidiasis
Mucous patches

5. Idiopathic "TRUE" leukoplakia

6. Erythroplakia

7.  Oral lichen planus
 Lichenoid reactions

8. Lupus erythematosus (systemic
)and discoid

9. :Miscellaneous lesions
 Oral submucous fibrosis.
 Skin graft.

10. :Hereditary White Lesions
 Leukoedema:
Leukoedema is a common mucosal
alteration that represents a variation of the
normal condition rather than a true
pathologic change.

11. : Features
 Faint, white, diffuse, and filmy appearance
 Numerous surface folds resulting in wrinkling
of the mucosa.
 It cannot be scraped off
 It disappears or fades upon stretching
the mucosa.
 Microscopic examination reveals thickening
of the epithelium, with significant intracellular
edema of the stratum spinosum. The
surface of the epithelium may demonstrate a
thickened layer of parakeratin.

12. Leukoedema

13. Treatment
 No treatment is indicated, no malignant
change has been reported.

14. :White Sponge Nevus
 The disease usually involves the oral
mucosa and (less frequently) the mucous
membranes of the nose, esophagus,
genitalia, and rectum.
 The lesions may be present at birth or may
first manifest or become more intense at
puberty.

15. :Features
 Bilateral symmetric white, soft, “spongy”, or velvety
thick plaques of the buccal mucosa.
 Other sites in the oral cavity may be involved,
including the ventral surface of the tongue, floor of
the mouth, labial mucosa, soft palate, and alveolar
mucosa.
 Asymptomatic and does not exhibit tendencies
toward malignant change.
 Histopathologic features are epithelial thickening,
parakeratosis, a peculiar perinuclear condensation
of the cytoplasm, and vacuolization of the
suprabasal layer of keratinocytes

16. :White Sponge Nevus

17. :Treatment
 No treatment is indicated for this benign and
asymptomatic condition.

18. Hereditary Benign Intraepithelial
:Dyskeratosis
1- Oral Lesions:
 Thick, corrugated, asymptomatic, white
“spongy” plaques involving the buccal and
labial mucosa.
 Other intraoral sites include the floor of the
mouth, the lateral tongue, the gingiva, and
the palate.
 Detected in the first year of life and gradually
increase in intensity until the teens.

20. 2- Eye Lesions
 Thick, gelatinous, foamy, and opaque
plaques form adjacent to the cornea.
 The plaques may exhibit seasonal
prominence, with many patients reporting
more-pronounced lesions in the Spring and
regression during the Summer months.
 Blindness due to corneal vascularization
may occur.

21. Histopathologic Features:
 Epithelium exhibits marked parakeratin
production with thickening of the stratum
spinosum and the presence of numerous
dyskeratotic cells (eosinophilic cells that
resemble epithelial pearls).

22.  Treatment:
 No treatment is required for the oral lesions.
For evaluation and treatment of the ocular
lesions, the patient should be referred to an
ophthalmologist.

23. Darrier’s Disease: (Keratosis
(Follicularis
 A genetic disorder characterized by a
persistent eruption of hyperkeratotic
papules.

24. :Pathology
 Fissures (lacunae) appear due to acantholysis
above the basal layer. They later extend
irregularly.
 Small groups of cells around the lacunae become
separated from their neighbours, enlarge and
present a darkly staining nucleus surrounded by
clear cytoplasm and a glistening ring simulating a
membrane. These corps ronds are cells showing
premature partial keratinization (dyskeratosis);
they give rise to the grains, small cells with
shrunken cytoplasm, seen in the upper layers of
the epidermis.

25.  Skin Lesions:
A firm, rather greasy, harsh papule, which
is skin coloured, yellow-brown or brown.
Coalescence of the papules produces
irregular warty plaques or papillomatous
masses, which in the flexures, become
vegetating and malodorous.

26.  Oral Lesions:
White umbilicate or cobblestone papules
on the palate, tongue, buccal mucosa,
epiglottis, pharyngeal wall, vulva,
oesophagus or rectum may occur, as may
hypertrophy of gums.
Confluence of the papules may form patches
simulating leukoplakia. Blockage of the
salivary glands may be associated

27. Nail Lesions:
Characteristic nail changes are seen:
 Broad, white, longitudinal bands;
 Broad, slightly translucent, red, longitudinal
bands;
 A sandwich of red and white longitudinal
bands, often with a V-shaped nick at the
free margin of the nail.

28. :Ear Lesions
 The external auditory meatus may be
blocked by accumulated keratotic debris

29. Reactive and Inflammatory White
Lesions:
Frictional Keratosis

30. :Cheek Chewing

31. Chemical Injuries of the Oral
:Mucosa

33. (:Actinic Keratosis (Cheilitis

34. Smokeless Tobacco-lnduced
:Keratosis

35. :Nicotine Stomatitis

40. Infectious White Lesions and
White and Red Lesions
Oral Hairy Leukoplakia:
 Corrugated white lesion
 Usually occurs on the
lateral or ventral
surfaces of the tongue
 In patients with severe
immunodeficiency. The
most common disease
associated with oral
hairy leukoplakia is HIV
infection.
 Epstein-Barr virus (EBV(
is the causative agent

41. :Histopathology
 Hyperparakeratosis with an irregular surface,
 Acanthosis with superficial edema,
 Koilocytic cells (virally affected "balloon" cells) in
the spinous layer. The characteristic microscopic
feature is the presence of homogeneous viral
nuclear inclusions with a residual rim of normal
chromatin.
 Demonstrating the presence of EBV through in
situ hybridization, electron microscopy, or
polymerase chain reaction

42. :Treatment and Prognosis
 The condition usually disappears when
antiviral medications such as zidovudine, or
acyclovir are used in the treatment of the
HIV infection .

43. Oral Candidosis
 Because Candida are normal oral
inhabitants, thrush and other forms of oral
candidiasis may be classified as specific
endogenous infections.

44. Important predisposing factors for
oral candidosis
– Immunodeficiency (e.g. diabetes mellitus or AIDS) or
immunosuppression (including steroid inhalers, cancer
chemotherapy, and radiotherapy).
– Poor oral hygiene
– Pregnancy
– Anaemia
– Suppression of the normal oral flora by antibacterial
drugs
– Xerostomia
– Haematologic malignancies

45. :Spectrum of oral candidosis
Acute candidosis
 Thrush (acute pseudomembranous candidosis).
 Acute antibiotic stomatitis (acute atrophic or erythematous)
Chronic candidosis
 Denture-induced stomatitis
 Chronic hyperplastic candidosis (candidal leukoplakia)
 Median rhomboid glossitis
 Chronic mucocutaneous candidosis
 Erythematous candidosis
Angular stomatitis (common to all types of oral candidosis).

46. Acute Pseudomembranous
(Candidosis (Thrush
Clinical Features:
 Painless, soft, friable, and creamy plaques on the
mucosa.
 Can be easily wiped off, to expose an
erythematous mucosa or shallow ulceration.
 Their extent varies from isolated small flecks to
widespread confluent plaques.
 Angular stomatitis is frequently associated as it is
with any form of intra-oral candidosis.
 Sometimes a prodrome of bad taste or loss of taste
sensation precedes the appearance of the lesions.

48. Pathology
 A Gram-stained smear shows large masses of
tangled hyphae, detached epithelial cells and
leucocytes.
 Biopsy shows hyperplastic epithelium infiltrated by
inflammatory oedema and cells, predominantly
neutrophils.
 Staining with PAS shows many candidal hyphae
growing down through the epithelial cells to the
junction of the plaque with the spinous cell layer.

49. Management
 Control of any local cause such as topical
antibiotic treatment .
 Nystatin or amphotericin lozenges (topical
antifungals) should allow the oral microflora
to return to normal.
 Failure of response to topical antifungals
suggests immune deficiency.
 In immunodeficient patients as in HIV
infection, candidosis may respond to
fluoconazole or itraconazole.

50. :Acute Antibiotic Stomatitis
 Overuse or topical oral use of antibiotics,
especially tetracycline, suppressing normal
competing oral flora.
 Clinically, the whole mucosa is red and
sore. Flecks of thrush may be present.
 Resolution may follow withdrawal of the
antibiotic but is accelerated by topical
antifungal treatment.

51.  Generalized candidal erythema which is
clinically similar, can also be a consequence
of xerostomia which promotes candidal
infection.
 It is a typical complication of Sjogren's
syndrome.
 Nystatin suspension or miconazole gel held
in the mouth is usually effective.

52. :Denture-induced Stomatitis
 Asymptomatic erythema sharply limited to
the area of mucosa occluded by a wellfitting upper denture or even an orthodontic
plate.
 Similar inflammation is not seen under the
more mobile lower denture which allows a
relatively free flow of saliva beneath it.
 Angular stomatitis is frequently associated
and may form the chief complaint.

54. :Pathology
 Gram-stained smears show candidal hyphae and
some yeast forms which have proliferated in the
interface between denture base and mucosa.

Histologically, there is typically mild acanthosis
with prominent blood vessels superficially and a
mild
chronic
inflammatory
infiltrate.
The
inflammation is probably a response to enzymes
such as phospholipases produced by the fungus

55. :Treatment
 Denture cleansing .Cleansers can be divided into groups according to
their primary components: alkaline peroxides, hypochlorites, acids,
disinfectants, and enzymes .Yeast lytic enzymes and proteolytic
enzymes are the most effective against the infection.
 Denture soak solution containing benzoic acid completely eradicates C
albicans from the denture surface as it is taken up into the acrylic resin
and eliminates the organism from the internal surface of the prosthesis.
 A protease-containing denture soak also effectively removes denture
plaque, especially when combined with brushing.
 An oral rinse containing 0.12% chlorhexidine gluconate results in
complete elimination of the presence of C albicans on the acrylic resin
surface of the denture and in reduction of palatal inflammation .
 Diet: High-sucrose diets should be avoided.

56. . Median Rhomboid Glossitis
 Erythematous patches
of atrophic papillae
located in the central
area of the dorsum of
the
tongue
are
considered a form of
chronic
atrophic
candidiasis.

57. :Chronic Hyperplastic Candidiasis
 Candidal leukoplakia is considered a chronic form
of oral candidiasis in which firm white leathery
plaques are detected on the cheeks, lips, palate,
and tongue.
 Mycelial invasion of the deeper layers of the
mucosa and skin occurs, causing a prolifertive
response of host tissue.
 The differentiation of candidal leukoplakia from
other forms of leukoplakia is based on finding
periodic acid-Schiff (PAS)-positive hyphae in
leukoplakic lesions.

58. Chronic Mucocutaneous
:Candidiasis
 Persistent infection with Candida usually
occurs as a result of a defect in cellmediated immunity or may be associated
with iron deficiency. Hyperplastic
mucocutaneous lesions, localized
granulomas, and adherent white plaques on
affected mucous membranes are the
prominent lesions that identify chronic
mucocutaneous candidiasis (CMC).

62. Two categories of CMC have been
described:
(1( Syndrome-associated CMC (further
categorized as either familial or chronic).
(2( Localized and diffuse CMC.

63. Candidiasis endocrinopathy
)syndrome (CES
 A rare autosomal recessive disorder
characterized by an onset of CMC during
infancy or early childhood, associated with
the appearance of hypoparathyroidism,
hypoadrenocorticism and other endocrine
anomalies
 Patients develop persistent oral candidiasis
and hyperplastic infections of the nail folds
at an early age.

64. Chronic candidiasis associated with
thymoma
 The other syndrome-associated form ,
which appears with other autoimmune
abnormalities such as myasthenia gravis.

65. Localized and diffuse CMC
 Localized CMC is a variant associated with
chronic oral candidiasis and lesions of the
skin and nails.
 The diffuse variant is characterized by
randomly occurring cases of severe
mucocutaneous candidiasis with
widespread skin involvement and
development of Candida granulomas.

66. Management
Both oral and cutaneous lesions of CMC
can be controlled by the continuous use of
systemic antifungal drugs.
Once treatment is discontinued, the
lesions rapidly reappear.

67. :Erythematous Candidosis
 This term applies to red mucosal macules
due to Candida albicans infection in HIV –
positive patients. Favoured sites, in order of
frequency, are the hard palate, dorsum of
the tongue and soft palate. Treatment with
intraconazole is usually effective.

68. :Angular Stomatitis
 Angular stomatitis is typically caused by
leakage of Candida- infected saliva at the
angles of the mouth. It can be seen in
infantile thrush ,in denture wearers or in
association with chronic hyperplastic
candidosis. It is a characteristic sign of
candidal infection.

70. :Treatment of Oral Candidiasis
Treatment of underlying predisposing factors
(if possible)
Antifungal Drugs




Antifungal antibiotics nystatin and amphotericin B.
Imidazole derivatives (clotrimazole, miconazole) are
available for topical use (cream, oral gel).
Systemic therapy includes the use of any one of these
three: ketoconazole, itraconazole, and fluconazole.
Fluconazole and amphotericin B may be used
intravenously for the treatment of the resistant lesions
of CMC and systemic candidiasis.

71.  Patients for whom predisposing factors such
as xerostomia and immunodeficiency
cannot be eliminated may need either
continuous or repeated treatment to prevent
recurrences.
 The consumption of yogurt two to three
times per week and improved oral hygiene
can also help.

72. :Idiopathic “TRUE” Leukoplakia
 Leukoplakia is a white oral precancerous
lesion with a recognizable risk for malignant
transformation.
 Leukoplakia is currently defined as “a white
patch or plaque that cannot be
characterized clinically or pathologically as
any other disease”.

73. Etiology
 A number of locally acting etiologic agents,
including
tobacco,
alcohol,
candidiasis,
electrogalvanic
reactions,
sunlight
and
(possibly) herpes simplex and papilloma
viruses, have been implicated as causative
factors for leukoplakia.
 Alcohol consumption alone is not associated
with an increased risk of developing leukoplakia,
but alcohol is thought to serve as a promoter that
exhibits a strong synergistic effect with tobacco.

74. :Clinical Features
More frequently found in men
Can occur on any mucosal surface
Infrequently causes discomfort or pain.
Causes change in physical characteristics of
tissues.
 Prevalence increases rapidly with age.
 Approximately 70% of oral leukoplakia lesions are
found on the buccal mucosa, vermilion border of
the lower lip, and gingiva.
 Lesions of the tongue and the floor of the mouth
account for more than 90% of cases that show
dysplasia or carcinoma.





75. Subtypes
 Homogeneous
leukoplakia
welldefined white patch,
that is slightly elevated
and
that
has
a
fissured, wrinkled, or
corrugated
surface.
On palpation, these
lesions
may
feel
leathery to “dry, or
cracked mud-like”.

76.  Nodular
(speckled)
leukoplakia
the
name
refers to a mixed red-and–
white lesion in which
keratotic white nodules or
patches are distributed over
an atrophic erythematous
background. This type of
leukoplakia is associated
with a higher malignant
transformation rate.

77. Nodular (speckled) leukoplakia

78. Verrucous leukoplakia
 Thick white lesions with
papillary surfaces .
 Usually heavily keratinized
 Most often seen in older
adults in the sixth to eighth
decades of life.
 Some of these lesions may
exhibit
an
exophytic
growth pattern.

79. Proliferative verrucous leukoplakia
Extensive papillary or verrucoid white
plaques that tend to slowly involve multiple
mucosal sites in the oral cavity and to
transform into squamous cell carcinomas
over a period of many years.

80. :Histopathologic Features
 Parakeratosis or orthokeratosis or both, alternately.
 The epithelium ranges from thinner than normal
(atrophic) to much thicker (acanthotic)
 Most leukoplakias show no dysplastic changes
 A minority display a range of dysplasia from mild to
severe and treatment is planned partly on this
basis.
 An inflammatory reaction of lymphocytes and
plasma cells is often present in the underlying
connective tissue.

81. :Diagnosis and Management
 If
a
leukoplakia
lesion
disappears
spontaneously or through the elimination of
an irritant, no further testing is indicated.
 For the persistent lesion, the definitive
diagnosis is established by tissue biopsy.
 Adjunctive methods as vital staining with
toluidine blue and cytobrush are helpful in
selecting the most appropriate spot for
biopsy .

82.  Toluidine blue staining uses a 1% aqueous
solution of the dye which stains dysplastic
and malignant cells and resists washing
away by rinsing with 1% acetic acid .
 Cytobrush technique utilizes a brush with
firm bristles that obtains individual cells from
the full thickness of epithelium for cytologic
examination .

83.  Definitive treatment involves surgical
excision although cryosurgery and laser
ablation are often preferred because of their
precision and rapid healing.

84. :Prognosis
 Clinical signs of malignant transformation of
leukoplakia include :
Ulceration , erythroplasia , bleeding ,
induration and lymphadenopathy
 After surgical removal long-term monitoring
of the lesion site is important since
recurrences are frequent and because
additional leukoplakias may develop.

85. Erythroplakia
 “Bright
red
velvety
plaque or patch which
cannot be characterized
clinically or histopathologically as being
due
to
any
other
condition”.

86. Erythroplakia

87. :Clinical Features
 Erythroplakia occurs predominantly in older
men, in the sixth and seventh decades of
life.
 Erythroplakias are more commonly seen on
the floor of the mouth, the ventral tongue,
the soft palate, and the tonsillar fauces, all
prime areas for the development of
carcinoma. Multiple lesions may be present.
 Almost all of the lesions are asymptomatic.

88. :Histopathologic Features
 80 to 90% of cases of erythroplakia are
histopathologically
severe
epithelial
dysplasia, carcinoma in situ, or invasive
carcinoma.

89. :Differential Diagnosis
 In view of the clinical significance of
erythroplakia, its differentiation from
other red inflammatory lesions of the oral
mucosa is critical.
 Clinically similar lesions may include
erythematous candidiasis, areas of
mechanical irritation, denture stomatitis,
vascular lesions, and a variety of
nonspecific inflammatory lesions

90. :Lichen Planus
 Lichen planus is a common chronic
inflammatory disease of skin and mucous
membranes. It mainly affects patients of
middle age or over. Oral lesions have
characteristic appearances and distribution

91. :Aetiology
 The predominantly T-lymphocyte infiltrate
suggests
cell-mediated
immunological
damage to the epithelium

92. :Clinical Features
Skin Lesions:
 Pruritic, polyangular, planar papules and plaques , 2 to 4
mm in diameter, with angular borders, a violaceous color,
and a distinct sheen in cross-lighting.
 Usually symmetrically distributed most commonly on the
flexor surfaces of the wrists, legs, trunk. The face is rarely
involved during the acute phase.
 New papules may appear at sites of minor skin injury
(Koebner’s phenomenon).
 Lesions may coalesce or change over time becoming
hyperpigmented, atrophic hyperkeratotic (hypertrophic LP)
or vesiculobullous.
 If the scalp is affected,there is patchy scarring alopecia

95. Nail Lesions:
 Nails are involved in up to 10% of cases.
Findings vary in intensity with nail bed
discoloration ,longitudinal ridging and lateral
thinning and complete loss of the nail matrix
and nail with scarring of the proximal nail
fold onto the nail bed.

97. :Oral Lesions




The reticular form
Atrophic lichen planus
Erosive lesions
Bullous lesions
 Atrophic or erosive lichen planus involving
the gingivae results in desquamative
gingivitis

100. :Histopathologic Features
 Three features are considered essential for the
histopathologic diagnosis of lichen planus:
 (1) Areas of hyperparakeratosis or
hyperorthokeratosis.
 (2) “liquefaction degeneration” or necrosis of the
basal cell layer which is often replaced by an
eosinophilic band.
 (3) A dense subepithelial band of lymphocytes.
This linear sub-basilar lymphocytic infiltration is
composed largely of T cells

102.  Isolated epithelial cells, shrunken with
eosinophilic cytoplasm and one or more
pyknotic nuclear fragments (Civatte bodies),
are often scattered within the epithelium and
superficial lamina propria. These represent
cells that have undergone apoptosis.

103. :Treatment
 Asymptomatic lesions require no treatment.
 Topical high-potency corticosteroids, as pastes or as gels.
 Erosive lesions may respond to oral dapsone or
cyclosporine rinses.
 Systemic steroids : Prednisone tablets with dosages
varying between 40 and 80 mg daily
 Intralesional injection of corticosteroid may be used in
lesions resistant to topical and systemic therapy
triamcinolone acetonide ampules are used (weekly
regimen).
 Systemically administered dapsone, hydroxychloroquine,
azathioprine and cyclosporine may help in cases resistant
to corticosteroids
 Drug combinations could also be used.

104. Lichenoid Reactions
 This term is given to lichen planus-like lesions
caused by either systemic drug treatment or those
where the histological picture is not completely
diagnostic.
 Oral lichenoid reactions are most frequently
responses to restorative materials, either amalgam
or polymeric. Lesions are localized to mucosa in
contact, not just close to, restorations.
 Lichenoid reactions are treated in exactly the
same way as lichen planus with withdrawal of
drug(s) if possible or removal of restoration.

105. :Lupus Erythematosus
 Lupus erythematosus is an autoimmune
connective tissue disease which has two
main forms namely systemic and discoid.
Either can give rise to oral lesions which
may appear similar to those of oral lichen
planus

106. Systemic Lupus Erythematosus
 Has varied effects. Any organ system can be affected. A
great variety of autoantibodies, particularly antinuclear, is
produced.
Pathological features of systemic lupus erythematosus:
Macroscopic:
 Pleurisy.
 Pericarditis.
 Libman-sacks endocarditis.
 Lymphadenopathy.
 Splenomegaly.
 May be none.

108. Microscopic:
 Immunoglobulins and complement at the
dermo-epidermal junction in skin lesions
(90%) and uninvolved skin (60%).
 Haematoxylin bodies in the endocardium,
renal glomeruli and elsewhere.
 Periarterial fibrosis of the spleen.
 Wire loop lesions in the kidneys.

109. immunoglobulin & complement
deposits at basement membrane
:zone & nuclei of epithelial cells

110. :Discoid Lupus
 A skin disease with mucocutaneous lesions
indistinguishable clinically from those of
systemic lupus. These may be associated
with arthralgias but rarely, significant
autoantibody production

111. Clinical Features:
:A) Skin Lesions
Cutaneous features of systemic lupus erythematosus.
 Butterfly rash.
 Facial oedema.
 Subacute cutaneous LE.
 Chronic discoid LE.
 Scarring DLE alopecia
 Non-scarring alopecia
 Photosensitivity
 Raynaud’s phenomenon
 Chronic urticaria
 Cutaneous vasculitis

116. :Histopathologic Features
 Liquefaction degeneration of basal cell layer.
 Degenerative changes in the connective tissue
(hyalinization, oedema,..).
 Lupus erythematosus shows more irregular
patterns of acanthosis and lacks the band-like
distribution of lymphocytes in the papillary corium
of lichen planus.
 The inflammatory infiltrate may have a
perivascular distribution.

117. : Management
 Oral lesions of discoid lupus erythematosus
may respond in some degree to topical
corticosteroids.
 Oral lesions in acute systemic lupus
erythematosus may not respond to doses of
corticosteroids adequate to control systemic
effects of the disease. Under such
circumstances, palliative treatment is
needed until disease activity decreases.

118. Miscellaneous Lesions:
Oral Submucous Fibrosis
 A slowly progressive chronic fibrotic disease
of the oral cavity and oropharynx,
characterized by fibroelastic change and
inflammation of the mucosa, leading to a
progressive inability to open the mouth,
swallow, or speak.

119.  These reactions may be the result of either direct
stimulation from exogenous antigens like Areca
alkaloids or changes in tissue antigenicity that may
lead to an autoimmune response.
 It occurs almost exclusively in the Indian
subcontinent.
 The inflammatory response releases cytokines and
growth factorsthat promote fibrosis by inducing the
proliferation of fibroblasts, up-regulating collagen
synthesis and down-regulating collagenase
production.

120. :Etiology
 General nutritional and vitamin deficiencies
and hypersensitivity to certain dietary
constituents such as chili peppers, chewing
tobacco, habitual use of betel and its
constituents (Areca catechu).

121. :Clinical Features
 The disease first presents with a burning sensation
of the mouth, particularly during consumption of
spicy foods.
 Often accompanied by the formation of vesicles or
ulcerations and by excessive salivation or
xerostomia and altered taste sensations.
 Gradually, patients develop a stiffening of the
mucosa, with a dramatic reduction in mouth opening
and with difficulty in swallowing and speaking.
 The mucosa appears blanched and opaque with the
appearance of fibrotic bands that can easily be
palpated.
 Usually involves the buccal mucosa, soft palate,
posterior pharynx, lips, and tongue.

124. :Histologic Features
 Severely atrophic epithelium with complete
loss of rete ridges.
 Varying degrees of epithelial atypia may be
present.
 The underlying lamina propria exhibits
severe hyalinization, with homogenization of
collagen. Cellular elements and blood
vessels are greatly reduced.

125. :Treatment and Prognosis
 Oral submucous fibrosis is regarded as a
premalignant condition.
 Oral submucous fibrosis is very resistant to
treatment.
 Submucosal injected steroids and hyaluronidase,
are some of the agents that have been used.
 In severe cases surgical intervention is the only
treatment but the fibrous bands and other symptoms
often recur within a few months to a few years.

126. :Skin Grafts
 A skin graft may be placed in the mouth to cover a
raw area left after excision of a lesion.
 Skin grafts typically appear sharply demarcated
smooth and paler than the surrounding mucosa
and occasionally contain hairs . Grafts on the
dorsum of the tongue may become corrugated and
less easy to differentiate from leukoplakia.