4. Definition:
White-appearing lesions of the oral mucosa, obtained their characteristic appearance from
the scattering of light through an altered surface.
Causes:
1. Increase in thickness of one or more of epithelial layers.
2. Abnormal character of keratin.
3. Abnormal permeability of epithelium.
5. Diagnosis of oral white lesions might be quite challenging
• These lesions represent a wide spectrum of lesions with different etiology and various prognoses.
• The diagnosis of white lesions varies from benign reactive lesions to more serious dysplastic and carcinomatous lesions.
• The onset of oral white lesions can be acquired or congenital, with a history of long-lasting existence in the latter form.
• Oral white lesions can be caused by a thickened keratotic layer or an accumulation of non-keratotic material.
• While there are some classic features that help distinguish these lesions, similar features may give rise to some
complications in diagnosis.
• Efforts should be made to establish a definite diagnosis to prevent time elapse in treatment of patients with more serious
lesions.
• Therefore, white lesions mandate an appropriate clinical diagnostic approach to exclude the possibility of malignancy.
6. There are three clinical steps to approach oral white
lesions: the first step is to determine whether the
lesion is congenital or acquired; the second and third
steps are to inspect if it can be wiped off or not and if
it has a special pattern or not.
9. Leukoedema
Clinical Picture:
o It presents as a diffuse, gray to white, non-scrapable and veil-like condition that can be described as a milky
and opalescent transformation of the oral mucosa.
o In more prominent cases, leukoedema is characterized by mucosal folds along with wrinkles or whitish streaks.
o This condition usually disappears temporarily after gentle stretching of the mucosa, which reappears after
quitting the manipulation
o Leukoedema often involves the buccal mucosa and sometimes the lateral borders of the tongue bilaterally.
o It may spread to the labial mucosa and rarely affects the floor of the mouth, palatopharyngeal and laryngeal
tissues.
o Leukoedema is asymptomatic with no potential for malignant transformation.
Leukoedema:
Accumulation of fluid within the epithelial cells of the buccal mucosa.
3
10. 3
Treatment:
No treatment is required for this condition.
Leukoedema
Histopathology:
▪ Acanthotic epithelium.
▪ Cells are flattened and show pyknotic nuclei.
▪ Cells of stratum spinosum are enlarged showing intracellular edema.
▪ Not infiltrated with inflammatory cells. Leukoedema-Epithelial hyperplasia and edema of the upper layers.
Leukoedema-Marked epithelial edema with pyknosis of nuclei.
Differential Diagnosis:
1. Leukoplakia
2. Linea Alba
3. Frictional Keratosis
4. Lichen Planus (LP)
5. White Sponge Nevus
11. White Sponge Nevus
White Sponge Nevus:
is a symptomless autosomal dominant disorder of keratins 3 and 13,
which manifests from early childhood.
a.k.a: FAMILIAL WHITE FOLDED GINGIVOSTOMATOSIS
Clinical Picture:
▪ The lesions generally present at birth or early in childhood.
▪ Intraoral lesions are symmetrical, thickened, white, corrugated or velvety, diffuse, spongy
plaques of variable sizes with an elevated, irregular, and fissural surface.
▪ Buccal mucosa is affected bilaterally in most patients.
▪ Other areas of the oral cavity such as the ventral surface of the tongue, labial mucosa,
soft palate, alveolar mucosa, and floor of the mouth can also be affected, but the amount
of involvement might vary from patient to patient.
▪ White sponge nevus can cause dysphagia when the esophagus is involved; otherwise,
the lesions are asymptomatic.
▪ Due to the benign nature of the lesion, good prognosis, and infrequent recurrence rate
2
12. Histopathology:
▪ Prominent acanthosis is seen accompanied by a marked intraepithelial edema
▪ Hyperparakeratosis
▪ Hydropic swelling of the epithelial cells that extends into the rete ridges but spares
the basal layer.
▪ Cells exhibit perinuclear and paranuclear dense eosinophilic intracytoplasmic
inclusions composed of disorganized aggregates of cytokeratin filaments and
clearing of peripheral cytoplasm.
▪ Basket weave appearance
Treatment:
No treatment is suggested for WSN
White Sponge Nevus
White sponge nevus.
A, Benign epithelial hyperplasia
with pale “spongy” appearance.
B, Intracellular
vacuolation and dyskeratosis
sparing basal cells; inset shows
PAS -positive, diastase-labile
intracytoplasmic granules
typical
for glycogen.
C, Perinuclear condensations
and cytoplasmic vacuolation
(not spongiosus).
A
B
C
2
14. Dyskeratosis Congenita
Dyskeratosis Congenita
is an inherited syndrome in which patients undergo premature aging and have a predisposition
to malignancy.
X-linked and autosomal dominant and recessive forms of the disease are recognized.
a.k.a Zinsser-Engman-Cole Syndrome
Clinical Picture:
▪ It usually emerges between the ages of 5 to 12 years.
• Reticulated skin hyperpigmentation of the upper chest and dysplastic nail changes
characterize the cutaneous manifestations.
▪ The most important oral manifestations are bullae formation.
▪ May be followed by erosions, which ultimately progress to leukoplakic lesions in the
buccal mucosa, tongue, and oropharynx .
▪ As well as rapidly progressive periodontal disease, gingival inflammation and
bleeding, gingival recession, bone loss, decreased root/crown ratio, and mild
taurodontism.
▪ Malignant transformation is reported in approximately 30% of the leukoplakic lesions
with a progression to Oral Squamous Cell Carcinoma (OSCC) within 10–30 years.
2
Dysplastic leukoplakia on the tongue
of a patient with dyskeratosis
congenita.
Dyskeratosis congenita
showing hands and nail
dystrophy
15. Histopathology:
▪ Thick keratin plug
▪ Intraepithelial clefting.
▪ Elongated rete ridges
Treatment:
The treatment is usually directed to the alleviation of symptoms
▪ Dyskeratosis congenita is a multi-organ-system disorder that needs regular follow-
ups.
▪ In severe conditions, allogeneic hematopoietic stem cell transplantation as the only
main treatment.
▪ Less successful treatments such as androgens and oral and topical vitamin e have
also been suggested for dc
2
Dyskeratosis Congenita
16. Hereditary Benign Intraepithelial Dyskeratosis
Clinical Picture:
▪ This disorder progresses during childhood
▪ oral manifestations are similar to WSN as thick, corrugated white plaques affecting
the buccal and labial mucosa.
▪ Milder cases show an opalescent appearance mimicking leukoedema.
▪ Other oral mucosal areas such as the floor of the mouth and lateral borders of the
tongue might also be involved.
▪ Another clinical manifestation of HBID is ocular lesions.
Treatment:
HBID is a benign lesion in the oral cavity; hence no treatment modality is needed unless
a superimposed infection with candida occurs, which requires antifungal therapy.
2
Hereditary Benign Intraepithelial Dyskeratosis:
is a rare autosomal dominant disease of the conjunctiva and the oral mucosa
caused by a duplication of chromosome 4q35
17. Histopathology:
▪ Acanthosis.
▪ parakeratosis.
▪ Hyperkeratosis.
▪ Enlarged, hyaline, waxy, eosinophilic cells (dyskeratotic elements)
▪ The dyskeratotic cells display central, homogenous, basophilic, pyknotic nuclei
surrounded by a clear halo
▪ Dyskeratotic cells may be surrounded by adjacent cells producing "cell within cell"
▪ An infiltrate of chronic inflammatory cells was present beneath the intact epithelial
basement membrane.
Differential Diagnosis:
• White sponge nevus shows perinuclear keratin condensations.
• Darier disease or warty dyskeratoma is acantholytic with dyskeratosis without the cell-within-a-
cell appearance.
Hereditary Benign Intraepithelial Dyskeratosis
Hereditary benign intraepithelial
dyskeratosis
A, Hyperparakeratosis and benign
papillary epithelial hyperplasia.
B, Prominent dyskeratosis within
the superficial keratinocytes.
C, Dyskeratotic
cells with “cell-within-a-cell”
morphology
A
B
C
2
18. DARIER DISEASE
Darier disease: diffuse, pebbly white papules on the
hard palate.
Darier Disease:
is an autosomal dominant disorder associated with a mutation of ATP2A2 gene (on
chromosome 12q) involved in cytoplasmic calcium transport that is required for proper
functioning of desmosomes and keratin formation, resulting in dyscohesion.
a.k.a Follicular keratosis
Warty Dyskeratoma is of unknown etiology but has the same
histology.
Clinical Picture:
• Darier disease characterized by white, painless, keratotic papules (seen in mild
disease) or plaques and cobblestoning of the mucosa (seen in more severe disease)
in 10% to 50% of patients with skin disease
• Onset in first and second decade
• Lesions is found on palate, gingiva or tongue
• Skin findings invariably present
• Up to one third of cases with parotid or submandibular swelling likely because of
• Strictures and obstruction
• Warty dyskeratoma: isolated white, warty papule usually of the palate or gingiva
2
19. Histopathology:
• Often umbilicated/crateriform hyperkeratosis
• Elongated, slender rete ridges 3 to 8 cells wide
• Suprabasilar acantholysis with villous-like projections of connective tissue papillae
rimmed by basal cells
• Dyskeratotic cells with dark nuclei in the form of slender grains (needle-shaped) or
corps ronds (round)
• may not be prominent; variable chronic inflammation
Differential Diagnosis
Pemphigus shows acantholytic cells, no dyskeratosis, and positive direct immunofluorescence
studies.
Treatment:
Darier disease is managed with topical steroids, whereas warty dyskeratoma is excised.
DARIER DISEASE
Warty Dyskeratoma
A, Crateriform architecture with
keratin plug.
B, Villous-like projections and
suprabasilar acantholysis.
C, Corps ronds and grains.
A
B
C
2
22. Frictional Keratosis
Frictional Keratosis:
is a name given to one type of white patch in the mouth.
Often this keratosis can appear as a thin white line across the length of the cheek (called
linea alba, 'white line') opposite where the teeth meet.
Clinical Picture:
• 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
3
Treatment:
• Observation, control of habit.
• Any lesion of questionable etiology, biopsy should be taken.
• Removal of the cause, the lesion may disappear in 2-3 weeks
23. Histopathology:
• Hyperkeratosis or hyperparakeratosis.
• Thickening of granular cell layer.
• Acanthosis but the individual cells are normal.
• Few chronic inflammatory cells in adjacent connective tissue.
Differential Diagnosis:
• Leukoplakia
• Linea alba
• Candidiasis
• Lichen planus
• Squamous cell carcinoma
Linea alba
A, Benign epithelial
hyperplasia and keratinocyte
edema.
B, Superficial
cells with perinuclear halos are
not koilocytes.
A
B
Frictional Keratosis
3
24. Morsicatio Mucosae Oris
▪ It is a subtype of frictional keratosis
▪ This lesion is caused by self-induced injury and chronic tissue irritation like habitual chewing
of buccal mucosa, chronic nibbling, biting, or sucking
Clinical Picture:
▪ A higher prevalence of classic morsicatio mucosae oris has been found in people who are
under stress or who exhibit psychologic conditions.
▪ Thickened, shredded, white areas may be combined with intervening zones of erythema,
erosion, or focal traumatic ulceration.
Treatment:
▪ Well-demarcated borders of the lesion of the mucosa, and the recognition of relevant habits of
each patient are considered to be important in making a diagnosis and the differential
diagnosis.
▪ Accurate diagnosis with history taking and educational modification of the patient's habitual
actions are essential in the treatment of morsicatio, and this should be included in the
differential diagnosis for hyperkeratotic lesion within the lips and mouth.
3
25. Histopathology
• Hyperkeratosis with basophilic debris on the surface
• Bacterial colonies were found
• The epidermis showed marked acanthosis and necrotic
keratinocytes. Beneath the surface
• Swollen keratinocytes were seen
Morsicatio Mucosae Oris
3
A
B C
Morsicatio mucosae
oris
A, Marked
hyperparakeratosis
with fissures and clefts
rimmed by bacteria
and keratinocyte
edema.
B, Marked
parakeratosis with
bacterial colonization
and no inflammation.
C, Prominent
keratinocyte edema
with degenerated
nuclei (not koilocytes).
26. • Smokeless tobacco lesions are caused by contact with caustic agents within the tobacco.
• Long-standing lesions occur from carcinogens within the tobacco and are essentially
lesions of leukoplakia
Clinical Findings:
• Early lesions are poorly demarcated, uniform graywhite, and edematous with wrinkles
and parallel ridges and fissures in the area where the tobacco is placed teeth may show
staining, gingival recession, and root exposure
• Lesions are usually reversible on stopping the habit
• More advanced lesions are dense, well-demarcated, keratotic plaques → these areas
must be biopsied for evaluation of dysplasia, and the lesions are unlikely to be reversible.
Smokeless Tobacco Lesion 3
Smokeless tobacco
lesion.
A, T ypical wrinkled and
ridged, poorly-
demarcated graywhite
lesion of the vestibule
where tobacco is placed.
B, T ypical wrinkled and
ridged, poorly
demarcated
gray-white lesion of the
vestibule where tobacco
is placed.
A
B
27. Histopathology:
• Early lesions: slight parakeratosis with prominent keratinocyte edema of superficial
cells that stops abruptly; karyopyknosis is common; keratin “chevrons” often are
seen, but this is not specific to this condition
• Epithelial hyperplasia is present with minimal reactive atypia and variable chronic
inflammation.
• May see amorphous amyloid-like eosinophilic deposits in the lamina propria and
within minor salivary gland parenchyma.
• More advanced keratotic lesions exhibit hyperparakeratosis or orthokeratosis with or
without dysplasia.
Treatment:
• Early lesions generally resolve if the habit is discontinued.
• Hyperkeratotic lesions should be regularly evaluated for dysplasia or excised/ablated
with discontinuation of habit.
Smokeless Tobacco Lesion 3
A
B
C
Smokeless tobacco
lesion
A, Oral mucosa with well-
demarcated area of degenerated
keratinocytes and salivary gland
involvement.
B, Very thin layer of parakeratin
on the surface and thick band of
degenerated keratinocytes, with
nuclear karyopyknosis.
C, Salivary glands containing
amyloid-like material.
D, P ale band of degenerated
keratinocytes and no epithelial
atypia. K aryopyknosis within
edematous keratinocytes.
D
28. • Nicotinic stomatitis is the most frequently occurring tobacco-related keratosis in the mouth.
• It can be associated with pipe, cigar, or cigarette
• smoking.
• The severity of the condition is proportional to the amount of the tobacco product that is
used.
• The hyperkeratosis of nicotinic stomatitis is reactive to the heat generated by the tobacco
product and the chemicals present.
Clinical Pictures:
• The characteristic site of involvement is the hard palate.
• Although predominantly white, there are areas of erythema with punctate red dots
representing inflamed minor salivary duct orifices.
• If a denture is worn, this will protect the covered mucosa in the hard palate and produce
an obvious distinction between affected and nonaffected areas.
Nicotinic Stomatitis 3
29. Histopathology:
• Hyperorthokeratosis or parakeratosis, benign epithelial hyperplasia, with or without
reactive epithelial atypia
• Variable chronic inflammation
• Squamous metaplasia of excretory salivary ducts and chronic sialodochitis
(periductal inflammation)
Treatment:
The patient should discontinue the tobacco habit.
• On the hard palate the condition does not usually progress to cancer
• Although it is an important indicator of tobacco use and may indicate a risk of dysplasia and
neoplasia at other susceptible sites in particular the floor of the mouth, the lateral margin of
the tongue, or the retromolar region.
Nicotinic Stomatitis 3
Nicotinic Stomatitis
A, Hyperorthokeratosis
and squamous metaplasia
of ducts forming a raised
papule.
B, Hyperorthokeratosis,
parakeratosis, and
squamous metaplasia of
ducts with periductal
chronic inflammation.
C, Periductal and
parenchymal chronic
inflammation of glands
A
B
C
30. Chemical Burn
A chemical burn of the oral mucosa occurs as a result of a noxious agent
placed in direct contact with the mucosa either by the patient or a dentist.
Clinical Picture:
• Changes in their color, texture, consistency, and vascularity.
• Superficial white to yellow, wrinkled lesion.
• Desquamation of the underlying tissue due to necrosis depends on the
duration of exposure to chemicals. As the duration of exposure
increases, the necrosis of the tissue increases.
• On removal of necrotic epithelium, the red bleeding connective tissue
can be observed subsequently covered by yellowish fibrinopurulent
membrane.
3
31. Histopathology:
• Features of coagulative necrosis.
• Salivary gland duct involvement might end up with transient obstructive sialadenitis, the
resulting scarring of ductal opening can end up with permanent obstruction.
• Chronic sialadenitis may require surgical excision of duct/gland.
• Chemical burns are often localized and are rarely confined solely to the anatomic distribution
of the masticatory mucosa.
Treatment:
• The early detection by the patient and the immediate institution of therapeutic measures will
ensure a rapid cure and possibly prevent further mucosal damage
• Permanent removal of the agent will be sufficient for the removal of the cause
• Copious irrigation with normal saline or betadine
• Analgesia if required
• Topical application of the corticosteroids and benzocaine
• Nutritional supplements in the form of multivitamins that would improve the healing
• If required, antibiotics to prevent secondary infections
• Advise the patient to be on soft and cold diet without spice for a week
• Recall after 1 week.
3
Chemical Burn
32. Thermal Burn
Thermal burns are ulcers of the oral mucosa cause by contact of hot
foods with the oral mucosa.
Clinical Picture:
• Vesicular or ulcerative lesions surrounded by an hyperemic edge .
• The severity of the lesions depends on the depth of the burn, which can
sometimes affect the nerve fibers with paresthesia of that district.
Treatment:
• It is important to know the severity of the lesion for an appropriate treatment
• If the lesion is not particularly extensive and painful, the normal tissue repair process
can be expected with topical gel application;
• for extensive and painful lesions, the cortisone therapy is evaluated by
considering a local anesthetic based on nervous involvement.
• For oral burns, the use of antibiotics is usually for the purpose of pre-operative
3
33. Electrical Burn
• Electrical burns in the oral cavity are usually of the arc type, where the
saliva conducts an electric arc from the source to the mouth.
• Most cases occur in young children biting live wires at the end of
extension cords.
Clinical Picture:
• Electric burns of the oral cavity can involve the lip, tongue, mucous
membranes, and underlying bone .
• The commissure of the mouth will show extensive damage from the
electrical current "arcing," resulting in gray-white tissue with elevated red
margins.
• Bleeding does not usually occur at this stage.
• Minor pain and swelling usually result.
3
34. Treatment:
• Emergency treatment is based on the extent of the wound.
• Debridement, systemic antibiotics, and a tetanus booster should be considered.
• Parents should be cautioned that the eschar will slough in 5-7 days and that significant
bleeding could occur at this time.
• symptomatic treatment can be done through the local application of aloe vera or
vitamin E in the post-surgical period in order to relieve pain and irritation .
• A commissure splint is fabricated within days of the injury and is worn for up to 12
months following the burn to prevent microstomia secondary to wound contraction.
• if the burn in the lips, vestibule or floor of the mouth is severe, the best
treatment is with the aggressive approach, employing early surgical debridement
followed by mucosal resurfacing.
• By contrast, a milder burn with limited anatomy involvement should be treated
with the conservative approach.
3
Electrical Burn
35. Actinic Cheilitis
Actinic cheilitis presents as diffuse or patchy dryness and variable thickening of the vermilion
of the lower lip.
The common form of actinic cheilitis is due to chronic sun exposure.
Clinical Picture:
• About 90 percent of cases involve the lower lip
• Common signs of actinic cheilitis include:
• overall dryness
• scaly plaques or scab-like lesions
• thin, delicate patches of skin
• loss of the demarcation between the lower lip and surrounding skin
• inflammation
• tenderness or soreness
• fissuring or skin breakage and separation
• leukokeratosis or white scaly patches
• discoloration
• more noticeable or prominent lip folds or lines
• tightness and wrinkled skin
3
36. Histopathology:
• the epithelium shows acanthosis
• often hyperkeratosis associated with varying degrees of dysplasia. Epithelial atrophy is
rare. Additionally,
• the underlying tissue demonstrates damage to elastic fibers and collagen (solar
elastosis).
• A mild lymphocytic inflammation is usually present.
Treatment:
• Smoking cessation and lifelong, year-round, daily sun protection are essential.
• Limit sun exposure
• Topical therapies for actinic cheilitis are unapproved. They include:
• Topical retinoids
• 5-fluorouracil cream
• Imiquimod cream
• Photodynamic therapy
• Physical treatments for actinic cheilitis include:
• Cryotherapy
• Electrocautery
• Vermilionectomy Laser ablation, eg with Er:YAG laser
Actinic Cheilitis
3
39. Hairy Leukoplakia
White patch on the side of the tongue with a corrugated or hairy
appearance. It is caused by Eptsein Barr Virus(EBV) and occurs usually
in persons who are Immunocompromised
Clinical Picture:
• Corrugated white lesion on lateral/ ventral tongue surface in immunodeficient
patients
• Association with HIV +v adults, AIDS, organ transplant, prolonged steroid therapy
25% - HIV +v adults
• Not common in HIV children
• Corrugated, shaggy/ frayed appearance or plaque like
4
40. Histopathology:
• Hyperparakeratosis
• Acanthosis
• koliocytic cells (viral infected Balloon Cells) in spinous layer
• Homogenous viral nuclear inclusions with residual rim of normal
chromatin
Treatment:
• Treatment is not necessary since the lesion is benign, however the person may
have aesthetic concerns about the appearance.
• The condition often resolves rapidly with high dose acyclovir or desiclovir but recurs
once this therapy is stopped, or as the underlying immunocompromise worsens.
• Topical use of podophyllum resin or retinoids[has also been reported to produce
temporary remission.
Hairy leukoplakia
A, Oral mucosa with sharply demarcated band of pale, ballooned cells with
overlying factitial/frictional hyperparakeratosis.
B, Cells with perinuclear halos and Cowdry inclusions.
C, Cells with perinuclear halos and Cowdry inclusions.
D, In situ hybridization study positive for nuclear Epstein-Barr virus.
A
C
B
D
Hairy Leukoplakia
4
41. Acute Pseudomembranous Candidiasis
(Thrush)
• Also known as moniliasis or thrush or candidosis
• Caused by the infection with yeast like fungus Candida albician.
• Other causative organism may be Candida tropicalis, Candida famata, Candida krusei
Clinical Picture:
• Thrush is the prototype of the oral infections caused by Candida.
• Superficial infection of the outer layers of the epithelium,
• Patchy white plaques or flecks on the mucosal surface
• Removal of the plaques by gentle rubbing or scraping usually reveals an area of
erythema or even shallow ulceration.
• Seen in children and in adults of all ages
• common in women 8
• Typical lesions cause inflammation, erythema, and painful eroded areas
4
42. Histopathology:
Microscopic examination of the lesions reveals
1. localized superficial inflammatory reaction
2. hyperparakeratosis
3. and ulceration of the surface covered with a fibrinoid exudate
4. In fibrinoid exudate large numbers of yeast and pseudohyphae are found .
Treatment:
• Carefully recording the medical history
• Predisposing factors should be treated or eliminated where feasible.
• Topical anti-candidal therapy is efficacious in the management of
oropharyngeal candidiasis
• The prognosis is good for oral candidiasis with appropriate and effective
treatment
4
Candidiasis
A, Psoriasiform epithelial hyperplasia with chronic inflammation; periodic
acid–Schiff (PAS) stain with diastase reveals candidal hyphae (inset).
B, Mild reactive epithelial atypia.
C, Neutrophilic exocytosis and early spongiotic pustules..
Acute Pseudomembranous Candidiasis
(Thrush)
A
B C
43. Chronic Mucocutaneous Candidiasis
A hereditary immunodeficiency disorder, is persistent or recurring infection with
candida due to malfunction of T cells (lymphocytes).
Clinical Picture:
• Chronic mucocutaneous candidiasis usually presents before the age of 3 years,
with one or more of the following:
• Chronic oral candidiasis (thrush)
• Napkin (diaper) dermatitis
• Paronychia and candida onychomycosis (nail infection)
• Widespread crusted plaques on the scalp, trunk, hands and feet
• Scarring alopecia (hair loss)
• Granulomas in the mouth, on the skin and/or nails
• Stenosis of esophagus, larynx or vagina
• Iron deficiency.
Causes:
• There is a genetic predisposition with either autosomal dominant inheritance or
autosomal recessive inheritance
• Autosomal dominant chronic mucocutaneous candidiasis in IL-17 deficiency.
• Chronic mucocutaneous candidiasis is associated with certain endocrine conditions:
hypoparathyroidism, hypothyroidism, hypoadrenalism, diabetes mellitus
• It is also associated with immune defects, include malfunctioning T lymphocytes and
low levels of immunoglobulin.
4
44. Histopathology:
• Multiple and widespread candida infectious lesions can be observed on the oral cavity of CMC
patients.
• Hyperplastic and nodule‐like lesion with irremovable whitish patches and deep fissure are the
most common oral manifestations.
Treatment:
• General measures to reduce the incidence and severity of candida infection:
• Practice good oral hygiene
• Avoid smoking and alcohol.
• Antifungal treatment
• Oral antifungal medications used for chronic mucocutaneous candidiasis include:
• Fluconazole
• Itraconazole
• Posaconazole
• Voriconazole
• Liposomal amphotericin B
• Immunological therapy to improve immune status include:
• Transfer factor
• JAK1/2 tyrosine kinase inhibitors,
• Intravenous immunoglobulin G (IVIg G)
• Granulocyte-macrophage colony-stimulating factor (GM-CSF) infusions
• Interferon-α.
4
Chronic Mucocutaneous Candidiasis
47. Oral lichen planus is a common disease and present in about 2%
of tbe adult population
Clinical Pictures:
• Interconnecting white striae and papules on an erythematous
background
• can also present as a white patch or as a desquamative gingivitis.
• Buccal mucosa, tongue, and gingiva.
• In adults, more often females.
Reticulated,
erythematous, and
ulcerated (yellow
fibrin membrane
Lichen planus on the
tongue:
symmetric white cast,
atrophy of filiform
papillae, and ulceration
on lateral aspects; lips
are also involved.
Oral Lichen Planus
5
48. Histopathology:
• Parakeratosis, orthokeratosis, epithelial hyperplasia, or atrophy
• Pointed rete ridges (Saw-tooth-like)
• Band-like lymphocytic infiltrate of the lamina propria hugging the epithelium
• Loss of basal cells in the involved lesional epithelium
• Civatte bodies (apoptotic keratinocytes with pyknotic or anucleate forms)
Special Stains/Immunopathology
• With direct immunofluorescence, an irregular band of fibrinogen is seen at the
basement membrane.
Histopathologic Differential
• Lichenoid mucositis has a deeper perivascular and nodular lymphocytic and
plasmocytic infiltrate.
Treatment and Prognosis
• Topical or systemic steroids
Oral Lichen Planus
5
Lichen planus
A, Hyper parakeratosis,
epithelial hyperplasia,
sawtooth rete ridges,
and
lymphocytic band.
B, Hyper parakeratosis,
spongiosus, leukocyte
exocytosis, and
lymphocytic band at
the interface.
C, Squamatized
(degenerated) basal cells
without colloid bodies.
A
B
C
49. Lichenoid Mucositis
Definition:
Reactive lesions caused by contact with allergenic materials such as
amalgam fiilings or ingestion of drugs such as nonsteroidal anti-
inflammatories or angiotensin converting enzyme inhibitors
Clinical Picture:
• Interconnecting white striae and papules on an erythematous
background
• Can also present as a white patch or as a desquamative gingivitis.
• Buccal mucosa. tongue, and gingiva.
• In adults, more often females. Usually related to drug intake.
5
Lichenoid drug reaction with
asymmetric distribution on the
tongue.
Lichenoid drug reaction
with asymmetric
distribution on
the buccal mucosa.
50. Microscopic Findings:
• Same as oral lichen planus but with deep, perivascular inftammatory
infiltrates predominantly lymphocytes but aha plasma cells.
Histopathologic Differential:
• Oral lichen planus has an identical histpathology but lacks the deeper
perivascular and nodular lymphocytic infiltrate.
Treatment and Prognosis:
• Removal of the offending material or discontinuation of medication.
Topical steroids.
Lichenoid Mucositis
Lichenoid Mucositis With Granulomatous Infiltrate
A, Hyperorthokeratosis, epithelial hyperplasia, and lymphohistiocytic
band.
B, Squamatization of the basal cells, colloid bodies, and epithelioid histiocytes in
the lamina propria.
C, Many epithelioid histiocytes admixed with lymphocytes in the lamina
propria.
A B
C
5
51. Drug-Induced Lichenoid Reactions
• Drug-Induced Lichenoid Reactions (DILRs) are related to a delayed
hypersensitivity reaction.
• It has been suggested that drugs or their metabolites precipitate the lichenoid
reaction.
• There are many drugs responsible for the development of these lesions such as
non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme
inhibitors.
• Other medications, such as anti-malarial and antihypertensive drugs, diuretics,
oral hypoglycemic agents, gold salts, penicillamine, and beta blockers are also
related to the evolution of DILRs.
Clinical Picture:
▪ DILRs are mostly unilateral with an ulcerative pattern, which might be quite
similar to OLP.
▪ Usually the lesions evolve several months after the patient starts a new drug.
Treatment:
▪ DILRs are not generally severe; however, if a patient has serious symptoms
withdrawal of the drug and use of topical steroids are often recommended.
5
54. Oral Leukoplakia
A white patch or plaque that cannot be scrapped off and also
characterized clinically or pathologically as any other disease.
Clinical Picture:
• Homogenous Leukoplakia
• Non Homogenous Leukoplakia
• Proliferative verrucous leukoplakia
• Erythroleukoplakia
• Sublingual keratosis
• Oral hairy leukoplakia
• Syphilitic leukoplakia
6
55. Histopathology:
1. Acanthosis/atrophy
2. Dysplasia and inflammatory cell
3. Cellular pleomorphism
4. Nuclear atypia
5. Increased number of cells seen undergoing mitosis, including both normal
and abnormal mitoses.
6. The distinction between the epithelial layers may be lost.
7. Abnormal keratinization
8. Alteration of the normal epithelial-connective tissue architecture
9. Rete pegs may become "drop shaped". wider at their base than more
superficially.
Treatment:
Most patches improve on their own and don’t require any treatment. It’s important
to avoid any trigger that may have caused leukoplakia
Oral Leukoplakia
6
Mild epithelial dysplasia.
Hyper parakeratosis and
mild epithelial dysplasia.
Basal cell hyperplasia in
the absence of
inflammation involving
less than one third the
thickness of
epithelium
Moderate epithelial
dysplasia. Bulbous
rete ridge and basal
cell hyperplasia and
discohesion. Basal
cell hyperplasia and
mitoses
A
B
56. Verrucous Carcinoma
A diffuse, largely exophytic,superficial spreading, highly keratinized, warty
form of well differentiated squamous cell carcinoma that is unlikely to
metastasize.
Clinical Picture:
• 5% of oral SCC
• Common sites: buccal mucosa and gingiva
• Early stage [verrucous hyperplasia] is benign or may arise from leukoplakia
• Indurate firm with invasion to the subjacent tissue
6
57. Histopathology:
• Papillary surface, acanthotic and highly keratinized epithelium
• Submucosal invasion by bulbous well differentiated epithelium
• Minimal atypia
• Epithelium seldom shows dysplastic features.
• Elephant foot like rete ridges is seen
• Parakeratin plugging is present
Treatment :
Because of its superficial and cohesive growth pattern and sharply demarcated
margins, verrucous carcinoma is ideally suited to treatment by either surgical excision
or laser therapy. The prognosis is good, because local excision is usually curative.
New lesions in adjacent sites may occur.
6
Verrucous
carcinoma
A, Bluntly
invasive
endophytic
growth with
parakeratin
plugging,
frondlike
bulbous rete
ridges, and
lymphocytic
band at
interface.
B, Minimal
cytologic
atypia.
.
Verrucous Carcinoma
A
B
58. Squamous Cell Carcinoma
(Epidermoid Carcinoma)
Malignant epithelial neoplasm exhibiting squamous differentiation as
characterized by the formation of keratin and/or the presence of
intercellular bridges
Clinical Picture:
• Rapid proliferation / growth of long standing, innoculous lesion.
• Unexplained color change.
• Growth / ulceration of pigmented area.
• Ulceration / erosion in otherwise.
• Homogenous white/red lesions.
• Longstanding ulcers with areas of sharp tooth or appliances insult.
• Induration in / around ulcer.
• Unexplained mobility, exfoliation of teeth.
• Unexplained paresthesia
• Unexplained dysphagia, hoarseness of voice.
• Unexplained restriction of tongue movements.
• Pain in ear
6
Contrasting appearance of
squamous cell carcinoma
as a smooth white patch
on the tongue (A)
compared with an
exophytic lesion
in the palate (B).
A
B
59. Squamous Cell Carcinoma 6
Well-differentiated squamous cell carcinoma, keratoacanthomatous pattern
A, Papillary proliferation of pale squamous cells with endophytic, cupped morphology.
Pale cells with broad pushing front and lymphocytic band.
B, Pale cells with glassy cytoplasm and darker basaloid cells.
C, Dyskeratotic cells and microabscesses at tips of rete ridges.
Histopathology:
1. Invasive islands and cords of malignant squamous epithelial cells
2. Irregular extension of lesional epithelium through the basement membrane and
into subepithelial connective tissue
3. Strong inflammatory or immune cell response to invading epithelium and
necrosis may be present
4. Dense fibrosis (desmoplasia or scirrhous change) and the formation of new
blood vessels (angiogenesis)
5. Dysplastic changes are also seen
Treatment:
• Either definitive radiation therapy or surgery
• In advanced stage - multimodal therapy involving various combinations of surgery,
radiation therapy, or chemotherapy
A B
C
60. Here we will go over the diagnostic scheme that will aid
in the correct differentiation and diagnosis of any white
lesion.
61.
62.
63. Thank You!
Conclusion
Proper history taking and
Proper clinical examination
along with a reliable diagnostic
scheme will definitely aid in the
correct differentiation and
diagnosis of any white lesion
