White Lesions Flashcards

(56 cards)

1
Q

What are the four variables that contribute to the normal pink color of the oral mucosa?

A

Keratinization,
melanin pigment,
vascularity, and
epithelial thickness.

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2
Q

What clinical term is often used to describe lesions appearing as white areas on the oral mucosa?

A

White patch.

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3
Q

Such lesions may be associated with :

A

increased surface keratin layer ( Hyperkeratosis ).
Increased thickness of the epitheliums the thickened ( acanthosis).
Abnormal permeability .
Reduced vascularity.
coagulation and opacity of the superficial tissue.
pseudo membranes.

submucosal deposits or hyperkeratinization

Fibrin exudates and surface debris

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4
Q

What is leukoedema and is it considered a disease?
And Etiology

A

a common oral mucosal condition that is considered a variation of normal rather than a disease.

To date, the cause of leukodema hasn’t been established.( suggest hereditary factors.)
Some - relationship between poor oral hygiene and abnormal
masticatory patterns

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5
Q

What are the clinical features of leukoedema regarding age, sex, site, and race?

A

Age: Adults and children;
Sex: No sex predilection;
Site: Typically occurs bilaterally on the buccal mucosa and may extend onto the labial mucosa;
Race: More common in blacks than whites.

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6
Q

What are the signs and symptoms of leukoedema?
Can leukoedema be rubbed off, and how can it be clinically diagnosed

A

It is asymptomatic

It cannot be rubbed off. It can be easily diagnosed clinically because the white appearance greatly diminishes يتضائل or disappears when the cheek is everted and stretched

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7
Q

What are the key histopathologic features of leukoedema

A

parakeratinized, acanthotic
show marked intracellular oedema with small pyknotic nuclei in clear cytoplasm.
These cells are vacuolated and contain glycogen. مفرغه
There are no alterations in the germinative layers or changes in the underlying connective tissue

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8
Q

What is white spongy nevus and how is it inherited?

A

also known as familial folded gingivostomatitis,
is a hereditary disorder transmitted as an autosomal dominant trait.
mutation in either keratin 4 or 13 genes, causing a defect in normal keratinization

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9
Q

What are the clinical features of white spongy nevus regarding age, sex, and site

A

Age: Appears at birth or in early childhood sometimes during adolescence; المراهقه
Sex: No sex predilection;
Site: Most commonly affects the buccal mucosa bilaterally,
Extraoral mucosal sites are less commonly affected.

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10
Q

: What are the signs and symptoms of white spongy nevus?

A

usually asymptomatic. The surface is shaggy or deeply folded اشعث مطوي with a wrinkled appearance. The edges are not well defined and merge gradually with

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11
Q

What are the main histopathologic features of white spongy nevus

A

The epithelium is acanthotic with marked surface parakeratosis,
is marked intracellular oedema of the prickle cell layer (spongiosis),
often beginning in the parabasal region.
Oedematous cells are swollen with faintly stained eosinophilic or clear cytoplasm and pyknotic eccentric nuclei, giving a (basket weave appearance.

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12
Q

What is Hereditary Benign Intraepithelial Dyskeratosis (HBID)

A

HBID, also known as Witkop’s disease, is a rare autosomal dominant hereditary condition.

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13
Q

What are the clinical features of HBID regarding age, and site?

A

Age: Early onset during childhood (usually within the first year)
Site: Affects the oral

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14
Q

What are the signs and symptoms of oral HBID?

A

Oral lesions consist of asymptomatic thick corrugated white plaques and folds of spongy mucosa,
Like white sponge nevas

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15
Q

What is the most notable feature of HBID, and what are its signs and symptoms?

A

The most interesting feature is the ocular lesions, which appear as thick, opaque, foamy gelatinous plaques on the bulbar conjunctiva adjacent to the cornea,
sometimes involving the cornea. When active, patients may experience tearing, photophobia, and itching. Ocular lesions may vary seasonally, being most prominent in spring and regressing in summer or autumn

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16
Q

What are the histopathologic features of HBID

A

parakeratin production (hyperkeratosis), epithelial hyperplasia and marked acanthosis,
and dyskeratotic cells (premature keratinization) waxy eosinophilic cells
dyskeratotic cells a cell-within-a-cell phenomenon.
Non-dyskeratotic cells are enlarged and oedematous with hydropic degeneration.
Normal cellular features are seen in the lower spinous and basal layers. The epithelial-connective tissue junction is well-defined,

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17
Q

What is Follicular Keratosis, also known as Darier’s disease

A

It is an uncommon genodermatosis with striking skin involvement and relatively subtle oral mucosal lesions.

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18
Q

How is Darier’s disease inherited?

A

condition is inherited as an autosomal dominant trait, though sporadic cases occur. حالات متفرقه

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19
Q

What do the skin lesions of Darier’s disease consist of

A

Symmetrically distributed small erythematous, often pruritic papular lesions that coalesce, ulcerate, and crust. Coalesced areas form vegetating to verrucous growths due to excessive keratin formation. Keratin accumulation may have a foul odor due to bacterial degradation.

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20
Q

What are some other signs of Darier’s disease besides skin lesions?

A

Thickening of palms and soles with pits and keratoses is not uncommon.

Fingernail changes can include fragility, longitudinal lines, and painful splintering

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21
Q

What do the oral lesions of Darier’s disease look like

A

They are typically asymptomatic and consist of multiple flat topped papules. If numerous and confluent, they result in a cobblestone mucosal appearance. Prominent palatal lesions may resemble inflammatory papillary hyperplasia. Lesions may extend to the oropharynx and pharynx.
15الي50 ‎%‎ من الحلات

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22
Q

What are the key histopathologic features of Darier’s disease

A

hyperkeratosis with a acanthosis, Intraepithelial clefting is seen as suprabasal lacunae containing acantholytic cells
. Specific benign dyskeratotic cells, corps ronds and corps grains,
Corps ronds are large abnormally keratinized cells with basophilic nuclei and eosinophilic cytoplasm with a clear perinuclear halo.
Corps grains are smaller flattened parakeratotic cells with pyknotic hyperchromatic nuclei

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23
Q

What is frictional keratosis and what causes it?

A

Frictional keratosis, or focal hyperkeratosis, is a hyperkeratotic white lesion caused by chronic friction from irritants like a sharp tooth, cheek biting, or ill-fitting dentures

24
Q

What are the clinical features of frictional keratosis

A

It appears as an asymptomatic lesion that becomes dense and white with a roughened surface over time.site It occurs in areas commonly traumatized

And Morsicatio mucosae oris

25
What is Morsicatio mucosae oris?
Morsicatio mucosae oris is a form of chronic oral frictional keratosis of the nonkeratinized oral mucosa, usually located on the buccal mucosa or lips (morsicatio buccarum, morsicatio labiorum)
26
What are the histopathologic features of frictional keratosis?
hyperkeratosis. acanthosis. • Dysplastic epithelial changes are not seen in this simple frictional hyperkeratotic lesion. • Few chronic inflammatory cells may be seen in the subjacent connective
27
What is nicotine stomatitis and what causes it?
Nicotine stomatitis is a common tobacco-related form of keratosis most typically associated with vipe and cigar smoking,
28
What are the clinical features of nicotine stomatitis regarding age, sex, and site?
Age & Sex: Most often found in men older than 45 years; Site: Most common in the hard palate
29
What are the signs and symptoms of nicotine stomatitis
erythematous-type reaction and overtime with increased keratinization → diffuse grey white palatal mucosa. numerous slightly elevated white papules with central red dots are noted. Such papules represent inflamed minor salivary glands and their ductal orifices.
30
What are the histopathologic features of nicotine stomatitis?
• Epithelium → hyperorthokeratosis & moderate acanthosis • Connective tissue → mild, patchy chronic inflammation • Minor salivary glands → mild to severe inflammatory changes as: • Squamous metaplasia of the excretory ducts • Inflammatory exudates • Hyperplastic ductal epithelium • Ductal dilatation, acinar atrophy • Chronic inflammatory cells
31
What causes white lesions associated with smokeless tobacco
chewing tobacco snuff ) in the mandibular vestibule India and Southeast Asi Oral mucosa responds to the irritating effects of tobacco Dysplastic changes may follow, with an associated risk of malignant change. This biologic alteration in tissues is thought to be a response to : - Tobacco constituents. - Other agents that are added to tobacco for flavouring or moisture retention. - Carcinogens such as nitrosamines and nitrosononicotine ( organic component of chewing tobacco and snuff ). - Alkaline PH of different forms of smokeless tobacco which ranges between 8.2 and 9.3
32
What are the clinical features of smokeless tobacco-associated lesions regarding age, sex, and site
Age & Sex: Predominantly seen in white teenage males. مراهقين Site: Develop in the immediate area where tobacco is placed, most commonly the mucobuccal fold of the mandible in the incisor or molar region.
33
What are the signs and symptoms of smokeless tobacco-associated lesions?
1 generally painless and asymptomatic, often discovered incidentally. 2New lesions are typically translucent plaque 3 advanced cases, becomes thickened and may appear leathery or nodular with a heavy folded character
34
What are the histopathologic features of smokeless tobacco keratosis?
Not specifica Squamous epithelium is hyperkeratinized and acanthotic (epithelial hyperplasia). epithelium may demonstrate vacuolization or oedema. Salivary gland alterations are seen in 40 % of biopsy specimens. Such changes are primarily inflammatory and include acinar atrophy, interstitial fibrosis and dilated excretory ducts.
35
What is actinic cheilitis and what causes it and most commonly affected
Actinic cheilitis, also known as solar cheilitis or actinic cheilosis, is a common premalignant alteration of the lower lip vermilion resulting from long-term or excessive exposure to ultraviolet sunlight. whites, especially those with fair skin. It is prevalent in those with outdoor occupations, leading to terms like farmer's lip and sailor's lip. بحار
36
What is the pathogenesis of actinic cheilitis
degeneration of the lower lip vermilion secondary to regular and prolonged sun exposure. UV light exposure can cause mutations in p53 tumor suppressor genes.
37
What are the clinical features of actinic cheilitis regarding age, sex, and site?
Age: Seldom occurs in persons younger than 45; Sex: Strong male predilection (up to 10:1 ratio); Site: Involves the vermilion portion of the lips, especially the lower lip
38
What are the signs and symptoms of actinic cheilitis
Earliest changes include atrophy of the lower lip vermilion border, characterized by a smooth, pale to silvery grey, glossy appearance with often fissuring and wrinkling. As it progresses, rough scaly areas develop on the drier vermilion, which can thicken and appear leukoplakic, especially near the wet line. The scaly material can be peeled off but reforms within days.
39
What are the histopathologic features of actinic cheilitis
The overlying epithelium is usually atrophic or focally and Various dysplastic changes (slight atypia to carcinoma in situ) may be seen. The underlying connective tissue shows striking basophilia (elastin replacement of collagen), known as solar (actinic)
40
What is lichen planus and how common is it in the oral mucosa?
Lichen planus is a chronic dermatological disease that often affects the oral mucosa and is by far the commonest.
41
What is the etiology of oral lichen planus?
Oral lichen planus is a known T-cell mediated chronic inflammatory response affecting the oral mucosa. The exact etiology is unknown, but implicated factors include genetic predisposition, infective agents, systemic diseases, vitamin deficiencies, psychiatric disorders or stresses. f systemic diseases, such as diabetes mellitus, hypertension, ulcerative colitis include genetic predisposition, infective agents, systemic diseases, vitamin deficiencies and psychiatric disorders or stresses. and liver diseases (such as hepatitis C)
42
What are the proposed pathophysiological mechanisms of oral lichen planus?
The two are antigen-specific and non-specific. The antigen-specific mechanism suggests antigen presentation leads to activation of CD4+ helper T cells, releasing pro-inflammatory cytokines (TNF-$\alpha$, IFN$\gamma$), which induces a CD8+ T cell-mediated cytotoxic reaction against basal cells resulting in keratinocyte apoptosis. The non-specific mechanism suggests mast cell activation releases pro-inflammatory mediators and upregulates matrix metalloproteinases, leading to T cell infiltration, basement membrane disruption, and keratinocyte apoptosis.
43
What are the six clinical subtypes of OLP, and which are most common?
reticular, papular, plaque, atrophic, erosive, and bullous. They can occur individually or in combination. The most common presentations are reticular, erosive, and plaque subtypes.
44
Describe the appearance of reticular OLP.
Reticular OLP has the most characteristic manifestation, displaying a white lacy network (Wickham striae) with hyperkeratotic plaques.
45
Describe the appearance of erosive or atrophic OLP.
Erosive or atrophic OLP typically presents with erythema and ulcerations, often associated with pain and sensitivity. Reticular keratotic striae may be present at the periphery.
46
Describe the appearance of papular or plaque OLP.
The papular or plaque subtypes appear as white keratotic papules or plaques that may resemble leukoplakia.
47
What is the typical distribution and common sites for OLP?
OLP typically has a(bilateral )distribution and most commonly appears on the buccal mucosa, tongue, and gingiva, followed by the labial mucosa and lower lip.oral وخلاص
48
What is the Koebner phenomenon and how might it relate to OLP?
The Koebner phenomenon is when lesions develop at sites of mechanical trauma دي المهم. It may explain why lesions appear more commonly on the buccal mucosa and tongue, which are prone to trauma.oral برضو
49
What are the characteristic histopathologic features of oral lichen planus?
saw-tooth pattern.اسنان المنشار colloid, hyaline or civatte bodies. eosinophilic band lymphocytic band ) liquefaction degeneratio
50
What is the classic and most common presentation of oral candidiasis?
Pseudomembranous candidiasis, also known as oral thrush.
51
What are common methods for identifying Candida?
10% potassium hydroxide stain and culture with Sabouraud dextrose agar.
52
Who is most susceptible to acute pseudomembranous candidiasis?
بتتقشر دا اللي متحتاج تعرفه بس
53
Can hyperplastic candidiasis be easily wiped off?
No, unlike oral thrush, hyperplastic candidiasis cannot be easily wiped off. Severe dysplasia or malignant Increase risk malignant
54
How does acute atrophic candidiasis present clinically?
It presents as generalized or localized erythema on the oral mucosa, most commonly on the palate, but also on the buccal mucosa and dorsum of the tongue.
55
What are the risk factors for acute atrophic candidiasis?
It is frequently secondary to broad-spectrum antibiotic treatment. Other risk factors include corticosteroids, HIV disease, iron deficiency anemia, vitamin B12 deficiency, and uncontrolled diabetes mellitus.
56
How common is denture stomatitis and what are the risk factors? Chronic
It is a common condition with an incidence up to 65%. Risk factors include poorly fitted dentures, prolonged use of dentures (especially wearing them for 24 hours), and poor oral hygiene.