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OPATH > White lesion > Flashcards

White lesion Flashcards

1
Q

White appearing lesions of the mucosal mucosa from the scattering of light through an altered mucosal surface

A

White Lesion

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2
Q

MUCOSAL ALTERATIONS of White Lesion

A

Hyperkeratosis- appears white
Hyperplasia of the stratum malpighi (basale)
Intracellular edema of epithelial cells
Reduced vascularity of subjacent CT
Color of exudate and other surface contaminants

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3
Q

Etiology of White Lesion

A

Physical trauma
Tobacco use
Genetic abnormalities
Mucocutaneous diseases
Inflammatory reactions

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4
Q

SUBCLASSIFIED ACCORDING TO:

A

Hereditary Conditions
Reactive Lesions
Other mucosal white lesions
Other non epithelial white lesions
Pre-neoplastic & neoplastic lesions

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5
Q

WHITE LESIONS HEREDITARY CONDITIONS

A

Leukoedema
White Sponge Nevus
Hereditary Benign Intraepithelial Dyskeratosis (HBID)
Follicular Keratosis

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6
Q

Generalized mild opacification of buccal mucosa
Variation of normal
No definitive cause
More prevalent in black population
Shows milder presentation in whites

A

LEUKOEDEMA

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7
Q

Etiology of Leukoedema

A

No definitive cause

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8
Q

Implicated factors of Leukoedema

A

Smoking
Alcohol Ingestion
Bacterial Infection
Salivary Conditions
Electrochemical Interaction
Poor oral hygiene and abnormal masticatory problems

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9
Q

CLINICAL FEATURES OF LEUKOEDEMA

A

Asymptomatic; Symmetrical
Gray-white, diffuse, filmy or milky, opalescent
Exaggerated cases result in wrinkling or corrugation (scalloped shaped areas) of the mucosa
Gentle stroking with gauze pad or tongue depressor will not remove it
Bilateral on the buccal mucosa

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10
Q

COMMON LOCATION OF LEUKOEDEMA

A

Bilateral on the buccal mucosa
border of the tongue

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11
Q

How to differentiate leukoedema from other white lesions

A

With stretching of the buccal mucosa, the opaque changes will dissipate

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12
Q

EPITHELIAL HISTOPATHOLOGY OF LEUKOEDEMA

A

Epithelium is parakeratotic

Epithelium is acantholytic (Irregular thickening of the epidermis/ epithelial layer)

Marked intracellular edema of spinous cells

Enlarged epithelial cells with small pyknotic nuclei in optically clear cytoplasm

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13
Q

DIFFERENTIAL DIAGNOSIS OF LEUKOEDEMA

A

Leukoplakia
White Sponge Nevus (Cannon’s Disease)
Hereditary Benign Intraepithelial Dyskeratosis (HBID)

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14
Q

TREATMENT OF LEUKOEDEMA

A

No treatment is required

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15
Q

PREMALIGNANT BA SI LEUKOEDEMA?

A

No premalignant tendencies

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16
Q

Clinical appearance commences during adolescence & has equal predilection for males and females

A

WHITE SPONGE NEVUS (CANNON’S DISEASE)

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17
Q

Rare genodermatosis that is inherited as an autosomal dominant trait - defects in the normal keratinization of the oral mucosa

A

WHITE SPONGE NEVUS (CANNON’S DISEASE)

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18
Q

Mistaken for leukoplakia

A

WHITE SPONGE NEVUS

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19
Q

CLINICAL FEATURES OF WHITE SPONGE NEVUS

A

Typical appearance: white lesion which is elevated and look irregular, have fissures and plaque formation

Painless

Deeply folder, white or gray lesions affecting the mucosa

Bilateral and symmetrical

Appears early in life (adolescence)

Keratosis in the buccal mucosa

Thicker than leukoedema

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20
Q

OTHER NAME FOR WHITE SPONGE NEVUS

A

CANNON’S DISEASE

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21
Q

HISTOPATHOLOGY OF CANNON’S DISEASE

A

Spongiosis

Acanthosis

Parakeratosis

Pronounced intracellular edema: edematous (fluid accumulation)

Mode of keratinization is characterized by the retention of the nuclei in the stratum corneum

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22
Q

DIFFERENTIAL DIAGNOSIS OF CANNON’S DISEASE

A

Hereditary Benign Intraepithelial Dyskeratosis (HBID)
Pachyonychia Congenita
Lichen Planus (Hypertrophy type)
Cheek biting or traumatic/ frictional keratosis

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23
Q

Affecting the nails and skin
Blisters in soles on their feet (painful) and palms
White patches on tongue and buccal mucosa

A

Pachyonychia Congenita

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24
Q

TREATMENT FOR CANNON’S DISEASE

A

No treatment - self limiting

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25
Q

IS WSP MALIGNANT

A

No malignant tendencies

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26
Q

CLINICAL FEATURES OF HBID

A

Syndrome

Early onset (first yr of life) - gradually intensifies until mid-adolescence

Bulbar Conjunctivitis

Oral lesions

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26
Q

Witkop’s Disease

A

HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS (HBID)

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27
Q

HBID

A

HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOS

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28
Q

Rare autosomal dominant disorder characterized by elevated epibulbar and oral plaques and hyperemic (increased blood volume) conjunctival blood vessels

A

HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS (HBID)

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29
Q

foamy plaques - triangular in shape in the eye area (corneal limbus)

A

Bulbar Conjunctivitis

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29
Q

HBID ORAL LESION IS FOUND IN

A

Buccal and labial mucosa
Labial commissures
Floor of the mouth
Lateral surfaces of the tongue
Gingiva
Palate
Except the dorsum of the tongue
Usually detected within the 1st yr of life
Gradually increase in intensity until mid adolescence
Variations: deeply folded, opaque, white lesions to more delicate, opalescent areas

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29
Q

Hypodontia
Accompanied by ocular lesions

A

HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS (HBID)

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29
Q

Vary seasonally
Patient complain of photophobia, especially in early life
Blindness secondary to corneal vascularization
Spontaneous shedding of the conjunctival plaques occurs on a seasonal basis

A

Ocular lesions

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30
Q

HISTOPATHOLOGY OF HBID

A

Similarities between oral and conjunctival lesions are noted microscopically
Cell within a cell
Non-dyskeratotic (Enlarged, edematous and elongated)

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30
Q

Ocular lesions

A

Vary seasonally
Patient complain of photophobia, especially in early life
Blindness secondary to corneal vascularization
Spontaneous shedding of the conjunctival plaques occurs on a seasonal basis

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31
Q

Similarities between oral and conjunctival lesions are noted microscopically (HBID)

A

Epithelial hyperplasia
Acanthosis
Significant hydropic degeneration
Enlarged, hyaline, and so called waxy eosinophilic cells present in the epithelium

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32
Q

Cell within a cell

A

Eosinophilic cells within the middle and superficial spinous regions become surrounded by adjacent cells (parang nakasandwich yung cells)

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32
Q

Darrier’s Disease / Darrier’s white-disease

A

FOLLICULAR KERATOSIS

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33
Q

TREATMENT OF HBID

A

No treatment is necessary unless it becomes invasive
Condition is self limiting

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34
Q

DIFFERENTIAL DIAGNOSIS OF HBID

A

White sponge nevus

Pachyonychia Congenita

Hypertrophic Lichen Planus

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35
Q

RISK OF MALIGNANCY OF HBID?

A

No risk of malignant transformation

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36
Q

Genetically transmitted disorder with an autosomal dominant mode of inheritance

A

FOLLICULAR KERATOSIS

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37
Q

CLINICAL FEATURES OF DARRIER’S DISEASE/FOLLICULAR KERATOSIS

A

Onset: childhood or adolescence
accompanied by skin lesions; has a predilections for the skin; 13% of its patients forming oral lesions
Skin manifestations
Oral Lesions

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38
Q

SKIN MANIFESTATION OF DARRIER’S DISEASE/FOLLICULAR KERATOSIS

A

small, skin-colored papular lesions, symmetrically distributed over the face, trunk, and intertriginous areas

Papules eventually coalesce and feel greasy because of excessive keratin production

Finger Nail Changes

Lesions may also occur unilaterally

Hyperkeratosis Palmaris et Plantaris)

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39
Q

ORAL LESION MANIFESTATION OF DARRIER’S DISEASE/FOLLICULAR KERATOSIS

A

Oral lesions closely resemble the cutaneous lesions

Asymptomatic

Favored oral mucosa sites/Predilection: attached gingiva and hard palate

Small, whitish papules producing an overall cobblestone appearance

Papules range from 2 to 3 mm in diameter may become coalescent (dikit-dikit)

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40
Q

HISTOPATHOLOGY OF FOLLICULAR KERATOSIS

A

Suprabasal lacunae (clefts) formation containing acantholytic epithelial cells

Dyskeratotic process characterized by a central keratin plug that overlies epithelium exhibiting a suprabasal cleft

Intraepithelial clefting phenomenon

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41
Q

DIFFERENTIAL DIAGNOSIS OF FOLLICULAR KERATOSIS

A

Dyskeratosis congenita (rare)

Acanthosis nigricans

Condyloma acuminatum

Nicotine stomatitis

Acantholytic dyskeratosis

Hailey-hailey disease

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42
Q

TREATMENT OF FOLLICULAR KERATOSIS

A

Vitamin A/ retinoids used - not advisable for long term therapy because the occurrence of systemic toxicity

Topical corticosteroids and Vitamin A analog retinoic acid

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43
Q

Side effects OF CORTICOSTEROIDS

A

cheilitis,

elevation of serum liver enzymes and triglycerides

severe dryness of the skin.

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44
Q

PROGNOSIS OF FOLLICULAR KERATOSIS

A

The disease is chronic and slowly progressive

Recurrence may be noted in some patient

Non malignant

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45
Q

WHAT DISEASE IS MALIGNANT UNDER HEREDITARY WHITE LESION

A

NONE

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46
Q

WHITE LESIONS: REACTIVE LESIONS

A

Focal (frictional) Hyperkeratosis

White lesions associated with smokeless tobacco

Nicotine stomatitis

Hairy Leukoplakia

Hairy Tongue

Dentifrices associated slough

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47
Q

Related to chronic rubbing or friction against an oral mucosa surface

A

FOCAL (FRICTIONAL) HYPERKERATOSIS

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48
Q

Chronic rubbing or friction against an oral mucosal surface — Resulting in Hyperkeratotic white lesion that is analogous to a callus on the skin

A

FOCAL (FRICTIONAL) HYPERKERATOSIS

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48
Q

commonly occur in highly traumatized areas such as the lips, lateral margins of the tongue, buccal mucosa along occlusal line and edentulous ridges

A

Frictional/Benign Hyperkeratosis

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49
Q

Other term: FOCAL (FRICTIONAL) HYPERKERATOSIS

A

Frictional/Benign Hyperkeratosis

Denture callous or ridge callus

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50
Q

Most common white lesion in the oral cavity

A

FOCAL (FRICTIONAL) HYPERKERATOSIS

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51
Q

May form due to chronic lip or cheek chewing that may result to keratinization that present itself as opacification at the affected area

A

FOCAL (FRICTIONAL) HYPERKERATOSIS

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52
Q

ETIOLOGY OF FOCAL (FRICTIONAL) HYPERKERATOSIS

A

Chronic Irritation
Broken tooth or restoration
Habitual cheek or lip biting
Vigorous tooth brushing
Hyperocclusion
Ill fitting denture

Hyperkeratotic white lesions (analogous to callus on the skin)

Protective action against low grade long term trauma

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53
Q

CLINICAL FEATURES OF FOCAL (FRICTIONAL) HYPERKERATOSIS

A

Lip
Lateral margin of tongue
Buccal mucosa along occlusal line
Edentulous alveolar ridges
Chronic cheek or lip chewing = opacification (keratinization) of the affected area
Chewing on edentulous alveolar ridges produces the same effect
Doesn’t often need biopsy

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54
Q

HISTOPATHOLOGY OF FOCAL (FRICTIONAL) HYPERKERATOSIS

A

Chronic Inflammatory Cells

Hyperkeratosis (thickened layer or keratin) or

Parakeratosis (keratin layers shows remnants of epithelial nuclei)

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55
Q

TREATMENT OF FOCAL (FRICTIONAL) HYPERKERATOSIS

A

Elimination of the cause Repair broken tooth, restoration or ill fitting denture (polish), wear mouth guard

Address the causative habit: encourage the patient to discontinue habit

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56
Q

ETIOLOGY OF WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO

A

Direct contact with smokeless tobacco and contaminants
Snuff form of tobacco
Chemical carcinogens liberated from smokeless tobacco (chewing and snuff)

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57
Q

DIFFERENTIAL DIAGNOSIS OF WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO

A

Frictional Keratosis
Hyperplastic Candidiasis
Leukoedema
Plaque-type Lichen Planus

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57
Q

CLINICAL FEATURES OF WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO

A

Prevalence associated with regional use
Mostly seen in white males
Asymptomatic in mucosa where tobacco is held
Most commonly seen in the mandibular vestibular mucosa (Snuff dipper’s pouch)
Wrinkled appearance
Damage seen in adjacent teeth and periodontium

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58
Q

HISTOPATHOLOGY OF WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO

A

Superficial epithelium may demonstrate vacuolization or edema

Slight to moderate parakeratosis often in form of chevrons (or pires/parulis) acanthosis

Diffused zone of basophilic stromal alterations

Epithelial Dysplasia

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58
Q

TREATMENT OF WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO

A

Smoking cessation (ask px to stop)
Biopsy may be required in persistent lesion, ulcerated and indurated lesions

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59
Q

RISK OF MALIGNANCY WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO

A

Risk of malignant transformation in palate except for reverse smokers

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60
Q

ETIOLOGY OF NICOTINE STOMATITIS

A

Chronic exposure to the heat from tobacco
caused by pipe cigar and cigarette smoking
Most severe changes seen in patients who reverse smoke
Common tobacco related form of keratosis
Opacification on the palate caused by heat and carcinogens

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61
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63
Q

CLINICAL FEATURES OF NICOTINE STOMATITIS

A

Diffuse, white thickening of the palatal mucosa with interspersed elevated white papules with a red central depression

Generalized white changes (hyperkeratosis) seen in hard palate

Red dots in the palate represent inflamed salivary duct orifices

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63
Q

PROGNOSIS OF NICOTINE STOMATITIS

A

Rarely evolves into malignancy
Except in reverse smoking

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63
Q

HISTOPATHOLOGY OF NICOTINE STOMATITIS

A

Hyperkeratosis and acanthosis of surface epithelium
Connective Tissue surrounding exhibits inflammation
Dilated salivary gland with squamous metaplasia of lining

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63
Q

TREATMENT OF NICOTINE STOMATITIS

A

Smoking cessation (ask px to stop)
Condition may regress
Re-evaluation - give them support system

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64
Q

Caused by superficial chemical reaction s/a burns, allergic reactions to a component of toothpaste or dentifrice → inclusion of detergents or flavoring compounds → may be related to essential oils

A

DENTIFRICE ASSOCIATED SLOUGH

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64
Q

Common phenomena associated with the use of a certain toothpaste brands

A

DENTIFRICE ASSOCIATED SLOUGH

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64
Q

A painless white lesion that is not known to progress or transform to any significant condition

A

DENTIFRICE ASSOCIATED SLOUGH

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64
Q

ETIOLOGY OF DENTIFRICE ASSOCIATED SLOUGH

A

Form of chemical burn or a reaction to an ingredient of a dentifrice
Possible causative component (Detergent; flavorings)
Can also be caused by mouthwash with similar causative agents

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65
Q

Overgrowth of the filiform papillae on the dorsal surface of the tongue

A

HAIRY TONGUE

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65
Q

PROGNOSIS OF DENTIFRICE ASSOCIATED SLOUGH

A

Benign white lesion
Lesion will resolve once the dentifrice/mouthwash is discontinued

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65
Q

Represents as increased keratin production of a decreased normal keratin production of a decreased normal keratin desquamation

A

HAIRY TONGUE

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65
Q

ETIOLOGY OF HAIRY TONGUE

A

Used of broad-spectrum antibiotics (like penicillin), systemic corticosteroids, hydrogen peroxide
Intense smoking
Head and neck therapeutic radiation
Not well understood, alteration in oral flora

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65
Q

CLINICAL FEATURES OF DENTIFRICE ASSOCIATED SLOUGH

A

Superficial whitish slough seen on the buccal mucosa
Commonly describe by the patient as “peeling” or “oral peeling”

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66
Q

HISTOPATHOLOGY OF HAIRY TONGUE

A

Presence of elongated filiform papillae, marked hyperkeratosis of filiform papillae with bacterial accumulation on the surface (dorsum of the tongue)
Surface contamination by clusters of microorganisms and fungi
Keratinization may extend into the mid-portions of the stratum spinosum
Mid inflammation occurring in the lamina propria

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66
Q

TREATMENT OF HAIRY TONGUE

A

Elimination of any predisposing factors
Brush, scrape tongue with baking soda

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66
Q

DIAGNOSIS OF HAIRY TONGUE

A

Biopsy is not necessary for confirmation
Clean the area
Know the cause and ask the patient

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67
Q

PROGNOSIS OF HAIRY TONGUE

A

Tongue will return to normal after physical debridement and proper oral hygiene

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67
Q

CLINICAL FEATURES OF HAIRY TONGUE

A

Represents overgrowth of filiform papillae and chromogenic microorganisms
Dense hairy like mat formed by hyperplastic papillae on the dorsal tongue surface
Asymptomatic
May be cosmetically objectionable because of color (usually black)
Extensive elongation of the papillae = gagging or a tickling sensation
Color may range from white to tan to deep brown or black
Depending on the Diet, Oral Hygiene, Oral medications, and the Composition of bacteria

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68
Q

White lesions commonly seen along the margins of the lateral borders of the tongue
First case was see in homosexual

A

HAIRY LEUKOPLAKIA

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69
Q

ETIOLOGY OF HAIRY LEUKOPLAKIA

A

Associated with local or systemic immunosuppression (esp. AIDS and organ transplantation)
Represents an opportunistic infection by Epstein-Barr Virus
Immunosuppression
Organ transplantation (medical induced immunosuppression)
Hematologic malignancy
Long Term use of systemic or topical corticosteroid
Can extend up to dorsal surface of tongue

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70
Q

CLINICAL FEATURES OF HAIRY LEUKOPLAKIA

A

Most commonly seen in lateral tongue, often bilateral
Asymptomatic
Papillary, filiform, or plaque like
May occur before or after the diagnosis of AIDS
May be secondarily infected by candida albicans

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71
Q

DIFFERENTIAL DIAGNOSIS OF HAIRY LEUKOPLAKIA

A

Idiopathic leukoplakia
Frictional hyperkeratosis
Lichen planus
Lupus Erythematosus
Hyperplastic Candidiasis

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72
Q

HISTOPATH OF HAIRY LEUKOPLAKIA

A

Acanthosis parakeratosis edema
Nuclear viral inclusions
EBV in infected nuclei

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73
Q

looks similar with fissured tongue
there’s mapping in the tongue
Distinct characteristic: red atrophic center
filiform papillae
Unknown etiolog

A

GEOGRAPHIC TONGUE

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73
Q

Erythema migrans or Benign migratory glossitis

A

Erythema migrans or Benign migratory glossitis

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73
Q

TREATMENT OF HAIRY LEUKOPLAKIA

A

None, unless cosmetically objectionable
Antiviral and antiretroviral agents likely to cause lesion to regress
Lesions usually improve and resolve with improvement in the patient’s immune system

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74
Q

WHITE LESIONS: OTHER MUCOSAL WHITE LESION

A

Geographic tongue
Lichen planus.
Lupus erythematosus

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75
Q

ETIOLOGY OF GEOGRAPHIC TONGUE

A

Numerous theories
emotional stress
fungal infections
bacterial infections

Associated with several different condition
psoriasis
seborrheic dermatitis
reiter’s syndrome
atopy

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75
Q

Geographic stomatitis - if its located at different sites

A
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76
Q

CLINICAL FEATURES OF GEOGRAPHIC TONGUE

A

Ring- shaped/ annular lesion affecting the dorsum and margin of the tongue
Atrophic patches surrounded by elevated keratotic margins
White, yellow, or slightly elevated peripheral zone
Desquamated area appears
Strong association between geographic tongue and fissured tongue
Symptoms may be more common when fissured tongue is present
affecting women slightly more often than men
children may occasionally affected
presence of small, round to irregular areas of dekaratinization and desquamation of filiform papillae
asymptomatic

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77
Q

HISTOPATHOLOGY OF GEOGRAPHIC TONGUE

A

Filiform papillae are reduced in number & prominence
Margins of the lesions demonstrate hyperkeratosis & acanthosis
Presence of neutrophils & lymphocytes
Histologic picture: psoriasiform type of intraoral eruption

77
Q

TREATMENT OF GEOGRAPHIC TONGUE

A

Not required
Self-limiting & asymptomatic
When symptoms occur, palliative treatment:
Topical steroids, esp. containing antifungal agent

78
Q

DIFFERENTIAL DIAGNOSIS OF GEOGRAPHIC TONGUE

A

Quite characteristic
Histopathology is rarely needed

79
Q

pre-malignant tendency OF WHITE LESIONS: OTHER MUCOSAL WHITE LESION

A

LICHEN PLANUS

80
Q

PROGNOSIS OF GEOGRAPHIC TONGUE

A

Lesion is totally benign
Reassure the patient that this does not represent any serious illness will relieve anxiety

81
Q

TYPES OF LICHEN PLANUS

A

Reticular form
Plaque type
Erythematous (Atrophic) form
Ulcerative Lesion
Bullous form
Papular type

82
Q

Immune system

A

Primary role in disease development
Subepithelial band formed infiltrate dominated by T- Lymphocytes and macrophages
Expression of the cell mediated arm of the immune system being involved in the pathogenesis through T- Lymphocyte cytotoxicity directed against antigens expressed by the basal cell layer
multifactorial- many factors that contribute to the condition

83
Q

stress

A

May establish the inflammatory process

84
Q

Cannot discriminate between inherent molecules of the body and foreign antigens. Activation of these cells may arise in other parts of the body

A

Autoreactive T lymphocytes

85
Q

CLINICAL FEATURES OF LICEHN PLANUS

A

Disease of middle age
Affects men & women in equal numbers
The severity of the disease parallels the patient’s level of stress
Prevalence of secondary oral candidiasis in patients with oral lichen planus (50%)
Altered status of cellular immunity may be responsible
most common
Presence of numerous interlacing keratotic lines or striae (Wickham’s striae) that produce an annular or lacy pattern
buccal mucosa

86
Q

most common LICHEN PLANUS

A

RETICULAR FORM

87
Q

Presence of numerous interlacing keratotic lines or striae (Wickham’s striae) that produce an annular or lacy pattern

A

RETICULAR FORM

88
Q

Striae may form a network but also show annular (circular) patterns

A

RETICULAR FORM

89
Q

Primary sites: OF PLAQUE TYPE

A

dorsum of the tongue & buccal mucosa

89
Q

Can be seen in all regions of the oral mucosa
Fine white lines or striae

A

RETICULAR FORM

89
Q

Resembles leukoplakia clinically

A

PLAQUE TYPE

90
Q

Striae display a peripheral erythematous zone which reflects subepithelial inflammation

A

RETICULAR FORM

90
Q

Most frequently in the buccal mucosa bilaterally
Vermillion border

A

RETICULAR FORM

90
Q

If in attached gingiva, without papules or striae and presents as

A

DESQUAMATIVE GINGIVITIS

90
Q

Small white dots, intermingle with the reticular from

A

PAPULAR TYPE

90
Q

May clinically be very similar to homogeneous oral leukoplakias
Difference is the simultaneous presence of reticular or papular structures in the case of plaque like Oral lichen planus
Smoker
film like material at buccal mucosa

A

PLAQUE TYPE

90
Q

Initial phase of lichen planus

A

PAPULAR TYPE

90
Q

Most disabling form
Fibrin coated ulcers are surrounded by erythematous zone displaying radiating white striae
Sharp sensation in conjunction with food intake

A

ULCERATIVE LESION

90
Q

ERYTHEMATOUS (ATROPHIC) FORM

A

attached/marginal gingiva
Symptomatic: burning or pain in the area of involvement
Homogenous red area
Buccal mucosa or palate
Striae in the periphery
If in attached gingiva, without papules or striae and presents as DESQUAMATIVE GINGIVITIS

90
Q

HAVE PREMALIGNANT TENDENCIES LICHEN PLANUS?

A

YES

90
Q

HISTOPATHOLOGY of LICHEN PLANUS

A

hyperorthokeratosis or hyperparakeratosis
ariable degrees of acanthosis
Within the epithelium, increase in numbers of langerhans cells
lymphocytes, immunoglobulin and fibrinogen
Liquefaction degeneration
Eosinophilic band
Dense subepithelial band shaped infiltrate of lymphocytes and macrophages

90
Q

unusual form
Bullae range from a few mm to cm in diameter
Bullae generally short - lived and or rupturing, leave a painful ulcer
Buccal mucosa: posterior and inferior regions adjacent to the 2nd and 3rd molars

A

BULLOUS FORM

90
Q

TREATMENT of LICHEN PLANUS

A

No specific tx
Palliative treatment
Corticosteroids- the single most useful group of drugs
Ability to modulate inflammation & immune response
topical application / local injection of steroids
Vitamin A ( retinoids)- systemic or topical
Cyclosporine –topical

90
Q

release inflammatory or chemotactic factors from mast cells or neutrophils

A

Dapsone(diaminoiphenylsulfone)

90
Q

the single most useful group of drugs
Ability to modulate inflammation & immune response

A

Corticosteroids

90
Q

Sub and supragingival plaque and calculus- oral prophylaxis
Optimal oral hygiene prior to steroid treatment

A

Erythematous OLP

90
Q

PROGNOSIS

A

Slightly higher rate of oral squamous cell carcinoma
Erosive / atrophic form are more common to develop into malignancy 0.4-2.5 %

90
Q

ETIOLOGY AND PATHOGENESIS
(LUPUS ERYTHEMATOSUS)

A

Classic prototype of autoimmune disease involving immune complex
Autoimmune disease involving both the humoral and cell-mediated arms of the immune system
Autoantibodies directed against various cellular antigens in both the nucleus and the cytoplasm

90
Q

FORMS OF LUPUS ERYTHEMATOSUS

A

Systemic (acute) lupus erythematosus (SLE)
Discoid (chronic) lupus erythematosus (DLE)
Subacute lupus (subacute cutaneous LE)

90
Q

Disorders that entail an increased risk of malignant transformation at some site of the oral mucosa, not necessarily associated with a pre existing lesion

A

Premalignant conditions

90
Q

A lesion that has an inherent increased risk to develop carcinomas compared with the surrounding tissues

A

Premalignant lesion

90
Q

Less aggressive form OF LUPUS ERYTHEMATOSUS

A

DISCOID (CHRONIC) LUPUS ERYTHEMATOSUS (SLE)

90
Q

LOCATION OF LUPUSERYTHEMATOUS

A

Buccal mucosa, gingiva and vermilion
Erythematosus or ulcerative lesions with delicate white, Keratotic striae radiating from the periphery

90
Q

Multisystem autoimmune inflammatory disorder of unknown etiology

A

SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)

90
Q

Main feature: SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)

A

formation of antibodies to DNA, which may initiate immune complex reactions in particular vasculitis

90
Q

Mild skin and mucosal lesions
Numerous autoantibodies directed against
nuclear and cytoplasmic antigens
Antibodies can cause lesions in nearly any tissue, resulting in a wide variety of clinical signs and symptoms
Affects several organs

A

SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)

90
Q

Most aggressive form OF LUPUS ERYTHEMATOSUS

A

SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)

90
Q

SYMPTOMS OF SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)

A

Fever, weight loss & malaise
With disease progression, many organs systems become involved

90
Q

Common Areas: SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)

A

vermillion buccal mucosa,
gingiva, and
palate

90
Q

Involvement of the skin results in an erythematous rash, seen over the malar process and bridge of the nose

A

Butterfly rash

90
Q

Skin lesions of mild to moderate severity
Mild systemic involvement and the appearance of some abnormal autoantibodies

A

SUBACUTE LUPUS (SUBACUTE CUTANEOUS LE)

90
Q

Expands peripherally, the center heals, with the formation of scar and loss of pigment
Involvement of hair follicles in permanent hair loss (ALOPECIA)

A

DISCOID (CHRONIC) LUPUS ERYTHEMATOSUS (SLE)

90
Q

Affecting predominantly the skin rarely progressing to the systemic form
Cosmetic significance because of its predilection for the face
Middle age, especially women
Skin, most commonly on the face and scalp
Oral and vermillion lesions are also commonly seen, but usually in the company of cutaneous lesions
Skin lesions appear as disk shaped erythematous plaques with hyperpigmented margins

A

DISCOID (CHRONIC) LUPUS ERYTHEMATOSUS (SLE)

91
Q

Intermediate between SLE and DLE

A

SUBACUTE LUPUS (SUBACUTE CUTANEOUS LE)

91
Q

DIFFERENCE OF DLE FROM SLE IN TERMS OF ORGAN

A

DLE
Skin and oral only

SLE
Skin, oral, heart, kidneys, joints

91
Q

DIFFERENCE OF DLE FROM SLE IN TERMS OF SYMPTOM

A

DLE
none

SLE
Fever, malaise, weight loss

91
Q

DIFFERENCE OF DLE FROM SLE IN TERMS OF HISTOPATOLOGY

A

DLE
Basal cell loss, lymphocytes at interface and prevascular keratosis

SLE
Similar to discoid

91
Q

DIFFERENCE OF DLE FROM SLE IN TERMS OF SEROLOGY

A

DLE
No detachable antibodies

SLE
Positive ANA, Anti- DNA antibodies

92
Q

SLE diagnosis with 4 of more of 11 criteria present at anytime T/F

A

TRU

93
Q

Criteria for SLE

A

Malar rash
Discoid lesions
Photosensitivity
Presence of oral ulcers
Nonerosive arthritis of two joints or more
Serositis
Renal disorder
Neurologic disorder (seizures or psychosis)
Hematologic disorder (hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia)
Immunologic disorder (anti-DNA, anti-SM, or antiphospholipid antibodies)

93
Q

DIFFERENCE OF DLE FROM SLE IN TERMS OF DIFFERENTIATION

A

DLE
Granular /linear basement
membrane deposits of IgG and C3

SLE
Similar to discoid

94
Q

DIAGNOSIS OF LUPUS ERYTHEMATOUS

A

Serologic test- for autoantibodies (+results)
The ANA (antinuclear antibody) test- matic suspecting SLE

94
Q

DLE DIAGNOSIS

A

Well-demarcated cutaneous lesions with round or oval erythematous plaques with scales and follicular plugging
These lesions may form butterfly-like rashes over the cheeks and nose known as Malar rash

95
Q

HISTOPATHOLOGIC CHARACTERISTICS OF LUPUS ERYTHEMATOUS

A

Hyperkeratosis with keratotic plugs
Atrophy of the rete pegs/ processes
Deep inflammatory infiltrate
Edema in the lamina propria
Thick patchy or continuous PAS- positive juxta epithelial deposits

96
Q

TREATMENT OF LUPUS ERYTHEMATOUS FOR DLE

A

topical corticosteroids

96
Q

DIFFERENTIAL DIAGNOSIS OF LUPUS ERYTHEMATOUS

A

Erosive lichen planus

Erythematous gingival Lupus

97
Q

TREATMENT OF LUPUS ERYTHEMATOUS FOR SLE

A

systemic steroids

98
Q

TREATMENT OF LUPUS ERYTHEMATOUS FOR Symptomatic intraoral lesions

A

topical steroids

99
Q

LE tend to be less symmetrically distributed

Keratotic striae of LE show characteristic radiation from a central focus are more delicate and subtle than Wickham’s striae of lichen planus

A

Erosive lichen planus

99
Q

SIDE EFFECTS OF TREATMENT OF LE

A

Fungal and viral infections
Immunologic defects
Mucosal ulceration caused by frequent exploitation of NSAIDS
Immunosuppressive drugs used to treat SLE

100
Q

Erythematous gingival Lupus

A

Mucous membrane pemphigoid
Erythematous lichen planus
Erythematous candidiasis
Contact hypersensitivity

101
Q

OTHER NON-EPITHELIAL WHITE LESIONS

A

Candidiasis
Mucosal burns
Submucosa fibrosis
Fordyce granules
Ectopic lymphoid tissue
Gingival cysts
Parulis
Lipoma

102
Q

causative agent: ORAL CANDIDIASIS

A

Candida albicans

102
Q

Most prevalent opportunistic infection affecting the oral mucos

A

ORAL CANDIDIASIS

103
Q

Common sites ORAL CANDIDIASIS

A

Mucosal linings
Rare systemic manifestations may have a fatal course

103
Q

accompanied by systemic mucocutaneous manifestations- other areas too & not just in oral region

A

Secondary infections

103
Q

Restricted to the oral and perioral sites

A

primary infections

103
Q

Oral candidiasis is divided into

A

Primary and secondary infections

104
Q

Human immunodeficiency virus (HIV) infections
Steroid inhalers

A

CHRONIC PSEUDOMEMBRANOUS

104
Q

PSEUDOMEMBRANOUS (CLINICAL FINDINGS)

A

Loosely attached membranes comprising fungal organisms and cellular debris
Leaves an inflamed, sometimes bleeding area if the pseudomembrane is removed

104
Q

PSEUDOMEMBRANOUS (SYMPTOMS)

A

Usually asymptomatic
Some discomfort
Brush biopsy

104
Q

TYPES OF ORAL CANDIDIASIS

A

DENTURE STOMATITIS
CHRONIC PLAQUE
ANGULAR CHEILITIS
CHRONIC PLAQUE
ORAL CANDIDIASIS ASSOCIATED WITH HIV
ERYTHEMATOUS CANDIDIASIS
PSEUDOMEMBRANOUS

104
Q

PSEUDOMEMBRANOUS

ACUTE FORM

A

Thrush/ Oral thrush
Grouped with the primary oral candidiasis
Classic candida infection

104
Q

Grouped with the primary oral candidiasis
Classic candida infection
whitish
Acute Form

A

PSEUDOMEMBRANOUS

104
Q

PSEUDOMEMBRANOUS
(PATIENTS)

A

Medicated with antibiotics or immunosuppressant drugs
Disease that suppresses the immune system

105
Q

reddish
Atrophic oral candidiasis
Erythematous surfac

A

ERYTHEMATOUS CANDIDIASIS

106
Q

A successor to PC but may also emerge de novo

A

ERYTHEMATOUS CANDIDIASIS

106
Q

Diffused border- medjo makalat you don’t know where specifically it starts & ends

A

ERYTHEMATOUS CANDIDIASIS

107
Q

type and Nodular Candidiasis

A

CHRONIC PLAQUE

108
Q

Inhalation steroids

A

Palate and dorsum of the tongue
Smoking
Treatment with broad spectrum antibiotics

108
Q

Site DENTURE STOMATITIS

A

Denture - bearing palatal mucosa

109
Q

White plaque- film like appearance
May be indistinguishable from an oral leukoplakia
Correlation with moderate to severe epithelial
dysplasia
Associated with malignant transformation
Nodular
Can be distinguished through inspection

A

CHRONIC PLAQUE

109
Q

CAUSE OF DENTURE STOMATITIS

A

DENTURE

109
Q

Localized to major part erythematous sites caused by trauma from the denture

A

Type I DENTURE STOMATITIS

110
Q

Protects microorganisms from physical influences such as salivary flow
- not included in the cleansing effect of the saliva
- If the patient doesn’t have good oral hygiene

A

DENTURE

111
Q

Affects a major part of the denture covered mucosa

Moderate

A

Type II DENTURE STOMATITIS

111
Q

Microorganisms DENTURE STOMATITIS

A

Candida

Bacteria from several genera, such as
Streptococcus,
Veillanella,
Lactobacillus,
Prevatella, and
Actinomyces

112
Q

Type II features

Granular mucosa in the central part of the palate

Affecting the granular mucosa and the central part of the palate

A

Type III DENTURE STOMATITIS

112
Q

mouth area

A

CHELITIS

112
Q

DIAGNOSIS AND PATHOLOGIC FINDINGS: ORAL CANDIDIASIS

A

Smear
From the infected area, which compromises
epithelial cells, creates opportunities for detection
of the yeast

Pseudomembranous oral candidiasis and angular cheilitis are suspected

Second scrape
Method is a valuable adjunct in the diagnostic
process of erythematous candidiasis and denture
stomatitis as these infections consist of fairly
homogenous erythematous lesions

Salivary culture techniques
Culture sensitivity testing

Histopathologic exam
Chronic plaque- type and nodular candidiasis,
cultivation techniques

Identify the possible presence of epithelial
dysplasia

112
Q

Causative agents: ANGULAR CHEILITIS

A

candida and staphylococcus aureus

112
Q

Infected fissures of the commissures of the mouth often surrounded by erythema

A

ANGULAR CHEILITIS

112
Q

Infection is considered a portent of Aids development

Advice the patient to do a work up

Pseudomembranous candidiasis, erythematous candidiasis, angular cheilitis, and chronic hyperplastic Candidiasis

A

ORAL CANDIDIASIS ASSOCIATED WITH HIV

112
Q

More than 90% of patients present with AIDS present oral candidiasis during course of HIV infections

A

ORAL CANDIDIASIS ASSOCIATED WITH HIV

112
Q

MANAGEMENT: ORAL CANDIDIASIS

A

Antifungal drug
Polyenes or azoles

Azoles
Miconazole for angular cheilitis
Topical treatment biostatic effect on S. Aureus and
fungistatic effect to candida
Systemic azoles for deeply seated primary
candidiasis, such as chronic hyperplastic
candidiasis, denture stomatitis, and median
rhomboid glossitis with a granular appearance
and for therapy- resistant infections, mostly
related to compliance failure
Known to interact with warfarin
Development of resistance is particularly
Compelling for fluconazole in HIV patients

Polyenes
Nystatin and amphotericin B
Negative effect on the production of ergosterol,
which is critical for the candida cell membrane
integrity. Polyenes can also affect the adherence
of the fungi

112
Q

SYMPTOMS: ANGULAR CHELITIS

A

Dry skin, red areas at the corner of the lips

112
Q

Predilection: CHRONIC PLAQUE

A

Denture wearers
Inhalation steroids

112
Q

Smokers and denture wearers = increased risk
dorsum of the tongue
Erythematous lesion in the center of the posterior part of the dorsum oval configuration
Atrophy of the filiform papillae

A

CHRONIC PLAQUE

112
Q

FOUND IN:CHRONIC PLAQUE

A

dorsum of the tongue w/ MRG

112
Q

Causative agents: CHRONIC PLAQUE

A

Mixed bacterial/fungal microflora

112
Q

SYMPTOMS: CHRONIC PLAQUE

A

Concurrent erythematous lesion may be observed in the palatal mucosa ( kissing lesions)
Asymptomatic and management is restricted to a reduction in predisposing factors

112
Q

ETIOLOGY: ANGULAR CHELITIS

A

Vitamin B12 iron deficiencies and loss of vertical dimension

112
Q

First sign OF SUBMUCOUS FIBROSIS

A

erythematous lesions

112
Q

Children who chew through electrical cords receive rather characteristic initial burn that are symmetric
Resulting to tissue damage, followed by scarring & reduction in the size of the oral opening

A

MUCOSAL BURN

112
Q

MANAGEMENT AND PROGNOSIS: Denture Stomatitis

A

Permanent removal of the denture

Improved denture hygiene and a recommendation not to use the denture while sleeping

If asymptomatic, pt may opt for no treatment

Type III denture stomatitis

112
Q

Surface of these lesions tends to be: thickened slough that extends deep into the surrounding tissue

A

MUCOSAL BURN

112
Q

MANAGEMENT AND PROGNOSIS: Type III denture stomatitis

A

Surgical excision if necessary to eradicate microorganisms present in the deeper fissures of the granular tissue

Continuous treatment with topical antifungal drugs
Need to remove because they have deeper
fissures

112
Q

MANAGEMENT AND PROGNOSIS: ANGULAR CHEILITIS

A

Mild steroid ointment for cases of inflammation

Prognosis is good if predisposing factors associated with the infection are reduced or eliminated

112
Q

MANAGEMENT AND PROGNOSIS: Persistent chronic plaque- type and nodular candidiasis

A

Increased risk for malignant transformation compared with leukoplakias not allied with candida Infection

Patients with primary candidiasis are also at risk if systemic predisposing factors arise

112
Q

THERMAL BURNS

A

Hard palatal mucosa
Hot sticky foods
Hot liquids

112
Q

Locations: SUBMUCOUS FIBROSIS

A

Lips
Buccal mucosa
Retromolar area
Soft palatal mucosa
May extend into pharyngeal region, pharynx and upper ⅔ of esophagus

112
Q

CLINICAL FEATURES: MUCOSAL BURN

A

Localized erythema
Short- term exposure

White slough or membrane
Long term chemical exposure/ increased concentration of offending agent

Friable and bleeds upon manipulation

With gentle traction, the surface slough will peel from the denuded connective tissue, producing tenderness and pain

112
Q

HAS PREMALIGNANT TENDENCY SUBMUCOUS FIBROSIS?

A

YES
The development of squamous cell carcinoma

112
Q

ETIOLOGY: MUCOSAL BURN

A

Topical applications of chemicals:
Aspirin or caustic agents (most common cause)

Chronic abuse of alcohol containing mouth washes

Topical abuse of drugs/medication

Accidental placement of phosphoric acid-etch solutions or gel by dentist

THERMAL BURNS

ELECTRICAL BURNS

112
Q

Electrical burn

A

MUCOSAL BURN

112
Q

INITIA CHANGE: SUBMUCOUS FIBROSIS

A

Whitish yellow change

112
Q

HISTOPATHOLOGY: MUCOSAL BURN FOR CHEMICAL BURN

A

Epithelial component show coagulative necrosis through its entire thickness

Fibrinous exudate is evident

Intensely inflamed underlying connective tissue

112
Q

HISTOPATHOLOGY: MUCOSAL BURN FOR ELECTRICAL BURN

A

Deep extension of necrosis, often into muscle

112
Q

Chronic, progressive, scarring, high-risk precancerous condition of the oral mucosa seen primarily on the Indian Subcontinent and in Southeast Asia

Areca quid chewing habit

Impaired degradation of normal collagen by fibroblast rather than excess production

Some people have a genetic predisposition for it

A

SUBMUCOUS FIBROSIS

112
Q

TREATMENT: MUCOSAL BURN FOR ELECTRICAL BURN

A

Co management

May need the services of pediatric dentist, OMS, and plastic surgeon

112
Q

LATER CHANGE: SUBMUCOUS FIBROSIS

A

the affected mucosa, especially the soft palate and

the buccal mucosa, loses its resilience and elasticity

fibrous bands are readily palpable in the soft palate and buccal mucosa

the clinical result is significant trismus and considerable difficulty in eating

112
Q

CLINICAL FINDINGS: FORDYCE SPOTS

A

Multiple areas, often seen in aggregates or in confluent arrangements

Often seen in Buccal mucosa & Vermillion border of the upper lip

Symmetrically distributed

112
Q

TREATMENT: MUCOSAL BURN FOR CHEMICAL BURN

A

Local symptomatic therapy with or without the use of systemic analgesics

Topical therapy: hydrocortisone acetate with or without benzocaine

Application of dilute solutions of topical anesthetics

112
Q

ETIOLOGY: FORDYCE’S GRANULES

A

Ectopic sebaceous glands- Normal tissues in an abnormal location; variation of the normal

A.k.a Sebaceous choristomas

Developmental in nature

112
Q

CLINICAL FEATURES: SUBMUCOUS FIROSIS

A

Fibrotic bands located beneath an atrophic epithelium

Increased fibrosis

112
Q

TREATMENT: SUBMUCOUS FIBROSIS

A

Cessation of the chewing habits

Eliminate causative agents

Stretching exercise

Intralesional injections of corticosteroids

Local injection of chymotrypsin, hyaluronidase and dexamethasone with placement of placental grafts

Topical and systemic steroids, supplement of vitamins and nutrients, repeated dilatation with physical devices and surgery

112
Q

HISTOPATHOLOGY: SUBMUCOUS FIBROSIS

A

Principal feature is atrophy of the epithelium and subjacent fibrosis

Epithelial dysplasia may occasionally be evident

Type I collagen predominates in submucosa whereas type III collagen tends to localize at the epithelium- connective tissue interface , and around blood vessels, salivary glands, and muscle

112
Q

DIAGNOSIS: SUBMUCOUS FIBROSIS

A

Needs to be palpated if its not stretchy as normal mucosa expect that it changed already

Palpable fibrous bands

Mucosal texture feels tough and leathery

Blanching of mucosa together with other histopathologic features

Features consistent with oral submucous fibrosis (atrophic epithelium with loss of rete ridges and juxta epithelial hyalinization of lamina propria)

112
Q

OTHER NAME FOR FORDYCE SPOT

A

FORDYCE’S GRANULES

112
Q

HISTOPATHOLOGY: FORDYCE SPOTS

A

Lobules of sebaceous glands aggregated around or adjacent to excretory ducts

Well formed heterotrophic glands and appear functional

112
Q

TREATMENT: FORDYCE SPOTS

A

Asymptomatic- leave it wag na galawin (not an emergency)

No treatment- removal if the glands would post or show abnormal qualities

112
Q

LOCATION: ECTOPIC LYMPHOID TISSUE

A

Anywhere in the oral cavity

112
Q

Aggregate of lymphoid tissue commonly seen in the soft palate, floor of the mouth, and tonsillar pillars.

A

ECTOPIC LYMPHOID TISSUE

112
Q

DIAGNOSIS: ECTOPIC LYMPHOID TISSUE

A

Entrapped epithelium within lymphoid tissue

Diagnosed on the basis of clinical features alone

112
Q

TREATMENT: GINGIVAL CYSTS

A

No treatment indicated for infants since it rupture spontaneously early in life

For adults, surgical excision with inclusion of the overlying epithelium is recommended

112
Q

TREATMENT: ECTOPIC LYMPHOID TISSUE

A

Normal tissue, no biopsy is necessary

112
Q

CLINICAL FEATURES: ECTOPIC LYMPHOID TISSUE

A

Yellow/yellow-white small dome shape elevations
Posterolateral aspect of tongue

112
Q

Occur in adults as well as infants

Odontogenic origin in adults

Frequency is highest in the neonatal phase- then disappear within 3 months due to rupture or exfoliate

A

GINGIVAL CYSTS

112
Q

Focus of or accumulation of pus in the gingiva

A

PARULIS

112
Q

COMMON TERM OF PARULIS

A

“Gum boil”

112
Q

Cysts noted along the palatal midline that had no relationship to the tooth-forming apparatus

A

Epstein pearls

112
Q

In neonatal: GINGIVAL CYSTS

A

Epstein pearls

Bohn’s nodules

112
Q

Cysts noted along the alveolar ridges that were believed to be related to salivary gland remnants

A

Bohn’s nodules

112
Q

TREATMENT: PARULIS

A

Treatment of the underlying condition
Know the cause of accumulation of pus

112
Q

CLINICAL APPEARANCE: PARULIS

A

Yellow-white gingival tumescence with an associated erythema

112
Q

ETIOLOGY: PARULIS

A

Derived from an acute infection either at the base of the occluded periodontal pocket or at the apex of a nonvital tooth

The path is of the least resistance

Pain is typical until the pus escapes to the surface

112
Q

CLINICAL APPEARANCE: LIPOMA

A

Asymptomatic

Yellowish submucosal mass

Intact overlying epithelium

Superficial blood vessels evident over the tumor

112
Q

LOCATION: PARULIS

A

Anywhere in the oral cavity soft tissues
Not expected to recur
Buccal mucosa, tongue, and floor of the mouth

112
Q

LOCATION: LIPOMA

A

Anywhere in the oral cavity soft tissues
Not expected to recur
Buccal mucosa, tongue, and floor of the mouth

112
Q

A well circumcised, lobulated mass of mature fat cells

A

LIPOMA

112
Q

DIFFERENTIAL DIAGNOSIS: LIPOMA

A

Granular cell tumor, neurofibroma

Traumatic Fibroma

Salivary gland lesions (mucocele, and mixed tumor)

112
Q

HAS NO PRE-MALIGNANCY TENDENCIES

A

Leukoedema
White Sponge Nevus
Hereditary Benign Intraepithelial Dyskeratosis
Follicular Keratosis
Focal Hyperkeratosis
Hairy Leukoplakia
Hairy Tongue
Dentifrice-associated slough
Candidiasis
Mucosal Burns
Gingival cysts
Parulis
Lipoma
Geographic tongue
Lupus Erythematosus

112
Q

TREATMENT: LIPOMA

A

Excision

112
Q

CLINICAL APPEARANCE: LIPOMA

A

Asymptomatic
Yellowish submucosal mass
Intact overlying epithelium
Superficial blood vessels evident over the tumor

112
Q

LOCATION: LIPOMA

A

Anywhere in the oral cavity soft tissues
Not expected to recur
Buccal mucosa, tongue, and floor of the mouth

112
Q

HAS PRE-MALIGNANCY TENDENCIES

A

Smokeless Tobacco Keratosis
Nicotine Stomatitis
Submucosal Fibrosis
Lichen Planus

OPATH (1 decks)

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