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22 Cards in this Set

  • Front
  • Back

White Lesions: What Causes Them?

* Hyperkeratosis


- Thickening of the horny layer of the epidermis or mucosa by increased keratin production which turns white when hydrated by saliva.




* Necrosis of epithelial cells


- Usually caused by an injury




* Ischemia


- Defective blood supply to the tissue

Variations of Normal:
Fordyce Granules

Variations of Normal:


Fordyce Granules

* Normal Sebaceous glands found in the oral mucosa


* Found in 80% of the population


* Not found in children - sebaceous glands form at puberty.

Variations of Normal:

Leukoedema

Variations of Normal:


Leukoedema

* Intracellular edema and tissue whiteness.


* More common in African Americans.


* Buccal Mucosa appears wrinkled


* Does not rub off - disappears when stretched.

Traumatic and Inflammatory:
Geographic Tongue

Traumatic and Inflammatory:


Geographic Tongue

* aka Benign Migratory Glossitis


* Rarely seen i nchildren.


* More common in females in early to mid-adulthood


* Cause of inflammation unknown


* Appears as de-papillated area


* Treated w/ corticosteroids

Traumatic and Inflammatory: 

Frictional Keratosis

Traumatic and Inflammatory:


Frictional Keratosis

* Physical irritation of oral mucosa produces keratin as protection against injury.


* White plaque that does NOT rub off.


* Not considered Leukoplakia because cause is known and does not become malignant lesion

Traumatic and Inflammatory:
Check Chewing

Traumatic and Inflammatory:


Check Chewing

* aka morsicatio buccarum and morsicatio labiorum


* Location on lip or at the occlusal plane helps w/ diagnosis


* Can be found on the tongue


* Pt should be discouraged from habit

Traumatic and Inflammatory:
Nicotine Stomatitis

Traumatic and Inflammatory:


Nicotine Stomatitis

* Keratotic change of palate mucosa by heat from smoking or chronically drinking hot fluids


* Heat and irritation produce keratosis and irritation of minor salivary gland ducts on palate (red ducts) and edema (white/raised rings)


* May lead to carcinoma

Traumatic and Inflammatory:
Hairy tongue

Traumatic and Inflammatory:


Hairy tongue

* Etiology Unknown


* Can be white, black or brown


* Elongation of filiform papillae w/ hair-like appearance


* Brush tongue or use rinse (i.e. chlorhexidine)


* Risk Factors: Antibiotics, Therapeutic radiation, Smoking, Oxygenated Mouthrinse, Overgrowth of oral flora

Infections:
Candidiasis.

Infections:


Candidiasis.

* Not in healthy people


* Predisposing Factors: Systemic broad-spectrum antibiotic therapy, Corticosteroids, Smoking, Xerostomia, Systemic Disorders, Diabetes, Immune Function Disorders.

Infections: 

Acute Pseudomembranous Candidiasis

Infections:


Acute Pseudomembranous Candidiasis



Candidiasis, Thrush


* White plaque that CAN BE RUBBED OFF


* Treatment: Nystatin oral suspension or glotrimazole croches or systemic fluconazole




* Organisms grow on mucosa and produce necrosis of superficial keratinocytes - dead cells lie on surface as white plaque due to hyphae (elongated form) of organism*

Infections: 

Chronic Hyperplastic Candidiasis

Infections:


Chronic Hyperplastic Candidiasis

* Rarest form


* very low risk of malignant transformation


* Thickened, raised, Whitish plaque that does NOT rub off


* Affects tongue, commissures, mucosa


* INDISTINGUISHABLE FROM LEUKOPLAKIA


* Systemic anti-fungals to treat


* Only candidiasis that shows malignant potential.

Infections:
Hairy Leukoplakia

Infections:


Hairy Leukoplakia

* Infection of Ebstein Barr virus secondary to immunosuppression


* Predictor of rapid progression - Latent HIV to AIDS


* Whitish plaques of raised vertical ridges that do NOT rub off, usually on lateral borders of tongue.


* Biopsy to diagnose


* Antifungal to treat

Infections:
Parulis

Infections:


Parulis

* Swelling of the gingiva


* Caused by draining of sinus tract from an odontogenic infection of periodontal or pulpal origin.


Listed as white because purulent exudate is seen clinically as yellow or white.

Immune System Disorders:
Lichen Planus

Immune System Disorders:


Lichen Planus

* Immune-mediated mucocutaneous disorder


* T-lymphocytes recruited to skin damage epithelium


* Wickham striae (lacy pattern) on buccal mucosa, usually bilaterally; gingiva (Koebner phenomenon), or tongue


* No treatment needed unless change/growth


* Suspicious for malignancy if erosive

Koebner Phenomenon

* aka isomorphic reaction (in same form)


* Most widely known phenomena in dermatology


* First described by Heinrich Koebner (1872)


* Some patients had developed psoriasis at site of excoriation (abrasion from scratching), a horse bite, or a tattoo.




* usually describes response where new lesions develop on healthy skin that has suffered trauma in patients with skin conditions


* Pt w/ psoriasis + trauma to healthy skin = new lesion resembling psoriasis lesions

Immune System Disorders:
White Sponge Nervus (WSN)

Immune System Disorders:


White Sponge Nervus (WSN)

* RARE - inherited mutation of certain keratin genes


* usually apparent in childhood


* widespread keratinization of buccal and labial mucosa


* Lesions do NOT rub off


* affect buccal mucosa folds - help in diagnosis since you can not bite buccal folds


* no treatment needed

Immune System Disorders:
Leukoplakia

Immune System Disorders:


Leukoplakia

* Most common form of premalignant lesion


* " White patch or plaque... does NOT rub off... can not be diagnosed clinically or pathologically as any specific disease"


* Diagnosis by exlusion of other conditions


* Frictional keratosis should not be mistaken for leukoplakia because leukoplakia is premalignant and frictional keratosis is not.


* Highly variable in size, shape, and location (any mucosal surface)


* Usually single and soft when palpated, some may feel leathery (degree of keratinization)


* Firm indurated mass indicates malignancy


* ventral tongue and floor of mouth (HIGHEST RISK AREAS) show more microscopic evidence of premalignancy or malignancy


* arises from microscopic mutations of epithelial cells following exposure to carcinogens


* 20% likely to become invasive


* Treatment includes eliminating risk factors (smoke/smokeless tobacco cessation), or surgical/laser removal w/ follow up observations


*other risk areas influde: lateral tongue, retromolar trigone, lateral soft palate, and lower lip from sun exposure (actinic cheilitis)

Immune System Disorders:
Speckled Leukoplakia

Immune System Disorders:


Speckled Leukoplakia

* Exhibits both red and white components


* May have redness, ulceration or pebbly appearance


* appears on lateral borders of tongue

Immune System Disorders:
Proliverative Verrucous Leukoplakia

Immune System Disorders:


Proliverative Verrucous Leukoplakia

* Aggressive


* High incidence of oral canver


* progressive


* Tendency to form on gingiva where associated w/ greatest potential for malignant transformation.


* biopsy should be performed to look for epithelial dysplasia, representing malignant change

Immune System Disorders:
Smoking-Related Leukoplakia

Immune System Disorders:


Smoking-Related Leukoplakia

* Most important etiologic factor is tabacco (smoked and smokeless)


* 50% of leukoplakias in smokers will resolve with smoking cessation and over 95% of smokeless tobacco will will resolve


* Lesions are painless and persistant

Immune System Disorders:
Leukoplakia of the Lower Lip

Immune System Disorders:


Leukoplakia of the Lower Lip

* aka actinic chelitis


* Related to chronic sun damage


* Atrophy of vermillion border


* erosion and crusted appearance

Immune System Disorders:
Oral Submucosal Fibrosis

Immune System Disorders:


Oral Submucosal Fibrosis

* Areca nut or betel nut chewing


* Genetic predisposition and genetic mutation


* Generalized stomatitis that develops numerous vesicles and ulcers


* Second tissue develops white thickening of tissue


* Third stage is formation of premalignant leukoplakia lesions in about 25% of cases


* NO treatment. Pt should stop chewing betel nut.