5. EPITHELIAL PATHOLOGY pt 1 ✅

ORAL SQUAMOUS PAPILLOMA

Benign proliferation of squamous epithelium, HPV- 6, 11

Common between 30 - 50 years, Equal frequency among sexes

Soft, painless, pedunculated

Exophytic, finger-like projections, "cauliflower“ appearance

White, slightly red, or normal color

Tongue and soft palate most common

Solitary, enlarge rapidly to 0.5 cm

no malignant potential

ORAL SQUAMOUS PAPILLOMA: Histopathology

Keratinized stratified squamous epithelium with finger-like projections

ORAL SQUAMOUS PAPILLOMA: Treatment

Conservative surgical excision

CONDYLOMA ACUMINATUM (Venereal Wart)

Papillary proliferation of genitalia, anus, larynx, mouth

• STD

HPV- 6, 11,16, 18

Develop at site of sexual contact, 20% of all STDs

Teenagers / young adults

Labial mucosa, soft palate, lingual frenum– Common sites

CONDYLOMA ACUMINATUM: appearance

Sessile, pink, well-demarcated, non tender, exophytic

Larger than papillomas

Multiple and clustered

Average size 1.0 to 1.5 cm

CONDYLOMA ACUMINATUM: Treatment and Prognosis

Conservative surgical excision

Should be removed - Contagious

VERRUCA VULGARIS

Benign, focal hyperplasia of squamous epithelium

HPV-2, 4, 40

Can spread by autoinoculation

Uncommon on oral mucosa

Extremely common on skin

Frequent in children, skin of hands usual site

Vermillion, labial mucosa, or anterior tongue

VERRUCA VULGARIS (Wart): appearance

Painless papules or nodules with papillary projections; occur in clusters

Usually surgically excised

2/3 disappear within 2 years, especially in children

in oral cavity this looks like papilloma

• can only differentiate under microscope bc focus of the lesion is in the center

Heck’s Disease Multifocal Epithelial Hyperplasia

Mostly in Native Americans, Eskimos, esp. kids

Familial predisposition

Lower socioeconomic status, poor hygiene, malnutrition, crowded living conditions – Additional etiologies

HPV 13, 32

Most regress spontaneously

Multiple lesions- Buccal / labial mucosa

Sessile, pink or white

HPV - HISTOPATHOLOGY

Squamous epithelial proliferation

Koilocytes - Hyperchromatic nuclei, clear perinuclear halo

SEBORRHEIC KERATOSIS

Positive correlation with chronic sun exposure

Acquired, benign proliferation of epithelial basal cells

Sudden multiple Seb K associated with internal malignancy

Skin of face, trunk, extremities

Multiple, small tan to brown macules initially, become papillary raised, Usually less than 2 cm

Appear "stuck onto" the skin

Except for aesthetic purposes, seldom removed

KERATOACANTHOMA (Self-Healing Carcinoma)

Self-limiting

Extremely well-differentiated squamous cell carcinoma , called “SCC, “keratoacanthoma type”

• MALIGNANT

Rarely before 45, male predilection

Does not occur intraorally

Rapid enlargement, diameter of 1 to 2 cm within 6 weeks

Regress spontaneously within 6 -12 months leaving depressed scar

KERATOACANTHOMA appearance + tx

Firm, non tender, dome-shaped nodule with central keratin plug

Epithelium at lateral edge of tumor normal

Epithelium exhibits a downward growth pattern

Treatment is surgical excision

well differentiated means very good prognosis, wont metastasize, likely to not return

ORAL MELANOTIC MACULE

Unknown etiology, focal increase in melanin, Unrelated to solar exposure

2:1 female predilection

Vermillion border (lower lip) >buccal mucosa >gingiva > palate

Solitary, uniform tan to dark-brown, round, oval macule, <7 mm, Lesions do not enlarge

flat

No treatment usually required

MELANOCYTIC NEVUS

“Nevus" - Congenital / Developmental

Skin, mucosa

Most common - Acquired nevus, or common mole

Benign, localized proliferation of neural crest cells

Sharply demarcated, brown / black macule

Intraoral nevi distinctly uncommon

Most arise on hard palate or gingiva

ACQUIRED MELANOCYTIC NEVUS (Mole)

White adults 10 - 40 cutaneous nevi

Head and neck region common site

Remains less than 6 mm

Melanoma can arise from nevi

The risk of transformation to melanoma is one in a million

ACQUIRED MELANOCYTIC NEVUS (Mole) Classified histopathologically

Junctional - Nevus cells nests within epithelium

Compound - Nevus cells within epithelium & connective tissue

Intramucosal– Nevus cells only within connective tissue (most common intraoral type)

No treatment for cutaneous nevi

CONGENITAL MELANOCYTIC NEVI

1% of newborns, Small (<20 cm), large (>20 cm)

Large – Brown/ black plaque, rough multi-nodular surface

Hypertrichosis, more prominent with age, called bathing trunk or garment nevus

Congenital nevi excised for aesthetic purposes

5 -10% of large congenital nevi change into melanoma

BLUE NEVUS

Benign proliferation of melanocytes, deep in connective tissue - Dark, sometimes blue color

Intraoral - Most common on palate (and all pigmented lesions)

Mimics an early melanoma

you do biopsy

LEUKOPLAKIA

"white patch" / plaque that can’t be characterized clinically or pathologically as any other disease

Cannot be scraped off

Clinical term, does not imply specific histopathology

Surface keratin or thickened spinous layer masks vascularity of connective tissue

Precancerous, dysplasia / carcinoma in 5 to 25%

Malignant transformation rate 4%

Increases with age, esp for males, 8% of men 70+

causes of LEUKOPLAKIA

Tobacco smoking - 80+% of patients

Heavy smokers - More / bigger lesions

Alcohol strong synergistic effect with tobacco

• Alcohol alone not associated with leukoplakia

UV radiation - Vermilion border

Candidal leukoplakia / candidal hyperplasia can → dysplasia

dysplasia

precancerous

LEUKOPLAKIA characteristics

70% - Lip vermilion, buccal mucosa, gingiva (low risk areas)

Tongue, oral floor, 90+% dysplasia / carcinoma (high risk areas)

Early lesions - Flat, fissured, wrinkled white plaques

2/3 of thin leukoplakia thicken, become distinctly white: homogeneous or thick leukoplakia

Exophytic / multiple projections:-verrucous leukoplakia

findings for leukoplakia biopsy

Hyperkeratosis - 80%

Dysplasia or ca-in-situ - 17%

Squamous cell carcinoma - 3%

you do incisional biopsy

• it is a big lesion all over

• you need to make sure it is not malignancy

LEUKOPLAKIA - DYSPLASIA stages

Mild - Limited to basal layer

Moderate - Basal layer to mid portion of spinous layer

Severe - Basal layer to level above midpoint of spinous layer

Ca-in-situ - Basal layer to surface ("top-to-bottom"), No invasion (high chance of SSC, frequent recall)

no histopathology on this but know the stage descriptions

LEUKOPLAKIA Histologic features of Dysplasia

(similar to squamous cell carcinoma)

• enlarged nuclei and cells

• increased nuclear/cytoplasmic ratio

• hyperchromatic nuclei

• pleomorphic nuclei and cells

• dyskeratosis (abnormal cellular keratinization)

• increased mitotic activity

• abnormal mitotic figures

TREATMENT for leukoplakia

Biopsy mandatory- Guides Tx *golden standard

Tissue sample from clinically most "severe" areas

Dysplasia or worse - Complete removal

Long-term follow-up, recurrences / additional lesions may develop

PROLIFERATIVE VERRUCOUS LEUKOPLAKIA

Extensive white plaques, Multiple sites, Invariable progression

Female 4:1, Usually nonsmokers, nondrinkers, HPV 16

Transform into carcinoma (verrucous carcinoma or SCC)

Recur after excision

main etiology for leukoplakia

smoking!!!

if not smoking, then likely hpv 16

ERYTHROPLAKIA

Red patch that can’t be clinically or pathologically diagnosed as any other condition

Related to alcohol and tobacco use

Older men, peak 65 – 74 years

Well-demarcated red macule or plaque, soft, velvety

Differential diagnosis: Inflammation, candidiasis, vascular lesions

ERYTHROPLAKIA; Histologic spectrum

Benign keratosis – 0%

Mild dysplasia - 10%

Severe dysplasia OR carcinoma-in-situ - 40%

Invasive carcinoma - 50%

Suspicious may be observed for 10-14 days, if persists biopsy

Recurrence & multifocal involvement common, long-term follow-up needed

TOBACCO POUCH KERATOSIS (Snuff Pouch)

Chewing tobacco / finely ground tobacco (snuff) : Smokeless tobacco or spit tobacco

Painless gingival "recession" & facial bone destruction

Correlates with quantity and duration

Thin gray-white, translucent plaque

• 1-5 years to become white

Fissured or rippled with pouch

Later becomes thickened leathery or nodular

TOBACCO POUCH KERATOSIS (Snuff Pouch) outcomes

 Hyperkeratosis, acanthosis, edema

Dysplasia uncommon, when present, is typically mild

Biopsy intensely white, granular/verruciform, ulcerated, mass forming, indurated, or hemorrhagic lesions

Cancer risk 4 times greater than non-users

• verrucous carcinoma is most common but SCC possible

Habit cessation normal mucosa within 1 to 2 weeks

• Lesions remaining after 1 month should be biopsied

NICOTINE STOMATITIS

Not premalignant, response to heat, not chemicals in tobacco, slightly elevated papules with punctate red centers

Inflamed & metaplastic salivary gland ducts

Completely reversible if habit discontinued

White lesion persisting after a month of habit cessation -True leukoplakia and biopsied

actinic

refers to sun exposure

ACTINIC CHEILITIS

Diffuse, premalignant alteration of lower lip vermilion, from excessive UV light

Light-complexioned, Strong male(45+)predilection(10:1)

Blurring of margin between vermilion & cutaneous portion of lip

Rough, scaly areas on drier portions of vermilion

can be reversable before its too bad

Ulcerations - Progression to squamous cell carcinoma

• shown in pic

• do incisional biopsy, NOT SHAVE

ACTINIC CHEILITIS outcomes

Marked hyperkeratosis, varying degrees of dysplasia

Degeneration of collagen fibers (solar elastosis)

Sunscreens prevent further degeneration

If severe – Vermilionectomy - Shave procedure

SCC- 6-10%

Enlarge slowly and metastasize late