Oral Pathology Exam I Practical Review Slides

Benign Epithelial Lesions

Items covered: Benign Epithelial Lesions Squamous Papilloma Verruca Vulgaris Condyloma Acuminatum Focal Epithelial Hyperplasia Verrucous Carcinoma Cowden Syndrome (Multiple hamartoma syndrome) Keratoacanthoma Seborrheic Keratosis Benign Melanocytic Lesions Ephelis Oral/Labial Melanotic macule Actinic Lentigo Nevus Blue Nevus Café-au-lait spots Neurofibromatosis Albright Syndrome Peutz-Jehgers Syndrome Addison Disease Smoker’s melanosis Exogenous pigments (amalgam tattoo) Heavy metal poisoning

Squamous Papilloma Exophytic, sessile or pedunculated Surface projections (Short cauliflower or long fingerlike) rough surface How to differentiate: Short and blunted at all same sites Cobblestone appearance Rough Granular surface Or long fingerlike projections Squamous papilloma Squamous Papilloma

Squamous Papilloma Exophytic, sessile or pedunculated Surface projections (Short cauliflower or long fingerlike) rough surface Hyperkeratinized (white lesions) epithelial fronds made up of purely epithelium with branched connective tissue cores. Each frond has central connective tissue vessels and branches into each branch of papilloma Squamous papilloma Squamous Papilloma Epithelial projections, (wavy like things sticking up) with thin core of connective tissue

Children who bite nails or suck fingers with warts on fingers. Identify Usually on anterior lips, gingiva and tongue (not shown in this case) Verrucous vulgaris Usually arise as multiple lesions (contrasting squamous papillomas) Verruca Vulgaris

Histology is same as squamous papilloma, except young lesions demonstrate Koilocytes (clusters of clear cells with shrunked raisin-like nuclei) Verrucous vulgaris This is a “young” lesion Verruca Vulgaris

Condyloma Acuminatum Multiple, fast-growing coalescing papillomas Identify Caused by HPV 2, 6, 11 (non-oncogenic), 16, 18 (oncogenic) History of oral sex with a partner with venereal warts (STD) Condyloma acuminatum Common in HIV patients Condyloma Acuminatum

Condyloma Acuminatum Large papilloma featuring many koilocytes appears as a benign proliferation of acanthotic stratified squamous epithelium with mildly keratotic papillary surface projections Thin connective tissue cores support the papillary epithelial projections, which are more blunted and broader than those of squamous papilloma and verruca vulgaris Condyloma acuminatum Condyloma Acuminatum

Focal epithelial Hyperplasia (Heck Disease) HPV 13 infection producing multiple ancanthotic (Thick epithelium) papules of same color as normal mucosa Individual lesions are small, discrete, and well demarcated, but they frequently cluster so closely together that the entire area takes on a cobblestone or fissured appearance mostly in Native American children; tends to resolve by themselves, but are very contagious when present Focal epithelial hyperplasia Focal epithelial Hyperplasia (Heck Disease)

Focal epithelial Hyperplasia (Heck Disease) Prominent acanthosis (an abnormal but benign thickening of the prickle-cell layer of the skin) of the epithelium with broad and elongated rete ridges The slightly papillary surface alteration noted here may or may not be present. Some superficial keratinocytes show a koilocytic change similar to that seen in other HPV infections. occasionally demonstrate an altered nucleus that resembles a mitotic figure (mitosoid cell), shown by arrows in bottom picture Focal epithelial hyperplasia Focal epithelial Hyperplasia (Heck Disease)

Exophytic papillary growth, much larger than any papilloma, sheer size of the lesion rules out squamous papilloma The most common sites of oral mucosal involvement include the mandibular vestibule, the buccal mucosa and the hard palate. The lesion appears as a diffuse, well–demarcated, painless, thick plaque with papillary or verruciform surface projections. Lesions are typically white but also may appear erythematous or pink. Verrucous Carcinoma Verrucous Carcinoma

Characterized by wide and elongated rete ridges that appear to "push" into the underlying connective tissue. Individual cells do not appear very dysplastic Lesions usually show abundant keratin (usually parakeratin) production and a rough papillary or verruciform surface Parakeratin typically fills the numerous clefts or crypts (parakeratin plugs) between the surface projections There is frequently an intense infiltrate of chronic inflammatory cells in the subjacent connective tissue. Bulbous rete ridges appearing to push into CT Verrucous Carcinoma Rough papillary or verruciform surface Verrucous Carcinoma

(multiple hamartoma syndrome) Multiple papules on gingiva, tongue, and buccal mucosa Multiple small facial hair follicle tumors (small and keratinized with sandpaper like texture) Warty growths all over face Macrocephaly in many cases Intestinal polyps, diarrhea Hyperkeratosis of palms and soles Development of malignant tumors of breast, thyroid Will only show epithelial hyperplasia Autosomal dominant Cowden syndrome Cowden Syndrome (multiple hamartoma syndrome)

Well demarcated, firm fleshy epithelial growth with a central keratin plug which may be yellow, brown or black Outer nodule may be erythematous Occurs on upper and lower lip with equal frequency Lesions on face and head become very large and grow aggressively Can occur on the lips, never in the oral cavity Grows rapidly (helps differentiate from Squamous Cell Carcinoma, which is slower growing), involutes, then falls off Male predilection, rare before 45 years of age Related to sun exposure Rapid Growth Keratoacanthoma Involutional stage Keratoacanthoma

Histologically looks very similar to squamous cell carcinoma (Pseudoepitheliomatous hyperplasia), important to note rate of growth Do not appear malignant, but invade in a similar manner as cancer Central plug of keratin Keratoacanthoma Keratoacanthoma

Soft, sessile, friable growth Never in oral cavity Can be pink, white or brown Well demarcated, with surfaces that are finely fissured, pitted, verrucous, or smooth Commonly seen on face and neck Common after age 40 Never become malignant Genetic predisposition + UV light contributes to development, although can occur in non UV-exposed areas A sudden multiple appearance of seborrheic keratosis is called the “sign of Leser-Trelat” and is an indicator of undiagnosed internal malignancy, usually stomach cancer. Seborrheic Keratosis Characteristic Similar to KA and Cowden’s syndrome Seborrheic Keratosis

Exophytic growth of basal cells showing hyperkeratosis, acanthosis, papillomatosis The entire epithelial hyperplasia extends upward Presence of keratin filled pseudocysts Seborrheic Keratosis Seborrheic Keratosis

Small macule (a perfectly flat lesion, non-palpable, differentiated from normal tissue only by color) only on skin that darkens with UV (invisible during the winter) Show increased melanin in the basal layer, with no increase in melanocytes No abnormal melanocytes, normal melanocytes produce excessive amount of pigment that is stored in basal epithelium No increase in number of melanocytes Does not occur in the oral cavity Ephelis Ephelis

Oral/Labial melanotic macule Single brown macule on lip, gingiva, or palate No larger than 7 mm Symmetrical outline No growth after reaching the final size Histology is the same as ephelis Dark independent of UV exposure Melanocytes are normal, but increased pigment is present Labial melanotic macule Oral/Labial melanotic macule

Oral/Labial melanotic macule Melanocytes are normal, but increased pigment is present Single brown macule on lip, gingiva, or palate No larger than 7 mm Symmetrical outline No growth after reaching the final size Histology is the same as ephelis Dark independent of UV exposure Note increased melanin at basal layer, normal melanocytes Oral melanotic macule Oral/Labial melanotic macule

Individual lesions appear as uniformly pigmented brown to tan macules with well-demarcated but irregular borders Show up on sun-exposed areas of elderly whites Lesions on skin, never in oral cavity Most lesions are smaller than 5mm Do not darken upon UV exposure Actinic lentigo Actinic Lentigo

Actinic Lentigo Increase in number of melanocytes Rete ridges are elongated and club shaped Thinning of epithelium above the connective tissue papillae The ridges sometimes seem to coalesce with one another. Within each rete ridge, melanin - laden basilar cells are intermingled With excessive numbers of heavily pigmented melanocytes. Actinic lentigo Actinic Lentigo

Nevus Small sessile exophytic growth, typically <6mm in diameter Macule or fleshy papule, sometimes with hairs growing from the center Symmetrical, brown, (may be light or dark) or amelanotic (same color as surrounding tissue) Common on skin, uncommon in mouth (occur on hard palate, buccal mucosa, gingiva and lips) Do not occur on the tongue or floor of the mouth Many lesions will involute and disappear throughout adult years, with fewer lesions detected in elderly Overgrowth of benign melanocytes Labial nevus Nevus

1) Lesions come in three types, all of which are characterized by theques (5 or more epidermal melanocytes) Junctional nevus 1) All theques are located intraepithelial; Always presents as a macule 2) 2) Theques in both epithelium and connective tissue -Theques continue to increase in density around the epithelium and begin to drop down into connective tissue Compound nevus 3) 3) Theques in connective tissue only Does not become malignant Presents as a papule Began as junctional, then became compound and finally this- Subepithelial (submucosal) nevus

Rare in mouth and almost exclusively on hard palate as a small, symmetrical blue macule or papule Lesion of true dermal melanocytes (in the connective tissue, not epidermis) Lesion is most commonly seen in children and young adults Common on skin of black and asian children as Mongolian spot, located on buttocks and lower back Eventually fades Blue nevus Blue Nevus

Blue Nevus Dermal melanocytes are spindly in apperance These cells are located deep within the dermis (or submucosa) or lamina propria and usually align themselves parallel to the surface epithelium Blue Nevus Blue nevus

Café-au-lait spots; coast of california outline These types of macules are associated with neurofibromatosis Note rounded edges of macule Café-au-lait spots; coast of california outline These types of macules are associated with Albright syndrome Note jagged edges of macule Café au lait (coast of maine lower left, coast of california upper right) Café-au-lait spots; coast of Maine outline

Peutz-Jeghers Syndrome Perioral and intraoral melanotic macules present at birth are very diagnostic of this Lesions appear on fingers as well Develop GI polyps (multiple hamartomas) and intusseptions Does not become malignant (contrasting Gardner’s Sx) Develop tumors of breast, thyroid, and pancreas (Compare to KA, SK and Cowden’s Sx) Autosomal Dominant Is a cancer Sx, (predisposes to multiple other cancers) Peutz Jegher sx Peutz-Jeghers Syndrome

Entire mucosa of mouth darkens, especially at sites of healed wounds Darkening of mucosa is followed by darkening of skin Excess pigment also shown in fingernails RECENT onset of diffuse oral pigmentation (Not to be mistaken for racial pigmentation) Failure of adrenal cortex causes excess release of ACTH, causing generalized melanosis Insidious onset of fatigue, irritability, depression , weakness, and hypotension is noted over a period of months. The patient usually complains of gastrointestinal upset with anorexia , nausea, vomiting, diarrhea, weight loss, and a peculiar craving for salt. Addisons disease intraoral pigmentation Addison’s Disease

RECENT onset of pigmented macules could suggest this disease (Not to be mistaken for racial pigmentation) Occurs on anterior ATTACHED gingiva (contrast to heavy metal poisoning) Increased incidence in women and more so if they are using birth control pills Does not mature into malignancy Melanin is formed as a protective response from smoke Develops approximately after 1 year after smoking Resolves 3 years post smoking cessation Smokers melanosis Smoker’s Melanosis

implantation of amalgam fragments into connective tissue Slate gray in appearance, can appear similar to melanoma can get larger over time Can verify via radiograph Amalgam Tattoo Amalgam tattoo

Amalgam Tattoo Fine to coarse pigment granules in connective tissue Black, brown or olive green Distributed along reticulin/elastin fibers appearing as loose tobacco strands Typically elicits no inflammatory reaction just leaves a tattoo or maybe the laceration could’ve left a scar Occasionally evokes fibrosis or giant cell reaction Amalgam tattoo Amalgam Tattoo

Symmetrical pigment distribution on FREE gingiva, but not on attached Heavy metal is in systemic circulation, and consequently is in crevicular fluid. Anaerobic bacteria reduce the heavy metals into sulfide salts, which are darkly pigmented Pigmentation is more apparent with higher levels of heavy metals More apparent in patients with poor oral hygiene Heavy metal (in this case lead) poisoning Heavy Metal Poisoning