1. Oral Pathology Exam I Practical Review Slides

2. Benign Epithelial Lesions

3. 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

4. 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

5. 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

6. 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

7. 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

8. 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

9. 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

10. 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)

11. 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)

12. 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

13. 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

14. (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)

15. 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

16. 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

17. 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

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

19. 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

20. 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

21. 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

22. 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

23. 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

24. 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

25. 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

26. 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

27. 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

28. 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

29. 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

30. 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

31. 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

32. 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

33. 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

34. 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