Exam 2

Question 1

Fibroma

Answer 1

• Hyperplasia of fibrous connective tissue
• most common tumor of the oral mucosa
• CT neoplasm (mesenchymal)
• usually sessile, smooth surfaced, normal color, asymptomatic
• ↑↑ cheek (buccal mucosa) but occurs almost anywhere
• usually sessile-the attachment of the tumor is the same size as the base of the tumor. Sometimes grow on a stalk or a pedicle, called pedunculated. Grow slowly but most of them stop
• Tx: surgical excision. Almost no regrowth potential

Question 2

Giant Cell Fibroma

Answer 2

• “papillary” tumor of fibrous connective tissue containing plump, stellate and often bi or trinucleated fibroblasts. Fibroblasts are exceedingly large and multinucleated
• ↑ children (most fibromas are in older adults)
• ↑↑ gingiva, ↑ tongue
• often confused clinically with papillomas
• look pebble like

Question 3

Peripheral odontogenic (ossifying) fibroma

Answer 3

• Reactive fibroblastic lesion of PDL (exclusively on the gingiva since come from PDL
• Strong predilection kids and young adults (more common in females), anterior regions
• ↑↑ 1-3 decades, occurs only on gingiva, asymptomatic; pedunculated or sessile mass ± red ± ulceration
• Histology: Cellular fibroblastic lesion with bone and/or cementum and/or dystrophic calcification
• Treatment: Excision including superficial PDL
• recurrence rate 15-20%, highest recurrence of any of the reactive gingival lesions

Question 4

Inflammatory Fibrous Hyperplasia (Epulis Fissuratum)

Answer 4

• Reactive folds of hyperplastic fibrous connective tissue along border of ill-fitting, over extend denture
• clinically called epilatus fissuratum, pathologically: inflammatory fibrous hyperplasia. Flabby folds
• Histology: Fibrous hyperplasia ± inflammation
• Treatment: Excision and remake/reline denture

Question 5

Inflammatory Papillary Hyperplasia (Papillomatosis)

Answer 5

• Hyperplastic response of palatal mucosa to ill-fitting denture
• Histology: Papillary hyperplasia + inflammation ± pseudoepitheliomatous (looks like cancer) Hyperplasia (PEH)
• Treatment: Excise + remake/reline denture

Question 6

Peripheral Giant Cell Granuloma

Answer 6

• Tumor of well vascularized fibrous connective tissue containing numerous multinucleated giant cells
• questionable histogenesis but occurs only on gingiva (↑ anterior) got to be over bone
• any age, asymptomatic
• usually reddish-brown-purple pedunculated or sessile mass
• peripheral ones are about 5x as common as central ones
• female:male; 2:1
• may produce cupping resorption of underlying bone (especially in edentulous areas)
• Treatment: Excision and removal of irritants, may recur

Question 7

Pyogenic Granuloma

Answer 7

• Pyo – pus genic – produces (misnomer) Do Not Have Pus
• reactive lesion representing hyperplasia of body’s basic reparative tissue –granulation tissue (lots of blood vessels, highly vascularized)
• reddish, ulcerated pedunculated or sessile mass
• ↑ 2-4 decades, ↑↑ gingiva but occurs anywhere including skin
• Asymptomatic but may bleed easily
• ↑ females, often in pregnancy “pregnancy tumor” bc when you are pregnant you develop more blood vessels to support another persons
• The angiogenic effect of pregnancy not uncommon in extraction sockets – epulis granulomatosa
• Histology: Hyperplastic granulation tissue, fibroblasts with delicate collagen, endothelial cells + capillaries and dilated larger vessels
• Treatment: Excision and removal of irritants, may recur

Question 8

Parulis (“gum boil”)

Answer 8

• Can occur anywhere but on gingiva, it represents draining from a source of odontogenic infection of either pulpal or periodontal origin
• pus (purulence, suppuration) = bacterial infection
• A sinus tract draining an odontogenic infection

Question 9

Localized juvenile spongiotic gingival hyperplasia

Answer 9

• Localized hyperplasia presumably from externalized sulcular epithelium on gingiva
• Developmentally some people are born with this epithelium exteriorized (on the gingiva) and if it gets irritated, this can develop.
• Almost exclusively 1-2 decades (children and teens), female 2:1,
• Almost all anterior gingiva, Max 5:1,
• Clinical: red often papillary gingival lesions
• Histology: Papillary proliferation of inflamed epithelium with intercellular edema (spongiosis)
• Very superficial and vascular
• Treatment: Excision

Question 10

Hemangioma

Answer 10

• Overgrowth of blood vessels (hamartoma – localized overgrowth of tissues native to the part, often developmental)
• rapid proliferation of endothelial cells at birth or shortly thereafter, characteristically involute most common tumor of infancy (5-10% incidence)
• ↑ females 3:1
• 60% H&N
• ↑↑↑ 0-5 years, rarely congenital, 90% complete but slow involution by age 10
• reddish to purple mass lesions that tend to blanch with pressure
• oral ones often later and don’t involute
• can occur in bone, often multilocular or soap bubble appearance (why you aspirate before bone biopsy)
• Histology: Endothelial cell proliferation with formation of small capillaries (capillary) or larger dilated vascular spaces (cavernous)
• Treatment: Natural history is involution laser pulse, excision, sclerosing agents, steroids both intralesional and systemic propranolol
• If traumatize, they will bleed very easily
• They can calcify

Question 11

Sturge-Weber Angiomatosis (Encephalotrigeminal angiomatosis)

Answer 11

• Nonhereditary developmental, congenital condition characterized by vascular proliferation of brain and face usually along distribution of ophthalmic branch of the trigeminal nerve. Stop at the midline
• Sturge-Weber and port wine stains are due to somatic activation mutation in GNAQ which encodes Gαq, a member of the q class of G-protein alpha subunits that mediates signals between G-protein–coupled receptors and downstream effectors. The difference is when and where the mutation occurs
• Large purplish lesions –identical clinically to port-wine stains, ipsilateral oral mucosal involvement common leptomingeal angiomas of cerebral cortex

Question 12

Lymphangiomas

Answer 12

• Developmental overgrowth of lymphatic vessels
• ↑↑ H&N, ↑↑ 0-5 years of age
• Orally: ↑↑ tongue (may produce macroglossia)
• Full of lymph, not blood

Superficial ones – pebbly surface covered by translucent vesicles

Deeper ones – more diffuse

Cystic hygroma: variant that infiltrates and becomes very large (↑ neck)

• Histology: Proliferation of thin walled lymphatic vessels capillary sized, Dilated (cavernous) or cystically dilated (cystic hygroma)
• Treatment: Lesions don’t involute; excision-deeper ones often recur; sclerosing agents

Question 13

Human Papilloma Virus (HPV) etiology

Answer 13

• Benign epithelial neoplasm
• All are papillary or verrucous growths.

1. Papilloma: exophytic (grow outward into air (path of least resistance), often pedunculated, pink to white, most common site: soft palate.
2. Verruca vulgaris (common wart): usually HPV2, similar to papilloma. Many patients have verruca on hands. Kids stick warty fingers in mouth-spread
3. Condyloma Acuminatum“venereal warts” usually HPV 6/11, often multiple, less exophytic than papillomas. Flatter, more sessile

Question 14

Keratoacanthoma (KA)

Answer 14

• benign epithelial neoplasm
• Clinical and histological features similar to skin cancer (squamous cell carcinoma), considered reactive, not neoplastic.
• Sun exposed areas of head and neck, ↑ older patients, 10% on lips/have been reported intraorally. Rapid growth, often umbilicated with rolled borders
• Natural history: Involution and healing.

Question 15

mesenchymal neoplasms

Answer 15

most look identical clinically and present as asymptomatic, slowly growing submucosal masses (fibrous, bone/cartilage, fat & vascular)

Question 16

Lipoma

Answer 16

• CT neoplasm (mesenchymal)
• Benign neoplasm of fat, may appear yellowish, very common in skin, less so orally
• Grow slowly, painless.
• Floats if biopsy

Question 17

Verruciform xanthoma

Answer 17

• CT neoplasm (mesenchymal)
• Reactive lesion with predilection for hard palate or gingiva.
• Most common orally but reported on skin and genitals
• Surface irregular (verrucous, “verruciform”)
• Pink to white
• Histology: Epithelium displays papillary hyperplasia. Connective tissue papillae contain phagocytic cells which have engulfed lipid (xanthoma cells)

Question 18

Leiomyoma (angioleiomyoma-blood inside lumen) (vascular leiomyoma)

Answer 18

• Benign neoplasm of smooth muscle (mesenchymal)
• Common in uterus (“fibroids”), rare orally, most normal color, can be reddish to purple

Question 19

Rhabdomyoma

Answer 19

• Benign neoplasm of skeletal muscle,↑ heart, rare orally, ↑ tongue
• To us will look benign and mesenchymal

Question 20

Granular Cell Tumor

Answer 20

• Muscular mesenchymal tumor
• Originally thought to arise from muscle (granular cell myoblastoma) now thought to be of nerve origin, possibly sheath. Common in skin and orally,
• ↑↑ tongue (most common site) but can affect other sites, may be firm and “fixed”, not freely movable on palpation-stuck to surrounding tissue.
• Histology: Large polygonal cells with granular cytoplasm, about 1/2 cause overlying epithelium to react in a pattern that simulates carcinoma called pseudoepitheliomatous hyperplasia (PEH)

Question 21

Congenital epulis of the newborn

Answer 21

• Muscular mesenchymal neoplasm
• Congenital tumor of anterior alveolar ridge
• Mx:Md/2:1
• F:M/8-10:1
• Varied size
• Histology: Identical cells to granular cell tumor but cells don’t react to immunohistochemical markers for nerve,
• No PEH
• May regress if incompletely “excised”

Question 22

Traumatic Neuroma

Answer 22

• not neoplasm but aberration of healing following trauma.
• Mass of tangled regenerating nerve in scar tissue
• ↑ lateral and anterior borders of tongue, lower lip, at mental foremen
• palpation produces pain

Question 23

Neurofibroma

Answer 23

• Benign neoplasm (mesenchymal) occurring in a nerve and composed of Schwann cells, axons and fibrous tissue
• Can occur in most tissues and organs of body, including oral cavity, soft tissue and bone, most asymptomatic
• Slow growing, symmetrical.

Question 24

Neurofibromatosis

Answer 24

• (Von Recklinghausens Disease of Skin)
• nerve mesenchymal neoplasm
• a developmental condition of neuroectoderm ranging from simple skin pigmentation to widespread involvement of central and peripheral nervous system.
• 1/2 inherited as autosound dominant trait, other 1/2 somatic mutations. (Gene for most on chromosome #17)
• Neurofibromas of skin and mucosa
• Light brown skin pigmentation (cafe-au-lait spots)
• Axillary freckling (pathoneumonic)
• pigmentary defects of iris (Lisch spots)
• 1-5% of patients develop malignancy in their neurofibromas

Question 25

Neurilemmoma (Schwannoma)

Answer 25

• Benign encapsulated neural neoplasm arising within the sheath or neurilemma of a peripheral nerve
• asymptomatic
• painless
• often freely movable
• Histology: Encapsulated neoplasm
• Antoni A: Acellular areas of replicated basement membrane material surrounded by Schwann cell nuclei
• Antoni B: Haphazardly arranged spindled Schwann cells in loose stroma.

Question 26

Melanotic neuroectodermal tumor of infancy

Answer 26

• Neural crest tumor occurring almost exclusively in jaws but does occur in

extragnathic sites.

• Most congenital - 1 year, anterior jaws, ↑ Mx.
• Rapidly growing destructive radiolucency, often pigmented (melanin) but technically not melanocytes
• tumor cells produce VMA (Vanilymandelic Acid) in serum and urine.
• Tx: Aggressive curettage 10-20% recur.

Question 27

Multiple Endocrine Neoplasia Type 3 (MEN 3)

Answer 27

• 95% of patients with mutation of RET gene, a proto-oncogene on chromosome 10.
• 50% - inherited as autosomal dominant-tall + skinny people
• 50% somatic mutation
  
  • Mucosal neuromas (predates other tumors)
  • Medullary carcinoma of thyroid
  • Pheochromocytoma of adrenal medulla

​oral cancer neuromas are usually the first they get

Question 28

Nevi (common mole)

Junctional

Intradermal

Compound

blue

Answer 28

• localized
• nevus cells migrate form neural crest to skin and occasionally mucous membranes
• palate, buccal mucosa and vermillion border are most common oral sites
• congenital - present at birth, about 1% of newborns, larger (“garmet nevus”);
• rarely occur intraorally, flat
• acquired - genetic influence and the average person has about 15.
• More common in whites
• junctional nevus - flat macule, nevus cell in basal epithelium at “junction” of epithelium and connective tissue
• intradermal nevus (intramucosal nevus) - nodule ± hair, nevus cells in dermis or lamina propria
• compound nevus - nodule, combination of junctional and intradermal
• blue nevus - dendritic nevus cells deep within connective tissue almost always occur on palate

Question 29

Melanoacanthoma

Answer 29

• reactive proliferation of intraepithelial dendritic melanocytes
• Most often from traumatic injury (sharp cusp tips)
• reactive, not neoplastic can simulate melanoma
• ↑↑ blacks, ↑cheek anyone with darker skin, women
• more commonly buccal mucosa; arises quickly
• resolves when irritant removed
• usually biopsy to double check
• localized

Question 30

Ephelis (freckle)

Answer 30

• localized overproduction of melanin, not an increase in number of cells
• very common, sun activated, ↑ H&N skin
• flat, tan macules, multiple

Question 31

Actinic or senile lentigo

Answer 31

• “age spots”,”liverspots”
• from chronic UV damage - not seen intraorally
• ↑ after 40, 90% of eldery
• ↑ face, hands, arms
• flat evenly discolored macules, multiple
• usually less than 5mm
• don’t treat unless for esthetics

Question 32

Melanotic macule

Answer 32

• tan to brown flat macule, like a big freckle but not sun related
• completely flat,
• female 2:1, average age 43 (1-80)
• average size 6.8mm
• 15% multiple
• ↑↑ lower lip (33%), ↑ palate, ↑ gingiva, then buccal mucosa

Question 33

Malignant Melanoma

Answer 33

• Malignancy of melanin-producing cells
• 3rd most common skin cancer (↑↑ basal cell carcinoma, ↑ squamous cell carcinoma) but incidence ↑↑ (8 4-6%/year since 1975),
• likelihood of a Caucasian today developing melanoma during their lifetime is
• Sites:
  
  • 25% H&N
  • 40% extremities
  • • Etiology
  • Risk factors (related to ultraviolet radiation damage from sun)
  • Acute sun damage (burns, blistering) probably more important than chronic exposure
  • Fair complexion, blond hair, blue eyes
  • Multiple moles, freckling, dysplastic nevi
  • Family history

Clinical features

Asymmetry - lesion asymmetric as well as surface with elevated, nodular areas

Borders - irregular and often notched

Color - ↑ variation, red, tan, brown, black

Diameter - history of growth or change or > 6mm

Evolution-evolves over time

Biologic Growth Phases

• Radial - malignant cells spread laterally through the epithelium, lesion remains flat but ↑ size can remain for years 75-85% of melanomas have radial growth phase
• Vertical - malignant cell grow down and invade producing a mass or tumor

Question 34

Superficial spreading melanoma

Answer 34

• About 70% of cutaneous melanoma
• ↑ trunk, 28% H&N
• short radial growth phase, develop nodules/vertical growth

Question 35

Nodular Melanoma

Answer 35

• 15% of cutaneous melanomas
• 30% in H&N
• Very short or non-existent radial growth
• Produce exophytic, pigmented nodules but rarely no pigment (amelanotic)

Question 36

Lentigo maligna melanoma

Answer 36

• 5-10% of cutaneous melanomas
• ↑↑ age, on sun exposed areas of face
• extremely long radial growth phase (lentigo maligna/Hutchinson’s freckle) which may last 15-20 years
• ultimately develops nodules/vertical growth

Question 37

Acral lentiginous melanoma

Answer 37

small subset affecting palms, soles, subungual and mucous membranes

Question 38

Oral Melanoma

Answer 38

• Most have radial growth (>50%) and many similar to acral lentiginous melanoma
• ↑↑ palate, Mx gingiva more common in men
• Treatment: Excision (resection) with minimum of 1cm margin
  
  • ± lymph node dissection
  • ± adjunctive chemotherapy, radiation and immunotherapy
• Prognosis
  
  • Depth of invasion is probably most important factor influencing survival
  • Metastasis ↓ survival, many patients have a sentinel lymph node biopsied as a staging procedure
  • Prognosis also affected by site affected and type of melanoma
• Overall survival is 79% for 10 years (on skin, and 98% 5-year prognosis)
• Oral melanomas much worse prognosis,

Question 39

What causes multifocal pigmentation

Answer 39

1. Physiologic
2. Drugs: Antimalarials, antiarrythmics (quinidine), tranquilizers (thorazine), cis-platinum
3. Addisons Disease: Adrenocortical insufficiency triggers hypothalamus to stimulate anterior pituitary to produce ACTH (and MSH - melanin stimulating hormone) Hyperpigmentation
4. Peutz - Jeghers Syndrome: Autosomal dominant skin and mucosal freckles, intestinal polyps (small bowel) (very low rate of malignant degeneration but will produce symptoms of obstruction) oral & perioral freckles, ↑ lips and cheeks
5. Any condition characterized by cafe au lait spots
   
   1. Neurofibromatosis
   2. McCune Albright syndrome (polyostotic fibrous dysplasia)
6. Smoker’s melanosis protective response to nicotine and heat ↑ palate, gingiva
7. Melanoma
8. Satelite lesions
9. Kaposi’s sarcoma
10. Petechiae, ecchymosis, purpura

Question 40

Odontogenesis

Answer 40

starts with surface ectoderm (epithelium) growing into jaw (dental lamina) and producing the tooth germ, a portion of which is the enamel organ.

Question 41

Odontogenic cyst

Answer 41

• Pathologic cavity lined by odontogenic epithelium and filled with fluid or semisolid material.
• Etiology:
  • Inflammation
  • Unknown, these are called developmental cysts but are not inflammatory
  • Radicular cyst and buccal bifurcation cyst are inflammatory, all the rest are developmental

Question 42

Primordial Cyst

Answer 42

• Cyst arising from degeneration of enamel organ prior to tooth formation aborts odontogenesis resulting in radiolucency in place of a missing tooth. ↑↑ Md3M.
• Odontogenic

Question 43

Dentigerous Cyst (Follicular Cyst)

Answer 43

• Odontogenic cyst resulting from separation of the follicle from around the crown of developing tooth.
• Any age, ↑ Md3M, ↑ MxCu, asymptomatic, usually no expansion
• Radiographic findings: Well circumscribed pericoronal radiolucency. From CEJ around crown.
• Histology: Stratified squamous epithelium without keratinization (this was originally the ameloblasts which following odontogenesis becomes reduced enamel epithelium).
• Treatment: Surgical removal of tooth and cyst if 3M. For Cu may be able to decompress and pull Cu in orthodontically

Variants:

• Eruption cyst – a dentigerous cyst that gets pushed into oral cavity by erupting tooth, may treat with decompression so tooth can erupt. Lateral - ↑Md 3M – laterally placed

Neoplastic potential – Exceedingly rare

• Ameloblastoma
• Squamous cell carcinoma
• Mucoepidermoid carcinoma

Question 44

Periodontal Cysts

Answer 44

Odontogenic Cyst

Apical Periodontal Cyst (radicular cyst)

Most common of all odontogenic cysts

Inflammatory origin secondary to devitalized pulp

• Lateral radicular cyst
• Residual cyst

Lateral Periodontal cyst – arises from cystic degeneration of rests of Malassez in PDL. Teeth vital, ↑↑ MdCu-Bi.

• Radiographic findings: Small well circumscribed radiolucency along lateral root surface of vital tooth.
• Histology: Nonkeratinizing stratified squamous epithelial lining.
• Treatment: Excision
• Variant: Botryoid odontogenic cyst – polycystic, multilocular, may recur after removal.

Question 45

Gingival Cysts

Answer 45

Newborn (dental lamina cyst) –

• Soft tissue cysts on gingiva or alveolar ridge from degenerating dental lamina
• Very common
• Congenital or early life
• Small yellowish elevations
• No treatment. Will self-marsupialize and heal

Adult –

• cysts of attached gingiva from degeneration of rests or glands of Serres (dental lamina), soft compressible swellings, ↑↑ MdCu-Bi clinically similar to mucocele but mucoceles don’t occur on gingiva.
• Treatment: Excision

Question 46

Buccal Bifurcation Cyst

Answer 46

Paradental Cyst

Inflammatory cyst occurring on buccal of erupting tooth

↑↑↑ children

↑↑ Md1M (often enamel extension into furcation)

Buccal swelling

Radiographic findings: unilocular lucency involving furcation of roots

Occlusal films: buccal location

Histologic findings: Inflamed cyst lined by stratified squamous epithelium

Treatment: Enucleation of cyst. If you recognize this clinically which you should, you do not have to extract the tooth.

Question 47

Glandular Odontogenic Cyst

Answer 47

↑ Md, may be large

Radiographic findings: Unilocular to multilocular radiolucency

Histologic findings: Cyst showing glandular differentiation (mucus cells, columnar epithelium with cilia, lumina)

Treatment: Surgical excision

30-50% recurrence.

Question 48

Calcifying odontogenic cyst (Gorlin Cyst)

Answer 48

• Any age, ↑ Md, maybe associated with unerupted teeth or odontomas.
• Asymptomatic, rarely expansion, occur extraosseously
• Radiographic findings: Radiolucent to mixed radiolucent/opaque
• Histologic findings: Fully or partially cystic, cystic epithelium contains ghost cells (prematurely keratinized) which tends to calcify
• Treatment: Conservative surgical removal – low recurrence

Question 49

Odontogenic Keratocyst

Answer 49

• developmental cyst from dental lamina
• 90% parakeratinized
• 10% orthokeratinized (orthokeratinized odontogenic cyst)

Parakeratinized

• All ages, ↑ 2-3 and 6-7 decades, Md:Mx, 2:1, ↑ post Md.
• ¼ expansion ± drainage and pain, clinically aggressive
• Radiographic findings: Unilocular or multilocular radiolucency, commonly mimics other types of odontogenic cysts.
• Histologic findings: Parakeratotic stratified squamous epithelial lining with well developed palisaded and hyperchromatic basal cells; often daughter or microcysts in wall.
• Treatment/Prognosis: Conservative surgical removal to resection to decompression.
• About 1/3 recur
• Basal cell nevus-bifid rib syndrome (Nevoid basal cell carcinoma syndrome)
• About 5% of patients with keratocyst have, almost all multiple OKCs
• Autosomal dominant (mutation of a tumor suppressor gene 9q22), basal cell carcinomas (not nevi; not limited to sun-exposed areas or elderly), calcification of falx cerebri, bone anomalies (bifid ribs), OKCs usually multiple, pits in palms and soles.
• Keratocysts known for:
  
  • Clinical aggressiveness
  • Recurrence after removal
  • Association with basal cell nevus-bifid rib syndrome

Orthokeratinized odontogenic cyst

• Smaller, less aggressive, minimal recurrence, not associated with syndrome.