1.

a. Macroglossia:
i. Occurs in numerous conditions: Down Syndrome, cretinism,
neurofibromatosis, lymphangioma, multiple endocrine neoplasia
tyupe III (MEN III, Williams-Poliack syndrome – mucosal
neuromas, medullary carcinoma of thyroid, pheochromocytoma)
ii. Acquired through edentulism, amyloidosis, acromegaly (no
containment of tongue-expands)
iii. Associated with noisy breathing, drooling, difficulty eating,
problematic speech
iv. Tongue may look crenated or searated from pressure on teeth and
embrasures
v. Characteristic feature of BECHWITH-WIEDEMANN
SYDROME:
1. Omphalocele---herniation of intestine through abdominal
wall of umbilicus
2. Visceromegaly ---big viscera (viscera—large organs within
the 3 body cavities
3. Gigantism –excessive size
4. Neonatal hypoglycemia
vi. psyndrome and multinodular or “lumpy” in amyloidosis,
lymphangioma, or MEN III
b. Akyloglossia
i. Tongue tie, high frenal attachment---tip of tongue to lingual
gingival—may affect speech
c. microglossia
i. small tongue: (the tongue may be missing, and this is called
aglossia)
ii. associated with oromandibular-limb hypogenesis syndromes—look
for limb abnormalities
iii. frequently associated with hypoplasia of mandible, tongue needs
space to achieve normal size
d. geographic tongue (Erythema migrans)
i. benign condition that primarly affects the tongue
ii. Females more than males affected
iii. Characteristics:
1. anterior 2/3 of the dorsal tongue mucosa
2. they appear as multiple, well demarcated zones of
erythema, concentrated at the tip and lateral borders of the
tongue.
3. Erythema---due to atrophy of filiform papillae, and these
atrophic areas are surrounded by slightly elevated,
yellowish-white, serpentine or scalloped border
e. Mueller’s glossitits
i. Patchy areas of mucosal erythema and atrophy
ii. Associated with Pernicious Anemia
 2. swollen lips
a. angioedema – rapid onset / nontender swelling / itching / can be allergic
b. orofacial granulomatosis = cheilitis granulomatosa (of Miescher) and
melkersson-rosenthal syndrome
c. cheilitis glandularis – lower lip / minor salivary glands /
d. hypothyroidism – cretinism
3. a. Sarcoidosis – abnormal response to antigenic material / lungs, lymphoid tissue,
skin, eyes, and salivary glands / elevated ACE levels
b. Wegeners Granulomatosis – necrotizing granulomatous inflammation of nose
and lungs / nasal discharge, chronic sinus pain, congestion, nasal ulcerations,
fever / c-ANCA levels for assessing tx
c. Angioedema = Quincke’s disease for GI and respiratory / histamine release
due to IgE-mediated hypersensitivity rxt / associated with the use of ACE-
inhibitors
4.
a. Attrition – loss of tooth structure caused by tooth-to-tooth contact during
occlusion and mastication…
b. Abrasion – pathologic loss of tooth structure or restoration secondary to the
action of an external agent…most common cause is toothbrushing ..pencils,
toothpicks, bobby pins… “V” shaped notches in incisal edges of ant teeth
c. Erosion – caused by a chemical process beyond that associated with bacterial
interaction with the tooth…typically acid is to blame..facial surfaces of max
anteriors mostly
d. Abfraction – wedge-shaped defects limited to cervical areas…clues to
diagnosis it include defects that are deep, narrow, and “V” shaped and often affect
a single tooth with the adjacent teeth unaffected
d. Abfraction – loss of tooth structure that results from repeated tooth flexure
caused by occulusal stresses..dentin can withstand the tensile stress better than
enamel…forces are concentrated at the cervical fulcrum
e. Dilacerations – trauma that causes displacement of the already formed hard-
tooth substance in relation to the soft tissue of the remaining developing tooth will
result in a bend of the tooth (dilaceration)…can affect either the crown or the root
f. Concrescence – union of two adjacent teeth by cementum alone without
confluence of the underlying dentin…may be developmental or postinflammatory
g. Germination / fusion– double teeth in both the primary and permanent
dentitions, with a higher frequency in the anterior and maxillary regions
5.
Hypoparathyroidism- delayed tooth eruption….Chovesteks Sign….Dec. Ca2+
Hypothyroidism- delayed eruption
Pituitary dwarfism- delayed eruption
Hypophosphatasia- dec. alkaline phos….inc. urinary phos….like rickets….premature
exfoliation…reduced cementum
Mucopolysaccriodoses- impacted teeth, large follicular spaces…GAG’s.....corneal
clouding, blindness…..Hunters and Hurlers(garoylism)
Ehlers-Danlos- collagen defect…Gorlin sign….dental abnormalities (hyperdontia)
Tuberous sclerosis- facial angiofibromas…..CNS, skin tumors….periunguinal….enamel
pitting
Turner’s Hypoplasia- periapical inflammatory disease of deciduous teeth…..varies with
timing+severity….white-yellowish brown…..affects perm bicuspids…..
Fluorosis-ingestion of excessive amts of F……Brownish yellow appearance…
Syphilis- Hutchingson’s incisors- crowns like screwdrivers…greatest circumference in
the middle 1/3……Mulberry molars- constricted occlusal tables and bumpy surface
projections.
Congenital porphoria- inc. synth and execretion of porphorins….reddish brown, when
exposed to UV light
Hyperbilirubinemia- grayish blue cervical portion more stained
Tetracycline- brownish color in perm dentition
Amelogenesis Imperfecta (AI)- Hypoplastic AI- generalized pin point pinhead sized
lesions scattered on buccal surface of teeth… Hypomaturation AI- snowcapped
mountain….
Dentinogenesis Imperfecta(DI)- similar to Osteogenesis Imperfecta….Shell teeth, normal
enamel, extremely thin dentin and enlarged pulps….more frequent in deciduous teeth..
Minocycline- green to brownish stain
Osteogenesis Imperfecta- type I collagen… opalescent teeth….similar to DI but different
mutation…..shell teeth….wormain bones
Clediocranial Dysplasia- defect in osteoblast differentiation and bone formation…
clavicles absent or hypoplastic…supernumary teeth…lack secondary cementum.
Pagets Disease-hypercemetosis, bulbous roots, “cotton wool”
Gardener’s Syndrome-supernumary, impacted, intestinal polyps
Odontoma- Compound-look like little teeth-anterior……Complex- don’t look like little
teeth-posterior

6. Acidic sources (diet, soft drink consumption and employment in acidic environments)
may cause erosion. Saliva aids by remineralization and contains bicarbonate (buffering
effect) however excess amounts of acid can overwhelm the protective effect of saliva.
-Affects facial surfaces of Maxillary anteriors (shallow spoon-shaped depressions in
cervical region).
-Occlusal surfaces of Posterior teeth and the edges of metallic restorations may be above
tooth structure

Farming in sandy soil may cause abrasion.

7) You prescribe Fluoride, chlorhexidine, etc rinses to patients undergoing radiation

therapy or patients with a high carries index because these agents are used to minimize
plaque buildup so no further bacteria can accumulate. Chlorhexidine gluconate is used to
treat redness, swelling and bleeding of inflamed gums as well.

8)Hypercementosis(p85/86)
 A nonneoplastic deposition of cementum that’s continuous with the normal
radicular cementum
  The pre molar are involved frequently and usually occurs in adulthood and many
cases suggest it to have some hereditary influence
 There are numerous conditions associated with increase cementum deposition but
it’s most commonly seen in Paget’s disease of bone
 Pts. require no treatment only problems encountered are during extraction
Radiographically
 Thickening /Blunting of root surrounded by the radiolucent pdl space and intact
lamina dura
 it appears as “round balls” attached at the apices of the roots

Cemento Osseous Dysplasia(p557-559)

 COD occurs in the tooth bearing areas of the jaws
 Most common to see in clinical practice
 Different types are Focal, periapical, florid

 Periapical COD
 Involves the Anterior Mandibular teeth
 Female’s 10:1 predilection with 70% in Blacks
 Never seen in pts under age 20
 Pulps are vital
 The pdl remains intact
 Does not expand cortex
 Diff. Diagnosis Hypercementosis/cementoblastoma/Radicular cyst or granuloma
Radiographically
 Final result is an opaque mass surrounding a thin radiolucent rim
 It appears as “round balls” attached at the apices of the roots
 Appear as periapical radiolucencies

Cementoblastoma(570-571, 637)
 Odontogenic benign tumor of cemento blasts (neoplastic)
 These are true cementomas not just hypercementosis
 Occur in the post. Md(Molar =50%, Premolar)
 Mostly in children and young adults
 Symptomatic, pain and swelling in 2/3 of patients
 Treated via surgical extraction

Radiographically
 radioopaque mass fused to one or more roots with thin radiolucent line
surrounding the mass
 Root resorption occurs
 The tumor fuses with the tooth so the outline of roots of the involved tooth are
obscured

9) Paget’s disease of bone (pg542)

 Is an abnormal anarchic resorption and deposition of bone
  Bones are distorted and weak with Pain being most common symptom
 The maxilla commonly enlarges needing new dentures frequently
 There’s an increase of serum alkaline phosphotase but normal calcium and
phosphate
Radiographically
 Patchy sclerosis or “Cotton Wool” appearance on lateral skull film

Fibrous dysplasia
 Its a fibrous osseous lesion of the jaw which means:-
1. Replacement of normal bone by fibrous tissue with newly formed
mineralized tissue
2. Is not a specific diagnosis it just describes a process
 Fibrous dysplasia is a non-neoplastic developmental disturbance of bone growth
2 diff. types (Monoostotic/Polyostotic)
Monoostotic=most common form
Polyostotic=Jaffe-Lichens syndrome and McCune –Albright syndrome
Radiographically
 diffuse uniform sclerosis “Ground glass” appearance
 The margins of the lesion blend in to the surrounding bone
 Narrowing of the pdl space
 Jaw lesions are radio opaque

Hyperparathyroidism (pg724)
 Increase pth = increase Serum calcium
 Primary HPT (due 2 adenoma) Secondary HPT (due 2 renal disease) =RENAL
OSTEODYSTROPHY

Primary HPT
Classic Triad (Stones, bones, abdominal groans)
Radiographically
 The Brown Tumor derives its name from the color of the tissue specimen and
appears as a well demarcated uniocular/multiocular radiolucency due to giant cell
resorptive lesions of bone in a long standing disease

Secondary HPT= RENAL OSTEODYSTROPHY

 Causes palatal enlargement
Radiographically
 “Ground Glass” appearance= due to alterations in the trabecular pattern
development, a decrease in trabecular density and blurring of the normal
trabecular pattern occur which causes the ground glass appearance
 A generalized loss of the lamina dura surrounding the roots of the teeth is seen as
an early manifestation.

Osteosarcoma(p574)
  A malignancy of mesenchymal cells that have the ability to produce osteoid or
immature bone
 Swelling, pain, displaced teeth occur
 Increase incidence seen in Paget’s disease of bone
 Mx and Md. Involved with equal frequency
Radiographically
 The classic “Sunburst”/sunray appearance is caused by osteophytic bone
production on the surface of the lesion is noted in about 25 % of jaw
osteosarcoma which is usually seen in an OCCLUSAL x-ray
 An important Early radiographic change in pts.=symmetric widening of the PDL
around the tooth
 Occasionally there is resorption of roots of teeth due 2 the tumor causing a
“spiking” resorption

10. Central Giant Cell Granuloma (benign tumorlike lesion) (pg. 545)
Age: Children and young adults
Gender: Female
Location: Anterior mandible

Brown Tumor (pg. 724) - histopathologically identical to Central Giant Cell Granuloma
Age: Older adults
Gender: Females
Location: mandible; may be solitary but often multiple
11. When considering root resportion, what is physiologic? Pathologic? Does
inflammation influence resportion?

Physiologic resorption is how the primary dentition is shed: it’s the pressure from
the erupting permeating teeth. Pathologic root resorption is due to inflammation,
impacted/unerupted teeth, replanted teeth, neoplasms or idiopathic.
Resportion can be internal which involves odontoclasts from the mesenchymal
pulp cells. Resorption can be external cementoclasts from cells of the PDL , shows as a
“moth eaten” appearance
Inflammation does influence resorption as seen in pathological root resorption.

12. What is the appearance of the incisive canal cyst? Is it the same as the
nasopalatine duct cyst?

An incisive canal cyst is a manifestation of the nasopalatine duct cyst (so the
incisive canal cyst is a type of nasopalatine duct cyst). Radiographically, this cyst appears
as a well-circumscribed radiolucency with a sclerotic rim in or near the midline of the
anterior maxilla between and apical to the central incisor teeth. There is characteristic
root resorption and the radiolucency usually looks like the shape of a heart.
Incisive canal cyst(26-27)
 The incisive canals begin on the
floor of the nasal cavity on either
side of the nasal septum, coursing
downward and forward to exit the
palatal bone via a common foramen
in the area of the incisive papilla; in
addition, the nasopalatine ducts
these canals contain the
Nasopalatine nerves plus other
branches
Nasopalatine duct cyst(26-30)
 Is the most common non-
odontogenic cyst of the oral cavity
 It arises from remnants of the
nasoplatine duct
 Displays the classic “Heart”shape
radiolucency b/x the max. Centrals

13. What would help you distinguish the amber brown crusts of impetigo from the
amber brown crusts of recurrent herpes labialis?

Impetigo is a skin infection that is caused by streptococcus pyogenes and

staphylococcus aureus either separately or together. This condition commonly occurs on
the skin of the face or extremities. Systemic manifestations such as fever are not present.
Recurrent herpes labialis is a viral condition that travels along nerves in an anterograde
and retrograde direction. The easiest way to determine whether or not herpes is present is
to perform a serological test to confirm the presence of virus.

Impetigo Rec. Herpes Labialis

 Due to a Staph/Strep skin infection  The recurrences of HSV-1 occurs
 In young children most commonly on the
 Amber crusts develop on the SKIN VERMILLION BORDER AND
OF THE FACE OR THE ADJACENT SKIN OF THE
EXTREMITIES LIPS(cold sore or face blister)

14. What is the oral appearance of Scarlet fever? Of Wegener’s granulomatosis?

The tonsils, soft palate, and pharynx become erythematous and edematous and the
tonsillar crypts may be filled with a yellowish exudate. The most telling sign of scarlet
fever is strawberry tongue. The most characteristic change of Wegner’s is strawberry
gingivitis – hemmoragic and friable gingiva. There may also be oral ulcerations and also
an enlargement of one or more salivary glands.

15. What is the difference between a tonsillolith and an oral lymphoepithelial cyst?

A tonsillith is a calcified structure that develops in an enlarged tonsillar crypt that

is packed with bacteria and organic debris. A lymphoepithelial cyst is a developmental
cyst that develops from the remnants of the brachial clefts. Clinically this occurs in the
lateral neck along the anterior border of the sternocleidomastoid muscle.
16.Oral manifestations of syphilis:

Primary-chancre (painless, infectious ulceration) develops at the site of injury (can be seen in mouth).
Chancre are common on lip (can be on tongue, palate, gingiva, or tonsils), regional lymphadenopathy.

Secondary-Primary lesion resolves, painless lymphadenopathy, sore throat, mucous patches (30%
patients-sensitive white areas of mucosa, may ulcerate, infectious, multiple lesions in mouth)

Tertiary-More major systemic than oral problems, gumma (active site of granulomatous inflammation
on mucosa; indurated, nodular, or ulcerated; may produce extensive tissue destruction).

Congenital-Tooth malformations-Hutchinson's incisors, mulberry molars.

17.Relationship of ANUG and NOMA

ANUG causes inflammation of dental papilla, resulting in papilla becoming blunted and producing "
"punched-out" craterlike necrosis that are covered with gray pseudomembrane" (pg 140). This can
lead to necrotizing infection and if it spreads through the mucosa to the skin of the face, you get
NOMA.

18.Clinical similarity of Scrofula and Cat-Scratch Disease:

Scrofula-disease caused by drinking contaminated milk

Cat-Scratch Disease-as name implies, bacterial infection from a cat scratch (b/c cats don't wash their
hands after they use the bathroom, thus they are dirty pussies (ha ha ha))

Similarity-caused by bacterial infection, regional (facial) lymphadenopathy (sco-cervical,cat-submand)

19. "Sulfur Granules" and refractory periapical lesions associated with:

Actinomycosis (pg 180)

20.Deep fungal infections, disseminated tuberculosis, and oral squamous cell carcinoma:
All three suck if you have it. The best I can get at is that there is a greater likelihood that patients that
have these diseases might also be IMMUNE COMPROMISED (possible AIDS, especially for the deep
fungal infections and disseminated TB).

21.) What do infections with EBV, VZV, and HSV look like? What are the oral mucosal
lesions called?

All of these viruses are members of the human herpesvirus (HHV) family. Herpes
simplex virus (HSV) is specially a DNA virus and a two types are known to exist: type I
(HSV-1) and type 2 (HSV-2). Other members of the HHV family include varicella zoster
virus (VZV) and Epstein-Barr Virus (EBV).

Epstein-Barr Virus (EBV)-

Most EBV infections (infectious mononucleosis) in children are asymptomatic.

Expressed symptoms in children younger than 4 years of age include -> fever,
lymphadenopathy, pharyngitis, hepatosplenomegaly, and rhinitis or cough. Children
older than 4 years of age are affected similarly (see above symptoms) but exhibit a much
lower prevalence of hepatosplenomegaly, rhinitis, and cough. EBV also establishes a
lifelong dormant infection in some cells of the body's immune system.

Varicella-zoster virus (VZV)-

Chickenpox represents the primary infection.
The symptomatic phase of VZV infection usually begins with malaise, pharyngitis, and
rhinitis. In older children and adults, additional symptoms (e.g. headache, myalgia,
nausea, anorexia, vomiting) occasionally are seen. This is followed by a characteristic,
intensely pruritic exanthem.

Herpes simplex virus (HSV)-

The most common pattern of symptomatic primary HSV infection (90% are the result of
HSV-1) is acute herpatic gingivostomatitis. Most cases of acute herpetic
gingivostomatitis arise between the ages of 6 months and 5 years, with the peak
prevalence occurring between 2 and 3 years of age. The onset is abrupt and often
accompanied by anterior cervical lymphadenopathy, chills, fever, nausea, anorexia,
irritability, and sore mouth lesions. Initially the affected mucosa develops numerous
pinhead vesicles, which rapidly collapse to form numerous small, red lesions. These
initial lesions enlarge slightly and develop central areas of ulceration, which are covered
by yellow fibrin.

22.) A morbilliform viral exanthem (skin rash) is associated with gray-white “salt grain-
like” oral mucosal lesion (enanthem). What is it?

Rubeola (Measles) is an infection produced by a paramyxovirus and exhibits a variable

prevalence that is correlated to the degree of vaccine use. Lesions, known as Koplik’s
spots, are the most distinctive oral manifestations of measles and develop early in the
course of the infection. Multiple areas of mucosal erythema are visible on the buccal and
labial mucosa or less often on the soft palate; within these areas, there are numerous
small, bluish-white macules. In addition, similar spots are noted rarely on the inner
conjunctival folds of the eye or the vaginal mucosa. These pathognomonic spots
represent foci of epithelial necrosis and have been describe as “grains of salt” on a red
back-ground. The height of the mucosal eruption occurs just as the exanthem begins to
develop and spread.

23.) A patient with a white “milk curd-like” pseudomembrane, purple maculopapular

lesions, white vertical plaques on the lateral border of the tongue, and persistent herpes
labialis suffers from what? What is the reason for the multi-pronged infectious
onslaught?

This patient is experiencing the best recognized form of candidal infection:

pseudomembranous candidiasis. Also, known as “thrush,” pseudomembranous
candidiasis is characterized by the presence of adherent white plaques that resemble
cottage cheese or curdled milk on the oral mucosa. The white plaques are composed of
tangled masses of hyphae, yeasts, desquamated epithelial cells, and debris. Also, note the
immune dysfunction seen in leukemic patients or those infected with HIV are often
associated with pseudomembranous candidiasis.

24.) Periodontal disease is a finding in cyclic neutropenia, AIDS, vitamin C deficiency,

uncontrolled diabetes mellitus, and Papillon-Lefeve syndrome. Why?

Cyclic Neutropenia: Characterized by regular periodic reductions in the neutrophil

population of the affected patient. When the neutrophil count is low, the patient
experiences problems with infection. From this clinical findings consist of oral
ulcerations develop on any oral mucosal surface that is exposed to even minor trauma.
Also, within the oral cavity the ginigiva is affected with severe periodontal bone loss with
marked gingival recession and tooth mobility.
AIDS: With a subsequent decrease in T-helper cells a resultant loss of immune function
takes place. The normal response to viruses, fungi, and encapsulated bacteria is
diminished.
Vitamin C deficiency: responsible for collagen synthesis (deficiency leads to scurvy,
poor wound healing, periodontal disease, capillary fragility, scorbutic gingivitis
Uncontrolled Diabetes Mellitus: microangiopathy, failure of neutrophilic migration
Papillon-Lefeve Syndrome: Mutation of the cathepsin C gene. This gene is important
in the structural growth and development of skin and is critical for appropriate immune
response of myeloid and lymphoid cells. Loss of appropriate function of this gene is
thought to result in an altered immune response to infection. In addition, the altered gene
may affect the integrity of the functional epithelium surround the tooth. From this teeth
are found floating in soft tissue due to extensive loss of alveolar bone.

25.) An African-American patient with a “hair on end” radiographic appearance on a

lateral skull film suffers from what? Why the “hair on end” appearance?
There are 2 conditions that could have the same background (African-American descent
& “hair on end” appearance)…
Sickle cell anemia: A condition that results in a hemoglobin molecule that, in the
deoxygenated state, is prone to molecular aggregation and polymerization.
Consequently, the red blood cells of patients with sickle cell anemia have a marked
tendency to undergo deformation from the normal biconcave disc shape to a rigid-and-
curved (sickle) shape. Is seen most frequently in populations, such as African,
Mediterranean, and Asian.Oral radiographic features of sickle cell disease are relatively
nonspecific. The consist of a reduced trabecular pattern of the mandible because of
increased hematopoiesis occurring the marrow spaces… “hair-on-end” appearance is seen
on the skull radiograph.
Thalassemia: represents a group of disorders of hemoglobin synthesis that are
characterized by reduced synthesis of either the alpha-globin or beta-globin chains of the
hemoglobin molecule. As those with sickle cell trait, increased frequency in
Mediterranean, African, Indian, and Southeast Asian populations. When two defective
genes for the beta-globin molecule are inherited. The disease is usually detected during
the first year of life because a severe microcytic, hypochromic anemia develops when
fetal hemoglobin synthesis ceases after 3 to 4 months of age. The red blood cells that are
produced are extremely fragile and survive for only a few days in the peripheral
circulation. In an attempt to maintain adequate oxygenation, the rate of hematopoiesis is
greatly increased, resulting in massive bone marrow hyperplasia…why the skull
radiograph shows a prominent “hair-on-end” appearance of the calvaria.

26.Leukemia, thrombocytopenia, and anemia have what oral consequences?

Leukemia:
Petechiae(pinpoint hemorrhagic lesions) of hard and soft palate
Spontaneous gingival hemorrhage
Deep, punched out ulcerations
Candidiasis and/or herpetic lesions on any surface (due to lower immune defense
cell)
Diffuse gingival enlargement with patients with (monocytic leukemia)
Ulcerated soft tissue nodule of the hard palate
Thrombocytopenia
Initially detected because of the oral lesions
Petechiae
Ecchymosis (bruise)
Hematoma (hemat= blood, oma= tumor)
Anemia
Oral mucosa may appear pale because of the decreased number of red blood cells.
Oral ulcers because of the infection may appear involving the gingival tissue. Gingival
hyperplasia may be also reported.

27. Punched out radiolucencies are associated with what.

Multiple Myeloma
 malignancy of plasma cells with multicentric involvement. Punched out or ragged
radiolucencies. Look for Bence Jones proteins in urine
Langerhans cell histocytosis
Punched out or scooped out radiolucencies usually in alveolar bone. Teeth appear
to be floating in air.( im not sure about the punched out thing, key is floating in air).

28. list and describe reactive lesions of the gingival in denture patients. In dentate
females.

Epulis fissuratum (inflammatory Fibrous hyperplasia)- Hyperplasia of fibrous connective

tissue that develops with ill-fitting dentures. Appears as single or multiple folds on facial
alveolar vestibule.
Inflammatory Pappillary Hyperplasia (Denture Papillomatosis) – Blebs or Cobblestone
like bumps of tissue usually on palate due to 24 hrs denture wearing, poor denture
hygiene
Denture Stomatitis- classified as erythematous candidiasis(chronic atrophic candidiasis).
Sometimes accompanied by petechial hemorrhage, localized to denture-bearing areas of
maxillary removable denture prosthesis. Patient wears denture continuously. May or
may not be associated to Candida albicans.
Pyogenic granuloma- affects pregnant females. Pink to red to purple color. Usually on
gingival, lip, tongue and buccal mucosa. Smooth or lobulated mass.

29. Why do smoking, xerostomia, diabetes and denture wear predispose to

candidiasis.
All theses seem to be associated with decreased cleansing and antimicrobial activity
normal to saliva.

30. What are the characteristics of recurrent aphthous stomatitis?

Occurs on non-keratinzed mucosa, Fiery red halo, occurs in stress time
Minor-80%, 4-6mm, 7-10 days duration
Major- 1cm, 4-6 weeks duration, scaring
Clusterform(herpetiform)- 2-3mm, 10-100 lesions, may extend into keratinzed tissue.

31. What forms of aphthous ulcers take, nad how are they distinguished from herpes
simplex lesions?
Aphthous ulcers occur on non-keratinized epithelium.

Minor Aphthous Stomaatitis- Most common form (80%); 1-5 painful ulcers between 3-
10mm; fewest recurrences (once per few years or twice per month); ulcers heal w/o scar
in 1-2 weeks.

Major Aphthous Stomaatitis aka Suttons Diesase- 1-10 ulcers between 3-10cm; heal with
scarring in 2-6 weeks.
Herpetiform Aphthous Ulceration- up to 100 ulcers between 1-3mm, which may
coalesce; resembles herpetic lesions but found on non-keratinized mucosa; heal in 7-10
days but common recurrences.

HSV lesions – fragile vesicles cluster on keratinized epithelium.

32. What is the purpose of staging oral SCC?

Staging is based on tumor size and metastatic spread. T= tumor size (cm) N=extent of
local nodal involvement M= distant mertastais. Staging is important b/c best predictor of
prognosis.

33. What does dysplasia mean?

Dysplasia is abnormal growth or development.. It is associated with increased nuclear to
cytoplasm ration, bit and prominent nucleoli, hyperchromatasia, pleomorphism,
dyskeratosis, and abnormal mitotic figures. Specifically in epithelium: budding of rete
ridges, loss of polarity, keratin pearl formation, and loss of cohesiveness.

34. The prognosis of melanoma depends on what?

For cutaneous lesions, th emost important prognostic indicator is histologic depth of
invasion. Oral melanoma has extremely poor prognosis and usually dies from distant
metastasis. .

35. What lesions are produced by HPV?

Squamous papilloma, Veruca Vulgaris aka common wart, Condyloma Acuminatum aka
venereal wart, Heck disease aka Focal Epithelial Hyperplasia, Sinonasal papilloma, and
Fungiform papilloma.

36) What is the significance of leukoplakia? Of Erythroplakia?

Leukoplakia is defined by the WHO as “a white patch that cannot be characterized

clinically or pathologically as any other disease.”
 considered premalignant since they are associated with a greater than
normal risk of malignant transformation
 lifetime risk of malignant transformation is 4% or more
 causes: tobacco, use of sanguinaria-containing products, UV radiation,
microorganisms
 “high risk” areas: tongue, lip, or floor of the mouth
 start as gray-white plaque which may disappear spontaneously; if
continues to grow, it becomes thicker and the surface corrugated,
wrinkled, or fissured
 biopsy worst areas
Erythroplakia is defined as a red patch that cannot be clinically or pathologically
diagnosed as any other condition.
 90% show severe dysplasia, carcinoma in situ, or carcinoma
 most common sites: tongue, soft palate, floor of the mouth
  biopsy

37) Mucous escape reactions cause psuedocysts known as what?

Mucoceles

38) What is a blue-gray, domed mass in the floor of the mouth?

Ranula

39) What is a creamy white, dome-shaped, doughy mass in the floor of the
mouth?
-lipoma

40) Sialoliths are common in the submandibular duct. Why? What radiographs
are necessary if you suspect a submandibular sialolith?
-Most common in the submandibular duct because of the long, tortuous, upward
path of Warton’s duct and the thicker, mucoid secretions of this gland may be
responsible for its greater tendency to form salivary calculi
-Occlusal radiographs best demonstrate submandibular sialoliths

41. What are the characteristics of Sjorgens Syndrome?

It is an autoimmune disease that is not considered to be hereditary. Patients form antibodies to

salivary, lacrimal, and other exocrine glands. There are two forms, primary and secondary. Primary
presents with xerostomia and xeropthalmia. Secondary presents with these two PLUS a connective
tissue disease, usually rheumatoid arthritis. Sjorgens syndrome can occur in conjunction with SLE.
Histologically, it presents as a "fruit laden branchless tree." It is usually diagnosed by testing for Anti
SSA-Anti Rho & Anti SSB-Anti La antibodies. A biopsy of labial salivary glands may be helpful but are
not 100% reliable. The xeropthalmia can produce blurred vision, a gritty sensation, and can be
diagnosed with a schirmer test.
Patients with Sjorgens Syndrome have a 40X greater risk of developing lymphoma.

42. The S-100 protein positive tumor tthat causes a firm nodular mass, commonly on the tongue, is a
what? Granular Cell Tumor

43.What vascular lesions are common in children? In adults? In children, hemangiomas are the most
common benign neoplasm of infancy. In adults, pyogenic granulomas along with telangiectasias (port
wine stains: big telangiectasias), are common. In either case, they may or may not be associated with
another disease or local factors (Port wine stains are associated with Sturge Weber). Lymphangiomas
can also be common in both populations.

44.The most common benign salivary gland tumor is what? Pleomorphic Adenoma

45. The most common malignant salivary gland tumor is what? Mucoepidermoid Carcinoma

46. What salivary gland tumors commonly occur in the palate? In the sublingual
gland? In children?
On the palate: pleomorphic adenoma and mucoepidermoid carcinoma
(parotid>palate>buccal mucosa)
Sublingual gland: none mentioned in the notes
In children: mucoepidermoid carcinoma
47. What benign parotid salivary gland lesion is commonly associated with
smoking? Why is there abundant lymphoid tissue associated with the lesion?
Warthin’s tumor (aka papillary cystadenoma lymphomatosum) is 8X more likely in
smokers, also the 2nd most common benign parotid tumor. Traditionally thought to arise
from heterotopic salivary gland tissue found within parotid lymph nodes.

48. Describe the survival pattern of adenoid cystic carcinoma. Why does it vary
over 5, 10 and 15 years? What is important about peri-neural invasion?
Because the tumor is prone to late recurrence and metastasis, the 5-yr survival rate has
little significance and does not equate to a cure. The 5-yr survival rate may be as high as
70%, but this rate continues to decrease over time. By 20 years, only 20% of patients are
still alive. Peri-neural invasion corresponds to the common clinical finding of pain in
these patients, but peri-neural invasion is NOT pathognomonic for this disease entity.

49. How would you characterize and what are the associations with:
All 4 are asymptomatic and well-defined.
a. Dentigerous cyst: MOST common developmental odontogenic cyst, dervied from
reduced enamel epithelium, mand. 3rd molar, crown of unerupted tooth, 2-4 cell layers
thick, unilocular, enucleation/marsupialization
b. Odontogenic keratocyst: developmental cyst, derived from dental lamina, mostly
posterior body/ramus of mandible, grows anteroposteriorly, if multiple  nevoid basal
cell carcinoma? uni/multilocular, 6-8 cell layers thick, difficult to enucleate
c. Periapical cyst: MOST common cyst of the jaw bone, dervied from rest of malassez,
NON-vital tooth with loss of lamina dura and +/- root resorption, contains calcification
and cholesterol clefts, extract with curettage, RCT or complete removal
d. Lateral periodontal cyst: adjacent to a VITAL tooth, mostly mandibular lateral-
canine-premolar region, enucleation. Polycystic variant  Botryoid odontogenic cyst.
Glandular feature that is aggressive and mostly in anterior jaws  glandular odontogenic
cyst.

50. What are the oral manifestations of:

a. Cleidocranial dysplasia: high/narrow palatal vault, mandibular prognathism, primary
teeth retained longer, delay/failure of eruption of teeth, supernumerary teeth.
b. Gardner syndrome: multiple osteomas at gonion region, odontoma, supernumerary
teeth, impacted teeth
c. Osteopetrosis: infant: delayed tooth eruption and facial deformity; adult: increased
bone density
d. Central giant cell granuloma: more common in mandible, 1st molars or regions
anterior to it; non-aggressive: no perforation or root resorption; aggressive: pain, bone
expansion, cortical perforation, root resorption
e: Simple bone cyst: more common in mandible, asymptomatic, some show swelling,
may scallop up between roots, vital teeth without root resorption
f: Aneurysmal bone cyst: mean age 20 yrs when occur in the jaw, mostly posterior jaw,
rapid swelling
g: Cemento-osseous dysplasia: 1). Focal: posterior mandible, asymptomatic. 2).
Periapical: anterior mandible, vital tooth, asymptomatic, PDL intact, does not expand
cortex. 3). Florid: all for quadrants, multifocal, asymptomatic.

51. Most significant odontogenic tumor: Ameloblastoma, a benign

aggressive neoplasm. Well circumscribed, multilocular
radiolucency, soap bubble or honeycomb, may be unilocular!!
Marked tendency to recur. POSTERIOR Mandible,

The unicystic type is much less aggressive than the solid type and
accounts for about 10% of all ameloblastomas. It occurs in younger patients around 18
to 20 years of age with a strong predilection for the posterior mandible. Almost 90% of
cases are associated with the crown of impacted third molar teeth with the radiographic
presentation similar to a dentigerous cyst. This type of ameloblastoma can arise from
a dentigerous cyst or de novo next to a cyst. The former is more commonly seen. In
about 10% of cases, it can present as a unilocular radiolucency simulating a residual
cyst, periapical, primordial cyst or Odontogenic keratocyst (OKC).
Radiographically, it is unilocular and corticated radiolucency and at times, the margins
are scalloped, simulating an OKC.
52.

Adenomatoid
Odontogenic
Tumor

Snowflake mineralizations
Calcifying
Epithelial
Epithelial
Odontogenic
Tumor
(Pindborg
tumor)

Amyloid calcified concentric rings

Flocculent radiopacity
Leisegang rings
Ameloblastic
fibro-
odontoma

Mixed radiopacities
Odontoma

Compound odontoma: tooth like radiopacities

Odontoma

Complex odontoms: disorganized radiopacities

Central Radiopaque flakes
odontogenic
fibroma
Calcifying Radiolucency with progressive calcification
Odontogenic
Cyst

NO calicification with Ameloblastic Fibroma odontogenic tumors

53. Ameloblastoma unicystic variety
Calcifying odontogenic cyst (gorlin cyst)

54. AOT: Odontogenic Adenomatoid Tumor

This is a totally innocuous odontogenic tumor which is locally expansive but which does
not infiltrate and does not recur. It can be treated by simple enucleation. F>M, <20yrs.,
MX>MD, Asymptomatic swelling often surrounds crown of impacted tooth (canine).
Well defined unilocular or multilocular. Tongues/strands of odontogenic epithelium
embedded in myxoid CT that resembles dental papilla or pulp.

55. Oral features of Reiter’s:

 Warning signs include stiff, tender joints. Usually only a few joints are affected. Most
often Reiter's syndrome affects the knees, ankles, feet, and wrists. You may also have
any of the other warning signs.
 Sore muscles.
 Pain in the lower back, or on the heel or bottom of the foot
 Possible mild fever.
 Frequent or painful urination.
 Dull pain in the pelvic area.
 Red, sore eyes. Sometimes the eyelids may stick together in the morning.
 Blurred vision.
 Sores in the mouth. These may be painful or painless.
 Thick, crusty red-purple sores on the palms of the hands or the soles of the feet.
 Sores on the genitals. These may be painful and can become infected.

Oral features of Behcet’s :

Almost everyone with this syndrome has recurring,
painful mouth sores, similar to canker sores. Sores
may also appear on the penis, scrotum, and vulva
and tend to be painful;

56. List the lip and cutaneous (skin) lesions associated with sun (actinic) exposure.
Basal Cell Carcinoma, Melanoma, Seborrheic Keratosis, Actinic Keratosis,
Keratoacanthoma, Leukoplakia, Actinic Cheiliosis (this is a broad question so there may
be some conditions I can be missing)
57. What are the similarities and the differences between:
a. Pemphigoid
b. Pemphigus
c. Lichen Planus
Pemphigoid:
- Autoimmune disease
- Desqaumative gingivitis is a feature
- Positive Nikolsky sign
- Vesiculo Bullous Disease
- Eye lesions (scarring of lid to conjuncitva)
- When bulla ruptures you obtain a raw red surface with a grey white
membrane
- Subepithelial seperation
- Greater resistance to being broken
Pemphigus:
- Uncommon Autoimmune disease
- More severe than Pemphigoid
- Positive Nikolsky sign
- Vesiculo Bullous Disease
- Intraepithelial seperation therefore vesicle is easier to break
- Bulla eruption yields jagged edges along with grey white membrane
- Tzanck cells
- “Tombstones” appearence
- Basal Cell Layer remains adherent to lamina propria
Lichen Planus
- “Civatte Bodies”
- Immunologically mediated
- Desquamative gingivitis
- White stria, white plaques, Wikham’s stria
- “Saw tooth” rete pegs
- T-lymphocyte infiltrate
- Contact with amalgam worsens lesion
- Degeneration of Basal Cell Layer

58. Radiolucencies of jaws, bleeding tendency, discoloration, gingival enlargement,

ulceration and macroglossia may be oral manifestations of systemic disease. Why?
Radiolucencies of the jaws: Multiple myeloma will result in punched out lesions of the
jaws (along with the skull), Non-hodgekin’s lymphoma, Burkett’s Lymphoma = teeth
floating in air,
Bleeding tendancy – vit. C, vit K deficiency, liver disease, Epidermolysis bullosa,
Hemophillia,
Discoloration-
Red- pyogenic granuloma, hormonal imbalance, Erosive lichen plannus
White = candadiasis = sometimes HIV,
Purple- lichen Plannus,
Gingival enlargement- gingival hyperplasia (dilantin (Anticonvulsants), Nifedipine (Ca++
channel blockers, Cyclosporin (Immunosuppressants), look at “Pulp 4” in the manual
Ulceration- apthous stomatitis, pemphigoid, pemphigus, erosive lichen plannus, crones
disease.
Macroglossia- Mekersons- Rosenthal syndrome, cretinism, neurofibromatosis, Beckwith
Widimenn Syndrome, Downs Syndrome,

59. What diseases are associated with pyostomatitis vegitans? With “snail trail” ulcers?
Inflammatory Bowel Disease
Crohn’s Disease
Ulcerative Colitis

60. What is:

a. Bell’s palsy
b. Frey Syndrome
c. Eagle Syndrome
d. Temporal arteries

Bell’s Palsy:
- motor neuron paralysis of CN 7-facial nerve
- due to HSVl in Geniculate ganglion
- triggered by cold, infection, trauma, pregnancy, Melkersson Rosenthal
Syndrome, ischemia at stylomastoid foramen
- abrupt loss of facial control on ONE side
- loss of taste, mass like appearence

Frey Syndrome:
- results from injury to Auriculotemporal Nerve, nerve regenerates in
misdirected pathway
- sensory to preauricular and temporal
- parasympathetic to parotid
- sympathetic sweat stiumulating fibers to preauricular skin
Eagle Syndrome:
- calcified stylohyoid ligament
- pain on turning head
Temporal Arteritis
- multifocal vasculitis of cranial arteries
- begins as Unilateral throbbing headache
- replaced by burning throbbing pain
- muscle pain and stiffness
- erythrocyte sedimentation rate is elevated
blindess occurs if untreated

61. Features of Nevoid Basal Cell carcinoma: also known as GORLIN syndrome, an inherited
syndrome characterized by multiple Basal Cell carcinomas(100s), Odontogenic Keratocysts,
Palmar/Plantar pits, Calcified Falx cerebri, Bifid ribs, Spina bifida
- may show Frontal bossing, Hypertelorism(wide-set eyes)
- OKCs tend to develop at a younger age
- mutation in PTCH gene, a tumor suppressor gene

62. Histological features of:

OKC-Parakeratinized cyst lined by a uniform layer of epithelium (6-8 cells thick) with a palisaded and
hyperchromatic basal cell layer, satellite cysts may be present within wall (pg 598).

Ameloblastoma:
conventional-mixed cystic and solid areas, nests and sheets of cells (surrounded by mature fibrous
tissue), peripheral cells of nests are columnar with nuclei polarized away from basement membrane
(reminiscent of enamel organ epithelium) (pg611-619).

CEOT-Islands,strands, and sheets of polyhedral epithelial cells, nuclei may show prominent
pleomorphism, large areas of hyalinized, eosinophilic material (amyloid), in amyloid material-get
distinctive calcifications with concentric rings.(pg 624)

Lichen Planus-*"saw-toothed" rete ridges, hydropic degeneration of basal cell layer with colloid bodies
(Civatte bodies), and a dense band-like infiltrate of lymphocytes below the basal cell layer, +/-
hyperkeratosis.

63. Lesion located at ange of mandible, beneath inferior alveolar canal, well-delineated radiolucency:
Stafne Bone defect

64. Lesions that push/displace teeth(erupted or unerupted) may be interepreted as a benign

process(although as you know there are slight exceptions to everything in pathology). Examples
include Ossifying Fibroma(erupted or unerupted), Dentigerous cyst, Calcifying Odontogenic/Gorlin
cyst, OKC, and inflammatory Paradental cyst(last 4 are assoc. with unerupted teeth). Ameloblastoma,
odontogenic myxoma, and brown tumors of renal osteodystrophy can be associated with tooth
displacement.
Lesions that cause spiking resorption of teeth suggest the presence of a malignant disease.
Normally a malignant process is too rapidly destructive to resorb teeth, but in cases with
chondrosarcoma, osteosarcoma, and myeloma a spiking resorptive pattern can be seen.
*little extra bonus - resorption of one or several teeth in association with an adjacent lesion is a sign of
a benign process with a more aggressive growth pattern, and RARE occasions a slow malignant
growth pattern. KNIFE EDGE resorption - AMELOBLASTOMA, resorption along MULTIPLE ROOT
PLANES - CENTRAL GIANT CELL GRANULOMA.

65. Multilocular radiolucencies - Ameloblastomas(Honeycomb initially, then soap bubble),

Odontogenic myxoma(Tennis racket), OKC(scalloped), Central Giant Cell
granuloma(multilocular/scalloped), Calcifying Epith. Odontogenic Tumor/Pindborg tumor(scalloped),
Clear cell odontogenic carcinoma(50/50 multi/uni).
*seen in association with locally aggressive benign conditions. Multilocular helps rule out
malignancy(exception - central mucoepidermoid carcinoma and clear cell odontogenic carcinoma)
*NOTE: Peripheral Giant Cell granuloma produces a saucerization/cupping of underlying bone.