Pathology Test I Diseases: 1

Pathology Test I Diseases:

Cherubism
Gardner syndrome
Epidermoysis Bullosa
Regional odontodysplasia
Progressive Hemifacial Atrophy
Primary herpetic Gingiovostomatitis
Acute Pseudomembraneous Candidiasis
Histoplasmosis

Squamous cell Carcinoma

Kaposi Sarcoma
Acute Leukemia
Ameloblastoma
Acromegaly
Hypothyroidism
Recurrent aphthous stomatitis-minor aphtha
Mucous membrane Pemphigoid
Desquamative gingivitis

Auto-immune Throbocytopenic purpura

Allergic contact stomatitis

Contact mucositis to nickel
Factitial injury

Sialadenosis in Bulimia
Sialadenosis in alcoholics
Epithelial hyperplasia
Fibrous hyperplasia
Inflammatory Papillary hyperplasia
Osseous hyperplasia
Sub-Pontic osseous hyperplasia
Hyperplatic dental follicle

DEVELOPMENTAL DISEASES:
Autosomally dominantly inheritedhave large jaws
See dense lesions in the jaw bone autosomally dominantly inherited; polyps in the
colon
Suffer a lot and phalanges on hands and feet often will fuse together
Teeth in specific segment of the arch are affected; large pulp chambers
Rhomberg Syndrome
INFECTIOUS DISEASES
Swollen sore gums with ulcerations on the mucosa (start as blister; ulcers are
white in the mouth)
Easily treated
This is a yeast from the environment; systemic fungal infectionfarmer that
chased chickens ex where developed pulmonary histoplasmosis
NEOPLASTIC
Lateral border of the tongue is the most common site for cancer
Uncommon until HIV and is virally induced
Liquid cancer of the bone marrow; gingiva packed with WBC is an example
Looks like black hole in the jaw
METABOLIC
Growth hormone-secreting pituitary adenoma; an excess of GH secreted after the
closure of the growth plates
Threat by deal with the pituitary adenoma
Short stature; generalized delayed dental eruption
IMMUNE MEDIATED
Canker soresimmune cells congregate beneath the mucosa and cause a
laceration to show the canker sore
Specific type of gingivitis that is known to be associated with a variety of diseases,
on of which is Pemphigoid (blistering disease)
Can see pustule that is a diagnostic sign of the disease
Can also see scar tissue in the eyecausing adhesion bands and in serious
cases blindness
See a separation in the epithelium and CT
See red spots all over the soft palate and the uvula representing bruising in those
areas; also see small hemorrhages on their skin because they form Abs against
their plateletsresults in significant decrease in platelets, can show up as large
bruises, and Ab platelets go to spleen which then enlarges and undergoes
hypertrophy
Lesion on the buccal mucosa
EX: Represents an allergic response to continual exposure to cinnamon gum
Rare allergy to nickel, can get with ortho bands/wires
Inflict injury on yourselfclass ex was brushing too hard and shows roots of the
teeth
HYPERTROPHY
Hypertrophy of the parotid glands even calluses on knuckles
Enlargement in salivary glands
HYPERPLASIA
Increase in the number of squamous cells you see pedunclated sore on the tip
On edentulous maxillary ridge you see irritation and proliferation of the fibrous CT
See a number of cobblestone bumps on the palate
Can see multiple firm sessile modules of bone growing from the maxillary alveolar
process
The level of bone under the pontic of a bridge grew
Can cause loosency around the tooth

Pathology Test I Diseases: 2

Hemifacial hyperplasia
Condylar hyperplasia
Gingival hyperplasia
Progressive hemifacial Atrophy (Romberg
syndrome)

Barrett esophagus
Necrotizing Sialometaplasia

Mandible-facial dysplasia Treacher Collins

Agenesis of multiple teeth
Pierre-Robin Sequence (complex/syndrome)

Ectodermal dysplasia
Osseous dysplasia
Fibrous dysplasia
Dentin dysplasia
Epithelial dysplasia
Precosiuos Periodontitis
The papillon-LeFerve syndrome

Brutons X-linked agammaglobulinemia

IgA deficiency
Hyper-IgM syndrome
Common variable immune deficiency (CVID)
DiGeorges Syndrome

Half of the face has enlargement of soft tissues and bone

Idiopathic unilateral growth of the mandibular condyle
Can lead to facial asymmetry
Height of mandible increased
Due to poor oral hygiene and or diabetes
Can be drug induced or inflammatory hyperplasia
ATROPHY
Slowly progresses over time
Atrophy of the soft tissues of the face they were symmetric at one time, bust
wasted away overtime
METAPLASIA
Has intestinal metaplasia in the esophagus
The normal squamous epithelium has undergone metaplasia and you can see a
change in the epithelium
Occurs in the oral cavity
Presents generally on the palate due to death of the minor salivary glands
The ducts of the necrotic salivary glands line by cuboidal columnar epithelium
undergo squamous metaplasia
APLASIA AND AGENESIS
Developmental defects of the 1st and 2nd brachial arches
External and middle ear defectsfrequently deaf
Teeth just dont develop
HYPOPLASIA
Mandibular hypoplasia
Palatal cleft
Glossophtosistongue doesnt drop and palatal shelves dont fuse
DYSPLASIA
x-linked inheritance
defective epidermal structures
Periapical cemento osseous dysplasia
There is replacement of normal bone with fibrous CT which causes an
enlargement of the jaw
Crown is formed normally but the root isnt
A precancerous change in the epithelium
INFLAMMATION/IMMUNITY
Dont have integrinscant stick to the epithelium
Impaired response for WBC to kill pathogens
Nonfunctional B2 integrins Mac-1 and LFA-1
Autosomal recessive inheritance
Prepubertal periodontitis (childhood onset)
Plamer/planter hyperkeratosis
Have a cathepsin C deficiency
HUMORAL DEFECTS
Affects maleslyonization protects females
Little/ no Ab failure of b lymphocytes maturation
Most common immune deficiency
Defect in differentiation of IgA secreting proteins
x-linked defect in switching from IgM to IgG and IgA
High IgM levels no IgG or IgA
Inherited or acquired abnormalities in producing all Ab classes
Treated by IV antibodies
CELLULAR IMMUNITY DEFECTS
Congenital absence of structures of the 3rd brachial pouch and 4th pharyngeal
pouchno thymus or parathymus and therefore NO cellular immunity

Pathology Test I Diseases: 3

patients will have hypoparathyroidism

Bare lymphocyte syndrome
Failure of APCs to express MHC II molecules due to mutations in genes for their
synthesis
B lymphocyte, macrophages, dendritic cells all lack MHC II molecules and cannot
present protein Ag to CD4 lymphocytes
Severe combined immune deficiency (SCID)
Defective development of both B and T cells
Lethal because lack both forms of immunity
AIDs
Failure due to HIV leading to death of CD4 lymphocyte
Both arms will fail (just cellular fails first)
OTHERS
Leukocyte adhesion molecule deficiency
No expression of integrins or selectins
(LAD)
Kids get prepubertal periodontitis (sometimes)
Chronic granulomatous disease of childhood
x-linked and autosomal recessive
mutation in genes encoding enzyme NADPH-Oxidase (which converts oxygen to
superoxide)
HOCl, major killing molecule, not formed
Chediak-Higashi syndrome
Characterized by oculocutaneous albinism and defects in humoral immune system
Failure of fusion between lysosome and phagosome
TYPE II HYPERSENSITIVITY REACTIONS
ITP
Develop antibodies against your plateletsso spleen takes the platelets out and
destroys themtreated with immune suppressing drugs
Mucous membrane Pemphigoid
IgG antibodies are made against ECM protein
Get inflammation and blistering
Myasthenia gravis
Muscle weakness disease
Can have tumor of the thymus associated with it
Sjogrens syndrome
Salivary glands swell in of people (parotid gland)
Immune system fails to recognize something in the salivary glands and becomes
intolerant to them in the ductal cells and then it destroys the glands (salivary and
lacrimal)
CD4 lymphocytes replace secretory cells
No saliva or IgA prone to xerostomia, dry eyes etc
TYPE III HYPERSENSITIVITY REACTIONS
Systemic lupus erythematosus
Mother of all autoimmune diseases
90% are female
Main problem is kidney diseasecauses problems with renal tubules
Form an antibody against your own blood cells (erythrocytes and platelets)
Post-streptococcal glomerulonephritis
Fails to recognize a whole host of tissues
Proinflammatory fragments of the complement system trigger a robust
inflammatory response that damages tissue
Streptococcal pharyngitis
After patient has this they will have blood in their urine
HUMAN HERPES VIRUS (HHV) FAMILY
Varicella Zoster Virus
Primary infection is varicella secondary is zoster
Characterized by skin eruptions/vesicles/blisters
Varicella
Transmission by inspiration of infected droplets
Skin lesions begin on face/ trunk
Vesicles in repeated waves
Heal without scarring
Oral mucosal lesion can occur it would be unusual to see oral lesion without
skin lesions
Zoster
Virus can be reactivated follow down the peripheral nerves and affects the body
at specific dermatome regionscausing a skin eruption and gives vesicles
Recurrent infections and can cause post-herpatic neuralgia
Epstein Barr Virus
Most adults are EBV +, Latency, Infects epithelial cells of oral mucosa
Tropism for B lymphocytestypically in waldeyers ring

Pathology Test I Diseases: 4

Cytomegalovirus

Association with human disease infectious mononucleosis, B cell non-Hodgkin

lymphomas (Burkitt lymphoma), nasopharyngeal carcinoma, oral hairy leukoplakia
Most of pop infected by 60 years
Most infections are asymptomatic
Acute infection: similar to infectious monocleosis, heterophile antibody negative,
rarely acute sialdentitis with painful swelling and xerostomia

Human herpes virus

Coxsackie virus infections:
Herpangina
Measles (Rubeola)

Infectious mononucleosis

Infectious parotitis (Mumps)

Histoplamosis

Disseminated histoplamosis

Coccidioidomycosis

Sarcoidosis

TB

Primary TB

Secondary TB

OTHER INFECTIONS
Constitutional symptoms
Begins as small vesicles that rupture and ulcerate
Posterior oral cavity and oropharynx
NOT caused by Herpes virus
Childhood infection
Communicable disease
Skin rash
MMRimmunization
If oral lesions getKoplik spots (grains of salt on an erythematous base)
Debilitating EBV infection
Self-limiting, occurs in young adults, salivary transmission, fatigue, malaises,
lymphadenopathy, lymphocytes NOT monocytes, can have pinpoint hemorrhages
on the palate, ANUG, symptomatic, heterophile antibody
Endemic parotitis, Childhood disease, Spread by droplets, 30% of subclinical
infections, Salivary gland swelling and discomfort, Elevated serum amylase,
sterility and hearing loss
FUNGAL DISEASE
Endemic to Mississippi River valley
Transmission by inhalation of spores
Sub-clinical infection usual
Flu-like symptoms, phagocytosis, specific immunity, killing of organisms, dystrophic
calcification, dimorphic fungus
Elderly, debilitated, immunosuppressed
Spreads to extra-pulmonary sites
Adrenal lesionsAddisons disease
Oral lesions
Coccidioides immitisexists as tiny structure in a larger circular structure
San Joaquin Valley Fever
Deep fungal infection of the lungs
GRANULOMATOUS DISORDERS
Multi-system granulomatous disorder
Hilar lymphadenopahty, skin and eye lesions
NON-caseating
Do a diagnosis of exclusion, Oral lesions are uncommon, Parotid enlargement,
xerostomia, facial nerve weakness
Treatment: mildobservation, no treatment, may resolve spontaneously, severe
system corticosteroids
BACTERIAL PATHOGENS
Mycobacterium tuberculosis; CASEAOUS NECROSIS
Pulmonary infection most common, IC pathogen, 1/3 of pop infected, leading
infectious cause of death behind AIDS
Transmissiondroplet nuclei
Previously unexposed person
Gohn complex (parenchymal lung lesion and hilar nodal lesion)
Cell-mediated immunity controls the infection
Fibrosis and calcification, viable organisms dormant in lesions (latent disease)
Reactivation of dormant primary lesions in a previously sensitized host

Pathology Test I Diseases: 5

Miliary TB
Scrofula
Acquired syphilis

Primary syphilis
Secondary syphilis
Tertiary
Congenital syphilis
Dentinogenesis imperfecta
Nevoid basal cell carcinoma syndrome

Downs syndrome

Turners syndrome

Klinefelters syndrome

Neurofibromatosis (von Rechinkhausenss)

Marfan syndrome

The Ehlers-Daniel syndrome

Caviation leads to erosion into airway and production of contaminated sputum,

Type IV response
Small tubercle granulomascan see on radiograph
Tuberculous lymphadenitis of neck
Mycobacterium bovis infection from infected milk
SYPHILIS
Sexual transmission
Primary 1 week-3 months if found here can use penicillin to cure it
Secondary 1-12 months
Tertiary 1-30 years
Chancrehard ulcerated nodule that arises a few days after contraction
If untreated it will progress to secondary
Skin rash, mucous patchoral lesion is infectious, condyloma lataon other
mucous tissues
Most destructive stage, Gumma, syphilitic glossitis, neurosyhpilistabes doralis
Aneurysm of the ascending aorta
Snuffles, saddle nose, Rhagedes, Hutchinsons incisors, mulberry molars
GENETIC DISEASES
Imperfection in the dentin and the enamel is secondarily affected and fractures off
On radiograph you can see the teeth have a narrow waist with the crown flaring off
Autosomal dominant, cerebral, has a lot of papules/pigmented spots all over the
body
Multiple keratocysts in the jaws, skeletal anomalies, enlarged calvaria, calcified falx
cerebri, mild hypertelorism, plamar/plantar pits
CHROMOSOME ABNORMALITIES
AKA mongolism trisomy G and trisomy 21
One of the most common diseases, tongue is a little large for the mouth, varying
degrees of mental retardation, epicample fold over the eyelids that gives an Asiatic
look, often have a semiant crease across the hand
1 in 25 births when maternal age is over 45
Vulnerable to congenital heart defects, 10-20 fold increased risk of acute leukemia,
Alzheimers if they live long enough, and abnormal immune responses
AKA: gonadal dysgenesis; female disease
Fold of skin comes from ear to shoulder giving a web neck
Generally of normal intelligence, little to no breastflat shield like, cant straighten
arms, infertile, aneuploid missing x-chromosome, most common chromosomal
abnormality in females; easy to see on karyogram
Aneuploid, more males than females are affected, breast tissue (glandular
epithelium), rounded hips (like female), atrophic/hypertrophic testies, infertile
Unequal distribution of chromosomes
AUTOSOMAL DOMINANT DISEASES
Gene on chromosome #17, neurofibromin cant see on karyogram
Caf au lait spotscan see pigmented spots on skin, six or more is strong
evidence
Lisch nodulespigmented spots on the iris
Neurofibromatosis type IIgene on chromosome 22, merlin, bilateral acoustic
nerve schwannomas, multiple meingiomas
Fairly uncommon, mutation in a gene that codes for a protein called fibrillin
Have long arms and legs, fingers are long, lens drifts off center, MAJOR
PROBLEM: fibrillin is imp in heart valves (thoracic aorta) so weakened are so they
tend to have aneurysms in the ascending aorta
Involves collagen fibers so skin ligaments, and joints become very elastic
They are very stretchy people

Pathology Test I Diseases: 6

Osteogenesis imperfecta
PKU
Hemophilia (factor VIII deficiency)
Ectodermal dysplasia

Also a collagen diseasetype I, collagen imperfection that doesnt allow correct

cross-linking so loss of tensile strength, cant support your own weight
AUTOSOMAL RECESSIVE DISEASES
Low IQ, pale skin, blue eyes, if dx early in life you can prevent it, enzyme problem
Cant convert phenylalanine to tyrosine, major cause of mental retardation,
SEX-LINKED DISEASES
If you are a male with zero factor 8 you will bleed, if female and have 50% you are
ok
Hypohydrotic ectodermal dysplasia, inherited, mostly x-linked, sparse fine hair,
oligodontia (very few teeth), reduced number of sweat glands (unable to regulate
body temp, learn to live inside because they will dive of hyperthermia if they go
outside, nail abnormalities