ORAL

PATHOLOGY 1

Name of the student

1. Cellular Adaptation –when there is excessive physiologic stress, or pathologic stimuli.
A. Atrophy – decrease in size and function of a cell.
B. Hypertrophy – increase in the size of a cell.
C. Hyperplasia – Increase in the number of cells in an organ
D. Metaplasia – a change of one differentiated type of cells to another.
Examples: Barrett’s esophagus; Smoker’s lungs
E. Dysplasia – alteration in the size, shape and organization of the cellular components of a
tissue; can be a sign of future neoplastic lesion
F. Anaplasia – hallmark of malignant cells (1:1) NOTE: Lack of differentiation.

2. Reversible Injury
Hypoxia → Cellular energy metabolism is altered → glycogen is depleted, decreased intracellular pH,
cellular swelling (mildest)

Types of Cell in Response to Tissue Injury

1. Labile: epithelium, urinary cell, hemotopoetic tissue

2. Stable/Quiescent: liver, kidney, pancreas
3. Permanent: neuron, skeletal

3. Irreversible Injury
Membrane injury →Intracellular release of lysozomal enzymes →damage of other cells

NECROSIS – cell death in living tissue, resulting from the progressive degradative action of enzymes.
*Nuclear changes : (1) karyolysis (2) pyknosis , and (3) karyorrhexis
Types of Necrosis

1. Coagulation – the most common pattern of necrosis. (myocardium, kidney, liver, and other solid
organs)
2. Liquefaction – necrotic area is soft and filled with fluid
3. Caseous – tuberculosis lesion, “cheesy material”
4. Fat – necrosis in adipose tissue (saphonification)
5. Fibrinoid – necrosis in blood vessels
6. Gangrenous – necrosis of a diabetic foot and in appendicitis

SALIVARY GLAND PATHOLOGY

a. Sjogren’s syndrome (Sicca syndrome) - an autoimmune disease of the salivary and lacrimal glands
Triad:
xerostomia, keratoconjunctivitis sicca and rheumatoid arthritis
b. Warthin’s tumor - a benign tumor of the parotid gland
c. Mixed tumor - the most common salivary gland tumor
d. Mucoepidermoid carcinoma - most common malignant tumor in parotid gland

Hepatitis
Hepatitis A. Picornavirus
Hepatitis B. Hepadnavirus
Hepatitis C Flavivirus
Hepatitis D. Deltavirus
Hepatitis E Calicivirus

PEUTZ-JEGHERS SYNDROME (Hereditary Intestinal Polyposis) - characterized by dark, freckle-like spots

that appear on the skin, lips, and oral mucosa.

MULTIPLE MYELOMA (plasma cell myeloma) - proliferation of monoclonal plasma cells Laboratory
findings: Bence-Jones proteins
Radiographic appearance: multiple punched-out (skull)
Radiographic technique: Lateral Cephalogram
DIGEORGE SYN - deficient T cells result from a failure of the third and fourth branchial pouches to
develop normally.
Note: Atrophy of thymus gland

Endocrine System

HYPOTHYROIDISM - decreased metabolism resulting in weight gain and retarded growth, bradycardia,
sensitivity to cold temperature

Clinical Manifestations

a. Myxedema –adult
b. Cretinism – children Note: Oral findings: macroglossia, prolonged retention of primary teeth c.
Hashimoto’s thyroiditis – autoimmune disease

HYPERTHYROIDISM - increased metabolism, resulting in weight loss, irritability, nervousness, and

tremor NOTE: Oral findings: early loss of primary teeth
Clinical Manifestations:
a. Grave’s disease - autoimmune disease, antibodies bind to TSH receptors. Sign: exophthalmus
b. Plummer disease - nodular growth or adenoma of the thyroid
NOTE: Never use epinephrine

HYPERPARATHYROIDISM (Von Recklinghausen’s disease of the bone)

Radiographic finding: “ground-glass”
a. Primary – caused by cancer
b. Secondary – result of chronic renal disease or kidney failure

4. HYPOPARATHYROIDISM - most commonly caused by accidental surgical removal of the thyroid gland.
NOTE: maybe associated with DiGeorge syndrome

LYMPHOMA - characterized by enlarged lymph nodes

NON-HODGKIN’S

HODGKIN’S Causative agent: EBV

-affects B-CELLS
Causative agent: REED – STENBERG CELLS -affects T-CELLS Example: Burkitt’s lymphoma
Example: nodular sclerosis

GH DEFICIENCY - dwarfism
a. abnormally short height
b. smaller maxilla and mandible
c. delayed eruption of permanent teeth

GIGANTISM– before epiphyseal plates have fused

ACROMEGALY – after epiphyseal plates have fused

OSTEOPOROSIS - decrease in bone mass

-a change in serum calcium or phosphorus or Vitamin D and decrease in level of estrogen

VITAMIN D - a deficiency that results in failure of new bone to mineralize

2 forms: osteomalacia and Rickets
Oral finding: delayed in eruption

OSTEOGENESIS IMPERFECTA - caused by defective formation of collagen I

Oral finding: dentinogenesis imperfecta
 Pathognomonic sign: blue sclera

PAGET’S DISEASE - characterized by abnormal bone remodeling leading to distortion of bone

architecture. Laboratory finding: increased serum alkaline phosphatase
Radiographic appearance: “cotton-wool appearance”
Histologic appearance: jigsaw-puzzle appearance

OSTEOMYELITIS - infection of the bone and bone marrow

Causative agent: staphylococcus aureus

FIBROUS DYSPLASIA - caused by replacement of normal bone with an irregular bone containing fibrous
connective tissue Radiographic appearance: “ground-glass”
Pathognomonic sign: Hockey-stick deformity
Types:

a. Monostotic- most common

b. Polyostotic – many bones

OSTEOSARCOMA - most common true primary bone tumor

Radiographic interpretation: Codman’s triangle with sun-burst
Histologic appearance: Touton giant cells

EWING’S SARCOMA (round cell myeloma) - most commonly found in long bones
ACHONDROPLASIA - caused by delayed or abnormal growth of cartilage
Oral manifestation: mandibular prognathism

CHONDROSARCOMA - the second most common primary bone tumor

RHEUMATOID ARTHRITIS - inflammation of the synovial membrane
Note: There is a formation of pannus

OSTEOARTHRITIS - most common arthritis; there is a formation of bony spurs at the margins
Clinical manifestations: nodules at the distal and proximal interpharangeal joint

MYASTHENIA GRAVIS - autoimmune disease caused by autoantibodies to Acol receptors at the

neuromuscular junction
Treatment: neostigmine

SEBORRHIC KERATOSIS (senile wart).

VERUCCA VULGARIS (common wart)
Causative agent: Human papilloma virus

ACTINIC KERATOSIS - dry, scaly plaques with an erythematous base

Etiology: sun damage

PSORIASIS - skin lesion that appear as scaly, white plaques caused by rapid proliferation of the epidermis
Treatment: Steroids

KELOID (proud flesh) - characterized by a progressively enlarging scar by an abnormal accumulation of

collagen
Note: most common in African-American

ERYTHEMA MULTIFORME - caused by allergic reaction in drugs

-lesions are seen in the skin, oral mucosa, eye and genital area
Treatment: steroids
Note: EM → Steven-Johnson syndrome → Toxic Ependymal Necrolysis
PEMPHIGUS - ulcerative lesions on the skin and oral mucosa
Note: Autoimmune disease in which patients have autoantibodies against hemidesmosal attachment
Histologic appearance: Tzanck cells
Oral manifestation: Nikolsky sign (blisters)

PEMPHIGOID - autoimmune disease in which patients have autoantibodies against basal cells
Note: There’s NO acantholysis

LICHEN PLANUS - appear as a cluster of purple papules.

Oral manifestation: Wickham striae in buccal mucosa
Histological appearance: presence of Civatte bodies

MARFAN SYNDROME - defective fibrillin type 1

Clinical findings: tall stature, joints that can hyperextend, and cardiovascular defects

EHLER-DANLOS SYNDROME (EDS) - defective collagen

TRISOMY 21 (47XX or 47XY)- most common chromosomal disorder

Oral findings: macroglossia, delayed eruption of teeth and hypodontia

TRISOMY 13 (47XX or 47XY)- extra copy of chromosome 13

Oral findings: cleft lip and palate

TRISOMY 18 (47XX or 47XY)- extra copy of chromosome 18

Oral finding: micrognathia

KLINEFELTER’S SYNDROME (47XXY) - one of the most common causes of male hypogonadism
Signs and symptoms: underdeveloped testes, gynecomastia, and lower IQ

TURNER’S SYNDROME (45X0) - one of the most important causes of amenorrhea Note: absence of barr
body

CRI-DU-CHAT (5p-) – high-pitched cry, intellectual disability, and delayed development

TREACHER-COLLIN SYN (bird-face) - abnormal development of first and second branchial arches,
zygoma, mandible and malformed ears
Oral findings: small or absent parotid gland and cleft palate

PIERRE-ROBIN SYNDROME (fish-face) – micrognathia (lower), tongue displaced backward

NOTE: commonly seen in patients with Stickler syndrome (flat-face)

CLEIDOCRANIAL DYSOSTOSIS - no clavicle

Oral manifestation: presence of impacted multiple supernumerary teeth
NOTE: presence of wormian bodies (occipital) in the skull bones

SUPERNUMERARY TOOTH
mesiodens – most common supernumerary teeth
distomolars – 4th molar
paramolar – facially or lingually in the maxillary posterior

CUSP OF CARABELLI – 5th cusp found in maxillary 1st molar (ML/MP)

TALON’S CUSP – lingual surface of maxillary incisor or canine
DOAK’S CUSP – accessory cusp found on buccal surface of molars
DENS EVAGINATUS – presence of additional cusp central groove of premolar
DENS INVAGINATUS – presence of deep pit fissure
GEMINATION – one tooth bud attempts to make two;
2 crowns in one root FUSION – two roots in one crown
DILACERATION – curvature of the root
ENAMEL PEARL – most commonly found in the furcation area molar
TAURODONTISM – “bull’s teeth” – presence of enlarged pulp chambers
CONCRESCENCE – fusion of teeth via cementum
ANKYLOSIS – fusion of alveolar bone to cementum
HYPERCEMENTOSIS – excessive production of cementum
AMELOGENESIS IMPERFECTA –enamel only is affected

hypoplastic – not formed to full normal thickness (pin-point pits)

hypocalcified – soft enamel that can be removed by a prophylactic instrument
hypomaturation – can be pierced by an explorer (scratches)

DENTINOGENESIS IMPERFECTA – dentin is affected

type I – associated with osteogenesis imperfecta
type II – not associated with osteogenesis imperfect
type III – “brandywine” type, with multiple pulp exposure

REGIONAL ODONTODYSPLASIA –teeth appear deformed clinically; enlarged pulp chamber

HYPOPHOSPHATASIA – decreased serum alkaline phosphatase

Dental Lamina Cysts of the Newborn

GINGIVAL CYST –white soft tissue nodules on alveolar ridge

EPSTEIN PEARLS – multiple small white nodules along midline of hard palate
BOHN’S NODULES – entrapped from minor salivary glands; primarily on soft and hard palate

Cysts of the Adult

NASOLABIAL CYST – nasolacrimal duct, swelling on the mucolabial fold and floor of the nose
NASOPALATINE DUCT CYST – most common non-odontogenic cyst
GLOBULOMAXILLARY CYST – found in between maxillary lateral and canine
BRANCHIAL CLEFT CYST – cystic transformation of salivary gland tissue present in cervical lymph nodes
Clinical appearance: freely movable mass along the anterior border of the SCM
THYROGLOSSAL DUCT CYST – remains in the foramen cecum
DERMOID CYST – it has sebaceous gland, hair follicles, and sweat glands.

Odontogenic Cysts and Tumors

APICAL PERIODONTAL CYST – most common odontogenic cyst
RESIDUAL CYST –cyst that persists after extraction
PARADENTAL CYST – buccal swelling adjacent to a molar (1st lower molar = children; mand 3rd
molar=adult) -occlusal radiograph will show lingual displacement of tooth

DENTIGEROUS CYST – the most common developmental cyst

Histologic appearance: Rushton bodies

PRIMORDIAL CYST – always associated with congenitally missing tooth

ERUPTION CYST -lesion appears as bluish-purple
LATERAL PERIODONTAL CYST – most common location: mand PM and canine area

*multilocular = Botryoid odontogenic cyst OKC – most common multilocular radiolucency.

Note: major component of the nevoid basal cell carcinoma

Odontogenic Tumors

EPITHELIAL MESENCHYMAL MIXED


1. AMELOBLASTOMA – aggressive 1. ODONTOGENIC FIBROMA –
in behavior
Note: lower 3rd molar area
2. CEOT – originated from stratum most common
intermedium
-amyloid can be seen
3. SQUAMOUS ODONTOGENIC
TUMOR – see teeth in floating air
1. ODONTOMA
4.1 Compound “toothlets”
composted of
most common in female;
maxilla
enamel, dentin and pulp (max ant)
4.2 Complex – unrecognizable dental
2. ODONTOGENIC MYXOMA –
tissue. (mand post)
-originated from cells that
2. ADENOMATOID ODONTOGENIC
would have formed the dental
TUMOR - slow growing and painless
(canine)
follicle
Note: the only odontogenic tumor
with duct-like tumor.

Oral Manifestation of Systemic Disease

SYPHILIS (Lues) – Treponema pallidum

a. Primary: Chancre (3 weeks)
b. Secondary: 4-10 weeks; maculopapular rash; condyloma lata (papillary lesions)
c. Tertiary stage- Gumma
*Luetic glossitis: atrophy and loss of dorsal tongue papilla

CONGENITAL SYPHILIS
Triad
(1) Hutchinson’s incisors and mulberry molars;
(2) interstitial keratitis; and
(3) deafness

WEGENER’S GRANULOMATOSIS
Triad: (1) Focal necrotizing vasculitis
(2) Necrotizing granuloma
(3) Necrotizing glomerular nephritis

HYPERPARATHYROIDISM (Von recklinghausen’s disease of the bone)

Clinical Features: Stones, Bones, Moans and Groans Stones – urinary tract stones
Bones – subperiosteal resorption
Moans – personality changes
Groans – abdominal pain
Radiographic appearance: ground glass

IRON DEFICIENCY ANEMIA – degeneration from low iron

NOTE: Plummer-Vinson Syndrome – chronic form
Clinical Feature: “spoon-shaped nail”

SICKLE CELL ANEMIA – a genetic disorder resulting from a substitution of thymine for an adenine in DNA
Radiographic appearance: “hair-on-end” appearance
NOTE: Hemoglobin S (abnormal)

THALASSEMIA – decreased in hemoglobin level

Radiographic appearance: salt and pepper
Clinical manifestation: flaring of anterior teeth
Bone Pathology of the Head and Neck

OSTEORADIONECROSIS – bone reaction to radiation with destruction of the blood vessels

Treatment: HBO2
BIONJ – associated to a drug.

CHERUBISM – bilaterally enlarged mandible, eyes upturned toward heaven, failure of teeth to erupt
Radiographic appearance: “Soap-bubble” bilateral

WHITE SPONGE NEVUS (Cannon’s disease) – white, rough, surface lesion due to epithelial thickening on
buccal mucosa bilaterally that mimics the cheek biting or squamous cell carcinoma

DARRIER’S DISEASE -a defect in the adhesion of epithelial cells -mimic papillary hyperplasia and nicotinic
stomatitis

SYSTEMIC LUPUS ERYTHEMATOSUS - antibodies are formed against cells and tissues
-Kidney disease: fatal to patient
-Heart disease: Libmann-Sach’s endocarditis
*Clinical Manifestation: Butterfly rash (malar rash)
ANGIOEDEMA - diffuse rapid swelling of soft tissues with unknown cause

KERATOACANTHOMA - superficial invasive squamous cell carcinoma

LEUKOPLAKIA – NOT A DISEASE; white patch or plaque that CANNOT be rubbed-off (pre-malignant
lesion)

SQUAMOUS CELL CARCINOMA (SCC)

a. Lip cancer - 90% lower lip

Note: MOST COMMON EXTRAORAL
b. Tongue - lateral and ventral surfaces are common
NOTE: tobacco and alcohol user
c. Floor of the Mouth - cervical lymph nodes metastasis can occur
d. Palatal Cancer - soft palate is most common

BASAL CELL CARCINOMA – benign in behavior Common location: upper face

RHABDOMYOSARCOMA – skeletal muscles

NOTE: most common soft tissue sarcoma in children
LEIMYOSARCOMA – smooth muscles (uterus)
LIPOSARCOMA – adipose
FIBROSARCOMA – fibroblasts, most common in males (30-40y/o)

INFLAMMATORY FIBROUS HYPERPLASIA - irritation to denture

Treatment: change the denture

FIBROMA – most common benign lesion of the oral cavity

-firm, asymptomatic nodule; buccal mucosa and lower lip

NEUROFIBROMATOSIS (Von Recklinghausen’s disease of the skin)

Clinical manifestation: presence of café-au-lait spots (smooth)
Skeletal abnormalities: macrocephaly

NEURILEMOMA (Schwannoma) - originates from Schwann cells

Histologic: presence of Antoni A and B

LYMPHANGIOMA – tumors in the lymph nodes of tongue, lips and neck (cystic hygroma)
SIALOLITHIASIS - formation of stone
-85% occur in submandibular gland; boys > girls

MUCOCELE - traumatized salivary gland duct caused by lip biting

Treatment: excision with the involvement of minor salivary gland

RANULA – swelling that crosses the midline of the floor of the mouth; most common in sublingual gland
lesion
Treatment: marsupialization

NECROTIZING SIALOMETAPLASIA - “My palate fell out”

-most common: posterior hard palate that exhibits crater-like ulcerations

BENIGN LYMPHOEPITHELIAL LESIONS- bilateral painless swelling of lacrimal and salivary glands (80% in
parotid)

EPHELIS / EPHELIDES - macular pigmented lesion in sun-exposed areas (vermillion border)

LENTIGO SIMPLEX - tends to occur in areas that are not exposed in sunlight
NEVUS - benign, pigmented tumor of melanocytes, found deep in connective tissue
a. junctional – “abtropfung effect”
b. compound
c. intradermal

a. Melanocytic nevi – most common human tumor

b. Congenital nevi – appears at birth, “bathing trunk” nevus
c. Blue Nevi – proliferation of dermal melanocytes
c.1 Common blue – palate and hands
c.2 Cellular blue – buttocks

MALIGNANT MELANOMA - tumors of melanocytes

Features: “ABCD”
A- asymmetry
B- orders, irregular
C- olor, brown, black
D- iamater, >6mm in diameter

Locations: BANS

B-ack (interscapular)
A- rm (posterior)
N-eck; posterolateral
S-calp

Types
Superficial – most common form of melanoma with radial growth
Acral lentigenous- most common form in oral cavity: hard palate, gingiva and alveolar mucosa
Nodular – lesions begin in vertical growth
Lentigo maligna melanoma

Syndromes of the Head and Neck

GARDNER SYNDROME – presence of polyps of large intestine

Clinical features: osteomas, fibromas of the skin, multiple unerupted permanent and supernumerary

CROUZON’S SYNDROME - “frog-like face” (mid face hypoplasia)

NOTE: Crouzon’s with syndactyly and hearing loss due to stapes fixation = Apert’s syndrome
NEVOID BASAL CELL CARCINOMA (Gorlin-Goltz)
Clinical features: Multiple OKC, bifid ribs, kyphoscoliosis, and calcification of the falx cerebri

PAPILLON-LEFEVRE SYNDROME - periodontitis in children with skin diseases

CHEDIAK-HIGASHI SYNDROME – periodontitis in children-adult with blood diseases
COWDEN SYNDROME - most common sites: tongue, buccal mucosa, and gingiva

NOTE:
Clinical Features: multiple nodular and papular lesions resulting in cobblestone appearance

Hereditary syndromes with intestinal polyposis

a. Garnder syndrome
b. Peutz-Jeghers syndrome (HIPS)
c. Turcot’s syndrome (with brain tumor)
d. Cowden syndrome