PATHOLOGY

HEAD AND NECK

DR. INOCENCIO

Teeth and Supporting Structures

Teeth
-

important fxns: mastication and proper speech.

firmly implanted in the jaw; surrounded by gingival mucosa
crown of the tooth projects into the mouth
covered by enamel, a hard, inert, acellular tissuehighly
mineralized tissue in the body.
enamel rests upon dentina specialized form of CT
makes up most of the remaining hard-tissue portion of the
tooth.
Cellular, contains numerous dentinal tubules, w/c contain
cytoplasmic extensions of odontoblasts.
pulp chamber is surrounded by dentin &consists of loose CT
stroma rich in nerve bundles, lymphatics, & capillaries.
in mammals, teeth attached to the alveolar ridge of the
jaws by the periodontal ligament, w/c provides a strong yet
flexible attachment can withstand forces of mastication.
The periodontal ligament attaches to the alveolar bone of the
jaw on one side and to cementum, present on the roots of the
teeth
acts as a cement anchor periodontal ligament to the
tooth.

CARIES (TOOTH DECAY)

-

Dental cariescaused by focal degradation of the tooth

structure
one of the most common dses throughout the world
most common cause of tooth loss before age 35.
Carious lesions result of mineral dissolution of tooth
structure by acid metabolic end products from bacteria
(present in oral cavity & capable of fermenting sugars.
improved oral hygiene & fluoridation of the drinking water
has become a standard practice.
Fluoride incorporates into crystalline structure of enamel,
forming fluoroapatite contributes to resistance to
degradation by bacterial acids.

GINGIVITIS

Gingiva squamous mucosa bet the teeth & around them.

Gingivitisinflamm of mucosa & assoc soft tissues.
result of a lack of proper oral hygiene accumulation of
dental plaque &calculus.
Dental plaquesticky, usually colorless, biofilm; builds in
bet &on surface of the teeth.
formed by a complex of oral bacteria, proteins from the
saliva, &desquamated epithelial cells.
If plaque continues to build mineralized to form calculus
(tartar).
Repeated erosions dental caries.
Plaque build-up beneath gumline gingivitis.

reversible disease; therapy primarily aimed at accumulation

of plaque &calculus via brushing, flossing, and regular dental
visits.

PERIODONTITIS
-

Periodontitis inflammatory process that affects the

supporting structures of the teeth: periodontal ligaments,
alveolar bone, and cementum.
periodontitis serious sequelae, including:
loss of attachment caused by complete destruction of the
periodontal ligament & alveolar bone. Loosening and
eventual loss of teeth are possible.
Devt of periodontal dse is now considered to be an
independent process,
reasons that are still unclear, assoc w/ a marked shift in the
types and proportions of bacteria along the gingiva.

Pathogenesis: poor oral hygiene!

facultative gram-positive organisms colonize healthy sites,
while plaque within areas of active periodontitis contains
anaerobic and microaerophilic gram-negative flora.
300 types of bacteria reside in oral cavity, adult periodontitis
assoc primarily w/
Aggregatibacter (Actinobacillus)
actinomycetemcomitans,
Porphyromonas gingivalis
Prevotella intermedia.
-

periodontal dse- component of several different systemic

diseases, including:
acquired immunodeficiency syndrome (AIDS), leukemia,
Crohn's disease, diabetes mellitus, Down syndrome,
sarcoidosis, and syndromes associated with
polymorphonuclear defects (Chdiak-Higashi syndrome,
agranulocytosis, and cyclic neutropenia).

Inflammatory/Reactive Tumor-like Lesions

-

tumor masses or ulcerationsreactive in nature & represent

inflamm induced by irritation or by unknown mechanisms.
All suspicious lesionsexamined by biopsy.
Reactive nodules of the oral cavity are fairly common and
microscopically diverse.

Most common fibrous proliferative lesions:

o
fibroma (61%),
o peripheral ossifying fibroma (22%), pyogenic
granuloma (12%),
o peripheral giant-cell granuloma (5%).

Most common inflammatory/reactive ulcerations of the oral

cavity traumatic and aphthous ulcers.

FIBROUS PROLIFERATIVE LESIONS

Chronic gingivitis is characterized by:
o gingival erythema,
o edema, bleeding, changes in contour,
o loss of soft-tissue adaptation to the teeth.
Gingivitis occurs at any age;most prevalent & severe in
adolescence (ranging from 40%-60%),

Aka. irritation fibroma primarily occurs in the buccal

mucosa along the bite line or @ gingivodental margin.
Consists of a nodular mass of fibrous tissue, w/ few
inflammatory cells, covered by squamous mucosa.
TX: complete surgical excision.

made up of a striking aggregation of multinucleate, foreign

bodylike giant cells separated by a fibroangiomatous
stroma.
not encapsulated, lesions are well delimited and easily
excised.
**should be differentiated from central giant-cell granulomas found
w/in the maxilla /mandible & from histologically similar but
frequently multiple brown tumors seen in hyperparathyroidism.
APHOTHOUS ULCERS (CANKER SORES)

Fibroma. Smooth pink exophytic nodule on the buccal mucosa.

-

Pyogenic granuloma highly vascular pedunculated lesion,

usuoccurring in the gingiva of children, young adults, and,
commonly, pregnant women (pregnancy tumor).
Surface of lesion ulcerated &red to purple color.
some cases growth alarmingly rapid, raising the fear of a
malignant neoplasm.
Histologically: highly vascular proliferation that is similar to
granulation tissue.
form of capillary hemangioma
either regress, particularly after pregnancy, or undergo
fibrous maturation, may develop into peripheral ossifying
fibroma.
TX: complete surgical excision.
peripheral ossifying fibroma relatively common growth
of the gingiva .
considered to be reactive in nature rather
etiology of lesion is unknown.
arise as a result of maturation of a long-standing pyogenic
granuloma.
peak incidence in young &teenage females,
appear as red, ulcerated, and nodular lesions of the gingiva.
TX: Complete surgical excision down to the periosteum
(recurrence rate of 15% to 20%.)

extremely common superficial ulcerations of the oral mucosa

more common in the first two decades of life
extremely painful and often recurrent
lesions appear as single or multiple, shallow, hyperemic
ulcerations
covered by a thin exudate
rimmed by a narrow zone of erythema
underlying inflammatory infiltrate is at first largely
mononuclear
SECONDARY BACTERIAL INFECTION introduces numerous
neutrophils
lesions may spontaneously resolve in 7 to 10 days or
stubbornly persistent for weeks
Most ulcers are more painful than serious and require only
symptomatic treatment

Recurrent apthous ulcers

May be associated with celiac disease and inflammatory
bowel disease

Aphthous ulcer. Single ulceration with an erythematous halo

surrounding a yellowish fibrinopurulent membrane.
GLOSSITIS
Pyogenic granuloma. Erythematous, hemorrhagic, and exophytic mass
arising from the gingival mucosa.
-

peripheral giant cell granuloma relatively common lesion

of the gingiva.
generally covered by intact gingival mucosa, but may be
ulcerated.
clinical appearance of peripheral giant-cell granuloma : more
bluish purple in color while the pyogenic granuloma is more
bright red.
Histologically: lesions are distinct.

implies inflammation of the tongue

sometimes applied to the beefy-red tongue encountered in
certain deficiency states
results from atrophy of the papillae of the tongue and
thinning of the mucosa
o exposing the underlying vasculature
atrophic changes do indeed lead to inflammation and even
shallow ulcerations
Such changes changes may be encountered in deficiencies of
o vitamin B12 (pernicious anemia)
o riboflavin
o niacin
o pyridoxine
Similar alterations are sometimes encountered with sprue
and iron-deficiency anemia
o complicated by deficiency in one of the B vitamins

HANSEL, CHINEE, JOAN 2

PATHOLOGY
HEAD AND NECK
DR. INOCENCIO

Plummer-Vinson or Paterson-Kelly syndrome - The

combination of iron-deficiency anemia, glossitis, and
esophageal dysphagia usually related to web

CHARACTERIZED BY
o ulcerative lesions

sometimes along the lateral borders of the

tongue
May also be seen with
o Jagged carious teeth
o ill-fitting dentures
o **Rarely with

syphilis

inhalation burns

ingestion of corrosive chemicals

INFECTIONS
-

oral mucosa is highly resistant to its indigenous flora

have many defenses including:
o
competitive suppression of potential pathogens by
organisms of low virulence
o elaboration of secretory IgA and other
immunoglobulins
submucosal collections of lymphocytes and plasma cells
o antibacterial effects of saliva
o
irrigating effects of food and drink
any lowering of these defenses sets the stage for oral
infections
o
immunodeficiency
o disruption of the microbiologic balance by
antibacterial therapy

HERPES SIMPLEX VIRUS INFECTIONS

-

Most orofacial herpetic infections are caused by HERPES

SIMPLEX VIRUS TYPE 1 (HSV-1)
changes in sexual habits = increase in HSV-2 (genital herpes)
has been observed in the oral cavity
Primary HSV infection typically occurs in CHILDREN AGE 2
TO 4 YEARS
o often asymptomatic
o does not cause significant morbidity
10 20% of the time = primary infection presents as acute
herpetic gingivostomatitis
o abrupt onset of vesicles and ulcerations throughout
the oral cavity
o ESPECIALLY in the gingiva
Lesions also accompanied by lymphadenopathy, fever,
anorexia, and irritability

Morphology
vesicles range from lesions of a few millimeters to large
bullae
o at first filled with a clear, serous fluid
o often rupture to yield extremely painful, redrimmed, shallow ulcerations
Microscopic Examination
intracellular and intercellular edema (acantholysis)
form clefts that may become transformed into macroscopic
vesicles

Individual epidermal cells

Margins of vesicles or lying free within the fluid
sometimes develop eosinophilic intranuclear viral inclusions
several cells may fuse to produce giant cells
aka multinucleate polykaryons
demonstrated by the diagnostic Tzanck test
vesicles and shallow ulcers USUALLY SPONTANEOUSLY
CLEAR within 3 to 4 weeks
virus treks along the regional nerves
eventually becomes dormant in the local ganglia (eg
trigeminal)
Usually in young adults, the virus becomes reactivated to
produce the common but usually mild cold sore
influences predisposing to activation are poorly understood

BUT MAY include:

Trauma
Allergies
exposure to ultraviolet light
upper respiratory tract infections
pregnancy
menstruation
immunosuppression
exposure to extremes of temperature
Recurrent herpetic stomatitis
o
In contrast to acute gingivostomatitis
o occurs either at the site of primary inoculation OR
o adjacent mucosal areas that are associated with the
SAME
GANGLION
-

groups of small (13 mm) vesicles

MOST COMMON LOCATIONS for recurrent lesions

o The lips (Herpes labialis)

o
nasal orifices
o
buccal mucosa
o gingival
o hard palate
**resemble those already described in the primary infections
much more limited in duration
are milder
usually dry up in 4 to 6 days
heal within a week to 10 days
OTHER VIRAL INFECTIONS
-

herpes zoster
Epstein-Barr virus (EBV; mononucleosis)
Cytomegalovirus
enterovirus (herpangina, hand-foot-and-mouth disease,
acute lymphonodular pharyngitis)
rubeola (measles)

ORAL CANDIDIASIS (THRUSH)

-

By far the most common fungal infection in the oral cavity

Candida albicans

normal component of the oral flora in 50% of the

population
o three factors that influence the likelihood of a
clinical infection:

immune status of the individual

the strain of C. albicans present

the composition of an individual's oral

flora
three major clinical forms of oral candidiasis
o pseudo-membranous (thrush) MOST COMMON
o erythematous
o hyperplastic
** with several different variations within these groups
Pseudo-membranous form
o aka thrush
o typically takes the form of a superficial, curdy, gray
to white inflammatory membrane
composed of matted organisms
enmeshed in a fibrinosuppurative exudates
reveal an underlying erythematous inflammatory base when
scraped off
causes mischief only in individuals who have some form of

IMMUNOSUPPRESSION
-

patients with diabetes mellitus

organ or bone marrow transplant recipients
those with neutropenia
chemotherapy-induced immunosuppression
AIDS
o broad-spectrum antibiotics
eliminate or alter the normal bacterial flora of the mouth
also result in the development of oral candidiasis

Infectious
Acute pharyngitis and tonsillitis that may
mononucleosis cause coating with a gray-white
exudative membrane; enlargement of
lymph nodes in the neck, palatal
petechiae
Diphtheria

Human
Predisposition to opportunistic oral
immunodeficie infections, particularly herpesvirus,
ncy virus
Candida, and other fungi; oral lesions of
Kaposi sarcoma and hairy leukoplakia
(described in text)
DERMATOLOGIC CONDITIONS[*]
Lichen planus

Reticulate, lacelike, white keratotic

lesions that rarely become bullous and
ulcerated; seen in more than 50% of
patients with cutaneous lichen planus;
rarely, is the sole manifestation

Pemphigus

Vesicles and bullae prone to rupture,

leaving hyperemic erosions covered with
exudates

Bullous
pemphigoid

Oral lesions resemble macroscopically

those of pemphigus but can be
differentiated histologically

Erythema
multiforme

Maculopapular, vesiculobullous eruption

that sometimes follows an infection
elsewhere, ingestion of drugs,
development of cancer, or a collagen
vascular disease; when it involves the lips
and oral mucosa, it is referred to as
Stevens-Johnson syndrome

DEEP FUNGAL INFECTIONS

Such fungi include:

Histoplasmosis

Blastomycosis

Coccidioidomycosis

Cryptococcosis

Zygomycosis

Aspergillosis

Characteristic dirty white,

fibrinosuppurative, tough, inflammatory
membrane over the tonsils and
retropharynx

HEMATOLOGIC DISORDERS
Pancytopenia
(agranulocytos
is, aplastic
anemia)

Severe oral infections in the form of

gingivitis, pharyngitis, tonsillitis; may
extend to produce cellulitis of the neck
(Ludwig angina)

Leukemia

With depletion of functioning

neutrophils, oral lesions may appear like
those in pancytopenia

ORAL MANIFESATIONS OF SYSTEMIC DISEASES

Monocytic
leukemia

Leukemic infiltration and enlargement of

the gingivae, often with accompanying
periodontitis

Systemic
Disease

MISCELLANEOUS

Due to increasing number of patients who are

IMMUNOCOMPROMISED

Associated Oral Changes

INFECTIOUS DISEASES
Scarlet fever

Fiery red tongue with prominent papillae

(raspberry tongue); white-coated tongue
through which hyperemic papillae
project (strawberry tongue)

Measles

Spotty enanthema in the oral cavity often

precedes the skin rash; ulcerations on the
buccal mucosa about Stensen duct
produce Koplik spots

Melanotic
pigmentation

May appear in Addison disease,

hemochromatosis, fibrous dysplasia of
bone (Albright syndrome), and PeutzJegher syndrome (gastrointestinal
polyposis)

Phenytoin
(Dilantin)
ingestion

Striking fibrous enlargement of the

gingivae

Pregnancy

A friable, red, pyogenic granuloma

protruding from the gingiva (pregnancy
tumor)

HANSEL, CHINEE, JOAN 4

PATHOLOGY
HEAD AND NECK
DR. INOCENCIO

Rendu-OslerWeber
syndrome

Autosomal dominant disorder with

multiple congenital aneurysmal
telangiectasias beneath mucosal surfaces
of the oral cavity and lips

Speckled leukoerythroplakia.- both leukoplakia and

erythroplakia

MANY SYSTEMIC DISEASES are associated with oral lesions

not uncommon for oral lesions to be the FIRST SIGN of some
underlying systemic condition

HAIRY LEUKOPLAKIA
-

distinctive oral lesion that is usually seen in

immunocompromised patients
Approximately 80% of patients with hairy leukoplakia are
INFECTED WITH THE HUMAN IMMUNODEFICIENCY VIRUS
(HIV)
20% of lesions are seen in patients who are
immunocompromised for other reasons (cancer therapy or
transplant immunosuppression)
takes the form of white, confluent patches of fluffy (hairy),
hyperkeratotic thickenings, almost always situated on the
LATERAL BORDER OF THE TONGUE
Unlike thrush, the lesion cannot be scraped off

Microscopic appearance:
Consists of hyperparakeratosis and acanthosis with balloon
cells in the upper spinous layer
Sometimes there may be koilocytosis of the superficial,
nucleated epidermal cells
o suggesting human papillomavirus (HPV) infection
- EBV is present in most cells and is NOW ACCEPTED AS THE
CAUSE of the condition
- Sometimes there is superimposed candidal infection
o Adds to the hairiness
- In HIV-positive individuals, with hairy leukoplarkia,
symptoms of AIDS follow in 2 to 3 years

Erythroplakia. A, Lesion of the maxillary gingiva. B, Red lesion of the

mandibular alveolar ridge. Biopsy of both lesions revealed carcinoma
in situ.
Morphology:
Leukoplakias- Oral cavity
o Favored location: buccal mucosa, floor of the
mouth, ventral surface of the tongue, palate, and
gingiva
o Appear as solitary or multiple white patches or
plaques, often with sharply demarcated borders
o
May be slightly thickened and smooth or wrinkled
and fissured, or they may appear as raised,
sometimes corrugated, verrucous plaques
Histologic examination
they present a spectrum of epithelial changes ranging from
hyperkeratosis overlying a thickened, acanthotic but orderly
mucosal epithelium to lesions with markedly dysplastic
changes sometimes merging into carcinoma in sit

Tumors and Precancerous Lesions

-

Oral squamous cell carcinoma and its associated

precancerous lesions

LEUKOPLAKIA AND ERYTHROPLAKIA

-

early detection in populations at risk have been proposed to

decrease the morbidity and mortality associated with oral
cancer
Leukoplakia- a white patch or plaque that cannot be
scraped off and cannot be characterized clinically or
pathologically as any other disease
o lesions that are present in the oral cavity for no
apparent reason
o lichen planus and candidiasis are not leukoplakias
o until it is proved otherwise via histologic
evaluation, all leukoplakias must be considered
precancerous.
Erythroplakia- red, velvety, possibly eroded area within the
oral cavity that usually remains level with or may be slightly
depressed in relation to the surrounding mucosa
o epithelium in such lesions tends to be markedly
atypical, incurring a much higher risk of malignant
transformation than that seen with leukoplakia

Leukoplakia. Clinical appearance of leukoplakias is highly variable and

can range from (A) smooth and thin with well-demarcated borders,
(B) diffuse and thick, (C) irregular with a granular surface, to (D)
diffuse and corrugated.
Histologic changes in erythroplakia only rarely consist of orderly
epidermal maturation; virtually all (approximately 90%) disclose
superficial erosions with dysplasia, carcinoma in situ, or already
developed carcinoma in the surrounding margins
SQUAMOUS CELL CARCINOMA
-

Multifactorial
Chronic abusers of smoked tobacco and alcohol
Actinic radiation (sunlight) and, particularly, pipe smoking
are known predisposing influences for cancer of the lower lip

Molecular Biology of Squamous Cell Carcinoma.

-

Several genetic alterations, some definitively identified and

some inferred from tumor-specific chromosomal alterations,
have been found in HNSCC

The first change is the loss of chromosomal regions of 3p and

9p21
Loss of heterozygosity (LOH) in conjunction with promoter
hypermethylation at this locus results in the inactivation of
the p16 gene, an inhibitor of cyclin-dependent kinase
Subsequent LOH at 17p with mutation of the p53 tumor
suppressor gene is associated with progression to dysplasia
gross genomic alterations as well as deletions on 4q, 6p, 8p,
11q, 13q, and 14q may act as predictors of progression to
malignancy
amplification and overexpression of the cyclin D1 gene
(located on chromosome 11q13), which constitutively
activates cell cycle progression, is a common late event

Clinical, histologic, and molecular progression of oral cancer. A, The

typical clinical progression of oral cancer. B, The histologic
progression of squamous epithelium from normal, to hyperkeratosis,
to mild/moderate dysplasia, to severe dysplasia, to cancer. C, The sites
of the most common genetic alterations identified as important for
cancer development. CIS, carcinoma in situ; SCC, squamous cell
carcinoma.
Morphology:
Favored locations are the ventral surface of the tongue, floor
of the mouth, lower lip, soft palate, and gingival

Epithelial lined cysts are quite common in jaws

DENTIGEROUS CYST
-

Originates around the crown of an unerupted tooth

Result of a degeneration of dental follicle
Radiographically unilocular lesions
Most associated with impacted 3rd molar
(wisdom) teeth

Histologically:
-

lined by thin layer of stratified squamous epithelium

Very dense chronic inflammatory cell infiltrate in the
connective tissue stroma
Complete removal of the lesion is curative
incomplete excision: may result in recurrence or very rarely
into an ameloblastoma or squamous cell carcinoma

KERATOCYSTIC ODONTOGENIC TUMOR formerly known as

Odontogenic Keratocyst (OKC)

Schematic representation of the sites of origin of squamous cell

carcinoma of the oral cavity, in numerical order of frequency.
Cancers of the oral cavity appear either as raised, firm, pearly
plaques or as irregular, roughened, or verrucous areas of mucosal
thickening, possibly mistaken for leukoplakia
Histologic examination, these cancers begin as dysplastic lesions,
which may or may not progress to full-thickness dysplasia (carcinoma
in situ) before invading the underlying connective tissue stroma
Squamous cell carcinomas range from well-differentiated
keratinizing neoplasms to anaplastic, sometimes sarcomatoid, tumors,
and from slowly to rapidly growing lesions
The favored sites of local metastasis are the cervical lymph nodes,
while the most common sites of distant metastasis are mediastinal
lymph nodes, lungs, liver, and bones.

Locally aggressive and has a high rate of recurrence

Patients between 10-40 years old
Most common in males within posterior mandible
Presents as well defined unilocular or multilocular
radiolucencies

Histologically:
-

cyst lining consists of a thin layer of parakeratinized or

orthokeratinized stratified squamous epithelium with a
prominent basal cell layer and corrugated appearance of the
epithelial surfaces
Treatment requires aggressive and complete removal
Recurrence rates 60%
Gorlin syndrome (nevoid basal cell carcinoma syndrome)
multiple OKC related to mutations in the tumor suppressor
gene PTCH located in 9q22

ODONTOGENIC CYSTS AND TUMORS

HANSEL, CHINEE, JOAN 6

PATHOLOGY
HEAD AND NECK
DR. INOCENCIO

PERIAPICAL CYST
-

Inflammatory in origin
Found at the apex of teeth
Develop as long standing pulpitis, which may be caused by
advanced carious lesions or by trauma to the tooth
Inflammatory process may result in necrosis of pulpal tissue
which can transverse the length of the root and exit the apex
of the tooth into the surrounding alveolar bone, giving rise to
periapical abscess
A lesion with granulation tissue may develop (periapical
granulomas is not appropriatee because it does not show
true granulomatous inflammation)
Lesions persist as a result of bacteria
Removal of offending material and appropriate restoration of
the tooth or extraction

ODONTOGENIC TUMORS
-

Complex group of lesions with diverse histologic

appearances and clinical behavior
True neoplasm or hamartomas
Derived from odontogenic epithelium, ectomesenchyme or
both

Two most common tumors:

1. Ameloblastoma arises from odontogenic epithelium and shows
no ectomesenchymal differentiation. Mostly in jaw bone and required
wide surgical resection to prevent recurrences
Cystic, slow growing, locally invasive Most are indolent
2. Odontoma most common type, arises from epithelium but shows
extensive deposition of enamel and dentin
Probably hamartomas, cured by excision

UPPER AIRWAYS

(Nose, Pharynx, Larynx and their related structures)

disorders are among the most common afflictions of humans, but
overwhelming majority are more nuisances than threats
NOSE
-

Inflammatory diseases in the form of common cold- Most

common disorders of the nose and its accessory sinuses
most are viral in origin but often complicated by
superimposed bacterial infections

INFLAMMATIONS
INFECTIOUS RHINITIS
-

Common cold
Caused by one or more viruses
Major offenders: adenoviruses, echoviruses, and
rhinoviruses
Profuse catarrhal discharge
Initial Acute stages: nasal mucosa is thickened, edematous
and red ;Nasal cavities are narrowed ;Turbinates are
enlarges
May produces concomitant pharyngotonsillitis
Secondary bacterial infections: enhances the inflammatory
reaction Produces mucopurulent or suppurative exudate

ALLERGIC RHINITIS
-

Hay fever
Hypersensitivity reactions to one of a large group of
allergens
Ig-E mediated immune reaction with an early and late
response phase
Marked mucosal edema
Redness
Mucus secretion, accompanied by leukocytic infiltration with
prominent eosinophils

NASAL POLYPS
-

recurrent attacks of rhinitis may eventually lead to focal

protrusions of the mucosa producing nasal polyps
may reach 3-4 cm in length

Histologically:
-

edematous mucosa having a loose stroma, often harboring

hyperplastic or cystic mucous glands, infiltrated with a
variety of inflammatory cells, including neutrophils,
eosinophils, and plasma cells with cluster of lymphocytes

When multiple or large, may encroach on the airway and

impair sinus drainage
if with absence of bacterial infection: mucosal covering is
intact; chronicity
may cause ulceration or infection

Variable inflammatory infiltrate of neutrophils,

lymphocytes, and plasma cells

SINUSITIS
-

Acute sinusitis: commonly preceded by acute/chronic

rhinitis
Maxillary sinusitis arises by extension of periapical infection
through the bony floor of the sinus
Offending agents: inhabitants of the oral cavity
Inflammatory reaction is non specific
Impairment of drainage of the sinus by inflammatory edema
of mucosa
Suppurative exudate producing empyema of the sinus
Obstruction of outflow most often from the frontal sinus
leads to accumulation of mucous secretions in the absence of
direct bacterial invasion producing mucocele
Component of Kartagener syndrome which also includes
bronchiectasis and and situs inversus.

Chronic sinusitis:
caused by fungi (e.g mucormycosis) especially in diabetics
Infection may spread into the orbit or penetrate the
surrounding bone to give rise to osteomyelitis or spread into
the cranial vault, causing septic thrombophlebitis of a dural
venous sinus
NECROTIZING LESIONS OF THE NOSE AND UPPER AIRWAYS
May be produced by:
-

Acute fungal infections (including mucormycosis particularly

in diabetics and immunosuppressed)
Wegener granulomatosis
Lymphoma of natural killer cells infected with EBV
previously known as Lethal midline granuloma or
polymorphic reticulosis
o
Ulceration and superimposed bacterial infection
complicate the process
o Uncontrolled growth of lymphoma possibly with
penetrating the cranial vault
o
Tumor necrosis with secondary bacterial infection
and blood borne dissemination of the infection

NASOPHARYNX
INFLAMMATIONS
a. nasal polyps. Low-power magnification showing adenomatous
masses lined by epithelium B. High power view, showing deem and
eosinophil-rich inflammatory infiltrates
CHRONIC RHINITIS
-

Repeated attacks of acute rhinitis

Either microbial or allergic in origin with the eventual
development of superimposed bacterial infection
Deviated nasal septum or nasal polyps with impaired
drainage of secretion
Superficial desquamation or ulceration of
mucosal epithelium

PHARYNGITIS AND TONSILLITIS

-

Multitudinous rhinoviruses, echoviruses and adenoviruses,

respiratory syncytial viruses and various strains of influenza
virus
Reddening and slight edema of nasopharyngeal mucosa
Reactive enlargement of related lymphoid structures
Inflamed mucosa may be covered by an exudative membrane
(pseudomembrane)
Nasopalatine and palatine tonsils are often enlarged and
covered by exudate
Most common offenders: B hemolytic streptococci ;
sometimes Staphylococcus aureus
Follicular tonsillitis- typical appearance of an enlarged,
reddened tonsils (due to reactive typhoid hyperplasia)

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PATHOLOGY
HEAD AND NECK
DR. INOCENCIO

dotted by pinpoints of exudates emanating from the tonsillar

crypts
Streptococcal sore throats may develop into rheumatic
fever (late sequelae) and glomerulonephritis

TUMORS OF THE NOSE, SINUSES AND NASOPHARYNX

-

Infrequent
Mesenchymal and epithelial neoplasm

NASOPHARYNGEAL ANGIOFIBROMA
-

Highly vascular tumor

Occurs almost exclusively in adolescent males
Tendency to bleed profusely during surgery (death caused by
haemorrhage)

SINONASAL (SCHNEIDERIAN) PAPILLOMA

-

Benign neoplasm
Arising from the sinonasal mucosa
Composed of squamous or columnar epithelium
HPV types 6 and 11 have been identified in the lesion

Three forms of lesions:

-

Exophytic (most common)

Inverted (most important biologically)
Cylindrical

INVERTED PAPILLOMAS
-

uniquely aggressive biologic behavior

Benign but locally aggressive neoplasm
Occurring in nose and paranasal sinuses
Papillomatous proliferation of squamous epithelium
Extends into the mucosa
High rate of recurrence
Serious complication of invasion of the orbit or cranial vault,
frank carcinoma may develop

Inverted papilloma. the masses of squamous epithelium are growing

inward; hence the term inverted.
OLFACTORY NEUROBLASTOMA (ESTHESIONEUROBLASTOMA)
-

Uncommon, malignant tumors

Composed of small round cells, resembling neuroblasts
Form lobular nests encircled by vascularized connective
tissue
Most often arise superiorly and laterally in nose from the
neuroendocrine cells dispersed in the olfactory mucosa
Differential diagnosis: lymphoma, Ewing sarcoma, and
embryonal rhabdomyosarcoma
Cells are of neuroendocrine origin
Are primitive neuroectodermal tumors
Some reveal trisomy 8
Exhibit membrane bound secretory granules
Express neuron specific enolase, synaptomhysin, CD56 and
chromogranin by immunohistochemistry (all look the same
sa stain will be needed)
many don not share the 11;22 translocation or fusion-gene
products typical of ewing sarcoma (has rosette formation) of
the bone and other primitive neuroectodermal tutors
5 year survival rate of 40-90%

NUT MIDLINE CARCINOMA

-

uncommon tumor that may occur in the nasopharynx, the

salivary gland or in other midline structures in the thorax or
abdomen
can occur at any age
extremely aggressive and resistant to conventional therapy
most patient survive for less than a year
associated with translocations that create fusion genes
encoding chimeric proteins comprised of most of NUT, a
chromatin regulator and a portion of a chromatin reader
protein, usually BRD1

NASOPHARYNGEAL CARCINOMA
-

Close anatomic relationship to lymphoid tissue and an

association with EBV infection

Three patterns:
Keratinizing squamous cell carcinoma (least radiosensitive)
Nonkeratinizing
Undifferentiated carcinomas (most radiosensitive)
-

Abundant non neoplastic, lymphocytic infiltrates

Lymphoepithelioma

Three factors that affect the origin:

- Heredity
Age
Infection with EBV (EBNA-1 in tumor epithelial cells)
Other factors:
Diets high in nitrosamines (fermented foods and salted fish)
Smoking
Chemical fumes

REACTIVE NODULES (VOCAL CORD NODULES & POLYPS)

-

Primary Nasopharyngeal Ca often occult for long periods and

present as metastases in cervical lymph nodes

Morphology
Histologically:
-

Keratinizing and nonkeratinizing squamous cell lesions

resemble usual well differentiated and poorly differentiated
squamous cell carcinoma arising from other locations
Undifferentiated: large epithelial cells with oval or round
vesicular nuclei, prominent nucleoli, and indistinct cell
borders dispodes in syncytium-like array
admixed with abundant, mature, normal appearing
lymphocytes, predominantly T cells

Polyps or reactive nodules develop on the - vocal cords

Often in heavy smokers or singers (singers nodules)
Adult men are most often affected
Singers nodules
Bilateral lesion and polyps are unilateral
Smooth, rounded, sessile or pedunculated excrescences
Located usually on the true vocal cords
Covered by squamous epithelium that may become keratotic,
hyperplastic or dysplastic
Core of nodule is loose myxoid connective tissue that may be
fibrotic or punctuated by numerous vascular channels
When nodules impinge each other, mucosa may undergo
ulceration
Change in character of voice and often progressive
hoarseness
Virtually never give rise to cancers -

SQUAMOUS PAPILLOMA AND PAPILLOMATOSIS

-

Nasopharyngeal Carcinoma, undifferentiated type. The syncytium-like

nests of epithelium are surrounded by lymphocytes

Histologically:
- papillomas are made up of multiple slender, finger like
projections supported by central fibrovascular cores and
covered by an orderly stratified squamous epithelium
- When papillomas are on the free edge, trauma may lead to
ulceration with hemoptysis
- Papillomas are usually single in adults; multiple in children
- Lesions are caused by HPV types 6 and 11
- Do not become malignant but may recur
- Juvenile laryngeal papillomatosis - Papillomas in children
-

LARYNX INFLAMMATIONS
LARYNGITIS
-

Sole manifestation of allergic, viral, bacterial or clinical insult

More commonly part of generalized URTI or result of heavy
exposure to environmental toxins (tobacco)
Occurs in association with gastroesophageal reflux due to
irritating effects of gastric content
Affected in systemic infections (TB or diphtheria)
Mucosal congestion, exudation or edema may
cause laryngeal obstruction
Heavy smokers: predisposes to squamous epithelial
mataplasia and sometimes carcinoma

Caused by Haemophilus influenza or B hemolytic

streptococci
Infants and children with small airways
Sudden swelling of the epiglottis and vocal cords

CROUP
-

Laryngotracheobronchitis in children
Inflammatory narrowing of the airway

Benign comparison of a benign papilloma and an exophytic

carcinoma of the larynx to highlight their quite different
appearances

CARCINOMA OF THE LARYNX

LARYNGOEPIGLOTTITIS
-

Benign neoplasm
Located on the true vocal cords
Soft, raspberry like excrescences rarely more than 1 cm in
diameter

Sequence of hyperplasia-dysplasia-carcinoma
Hyperplasia, dysplasia, carcinoma in situ to invasive
carcinoma
typically a squamous cell carcinoma seen in male chronic
smokers
those confined within the larynx proper are termed intrinsic,
whereas those that arise or extend outside the larynx are
called extrinsic
Epithelial changes vary from smooth, white or reddened
focal thickenings, sometimes roughened by keratosis, to
irregular verrucous or ulcerated white-pink lesions that are
similar in appearance to carcinoma
There are all gradations of epithelial hyperplasia of the true
vocal cords, and the likelihood of the development of an
overt carcinoma is directly proportional to the level of atypia
when the lesion is first seen
Orderly hyperplasias have almost no potential for malignant
transformation
Changes are often related to tobacco smoke The changes
often regress after cessation of smoking
Alcohol is also a risk factor

HANSEL, CHINEE, JOAN 10

PATHOLOGY
HEAD AND NECK
DR. INOCENCIO

Nutritional factors, exposure to asbestos, irradiation and

infection with HPV may contribute to increased risks
Persistent hoarseness
Tumors may produce pain, dysphagia, and hemoptysis
Vulnerable to secondary infection of the ulcerating lesion
Surgery, irradiation, combination therapy

OTITIS MEDIA (ACUTE/CHRONIC)

-

Morphology
-

INFLAMMATORY LESIONS

95 % are typical squamous tumors

Develops directly on the vocal cords but may arise above or
below, on the epiglottis or aryepiglottic folds or pyriform
sinuses
Intrinsic: confined within larynx
Extrinsic: outside the larynx
Begins as in situ lesions that later appear as pearly gray,
wrinkled plaques on the mucosal surface, ultimately
ulcerating and fun gating
Adjacent mucosa may demonstrate squamous cell
hyperplasia with foci or dysplasia or even carcinoma in situ

Inflammation of the ear

Occur mostly in infants and children
Viral in nature
Produce a serous exudate but may become suppurative with
superimposed bacterial infection
Most common offenders: Streptococcus, pneumonia, non
typeable H. influenza, Moraxella catarrhalis,
Pseudomonas aeroginosa (chronic om), Staphylococcus
aureus, or a fungus
In diabetic person, is aggressive and spreads widely causing
destructive necrotizing otitis media

CHRONIC OTITIS MEDIA

-

Has potential to perforate the eardrum

Encroach on the ossicles or labyrinth
Spread into the mastoid space
Even penetrate into the cranial vault to produce a temporal
cerebritis or abscess
with serous accumulation, may rupture

CHOLESTEATOMAS
-

A. Larngeal Carcinoma, Note the large, ulcerated, fun gating lesion

involving the vocal cord and pyriform sinus. B, Histologic appearance
of laryngeal squamous cell carcinoma. note the atypical lining
epithelium and invasive keratinising cancer cells in thesubmucosa

Associated with chronic otitis media

Not neoplasms, nor do they always contain cholesterol
Cystic lesions 1-4 cm in diameter
Lined by keratinizing squamous epithelium or metaplastic
mucus- secreting epithelium
Filled with amorphous debris
Sometimes contain specules of cholesterol
Chronic inflammation and perforation of the eardrum with
ingrowth of squamous epithelium or metaplasia of secretory
epithelial lining of the middle ear are responsible for
formation of a squamous cell nest that become cystic
Sometimes, the cyst ruptures, increasing the inflammatory
reaction and inducing the formation of giant cells that
enclose partially necrotic squames and other debris
Can erode ossicles, labyrinth, adjacent bone or surrounding
tissues
Sometimes produce visible neck masses

OTOSCLEROSIS
EARS
-

Most common aural disorders in descending order of

frequency:
Acute and chronic otitis (most often middle ear and mastoid),
sometimes leading to cholesteatoma
symptomatic otosclerosis
aural polyps
labyrinthitis
carcinomas, largely of external ear
paragangliomas, found mostly in the middle ear

Abnormal bone deposition in the middle ear about the rim of

the oval window into which the footplate of the stapes fit
Both ears are usually affected
First, there is fibrous ankylosis of the footplate followed by
bony overgrowth anchoring it into the oval window
degree of immobilization governs the severity of the hearing
loss
basis for osseous overgrowth appears to represent
Uncoupling of normal bone resorption and bone formation
Begins with bone resorption, followed by fibrosis and
vascularization of the temporal bone in the immediate
vicinity of the oval window, in time replaced by dense new
bone anchoring the footplate of the stapes

Usually begins in the early decades of life

May be familial autosomal dominant
May lead to marked hearing loss

Thyroglossal Duct Cyst

-

TUMORS
-

Epithelial and mesenchymal tumors external, middle,

internal
Basal cell or squamous cell carcinomas of the pinna (external
ear)
Tend to occur in elderly men
Associated with actinic radiation
Locally invasive but rarely spread

Squamous cell carcinomas within canal

-

Middle aged to elderly women

Not associated with sun exposure
Beginning as papules that extend, crode and invade locally
May invade the cranial cavity or metastasize to regional
nodes

NECK
The following are uncommon but unique to the neck:

1 to 4 cm in diameter
lined by stratified squamous epithelium - near the base of the
tongue, or by pseudostratified columnar epithelium - lower
locations
Transitional patterns are also encountered
Possible of malignant transformation but rare!
Tx: excision

Paraganglioma (Carotid Body Tumor)

-

most common location of the tumor is within the adrenal

medulla, where they give rise to pheochromocytoma
approximately 70% of estra- adrenal paragangliomas occur
in the head and neck region
pathogenesis is not fully understood
chiefly composed of nests (zellballen) of round to oval chief
calls (neuroectodermal in origin) that are surrounded by
delicate vascular septae
tumors cell contain abundant, clear or granular, eosinophilic
cytoplasm and uniform, round to ovoid, sometimes vesicular
nuclei
slow-growing and painless masses
usually arise in the fifth and sixth decades of life
associated with the sympathetic and parasympathetic
nervous systems
can be seen throughout various regions of the body

Branchial Cyst (Cervical Lymphoepithelial Cyst)

-

thought to arise from remnants of the second brachial arch

and are most commonly observed in young adults between
ages 20 and 40
appear on the upper lateral aspect of the neck along
sternocleidomastoid muscle
cyst are well circumscribed, 2 to 5 cm in diameter, with
fibrous walls usually lined by stratified squamous epithelium
or pseudostratified columnar epithelium
cyts wall typically contains lymphoid tissue with prominent
germinal centers.
contents of the cyst may be clear and watery or mucinous
and may contain desqwuamated, granular cellular debris.
benign cysts
slowly progressive
readily excised

possible cause: succinate oxidoreductase, an enzyme

involved in mitochondrial respiration
microscopic features - remarkably uniform

locations of possible growth:

1.

2.

upper lateral aspect of the neck along the

sternocleidomastoid muscle
arise from remnants of second branchial arch

Paravertebral paraganglia - tumors have sympathetic

connections chromaffin-positive - a stain that detects
catecholamines
Paraganglia related to the great vessels of the head and
neck, the so- called aorticopulmonary chain, including
carotid bodies; aortic bodies; jugulotympanic ganglia;
ganglion nodusom of the vagus nerve; and clustersw
located about the oral cavity, nose, nasopharynx, larynx,
and orbit. These are innervated by parasympathetic
nervous sytem and release cathecholamines.

Morphology:
Carotid body tumor:

HANSEL, CHINEE, JOAN 12

PATHOLOGY
HEAD AND NECK
DR. INOCENCIO

prototpye parasympathetic ganglioma

rarely exceeds 6cm in diameter
arises close to or envelops the bifurcation of the common
carotid artery
red-pink to brown
composed of nests (Zellballen) of round to oval chief cells
(neuroectodermal in origin) that are surrounded by delicate
vascular septae
abundant, clear or granular, eosinophilic cytoplasm
uniform, round to ovoid, sometimes vesicular, nuclei
little cellular pleomorphism, and scant mitoses
sustentacular cells - positive for S-100 protein
** chief cells that stain in chromogranin, synaptophysin,
neuron-specific enolase, CD56, and CD57

analgesic
antihistamine agents

Complications:
-

increased rates of dental caries

candidiasis
difficulty in swallowing and speaking.

Inflammation (Sialadenitis)
-

traumatic, viral, bacterial, or autoimmune

Mucoceles are the most common type of lesion
keratoconjunctivitis sicca dry eyes

Mumps
-

most common form of viral sialadenitis

parotid glands are affected

Mucocele
FIGURE 16-14 Carotid body tumor. A, Low-power view showing tumor
clusters separated by septa (Zellballen). B, High-power view of large,
eosinophilic, slightly vacuolated tumor cells with elongated
sustentacular cells in the septa
-

may be familial
with autosomal dominant transmission
frequently recur after incomplete resection
benign but may metastasize to regional lymph nodes and
distant sites
**mitoses, pleomorphism, and even vascular invasion are not
reliable indicators**

most common lesion of the salivary glands

results from the blockage or rupture of salivary gland duct,
with consequent leakage of saliva into the surrounding
connective tissue stroma.
most often found in lower lip and the result of trauma
typically seen in toddlers and young adults and elderly, ho
are more prone to falling

histologically,
- has a cystlike space (filled with mucin and inflammatory
cells)that is lined by inflammatory granulation tissue or by
fibrous connective tissue
-

Complete excision of the cyst with the minor salivary gland

lobule origin is required
to avoid recurrence.

SALIVARY GLANDS
-

parotid, submandibular, and sublingual

Xerostomia
-

decreased saliva production

aka dry mouth
major feature of the autoimmune disorder Sjgren
syndrome
major complication of radiation therapy

drug-induced:
- anticholinergic
- antidepressant/antipsychotic
- diuretic, antihypertensive
sedative
- muscle relaxant

FIGURE 16-15 Mucocele. A, Fluctuant fluid-filled lesion on the lower

lip subsequent to trauma. B, Cystlike cavity filled with mucinous
material and lined by organizing granulation tissue
Ranula identical to mucocele in which duct of the sublingual gland
has been damaged; can become extremely large and develop into a
plunging ranula

Sialolithiasis and Nonspecific Sialadenitis

-

major salivary glands

submandibular glands
usually secondary to ductal obstruction produced by stones
(sialolithiasis)
common etiology: S. aureus and Streptococcus viridians
unilateral involvement

Most common Salivary Gland Tumors

Benign:
Pleomorphic adenoma. i.e. Mixed Tumor
warthin Tumor (Papillary Cystadenoma Lymhpomatosum)
Malignant:
all are adenocarcinoma
muciepidermoid carcinoma
adenoid cystic carcinoma
Neoplasms
-

About 65% to 80% arise within the parotid, 10% in the

submandibular gland, and the remainder in the minor
salivary glands, including the sublingual glands
The likelihood of a salivary gland tumor being malignant is
more or less inversely proportional to the size of the gland.
Adults, slight female predominance

Warthin tumors
-

Palate capsule (not fully developed)

expansile growth produces protrusions into the surrounding
gland
enucleation of the tumor hazardous
cut surface gray-white with myxoid and blue translucent
areas of chondroid (cartilage-like)
epithelial resembling ductal cells or myoepithelial cells
arranged in acini, irregular tubules, strands, or sheets of
cells
typically dispersed within a mesenchyme-like background of
loose myxoid tissue containing islands of chondroid and,
rarely, foci of bone

Males
Benign - often appear in the fifth to seventh decades of life
Malignant ones later in life
no reliable criteria to differentiate benign from malignant
tumors.

PLEOMORPHIC ADENOMA/MIXED BENIGNBENIGN TUMOR

-

60% of tumors in the parotid

Dominant histologic feature:

- great heterogeneity
- mixture of ductal (epithelial) and myoepithelial cells
- Epithelial - myxoid, hyaline, chondroid (cartilaginous), and
even osseous tissue
- Resembles ductal cells or myoepithelial cells
- arranged in duct formations, acini, irregular tubules, strands,
or sheets of cells
Morphology
Pleomorphic adenomas rounded, well-demarcated
masses (encapsulated)

lined by cuboidal to columnar cells with an underlying layer

of deeply chromatic, small myoepithelial cells
no difference in biologic behavior between the tumors
composed largely of epithelial elements and those composed
largely of seemingly mesenchymal elements

Clinical Features
- tumors: painless, slow-growing, mobile discrete masses
within the parotid or submandibular areas or in the buccal
cavity (image earlier)
- carcinoma ex pleomorphic adenoma or a malignant mixed
tumor carcinoma arising in a pleomorphic adenoma
- cancer usually takes the form of an adenocarcinoma or
undifferentiated carcinoma
WARTHIN TUMOR (PAPILLARY CYSTADENOMA
LYMPHOMATOSUM)
-

benign neoplasm

HANSEL, CHINEE, JOAN 14

PATHOLOGY
HEAD AND NECK
DR. INOCENCIO

second most common salivary gland neoplasm

arises almost exclusively in the parotid gland (the only tumor
virtually restricted to the parotid)
more commonly in MALES
Smokers have higher risk

Morphology
round to oval, encapsulated masses, 2 to 5 cm in diameter
superficial parotid gland palpable
transaction: pale gray surface punctuated by narrow cystic
or cleftlike spaces filled with a mucinous or serous secretion

contain small, mucin-containing cysts

histologic pattern:
cords, sheets, or cystic configurations of squamous, mucous,
or intermediate cells
hybrid cell types squamous features, with small to large
mucus-filled vacuoles (highlighted with mucin stains)
tumor cells regular and benign appearing OR highly
anaplastic and unmistakably malignant
subclassified: low, intermediate, or high grade

microscopic:
- lined by a double layer of neoplastic epithelial cells resting
on a dense lymphoid stroma sometimes bearing germinal
centers
spaces: narrowed by polypoid projections of the
lymphoepithelial elements
- double layer of lining cells consists of a surface palisade of
columnar cells having an abundant, finely granular,
eosinophilic cytoplasm (oncocytic appearance) rests on a
layer of cuboidal to polygonal cells
Oncocytes epithelial cells stuffed with mitochondria
- Secretory cells dispersed in the columnar cell layer

OTHER SALIVARY GLAND TUMORS ADENOID CYSTIC

CARCINOMAS
-

uncommon tumor
50% cases minor salivary glands (palate)
(major) parotid and submandibular glands most common
locations

Morphology
MUCOEPIDERMOID CARCINOMA
Composed of:
Squamous cells
Mucus-secreting cells
Intermediate cells
-

15% of ALL salivary gland tumors

60-70% in the PAROTIDS
MECT1-MAML2 gene play a key role in the genesis of this
tumor, possibly by perturbing the notch and cAMPdependent signaling pathways
most common form of primary malignant tumor of the
salivary glands

Morphology
can grow as large as 8 cm in diameter
circumscribed but lack well-defined capsules (infiltrative at
the margins
Transection:
- pale and gray-white

Gross:
-

small, poorly encapsulated, infiltrative, gray-pink lesions

Histologic:
- composed of small cells having dark, compact nuclei and
scant cytoplasm
- Cells disposed in tubular, solid, or cribriform patterns
reminiscent of cylindromas arising in the adnexa of the skin
- Spaces: filled with a hyaline material thought to represent
excess basement membrane

ACINIC CELL TUMOR

-

Composed of resembling serous acinar cells of salivary

glands
uncommon (2-3% of salivary gland tumors)
most arise in the parotids; remainder arise in the
submandibular glands
sometimes bilateral or multicentric

Gross:
- small, discrete lesions that may appear encapsulated
Histologic:
- cells clear cytoplasm but the cells are sometimes solid and
at other times vacuolated
- disposed in sheets or microcystic, glandular, follicular, or
papillary patterns
- course of these neoplasms dependent on the level of
pleomorphism
- recurrence after resection is uncommon

_________________________________________________________________________________
END.
Hansel, chinee, joan
REFERENCES:
1. Kumar et al. 2010. Robbinsand Cotran Pathologic Basis of Disease.
8th ed. Pp. 3-42
2. DR. nocencios lecture
3. Trascription from Batch 2016

HANSEL, CHINEE, JOAN 16