Alimentary system pathology (part 1)

Pyogenic Granuloma (12st)

Highly vascular pedunculated lesion,
usually in children, young adults,
and pregnant women (pregnancy
tumor).
Over 60% of between 11 and 40
years of age
painless, exophytic nodular mass
usually pedunculated or sessile
Elevated. Soft
deep red/purple color
Erythematous, hemorrhagic
Benign polypoid nodule primarily
occurring on mucous membranes
Gingiva 70 - 75%, followed by the
tongue, lips, and buccal mucosa
Composed of lobules of dense,
proliferating capillaries (capillary
hemangioma), often with edema
and inflammatory infiltrate
Dilated, irregular vascular spaces
surrounded by granulation tissue
with chronic inflammatory
infiltrate
Keratinized, squamous
epithelium.
Grows rapidly. Size from a few
millimeters to several centimeters
Budding of the capillaries takes place
around the small, thin-walled blood
vessels, which are often considerably
expanded. Thus comes the another
Latin name granuloma
teleangiectaticum
Slide:
Granulation tissue proliferative
connective tissue (fibroblasts and
fibrocytes) and newly formed
capillary channels, with interspersed
chronic inflammatory cells.
Numerous thin-walled capillaries
containing erythrocytes

Vascular space

Giant cell epulis (Epulis gigantocellularis) (13st)

Peripheral giant cell granuloma (giant
cell epulis) is a relatively uncommon
reactive tumor of the oral cavity
All age groups. More common in
females. Predominant in white
persons. Often > 20 years of age.
Maxilla and mandible are affected
with equal frequency
A soft-to-firm mass forms in the
gingiva
Pushes the teeth aside, may erode
the underlying bone
Benign and probably of reactive
nature
Typically well-circumscribed sessile
or pedunculated mass, dark red in
color, which hemorrhages easily and
may or may not be ulcerated.
The lesion is relatively elastic on
palpation, and the size ranges from
0.5 cm to 2 cm in diameter.
Etiology
Local irritation or trauma. Injury
to soft tissues. The trauma may be
caused by tooth extraction
Chronic infection
Fibroblasts between the giant
cells produce the stroma
It seems to originate from either
periodental ligament or
mucoperiosteum
The lesion occurs exclusively on the
gingiva or edentulous alveolar ridge
Treatment excision with borders of
normal tissue with entire base of
lesion, so that recurrence is avoided.
Active stroma with numerous:
osteoclast-like giant cells
blood vessels
Fibroangiomatous stroma

Squamous epithelium of the

gingiva is seen on the surface

Keratosis of the epithelium of the oral cavity (Leukoplakia) (23st)

Leukoplakia (from Greek, leukos, white and palx, plaque) is an asymptomatic white patch on
oral mucosa that cannot be scraped off. Some of these lesions undergo transformation to
squamous cell carcinoma (premalignant lesion)!
Always biopsy these lesions because of the high risk to progress to oral cancer
5-25% of cases are premalignant.
Is a clinical term used to describe patches of keratosis. It is visible as adherent white patches on
the mucous membranes of the oral cavity. The clinical appearance is highly variable:
Solitary or multiple
Small lesions to large patches
Usually well defined borders
Clinical appearance of leukoplakias can range from:
a) smooth and thin with well demarcated borders
b) diffuse and thick
c) irregular with a granular surface
d) diffuse and corrugated
Locations: leukoplakia occurs most often on the buccal mucosa, tongue, and floor of the mouth
Lekoplakia of the tongue with invasive squamous cell carcinoma. Discrete raised white patches
are evident on both sides of the tongue.
The disorders occur with equal frequejcy in both sexes, mostly after the third decade of life
Etiology - the causes of leukoplakia are diverse:
a) chronic local irritation (e.g. dentures)
b) all forms of tobacco use major risk factor (associated with smoking!)
c) alcohol abuse
d) human papilloma virus (HPV)
Treatment: complete removal (surgical excision, cryosurgery, CO2-laser surgery). Preserve
specimen for histological exam!
A variety of diseases appear clinically as leukoplakia.
Candidiasis, lichen planus, psoriasis, syphilis, various kerotoses, hyperkerotosis, squamous
carcinoma in situ, chemical injury (aspirin burn)
Must distinguish from diseases that may cause similar white lesions. The lesions of leukoplakia
cannot be scraped off easily
The typical clinical progression of oral cancer:
Leukoplakia may show a spectrum of histopathologic changes, from increased surface
keratinization without dysplasia to invasive keratinizing squamous carcinoma. The frequency
of malignant transformation in leukoplakia is about 10-30%
The histologic progression of squamous epithelium:
Hyperkeratosis mild/moderate dysplasia to severe dysplasia carcinoma in situ
(CIS) squamous cell carcinoma (SCC)
Histopathological features: presence or absence of epithelial dysplasia, epithelial hyperplasia,
surface hyperkeratosis, marked atypia, and parakeratosis.

Keratosis of the epithelium of the oral cavity (Leukoplakia) (23st)

Keratin

Submucosa

Mucous gland

Epithelium

Lamina propria
(underlies epithelium)

Leukoplakia
Epithelial changes can range from hyperkeratosis overlying a thickened, acanthotic but orderly
mucosal epithelium to lesions with markedly dysplastic changes sometimes merging into
carcinoma in situ.
The more dysplastic or anaplastic, the more likely inflammatory infiltrate is present.

Squamous papilloma (17st)

The papilloma (squamous papilloma) is a benign, exophytic proliferation of stratified squamous
epithelium arranged in fingerlike projections
Develops in all age groups but is most often seen in the third to fifth decade of life
Etiology: presumably human piapillomavirus (HPV)
Treatment is conservative surgical excision, including a small amount of normal epithelim at the
base. Recurrance is rare 4%.
Most commonly seen on the hard and soft palate-uvula complex, but is often seen on the ventral
and dorsal tongue, the gingiva, and the buccal mucosa.
Pink, pedunculated and papaillary lesion attached to the lingual frenum.
Clinically, this configuration may appear cauliflowerlike
The base may be either pedunculated or sessile
Color ranges from that of normal mucosa to white or red
Soft, painless
papillomas are generally less than 1 cm in diameter, but they have grown as large as 2 to 3 cm
(75% are less than 1 cm)
In most situations, the lesion is solitary; however, an occasional patient may have multiple
papillomas. In addition, multiple papillomalike epithelial proliferations may develop in
immunocompromised persons
The covering squamous epithelium shows a normal maturation pattern, although occasional
papillomas demonstrate basilar hyperplasia an mild mitotoc activity which could be mistaken for
mild epithelial dysplasia
Micro: delicate fibrovascular cores surrounded by squamous epithelium; hyperkeratosis in 82%,
parakeratosis in 72%; variable hyperplasia of basilar cell, individual cell keratinization, abnormal
mitotic figures; often no koilocytotic changes; no pushing growth into lamina propria.

Squamous papilloma (17st)

Histology:
papillary configuration
Finger-like projections of
thickened (acanthotic) epidermis
overlying a fibrovascular core
variable inflammation
Hyperkeratosis and parakeratosis
often present.

Keratinized, stratified
squamous epithelium

Branching fronds of
squamous epithelium
with fibrovascular cores

Fibrovascular
connective tissue

Granular cell tumor (myoblastoma) (10st)

This granular cell tumor is relatively
uncommon neoplasm that shows a
predilection to the oral cavity,
especially the tongue
Formerly called the granular cell
myoblastoma because of its suspected
skeletal muscle origin.
Most investigators now believe it
arises from either the Schwann
cell or an undifferentiated
mesenchymal cell.
It is most common in young and
middle-aged adults and is twice as
common in women.
The typical presentation:
A sessile swelling on the tongue
covered by normal appearing
epithelium
Slow-growing, nonulcerated
nodular mass that is usually pink
but sometimes may appear yellow
Multiple granular cell tumors
occasionally may occur
Benign
Treatment: Local surgical excision;
recurrence uncommon
Micro: associated with
pseudoepitheliomatous hyperplasia of
the overlying epithelium. It is
important that the pathologist not
mistake it for squamous cell
carcinoma.
Large polygonal oval or bipolar
cells with eosinophilic cytoplasm.
A small nuclei acentrically located
in the cell.
Minimal or no background
stroma.
Large cells with abundant granular
cytoplasm and nuclei
Large cells with no
background stroma.
Small nuclei.

Ameloblastoma (5st)
Ameloblastomas are slow-growing,
locally invasive tumors that generally
follow a benign course
The most common tumor of
odontogenic epithelial origin that
primarily affects jaws
Confluent islands of
odontogenic epithelium.
Irregular cords of epithelial cells
form plexiform pattern.
Central portion of epithelial cord is
composed of loose network of
triangular shaped cells resembling
stellate reticulum
Etiology:
Ameloblastoma probably arises
from dental lamina rests or from
basal epithelial cells
Remember! Ameloblastoma is
characterized by infiltrative
growth and tendency to recur.
Rarely, it may metastasize.
Usually present as painless, slow
growing, non-ulcerated, sessile red
mass
size between 1 and 2 cm
Mandible most arise in mandibular
ramus or molar area
Fibrous connective
tissue stroma
Micro:
Cells tend to move the nucleus
away from basement membrane.
This process is called reverse
polarization
inner zone composed of cells
resembling stellate reticulum
Peripheral cells form bands that
separate the tumor from the
stroma. The outermost cells
resemble the ameloblastic layer of
developing tooth follicle.
Basement membrane
Odontogenic epithelium cells with
palisading and polarizing nuclei
oriented vertically to the basement
membrane.

Chronic sialadenitis (514)

Septa

Duct
A form of mild lymphocytic
infiltration of major salivary gland
Some cases are focal obstructive,
accompanied by various degree of
parenchymal atrophy and fibrosis.
Other, more common in females, are
age related, have high statical
association with rheumatoid arthritis,
and probably immune related.
Sialolithiasis is the most common
cause in clinically apparent cases.
Mainly involves submandibular gland
Treatment depends on position of
stone. If the stone is in the duct, it can
be removed with the duct. But if
inside gland, the entire gland will
have to be removed.
Salivary gland (acini)
Slide:
Hyperplastic lymphoid infiltrates
with loss of salivary gland acini;
ducts are surrounded and infiltrated
by lymphoid cells
Fibrosis and parenchymal atrophy
Inflammatory infiltrate everywhere
Many glands (mixed glands)
Bands of fibrous connective tissue,
divide salivary gland into nodules
(septa)
Dense inflammatory
infiltrate (lymphocytes)
surrounding acinar glands

Capsule

Pleomorphic adenoma of the salivary gland (515)

Benign mixed tumor (pleomorphic
adenoma of parotid gland)
Epithelial and mesenchymal part
in are mixed together
Pleomorphic adenomas:
Epidemiology: 60% of tumors of
parotid gland are pleomorphic
adenomas.
Rare in minor salivary glands.
The most common neoplasm of
the salivary gland.
Radiation exposure
Female dominant
Micro: Nests of epithelial and
myoepithelial cells forming ducts,
trabeculae or solid sheets.
Loose myxoid and chondroid
tissue (differentiation of a part of
the stroma into cartilage)
Myoepithelial cells undergoing
cartilaginous metaplasia
Ductal cells, myoepithelial cells,
matrix (myxoid, hyaline,
chondroid).
Usually no epithelial dysplasia or
mitotic activity.

Chondroid matrix

Slow growing, painless, movable

mass at the angle of jaw
Tumor with stromal metaplasia
The capsule tends to be thicker and
less likely to be penetrated by the
tumor when the lesions are located in
the deeper lobes.
Benign tumor, but may recur when
removed from capsule without the
surrounding tissue.
Gross: well-demarcated, rarely
exceed 6 cm. The consistency
depends on the relative amount of
epithelial cells and stroma. Cut
surface is yellow-white with myxoid.
Island of cartilage can be recognized
by their translucent appearance.
Myxoid

Duct formation