DISORDER OF HEAD & NECK

DISORDER OF HEAD & NECK

Topics include-
 Ear

 Nasal cavity

 Oral cavity

 Neck

 Salivary gland

 Odontogenic cysts & Neoplasms

EAR INFECTION
Ear infections are found in all age groups, but they are
considerably more common in children, especially those aged six
months to three years.

Boys are affected more commonly than girls. Other children at

higher risk include those from poor families, Native Americans,
children born with cleft palate or other defects of the facial
structures, and children with Down syndrome .

Exposure to cigarette smoke and early entrance into daycare also

increase the risk. Otitis media occurs more frequently in winter
and early spring
MIDDLE EAR
• Acute otitis media (AOM) is most often purely viral and
self-limited, as is its usual accompanying viral upper
respiratory infection. There is congestion of the ears and
perhaps mild discomfort, but the symptoms resolve with
the underlying URI.
• If the middle ear, which is normally sterile, becomes
contaminated with bacteria, pus and pressure in the
middle ear can result, and this is called acute bacterial
otitis media.
• Bacterial cases may result in perforation of the ear drum,
infection of the mastoid space (mastoiditis) and in very
rare cases further spread to cause meningitis
MIDDLE EAR
• Acute suppurative otitis media is most frequently caused
by streptococcus pneumonia or H. influenza.
• Clinical features : Bulging, hyperemic tympanic
membrane, the result of accumulation of fluid in the
middle ear.
• Ear pain, tenderness & fever.
• Treatment: Incision of the tympanic membrane releases
the exudate, reduces pressure & diminish the pain .
• Complication : Mastoiditis, meningitis.
OTITIS MEDIA IMAGE
Acute otitis
media presents
with a bulging
tympanic
membrane,
increased
vascularity,
erythema and
distortion of
normal
landmark
CHRONIC OTITIS MEDIA
 Chronic suppurative otitis media (CSOM) is a chronic
inflammation of the middle ear and mastoid cavity.
Clinical features are recurrent otorrhoea through a
tympanic perforation, with conductive hearing loss of
varying severity.

 Experts dispute the duration of otorrhoea required to

determine it as a chronic infection - the World Health
Organization's definitions suggest more than two weeks;
others contend longer (e.g. up to six weeks).
CSOM
• Risk factors
• Multiple episodes of acute otitis media (AOM).
• Living in crowded conditions.
• Being a member of a large family.
• Attending daycare
• Craniofacial anomalies increase risk: cleft lip or
palate, Down's syndrome, , and microcephaly all
increase the risk of CSOM.
CHRONIC SUPPURATIVE OTITIS MEDIA
(CSOM)
 Gross appearance : Polypoid granulation tissue may be
present in external canal, attached to the tympanic
membrane or middle ear structures.
 Granulomatous lesions such as tuberculosis & fungal
infection are also causes of chronic otitis media.
CSOM
 Clinical features : Persistent drainage from the ear
associated with tympanic membrane perforation & some
degree of hearing impairment.
 Treatment:Surgeries include tympanoplasty,
mastoidectomy, or typanomastoidectomy
CHOLESTEATOMA
 This tumor most often found in the middle ear or
mastoid .
 It is thought to be the post inflammatory
Nonneoplatic condition.
 Grossly it resemble a pearl.

 Microscopically it consist of an epidermal cystic

structure filled with fibrillar layer of keratin
debris admixed with cholesterol crystals.
CHOESTEATOMA
CHOESTEATOMA(MICRO)
CHOESTEATOMA
 Pathogenesis : Ingrowth of squamous epithelium from
the external ear into the middle ear following an ottitis
media.
 Complication : Produce hearing impairment & erode into
mastoid bone.
 Treatment : surgical removal.
INNER EAR
 Ménière's disease: In 1861, the French physician Prosper
Ménière described a condition which now bears his
name. Ménière's disease is a disorder of the inner ear
which causes episodes of vertigo, ringing in the ears
(tinnitus), a feeling of fullness or pressure in the ear, and
fluctuating hearing loss
INTERNAL EAR
 Internal ear:
 Internal ear contains
 1) Bony labyrinth which consists of a series of
channels(Present in the petrous portion of
temporal bone) The bony labyrinth contains a
fluid called perilymph.
 2) Membranous labyrinth which lies within the
bony labyrinth.The membranous labyrinth is
filled with a fluid called endolymph.
 MÉNIÈRE'S DISEASE
An acute attack of Ménière's disease is generally
believed to result from fluctuating pressure of the fluid
within the inner ear. A system of membranes, called the
membranous labyrinth, contains a fluid called
endolymph. The membranes can become dilated like a
balloon when pressure increases. This is called
"hydrops".
However, for the most part the underlying cause of
Menieres disease is unknown. It is most often attributed
to viral infections of the inner ear, head injury, a
hereditary predisposition, and allergy
MÉNIÈRE'S DISEASE

Normal membranous Dilated membranous labyrinth in Meniere's

labyrinth disease (Hydrops)
MÉNIÈRE'S DISEASE
 Treatment :
 Most patients are advised to adopt a low-sodium
diet, avoid caffeine, alcohol and tobacco, all of
which can aggravate symptoms of Ménière's
disease.

 Medicine
-Include antihistamines, anticholinergics, steroid
s, and diuretics
NASAL CAVITY
 
 Inflammatory disease are most common
disorders to affect the nose & nasal sinuses-
common cold.
 Rhinitis – Inflammation of nasal cavity by one
of the many viruses –adenovirus produce
nasopharyngitis or phyryngotonsilitis.
 These virus aggravates or evoke a profuse
catarrhal discharge.
RHINITIS
 During the acute stage of rhinitis the nasal mucosa is
thickened, edematous & red.
 Secondary bacterial infection produces mucopurulent or
suppurative exudate.
ALLERGIC RHINITIS
 Allergic rhinitis (Hay fever): It is sensitivity
reaction to one of the large group of allergens.
 Most common allergens are plant pollens.
 Allergic rhinitis is an IgE mediated immune
reaction.
 Acute response mediated by mast cell
degranulation.
 Late persistent response caused by infiltration of
eosinophils, basophis, neutrophils &
macrophages.
ALLERGIC RHINITIS
NASAL POLYP
 Nasal polyp : Result of recurrent allergic rhinitis.
 It is not true neoplasm but inflammatory
hypertrophic swelling of nasal mucosa.
 Grossly nasal polyp can reach over 5 cm in
diameter.
 Histologically polyp consist of loose edematous
stroma with inflammatory cells- neutrophils,
eosinophils & plasma cells.
NASAL POLYP
Nasal polyp has
inflammatory cells in the
edematous stroma. Seen
here are many
eosinophils, which are
characteristic for allergic
inflammatory responses.
However, neutrophils,
plasma cells, and
occasional clusters of
lymphocytes can also be
seen.
ORAL CAVITY
Oral candidiasis-
 Candida albicans is a normal inhabitant of the
oral cavity- 30% to 40%.
 It causes disease only when there is some
impairment of protective mechanism-DM,
anemia, steroid therapy, disseminated cancer etc,
 Persons with the acquired immunodeficiency
syndrome (AIDS) are at particular risk.
ORAL CANDIDIASIS

 Morphology: White , curd like, circumscribed

plaque anywhere within the oral cavity- pseudo
membrane.
 It can be scrapped of to reveal an underlying
granular erythematous base.
 Microscopy: Pseudo membrane is composed of
fungal organism attached to necrosed mucosa.
 The fungi can be identified as box-like chain or
tubular cells.
ORAL CANDIDIASIS

-Candidiasis may spread into the esophagus.

-It may gains entry into the blood stream & produced
widespread visceral infection
- Disseminated candidiasis is a life threatening infection.
Oral candidiasis is an
infection of yeast fungi of the
genus "Candida" on the
mucous membranes of
the mouth. It is frequently
caused by "Candida
albicans", or less commonly
by "Candida glabrata" or
"Candida tropicalis
 Oral candidiasis -PAS stain  KOH preparation
LEUKOPLAKIA
 Leukoplakia : It is a white patch or plaque that
cannot be scraped off
 Thus the term is not applied to other white
lesions, such as candidiasis,lichen planus or any
other disorders.
 It is whitish, well defined mucosal patch or
plaque caused by epidermal thickening or
hyperkeratosis.
LEUKOPLAKIA
 The plaques are most often on the vermillion border
of the lower lip ,buccal mucosa & the hard & soft
palates.
 Etiology : associated with use of tobacco-pipe
smoking, pouch,snuff, chewing.
 Alcohol abuse.
 Chronic friction from ill –fitting denture or jagged
teeth.
 Recently human papilloma virus antigen has been
identified in some tobacco-related lesions.------SCC
(squamous cell carcinoma)
LEUKOPLAKIA
 Microscopic appearance is vary from hyperkeratosis to
mild to severe dysplasia.
 3 to 25% lesions undergo transformation to squamous
cells carcinoma.
 Transformation rate is greatest with tongue lesion &
those on the floor of the mouth.
Hairy leukoplakia (also known as "oral hairy leukoplakia“) is a white patch on
the side of the tongue with a corrugated or hairy appearance

Hairy leukoplakia is seen in severe defects of immunity, particularly

in HIV infection
ERYTHROPLAKIA
 Erythroplakia – It is red, velvety circumscribed area that
may or may not be elevated.
 Histologically erythroplakia almost invariably reveals
epithelial dysplasia.
 Malignant trasformation rate is >50%.

 100% dysplasia on erythroplakia rather than hairy cell

leukoplakia.
 ERYTHROPLAKIA
Treatment involves biopsy of
the lesion to identify extent of
dysplasia. Complete excision
of the lesion is sometimes
advised depending on the
histopathology found in the
biopsy. Even in these cases,
recurrence of the
erythroplakia is common
and, thus, long-term
monitoring is needed
EPITHELIAL DYSPLASIA
ORAL MANIFESTATIONS IN
SYSTEMIC DISEASES
 HAIRY LEUKOPLAKIA
 Immunocompromised or
immunosuppressive patients
(HIV)
 Related to EBV infection

 Appears as white, confluent

patches of fluffy (hairy)
hyperkeratotic thickenings on
lateral border of tongue.
 Microscopy :

 Hyperkeratosis

 Acanthosis

 Balloon cells in upper spinous

layer.
 MEASLES - KOPLIKS SPOTS

They are characterized as

clustered, white lesions on
the buccal mucosa and
are pathognomonic for
measles

They are described as

appearing like "grains of salt
on a wet background
GUM ENLARGMENT

 Assoc w/ phenytoin
(Dilantin) therapy
 Thickened gums not
hyperplastic
 PEUTZ-JEGHER SYNDROME

Disease characterized by
the development of benign
hamartomatous polyps in
the gastrointestinal tract
and hyperpigmented
macules on the lips and
oral mucosa
CANCER OF ORAL CAVITY
Cancer of oral cavity & tongue.
 Most of the oral cavity cancers are squamous
cells carcinoma.
 They represent only 3% of all cancers in the
USA.
 Readily accessible to biopsy & early
identification.
 Age is rarely before 40 years.
 When these cancers are discovered at an early
stage, 5 year survival can exceed 90 %.
CANCER OF ORAL CAVITY & TONGUE
 Risk factors:
 Preexisting lesions- leukoplakia or erythroplakia.

 Tobacco- Pipe smoking & smokeless tobacco.

 HPV type 16 & 18 : The antigen identified in

30% to 59% of lesions.
 Alcohol abuse: Weaker influence then tobacco
but two habits interact to greatly increases risk.
CANCER OF ORAL CAVITY & TONGUE
 Practical method of grading the tumors:
 1) Tumors of lips to teeth- mostly low grade tumors

 2) Tumors from teeth to back of tongue- more malignant.

 3) Tumor of pharynx: Having High grade of maliganacy.

 Velscope Oral Mucosal Screening
 A new tool for oral mucosal examination Velscope
  It is based on the direct visualization of tissue fluorescence and
the changes in fluorescence that occur when abnormalities are
present
 View of healthy tissue through the
VELscope

View of abnormal tissue through the

VELscope. Lesions identifiable by dark
color and irregular shape
CARCINOMA OF LIP
Carcinoma of lip :
 One of the most common cancer

 More common in males

 More common site is lower lip. Because more exposed

to actinic rays
CARCINOMA OF LIP
 Gross appearance : Lesion begins as a local
thickening & indurations.
 If growth is mainly toward the surface a warty
nodule is formed which soon become ulcerated.
 If growth is deep – It represents as a deep seated
indurations.
 Microscopically the tumors is squemous cell
carcinoma.
CARCINOMA OF LIP
 Spread of lip carcinoma :
 Tumor may destroy the lip, skin of the chin &
involve the mandible.
 Tumor cells spread by lymphatics- submaxillary
& submental lymph nodes are involved.
 Inferior cervical & supraclavicular nodes are
seldom involved.
 Prognosis is excellent.

 Treatment- Surgery or radiotherapy.

Actinic chelitis is caused by Excessive exposure to UV rays
chronic and excessive can also lead to squamous cell
exposure to the ultraviolet carcinoma
radiation in sunlight
CARCINOMA OF MOUTH
 Carcinoma of mouth : Occurs commonly in the lower
oral cavity, chiefly on the floor of the mouth, chin & the
mandible.
 Leukoplakia- frequent present

 Other predisposing factors- Tobacco, lack of vitamin B,

badly fitting dental plate.
CARCINOMA OF MOUTH
 In Indian subcontinent it is known as betal-nut
cancer.
 People have a habit of chewing quid composed
of-
 1) Leaf of betel vine

 2)Nut of areca palm

 3)Slaked lime

 4)Uncured tobacco

 And result is oral carcinoma.

 INDIA( RISK FACTOR FOR ORAL
CANCERS) Areca nut

Betel leaf Tobacco

Slaked lime
The picture to the right shows the removed surgical specimen. 

Although smoking is a risk factor for development of oral cancer,

the human papillomavirus is an even greater risk in developing
cancer of the base of tongue and tonsil
CARCINOMA OF MOUTH
 Microscopy : Squemous cells carcinoma, but high grade
& much more severe.
CARCINOMA OF TONGUE
Carcinoma of tongue :
 It is quite rare in women & in a healthy tongue.
 Tongue is divided in to two portions by V –shaped
line of circumvallate papillae, the anterior two third
& posterior one third.
 Cancer of the anterior two-third is epidermoid in
nature & of high grade malignancy.
 Cancer of posterior third is rare but usually markedly
malignant & occasionally a transitional cell carcinoma
 Tumors on the base
of the tongue are
usually larger when
diagnosed because in
the early stages the
tumor is difficult to
see. The only early
symptom is ear pain.
Voice changes and
difficult swallowing
occur later
CARCINOMA OF TONGUE.
 Spread is rapid because-
 1) Rich lymphatic drainage.

 2) Constant muscular movement

 3) High grade of malignancy.

 Lymphyetic spread takes place into the submental &

submaxillary lymph nodes.
 Superior , inferior deep cervical & even supraclavicular
nodes are involved.
Carcinoma of tongue
Any lesion in the mouth which
does not go away within a few
days needs investigation.   A
malignancy may present as a
white lesion (sometimes white
and red), an ulcer which does
not heal.
 LUDWIG'S ANGINA
Ludwig's angina, is a serious, potentially life-
threatening cellulitis infection of the tissues of the floor
of the mouth, usually occurring in adults with dental
infections
The cause is usually a bacterial infection, most often
Streptococcus spp, although other bacteria can also
cause.
Since the advent of antibiotics, Ludwig's angina has
become a rare disease
 LUDWIG'S ANGINA
The route of infection in most cases is from infected
lower third molars or from pericoronitis, which is an
infection of the gums surrounding the partially erupted
lower third molars
Thus, it is very important to obtain dental consultation
for lower third molars at the first sign of any pain,
bleeding from the gums
 LUDWIG'S ANGINA
The symptoms include swelling, pain and raising of the tongue,
swelling of the neck and the tissues of the submandibular and
sublingual spaces, malaise, fever, dysphagia (difficulty
swallowing) and, in severe cases, stridor or difficulty breathing.

Swelling of the submandibular and/or sublingual spaces are

distinctive in that they are hard and classically 'boardlike'.

Important signs include the patient not being able to swallow

his/her own saliva and the presence of audible stridor as these
strongly suggest that airway compromise is imminent
LUDWIG'S ANGINA
 LUDWIG'S ANGINA

Treatment involves appropriate antibiotic

medications & management of the airway. 
NECK
Cysts of neck-
 A cyst of neck may be central or lateral

 1) Thyroglossal cyst- central

 2) Branchial cyst- lateral

 3) Lymphangioma- lateral.
THYROGLOSSAL CYST
 The thyroglossal duct is a vestigial structure which
passes from the foramen cecum at the base of tongue to
the isthmus of the thyroid gland.
 If a portion of the duct remain unclosed a cyst is
formed ,lined by columnar epithelium.
 Cyst is in the middle line & below hyoid bone but
occasionally is at the base of the tongue.
 THYROGLOSSAL CYST
It usually presents as a midline neck lump (in the region of the
hyoid bone) that is usually painless, smooth and cystic, if
infected pain can occur

There may be difficulty breathing, dysphagia (difficulty

swallowing), especially if the lump becomes large

A thyroglossal cyst will move upwards with protrusion of

the tongue

Treatment for a thyroglossal cyst is surgical resection, often

requiring concomitant removal of the midsection of the hyoid
bone (sistrunk procedure)
THYROGLOSSAL CYST
BRANCHIAL CYST

 Branchial cyst : This is formed from an unclosed portion of

branchial cleft, usually the third cleft.
 If it arises from the second cleft it lies just below the mastoid
process & projects in to the mouth.
 Cyst is lined by columnar ciliated epithelium but when
superficial it is lined by stratified epithelium.
 Wall contains lymphoid tissue. If the outer end of the cleft
remain open the condition is a branchial fistula, which opens
on the neck at the level of the angle of the jaw.
BRANCHIAL CYST
Symptoms
 Most branchial cleft cysts are asymptomatic, but
they may become infected.
Treatment
 Conservative (i.e. no treatment), or
surgical excision. As complete surgical excision
may be difficult (due to the close proximity of
the internal jugular vein and carotid vessels that
lie deep to the swelling), they can recur
BRANCHIAL CYST
BRANCHIAL CYST(MICRO)

Cyst is lined by columnar ciliated

epithelium or stratified epithelium

Wall contains lymphoid tissue

 CYSTIC LYMPHANGIOMA
A cystic hygroma — or lymphangioma — is a birth
defect that appears as a sac-like structure with a thin
wall that most commonly occurs in the head and neck
area of an infant.
Cystic hygromas are now more commonly referred to
as lymphangiomas or lymphatic malformations.

Soft  lymph  filled masses within a thin-walled "sac" 

generally appearing on the neck (75%), axilla (20%), or
trunk or extremity (5%)
 CYSTIC LYMPHANGIOMA

A cystic lymphangioma is a
fluid-filled sac that occurs
when there is a blockage in
the lymphatic system. They
appear as single or multiple
cysts and are usually found
on the neck
CYSTIC LYMPHANGIOMA
Symptoms
 A common symptom is a neck mass found at
birth, or discovered later in an infant after an
upper respiratory tract infection
Treatment
 Treatment involves surgical removal of the
abnormal tissue whenever possible. However,
cystic hygromas can often invade other parts of
the neck, making this impossible
 SIALADENITIS
Sialadenitis is inflammation of a salivary gland. It may be
subdivided temporally into acute, chronic and recurrent forms

Acute form
Predisposing factors:
•decreased flow (dehydration, post-op, drugs)
•poor oral hygiene
Clinical features:
•Painful swelling
•Reddened skin
•Oedema of the cheek, Periorbital region and neck
•low grade fever
•purulent exudate from duct punctum
 SIALADENITIS
Chronic Form
Clinical Features:
unilateral
mild pain / swelling common after meals
duct orifice is reddened and flow decreases
may or may not have visible/palpable stone
SIALADENITIS
Bacterial sialadenitis:
 Most common bacteria are Staph. Aureus & Strep.
viridan. Inflammation may be largely interstitial or may
cause focal area of suppurative necrosis or abscess
formation.
 Virus sialadenitis(Mumps) most common viruses are
influenza & para-influenza.
 It produces a diffuse, interstitial inflammation,
mononuclear cells infiltration & edema.
 Childhood mumps is self –limited.
SIALADENITIS

Tissue: Salivary Gland
Enlarged parotid gland
Diagnosis: Lymphocytic infiltration and
desmoplastic reaction
SJÖGREN'S SYNDROME
Sjögren's syndrome  (also known as "Mikulicz disease"
and "Sicca syndrome") is an autoimmune disorder in
which immune cells attack and destroy the exocrine
glands that produce tears and saliva.

Nine out of ten Sjögren's patients are women and the

average age of onset is late 40s.

The hallmark symptoms of the disorder are dry

mouth and dry eyes. In addition, Sjögren's syndrome may
cause skin, nose, and vaginal dryness, and may affect
other organs of the body, including the kidneys, blood
vessels, lungs, liver, pancreas, and brain.
 SJÖGREN'S SYNDROME

Sjogren's syndrome with gland inflammation that is not

associated with another connective tissue disease is referred to
as primary Sjogren's syndrome.

Sjogren's syndrome that is also associated with a connective

tissue disease, such as rheumatoid arthritis, systemic lupus
erythematosus, or scleroderma, is referred to as secondary
Sjogren's syndrome.
 SJÖGREN'S SYNDROME
Patients with Sjogren's syndrome typically produce an
antibodies against a variety of body tissues (autoantibodies).
include antinuclear antibodies (ANAs), which are present in
nearly all patients
 SJÖGREN'S SYNDROME

Enlarged parotid gland Histopathologic image of focal lymphoid

infiltration in the minor salivary gland
associated with Sjögren syndrome.
TUMORS OF SALIVARY GLAND
The salivary glands are divided into major and minor
salivary gland categories.

The major salivary glands are the parotid, the

submandibular, and the sublingual glands.

The minor glands are dispersed throughout the upper

aerodigestive submucosa (ie, palate, lip, pharynx,
nasopharynx, larynx, parapharyngeal space).
TUMORS OF SALIVARY GLAND
Most (70%) salivary gland tumors (SGTs) originate in
the parotid gland.
The remaining tumors arise in the submandibular
gland (8%) and in the minor salivary glands (22%).

Although 75% of parotid gland tumors are benign,

slightly more than 50% of tumors of the
submandibular gland and 60-80% of minor SGTs are
found to be malignant
TUMORS OF SALIVARY GLANDS
 Most common tumor arising in the parotid gland is benign
pleomorphic adenoma (Mixed tumor of parotid gland)
 Less frequent benign tumor is papillary cystadenoma
lymphomatosum (Warthin tumor).
 Collectively, these two types account for three-fourths of
parotid tumors.
 Malignant tumor is mucoepidermoid carcinoma .

 Malignant transformation of pleomorphic adenoma may

occur.
PLEOMORPHIC ADENOMA
Pleomorphic adenoma :
 It is a slow –growing well-demarcated encapsulated
lesion.
 Most often arising in the parotid gland -usually causes
painless swelling at the angle of the jaw.
  Its pleomorphic appearance is due to its dual origin from
epithelial and myoepithelial elements
 Although it is "benign", it can recur after resection, it
invades normal adjacent tissue and distant metastases
have been reported after long (+10 years) time intervals
 PLEOMORPHIC ADENOMA
The tumor is not enveloped, but it is surrounded by a
fibrous pseudocapsule of varying thickness.

The tumor extends through normal glandular

parenchyma in the form of finger-like pseudopodia,
but this is not a sign of malignant transformation
PLEOMORPHIC ADENOMA
Histologically, it is highly variable in appearance,
even within individual tumors.

Classically it is biphasic and is characterized by an

admixture of polygonal epithelial and spindle-
shaped myoepithelial elements in a variable
background stroma that may be mucoid, myxoid,
cartilaginous or hyaline
 PLEOMORPHIC ADENOMA
The tumor on the right is
well circumscribed due to
predominantly pushing
margins.
Cut surface of the tumor is
typically gray-white or tan-
white
Pleomorphic adenoma
consists of mixed
epithelial (left) and
mesenchymal cell
components (right). The
latter often exhibits
myxofibrous appearance
and in some instances
shows chondromatous
differentiation
WARTHIN’S TUMOR
 Warthin’s tumor (Papillary cystadenoma
lymphomatosum) :
 It occurs virtually only in the parotid gland

- Its etiology is unknown, but there is a strong

association with cigarette smoking. Smokers are
at 8 times greater risk of developing Warthin's
tumor than the general population.
About half of reported cases have prior radiation
exposure.
WARTHIN’S TUMOR
 Tumor is small , well
encapsulated, round to
ovoid mass. The tumor,
at the right of the image,
is well-demarcated from
the adjacent parotid
tissue and tends to shell
out from it
WARTHIN’S TUMOR
 Microscopically, it exhibit two features
 1)Two tired epithelial layer lined the cystic or cleft like
spaces.
 2)Below epithelial cells, well –developed lymphoid
tissue sometimes forming germinal centers.
 Warthin’s tumor

There are cystic spaces

surrounded by two uniform
rows of cellswith centrally
placed pyknotic nuclei.

The cystic spaces have

epithelium referred to as
papillary infoldings that
protrude into them.

Additionally, the epithelium

has lymphoid stroma with
germinal center formation
MALIGNANT SALIVARY GLAND TUMORS
  Malignant tumors are less common and are
characterized by rapid growth.
 They are firm, nodular, and can be fixed to adjacent
tissue, often with a poorly defined periphery.
 Pain and neural involvement are common.
 Eventually, the overlying skin or mucosa may become
ulcerated or the adjacent tissues may become invaded.
Surgery, followed by radiation therapy, is the treatment
of choice for resectable disease.
 Currently, there is no effective chemotherapy for salivary
cancer
ADENOID CYSTIC CARCINOMA
 Adenoid cystic carcinoma is the most common
malignant tumor of minor salivary glands (and of the
trachea).
 Its peak incidence is between ages 40 and 60, and
symptoms include severe pain and, often, facial nerve
paralysis
 Lymphatic spread is not a common feature of this tumor,
so elective nodal treatment is less common.
 Although the 5- and 10-yr survival rates are quite good.
 Pulmonary metastases are common, although patients
can live quite long with them
Here is an adenoid cystic carcinoma of salivary gland. It is not common in the
parotid gland, but it is the most common neoplasm of minor salivary glands.
Though often small, they are infiltrative and have a tendency to recur. Half of
them eventually metastasize to a distant site. The microscopic pattern shown
here is that of a solid to tubular to cribriform pattern, with the neoplastic cells
surrounding mucinous secretions
ODONTOGENIC CYSTS &
NEOPLASMS
DENTIGEROUS CYST
 Around crown of unerupted tooth
 Radiographically – unilocular radiolucency often
assoc. with impacted 3rd molar tooth
 Histolgically, cysts are lined by layer of stratified
squamous epithelium, dense chronic
inflammatory infiltrate.
 Treatment – complete removal of cyst

 Incomplete excision result in recurrance or

transformation into an Ameloblastoma
DENTIGEROUS CYST
AMELOBLASTOMA
 Ameloblasts are cells, present only during tooth
development, that deposit tooth enamel
 Ameloblastoma is a rare,benign tumor of odontogenic 
epithelium 
Locally invasive involving the molar area of the
mandible
 Rarely metastasize

 “Soap bubble” appearance on x-ray

 Grossly, the lesions consist of multiple cysts filled with a

thick, “motor oil”–like fluid
AMELOBLASTOMA

“soap-bubble” appearance, radiographs

 AMELOBLASTOMA
HISTOLOGIC FEATURES

 Mature fibrous
connective tissue
stroma,
 Islands of epithelial
elements within the
stroma, showing
peripheral tall columnar
cells (ameloblasts)
enclosing stellate
reticulum (loose cells in
the center)