THE PHARYNX & SALIVARY

GLANDS
Dr. Melita Jesusa Uy
February 24, 2014
Notetakers: AAB, OSG, GMO
(#TeamLouise)

THE PHARYNX
3 divisions:

Nasopharynx or Epipharynx

Oropharynx or Mesopharynx

Hypopharynx or Laryngopharynx

Oropharynx
Continuous with the nasopharynx at the free margin
of the soft palate
2nd, 3rd, 4th vertebral bodies form the posterior
wall and is the only solid wall of the oropharynx
base of the tongue and the oral cavity form the
anterior limits
includes facial or palatine tonsils and the pillars of
these tonsils
Lining mucosa of the oropharynx is stratified
squamous epithelium

Figure 3. Waldeyers ring

Figure 1. regions of the pharynx
Pharynx

Free border of the soft palate divides the

nasopharynx from the oropharynx

A horizontal line at the level of the epiglottis

separates the oropharynx from the nasopharynx

Posterior pharyngeal wall is continuous in all

three divisions

Nasopharynx
Continuous with the nasal airways at the
posterior choanae
respiratory portion of the pharynx
soft palate forms the floor
occipital bone and upper cervical vertebrae
forms the roof
posterior pharyngeal wall make up the lateral
walls

Nasopharynx borders
Superiorly: adenoids
Laterally: opening of ET, Fossa of Rosenmuller, Torus
tubarius

Waldeyers ring - lymphatic encirclement of the

pharynx ; composed of the palatine tonsils,
adenoids and lingual tonsils

Figure 3. The oral cavity

Hypopharynx
An imaginary horizontal line at the level of the
valleculae separates the oropharynx from
hypopharynx
Valleculae - two shallow depressions located
between the base of the tongue anteriorly and the
epiglottis posteriorly
Glottis
Pyriform sinus

Figure 2. the nasopharynx

Figure 4. the hypopharynx

Diseases of the Nasopharynx
Adenoids
Hyperplasia of the pharyngeal tonsils
3-6 years old

Clinical Manifestations
Chronic airway obstruction (mouth breathing)
Nasal discharge
Snoring
Anorexia
Hyponasal voice
Frequently recurring infections of the nose and
paranasal sinuses
Otitis media- from encroachment of opening of
Eustachian tube producing effusion in middle ear
Eustachian tube dysfunction
Prolonged conductive hearing loss ~ delays in speech
development
Maxillary deformity and dental malalignment
Level 2 lymph nodes are involved

Figure 5. Level 2 lymph nodes involved

Diagnosis
Posterior rhinoscopy/endoscopy
Otoscopy
Pure tone audiometry

Figure 6. endoscopic view of hyperplasia of tonsils

Treatment
Adenoidectomy under general endotracheal anesthesia
Myringotomy with ventilation tube insertion
Medical management
Juvenile Nasoangiofibroma
Benign Tumors

Epidemiology
Most common of benign tumors of the
nasopharynx
Less than 0.05% of all ear, nose and throat
Occurs in boys of 10-18 years of age

Symptoms
Obstructed nasal breathing
Recurrent epistaxis
Headache- with encroachment of cranial
vault
Impaired eustachian tube ventilation with
middle ear effusion
Conductive hearing loss

Diagnosis
Endoscopy: well-circumcribed, vascularized
mass with superficial vascular markings in
the nasopharynx or posterior part of the
nasal cavity
Important: if angiofibroma is suspected, do
not do biopsy (because they bleed)
Diagnosis
MRI or CT Scan
Angiography

Treatment
Surgical Removal
Preoperative embolization of the feeding
vessels- do surgery 24-48 hours after
embolization
Malignant Tumors

Epidemiology
Squamous cell carcinoma account for great
majority of malignant tumors of the
nasopharynx
Lymphoepithelial carcinomas

Adenocarcinoma
Adenoid cystic carcinoma
Malignant melanoma
Sarcoma
lymphoma
Nasopharyngeal ca common in Chinese
Etiology
Epstein-Barr virus (EBV) ~ undifferentiated
lymphoepithelial carcinoma
Signs & Symptoms
Neck mass- may be the only complaint i.e.
nasopharyngeal carcinoma
Unilateral conductive hearing loss with
middle ear effusion
Cervical lymph node metastasis
Recurrent epistaxis
Nasal airway obstruction
Headache
Cranial nerve palsies
Diagnosis
Endoscopy: smooth, well-circumscribed
tumor surfase to mucosal ulceration
Some of these tumors are initially
submucosal and are easily missed at
endoscopy
Otoscopy: unilateral tympanic membrane
retraction and middle ear effusion as a
result of impaired eustachian tube
ventilation
EBV titer- not really done
MRI / CT scan
Must refer to ENT specialist because
primary location of mass cannot be
ascertained by FNAB (fine needle biopsy)
Treatment
Primary high-voltage radiotherapy because
most of the tumors are very radiosensitive
Cannot be totally removed by surgery

Diseases of the oropharynx and hypopharynx

Injuries and Foreign Bodies: Scalds and Corrosive
Injuries
Etiology
Accidental drinking of hot liquids
Corrosive injuries more common in adults die to
injestion of caustic liquids with suidical intent
Symptoms
Severe pain
Increased salivation
Rule out mediastinitis
Diagnosis
Initially, the mucosa appears erythematous
Blistering then formation of a whitish fibrin
coating
Exclude injuries in lower levels of alimentary
tract
Chest Xray to rule out widening of mediastinum
due to esophageal perforation
Early endoscopy
Treatment
Rinse the oral cavity with cold water
If lips are affected: corticosteroid-containing
ointment
Severe injuries: systemic corticosteroids,
antibiotics and analgesics

Nasogastric feeding tube- insert within 24 hours

to reduce risk of perforation
Total parenteral nutrition (TPN) is also a choice
for those who can afford

Injuries and Foreign Bodies: Foreign Bodies

Most commonly located in the tonsils and at the
tongue base
Fish bone and bone fragments
Well-localized pain on swallowing
Treatment: removal
-

Acute Inflammation: Acute Tonsillitis

Etiology
Bacterial inflammation of the palatine tonsils
Group A -hemolytic streptococci
Staphylococci
Haemophilus influenzae
Pnemococci
Symptoms
High fever
Odynophagia
Swollen tonsillar lymph nodes
Muffled speech
Common in level 2 lymph nodes
Diagnosis
Swollen, bright red, coated tonsils
Leokocytosis
Culture
Rapid immunoassay

Figure 7. Tonsillar inflammation

Treatment
10-14 day treatment of Penicillin V
Macrolides or oral cephalosporins
Analgesic
Acute Inflammation: Scarlet Fever
Etiology
Group A -hemolytic streptococci
Exotoxin
Clinical Manifestations
Rash ( begins on the trunk)
Perioral pallor
Rasberry tongue (bright red tongue with
glistening surface and hyperplastic papillae)
Tonsils are greatly swollen with a deep red color
Diagnosis
by clinical picture and positive rapid
streptococcal test
Treatment

Penicillin
Mild antiseptic solution gargles
Pain reliever

Figure 9. Pseudomembrane of Diphtheria

Figure 8. Raspberry tongue

Acute Inflammation: Diphtheria
Etiology
Causative Organism
Corynebacterium diphtheriae
Droplet inhalation
Skin-to-skin contact
Very infectious
Incubation period: 1-5 days
Pathogenesis
Special endotoxin that causes cell necrosis and
ulcerations
Clinical Manifestations
Two main forms:
Local, benign pharyngeal diphtheria
Primary toxic, malignant diphtheri
Begins with moderate fever and mild swallowing
difficulties
Fully developed in ~ 24 hours with severe
malaise, headache, and nausea
Diagnosis
Grayish-yellow pseudomembranes firmly
adherent to the tonsils and may spread to the
palate and pharynx
Tissue bleeds when coating removed
Slightly sweet breath smell
Smear findings
Treatment
Isolation
Diphtheria antitoxin 200-1000IU/kg body
weight/IV or IM (after a negative skin test)
Penicillin G
Discharge after 3 consecutive 1-week interval
smears show negative resutls
2% may continue to carry the bacterium and
should undergo tonsillectomy
Complications
Toxic myocarditis (usually with the primary toxic
malignant form): can be fatal
Interstitial nephritis
ECG and urinalysis follow-ups should be
continued for at least 6 weeks after onset of
disease

Acute Inflammation: Tuberculosis

Epidemiology
Usually in advanced organ tuberculosis
Very rare
Clinical Manifestations
Primary complex
Commonly in children
Typical ulcerative lesion of the oral mucosa and
tonsil with regional cervical lymphadenopathy
Organ tuberculosis with ulcerative
mucocutaneous lesions
In regions that may come into contact
o Lesions may appear as mucosal
ulcerations on the lips and dorsum of
the tongue or as slightly raised, nodular
eruptions on the palate
o Skeletal involvement (cold abscesses)
causing bulging of the posterior wall of
the pharynx (like retropharyngeal or
parapharyngeal abscess)
Miliary tuberculosis
Hematogenous spread, appearing as multiple
pinhead-size papules, some hemorrhagic, that
form on the oral mucosa
Diagnosis
Acid-Fast bacilli smears, sputum, bronchial
secretions, gastric juice, or biopsy material
Biplane chest radiograph
Tuberculin skin test
Calcifications by ultrasound in enlarged cervical
lymph nodes ~ pathognomonic
Cervical lymph node biopsy
Treatment
Inpatient antituberculous polychemotherapy
Triple or quadruple regimen
Acute Inflammation: Acute Viral Pharyngitis
Etiology, symptoms
Influenza or parainfluenza viruses
Sudden onset of fever, sore throat and
headache
Coughing and catarrhal symptoms
Cervical adenopathy
Diagnosis
Pharyngeal mucosa appears red and coated on
mirror examination
If bacterial etiology is suspected ~ rapid
streptococcal test
Treatment
Supportive

Analgesics, cold compresses, warm liquids

-

Acute Inflammation: Infectious Mononucleosis

kissing disease
Causative Organism
Epstein-Barr virus
Adolescents and young adults
Incubation period: 7-9 days
Clinical manifestations
Systemic disease but commonly presents as
tonsillitis as the initial or cardinal symptoms
Fatigue, anorexia and moderate temperature
elevation
Severe pain on swallowing
Headache
Limb pains
Diagnosis: Clinical Examination
Tonsillar, nuchal, axillary and inguinal nodes are
enlarged
Liver spleen enlargement
Tonsils are bright red, swollen, and covered with
grayish fibrin coating
Diagnosis: Laboratory tests
Initially leukopenia followed by luekocytosis
80-90% atypical lymphocytes
EBV serology
Hepatic enzymes
Upper abdominal ultrasound and ECG
Treatment
Symptomatic relief of pain and fever
Aspirins not recommended as they cause
bleeding problems if tonsillectomy is required
Antibiotics
Ampicillin and amoxicillin avoided since they
frequently induce a pseudoallergic rash
Tonsillectomy
Severe course
Tonsillogenic Complications: Peritonsillar Abscess
Unilateral inflammatory process that includes
the peritonsillar tissue
Pronounced unilateral redness and swelling of
the soft palate, muffled speech, and possible
trismus
Uvular edema
May involve tongue base and lateral pharyngeal
wall

Peritonsillar infections may readily spread to the

parapharyngeal space.
Removal or incision of the affected tonsil under
antibiotic coverage
Tonsillogenic sepsis
Rare
Immune-compromised patients
Hematogenous or lymphogenous route

Figure 11. Peritonsillar abscess

Tonsillogenic Complications:
Retropharyngeal and parapharygeal abscess
Inflammation or abscess from prevertebral or
parapharyngeal lymph nodes or by
hematogenous spread as a result of minor
foreign-body injury or upper respiratory
inflammation
Clinical hallmarks
Severe pain on swallowing, progressive
dysphagia, muffled speech and possible trismus
and dyspnea
Routes of entry: direct spread from the
parapharyngeal space, or lymphatic spread from
the paranasal sinuses or nasopharyngeal region
Diagnosis
Pronounced swelling in the oropharynx or
hypopharynx usually at prevertebral or
parapharyngeal region
Leukocytosis
Contrast CT scan

Figure 10. Tonsils in Infectious Mononucleosis

Figure 12. Bulging of post. Pharyngeal wall in xray

NOTE: Danger Space
Potential Space, dangerous for rapid inferior
spread of infection to the posterior mediastinum
through its loose areolar tissue
Between retropharyngeal and pre-vertebral
space

Figure 13. Danger space colored orange

-

Routes of entry: retropharyngeal,

parapharyngeal, or prevertebral spaces

Treatment
Surgical incision and drainage under general
endotracheal anesthesia
Transoral or external approach
Antibiotics
Steroids
Intubation or tracheostomy
Chronic Inflammations: Chronic Pharyngitis
Etiology
Long term exposure to various noxious agents
(nicotine, alcohol, chemical, gaseous irritants)
Chronic mouth breathing due to nasal
obstruction
Accompanying feature of chronic sinusitis
Symptoms
Dry-throat sensation with frequent throat
cleaering and drainage of viscous mucus
Dry cough and foreign-body sensation in the
pharyx
Diagnosis
History
Pharygeal mucosa appears red and grainy due
to the hyperplasia of lymphatic tissue on the
posterior pharyngeal wall
In some cases the mucosa may appear smooth
and shiny
Nasal examination to exclude nasal airway
obstruction
Treatment
Avoid causing agents
Sage or chamomile in steam inhalation to
moisten
Surgery for those with nasal airway obstruction
Chronic Inflammations: Chronic Tonsillitis
Pathogenesis
Recurrent inflammations of the tonsils and
peritonsillar tissue can lead to permanent
structural changes with scarring
Bacteria can grow on cellular debris in poorly
drained crypts
Symptoms
Recurrent episodes of pain or asymptomatic
Lethargy, poor appetite, bad taste in mouth and
fetid breath odor
Diagnosis
Reveals small, firm immobile tonsils with
associated peritonsillar redness
Occasionally, purulent liquid can be expressed
from the crypts
Smears: group A -hemolytic streptococci
Tonsillar lymph nodes may be enlarged
Antistreptolysin titer > 400IU/mL
Treatment
Tonsillectomy
Peripheral Obstructive Sleep Apnea Syndrome (OSAS)
Etiology and Pathogenesis
Tendency for the velum, oropharynx, and/or
hypopharynx to collapse during sleep narrowing
airway and causing periods of apnea or
hypopnea
Frequent arousal from sleep and gasping for air
preventing normal sleep pattern

Long-term effects due to reduction in blood

oxygen levels with potential for damage to the
cardiopulmonary system
Signs in the patients history that are suggestive
of OSA
Loud, irregular snoring
Periods of apnea during sleep (witnessed)
Unusual daytime sleepiness or fatigue
Intellectual deterioration (poor concentration
and impaired memory)
Personality changes
Loss of libido, impotence
Nycturia, enuresis
Table 1. Factors and Conditions that promote snoring
and apnea
Classification
Pharyngeal
obstruction

Common Factors
Overweight, obesity
Adenoids
Tonsillar hyperplasia
Tumors in oral cavity, pharynx,
larynx, neck
Dysgnathia
Acromegaly

Nasal
Obstruction

Turbinate hyperplasia
Septal deviation
Nasal Polyps
Deformities of the external nose
Tumors of the nose

Decreased
Muscle Tone

Alcohol
Nicotine
Drugs (sedatives, hypnotics,
muscle relaxants)
Sleep deprivation
Shift work

Other

Sex (male predominate)

Genetic predisposition
Sleeping in supine position

Diagnosis
Elongated uvula,
Narrow velopharyngeal passage
Bulky soft palate with a small oropharyngeal
lumen
Hyperplastic tongue base
Hyperplastic palatine tonsils
Nasal obstruction
Flexible transnasal endoscopy

Mller maneuver-Negative inspiratory pressure

(let patient swallow while nose and mouth are
closed) during the maneuver produces various
collapse effects in the pharynx when OSAS is
present
Diagnosis: Objective Measuring Techniques
Screening
Outpatient basis: oxygen saturation, respiratory
sounds, heart rate during sleep
Madaus Electronic Sleep Apnea Monitor
(MESAM)
Not accurate since no EEG
Confirming the diagnosis
Polysomnography: gold standard-Inpatient
procedure
Additional thoracic and abdominal respiratory
excursions, transcutaneous PO2 and records an
EEG evaluation
Treatment
Weight reduction
Abstinence from alcohol and nicotine
Avoiding big meals
Establish regular sleep-wake patter
Splint- Occlusive splint that advances the lower
jaw
Widens the airway
Continuous positive airway pressure (CPAP)
In severe OSAS or failed occlusive splint
Pneumatic splint
Surgery-Careful patient selection
Uvulopalatopharyngoplasty (UPPP) with
tonsillectomy
Intranasal surgery: septorhinoplasty, turbinate
reduction
Differential Diagnosis of sleep apnea
Occasional or habitual nonobstructive snoring
Upper airway resistance syndrome
Narcolepsy
Underlying hear disease with Cheyne-Stokes
respiration
Nocturnal bronchial asthma
Periodic hypersomnia, hypersomniac form of
endogenous depression
Insomnia
Chronic alcohol and drug abuse
Tumors: Benign Tumors
Can arise from all epithelial and mesenchymal
tissues in the head and neck region
Papillomas, pleomorphic adenoma
Fibromas, lipomas, chondromas
Hemangiomas and lymphangiomas
Treatment
Generally surgical
Hemangiomas and lymphangiomas
Due to high rate of spontaneous remission
during first years of life surgery is advised if
tumor persist beyond that period or there are
already symptoms of dyspnea or dyphagia
-

1.
-

Figure 14. Leukoplakia

2. Bowens Disease
Chronic inflammatory disease caused by an
intraepidermal carcinoma
Similar to leukoplakia
Tumors: Malignant Tumors
Majority are squamous cell carcinoma
80% are located in the palatine tonsils or tongue
base
Less common sites are the soft palate and
posterior wall of the pharynx
Etiology
Chronic nicotine and alcohol abuse
Smokeless tobacco use
Betel nut use
Reverse smoking
Poor oral hygiene, ill-fitting dentures
Symptoms
Some may remain clinically silent
Depend on location and extent
Dysphagia, odynophagia
Blood-tinged saliva
Fetid breath odor
trismus
Diagnosis
Tonsillar carcinoma may appear as exophytic
lesions or an ulcerating infiltrating type
Occasionally not grossly visible
CT and MRI
Biopsy
Treatment
For most cases is surgical removal
Neck dissection
Postoperative radiation
Alternatively, primary radiotherapy or combined
radiation and chemotherapy
-

Tumors: Precancerous Lesions

Leukoplakia
Most common precancerous lesion
Asymptomatic
Exogenous irritants such as denture pressure or
alcohol/nicotine abuse
Complete surgical removal

Figure 15. Malignant tumor at pyriform sinus

THE SALIVARY GLANDS

The Major Salivary Glands

Parotid
Submandibular
Sublingual

There are 3 major

salivary glands. The
parotid, submandibular
and sublingual glands.
These glands along
with the numerous
small glands
associated with the
oral cavity, secrete
saliva into the mouth
thru the ducts (after
mechanical, thermal,
chemical, psychic, or
olfactory stimuli due to presence, or anticipated
presence of food)
The minor salivary glands(located in the mucosa and
submucosa of the oral cavity) secrete 5-10% of the total
daily salivary output, but they account for about 70% of
the mucus secretion.

The Minor Salivary Glands

Labial, buccal, palatoglossal, palatal, and
lingual mucosae
Not present in gingivae and dorsum of
anterior 2/3 of the tongue

o Neurovascular space
o IJV, ICA, cranial nerves IX to XII
Stylomandibular ligament
o separates parotid gland from
submandibular gland
Stensens Duct
Arises from anterior border
~1-1.5 cm inferior to zygomatic arch
Pierces Buccinator at 2nd upper molar
4-6 cm in length
5 mm in diameter
CN VII
Pes Anserinus
1.3 cm
Temperofacial
Division
Cervicofacial
Division
5 Terminal
branches
o Temporal
o Zygomatic
Crosses the zygoma over the
periosteum
o Buccal
o Mandibular
o Cervical

EMBRYOLOGY
6th-8th Weeks of Gestation
Oral ectoderm
Parotid
First to develop
Last to become encapsulated
Autonomic Nervous System: Crucial

Variations
PAROTID GLAND

Largest
~ 25 grams
Wedge shaped
Superficial
lobe
Deep lobe
Parotid
Compartment
Superior
Zygoma
Posterior
EAC
Inferior
Styloid, ICA, Jugular veins
80% overlies Masseter & Mandible
20% Retromandibular
Deep portion in contact with parapharyngeal
space
Parapharyngeal Space
Prestyloid Compartment
o Muscles and fat
Poststyloid Compartment (Paragangliomas)

Most common is type III (28%)

Localization of CN VII
Tragal pointer
Tympanomastoid suture
Posterior belly Digastric
Styloid process
Retrograde dissection
Mastoidectomy
Neural compartment
VII, Great Auricular, Auriculotemporal

10

Venous compartment
Retromandibular vein
Arterial compartment
Superficial Temporal/Transverse Facial
Parasympathetic supply
inferior salivatory nucleusglossopharyngeal
nerve then Jacobsons nerveotic ganglion
(synapses)
Postganglionic fibers (auriculotemporal
branch of V3)gland
Sympathetic Supply
Spinal cordexit with superior thoracic
nervessuperior cervical ganglion
Postganglionic fibersarterial plexuses and
sensory nervessalivary and sweat glands
and cutaneous blood vessels
Postganglionic sympathetic and
parasympathetic nerves
Acetylcholine
OTIC GANGLION SCHEMA

Whartons duct
Exits medial surface
Between Mylohyoid & Hyoglossus
5 cm in length
Opens lateral to the frenulum at floor of
mouth
Lingual nerve & CN XII

Innervation
Parasympathetic
o Superior salivatory nucleus
(pons)nervus intermedius and chorda
tympani (lingual nerve)submandibular
ganglion/gland
Sympathetic (superior cervical ganglion)
Artery: Submental branch of Facial a.
Vein: Anterior Facial v.
Lymphatics: Deep Cervical and Jugular chains
Facial artery nodes

Lymphatics
Paraparotid & Intraparotid nodes
Superficial & Deep Cervical nodes

SUBMANDIBULAR GLAND
The Submaxilla
Submandibular Triangle
Mylohyoid C
Marginal Mandibular branch
Passes through the superficial layer of deep
cervical fascia and is directly superficial to
the gland
Capsule from superficial layer of Deep Cervical
fascia

SUBMANDIBULAR GANGLION

11

Imaging
CT Inflammatory
MR Tumor
Children: U/S & MR
NO sialogram during active infection

SUBLINGUAL GLAND
Between Mandible & Genioglossus
No capsule
Ducts of Rivinus +/- Bartholins duct
Sialogram not possible
Innervation: Same as Submandibular
Artery/Vein: Sublingual branch of Lingual &
Submental branch of Facial
Lymphatics: Submandibular nodes
Anatomy: Sublingual Gland

Microanatomy
The Secretory Unit (MAISE)
Myoepithelial cells
Acinus (serous, mucinous mixed)
Intercalated duct
Striated duct
Excretory duct

Minor Salivary Glands

600-1,000
Simple ducts
Buccal, Labial, Palatal, Lingual
Tumor sites: Palate, upper lip, cheek
Lingual & Palatine nn.

Parotid: serous cells predominate

Submandibular: mixed serous
Sublingual: mixed mucinous
Minor salivary: seromucinous
Stroma: Plasma cells
Striated & Intercalated ducts well developed in
serous, NOT mucous glands
Striated duct: HCO3 into, Cl from lumen
Intercalated duct: K into lumen, Na from lumen,
producing hypotonic fluid
Excretory ducts do NOT modify saliva
The Reserve Cell/ Bicellular Theory
Intercalated duct
o Differentiate into acinar cells,
intercalated duct cells, striated duct
cells, myoepithelial cells
o Adenoid cystic and acinic cell carcinoma
Excretory duct
Excretory duct columnar and squamous
cells
Mucoepidermoid, squamous cell carcinoma
The Multicellular Theory
Neoplasm arise from differentiated cells
along the salivary unit
Squamous cell CA from excretory duct cells;
acinic cell carcinoma from acinar cells

12

SALIVA
Function of Saliva
Lubrication
Mucin
Physical protection of oral mucosa
Taste
Antibacterial and immunity
Lysozyme
IgA produced by plasma cells
Digestion
Amylase, lingual lipase
Buffering
Minerals
Helps in maintaining the integrity of enamel
Wound healing and upper GI mucosal integrity
Epidermal Growth Factor produced and
secreted by the submandibular salivary
glands
Blood coagulation
Kallikrein
Synthesis of Saliva
Active secretory process
Not a blood ultra-filtrate
Serous cells
Watery proteinaceous fluid contains
amylase
Mucous cells
Proteins linked to a greater amount of
carbohydrates
Plasma cells
IgA
Production of Saliva
Primary secretion
Ductal secretion
The secretory potential (hyperpolarizes)
Increased flow rate yields decreased
hypotonicity & K
Saliva is always hypotonic to plasma

Autonomic Innervation
Parasympathetic
Abundant, watery saliva
Amylase down
Sympathetic
Scant, viscous saliva
Amylase up
Salivary Flow
1-1.5 L/day (1 cc/min)
Unstimulated state
Submandibular
Stimulated state
Parotid
Sublingual & minor
Mucin
Function of Saliva
Salivary hypofunction
Candidiasis
Burning Mouth
Aphthous ulcers
Dental caries
Xerostomia

13

EFFECTS OF AGING
Total salivary flow independent of age
Acinar cells degenerate with age
Submandibular gland more sensitive to
metabolic/physiologic change
Unstimulated salivary flow more greatly affected
by physiologic changes
SUMMARY
Parotid
Submandibu
Sublingu
lar
al
A.
below
floor of the
collections
Location
and
mouth
of
anterior
beneath the
numerous
to the
body of the
glands
ear
mandible
lying close
to the
Whartons
duct
B. Main
Stensen
Whartons
open at
Duct
s duct
duct opens
the base of
opens
beneath the
the tongue
opposite
tips of the
the 2nd
tongue
upper
molar
c. Type of
serous
mixed but
mixed but
Secretion
more serous
more
arranged in
mucous
characteristic
s pattern serous
demilunes
D.
high
weak amylase insignifica
Secretory
amylase
activity
nt
Product
activity
E.Intercal
long &
shorter &less
shortest &
ated
prominen prominent
least
Ducts &
t
prominent
Striated
among the
Ducts
three
F. Size

Largest
salivary
gland
20-30 g

In between
12-15 g

Smallest
2-3 g

G. Total
salivary
output

30%

60%

5%

14

DISEASES OF THE SALIVARY GLANDS

Symptoms of Salivary Gland Disease

Pain
Swelling
Purulent Discharge
Dryness
Pain
Obstruction

At mealtime

Intermittent swelling
Infection
Swelling
Neoplasm

Unilateral, non-painful, long term

Obstruction

Unilateral, painful, short term

Systemic

bilateral

Submandibular Gland Swelling

Amount of saliva
Character of saliva
Infection
Culture and sensitivity
Sialography

Salivary calculi

Ductal stricture and irregularities

Filling defects

Acinar destruction
Indications:
1. Presence and / or position of calculi or other
blockages
2. Extent of ductal and glandular destruction
secondary to an obstruction
3. To determine the extent of glandular breakdown
4. Assessment of function in cases of dry mouth
5. To determine the location, size, nature and
origin of a swelling or mass
6. Post operative or post traumatic salivary fistula
7. Surgical consideration
8. Amount of damage to gland and its
salvageability
9. Choose site of biopsy
10. Differentiate intrinsic or extrinsic mass
11. Relation of mass to facial nerve

Contraindications:
1. Allergy to compounds containing iodine
2. Periods of acute infection/inflammation
3. Painful
4. Retrograde infection
5. Calculus close to the duct opening : push the
calculus back
6. Anticipated thyroid function tests

Parotid Gland Swelling

Purulent Discharge

Infection
Possible obstruction
Dryness
Obstruction
Radiation
Dehydration
Chronic Illness
Drugs
Sjgrens Syndrome
Evaluation and Diagnosis
Physical Examination
Bimanual Palpation

Normal = non palpable

Tenderness ~ infection
Firm mass floor of mouth

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Non-neoplastic Salivary Gland Disease

A. Infectious Inflammatory
B. Noninfectious Inflammatory
C. Non inflammatory

Infectious Inflammatory Disease

1. Acute Viral Inflammatory Disease
Mumps (paramyxovirus)-most common

Children 4-6yo

Incubation period 14-21 days (contagious)

Clinical findings

Bilateral swelling

Pain

Erythema

Tenderness

Fever

Occasional trismus
Treatment

Self-limiting

Symptomatic

Vaccine
2.

1.

Acute SuppurativeSialadenitis
Bacteria
Stasis of salivary flow
Dehydration, immunosuppression, trauma,
debilitation
Swelling, erythema, pain, tenderness, trismus,
purulent discharge
S. aureus, S. pneumoniae, E. coli, H. influenza
May lead to abscess
Treatment

Rehydration

IV antibiotics

Warm compress

Sialagogues

Oral hygiene

I and D for abscess

3. Chronic Granulomatous Sialedinitis
Chronic unilateral or bilateral swelling
Minimal pain
Primary TB if with risk factors for exposure
Diagnosis

AFB smear

Culture of saliva

PPD test
Multidrug antituberculous therapy
Noninfectious Inflammatory Disease
Sialolithiasis
80-90% submandibular gland, 10-20% parotid
gland
Any age
Male>female
Risk factors

Long illness with dehydration

Gout, diabetes, hypertension

Submandibular calculi more radioopaque
Recurrent swelling and pain exacerbated by
eating
Prolonged obstruction acute infection
Occasional gritty, sandlike foreign bodies

X-rays
Sialography
Treatment

Antibiotic therapy

Stone removal by manipulation

Surgical removal of stone

Surgical removal of gland

2.

Chronic Sialadenitis
Decreased production of saliva
Salivary stasisrisk for infection
+/- obstruction
Chronic intermittent painful swelling especially
on eating
May or may not be associated with infection
Conservative/Surgical removal of gland

3.

1.

2.

Sjgrens Syndrome
Autoimmune
Parotid enlargement, xerostomia,
keratoconjuctivitissicca
Rheumatoid arthrtis/SLE
Females 90%, 6th decade
Bilateral, nontender salivary gland enlargement
Swelling may occur intermitently or stary
constant
Dry eye, dry mouth, altered taste, dry skin,
myalgia, vasculitis, arthritis
SS-A or SS-B auto antibodies, rheumatoid factor
or antinuclear antibodies
Treatment

Symptomatic and supportive

Steroids and topical steroids

Superficial parotidectomy for severe

recurrent parotid infections
Noninflammatory Diseases
Sialadenosis
Sialosis
Rare
Bilateral, diffuse and painless swelling
May cause degenerative changes to the
autonomic innervation of the glands
Parotid gland>submandibular gland
Unclear etiology

Obesity, alcoholic cirrhosis, diabetes,

hyperlipidemia, hypothyroidism,
anemia, pregnancy, malnutrition,
menopause
Treatment

Underlying causes

Parotidectomy if glandular enlargement

is cosmetically unacceptable

Surgical removal of submandibular

gland
Parotid cysts
Congenital Parotid Cysts

Branchial Cleft anomalies

Dermoid Cysts - Trapped embryonic

epidermis
Acquired Parotid Cysts

May result from other parotid disorders

such as tumors, trauma, chronic

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sialadenitis, sialolithiasis and radiation

injury
3.

Mucoceles
Mucous retention cyst
Dilatations of minor salivary gland ducts

Accumulated mucous secretions

Mucous extravasation into the

connective tissue
Fairly common
Lip (60-70%), buccal mucosa, floor of mouth and
palate
Differentials

Cystic hygroma, lymphangioma,

thyroglossal duct cyst, dermoid cyst
Complete surgical excision
Recurrences can occur with inadequate excision

RANULA (floor of mouth)

May involve sublingual and submandibular

glands

Round fluctuant masses in floor of mouth

Usually unilateral

Any age group, any gender

Infections can occur

Simple ranula

True cyst with epithelial lining that

occurs intraorally with elevation of the
mouth floor

Plunging ranula

Extends below the mylohyoid muscle,

beyond the sublingual space, and
involves the submandibular space

May present as painless submandibular

mass or cervical mass

Does not have an epithelial lining and

therefore is classified as pseudocyst

Treatment

Underlying conditions

Symptomatic treatment: fluids,

sialagogues, mouthwashes, artificial
saliva

Salivary Gland Tumors

A. Benign Salivary Gland Tumors
B. Malignant Salivary Gland Tumors
Benign Salivary Gland Tumors
1.
2.
3.
4.

Pleomorphic Adenoma
WarthinsTumor
Monomorphic Adenoma
Hemangiomas
Pleomorphic Adenoma
benign mixed tumor
Occurrence:

70% parotid tumors

50% submandibular tumors

45% minor salivary gland tumors

6% of sublingual tumors
Location

parotid (85%)

minor salivary glands (10%): palate,

upper lip and buccal mucosa
4th to 6th decades of life
uncommon in children although they are second
only to hemangiomas
female-to-male ratio of 3-4:1
Clinical Presentation:

slow-growing, painless firm

fixed with advanced growth

nearly always solitary

facial nerve paralysis almost never

occurs

Mucoceles

4.

Ranula
Xerostomia
Dry mouth
Altered sense of taste, dysphagia and
complications related to dental decay
Disorders in salivary flow
Sjgren syndrome, stress, diabetes, chronic
infection and irradiation

Gross Pathology
smooth or lobulated, well-encapsulated tumor
typically solid tumors and may have areas of
gelationousmyxoidstroma
cystic degeneration or tumor infarction and necrosis are
rarely seen except in large, long-standing lesions
Microscopic Pathology

varying proportions of gland-like epithelium and

mesenchymalstroma

epithelial cells: may display several different

patterns of growthsmall nests, solid sheets, ductal
structures or anastamosingtrabeculae

Stroma: myxoid, chondroid, fibroid or osteoid

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incomplete encapsulation and transcapsular growth

of tumor pseudopods
Treatment
complete surgical excision with a surrounding margin of
normal tissue
superficial parotidectomy with facial nerve
preservation
submandibular gland excision
wide local excision for a minor salivary gland
Simple enucleation
high local recurrence rates
Rupture of the capsule and tumor spillage
increase the risk of recurrence

Warthins Tumor
papillary cystadenomalymphomatosum
10% of cases of parotid tumors and has only rarely
been described as occurring outside the parotid gland
older white males
4th to 7th decades
male-to-female ratio ~5:1
Bilateral or multicentric ~10% of cases
3% are associated with other benign or malignant
tumors
Clinical Presentation

slowly enlarging, painless mass

firm or rubbery in texture and may be nodular

minority of patients may report rapid

enlargement of the tumor with associated pain
or pressure

Gross
Pathology

smooth lobulated surface and a thin but tough

capsule.

cut surface of the tumor: Multiple cysts of

varying diameter and containing variably
viscous fluid

lining of the cysts appears shaggy and irregular

lymphoid component makes up the solid areas

of the tumor and lymphoid follicles can
occasionally be seen
Microscopic Pathology

Pathognomonic: epithelial cells forming papillary

projections into cystic spaces in a background of
a lymphoid stroma

epithelium ~double cell layer with tall columnar

cells lining the cystic spaces and cuboidal cells
along the basement membrane

nuclei of the columnar cells~oriented toward

the cystic space while the cuboidal cell nuclei is
oriented toward the basement membrane
Treatment

surgical resection

Enucleation

Basal

superficial parotidectomy with facial nerve

preservation is the standard management
Monomorphic Adenoma
Slow growing
<5%
One morphologic cell type
Basal cell adenomas, canalicular adenomas,
oncocytomas and myoepitheliomas
Cell Adenomas
2% of all epithelial salivary gland tumors
male=female
4th to 9th decades
Parotid gland

Canalicular Adenomas

Minor salivary glands

Tends to be multifocal

Upper lip mucosa

Elderly

Complete resection
Oncocytomas

Oncocytes (large polyhedron shaped epethelial

cells packed with eosinophlic cytoplasm and
mitochondria)

<1% of all salivary gland neoplasms

No gender predilection

6th to 8th decade

Parotid gland>submandibular gland

7% bilateral

Surgical excision
Myoepitheliomas

< 1%

No gender predilection

3rd to 6th decades

Parotid gland in 40%

Well-encapsulated
Hemangiomas
Significant differential diagnosis especially in
children

Endothelial in origin

<5%

Capillary hemangioma- most common salivary

gland tumor in children

Female>male

90% parotid gland

Clinical Presentation

Unilateral, painless mass

Rapid proliferative growth

Cosmetic deformity

CT scan/MRI

Differential Diagnosis: lymphangioma and

cavernous hemangioma

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The cystic spaces contain viscous or mucoid

material
Microscopy

the mucus cells and the epidermoid cells, the

proportion of which helps to define the grade of
the tumor
o

Treatment

Spontaneous regression

Complete excision : significant cosmetic or

functional compromise

Malignant Salivary Gland Tumors

Mucoepidermoid Carcinoma
Adenoid Cystic Carcinoma
Acinic Cell Carcinoma
Adenocarcinoma
Carcinoma ex-pleomorphic adenoma
Squamous Cell Carcinoma
Undifferentiated Carcinoma

Mucoepidermoid Carcinoma
most common
5 and 9% of all salivary gland neoplasms
most commonly in the major salivary glands

parotid (45-70%)

palate (18%)
o 20 and 70 years
o rare before age 20, it is the most common
salivary gland malignancy in the pediatric and
adolescent populations
o female> male
Clinical Presentation
o similar to that of a benign lesion
o enlarging but asymptomatic mas
o Occasionally patients will report a rapid
enlargement of a previously stable mass
o pain, fixation to the surrounding tissues or skin
o facial paralysis are uncommon ~ increase
suspicion for a high-grade tumor
o intraoral minor salivary gland: mistaken for a
benign or inflammatory process.
o bluish or red-purple, soft and smooth growth
o Others may present with a papillomatous
appearance or as a hard submucosal mass,
identical to a torus
o intraoral minor salivary gland:mistaken for a
benign or inflammatory process.
o bluish or red-purple, soft and smooth growth
o Others may present with a papillomatous
appearance or as a hard submucosal mass,
identical to a torus
o
o
o

Gross Pathology
o well-circumscribed and may be partially
encapsulated
o Others are poorly defined and infiltrative
o cut surface of the tumor may contain solid
areas, cystic areas or both

Low-grade mucoepidermoid carcinoma

o prominent cystic structures and mature
cellular elements
o proportionally more mucus cells, which
may form gland-like structures, and fewer
epidermoid cells.

Intermediate-grade tumors
o fewer and smaller cysts and occasional
solid islands of epidermoid tumor cells
o Although mucus cells are still present,
there is an increasing proportion of
epidermoid cells and occasional keratin
pearl formation

High-grade carcinomas
o hypercellular, solid tumors with noticeable
cellular atypia and frequent mitotic figures
o often mistaken for a squamous cell
carcinoma and the differentiation between
the two can be quite difficult
o Positive immunohistochemical staining for
mucin indicates a high-grade
mucoepidermoid carcinoma rather than a
squamous cell carcinoma
Treatment

stage of disease

Also influenced by tumor grade and location

Stage I and II disease

can often be treated by surgical excision
alone

parotidectomy with facial nerve

preservation, submandibular gland
excision or wide local excision of an
involved minor salivary gland

Stage III and IV disease

often require more radical excision and
may warrant additional intervention such
as a neck dissection or postoperative
radiation therapy
Adenoid Cystic Carcinoma
2nd most common salivary gland malignancy
overall

most common in the submandibular, sublingual

and minor salivary glands

Men=women

5th decade of life

more common in Caucasians

Clinical Presentation

often an asymptomatic mass

pain or paresthesias

Facial paralysis remains rare, but again, may be

seen more frequently with adenoid cystic than
with other tumors

Minor salivary gland involvement is

characterized by a submucosal mass with or
without pain and ulceration
Gross Pathology

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well defined but not encapsulated mass that can

be seen infiltrating surrounding normal tissue

these are solid tumors that rarely display

obvious cystic spaces on the cut surface
Microscopy

cribriform, tubular or solid

cribriform pattern
most common and most easily
recognizable
swiss cheese pattern
tumor cells are arranged in nests around
cylindrical spaces that may contain a
mucinous or hyalinized material

tubular pattern
cells that are arranged in layers and form
ductal structures

solid pattern
sheets of tumor cells with no intervening
spaces
Treatment

complete surgical resection and postoperative

radiation therapy

Perineural invasion
sacrifice of the facial nerve may be
necessary for tumor eradication

Elective neck dissection

usually not indicated because this tumor
rarely involves the cervical lymph nodes

local recurrence of adenoid cystic carcinoma

tumor recurrence rates vary in the
literature but reportedly can be as high
as 42%.

distant metastasis : most common site being

the lung

Both local recurrence and distant metastasis

can develop many years after initial treatment
and multiple recurrences in the same patient
have been reported

prognosis for complete cure is poor

the course of disease is often indolent
and patients with adenoid cystic
carcinoma may survive for many years
before eventually succumbing to the
disease
Acinic Cell Carcinoma
second most common parotid malignancy
second most common pediatric salivary gland
malignancy.

rare tumor that accounts for about 1% of all

salivary neoplasms.

5th decade of life and is more common in women

and Caucasians

Bilateral parotid disease occurs in approximately

3% of cases.
Gross Pathology

well circumscribed but lacks a true capsule

cut surface
grayish, friable, and displays solid and
cystic areas
Microscopy

solid, microcystic, papillary cystic and follicular

Tumor cells are dark staining and have granular

or honeycomb cytoplasm

stroma often demonstrates a lymphoid infiltrate.

Treatment

Surgical excision

Elective neck dissection is not warranted

demonstrates a benign course in early years

long-term follow-up studies have shown a

decline in survival approaching 50% at 20 years
after therapy
Adenocarcinoma
rare but aggressive tumors
40 years of age
Men = female
most commonly occurs in the minor salivary
glands, followed by the parotid gland and
represents about 15% of malignant parotid
neoplasms

arise from the terminal tubules and intercalated

duct cells
Clinical Presentation

enlarging mass

25% of patients will complain of pain or facial

weakness at presentation
Treatment

more aggressive tumors, treatment for

adenocarcinoma is more aggressive

Complete local excision mainstay of therapy

postoperative radiation therapy of some benefit

Palpable neck disease : neck dissection is

warranted

Elective neck dissection :patients with extensive

local disease or high-grade lesions

Carcinoma ex-pleomorphic adenoma

has arisen from a preexisting pleomorphic

adenoma

2% to 5% of salivary gland tumors

Clinical Presentation

slowly growing mass

usually been present for 10 to 15 years
and suddenly increases in size.

Malignant transformation of the benign mixed

tumor is more likely to occur in long-standing
tumors
Gross Pathology

tumors are nodular or cystic with minimal

encapsulation

Cut tumor
similar to a pleomorphic adenoma but
reveals necrosis and hemorrhage
Microscopy

malignant neoplasm arises in a neoplasm that

has the characteristics of a mixed tumor.
The malignant portion of the tumor may appear
Adenocarcinoma, squamous cell
carcinoma, undifferentiated carcinoma,
or some other form of malignancy
Local and distant metastases are common
very poor prognosis
Combination surgery and postoperative
radiation therapy

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Patients with pleomorphic adenoma should be

encouraged to undergo surgery as soon as
possible to avoid malignant degeneration
Squamous Cell Carcinoma
Rare
0.3% to 1.5%
high incidence of regional and distant
metastases
Poor prognosis
Total parotidectomy with postoperative radiation
therapy
Undifferentiated Carcinoma
Rare
men = women
high incidence in Greenlandic thought to be
related to the Epstein-Barr virus

extremely aggressive, with marked local

invasion and early distant metastases
These tumors have low survival rates

Complications of Parotidectomy
Freys Syndrome
Gustatory sweating
Cross reinervation of autonomic supply
Scopolamine, Jacobsons nerve
resection, SCM muscle flap,goretex
patch

Facial nerve paralysis

Salivary fistula

-End -

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