NON SPECIFIC DISEASE
OF PAROTID
Babak Saedi.MD
Tehran university of Medical sciences
Imam Khomeini Hospital
ANATOMY & PHYSIOLOGY
Parotid
• Serous
Sublingual
• Mucous
Submandibular
• Mixed
Minor salivary glands
Controlled by sympathetic & parasympathetic
SALIVARY GLAND LESSIONS
Non-Neoplastic Disease
Benign Tumors
Malignant Tumors
Acute & Chronic
Non-Autoimmune
Pleomorphic
Adenomas
Adenoid Cystic
Carcinoma
Autoimmune
Sialadenitis
Basal Cell
Adenomas
Mucoepidermoid
Carcinoma
Necrotizing
Sialametaplasia
Myoepitheliomas
Sialadenosis
Oncocytoma and
Oncocytosis
Salivary
Lymphoepithelial
Cysts
Warthin’s Tumor
Sclerosing
Polycystic Adenosis
SIALADENOSIS
 Non-specific term used to describe a non-inflammatory nonneoplastic enlargement of a salivary gland, usually the parotid.
 May be called sialosis
 The enlargement is generally asymptomatic
 Mechanism is unknown in many cases.
SIALADENOSIS (SIALOSIS)
Parotid glands most commonly.
Probably due to abnormalities
of neurosecretory control.
SIALADENOSIS (SIALOSIS )

Cause maybe due to:
a.
b.
c.
Nutritional (Alcoholism, Cirrhosis, Kwashiorkor and Pellagra
Endocrine (Diabetes, Thyroid diasease, Gonadal dysfunction)
Neurochemical (Vegetative state, Lead, Mercury, Iodine,
Thiouracil)
RELATED TO…
a.
Metabolic “endocrine sialendosis”
b.
Nutritional “nutritional mumps”
a.
b.
c.
Obesity: secondary to fatty hypertrophy
Malnutrition: acinar hypertrhophy
Any condition that interferes with the absorption of nutrients
(celiac dz, uremia, chronic pancreatitis, etc)
RELATED TO…
a.
Alcoholic cirrhosis: likely based on protein deficiency &
resultant acinar hypertrophy
b.
Drug induced: iodine mumps
e. HIV
SIALADENOSIS (SIALOSIS)
Histopathology:
1.
Hypertrophy of serous acinar cells to about twice their normal
size.
2.
Cytoplasm is densely packed with secretory granules.
ALLERGIC SIALADENITIS
 Caused by drugs or allergens
 Clinical presentation:
1.
2.
3.
Acute salivary gland enlargement
Itching over the gland
With/without rash
 Treatment
•
•
•
Self-limiting
Avoid allergen
hydration
SALIVARY
GLAND
OBSTRUCTIVE
SALIVARY GLAND DISORDERS
Sialolithiasis
Mucous retention/extravasation
MUCOCELE 9
 Mucus is the exclusive secretory product of the accessory minor
salivary glands and the most prominent product of the sublingual
gland.
 The mechanism for mucus cavity development is extravasation or
retention
MUCOCELES & RANULA

Etiology
•
•
Trauma  extravasation labial mucosa
Obstruction  retention  palate & floor of mouth

Clinical appearance

Ranula
•
•
•
extravasation / retention in floor of mouth
Obstruction of Sublingual salivary gland duct
Usually unilateral
MUCOCELE
 Mucoceles, exclusive of the irritation fibroma, are most common of the
benign soft tissue masses in the oral cavity.
Muco: mucus , coele: cavity. When in the
oral floor, they are called ranula.
MUCOCELE 9
Extravasation is the leakage of fluid from the ducts or acini
into the surrounding tissue.
Extra: outside, vasa: vessel
Retention: narrowed ductal opening that cannot adequately
accommodate the exit of saliva produced, leading to ductal
dilation and surface swelling. Less common phenomenon
MUCOCELE
 Consist of a circumscribed cavity in the connective tissue and submucosa
producing an obvious elevation in the mucosa
MUCOCELE
 The majority of the mucoceles result from an extravasation of
fluid into the surrounding tissue after traumatic break in the
continuity of their ducts.
 Lacks a true epithelial lining.
RANULA 9
Is a term used for
mucoceles that occur in the
floor of the mouth.
The name is derived form
the word rana, because the
swelling may resemble the
translucent underbelly of the
frog.
RANULA 9
 Although the source is usually the sublingual gland,
• may also arise from the submandibular duct
• or possibly the minor salivary glands in the floor of the mouth.
RANULA
Presents as a blue dome shaped swelling in the
floor of mouth (FOM).
They tend to be larger than mucoceles & can fill
the FOM & elevate tongue.
Located lateral to the midline, helping to
distinguish it from a midline dermoid cyst.
PLUNGING OR CERVICAL
RANULA
 Occurs when spilled mucin dissects through the mylohyoid muscle
and produces swelling in the neck.
 Concomitant FOM swelling may or may not be visible.
TREATMENT OF MUCOCELES 9
IN LIP OR BUCCAL MUCOSA
 Excision with strict removal of any projecting peripheral salivary glands
 Avoid injury to other glands during primary wound closure
RANULA TREATMENT 9
 Marsupialization has fallen into disfavor due to the excessive
recurrence rate of 60-90%
 Sublingual gland removal via intraoral approach
SALIVARY
GLAND
IMMUNOLOGIC DISEASE
SJÖGREN’S SYNDROME 7
 Most common immunologic disorder associated with salivary gland disease.
 Characterized by a lymphocyte-mediated destruction of the exocrine glands
leading to xerostomia and keratoconjunctivitis sicca
SJÖGREN’S SYNDROME 7
 90% cases occur in women
 Average age of onset is 50y
 Classic monograph on thediease published in 1933 by Sjögren, a
Swedish ophthalmologist
SJOGREN’S SYNDROME
All the above conditions plus;
Dry eyes
Generalized arthritis
P R I M A RY S S - CLINICAL PICTURE
Mostly parotid gland is affected
Persistent / intermittent gland enlargement
bilateral, non-tender, firm, and diffuse
swelling
 saliva and altered saliva composition
Check of any recent changes to the
character of the glands (nodularity)
• significantly increased risk of developing B-cell
lymphoma
Keratoconjunctivitis sicca
S E C O N DA RY S S - C L I N I CAL
PICTURE
Dryness of the skin & pruritis
Dry and persistent cough
>50% have arthralgia with or without arthritis
Dysphagia, nausea, dyspepsia, and epigastric pain
Peripheral & cranial neuropathy
SJÖGREN SYNDROME DIAGNOSIS
 Different diagnostic criteria
1. Objective measurement of decreased salivary &
lacrimal gland function
2. +ve autoimmune serologies
3. Minor salivary gland biopsy
•
Lymphocytic infiltration
4. Silagoraphy is also useful
SJÖGREN’S SYNDROME
Keratoconjuntivitis sicca: diminished tear production caused by
lymphocytic cell replacement of the lacrimal gland parenchyma.
Evaluate with Schirmer test. Two 5 x 35mm strips of red
litmus paper placed in inferior fornix, left for 5 minutes. A
positive finding is lacrimation
of 5mm or less.
Approximately 85% specific & sensitive
SJÖGREN’S LIP BIOPSY 15
Biopsy of SG mainly used to aid in the diagnosis
Can also be helpful to confirm sarcoidosis
SJÖGREN’S LIP BIOPSY 15
Single 1.5 to 2cm horizantal incision labial mucosa.
Not in midline, fewer glands there.
Include 5+ glands for identification
Glands assessed semi-quantitatively to determine
the number of foci of lymphocytes per 4mm2/gland
SJÖGREN SYNDROME - TREATMENT

Symptomatic

Systemic cholinergic (Pilocarpine)
•

5mg TID/QID (should not exceed 30mg/day)
Follow up
SJÖGREN’S TREATMENT 15
Avoid xerostomic meds if possible
Avoid alcohol, tobacco (accentuates xerostomia)
Sialogogue (eg:pilocarpine) use is limited by other
cholinergic effects like bradycardia & lacrimation
Sugar free gum or diabetic confectionary
Salivary substitutes/sprays
M I C K U L I CZ’ S S Y N D RO M E
1) Symmetrical enlargement of salivary
2) Enlargement of the lachrymal glands
3) Dry mouth
glands
R A D I A T I O N I N D U C E D PA T H O L O G Y

Permanent salivary damage caused by doses 50Gy

Radioactive iodine for thyroid cancer treatment has similar but less
severe effect

Clinical presentation
1.
2.
3.
Salivary gland dysfunction signs & symptoms
Osteonecrosis
Increased risk of tumors affecting radiated tissues
M A N A G E M E N T S T E P S F O R PA T I E N T S
WITH RADIATION-INDUCED
XEROSTOMIA
RADIATION INJURY 7
 Low dose radiation (1000cGy) to a salivary gland causes an acute
tender and painful swelling within 24hrs.
 Serous cells are especially sensitive and exhibit marked
degranulation and disruption.
 Continued irradiation leads to complete destruction of the serous
acini and subsequent atrophy of the gland7.
 Similar to the thyroid, salivary neoplasm are increased in incidence
after radiation exposure7.
GRANULOMATOUS
DISEASE 7
Primary Tuberculosis of the salivary glands:
• Uncommon, usually unilateral, parotid most common affected
• Believed to arise from spread of a focus of infection in tonsils
 Secondary TB may also involve the salivary glands but tends to
involve the SMG and is associated with active pulmonary TB.
61.
2.
•
GRANULOMATOUS CONDITIONS
Tuberculosis
Granulation tissue formation in salivary gland
1.
2.
•
•
•
Xerostomia
Salivary gland enlargement
Sarcoidosis
Granulomas (T lymphocytes) affecting several organs
•
•
•
•
Lungs
Skin
Eyes
Parotid glands
Severity and duration of disease varies
Mild improvement noticed with steroid therapy
G R A N U L O M A TO U S C O N D I T I O N S
1.
2.
•
Tuberculosis
Granulation tissue formation in salivary gland
1.
2.
•
•
•
Xerostomia
Salivary gland enlargement
Sarcoidosis
Granulomas (T lymphocytes) affecting several organs
•
•
•
•
Lungs
Skin
Eyes
Parotid glands
Severity and duration of disease varies
Mild improvement noticed with steroid therapy
GRANULOMATOUS
DISEASE 7
Sarcoidosis: a systemic disease characterized by
noncaseating granulomas in multiple organ systems
Clinically, SG involvement in 6% cases
Heerfordts’s disease is a particular form of
sarcoid characterized by uveitis, parotid enlargement
and facial paralysis. Usually seen in 20-30’s. Facial
paralysis transient.
GRANULOMATOUS
DISEASE 7
Cat Scratch Disease:
 Does not involve the salivary glands directly, but involves the
periparotid and submandibular triangle lymph nodes
 May involve SG by contiguous spread.
 Bacteria is Bartonella Henselae(G-R)
 Also, toxoplasmosis and actinomycosis.
CYSTS 7
True cysts of the parotid account for 2-5% of all parotid lesions
May be acquired or congenital
Type 1 Branchial arch cysts are a duplication anomaly of the membranous external
auditory canal (EAC)
Type 2 cysts are a duplication anomaly of the membranous and cartilaginous EAC
CYSTS
Acquired cysts include:
Mucus extravasation vs. retention
Traumatic
Benign epithelial lesions
HIV
Association with tumors
•
•
•
•
Pleomorphic adenoma
Adenoid Cystic Carcinoma
Mucoepidermoid Carcinoma
Warthin’s Tumor
OTHER: PNEUMOPAROTITIS
In the absence of gas-producing bacterial
parotitis, gas in the parotid duct or gland is
assumed to be due to the reflux of pressurized
air from the mouth into Stensen’s duct.
May occur with episodes of increased
intrabuccal pressure
• Glass blowers, trumpet players
Aka: pneumosialadenitis, wind parotitis,
pneumatocele glandulae parotis
PNEUMOPAROTITIS 8
 Crepitation, on palpation of the gland
 Swelling may resolve in minutes to hours, in some cases, days.
 US and CT show air in the duct and gland
 Consider antibiotics to prevent superimposed infection
N E C RO T I Z I N G S I A L O M E TA P L A S I A

Benign self-limiting reactive inflammatory disorder

Etiology
•
•

Clinical presentation
•
•
•
•
•

Unknown
Trauma (LA)
Red nodule
Deep ulcer with rolled margin
Necrosis
Moderate dull pain
6-8 weeks
Treatment
OTHER: NECROTIZING
SIALOMETAPLASIA
 Cryptogenic origin, possibly a reaction to ischemia or injury
 Manifests as mucosal ulceration, most commonly found on hard
palate.
 May have prodrome of swelling or feeling of “fullness” in some.
 Pain is not a common complaint
NECROTIZING
SIALOMETAPLASIA
Self limiting lesion, heals by secondary intention over 6-8
weeks
Histologically may be mistaken for SCC
IMPORTANCE OF SALIVA
Oral hygiene
Taste acuity
Mastication
Deglutition
Digestion
Voice acuity
Speech articulation
XEROSTOMIA
 22 – 26% of total population
 Occurs most common among elderly
 Associated with immunotherapy,
radiotherapy
 Treatment
1.
2.
3.
4.
Stringent oral and dental care
Radiation therapy protectants
Gene therapy
Pharmacologic options
D I AG N O ST I C A P P ROAC H
1- EVALUATION OF DRY MOUTH
Symptoms of salivary gland
dysfunction
1.
Dryness of all oral mucosal surfaces
2.
Difficulty chewing, speaking
3.
Increased sensitivity to spicy food
4.
Increased caries activity
D I AG N O ST I C A P P ROAC H
2- PAST & PRESENT
MEDICAL HISTORY

Radiotherapy

Dryness at other body sites (eye,

Medication
•
•
•
•
Tricyclic antidepressant
Antihypertensive
Antihistamines
Decongestants
nose, skin)
D I AG N O ST I C A P P ROAC H
3- CLINICAL EXAMINATION
 Intra-Oral examination
• Notice signs of salivary gland dysfunction
•
•
•
•
•
Red depapillated tongue
Oral mucosa adhere to mirror
Lipstick/food debris on anterior teeth
Candidaiasis
Increase caries & erosion
• If could detect mass
• Any mucosal ulcerations over the mass
• Milking of saliva
D I AG N O ST I C A P P ROAC H
3- CLINICAL EXAMINATION
 Extra-Oral examination
• Palpate cervical lymph nodes
• Palpate the gland
• Slightly rubbery
• Painless unless infected/inflamed
• Check motor function of facial nerve
D I AG N O ST I C A P P ROAC H
4- SALIVA COLLECTION
 Different methods to determine salivary flow rate
 Salivary flow rate fluctuate
 Abnormal low salivary flow rate
• Unstimulated whole saliva flow rate <0.1ml/min
• Stimulated whole saliva flow rate <1.0ml/min
TREATMENT OF XEROSTOMIA
1.
2.
3.
Preventive therapy
1.
2.
Florid rinses & gel
Oral hygiene
Symptomatic treatment
1.
2.
•
Water
Artificial saliva
Avoid products containing sugar, alcohol
Salivary stimulation
1.
2.
Local / topical stimulation
1.
Chewing (flavoured)
1.
Pilocrpine HCl
Systemic stimulation (sialogogues)
FREY’S SYNDROME
Etiologies:
1. Trauma to parotid regions
a. Parotidectomy
b. Penetrating trauma
c. Closed mandibular fractures
2. Trauma to cervical sympathetic chain
3. Diabetic neuropathy
4. Aberrant regeneration location
a. CP angle
b. Middle ear
c. OTIC Ganglions
TREATMENT OF FREYS
SYNDROME
1.
External radiotherapy
2.
Local or systemic applications of anticholinergic drugs
3.
Section of some portion of efferent arc
4.
Interposition of subcutaneous barrier
5.
Botox injection
SIALORRHEA
Causes:
1. Change in oral perception
1.
2.
2.
Neurologic changes (CVA, Parkinson’s)
Extensive oral surgical procedure
Decrease swallowing
Treatment:
1. Speech pathologist
2. Xerostimia inducing drugs (antihistamine)
3. Botulinum toxins (Botox injection)
4. Surgery
AGE CHANGES IN
SALIVARY GLANDS
Reduction in weight of parotid and
submandibular glands related to atrophy of
secretory tissue & replacement by fibrofatty tissue.
Similar changes in labial minor glands.
Oncocytic change in ductal epithelium.
Reduction in flow rate in submandibular gland.
REFERENCES
1.
McQuone, SJ: Acute viral and bacterial infections of the salivary glands. Oto
Clinics North America, 32:793,1999
2.
Marchal F, Dulguerov P. Sialolithiasis Management. Arch Oto, 129:951, 2003
3.
Escudier MP, McGurk M. Symptomatic sialodenitiis and sialolithiasis in the
english population:an estimate of the cost of hospital treatment. Br Dent J.
1999;186:463
4.
Lustmann J, Regev E, Melamed Y. Sialolithiasis: a survey on 245 patients and a
review of the literature. Int J Oral Maxillofacial. 1990; 19, 135
5.
Crabtree GM, Yartington CT. Submandibular gland excision. Laryngoscope.
1988;98:1044
Sialadenitis
Treatment:
• The first step is to make sure about fluid balance.
•Patient needs to receive fluids intravenously
•Antibiotics to destroy the bacteria.
•Sugarless sour candies or gum is recommend ,they can
stimulate the glands to produce more saliva.
•If the infection is not improving, surgery may be needed to
open and drain the gland.
Prevention:
Always drink plenty of fluids. This is especially important after
surgery, during illness or in elderly people