Anatomy and Physiology of the Salivary Glands

The Major Salivary Glands - Parotid - Submandibular - Sublingual

The Minor Salivary Glands

Anatomy: Parotid Gland

• Nearly 80% of the parotid gland (PG) is found below the level of the external auditory canal, between the mandible and the SCM.

• Superficial to the posterior aspect of the masseter mm

• CN VII branches roughly divide the PG into superficial and deep lobes while coursing anteriorly from the stylomastoid foramen to the muscles of facial expression.

Anatomy: Parotid Duct

• Small ducts coalesce at the anterosuperior aspect of the PG to form Stensen’s duct.

• Runs anteriorly from the gland and lies superficial to the masseter muscle

• Follows a line from the EAM to a point just above the commissure.– Is inferior to the transverse facial

artery– It is 1-3 mm in diameter– 6cm in length

• At the anterior edge of the masseter muscle, Stensen’s duct turns sharply medial and passes through the buccinator muscle, buccal mucosa and into the oral cavity opposite the maxillary second molar.

• Gland encapsulated by a fascial layer that is continuous the deep cervical fascia (DCF).

• The stylomandibular ligament (portion of the DCF) separates the parotid and submandibular gland.

Anatomy: Parotid Fascia

• Preganglionic parasympathetic (from CN9) arrives at otic ganglion via lesser petrosal n.

• Postganglionic parasympathetic leaves the otic ganglion and distributes to the parotid gland via the auriculotemporal nerve.

Parotid: Parasympathetic Innervation

• Postganglionic innervation is provided by the superior cervical ganglion and distributes with the arterial system

Parotid:Sympathetic Innervation

• Located in the submandibular triangle of the neck, inferior & lateral to mylohyoid muscle.

• The posterior-superior portion of the gland curves up around the posterior border of the mylohyoid and gives rise to Wharton’s duct.

Anatomy:Submandibular gland

Anatomy: Submandibular Duct

Wharton’s duct passes forward along the superior surface of the mylohyoid adjacent to the lingual nerve. Between Mylohyoid & Hyoglossus

5 cm in length ,2-4mm in diameter

• Innervation– Superior Cervical Ganglion (symp)– Submandibular Ganglion (para)

• Artery: Submental branch of Facial a.• Vein: Anterior Facial vn.• Lymphatics: Deep Cervical and Jugular chains

– Facial artery nodes

AnatomySubmandibular gland

Submandibular duct

Lie on the superior surface of the mylohyoid muscle and are separated from the oral cavity by a thin layer of mucosa.

Anatomy: Sublingual glands

The ducts of the sublingual glands are called Bartholin’s ducts. In most cases, Bartholin’s ducts consists of 8-20 smaller ducts of Rivinus. These ducts are short and small in diameter.

• Between Mandible & Genioglossus• No capsule• Ducts of Rivinus +/- Bartholin’s duct• Sialogram not possible• Innervation: Same as Submandibular• Artery/Vein: Sublingual branch of Lingual &

Submental branch of Facial• Lymphatics: Submandibular nodes

Anatomy: Sublingual glands

• Acute bacterial sialdenitis

• Chronic bacterial sialdenitis

• Viral infections

Salivary Gland Infections

Sialadenitis represents inflammation mainly involving the acinoparenchyma of the gland.

Sialadenitis

Acute infection more often affects the major glands than the minor glands1

Pathogenesis

1. Retrograde contamination of the salivary ducts and parenchymal tissues by bacteria inhabiting the oral cavity.

2. Stasis of salivary flow through the ducts and parenchyma promotes acute suppurative infection.

Acute Suppurative

• More common in parotid gland. • Suppurative parotitis, surgical parotitis, post-

operative parotitis, surgical mumps, and pyogenic parotitis.

• The etiologic factor most associated with this entity is the retrograde infection from the mouth.

• 20% cases are bilateral7

• Systemic dehydration (salivary stasis)• Chronic disease and/or immunocompromise

– Liver failure– Renal failure– DM, hypothyroid– Malnutrition– HIV– Sjögren’s syndrome

Risk Factors for Sialadenitis

Risk Factors continued…

• Neoplasms (pressure occlusion of duct)• Sialectasis (salivary duct dilation) increases

the risk for retrograde contamination. Is associated with cystic fibrosis and pneumoparotitis

• Extremes of age• Poor oral hygiene• Calculi, duct stricture• NPO status (stimulatory effect of mastication on

salivary production is lost)

Acute Suppurative Parotitis - History

• Sudden onset of erythematous swelling of the pre/post auricular areas extend into the angle of the mandible.

• Is bilateral in 20%.

Bacteriology

• Purulent saliva should be sent for culture.– Staphylococcus aureus is most common – Streptococcus pnemoniae and S.pyogenes– Haemophilus Influenzae also common

Lab Testing

• Parotitis is generally a clinical diagnosis• However, in critically ill patients further diagnostic

evaluation may be required• Elevated white blood cell count• Serum amylase generally within normal • If no response to antibiotics in 48 hrs can perform

MRI, CT or ultrasound to exclude abscess formation• Can perform needle aspiration of abscess

Treatment of Acute Sialadenitis

• Reverse the medical condition that may have contributed to formation

• Discontinue anti-sialogogues if possible

• Warm compresses, maximize OH, give sialogogues (lemon drops)

• External salivary gland massage if tolerated

Treatment of Acute Sialadenitis/Parotitis

• Antibiotics!• 70% of organisms produce B-lactamase or

penicillinase• Need B-lactamase inhibitor like Augmentin or

Unasyn or second generation cephalosporin• Can also consider adding metronidazole or

clindamycin to broaden coverage

Surgery for Acute Parotitis

• Limited role for surgery

• When a discrete abscess is identified, surgical drainage is undertaken

• Approach is anteriorly based facial flap with multiple superficial radial incisions created in the parotid fascia parallel to the facial nerve

• Close over a drain

Chronic Sialadenitis

• Causative event is thought to be a lowered secretion rate with subsequent salivary stasis.

• More common in parotid gland. • Damage from bouts of acute sialadenitis

over time leads to sialectasis, ductal ectasia and progressive acinar destruction combined with a lymphocyte infiltrate.

Chronic Sialadenitis

• Of importance in the workup…

• The clinician should look for a treatable predisposing factor such as a calculus or a stricture.

Acute viral infection (AVI)

• Mumps classically designates a viral parotitis caused by the paramyxovirus

• However, a broad range of viral pathogens have been identified as causes of AVI of the salivary glands.

Viral Infections

As opposed to bacterial sialadenitis, viral infections of the salivary glands are SYSTEMIC from the onset!

Virology

• Classic mumps syndrome is caused by paramyxovirus, an RNA virus

• Others can cause acute viral parotitis:– Coxsackie A & B, ECHO virus,

cytomegalovirus and adenovirus

• HIV involvement of parotid glands is a rare cause of acute viral parotitis, is more commonly associated with chronic cystic dz

Clinical presentation

• 30% experience prodromal symptoms prior to development of parotitis

• Headache, myalgias, anorexia, malaise

• Onset of salivary gland involvement is heralded by earache, gland pain, dysphagia and trismus

Physical exam

• Glandular swelling (tense, firm) Parotid gland involved frequently, SMG & SLG can also be affected.

• May displace ispilateral pinna• 75% cases involve bilateral parotids, may

not begin bilaterally (within 1-5 days may become bilateral)….25% unilateral

• Low grade fever

Treatment

• Supportive

• Fluid

• Anti-inflammatories and analgesics

Complications

• Orchitis, testicular atrophy and sterility in approximately 20% of young men

• Oophoritis in 5% females• Aseptic meningitis in 10%• Pancreatitis in 5%• Sensorineural hearing loss <5%

– Usually permanent – 80% cases are unilateral

Immunologic Disease

• 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

• 90% cases occur in women• Average age of onset is 50y• Classic monograph on the disease published

in 1933 by Sjögren, a Swedish ophthalmologist

Sjögren’s Syndrome

Two forms:• Primary: involves the exocrine glands only• Secondary: associated with a definable

autoimmune disease, usually rheumatoid arthritis.– 80% of primary and 30-40% of secondary

involves unilateral or bilateral salivary glands swelling

Sjögren’s Syndrome

• Unilateral or bilateral salivary gland swelling occurs, may be permanent or intermittent.

• Rule out lymphoma

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 finiding is lacrimation

of 5mm or less. Approximately 85% specific & sensitive

Sjögren’s Treatment

• 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

Sialadenosis

• Non-specific term used to describe a non-inflammatory non-neoplastic enlargement of a salivary gland, usually the parotid.

• May be called sialosis• The enlargement is generally asymptomatic• Mechanism is unknown in many cases.

Related to

a. Metabolic “endocrine sialendosis”

b. Nutritional “nutritional mumps”

a. Obesity: secondary to fatty hypertrophy

b. Malnutrition: acinar hypertrhophy

c. 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

c. Mumps

d. HIV

Granulomatous Disease

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.

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.

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.

Sialolithiasis

• The exact pathogenesis of sialolithiasis remains unknown.

• Thought to form via…. an initial organic nidus that progressively grows by

deposition of layers of inorganic and organic substances.

• May eventually obstruct flow of saliva from the gland to the oral cavity.

Acute ductal obstruction may occur at meal time when saliva producing is at its maximum, the resultant swelling is sudden and can be painful.

Gradually reduction of the swelling can result but it recurs repeatedly when flow is stimulated.

This process may continue until complete obstruction and/or infection occurs.

Etiology

• Water hardness likelihood? …Maybe….• Hypercalcemia…in rats only• Xerostomic meds• Tobacco smoking, positive correlation• Smoking has an increased cytotoxic effect on saliva,

decreases PMN phagocytic ability and reduces salivary proteins

Gout is the only systemic disease known to cause salivary calculi and these are composed of uric

acid.

Stone Composition

• Organic; often predominate in the center– Glycoproteins– Mucopolysaccarides– Bacteria!– Cellular debris

• Inorganic; often in the periphery– Calcium carbonates & calcium phosphates in the

form of hydroxyapatite

Reasons sialolithiasis may occur more often in the SMG

• Saliva more alkaline• Higher concentration of calcium and phosphate in

the saliva• Higher mucus content• Longer duct• Anti-gravity flow

Other characteristics:

• Despite a similar chemical make-up,

80-90% of SMG calculi are radio-opaque7

50-80% of parotid calculi are radiolucent7

• 30% of SMG stones are multiple

60% of Parotid stones are multiple

Clinical presentation

• Painful swelling (60%)

• Painless swelling (30%)

• Pain only (12%)– Sometimes described as recurrent salivary

colic and spasmodic pains upon eating

Diagnostics: Plain occlusal film

• Effective for intraductal stones, while….

• intraglandular, radiolucent or

small stones may be missed.

Diagnostic approach: Diagnostic Sialendoscopy2

• Allows complete exploration of the ductal system, direct visualization of duct pathology

• Success rate of >95%2

• Disadvantage: technically challenging, trauma could result in stenosis, perforation

Sialolithiasis Treatment

• None: antibiotics and anti-inflammatories, hoping for spontaneous stone passage.

• Stone excision:– Lithotripsy– Interventional sialendoscopy– Simple removal (20% recurrence)7

• Gland excision

• If patients DO defer treatment, they need to know:• Stones will likely enlarge over time• Seek treatment early if infection develops• Salivary gland massage and hyper-hydration when symptoms

develop.

Transoral vs. Extraoral Removal

• Some say: – if a stone can be palpated thru the mouth, it can be

removed trans-orally (TO)– Or if it can be visualized on a true central occlusal

radiograph, it can be removed (TO).– Finally, if it is no further than 2cm from the punctum,

it can be removed (TO).

Gland excision indicated

• Very posterior stones• Intra-glandular stones• Significantly

symptomatic patients• Failed

transoral

approach