oral medicine

Salivary Glands& Disease

Embryology

• The parotid anlagen are the first to develop, followed by the submandibular gland, and finally the sublingual gland.

• Parenchymal tissue (secretory) of the glands arises from the proliferation of oral epithelium.

Embryology

• The stroma (capsule and septae) of the glands originates from mesenchyme that may be mesodermal or neural crest in origin.

Parotid development

• Although the parotid anlagen are the first to develop, they become encapsulated AFTER the SMG and SLG.

• This delayed encapsulation is critical because after the encapsulation of the SMG and SLG but BEFORE encapsulation of the parotid, the lymphatic system develops.

Parotid development

• Therefore, there are intraglandular lymph nodes and lymphatic channels entrapped within the parotid gland (PG).

• PG is also unique because its epithelial buds grow, branch and extend around the divisions of the facial nerve.

Embryology

• The epithelial buds of each gland enlarge, elongate and branch initially forming solid structures.

• Branching of the glandular mass produces arborization.

• Each branch terminates in one or two solid end bulbs.

Embryology

• Elongation of the end bulb follows and lumina appears in their centers, transforming the end bulbs into terminal tubules.

• These tubules join the canalizing ducts to the peripheral acini.

Duct Canalization

• Canalization results from mitotic activity of the outer layers of the cord outpacing that of the inner cell layers

• Canalization is complete by 6th month post conception.

Acinar cells

• At around the 7-8th month in utero, secretory cells (acini) begin to develop around the ductal system.

Acinar cells of Salivary Glands

Classified as either:• Serous cells: produce a thin watery secretion

• Mucous cells: produce a more viscous secretion

Salivary gland secretory unit

• Composed of terminal acini

• Intercalated, striated and excretory ducts

• Myoepithelial cells

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 muscle.

Anatomy:Parotid Gland

• Extensions of PG project to mastoid process– Down the anterior aspect of the SCM for a

short distance– Around the posterior border of the mandible.– Superiorly to the to inferior margin of the

zygomatic arch

Anatomy:Parotid Gland

• 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: Deep Lobe

• The remaining 20% extends medially through the stylomandibular tunnel, which is formed – ventrally by the posterior edge of the ramus – dorsally by the anterior border of the SCM &

posterior digastric muscle– deeply and dorsally by the stylomandibular

ligament.

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

Anatomy: Parotid Duct

• 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.

Anatomy: Parotid Fascia

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

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

Anatomy: Parotid Lymphatics

• Lymphatic drainage is to the superficial and deep cervical nodes

• Preauricular lymph nodes (LN) in the superficial fascia drain the temporal scalp, upper face, anterior pinna

• LN within the gland drain the parotid gland, nasopharynx, palate, middle ear and external auditory meatus

Parotid: Parasympathetic Innervation

• 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: SympatheticInnervation

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

Parotid Anatomy: Great Auricular Nerve (C2,C3)

• Emerges from the posterior border of the SCM at Erb’s point.– It crosses the mid-portion of the SCM about

6.5cm beneath the EAM.

• Passes parallel and superior to the external jugular vein to supply the ear and pre-auricular region.

Parotid Anatomy: Auriculotemporal Nerve

• Branch of V3

• Traverses the upper part of the parotid gland and emerges from the superior surface with the superficial temporal vessels.

• It carries sensory fibers from the trigeminal and post-ganglionic parasympathetic (secretory)fibers.

Parotid Anatomy: Facial Nerve

• Emerges at the level of the digastric muscle, through the stylomastoid foramen.

• Main trunk divides at the pes anserinus (intraparotid plexus of CN7) into the upper temporofacial and lower cervicofacial divisions.

• Before it enters gland, gives off 3 branches:– Posterior auricular, posterior digastric, stylohyoid

Parotid Anatomy: Vessels

• Retromandibular Vein: located within the substance of the gland

• External carotid : at the inferior level of the gland, the external carotid divides into the superficial temporal and internal maxillary artery.

Parotid Bed: Deep lobe lies on...14

• V: internal jugular vein• A: external and internal carotid arteries• N: glossopharyngeal N vagus N spinal accesory N hypoglossal N• S: styloid process styloglossus mm stylohyloid mm

Anatomy:Submandibular gland

• 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 Lymphatics

Submandibular gland drains into submandibular nodes.

Anatomy: Submandibular Duct13

• Wharton’s duct passes forward along the superior surface of the mylohyoid adjacent to the lingual nerve.

• The nerve winds around the duct, first being lateral, then inferior, and finally medial.

Anatomy: Submandibular duct

• 2-4mm in diameter & about 5cm in length.

• It opens into the floor of the mouth thru a punctum.

• The punctum is a constricted portion of the duct to limit retrograde flow of bacteria-laden oral fluids.

Anatomy: Sublingual glands

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.

Anatomy: Sublingual glands

• The ducts of Rivinis either open…

– individually into the FOM near the punctum of Wharton’s duct

– on a crest of sublingual mucosa called the plica sublingualis

– open directly into Wharton’s duct

Diseases of Salivary Glands

Physiology

• Physiologic control of the SG is almost entirely by the autonomic nervous system; parasympathetic effects predominate.

• If parasympathetic innervation is interrupted, glandular atrophy occurs.

• Normal saliva is 99.5% water

• Normal daily production is 1-1.5L

Major glands/Secretions

• Major SG are paired structures and include the parotid, submandibular and sublingual

• Parotid: serous• Submandibular: mucous & serous

• Sublingual: mucous

Salivary Function

• Aid is mastication, deglutination

• Salivary lysozyme, IgA and other antibacterial substances protect against caries and oral cavity infections

• Saliva also aids in speech

ObstructiveSalivary Gland Disorders

• Sialolithiasis

• Mucous retention/extravasation 

Obstructive SG Disorders: Sialolithiasis

• Sialolithiasis results in a mechanical obstuction of the salivary duct

• Is the major cause of unilateral diffuse parotid or submandibular gland swelling

Sialolithiasis Incidence

• Escudier & McGurk 1:15-20 000

• Marchal & Dulgurerov 1:10-20 000

Sialolithiasis remains the most frequent reason for submandibular gland resection

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.

Sialolithiasis

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

Etiology

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

Parotid (PG) vs. Submandibular Gland (SMG)….

• Most authorities agree obstructive phenomemnon such as mucous plugs and sialoliths are most commonly found in the SMG– Escudier et al – Lustmann et al– Rice

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-opaque

50-80% of parotid calculi are radiolucent

• 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

Clinical History

• History of swellings / change over time?• Trismus?• Pain?• Variation with meals?• Bilateral?• Dry mouth? Dry eyes?• Recent exposure to sick contacts (mumps)?• Radiation history?• Current medications?

Exam: Inspection

• Asymmetry (glands, face, neck)• Diffuse or focal enlargement• Erythema extra-orally• Trismus• Medial displacement of structures intraorally?• Examine external auditory canal (EAC)• Cranial nerve testing ( Facial Nerve )

Exam: Palpation

• Palpate for cervical lymphadenopathy• Bimanual palpation of floor of mouth in a

posterior to anterior direction– Have patient close mouth slightly & relax oral

musculature to aid in detection– Examine for duct purulence

• Bimanual palpation of the gland (firm or spongy/elastic).

Diagnostics: Plain occlusal film

• Effective for intraductal stones.

• intraglandular, radiolucent or

small stones may be missed.

Diagnostic approaches

CT Scan:

• large stones or small CT slices done

also used for inflammatory disorders

Ultrasound:

• operator dependent, can detect small stones (>2mm), inexpensive, non-invasive

Diagnostic approaches: Sialography

• Consists of opacification of the ducts by a retrograde injection of a water-soluble dye.

• Provides image of stones and duct morphological structure

• May be therapeutic, but success of therapeutic sialography never documented

Sialography

• Disadvantages: – irradiation dose

– pain with procedure

– Possible perforation

– infection

– dye reaction

– push stone further

– contraindicated in active infection.

Diagnostic approach: Radionuclide Studies

• Useful to image the parenchyma• T99 is an artificial radioactive element (atomic

#43, atomic weight 99) that is used as a tracer in imaging studies.

• T99 is a radioisotope that decays and emits a gamma ray. Half life of 6 hours.

• Helman & Fox 1987, found that Technitium-99 shares the Na-K-Cl transport system on the basement membrane of the parotid acinar cells

Diagnostic Approaches: Radionuclide Studies

• Some say T99 is useful preoperatively to determine if gland is functional.

• However, no evidence to suggest gland won’t recover function after stone removed. Not advised for pre-op decision making!

Diagnostic Approach: MR Sialography

• T2 weighted fast spin echo slides in sagittal and axial planes. Volumetric reconstruction allows visualization of ducts

• ADV: No dye, no irradiation, no pain

• DIS: Cost, possible artifact

Diagnostic approach: Diagnostic Sialendoscopy

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

• Success rate of >95%

• 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)

• Gland excision

Sialolithiasis Treatment

• 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.

Stone excision

• External lithotripsy– Stones are fragmented and expected to pass

spontaneously– The remaining stone may be the ideal nidus for

recurrence

• Interventional Sialendoscopy– Can retrieve stones, may also use laser to

fragment stones and retrieve.

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.

Posterior Stones

• Deeper submandibular stones (~15-20% of stones) may best be removed via sialadenectomy.

• Some surgeons say can still remove transorally, but should be done via general anesthetic.

• Floor of mouth (FOM) opened opposite the first premolar, duct dissected out, lingual nerve identified.

• Duct opened & stone removed, FOM approximated.

Submandibular Sialoliths: Transoral Advantages

• Preserves a functional gland

• Avoids neck scar

• Possibly less time from work

• No overnight stay in hospital

• Avoids risk to CN 7 & 12

Gland excision

• After SMG excision, 3% cases have recurrence via:– Retention of stones in intraductal portion or

new formation in residual Wharton's duct

• No data regarding recurrence after parotidectomy

Gland excision indicated

• Very posterior stones

• Intra-glandular stones

• Significantly symptomatic patients

• Failed

transoral

approach

Gland excision

• While some believe that a gland with sialolithiasis is no longer functional, a recent study on SMGs removed due to sialolithiasis found there was no correlation between the degree of gland alteration and the number of infectious episodes.

• 50% of the glands were histopathologically normal or close to normal

• A conservative approach to the gland/stone seems to be justified

ObstructiveSalivary Gland Disorders

 • Sialolithiasis

• Mucous retention/extravasation

Mucocele

• 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

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

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• 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

• 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 Mucocelesin 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

• Marsupialization has fallen into disfavor due to the excessive recurrence rate of 60-90%

• Sublingual gland removal via intraoral approach

Salivary Gland Infections

• Acute bacterial sialdenitis

• Chronic bacterial sialdenitis

• Viral infections

Sialadenitis

Sialadenitis represents inflammation mainly involving the acinoparenchyma of the

gland.

Sialadenitis

Awareness of salivary gland infections was increased in 1881 when President Garfield died from acute parotitis following abdominal surgery and associated systemic dehydration.

Sialadenitis

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

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 bilateral

Predilection for ParotidSalivary Composition

The composition of parotid secretions differs from those in other major glands.

Parotid is primarily serous, the others have a greater proportion of mucinous

material.

Salivary Composition

• Mucoid saliva contains elements that protect against bacterial infection including lysozymes & IgA antibodies (therefore, parotid has bacteriostatic activity)

• Mucins contain sialic acid which agglutinates bacteria and prevents its adherence to host tissue.

• Specific glycoproteins in mucins bind epithelial cells competitively inhibiting bacterial attachment to these cells.

Parotid PredilectionAnatomic factors

• Minor role in formation of infections

• Stensen’s duct lies adjacent to the maxillary mandibular molars and Wharton’s near the tongue.– It is thought that the mobility of the tongue may

prevent salivary stasis in the area of Wharton's that may reduce the rate of infections in SMG.

Risk Factors for Sialadenitis

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

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

Risk Factors continued…

• Neoplasms (pressure occlusion of duct)

• Sialectasis (salivary duct dilation) increases the risk for retrograde contamination.

• cystic fibrosis and pneumoparotitis• Extremes of age• Poor oral hygiene• Calculi, duct stricture• NPO status (stimulatory effect of mastication on salivary

production is lost)

Complex picture

• There must be other factors at work…..

• Sialolithiasis can produce mechanical obstruction of the duct resulting in salivary stasis and subsequent gland infection.

• Calculus formation is more likely to occur in SMG duct (85-90% of salivary calculi are in the SMG duct) However, the parotid gland remains the site of acute suppurative infection!

Differential Diagnosis of Parotid Gland Enlargement

• Lymphoma

• Actinomycoses

• Cat-scratch disease

• Sjogren’s syndrome

• Wegener’s granulomatosis

• Viral infection

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 – 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

Failure to respond

• After 48 hours the patient should respond

• Consider adding a third generation cephalosporin

• Possibly add an aminoglycoside

• The preponderance of MRSA in nursing homes and nosocomial environments has prompted the recommendation of vancomycin in these groups

Surgery for Acute Parotitis1

• 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

Complications of Acute Parotitis

• Direct extension– Abscess ruptures into external auditory canal

and TMJ have been reported

• Hematogenous spread

• Thrombophlebitis of the retromandibular or facial veins are rare complications

Complications

• Fascial capsule around parotid displays weakness on the deep surface of the gland adjacent to the loose areolar tissues of the lateral pharyngeal wall (Achilles’heel of parotid)

• Extension of an abscess into the parapharyngeal space may result in airway obstruction, mediastinitis, internal jugular thrombosis and carotid artery erosion

Complications

• Dysfunction of one or more branches of the facial nerve is rare.

• Occurs secondary to perineuritis or direct neural compression ; but resolves with adequate treatment of the parotitis.

• These patients need to be followed to ensure resolution….must rule out TUMOR.

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.

No treatable cause found

• Initial management should be conservative and includes the use of sialogogues, massage and antibiotics for acute exacerbations.

• Should conservative measures fail, consider removing the gland.

• Dilatations & Irrigation

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.

AVI

• Derived from the Danish word “mompen”

• Means mumbling, the name given to describe the characteristic muffled speech that patients demonstrate because of glandular inflammation and trismus.

Viral Infections

As opposed to bacterial sialadenitis, viral infections of the salivary glands are

SYSTEMIC from the onset!

Viral infection

• Mumps is a non-suppurative acute sialadenitis

• Is endemic in the community and spread by airborne droplets

• Communicable disease

• Enters through upper respiratory tract

Mumps

• 2-3 week incubation after exposure

• 3-5 day viremia

• Then localizes to biologically active tissues like salivary glands, germinal tissues and the CNS.

Epidemiology

• Occurs world wide and is highly contagious

• Prior to the widespread use of the Jeryl Lynn vaccine (live attenuated), cases were clustered in epidemic fashion

• Sporadic cases are observed today likely resulting from non-paramyxoviral infection, failure of immunity or lack of vaccination

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

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 exam1

• 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

Diagnostic Evaluation

• Leukocytopenia, with relative lymphocytosis

• Increased serum amylase (normal by 2- 3 week of disease)

• Viral serology essential to confirm:

• Complement fixing antibodies appear following exposure to the virus

Serology

• “S” or soluble antibodies directed against the nucleoprotein core of the virus appear within the first week of infection, peak in 2 weeks.

• Disappear in 8-9 months and are therefore associated with active or recent infection

Serology

• “V”, or viral antibodies directed against the outer surface hemagglutinin, appear several weeks after the S antibodies and persist at low levels for about 5 years following exposure.

• V antibodies are associated with past infection, prior vaccination and the late stages of active infection

Serology

• If the initial serology is noncontributory, then a non-paramyxovirus may be responsible for the infection.

• Blood HIV tests should also be obtained• The mumps skin test is not useful in

diagnosis an acute infection because dermal hypersensitivity does not develop until 3 or 4 weeks following exposure.

Treatment

• Supportive

• Fluid

• Anti-inflammatories and analgesics

Prevention

• The live attenuated vaccine became available in 1967

• Commonly combined with the measles and rubella vaccines, the mumps vaccine is administered in a single subcutaneous dose after 12 months of age. Booster at 4-6yr

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 Sjögren’s Syndrome

• 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 diease 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 Lip Biopsy

• Biopsy of SG mainly used to aid in the diagnosis• Can also be helpful to confirm sarcoidosis

Sjögren’s Lip Biopsy

• 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’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 mumps

e. HIV

Radiation Injury

• 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 gland.

• Similar to the thyroid, salivary neoplasm are increased in incidence after radiation exposure.

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.

Granulomatous Disease

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

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.

CystsTrue 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• Association with tumors

– Pleomorphic adenoma– Adenoid Cystic Carcinoma– Mucoepidermoid Carcinoma– Warthin’s Tumor

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

• 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

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

Neoplasms

• Benign:

- Pleaomorphic Adenoma:

Commonest (2/3 of all salivary tumors)

85% in Parotid Gland.

? Capsulated with Psudopods

30% recurrence rate

Neoplasms

• Benign:

- Warthins Tumor:

2nd most common

almost exclusive to tail of parotid

Well encapsulated

Bil in 10%

Neoplasms

• Benign:

- Monomorphic Adenoma

- Oncocytomas

- Hemangiomas

Neoplasms

• Malignant:make up a relatively small percentage

of all cancer occurring in the head and neck region.

Radiation exposure is one known risk factor

Pain is present in 10 to 29% of patients with cancer

in the parotid gland.

Facial paralysis is detected in 10 to 15% of parotid gland malignancies

Neoplasms

• Malignant:

- Mucoepidermoid Carcinoma

most common (1/2 in Parotid )

High Grade & Low Grade.

Neoplasms

Malignant:

- Adenoid Cystic Carcinoma

2nd most common

most common in submandibular & minors

perineural invasion is hallmark

High grade & low grade.

Neoplasms

• Malignant:

- Polymorphus low grade Adenocarcinoma

- Acinic Cell Carcinoma

- Malignant Mixed Tumors

- Sqaumous Cell Carcinoma

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

References

6. Marchal F, Kurt AM, Dulgeurov P, Becker M et al. Histopathology of submandibular glands removed for sialolithiasis. Ann Oto Rhinol.2001;110, 464

7. Rice DH. Salivary Gland Disorders. Med Clin North Am. 1999; vol 83, 197.

8. Kirsh CM, Shinn J, Porzio R et al. Chest. 1999, vol 116, 14769. Baurmash HD. Mucoceles and Ranulas. J Oral Maxillo Surg. 2003, vol

61, 36910. Ellies M, Laskawi R, Arglebe C, et al. Surgical management of

nonneooplastic disease of the submandibular gland. Int J Oral Maxillofac Surg. 25:1996, 285

11. Williams MF. Salivary gland diseases: sialolithiasis. Oto Clin North America. Vol 32, 819, 1999

References

• 12: Krause GE, Meyers AD. Management of parotid swelling. Comprehensive Therapy. 1996, 22:256.

• 13. Silvers AR, Som PM. Head and Neck Imaging: the Salivary Glands. 1998, 36:941

• 14. Carlson GW. The salivary glands. Surgical Clin North America. 2000, 80:261

• 15. Feinberg SE. Diagnosis and management of salivary gland disorders. Ch.34