Slivary Glands & Diseases

by: dr nikil

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

secretionMucous cells: produce a more viscous

secretion

Salivary gland secretory unit

Composed of terminal aciniIntercalated, striated and excretory ductsMyoepithelial cells

Major glands/Secretions

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

Parotid: serousSubmandibular: mucous & serousSublingual: mucous

Salivary Function

Aid is mastication, deglutinationSalivary lysozyme, IgA and other

antibacterial substances protect against caries and oral cavity infections

Saliva also aids in speech

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

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: Sympathetic Innervation

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 V3Traverses 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...

V: internal jugular veinA: external and internal carotid arteriesN: glossopharyngeal N vagus N spinal accesory N hypoglossal NS: 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 Duct

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 glandsLie 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 ducton a crest of sublingual mucosa

called the plica sublingualisopen directly into Wharton’s duct

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% waterNormal daily production is 1-1.5L

ObstructiveSalivary Gland Disorders

SialolithiasisMucous 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 swelling2

Sialolithiasis Incidence

Escudier & McGurk 1:15-20 0003

Marchal & Dulgurerov 1:10-20 0002

Sialolithiasis remains the most frequent reason for submandibular gland resection5

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 onlyXerostomic medsTobacco smoking, positive correlationSmoking 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 al3 Lustmann et al4

Rice7

Others note that parotid glands are most commonly affected2

Reasons sialolithiasis may occur more often in the SMG

Saliva more alkalineHigher concentration of calcium and

phosphate in the salivaHigher mucus contentLonger ductAnti-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

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 enlargementErythema extra-orallyTrismusMedial displacement of structures

intraorally?Examine external auditory canal (EAC)Cranial nerve testing

Exam: Palpation

Palpate for cervical lymphadenopathyBimanual 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, while….

intraglandular, radiolucent or

small stones may be missed.

Diagnostic approaches

CT Scan:large stones or small CT slices done

also used for inflammatory disordersUltrasound: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 continued…Disadvantages:

irradiation dose pain with procedure poss.perforation infection dye reaction push stone further contraindicated in active infection.

Diagnostic approach: Radionuclide Studies

Useful to image the parenchymaT99 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 painDIS: Cost, possible artifact

Diagnostic approach: Diagnostic Sialendoscopy

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

Sialolithiasis Treatment

If patients DO defer treatment, they need to know:

Stones will likely enlarge over timeSeek treatment early if infection developsSalivary 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

recurrenceInterventional 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 glandAvoids neck scarPossibly less time from workNo overnight stay in hospitalAvoids 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 ductNo data regarding recurrence after

parotidectomy

Gland excision indicatedVery posterior stonesIntra-glandular stonesSignificantly symptomatic patientsFailed transoral approach

Gland excisionWhile 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

SialolithiasisMucous 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.

RanulaPresents 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 sialdenitisChronic bacterial sialdenitisViral 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 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

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 Predilection : Anatomic factors

Minor role in formation of infectionsStensen’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. Is associated with cystic fibrosis and pneumoparotitis

Extremes of agePoor oral hygieneCalculi, duct strictureNPO 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 MC site of acute suppurative infection!

Differential Diagnosis of Parotid Gland Enlargement

LymphomaActinomycosesCat-scratch diseaseSjogren’s syndromeWegener’s granulomatosisViral 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 and S.pyogenes Haemophilus Influenzae also common

Lab Testing

Parotitis is generally a clinical diagnosisHowever, in critically ill patients further

diagnostic evaluation may be requiredElevated white blood cell countSerum 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 possibleWarm 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

penicillinaseNeed B-lactamase inhibitor like Augmentin or

Unasyn or second generation cephalosporinCan also consider adding metronidazole or

clindamycin to broaden coverage

Failure to respond

After 48 hours the patient should respondConsider adding a third generation cephPossibly add an aminoglycosideThe preponderance of MRSA in nursing

homes and nosocomial environments has prompted the recommendation of vancomycin in these groups

Surgery for Acute Parotitis

Limited role for surgeryWhen a discrete abscess is identified,

surgical drainage is undertakenApproach 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 reportedHematogenous spreadThrombophlebitis 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.

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 diseaseEnters through upper respiratory tract

Mumps

2-3 week incubation after exposure (the virus multiplies in the URI or parotid gland)

3-5day viremiaThen 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, 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

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

SupportiveFluidAnti-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% femalesAseptic 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 womenAverage age of onset is 50yClassic monograph on thediease published in

1933 by Sjögren, a Swedish ophthalmologist

Sjögren’s Syndrome

Two forms:Primary: involves the exocrine glands onlySecondary: 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 identificationGlands assessed semi-quantitatively to

determine the number of foci of lymphocytes per 4mm2/gland

Sjögren’s Treatment

Avoid xerostomic meds if possibleAvoid alcohol, tobacco (accentuates xerostomia)Sialogogue (eg:pilocarpine) use is limited by other

cholinergic effects like bradycardia & lacrimationSugar 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”

a. Nutritional “nutritional mumps” a. Obesity: secondary to fatty hypertrophyb. Malnutrition: acinar hypertrhophyc. 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

c. 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.

Cysts

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. retentionTraumaticBenign epithelial lesionsAssociation 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

Crepitation, on palpation of the glandSwelling may resolve in minutes to hours, in

some cases, days. US and CT show air in the duct and glandConsider 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

References

1. Tex book of oral surgery- Peter wardbooth2. Principles of oral surgery – Peterson 3. Salivary glands disorder – Mayors