sialodenosis

7/26/2019 Sialodenosis

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SIALODENOSIS


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TERMINOLOGY:

Sialadenitis refers to inflammation of a salivarygland and may be acute or chronic, infective orautoimmune.

Sialolithiasis refers to stone-related diseasewithin the ductal systems of a gland.

Sialectasis refers to the dilation of a duct due tostones or strictures.

Sialadenosis refers to non-neoplastic non-inflammatory swelling with acinar hypertrophyand ductal atrophy.


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Sialosis (sialadenosis) is a chronic, bilateral,diffuse, non-inflammatory, non-neoplasticpainless swelling of the major salivary glandsthat primarily affects the parotid glands, butoccasionally involves the submandibular

glands and rarely the minor salivary glands(Scully 2008)

Enlargement of the salivary gland, usually the

parotids, often seen in conditions such asalcoholism and malnutrition


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Sialadenosis is a non-specificterm used to describe anuncommon, benign, non-

inflammatory, non-neoplasticenlargement of a salivarygland, usually the parotid gland

but occasionally affects thesubmandibular glands andrarely, the minor salivary

glands


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Sialadenosis or sialosis is an

uncommon disease of the salivaryglands, characterized byasymptomatic, bilateral, diffuse

swelling of the major salivary glands,particularly the parotid gland . Thiscondition usually does not affect

salivary gland function. Since systemicdiseases or conditions such as diabetesmellitus and alcoholism


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Sialadenosis is a non-neoplastic,

noninflammatory enlargement of thesalivary gland that more commonlyaffects the parotid gland and is often

bilateral. It results from acinar cellhypertrophy, and has been associatedwith a wide range of etiologies,

including endocrine abnormalities likediabetes mellitus, nutritionaldeficiencies, alcoholism, cirrhosis, andcertain drugs, especially

antihypertensives.


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Sialadenosis usually occursbetween 30-70 years of age,

and is usually associated with an

underlying disease such as

diabetes mellitus, nutritional

deficiencies, neurologicdiseases, or alcoholic-liver

disease


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Sialosis may be idiopathic or maybe associated with the following:

chronic malnutritionobesity

diabetes mellitus

alcoholism

liver disease

eating disordersdrugs (ie antihypertensives)


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Drugs

anti-hypertensive agentsAlcohol

Sympathomimeticssuch as

isoprenaline

Phenylbutazone

Anti-thyroids&phenothiazines


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Endocrine (Hormonal)

Diabetes Mellitus(prevalence10% to 80%)

Pregnancy

Acromegaly

Nutritional Disorders


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Histological characteristics of

sialadenosis include hypertrophy of the

acinar cells with basally located small

round nuclei with zymogen granules in

the cytoplasm

The normal size of parotid acini is about40m. The size of parotid glands may

increase to as much as 100m


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DIAGNOSIS:

There are no symptoms associated withparotid gland enlargement. A comprehensivemedical history should be taken andinflammatory and infectious diseases such

as Sjgrenssyndrome, HIV, and hepatitis Cshould be excluded.14 Saliva may beincreased or decreased depending upon theunderlying etiology.

Various imaging techniques such ascomputed tomography (CT), sialography,ultrasonography (US) and magneticresonance imaging (MRI) may be used


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Blood Tests:

glucose levels

Abnormal liver function tests

potassium levels

calcium levels

Evaluation of the clinical and medical history,imaging, serology, or fine-needle aspiration, maybe necessary to reach a definitive diagnosis.


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BIOPSY:

Rarely indicated. If done, the biopsy shows theacinar cellsto be enlarged toalmost twice the normal diameter and thecytoplasmpacked with enzyme granules.

Clin ical Find ings:

Soft, painless, general enlargement of both

parotids.


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TR TM NT:

None necessary.As the condition is asymptomatic, notreatment is indicated and periodic follow-up is advised. In patients who areesthetically concerned, surgery isrecommended.

Sialosismay resolve if diabetes mellitus- &alcoholism-related sialosisis treated


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One explanation is that the sympathetic nerve supply tothe secreting acinar cellisconcerned with the production and secretion of zymogen,the precursor ofamylase. Because of sympathetic nerve dysfunction,

there may be an increase inzymogen storagein the cell, owing to increasedproduction, decreased secretion ofthe granules or both. The ensuing cellular enlargement,which is evidenced by fine-

needle aspiration biopsyand electron microscopy, leadsto the clinically visiblegland enlargement.


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AnatomyThe submandibular gland, along with the

parotid and sublingual glands, comprise

the major salivary glands. The minor

salivary glands are scattered along the

upper aerodigestive tract, including thelips, mucosa of the oral cavity, pharynx,

and hard palate.

The submandibular gland is the second

largest (approximate weight, 10 g) of the

major salivary glands (the parotid gland is

the largest). Anatomically, it is situated inthe submandibular triangle of the neck.


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The gland itself can be arbitrarily divided into superficialand deep lobes based on its relationship to the mylohyoidmuscle, the former lying superficial to the muscle, and thelatter wrapping around the posterior aspect of the muscle.The gland itself lies on the hyoglossus muscle, superficial

to both the hypoglossal and the lingual nerves, the lattersupplying parasympathetic innervation by way of thechorda tympani nerve (from cranial nerve VII) and thesubmandibular ganglion. The duct of the submandibulargland, also known as the Wharton duct, exits the gland

from the deep lobe, passing through the floor of themouth, and opening in close proximity to the lingualfrenulum. See the image below.


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Pathophysiology The salivary glands serve numerous functions, including

lubrication; enzymatic degradation of food substances;production of hormones, antibodies, and other bloodgroupreactive substances; mediation of taste; andantimicrobial protection. The regulation of salivary flow isprimarily through the autonomic system and, mostimportantly, the parasympathetic division. In the case ofthe submandibular gland, this is mediated through thesubmandibular ganglion. Presynaptic fibers are derived

from the superior salivatory nucleus and carried by thechorda tympani nerve, which joins the lingual nervetraveling towards the ganglion. Postsynaptic fibers extendfrom the ganglion to the gland itself.


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Saliva is produced in the glandular subunit. Thefluid component of the saliva is derived from theperfusing blood vessels in proximity to thegland, while the macromolecular composition isderived from secretory granules within theacinar cells. The saliva is produced in theacinus. Myoepithelial cells, containing

contractile elements, are located along theperiphery of the acinus. Upon contraction ofthese myoepithelial cells, the saliva is secretedinto the ductal system.


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The exact mechanism of salivary secretion isnot completely understood but is believed tobe under the influence of a cyclic AMP

(adenosine 3,'5'-cyclic monophosphate) anda calcium-activated phosphorylationmechanism. The salivary secretions are thenmodified by a variety of cell types along a

series of ducts, including the striated,intercalated, and excretory ducts, beforefinally being excreted through the Whartonduct into the oral cavity.


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The concentration of mucus is higher in the

submandibular gland, accounting for the

viscous nature of its secretions relative to the

other salivary glands. This increasedviscosity, and subsequent relatively slower

flow, contributes to the propensity for salivary

gland calculi and stasis in certain diseasestates.


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Epidemiology Frequency

United States

The exact frequency of submandibularsialadenitis is unclear. The incidence of acutesuppurative parotitis has been reported at 0.01-0.02% of all hospital admissions. Thesubmandibular gland is suggested to accountfor approximately 10% of all cases ofsialadenitis of the major salivary glands.Extrapolation would suggest an incidence of0.001-0.002%, but this is unconfirmed.


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Race

No race predilection per se exists.

Sex

No sex predilection per se exists.

Age

Although no obvious age predilection exists,per se, sialadenitis as a whole tends to occur

in the older, debilitated, or dehydrated

patient.[1]


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History Submandibular sialadenitis takes several forms. The

diagnostic workup of any submandibular enlargementbegins with a thorough history. This should include onset,duration of symptoms, recurrence, recent operativehistory, recent dental work, and thorough drug history,immunization history (specifically measles , mumps ,rubella [MMR] vaccine), past medical (specificallyautoimmune) history, past surgical history, and history ofradiation therapy. Inquire as to associated fever or chills,

weight loss, presence of a mass, bilaterality orunilaterality, skin changes, lymphadenopathy, keratitis,shortness of breath, oral discharge, dental pain, or skindischarge.
http://emedicine.medscape.com/article/1194028-overviewhttp://emedicine.medscape.com/article/1194028-overview


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History Submandibular sialadenitis takes several forms. The

diagnostic workup of any submandibular enlargementbegins with a thorough history. This should include onset,duration of symptoms, recurrence, recent operativehistory, recent dental work, and thorough drug history,immunization history (specifically measles , mumps ,rubella [MMR] vaccine), past medical (specificallyautoimmune) history, past surgical history, and history ofradiation therapy. Inquire as to associated fever or chills,

weight loss, presence of a mass, bilaterality orunilaterality, skin changes, lymphadenopathy, keratitis,shortness of breath, oral discharge, dental pain, or skindischarge.


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Physical Physical examination should begin with the gland itself. The gland

should be palpated for the presence of calculi. Examine theductal opening for purulence. Palpation should extend into thefloor of mouth as well as the soft tissue of the tongue, cheek, and

neck. Lingual papillary atrophy should be looked for, as well asloss of enamel from the tooth surface (the latter may beassociated with bulimia). All of the major salivary glands shouldbe examined for masses, symmetry, and the presence ofdischarge. The presence of lymphadenopathy should be noted.The eyes should be examined for any presence of interstitial

keratitis. A quick cranial nerve examination should be conductedwith particular attention to cranial nerves VII and XII. The lungsshould be examined and a chest radiograph ordered if suspectedpulmonary involvement exists.


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Causes Acute sialadenitis

Acute sialadenitis is an acute inflammation of asalivary gland.

Patients typically present with erythema over thearea, pain, tenderness upon palpation, and swelling.Frank cellulitisand induration of adjacent soft tissuesmay be present. Purulent material may be observedbeing expressed from the Wharton duct, particularlyupon milking the gland. Rarely, a cutaneous fistulamay occur, with spontaneous drainage of purulentmaterial. The inflammation is secondary to aninfectious proces


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The most common organism is Staphylococcusaureus. Other bacterial organisms includeStreptococcus viridans, Haemophilusinfluenzae, Streptococcus pyogenes,andEscherichia coli. The infection is often the resultof dehydration with overgrowth of the oral flora.The most common causes are postoperative

dehydration, radiation therapy, andimmunosuppression (eg, diabetes mellitus,organ transplant, chemotherapy, humanimmunodeficiency virus).
http://emedicine.medscape.com/article/211316-overviewhttp://emedicine.medscape.com/article/211316-overviewhttp://emedicine.medscape.com/article/211316-overviewhttp://emedicine.medscape.com/article/211316-overview


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Of note, infection of the submandibular glandis rare in the neonate and prepubescentchild. When it does occur, similar pathogens

have been identified, includingPseudomonas aeruginosaand group Bstreptococci. Physical examination, inaddition to the symptoms described above,

includes failure to thrive and irritability.Progression may occur, involving thecontralateral gland. The etiology of this entityis unclear.


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Although less common than bacteria, several

viruses have been implicated in

submandibular sialadenitis. These include

the mumps virus, which typically affects theparotid gland but can affect the

submandibular gland as well. Other viruses

include HIV, coxsackievirus, parainfluenzatypes I and II, influenza A, and herpes


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Infection of the submandibular gland can resultin the formation of a submandibular abscess. Inthis state, the patient may appear toxic, withfeatures similar to acute submandibular

sialadenitis. Spiking fevers are not uncommon.This is a serious condition requiring strictattention because of the possibility that theabscess may spread to involve other deep neck

spaces of the neck. Trismus may be indicativeof parapharyngeal involvement. Progression toLudwig angina, a life-threatening infection of thesubmental and sublingual spaces, althoughrare, can occur.


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Chronic sialadenitis

Chronic sialadenitis, in contrast, is typically lesspainful and is associated with recurrent

enlargement of the gland (often following meals)typically without erythema. The chronic form ofthe disease is associated with conditions linkedto decreased salivary flow, rather than

dehydration. These conditions include calculi,salivary stasis, and a change in the fluid andelectrolyte composition of the gland.


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Sialolithiasis Salivary calculi (sialolithiasis) relate to the formation

and deposition of concretions within the ductalsystem of the gland.

Eighty percent of all salivary calculi occur in thesubmandibular gland, with approximately 70% ofthese demonstrable as radio-opacities on routineplain radiography consisting of intraoral occlusalradiographs.

The calculi vary in size and may be single or multiple.The formation of calculi is associated with chronicsialadenitis, and in particular, the recurrent nature ofthe problem.


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The exact mechanism of stone formation is unclear,but it appears to be related to the followingconditions:

Salivary stagnation

Epithelial injury along the duct resulting in sialolithformation, which acts as a nidus for further stoneformatio

Precipitation of calcium salts

The stones themselves are typically composed ofcalcium phosphate or calcium carbonate inassociation with other salts and organic material suchas glycoproteins, desquamated cellular residue, andmucopolysaccharides.


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Patients most often present with a colicky

postprandial swelling of the gland. The

course of the disease is typically relapsing

and remitting until a final definitive treatment,usually in the form of surgery, is undertaken.


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Autoimmune sialadenitis Autoimmune diseases, in particular Sjgren

syndrome, can be associated with sialadenitis.Although preferentially affecting the parotid gland, the

submandibular and minor salivary glands are alsoaffected. The disease, which is associated withkeratoconjunctivitis sicca, xerostomia, salivary glandenlargement, and lingual papillary atrophy, isconfirmed through biopsy of the minor salivary glands

of the lip. Numerous laboratory tests are also used toconfirm the diagnosis, such as autoantibodiesSjgren syndrome A (SS-A) and Sjgren syndrome B(SS-B), rheumatoid factor, and antinuclear antibodies.


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Sialadenosis Sialadenosis refers to nonneoplastic noninflammatory swelling in

association with acinar hypertrophy and ductal atrophy.

Etiologies fall into 5 major categories.

Nutritional (eg, vitamin deficiency, bulimia)

Endocrine (eg, diabetes mellitus, hypothyroidism) Metabolic (eg, obesity, cirrhosis, malabsorption)

Inflammatory/autoimmune (eg, Sjgren disease, Heerfordtsyndrome)

Drug induced (eg, thiourea)

Physical examination shows a nontender swelling that is oftenbilateral and symmetric but can be unilateral and asymmetric.
http://emedicine.medscape.com/article/122393-overviewhttp://emedicine.medscape.com/article/185856-overviewhttp://emedicine.medscape.com/article/185856-overviewhttp://emedicine.medscape.com/article/122393-overview


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Laboratory Studies In evaluating the patient with sialadenitis, steps should be

taken in the following order: history, physical examination,culture, laboratory investigation, radiography, and ifindicated, fine-needle aspirationbiopsy (see History and

Physical). Laboratory investigations should begin with culture of the

offending gland (if possible, prior to the administration ofantibiotics).

Blood cultures should be obtained in the patient exhibitingbacteremia or sepsis.

As a rule, needle aspiration of a suspected abscess is notindicated.
http://emedicine.medscape.com/article/882291-overviewhttp://emedicine.medscape.com/article/234587-overviewhttp://emedicine.medscape.com/article/234587-overviewhttp://emedicine.medscape.com/article/882291-overviewhttp://emedicine.medscape.com/article/882291-overviewhttp://emedicine.medscape.com/article/882291-overview


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Routine electrolytes and complete blood cell

count with differential should be obtained to

assess for any evidence of dehydration or

systemic infection. If a diagnosis of autoimmunity is entertained,

serum analysis for antinuclear antibody, SS-

A, SS-B, and erythrocyte sedimentation rateshould be conducted.


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Imaging Studies

Numerous radiologic techniques are available in

submandibular imaging. Deciding which study to

obtain first is often difficult. Examinationselection should be based in part on the

suspected cause of the problem. The authors'

institution tends to begin with plain radiography,

followed by the use of computed tomography

scanning with combined sialography


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Of all the radiologic examinations available,one of the simplest is conventional plainradiography.[2]Anteroposterior, lateral, and

oblique intraoral occlusal views are used.This technique is particularly valuable inevaluating the presence of calculi, which areradio-opaque in approximately 70% of cases.

These radiographs are limited in that they donot provide any information about the ductalsystem or soft tissues.


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ialography can be used to evaluate sialolithiasis or otherobstructive entities, as well as inflammatory andneoplastic disease. In this technique, a water-solublemedium such as meglumine diatrizoate is injected into theWharton duct and lateral, oblique, and anteroposterior

plain radiographs are obtained in order to assess theductal arborization.

Contraindications for this test are iodine allergy and acutesialadenitis.

Any filling defects (eg, calculi), retained secretions (eg,

chronic sialadenitis), stricture formation (eg,inflammation), extravasation (eg, Sjgren disease), orirregularly contoured borders (eg, neoplasm) are noted.


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Ultrasonography can be used to differentiatebetween solid versus cystic lesions of thegland. It can also be used to differentiate

intrinsic from extrinsic disease and can behelpful in identification of abscess formation.A 2009 study by Bozzato et al determinedthat application of ascorbic acid (vitamin C)

as a contrast agent can aid in the ultrasoundassessment of obstructive sialadenitis of theparotid and submandibular glands.[3, 4]


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Computed tomography scanning is an excellentmodality in differentiating intrinsic versus extrinsicglandular disease. It is also extremely valuable indefining abscess formation versus phlegmon. It islimited in evaluating the ductal system unlesscombined with simultaneous sialography.

Magnetic resonance imaging is of little utility insialadenitis or sialadenosis. It does not allowevaluation of the ductal system, and it is not helpful in

defining calcifications. It is an excellent tool for softtissue definition and is invaluable in instances ofsuspected neoplasia.


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Procedures

Fine-needle aspiration and biopsy Open biopsyof the lip should be considered when the

diagnosis of Sjgren disease is contemplated. If suspicion of a solid neoplasm masquerading

as sialadenitis is significant, a fine-needleaspiration with biopsy should be undertaken.

The management and differential diagnosis ofsubmandibular neoplasms is beyond the scopeof the current discussion.


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Medical Care Management of submandibular sialadenitis and

sialadenosis involves a wide range of approaches, fromconservative medical management to more aggressivesurgical intervention.

One management scheme is as follows: Acute sialadenitis Medical management - Hydration,

antibiotics (oral versus parenteral), warm compresses andmassage, sialogogues

Surgical management - Consideration of incision anddrainage versus excision of the gland in cases refractoryto antibiotics, incision and drainage with abscessformation, gland excision in cases of recurrent acutesialadenitis


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Salivary calculi Medical management - Hydration,compression and massage, antibiotics for theinfected gland

Surgical management - Duct cannulation with stone

removal, gland excision in recurrent case Sjgren disease Medical management - Hydration,

dental hygiene, rheumatology and dental referral

Surgical management - Gland excision not usuallyneeded unless recurrent acute sialadenitis

Sialadenosis Medical management - Treatment ofunderlying cause

Surgical management - Not indicated


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Medical management centers on eliminating thecausative factor.

Acute sialadenitis In cases of acute sialadenitis,adequate hydration should be ensured and

electrolyte imbalances corrected. Patients are most often treated on an outpatient

basis, with the administration of a single dose ofparenteral antibiotics in an emergency department,

followed by oral antibiotics for a period of 7-10 days.Clindamycin (900 mg IV q8h or 300 mg PO q8h) is anexcellent choice and provides good coverage againsttypical organisms.


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Patients who exhibit significant morbidity, aresignificantly dehydrated, or are septic shouldbe admitted to hospital. In this latter group of

patients, CT scanning of the area should beperformed. If a large abscess is noted,incision and drainage should be considered.Small abscesses typically respond to

conservative methods. In cases refractory toantibiotics, viral and atypical bacterial causesshould be considered.


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Sialolithiasis Patients with sialolithiasis should beinitially treated with hydration, warm compresses, andgland massage.

Antibiotics are indicated in patients exhibiting

infection. Sjgren disease In those patients with Sjgren

disease, hydration and prevention of complicationsshould be undertaken.

Dental hygiene should be strictly maintained in orderto prevent carries, and dental and rheumatologyconsults should be sought. Gland excision is rarelyindicated.


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Sialadenosis: Sialadenosis should bemanaged expectantly. Treatment should be

directed towards managing the underlying

problem and achieving homeostasis. Glandexcision is not indicated.


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Surgical Care Acute sialadenitis Patients who exhibit significant

morbidity, are significantly dehydrated, or are septicshould be admitted to hospital. In this latter group ofpatients, CT scanning of the area should be performed. If

a large abscess is noted, incision and drainage should beconsidered. Small abscesses typically respond toconservative methods.

In patients with recurrent acute attacks, gland excisionduring a period of quiescence should be considered.

Serial CT scanning is often useful. Endoscopic management of sialadenitis frequently

obviates the need for gland removal. Results follow alearning curve.[5]


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Sialolithiasis In patients with calculi inproximity of the opening of the Wharton duct,the duct can be cannulated, dilated, and the

stone removed via a transoral approach. Patients with deep intraparenchymal stones

or multiple stones should have their glandsexcised on an elective basis. Ultrasonic

lithotripsy is rarely effective and is not offeredat the authors' institution


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Medication Summary

The goals of pharmacotherapy are to

eradicate the infection, reduce morbidity, and

prevent complications.


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Antibiotics Class Summary

Therapy must cover all likely pathogens in the context ofthis clinical setting.

View full drug information Clindamycin (Cleocin)

Lincosamide for treatment of serious skin and soft tissuestaphylococcal infections. Also effective against aerobic

and anaerobic streptococci (except enterococci). Inhibitsbacterial growth, possibly by blocking dissociation ofpeptidyl tRNA from ribosomes, causing RNA-dependentprotein synthesis to arrest.
http://reference.medscape.com/drug/cleocin-clindesse-clindamycin-342558http://reference.medscape.com/drug/cleocin-clindesse-clindamycin-342558http://reference.medscape.com/drug/cleocin-clindesse-clindamycin-342558http://reference.medscape.com/drug/cleocin-clindesse-clindamycin-342558http://reference.medscape.com/drug/cleocin-clindesse-clindamycin-342558http://reference.medscape.com/drug/cleocin-clindesse-clindamycin-342558http://reference.medscape.com/drug/cleocin-clindesse-clindamycin-342558http://reference.medscape.com/drug/cleocin-clindesse-clindamycin-342558


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Further Inpatient Care Patients requiring inpatient management should

be monitored on a daily basis and preferablytwice daily.

In order to ascertain the progression orimprovement of acute sialadenitis, serial CTscanning may be warranted.

Patients with sialolithiasis should be treated

conservatively during the acute exacerbationstage and should be monitored after dischargefor definitive surgical intervention.


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Further Inpatient Care Patients requiring inpatient management should

be monitored on a daily basis and preferablytwice daily.

In order to ascertain the progression orimprovement of acute sialadenitis, serial CTscanning may be warranted.

Patients with sialolithiasis should be treated

conservatively during the acute exacerbationstage and should be monitored after dischargefor definitive surgical intervention.


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Further Outpatient Care For patients with acute sialadenitis not

requiring admission, follow-up visit should be

3 days from the first visit and then 1 weeklater (with improvement).

Patients with chronic sialadenitis/sialolithiasisand autoimmune sialadenitis or sialadenosisshould be seen on a regular basis and ifacute exacerbation of the problem occurs.


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Inpatient & Outpatient Medications In addition to the antibiotics, patients may be treated

with any form of nonsteroidal anti-inflammatorymedications. Narcotics may be needed in severecases, and increasing pain refractory to medicationsis often an indication for admission for furtherevaluation.

In addition, medications predisposing to xerostomiashould be avoided where possible. These include

antiparkinsonian, antiemetics, antinauseants, over-the-counter and prescription cold medications,antidepressants, antihypertensive agents, diuretics,anticholinergics, antianxiety agents, anddecongestants.


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Complications The most serious complication of acute sialadenitis is

the formation of an abscess. Management isdescribed above.

Complications of chronic sialadenitis andautoimmune sialadenitis are most often dental innature because of the decreased function of thegland and the protective effect provided against

caries. Chronic inflammation of the gland with or without

calculi often renders the gland difficult to excisebecause of the loss of normal tissue planes.


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Prognosis The prognosis of acute sialadenitis is very good.

Most cases are easily treated with conservativemedical management, and admission is theexception, not the rule. Acute symptoms resolvewithin 1 week; however, edema in the area maylast several weeks.

Postsurgery, patients are often already admittedwith appropriate intravenous antibiotics. Thesepatients have a similar prognosis.


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Patients with chronic sialadenitis often have a relapsingand remitting course. Prognosis is dependent on theetiology.

Patients with sialolithiasis require definitive surgicaltreatment in most cases, which results in an excellent

prognosis. Patients with Sjgren or other autoimmune diseases are

likely to have a protracted course related to systemicinvolvement.

Patients with sialadenosis have a good prognosis, if their

underlying problem is adequately controlled. Even ifcontrol is attained, bilateral swelling may be persistent.


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Patient Education Patients with any form of sialadenitis should be

educated as to the value of hydration andexcellent oral hygiene. This lessens the severity

of the attacks and prevents dentalcomplications. Patients with sialadenosis shouldbe educated regarding the mechanism of theirunderlying pathology and methods of

maintaining control over them. For excellent patient education resources, visit

eMedicineHealth's Oral Health Center.
http://www.emedicinehealth.com/collections/CO1601.asphttp://www.emedicinehealth.com/collections/CO1601.asp


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Sialosis (sialadenosis) is a chronic,

bilateral, diffuse, non-inflammatory, non-

neoplastic painless swelling of the major

salivary glands that primarily affects theparotid glands, but occasionally involves

the submandibular glands and rarely the

minor salivary glands (Scully 2008)


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Acute Predisposing factors

decreased flow (dehydration, post-operative, drugs)

poor oral hygiene

exacerbation of low grade chronic sialoadenitis

Clinical features Painful swelling

Reddened skin

Edema of the cheek, Periorbital region and neck

low grade fever

malaise

raised ESR, CRP, leucocytosis

purulent exudate from duct punctum


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Chronic Clinical Features

unilateral

mild pain / swelling

common after meals duct orifice is reddened and flow decreases

may or may not have visible/palpable stone.

Parotid gland Recurrent painful swellings

Submandibular gland Usually secondary to sialolithiasisor stricture
http://en.wikipedia.org/wiki/Parotid_glandhttp://en.wikipedia.org/wiki/Submandibular_glandhttp://en.wikipedia.org/wiki/Sialolithiasishttp://en.wikipedia.org/wiki/Sialolithiasishttp://en.wikipedia.org/wiki/Submandibular_glandhttp://en.wikipedia.org/wiki/Submandibular_glandhttp://en.wikipedia.org/wiki/Submandibular_glandhttp://en.wikipedia.org/wiki/Parotid_gland


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Treatment In chronic recurrent sialadenitis or chronic

sclerosing sialadenitis, acute attacks aremanaged with conservative therapies such as

hydration, analgesics(mainly NSAIDs),sialogoguesto stimulate salivary secretion, andregular, gentle gland massage.[1]If infection ispresent, appropriate cultures should be

obtained, followed by empirical antibiotictherapy initially,[1]for exampleamoxicillin/clavulanateor clindamycinwhichcover oral flora.
http://en.wikipedia.org/wiki/Analgesicshttp://en.wikipedia.org/wiki/NSAIDshttp://en.wikipedia.org/wiki/Sialogoguehttp://en.wikipedia.org/wiki/Sialadenitishttp://en.wikipedia.org/wiki/Sialadenitishttp://en.wikipedia.org/wiki/Amoxicillin/clavulanatehttp://en.wikipedia.org/wiki/Clindamycinhttp://en.wikipedia.org/wiki/Clindamycinhttp://en.wikipedia.org/wiki/Amoxicillin/clavulanatehttp://en.wikipedia.org/wiki/Amoxicillin/clavulanatehttp://en.wikipedia.org/wiki/Sialadenitishttp://en.wikipedia.org/wiki/Sialadenitishttp://en.wikipedia.org/wiki/Sialogoguehttp://en.wikipedia.org/wiki/NSAIDshttp://en.wikipedia.org/wiki/Analgesics


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If there are attacks more than approximately 3times per year or severe attacks, surgicalexcision of the affected gland should beconsidered.[1]

See alsoSialadenitis of the submandibular glandis a relatively commonly encountered yetinfrequently discussed topic. Causes range fromsimple infection to autoimmune etiologies.

Although not as frequent as sialadenitis of theparotid gland, it represents an important area ofclinical relevance to the otolaryngologist andother specialists. The following discusses thebasic
http://en.wikipedia.org/wiki/Sialadenitishttp://en.wikipedia.org/wiki/Sialadenitis


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science of the submandibular gland, as well as the morecommon causes of sialadenitis and sialadenosis of thesubmandibular gland.

Anatomy

The submandibular gland, along with the parotid and

sublingual glands, comprise the major salivary glands.The minor salivary glands are scattered along the upperaerodigestive tract, including the lips, mucosa of the oralcavity, pharynx, and hard palate.

The submandibular gland is the second largest

(approximate weight, 10 g) of the major salivary glands(the parotid gland is the largest). Anatomically, it issituated in the submandibular triangle of the neck.


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The gland itself can be arbitrarily divided into superficialand deep lobes based on its relationship to the mylohyoidmuscle, the former lying superficial to the muscle, and thelatter wrapping around the posterior aspect of the muscle.The gland itself lies on the hyoglossus muscle, superficial

to both the hypoglossal and the lingual nerves, the lattersupplying parasympathetic innervation by way of thechorda tympani nerve (from cranial nerve VII) and thesubmandibular ganglion. The duct of the submandibulargland, also known as the Wharton duct, exits the glandfrom the deep lobe, passing through the floor of themouth, and opening in close proximity to the lingualfrenulum. See the image below.

Sialogram with stenosis secondary to chronicsialadenosis.


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sialodenosis

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