sailedinitis.pdf

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Microbiology andManagement of Sialadenitis

Patrick J. Bradley, MB, FRCS

AddressDepartment of Otorhinolaryngology Head and Neck Surgery,University Hospital, Queens Medical Centre,Nottingham NG7 5EU, England.E-mail: [email protected]

Current Infectious Disease Reports 2002, 4:217224Current Science Inc. ISSN 1523-3847Copyright 2002 by Current Science Inc.

IntroductionSialadenitis is an acute, chronic, or recurrent infectionor inflammation condition affecting the salivary glands.The condition of sialadenitis has been classified by Seif-ert [1] according to known etiologic and histologicfactors (Table 1). Sialadenitis includes a number of con-ditions ranging from acute infections to immunologi-cally mediated diseases, the parotid gland being most

frequently involved. Infections of the salivary glands arecaused by a variety of microbial agents including bacte-ria, viruses, fungi, parasites, and protozoa. The clinicalcondition of infective or suppurative sialadenitis pre-sents most frequently in young children [2] and the eld-erly [3]. This article reviews the microbiology of acuteand chronic sialadenitis, which presents clinically inthe parotid and submandibular gland, as presented inthe current literature. I also attempt to highlight the dif-ficult decisions that may need to be made in the man-agement of patients with sialadenitis.

Etiologic FactorsBacterial infection of the salivary glands results from one oftwo important physiologic mechanisms. The first is retro-grade contamination of the salivary ducts and parenchymaltissues by bacteria inhabiting the oral cavity, which providesthe bacterial source of the infection. The second is stasis ofsalivary flow through the ducts and parenchyma, whichpromotes acute or recurrent suppurative infection. Theseprocesses can affect any of the major or minor salivary

glands, but most commonly involve the parotid and thenthe submandibular gland.Viral infections of the salivary glands are systemic from

the onset. The viruses are endemic in the community, spreadby airborne droplets, and enter the body through the upperrespiratory tract. Patients experience a 2- to 3-week incuba-tion period after exposure, during which the virus multipliesin the upper respiratory tract, followed by a 3- to 5-dayperiod of viremia. The virus then localizes to biologicallyactive tissue, such as salivary glands, germinal tissues, and thecentral nervous system. Although the viruses causing themumps syndrome demonstrate a strong predilection forparotid tissue, the infection can involve the submandibular

or sublingual glands.Chronic recurrent bacterial sialadenitis more characteristi-

cally affects the parotid gland, and occasionally may be bilat-eral. The most common etiology is ductal obstruction, butthere may be a history of an antecedent pyogenic infection ormumps. The interrelationship of acute and chronic inflam-matory diseases has been hypothesized and is illustrated inFigure 1. The primary pathogenic event is considered to be adecrease in the parotid saliva secretion rate, which results instasis and inspissation of secretions with resultant ascendingbacterial invasion of the ductal system. When the bacteria arepyogenic, most usually staphylococcal, acute suppurativesialadenitis occurs; this leads to destruction and fibrosis of

acinar elements, and ductal ectasia results. Most commonly,however, the chronic reduced salivary flow leads to frequentopportunistic infections leading to chronic sialadenitis andsialectasia [4]. Management of intractable chronic disease issurgical excision [5].

Acute InfectionsAcute bacterial sialadenitis

Acute, mostly ascending bacterial inflammation from the oralcavity localizes most frequently to the parotid gland, whereas

Acute and chronic inflammatory diseases of the major

and minor salivary glands constitute the most commonclinical syndrome of salivary glands. During the pastdecade, the use of antibiotics along with fluid hydration

and electrolyte management has almost eliminated thedevelopment of fulminating acute suppurative parotitis inhospital surgical patients. Although acute bacterial and

viral sialadenitis persists, the clinical challenge haschanged, with more focus on the chronic inflammatory

group of diseases. The pathogenesis of the chronic sali-vary inflammatory disease spectrum has also changed,

with the interplay between sialadenitis, sialectasia, andsialolithiasis. There also exists a heterogeneous group ofdisorders in chronic inflammatory sialadenitis, which

include the group of specific and nonspecific granuloma-tous diseases.


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218 Upper Respiratory, Head, and Neck Infections

such acute inflammations of the submandibular gland aremore rare. Suppurative sialadenitis can present as an acutesingle episode, or multiple recurrent episodes. Acute suppura-tive parotitis may arise from a septic focus in the mouth, suchas chronic tonsillitis or dental sepsis, and may be found inpatients taking sedative drugs, which suppress saliva excre-tion. The reduction of the secretory flow is an importantpathogenic factor, most often seen in debilitated and dehy-drated patients following major surgery, and also seen in

coma patients. Typically, the disorder is of acute onset, withtender, painful swelling of one or both of the parotid or sub-mandibular glands. External and bimanual palpation revealsa firm, indurated, tender salivary gland. The duct orifice maybe red and swollen with pus discharging into the mouth. Insome cases pus may be localized to produce abscesses thatdischarge directly through the skin.

Recommended treatment should commence after aculture from the appropriate duct on suspicion of the dis-ease. A blood culture should be obtained, as well as anassessment of the fluid and electrolyte balance in surgicalpatients. Penicillin-resistant coagulase-positive Staphylococ-cus aureus is the most common organism cultured in acute

parotitis. Streptococcus pneumonia and -hemolyticStrepto-coccus have also been identified. Management consists ofhydration and systemic antibiotics appropriate for penicil-linase-resistantStaphylococcus, such as methicillin. If septi-cemia is present, a broad-spectrum antibiotic such as acephalosporin should be used. If the suppurative event hasprogressed or a delay in making the correct diagnosis hasoccurred, then consideration should be made for the surgi-cal drainage of the abscess. A fluctuant abscess of the sub-mandibular gland will respond to incision and drainagewith subsequent excision of the gland recommended some

weeks following antibiotic therapy. Because of the verticalseparation of the parotid fascia, however, a fluctuant massof the parotid is seldom present even in the most advancedstages of suppuration. Progressive edema, induration, andsepsis are the indications for incision of a parotid abscess.A flap is elevated in the usual manner with a modifiedBlair incision, and a hemostat is introduced into theparotid gland and spread in the direction of the branchesof the facial nerve. The wound is drained and dressed. Res-olution may occur promptly with antibiotics or surgicaldrainage. In some cases, extensive acinar destruction andsubsequent fibrosis leads to atrophy of the gland withrecurrent chronic sialadenitis.

Pediatric bacterial parotitis

Although bacterial parotitis can affect individuals of anyage, suppurative parotitis in the neonate is a well-knownentity, generally occurring in the first 2 weeks of life [6].Thirty-five percent to 40% of cases occur in premature

infants, who demonstrate a greater propensity for dehydra-tion than term infants. Unlike parotitis in the adult popu-lation, neonatal parotitis is often bilateral. Recently, casesof submandibular sialadenitis have been reported in theneonatal group without parotitis [7,8]. Although S. aureusis the most common responsible organism, streptococci,Esherichia coli, Pseudomonas aeruginosa, andNeisseriacatarrhalis have been reported as causative agents in neona-tal sialadenitis. It is therefore recommended that Gramstaining and culture with antibiotic sensitivity should beobtained to ensure proper selection of antimicrobial agent.Antimicrobial therapy is the mainstay for suppurativesialadenitis; oxacillin or methicillin seems to be the logical

first-line antibiotic for treatment. Recently, two cases ofmethicillin-resistantS. aureus (MRSA) have been reportedfrom Japan, and as the authors suggest, these cases reflect aserious situation with MRSA contamination in neonatalintensive care units [9].

Bacteriology of sialadenitisStaphylococcus aureus is the most common bacterial cause ofacute suppurative parotitis and has been cultured in 50% to90% of cases. Streptococcal species, includingS. pneumoniaand Streptococcus pyogenes (-hemolyticStreptococcus), as wellas Haemophilus influenzae, have been recognized as commoncauses of acute pyogenic sialadenitis. It has been shown that

the fibronectin found in saliva promotes the adherence ofstaphylococcal and streptococcal species.

Less frequently, gram-negative organisms, includingE.coli, Klebsiella pneumoniae, and P. aeruginosa have been cul-tured from salivary infections. A parotid abscess due to aSalmonella species has also been reported in a patient withHIV [10]. In Southeast Asia, Pseudomonas pseudomallei, anorganism found in soil and surface water, is a commoncause of acute parotitis, especially in children. Recently,anaerobic organisms in acute bacterial infections withinthe salivary glands have been recognized. Bacteroides,

Table 1. Etiologic classification of sialadenitis

Acute bacterial sialadenitisAcute purulent parotitisAcute postoperative parotitis

Chronic recurrent parotitisChronic sclerosing sialadenitis of submandibular gland

(Kuttner tumor)Obstructive sialadenitisRadiation sialadenitisViral sialadenitis

Parotitis epidemica (mumps)Cytomegalovirus infections (salivary gland viral disease)Other types (Coxsackie virus, infectious mononucleosis,

measles, echovirus)HIV-associated lesions

Immune sialadenitisAcute immune complex typeEpithelioid cell sialadenitisAutoimmune myoepithelial sialadenitis

Other granulomatous types of sialadenitisGiant cell sialadenitis

TuberculosisSialadenitis of minor salivary glands


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Microbiology and Management of Sialadenitis Bradley 219

peptostreptococcal, and fusobacterial species have been

cultured from as many as 43% of infections [11]. Thesefindings are considered to be due to improved culture tech-niques rather than a change in microbiology. Others postu-late that this increase in anaerobic and gram-negativeorganisms reflects nosocomial disease, because this infec-tion demonstrates a predisposition for debilitated andpostsurgical patients. Cases of unusual pathogens generallyare identified in infections of the parotid gland, because925 of acute submandibular infections are communityacquired, resulting from the more common staphylococcalspecies [12].

Mycobacterium tuberculosis [13] and Treponema pallidum[14] have been reported as extremely rare etiologic agents

in acute parotitis, but tuberculosis and syphilis usually areassociated with a painless, chronic salivary gland infectionthat can be confused with neoplasm.

Chronic SialadenitisChronic sialadenitis may occur as a result of an unresolvedacute parotitis and usually follows a persistently reducedsalivary flow. Chronic sialadenitis in the submandibulargland is relatively common and is usually the result of ductobstruction by a calculus. At first this is characterized byrecurrent swelling due to retention of secretions, but aschronic infection supervenes, the gland becomes inflamed

and eventually fibrosed to produce a firm tumorlike mass:Kuttners tumor.

Sialography may demonstrate ductal ectasia or dilata-tion with atrophy of acinar elements; however, the degreeof ectasia may be more severe than the histopathologicgrade and the patients expressed symptoms [15]. Patienthistory of recurrent swelling of one or more salivarygland, occasionally accompanied by pain typically whileeating, suggests the diagnosis. Palpation reveals a swol-len, indurated, and mildly tender gland. Digital palpation

demonstrates reduced salivary flow, or mucopus that can

be expressed.Treatment should be conservative. Sialagogues such aslemon or chewing gum stimulate salivary flow and ductalirrigation. Periodic massage of the affected gland by thepatient may also be of assistance. Acute exacerbationsshould be treated as acute suppurative sialadenitis. Salicy-lates may help in the control of pain, and hydration isimportant. Ductal probing has been recommended to eval-uate the possibility of a stricture or stone, but it is not rec-ommended in the acute phase of the disease. Surgicalprocedures have been offered as cures and include periodicdilatation of the ductal orifice, ligation of the duct, totalgland irradiation, and avulsion of the auriculotemporal

nerve in the infratemporal fossa. Tympanic neurectomyhas been advocated for the treatment of chronic recurrentparotitis without suppuration. Cessation of function andatrophy of the acinar elements appears to be the theoreticalbasis for the reported success of these cases. However, ifprolonged, conscientious, conservative management fails,then surgery (either superficial or total parotidectomy orexcision of the submandibular gland) is the only effectivemeans of managing this disease.

Chronic sialectasiaChronic sialectasia may represent the end stages ofchronic recurrent sialadenitis. It may follow severe

inflammatory viral or bacterial infections. The most com-mon complaint by the patient is diffuse swelling of oneparotid gland, which may slowly increase over severalmonths or years. Differential diagnosis includes benignlymphoepithelial lesion and neoplasm. Histologically,sacculation of the ductal and acinar elements is found,with lymphocytic infiltration of the interstitim and atro-phy of the myoepithelial elements. Other parts of thegland may show fibrosis and atrophy. Acute suppurationmay develop terminally.

Figure 1. The interrelationship of acute andchronic inflammatory diseases.


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Sialolithiasis

Sialolithiasis is both a cause and consequence of chronicrecurring sialadenitis, and in addition is frequently a causeof acute suppurative sialadenitis. Sialolithiasis is muchmore common in the submandibular than in the parotidgland (83% as opposed to 10%), with the remainder beingin the minor salivary glands or even the sublingual glands[16]. The submandibular gland is alleged to produce morestones than the parotid gland for the following reasons: 1)longer and larger caliber duct with slower rates of flow, 2)flow of saliva against gravity, 3) more alkaline saliva, and4) high mucin and calcium content of saliva [17]. Thisallows inspissation of the mucus to occur, particularly attimes of dehydration or febrile illness. A nidus formsaround which calcification can occur. Small stones may bedischarged spontaneously from the duct, followed by agush of turbid saliva. The stone in the duct will usually giverise to repeated episodes of duct obstruction and swelling.Ultimately the gland will become atrophic and fibrosed

unless an acute abscess supervenes. The treatment of thesalivary calculus is determined by the symptoms and bythe position of the stones. Stones can be removedintraorally or by the use of a wire basket. The use of extra-corporial shock wave lithotripsy has been described, but todate has only been available in specialist centers [18].

Animal scratch diseaseAnimal scratch disease does not involve the salivary glandsdirectly but may involve the parotid and submandibulartriangle lymph nodes; these in turn may involve the sali-vary glands by contiguous spread. Cat scratch disease isone such entity, which primarily involves children and

young adults. A history of animal contact, usually with catsor even kittens (scratches, bites or even licks by a cat), hasbeen elicited in 67% to 90% of reported cases. Recently,the true origin of this disease has been implicated as Bar-tonella henselae, a gram-negative bacterium. A polymerasechain reaction assay to detectBartonella DNA has beenused to identify the agent. A serology test for cat scratchdisease patients has shown titers of at least 1:64 forB.henselae antibodies [19]. Treatment consists of supportivetherapy and reassurance, as antibiotics have not beenshown to be effective in shortening the course of the dis-ease. The lymphadenopathy usually disappears within 2 to3 months without complications.

Granulomatous sialadenitisGranulomatous sialadenitis is a form of chronic sialadeni-tis with many potential causes (Table 2). Duct obstructionsecondary to stone or tumor is the most commonly identi-fied cause [20]. Rarely the salivary glands may be involvedin a specific inflammatory disorder, such as tuberculosis,syphilis, gonorrhea, or actinomycosis. Of these, tuberculo-sis is the most common and often affects the parotid glandas a result of involvement of the intraparotid lymph nodes.As well as the specific infections, the parotid gland may be

involved in up to 5% of patients with sarcoidosis. In addi-tion to the usual systemic manifestations, there is painless,firm nodular swelling of the parotid glands, which containtypical noncaseating granulomata. The minor salivaryglands of the palate and the lip may also be involved. InWageners granulomatosis, a unilateral tumorlike swellingespecially of the parotid gland is observed. The granuloma-tous reaction is characterized by giant cells, necrosis, and anecrotizing vasculitis.

TuberculosisMycobacterial lymphadenitis of the parotid gland is themost common form of mycobacterial infection to affectthe salivary glands. Both tuberculosis and atypical infec-tions occur [21]. Parenchymal infection is rare [22,23].Intraparotid and periparotid lymph nodes becomeinfected as a result of lymphatic drainage of the glandularduct system from an infection originating in the mouth orpharynx [24], or as a result of dissemination of pulmonary

disease. The differences in presentation and age of presen-tation may be the key to diagnosis, however, the final diag-nosis is reliant on special investigations, as physicalexamination is usually unrewarding. The most valuableinvestigation currently appears to be the use of fine needleaspiration biopsy (FNAB), which frequently can confirmthe suspected diagnosis and avoid the sequelae of exci-sional surgery. The role of FNAB must in part be to excludethe possibility of malignancy; a positive diagnosis of gran-ulomatous disease would be a benefit in terms of possiblyavoiding surgery, although other disease processes requireserologic exclusion (Fig. 2). Imaging of the lesion is per-formed initially with ultrasound, which distinguishes solid

from cystic masses. Incisional biopsy is deplored in boththe management of tuberculosis and in tumors of thisregion. Definitive histologic diagnosis is based on surgicalexcision if FNAB is equivocal. Upon diagnosis, medicalmanagement of the tuberculous disease involves the use ofisoniazid, rifampicin, and pyrazinamide. In the atypicaldisease, chemotherapy is normally ineffective but mayhave a role in suboptimal surgery.

SarcoidosisSarcoidosis is a systemic, multifocal, granulomatous disor-der of unknown etiology. Although the etiology of the dis-ease is unknown, hypothetical causative agents include

infectious organisms, environmental agents, or autoanti-gens [25]. Salivary gland involvement in sarcoidosis is fre-quently observed and presents in a variety of clinicalpatterns. Most commonly, there is bilateral swelling of theparotid glands. Xerostimia is frequently present. Heer-fordts syndrome (uveoparotid fever) is a triad manifestingas inflammation of the uveal tract of the eye, bilateralparotid gland swelling, and cranial nerve involvement. Sal-ivary gland flow and enzyme content of amylase and kal-likrein are significantly reduced in many patients duringthe active phase of the disease.


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Up to one third of patients will experience prodromalsymptoms prior to developing parotitis consisting of head-ache, myalgia, arthralgia, anorexia, and malaise. The onsetof salivary involvement is heralded by otalgia followed bypain localized to the gland, trismus, and dysphagia. Painoften is exacerbated by stimulation of salivary flow duringchewing or eating. Systemically the patient also may have alow-grade fever during the prodromal period.Viral parotitis usually reveals a leucocytopenia with relativelymphocytosis and an increased serum amylase. Serumamylase peaks during the first week, and may normalize bythe second or third week of disease. Viral serology is essen-tial to confirm the diagnosis of viral parotitis. Complement-

fixing antibodies appear following exposure to the paramyx-ovirus. Soluble antibodies directed against the nucleopro-tein core of the virus appear within the final week ofinfection, and peak within 2 weeks. Soluble antibodies dis-appear within 8 to 9 months, and therefore are associatedwith active infection or recent vaccination. Viral antibodiesdirected against the outer surface hemagglutinin appear sev-eral weeks after the soluble antibodies, and persist at lowlevels for approximately 5 years following exposure. Viralantibodies, therefore, are associated with past infection,prior vaccination, and the late stages of acute infection.

If initial serology is noncontributory, a nonparamyx-ovirus may be responsible for acute viral salivary infection.Antibody titers against such viral antigens as influenza,parainfluenza, Coxsackie virus, echoviruses, and lympho-cytic choriomeningitic viruses can be obtained. An increasein antibody titer, four times from the normal, is diagnosticof acute infection. Rarely the virus can be cultured fromblood, saliva, breast milk, or cerebrospinal fluid. Bloodtests for HIV virus should be obtained in these cases,because this disease has been a reported cause of acuteparotid inflammation.

Treatment of viral salivary gland infection is primarilysupportive, including rest and adequate hydration because

the disease is self-limiting. Antipyretics and anti-inflamma-tory medications are of benefit.

HIV

Clinically, patients with HIV infection are at risk for thedevelopment of infective sialadenitis. Lymphoid lesionsoccurring in the salivary glands, especially the parotidglands, have been reported extensively in the literatureand have been associated with an increased incidence ofcystic lesions of the parotid gland in these patients [31].Potential opportunistic pathogens include cytomegalovi-

Figure 2. Diagnostic tests and investigation ofparotid granulomatous disease. ACEangio-tensin converting enzyme; ANCAantineutro-phil cytoplasmic antibody; FNABfine needleaspiration biopsy.


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Microbiology and Management of Sialadenitis Bradley 223

rus (CMV), Pneumoncystis carinii, adenovirus, and Histo-plasma. Clinical presentations are variable, and eitherinfection or neoplasm is suspected. Pronounced CMV

salivary gland disease is rare, even though many patientswith AIDS excrete CMV in their saliva [32]. The chronicparotid swelling observed in some infants with AIDS isbelieved to be due to acute CMV parotitis.

Sialadenitis of minor salivary glandsAnalogous to the major salivary glands, the minor sali-vary glands show local inflammatory reactions as well asjoint reactions with systemic diseases (Table 3). Obstruc-tive sialadenitis of the palate is the most frequent type ofsialadenitis presenting in clinical practice. Surgicalbiopsy may be required to diagnose and treat several ofthese conditions that most frequently present acutely in

the oral cavity, but can be found elsewhere in the headand neck region.

ConclusionsAcute bacterial and viral infections of the salivary glandspresent with a broad spectrum of severities, but are notassociated with the same potential morbidity and mor-tality. The majority of viral infections are caused by theparamyxoviruses and are associated with the mumps syn-drome. In chronic or recurrent sialadenitis, the clinicalchallenge remains the suspicion that there may exist aspecific granulomatous disease, which presents a sub-

acute or chronic clinical picture. The clinician needs tobe vigilant that a possible underlying neoplasm is notbeing missed, and serious consideration to aspiration oreven biopsy of the salivary glands should be consideredin resistant cases.

References and Recommended ReadingPaper of particular interest, published recently, have beenhighlighted as: Of importance Of major importance

1. Seifert G:Aetiology and histological classification of sialad-enitis. Pathologica 1997, 89:717.

This paper is the only available attempt at classification of sialadeni-tis.

2. Pershall KE, Koopmann CF, Coulthard SW: Sialadenitis in chil-dren. Int J Paediatr Otolaryngol 1986, 11:199203.

3. Pajukoski H, Meurman JH, Odont D, et al.: Salivary flow andcomposition in elderly patients referred to an acute geriatricward. Oral Surg Oral Med Oral Pathol Oral Radiol Endo 1997,84:265271.

4. Travis LW, Hecht DW:Acute and chronic inflammatory dis-eases of the salivary glands: diagnosis and management. Oto-laryngol Clin North Am 1977, 10(2):329338.

5. Bates D, OBrien CJ, Tikeram K, Painter DM: Parotid and sub-mandibular sialadenitis treated by salivary gland excision.Aust N Z Surg1998, 68:745748.

This paper is an honest report of a single surgeons experience withexcision of a parotid and submandibular gland in chronic sialadenitisthat was resisitant to conservative medical management. The risks of

surgery are not minimal!6. Chiu CH, Lin TY: Clinical and microbiological analysis of six

children with acute suppurative parotitis.Acta Paediatr1996,85:106108.

7. Ungkanont K, Kolatat T, Tantinikorn W: Neonatal suppurativesubmandibular sialadenitis: a rare clinical entity. Int J Paedi-atr Otolaryngol 1998, 43:141145.

8. Bafaqeeh SA: Complicated neonatal submandibular suppura-tive sialadenitis. Int J Paediatr Otolaryngol 1998, 44:267271.

9. Takahashi R, Chikaoka S, Ito T, et al.: Neonatal submandibularsuppurative sialadenitis. Eur J Paediatr2000, 159(11):868.

A short report on methicillin-resistantS. aureus infection of a neona-tal submandibualar sialadenitis.

10. Knee TS, Ohl CA:Salmonella parotitis with abscess formationin a patient with human immunodeficiency virus infection.Clin Infect Dis 1997, 24:10091010.

11. Brook I, Frazier EH, Thompson DH:Aerobic and anaerobicmicrobiology of acute suppurative parotitis. Laryngoscope1991, 101:170172.

12. Raad II, Sabbagh MF, Caransos GJ:Acute bacterial sialadenitis:a study of 29 cases and review. Rev Infect Dis 1990, 12:591601.

13. OConnell JE, Speculand GB, Pahor AL: Mycobacterial infec-tion of the parotid gland: an unusual cause of parotid swell-ing.J Laryngol Otol 1993, 107:561564.

14. Hira SK, Hira RS: Parotitis with secondary syphilis. Br J VenDis 1984, 60:121122.

15. Tighe J, Bailey BMW, Khan MZ, et al.: Relation of preoperativesialagraphic findings with histopathological diagnosis incases of obstructive sialadenitis of the parotid and subman-dibular glands: retrospective study. Br J Oral Maxiofac Surg1999, 37:290293.

16. Rauch S: Die Speicheldrusen des Menschen. Stuttgart: Thieme;1959.

17. Williams MF: Sialolithiasis. Otolaryngol Clin North Am 1999,32(5):819834.

18. Bull PD: Salivary gland stones: diagnosis and treatment. HospMed 2000, 62(7):396399.

19. Malatskey S, Fradis M, Ben-Davis J, Podoshin L: Cat-scratchdisease of the parotid gland.Ann Otol Rhinol Laryngol 2000,109:679682.

A case report that highlights the importance of culture and appropri-ate history taking in selected cases of sialadenitis.

Table 3. Types of sialadenitis of minorsalivary glands

Traumatic sialadenitisChelitis glandularis apostematosaStomatitis glandularis

Subacute necrotizing sialadenitisObstructive sialadenitisSialadenitis in systemic disease

Graft-versus-host reactionLupus erythematodesProgressive systemic sclerosisChronic rheumatoid arthritisMyasthenia gravis

GlossodyniaSjgren's syndrome


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20. Ericson S, Zetterlund B, Ohman J: Recurrent parotitis and sia-lectasis in childhood: clinical radiological, immunologic,bacteriologic, and histologic study.Ann Otol Rhinol Laryngol1991, 100:527535.

21. Perlman DC, DAmico R, Salomon N: Mycobacterial infectionsof the head and neck. Curr Infect Dis Rep 2001, 3:233241.

An up-to-date review of typical and atypical mycobacterial infectionsof the head and neck.

22. Holmes S, Gleeson MJ, Cawson RA: Mycobacterial disease ofthe parotid gland. Oral Surg Oral Med Oral Pathol Oral RadiolEndo 2000, 90:292298.

A clinicians view of mycobacterial disease of the parotid gland withrecommendations for a paradigm for the investigation of such cases.

23. Handa U, Kumar S, Punia RS, et al.:Tuberculous parotitis: aseries of five cases diagnosed on FNAC.J Laryngol Otol 2001,115:235237.

24. Jervis PN, Lee JA, Bull PD: Management of non-tuberculousmycobacterial perisialadenitis in children. Clin Otolaryngol2001, 26:243248.

25. Batal H, Chou L, Cottrell DA: Sarcoidosis: medical and dentalimplications. Oral Surg Oral Med Oral Pathol Oral Radiol Endo1999, 88:386390.

An attempt at a modern view of sarcoidosis as it presents in the head andneck. Not very detailed information, but a good start for further reading.

26. Cahn L, Eisenbud LR, Blake MN, Stern D: Biopsies of normal-

appearing palates of patients with known sarcoidosis. OralSurg Oral Med Oral Pathol 1964, 18:342345.

27. Marx RE, Hartman KS, Retman KA:A prospective study com-paring incisional labial to incisional parotid biopsies in thedetection and confirmation of sarcoidosis, Sjogrens disease,sialosis and lymphoma.J Rheumatol 1988, 15:621629.

28. de Norman JE, Mitchell RD: Unusual conditions of the majorand minor salivary glands. Int J Oral Maxillofac Surg1998,7:157171.

This author is an authority and has written widely on all aspects ofsalivary pathology. This paper is an excellent review of unusual condi-tions and is illustrated by colored pictures throughout (worth gettinga reprint in color).

29. Belmont MJ, Behar PM, Wax MK:Atypical presentation of acti-nomycosis. Head Neck 1999, 21:264268.

An excellent review of actinomycosis as it presents to the head andneck surgeon.

30. McQuone S:Acute viral and bacterial infections of the sali-vary glands. Otolaryngol Clin North Am 1999, 32(5):793811.

The most recent publication on acute viral and bacterial infections.Covers all aspects of clinical presentations, diagnostic examinations,treatment, and complications.

31. Huang RD, Pearlman S, Friedman WH, Loree T: Benign cysticvs. solid lesions of the Parotid Gland in HIV Patients. HeadNeck 1991, 13:522527.

32. Scott GB, Buck BE, Leterman JG:Acquired immunodeficiencysyndrome in infants.N Engl J Med 1984, 310:7681.

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