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BACTERIAL SIALADENITIS

Acute Chronic Recurrent Parotitisrare Rare for children & adults

SG Parotid Submandibular > parotid parotid

ascending infection from mouth -In major glands, usually non-specific, asocc. with ductobstruction (salivary calculi) & low grade ascendinginfection

-progressive chronic inflammation of SM complete

replacement of parenchyma by fibrous tissue mistakenfor chronic sclerosing sialadenitis (a tumor)

Rarely, adult for may follow onfrom childhood type but mostlydue to persistence ofpredisposing factors (calculi,

duct strictures)

Childhood type:1. Abnormally secretion

rate2. Immature immune

response3. Congenital abnormalities

of ductal system

Clinical features:1. Unilateral or bilateral

2. Recurrent painfulswelling

3. Pus from orifice4. Often resolve

spontaneously by earlyadulthood

bacteria Strep. PyogenesStaph. AureusHaemophilus species

Black-pigmented Bacteroides

Factors 1. salivary flow-Sjogren syndrome-drugs with xerostomicS/E

2. Postoperativecomplication indebilitated dehydratedpts after abdominalsurgery

3. Immunocompromized pts4. Acute exacerbation of

chronic sialadenitis

salivary flowDisorder of salivary secretion

Clinicalfeatures

1. Rapid onset2. Swelling3. Pain, fever, malaise4. Redness of overlying skin5. Pus from duct

1. Unilateral2. Recurrent, tender swelling3. Inflammation of duct orifice4. Purulent, salty discharge (in acute exacerbation)

histopathology

1. Vary degrees of ductal dilatation2. Hyperplastic ductal epi.3. Periductal fibrosis

4. Acinar atrophy, replaced by fibrous tissue5. Chronic inflammatory infiltration

Sialography :

1. Duct obstruction

2. Glandular tissue

obstruction

3. Ductal dilatation

Cellul

ar

Dilat

edAtrophi

c acini

Fibrosis

with

collage

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VIRAL SIALADENITISMUMPS (EPIDEMIC PAROTITIS)

mumps 1

mumps 2

CYTOMEGALIC INCLUSION DISEASE(SG INCLUSION DISEASE)

Paramyxovirus Cytomegalovirus (herpervirus gp)Acute, contagious infection, often in minor epidemicsCommonest cause of parotid enlargement

Commonest of all SG diseaseDiagnosis usually clinicalConfirmed diagnosis by (within 1st week)

detection of IgM Ab

in serum titer to mumps virus AgImmunity after an attack is long-lastingRare recurrent infection

Infection is common in humansworldwide

Most 1 infections are asymptomaticCausing severe disseminated disease inneonates & immunocompromised hosts(transplant, HIV pts)Maybe assoc. with xerostomia & HIVinfection

Clinically:1. Most common in childhood2. Transmitted by direct contact with infected saliva &

droplet spread3. Incubation period: 2-3 weeks

4. Prodromal symptoms: fever, malaise5. Sudden onset of painful swelling of 1 or more SG

-parotid (70%)6. occasional involvement of SM & SL but rarely w/out

parotid7. enlargement gradually subsides () over 1 week8. virus present in saliva

-2-3 days before onset-6days after

9. occasional involve of other organs in adults; testes,ovaries, CNS

10. orchitis (inflamme testes):most common

complication (20%)

Histopathology:1. SG involvement usually an

incidental finding2. Large, doubly contoured owl-eye

inclusion bodies within nucleus or

cytoplasm of duct cells of parotidgland

3. In disseminated disease, similarinclusions are found in kidneys,liver, lungs, brain & other organs

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SIALADENOSIS (SIALOLIS) HIV-ASSOCIATED SG DISEASE

Non-inflammatory, non-neoplastic, recurrent bilateral swelling of SGMost common: parotid (due to abnormal of neurosecretory control)

-A small feature in small # of adults HIV pts-Prevalence higher in children-xerostomia and/or swelling of major SG, esp parotid-xerostomia caused by SS-like process associated with

myoepithelial sialadenitis-however, no auto-Ab profile as seen with SS-HIV-related parotid enlargementdue to:

1. Persistent glandularlymphadenopathy

2. Multiple lymphoepitelialcyst

Reported with:1. Hormonal disturbances

2. Malnutrition3. Liver cirrhosis4. Chronic alcoholism

Various drugs

Histopathology:1. Hypertrophy of serous acinar cells to about 2x their normal size

Cytoplasm is densely packed with secretory granules

POSTIRRADIATION SIALADENITIS SARCOIDOSIS SIALADENITIS OF MINOR GLANDSCommon complication of radiotheraphyDirect correlation btwn-dose of irradiation-severity of damageDamage is often irreversible, leading to:-fibrous replacement of damaged acini-squamous metaplasia of ductsIn less severe cases, some degree of fx mayreturn after several monthsSerous acini are more sensitive than mucousacini

-May affect parotid & minor salivary glands-Parotid involvement present as persistent,often painless enlargement-may be assoc. with involvement of lacrimalglands in Heerfordt syndrome

-often an incidental & insignificant finding-may however be of diagnosticsignificance, such as in Sarcoidosis &Sjogren syndrome-Most frequently seen in assoc. withmucous extravasation cysts & nicotinicstomatitis-Very rarely may present with multiplemucosal swellings assoc. with cysticdilatation of ducts & chronic suppuration(stomatitis glandularis)

-most commonly on the lips, probably asan acute exacerbation of a chronic formassoc. with obstruction or reduction insalivary flow (cheilitis glandularis)

Clinically Histopathology

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Obstructive&

TraumaticLesions

Obstructive&

TraumaticLesions

SALIVARYCALCULI(SIALOLITHS)

Most common in middle-aged adultsMay form in ducts withinthe gland, or in mainexcretory ductSubmandibular (79-90%)> parotid > Sublingual orminor glands (2%)

UnilateralMay be multiple in thesame gland

-when symptomatic, they cause pain &sudden enlargement of affected gland(esp at meal times when salivaryscrtn)- in flow predispose to ascendinginfection & chronic sialadenitis-calculi may be detected by palpation &on radiographs

Form by gradual deposition of Ca saltsaround an initial organic nidus (whichmay consists of altered salivarymucins with desquamated cells &microorganisms)

NECROTIZINGSIALOMETAPLASIA

UncommonMay be mistaken clinically& histologically formalignant diseaseMost frequent on hardpalate in middle aged pts,males

Etiology unknown, butprobably due to:

-most common as deep, crater-like ulcer(mimic malignant ulcer)-10-12 weeks to healUlcer may be preceded by induratedswelling

Lobular necrosisSq metaplasiaof ducts & aciniMucous extravasationInflammatory cell infiltration-Overlying palatal mucosa:pseudoepitheliomatous hyperplasia-features may be mistaken for SCC or

mucoepidermoid carcinoma

Sialoliths at the

orifice of

submandibular

Multiple

sialoliths

Duct

metapla

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-ischemia leading toinfarction of Salivarylobules-trauma (eg LA injection,previous surgery)

MUCOCELES

SJOGREN SYNDROMEChronic autoimmunedisease

1. Primary (Sicca Sydrome)-dry mouth (xerostomia)

-dry eyes (xerophtalmia or keratoconjunctivitis sicca)-more severe ocular & oral manifestations

Manifestation of keratoconjunctivitis sicca:-dryness of eyes-conjunctivitis-gritty, burning sensation

2. Secondary-xerostomia

-xerophtalmia-Autoimmune CT disease

:: Rheumatoid Arthritis (most common):: SLE:: Systemic sclerosis:: Primary billiary cirrhosis:: mixed CT disease

Lymphocytic infiltrationAcinar destruction oflacrimal & SG

Histophatology of major glands:

-lymphocytic infiltration, initially around intralobular ducts,eventually replacing the whole effected lobules

-20% B cells, 80% T cells (mostly T helper)

Histopatholohy of minor glands

-focal collection of lymphoid cells, initiallyaround intralobular ducts

-# of foci reflects the severity of disease

Coagulati

ve

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-acinar atrophy-proliferation of duct epithelium to form epimyoepithelial islands(myoepithelial sialadenitis or benign lymphoepithelial lesions)-unlike lymphoma, the infiltrate x cross interlobular CT septa

-the semi-quantitative assessment of thisfocal lymphocytic sialadenitis in labial minorSG biopsies is an imp. Investigation inestablishing a dx, & is one of the dx criteria-however, since the appearance is x specific,it must be interpreted in the presence ofclinical features & serological investigations.

i. Ocular symptoms

ii. Ocular signsiii. Oral symptomsiv. SG fxv. Labial SG histologyvi. Ro & La autoAb

(fulfill 4/6 criteria todiagnose as SS)

Investigations:

-minor SG biopsy-estimation of parotid salivary flow rates, usually -sialography: shows sialectasia (snowstorm pattern, cherry-tree in blossom appearance)

-salivary scintiscanning with [99Tcm] shows uptake-serological findings: Anti-Ro & Anti-La**Although neither Anti-Ro nor Anti-La are specific for SS, theyare diagnostically helpful since they may be detected some time

before clinical picture develops

Etiology & pathogenesis

- autoimmune-genetic factors important in susceptibilityto external factors that trigger SS- frequency in pts with HLA class II MHCgenes-EBV as potential trigger-immunological mechanisms (T cells & theircytokines) causing destruction of glandulartissue-pathogenic significance of the range ofcirculating auto-Ab is uncertain

Middle-aged females (F:M.9:1)Most common symptomsrelated to xerostomia &xerophtalis

Malignant transformation-risk of B cell lymphoma developing in affected glands 44x thanof general ppltn-risk varies from

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of mucosa assocwith candisosis

5. rapidly progressivecaries

6. Acute bacterialsaladenitis

Oral mucosa appears dry,smooth & glazed

Dorsum of tongue appearred & atrophic with variabledegrees of fissuring &lobulation

xerophtalmia

Salivary gland enlargement is variable

What are the other causes of SG swelling?

Sarcoidosis

Mumps

Sometimes in conditions like starvation,diabetes mellitus, HIV pts

Variable SG enlargement-30% pts give hx ofenlargement-only 15% present withenlargement-usually bilateral-predominantly: parotid

gland-seldom painful

Lacrimal gland enlargementis uncommon

High incidence of cariescaused by low salivary

The antinuclear Ab are

mostly found in the

secondary Sjgren

Syndrome. What Ab

are the most helpful in

our diagnosis? It isAnti-Ro and Anti-La or

also known as anti SSA

and anti SSB. SS refers

to Sjgren Syndrome.

These can be found in

other diseases but

when present they are

good indication of

Sjgren Syndromebecause they are

found early. This

makes it as the most

Epimyoepithe

lial island

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scretion

This is the serological abnormalities & autoantibodies in

primary & secondary Sjgren Syndrome. Just look andunderstand. You dont need to memorize them. Just to

help you in understanding this disease.

Here is example in minor SG. The minorSG biopsy is very important to diagnoseSjgren Syndrome & of course withassociation to other clinical symptomslike the presents of Ab, enlargement,xerostomia, etc.

Parotid SG Submandibular SG Sublingual SG

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serous, proteinaceous (more watery) mix of serous and mucous. Butmainly serous

mainly mucous

Minor SGmucous, some of them are(mostly on the tongue) are mix.

Areas where we cant findminor SG are:

Attached gingiva

Ant. part of hard palateuntil molar area

Mid palatal raphe

This is a sample from labial minorSG where we have mostlymucinous but sometimes seroussecretion.

DEVELOPMENTAL ANOMALIES OF SG

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The most famous is Stafnes Idiopathic Bone Cavity. At the lingual aspect of

the mandible, we have a slight depression called submandibular fossae.

Sometimes during development, some SG tissue entrapped within the

submandibular fossae, either completely surrounded by bone or partially.

Radiographically, we can see this area as a well-defined area beneath theinferior alveolar canal.

*Assalamualaikum. Selamat study semua. Smg Allah permudahkan kita utk memahami, menghafal dan menjawab soalan2 dgn

baik. Notes ni x termasuk buku. Kalau ada masa, boleh la tmbh2 maklumat dr buku ye. Bukan ape, selain mun x ckp rajin , lg

pun kalau masukkn semuasgt tebaaaal la notes ni.dn namenye pn notes kan. Mestilah ringkas dn padat. Hehedn jugekalauboleh baca la at least sekali lecture notes for labx semua mun masukkn kt cni. Alasan spt d atsok. Selamaaat!

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