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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 µorganisms)
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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