Acute SG bacteria rare Parotid ascending infection from mouth Strep. Pyogenes Staph.

Aureus Haemophilus species Black-pigmented Bacteroides 1. salivary flow -Sjogren syndrome -drugs with xerostomic S/E 2. Postoperative complication in debilitated dehydrated pts after abdominal surgery 3. Immunocompromized pts 4. Acute exacerbation of chronic sialadenitis 1. Rapid onset 2. Swelling 3. Pain, fever, malaise 4. Redness of overlying skin 5. Pus from duct

BACTERIAL SIALADENITIS Chronic Submandibular > parotid -In major glands, usually non-specific, asocc. with duct obstruction (salivary calculi) & low grade ascending infection -progressive chronic inflammation of SM complete replacement of parenchyma by fibrous tissue mistaken for chronic sclerosing sialadenitis (a tumor) salivary flow Sialography : Disorder of salivary secretion 1. Duct obstruction 2. Glandular tissue obstruction 3. Ductal dilatation

Recurrent Parotitis Rare for children & adults parotid Rarely, adult for may follow on from childhood type but mostly due to persistence of predisposing factors (calculi, duct strictures) Childhood type: 1. Abnormally secretion rate 2. Immature immune response 3. Congenital abnormalities of ductal system Clinical features: 1. Unilateral or bilateral 2. Recurrent painful swelling 3. Pus from orifice 4. Often resolve spontaneously by early adulthood

Factors

Clinical features

1. 2. 3. 4. 1. 2. 3. 4. 5. Cellul ar debri

Unilateral Recurrent, tender swelling Inflammation of duct orifice Purulent, salty discharge (in acute exacerbation) Vary degrees of ductal dilatation Hyperplastic ductal epi. Periductal fibrosis Acinar atrophy, replaced by fibrous tissue Chronic inflammatory infiltration Dilat ed duct Atrophi c acini

histopat hology

Fibrosis with collage n

VIRAL SIALADENITIS MUMPS (EPIDEMIC PAROTITIS) Paramyxovirus Acute, contagious infection, often in minor epidemics Commonest cause of parotid enlargement Commonest of all SG disease Diagnosis usually clinical Confirmed diagnosis by (within 1st week) detection of IgM Ab in serum titer to mumps virus Ag Immunity after an attack is long-lasting Rare recurrent infection Clinically: 1. Most common in childhood 2. Transmitted by direct contact with infected saliva & droplet spread 3. Incubation period: 2-3 weeks 4. Prodromal symptoms: fever, malaise 5. Sudden onset of painful swelling of 1 or more SG -parotid (70%) 6. occasional involvement of SM & SL but rarely w/out parotid 7. enlargement gradually subsides () over 1 week 8. 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%) CYTOMEGALIC INCLUSION DISEASE (SG INCLUSION DISEASE) Cytomegalovirus (herpervirus gp) Infection is common in humans worldwide Most 1 infections are asymptomatic Causing severe disseminated disease in neonates & immunocompromised hosts (transplant, HIV pts) Maybe assoc. with xerostomia & HIV infection Histopathology: 1. SG involvement usually an incidental finding 2. Large, doubly contoured owl-eye inclusion bodies within nucleus or cytoplasm of duct cells of parotid gland 3. In disseminated disease, similar inclusions are found in kidneys, liver, lungs, brain & other organs

mumps 1

mumps 2

SIALADENOSIS (SIALOLIS) Non-inflammatory, non-neoplastic, recurrent bilateral swelling of SG Most common: parotid (due to abnormal of neurosecretory control) Reported with: 1. Hormonal disturbances 2. Malnutrition 3. Liver cirrhosis 4. Chronic alcoholism Various drugs Histopathology: 1. Hypertrophy of serous acinar cells to about 2x their normal size Cytoplasm is densely packed with secretory granules

HIV-ASSOCIATED SG DISEASE -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 enlargement due to: 1. Persistent glandular lymphadenopathy 2. Multiple lymphoepitelial cyst

POSTIRRADIATION SIALADENITIS Common complication of radiotheraphy Direct correlation btwn -dose of irradiation -severity of damage Damage is often irreversible, leading to: -fibrous replacement of damaged acini -squamous metaplasia of ducts In less severe cases, some degree of fx may return after several months Serous acini are more sensitive than mucous acini

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

SIALADENITIS OF MINOR GLANDS -often an incidental & insignificant finding -may however be of diagnostic significance, such as in Sarcoidosis & Sjogren syndrome -Most frequently seen in assoc. with mucous extravasation cysts & nicotinic stomatitis -Very rarely may present with multiple mucosal swellings assoc. with cystic dilatation of ducts & chronic suppuration (stomatitis glandularis) -most commonly on the lips, probably as an acute exacerbation of a chronic form assoc. with obstruction or reduction in salivary flow (cheilitis glandularis) Histopathology

Clinically

Obstructi ve & Traumatic Lesions

SALIVARY CALCULI (SIALOLITHS)

Most common in middleaged adults May form in ducts within the gland, or in main excretory duct Submandibular (79-90%) > parotid > Sublingual or minor glands (2%) Unilateral May be multiple in the same gland

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

Form by gradual deposition of Ca salts around an initial organic nidus (which may consists of altered salivary mucins with desquamated cells & microorganisms)

Sialoliths at the orifice of submandibular duct

Multiple sialoliths fused

Obstructi ve & Traumatic Lesions

NECROTIZING SIALOMETAPL ASIA

Uncommon May be mistaken clinically & histologically for malignant disease Most frequent on hard palate in middle aged pts, males Etiology unknown, but probably due to:

-most common as deep, crater-like ulcer (mimic malignant ulcer) -10-12 weeks to heal Ulcer may be preceded by indurated swelling

Lobular necrosis Sq metaplasiaof ducts & acini Mucous extravasation Inflammatory cell infiltration -Overlying palatal mucosa: pseudoepitheliomatous hyperplasia -features may be mistaken for SCC or mucoepidermoid carcinoma Duct metapla

-ischemia leading to infarction of Salivary lobules -trauma (eg LA injection, previous surgery)

Coagulati ve necrosis MUCOCELES

Chronic autoimmune disease

SJOGREN SYNDROME 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 Histopatholohy of minor glands -focal collection of lymphoid cells, initially around intralobular ducts -# of foci reflects the severity of disease

Lymphocytic infiltration Acinar destruction of lacrimal & 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)

-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

i. Ocular symptoms ii. Ocular signs iii. Oral symptoms iv. SG fx v. Labial SG histology vi. Ro & La autoAb (fulfill 4/6 criteria to diagnose as SS)

Investigations: -minor SG biopsy -estimation of parotid salivary flow rates, usually -sialography: shows sialectasia (snowstorm pattern, cherrytree in blossom appearance) Sialography is where they inject a contrast medium in the stensons duct (main duct) and after a while they take a radiograph. This picture shows snowstorm pattern or cherry tree in blossom. The ducts are dilated and the acini are atrophy. Thats why only these areas contain the contrast medium and -salivary scintiscanning with [99Tcm] shows uptake -serological findings: Anti-Ro & Anti-La **Although neither Anti-Ro nor Anti-La are specific for SS, they are diagnostically helpful since they may be detected some time before clinical picture develops

-the semi-quantitative assessment of this focal lymphocytic sialadenitis in labial minor SG biopsies is an imp. Investigation in establishing a dx, & is one of the dx criteria -however, since the appearance is x specific, it must be interpreted in the presence of clinical features & serological investigations. Etiology & pathogenesis - autoimmune -genetic factors important in susceptibility to external factors that trigger SS - frequency in pts with HLA class II MHC genes -EBV as potential trigger -immunological mechanisms (T cells & their cytokines) causing destruction of glandular tissue -pathogenic significance of the range of circulating auto-Ab is uncertain

Middle-aged females (F:M. 9:1) Most common symptoms related to xerostomia & xerophtalis Xerophtalmia assoc with: 1. difficulty in speaking & swallowing 2. fluid intake 3. disturbance of taste 4. Soreness & redness

Malignant transformation -risk of B cell lymphoma developing in affected glands 44x than of general ppltn -risk varies from <1%-6% of SS pts -risk may be slightly greater in primary SS than secondary -malignancy usually occurs late -assoc with swelling of gland -assoc. lymphoma share many similarities with MALT lymphoma (they tend to pursue indolent course & remain localized until late)

of mucosa assoc with candisosis 5. rapidly progressive caries 6. Acute bacterial saladenitis Oral mucosa appears dry, smooth & glazed Dorsum of tongue appear red & atrophic with variable degrees of fissuring & lobulation Variable SG enlargement -30% pts give hx of enlargement -only 15% present with enlargement -usually bilateral -predominantly: parotid gland -seldom painful Lacrimal gland enlargement is uncommon

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

Epimyoepithe lial island

The antinuclear Ab are mostly found in the secondary Sjgren Syndrome. What Ab are the most helpful in our diagnosis? It is Anti-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 High incidence of caries Sjgren Syndrome caused by low salivary because they are found early. This makes it as the most

scretion

This is the serological abnormalities & autoantibodies in primary & secondary Sjgren Syndrome. Just look and understand. You dont need to memorize them. Just to help you in understanding this disease.

Here is example in minor SG. The minor SG biopsy is very important to diagnose Sjgren Syndrome & of course with association to other clinical symptoms like the presents of Ab, enlargement, xerostomia, etc.

Parotid SG

Submandibular SG

Sublingual SG

serous, proteinaceous (more watery)

mix of serous and mucous. But mainly serous Minor SG mucous, some of them are (mostly on the tongue) are mix. Areas where we cant find minor SG are: Attached gingiva Ant. part of hard palate until molar area Mid palatal raphe

mainly mucous

This is a sample from labial minor SG where we have mostly mucinous but sometimes serous secretion.

DEVELOPMENTAL ANOMALIES OF SG

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 the inferior 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 jugekalau boleh baca la at least sekali lecture notes for labx semua mun masukkn kt cni. Alasan spt d atsok. Selamaaat! Slm syg