Non-neoplastic salivary gland disorders

Presented byDr. Anjum Baker

II MDS PostgraduateDept of Oral Pathology, VIDS & RC

SEMINAR #10

CONTENTS• Introduction• Classification• Developmental Disorders• Infections• Traumatic/Ischaemic Disorders• Autoimmune Disorders• Obstructive disorders• Endocrine disorders• Others

INTRODUCTION• Non neoplastic disorders of salivary glands include a

spectrum of conditions ranging from developmental to

inflammatory to functional disorders

• Commonly the major salivary glands are affected by these

conditions, however, minor salivary gland involvement is

also seen, especially in traumatic and autoimmune

disorders

CLASSIFICATION• I. Rice (1999)• 1. Acute inflammatory lesions• Mumps• Acute suppurative sialadenitis• 2. Chronic inflammatory lesions and disorders• Sjogren’s syndrome• Mickulicz disease• Necrotising Sialometaplasia• Chronic suppurative & Sclerosing sialadenitis• 3. Granulomatous diseases• Primary TB of salivary gland• Animal scratch disease

• Sarcoidosis• Sialolithiasis• 4. Cystic Lesions• 5. Radiation injury• 6. Trauma• 7. Sialadenosis• 8. Others

Rice DH. Neoplastic and Nonneoplastic salivary gland lesions. Medical Clinics. 1999 Jan 1;83(1):197-218.

• II. Rosen (2001)• 1. Inflammatory• Mumps• CMV parotitis• Acute suppurative sialadenitis• Chronic suppurative sialadenitis• Recurrent parotits of childhood• Benign lymphoepithelial lesion• TB• Actinomycosis• Atypical Mycobacterial infection• Sarcoidosis• Sjogren’s syndrome

• 2. Non inflammatory• Sialolithiasis• Cysts• Radiation• Trauma• Sialadenosis• Pneumoparotitis• Cheilits Glandularis• Necrotising sialometaplasia

Rosen SF. Non neoplastic salivary gland disorders. MD Anderson Cancer Research Centre. Special issue. Oct 2001. SP 019-024

Working Classification based on etiology• I. Developmental

• Aplasia/ Hypoplasia• Agenesis• Ductal atresia• Aberrancy• Accessory ducts/lobes• Polycystic disease of parotid• II. Traumatic / Ischaemic• Cheilitis Glandularis• Mucocoele• Stomatitis Nicotina• Necrotising sialometaplasia

• III. Infections• Bacterial- Acute sialadenitis• - Chronic sialadenitis - Subacute necrotizing sialadenitis _Actinomycosis Viral – Mumps, CMV, ECHO, influenza - HIV-SGD Fungal – Aspergillosis IV. Autoimmune• Sjogren’s syndrome• Mickulicz disease• Chronic sclerosing sialadenitis• V. Cysts• Lymphoepithelial cysts

• VI. Functional• Sialorrhea• Xerostomia• VII. Obstructive• Sialolithiasis• Strictures• VIII. Endocrine – Sialosis• IX. Drug Induced• Chlorhexidine• Iodine• Phenyl butazone• X. Miscellaneous- Sarcoidosis, Radiation damage

I. Developmental Disorders• Developmental disorders of salivary glands are very rare.

• 1. Aplasia/Hypoplasia

• Affects one or more lobes or whole of salivary gland

• Major salivary glands are involved

• M>F,2:1

• Hypoplasia associated with Melkerson Rosenthal syndrome

• Severe xerostomia, leathery tongue, predisposition to caries.

• Active minor SG provide some degree of relief

• Diagnosis by CT/MRI/Tc pertechnetate scintiscan

• 2. Agenesis

• Total absence of glands

• Unilateral or bilateral

• Syndrome associated- Treacher Collins syndrome,

hemifacial macrosomia, Xerostomia, burning sensation,

infections, caries

• Site of SG occupied by adipose/connective tissue

• Diagnosis- CT/MRI/Tc-99 scan

• 3. Ductal Atresia

• Congenital blockage or absence of the orifice of a major

salivary gland duct or part of the duct itself.

• The submandibular salivary gland duct is usually involved

• Occurs due to failure of duct to cannulate during

embryological development.

• The condition first becomes apparent in the first few days

after birth where a submandibular swelling caused by a

retention cyst is noticed.

• 4. Aberrency

• Development of salivary gland away from normal site

(ectopic)

• Usually seen in ramus or body of mandible posterior to Ist

molar

• Site for development of cyst/neoplasm

• 5. Accessory ducts/lobes

• Increased proliferative activity during embreyogenesis

• No clinically evident disease

• May posed difficulty during surgical manipulation

• 6. Polycystic disease of parotid

• First described by Seifert et al

• F>M,4:1

• Congenital/ early childhood

• Bilateral non tender enlargement of parotid

• CT- glandular enlargement with multiple cystic areas

• H/P- small epithelium lined cysts replacing whole of SG

parenchyma

• Presence of vacuolated cells and sloughing of cell debris

into cyst lumen

II. Traumatic/ Ischaemic• 1. Cheilitis Glandularis

• First described by Volkmann in 1870

• Uncommon inflammatory disorder characterized by

progressive enlargement and eversion of labial mucosa.

• Etiology- chronic irritation/trauma/wetting

• C/F- onset- 3-12 months

• 4th -7th decade

• M>F

• Asymptomatic swelling to swelling with mucopurulent

exudate from ductal orifice

• Pain +/-

• Burning sensation, ulceration with crusting

• Risk of development of SCC

Classification

• Simple

• Superficial suppurative/ Baelz disease

• Deep suppurative

• H/P-

• Non specific sialadenitis

• Atrophy/distention of acini

• Ductal ectasia with or without squamous metaplasia

• Replacement of glandular parenchyma with chronic inflammatory

cell infiltrate

• Fibrosis

• Suppuration/ stromal edema

• Rx• Removal of source of irritation• Culture and sensitivity tests if suppuration is present

• 2. Mucocoele• Most common salivary gland pathology• Considered to be of traumatic origin• Involves ducts of minor SG• Etiology- traumatic severance of duct or chronic partial

obstruction• C/F- • No age/ gender predilection• Site- lower lip,buccal mucosa, palate, cheek, floor of

mouth.• Raised circumscribed vesicle with bluish translucency.• May rupture to release thick mucinous material.• Deep seated lesions – overlying mucosa appears normal• Recurrent swelling• May enlarge during meal times

• Types-

• Mucous extravastion cyst (Pseudocyst)

• No epithelial lining

• Extravastion of mucous into connective tissue

• Mucous retention cyst (True cyst)

• Result from dilatation of duct

• Epithelium lined

Mucous extravastion cyst

• Normal minor salivary gland tissue is usually seen along with poorly defined

pools containing faintly eosinophilic mucinous material muciphages’.

• One or more dilated ducts may be present and sometimes a breach may be

seen in a duct.

• Sometimes inflammatory

infiltrate is seen

• Mucous Retention Cyst

• Well defined cysts may be partially or completely lined by epithelium. Thin

fibrous capsule may be present

• The epithelium may consist of flattened cells or may be stratified squamous

or cuboidal cells or a thicker pseudostratified columnar epithelium.

• Cystic lumen may contain mucous secretions, mucinophages and

inflammatory cells

• Rx

• May resolve spontaneously

• Surgical excision if it is problematic

• Cyst should be excised with associated minor salivary

gland in toto to prevent recurrence.

• Ranula

• Mucocele that occur in the floor of the mouth.

• Latin-rana, means frog.

• the swelling may resemble a

frog' s translucent underbelly.

• C/F

• blue, dome-shaped , fluctuant swelling in the floor of the

mouth

• fills the floor of the mouth,elevates the tongue.

• located lateral to the midline,

• may rupture, release their mucin contents and reform .

• plunging or cervical ranula - occurs when the spilled

mucin dissect s through the mylohyoid muscle and

produces swelli ng within the neck

• H/P

• similar to that of a mucocele in other locations.

• Rx- Surgical excision

• 3. Stomatitis Nicotina

• Seen in cigar smokers and pipe smokers

• Etiology- inflammation of minor salivary glands and their

orifices due to chronic irritation from tobacco smoke

• C/F-

• M>F, 5th-7th decade of life

• Seen commonly in reverse smokers.

• Minor SG of hard palate is affected

• Palatal mucosa becomes diffusely grey or numerous

elevated papules with punctate centres maybe seen

• ‘Dried mud appearance’ - keratinized palatal epithelium

• H/P

• Hyperkeratosis/ acanthosis of palatal epithelium

• Mild patchy inflammation of subepithelial connective

tissue and mucous glands

• Squamous metaplasia of excretory ducts

• Inflammatory exudate within ductal lumina

• Hyperplastic ductal epithelium near the orifices

• Rarely, epithelial dysplasia is seen

• Rx

• Completely reversible with smoking cessation within 1-2

weeks

• 4. Necrotising Sialometaplasia

• Ist reported by Abrams et al in 1973

• Non neoplastic inflammatory lesion that may clinically

resemble SCC/MEC

• Etiology- h/o trauma,surgery,radiation

• Vascular ischaemia is said to be the main cause

• Associated with smoking

• C/F

• M:F-2:1

• Peak incidence-5th dec

• Involves minor SG especially of palate

• Painless swelling with or without ulceration.

• 1-3cm size

• unilateral/rarely bilateral

• Typical presentation with crateriform ulcer similar to

malignancy

• Erosion of palatal bone maybe

seen

• H/P• Coagulative necrosis of glandular acini, Squamous metaplasia of

ducts

• Mucin pooling

• Mixed inflammatory

infiltrate

• Rx

• Resolves spontaneously within 2 weeks, upto 5 weeks in

palate

III. Infections

• Sialadenitis – inflammation of salivary gland

• Acute/Chronic

• Specific/Non specific

• Suppurative/Non suppurative

• Bacterial- Staph, Strep, Primary TB

• Viral – Mumps, CMV

• Fungal- Actinomycosis

• 1. Bacterial sialadenitis

• Acute Bacterial Sialadenits

• Most common in parotid

• Bilateral in 10%-25% cases

• Commonly due to ductal

obstruction or decreased salivary flow causing retrograde

infection

• Etiology- Commonly S. aureus & Strep viridans

• Swollen painful gland, overlying skin is erythematous

• Low grade fever, trismus

• Purulent discharge from duct

• Chronic Sialdenitis

• Periodic swelling

• Pain- mild to moderate

• Periods of excacerbation and

remission

• Fever +/-

• Subacute necrotizing sialadenitis

• Commonly seen in young adults

• Involves minor SG of hard and soft palate

• Presents as painful nodule covered by intact erythematous mucosa

• No ulceration or sloughing of surface mucosa

• Imaging

• Acute cases- sialography shows ductal dilatation

• Chronic sialadenitis- Characteristic ‘sausaging pattern’ of

stenson’s duct- alternate dilatations and strictures.

• H/P

• Acute sialadenitis – accumulaton of neutrophils in ductal

system, dilatation of ducts

• Marked edema

• No changes in acinar architecture

• Chronic sialadenitis- • scattered patchy

Inflammatory infiltrate

composed of lymphocytes and

plasma cells

• Atrophy of acini

• Ductal dilatation

• Subacute necrotizing sialadenitis – intense mixed

inflammatory infiltrate of lymphocytes, plasma cells,

neutrophils, histiocytes and eosinophils

• Necrosis of acini

• Atrophy of ducts

• (Autoimmune etiology has been postulated)

• Rx

• Antibiotic therapy

• Hydration to stimulate salivary flow

• Analgesics, Sialogogues

• Subacute necrotizing sialadenitis- self limiting, resolves

in 2-3 weeks

• Abscess formation- surgical drainage

• Actinomycosis

• Infection from tonsil or teeth

• Trauma to the region or extension from adjacent site

• C/F

• pain+/- , visible sinus tracts oozing pus/ granules – sun ray

appearance,

• enlargement of salivary gland (parotid)

• some have purplish skin discoloration

• H/P

• Necrosis of acini, chronic inflammatory cell infiltrate,

granulomatous reaction, sulfur granules

• Diagnosis: culture

• Rx

• I&D

• Antibiotic therapy- Pencillin G ,2-6 weeks

• 2. Viral Sialadenitis

• Mumps- paramyxovirus

• Coxsackie A, ECHO, parainfluenza, CMV

• Viral Parotitis/Mumps

• Contagious infection of parotid gland

• Rarely SMG & SLG involved

• Commonly affects children

• Unilateral or bilateral enlargement of parotid salivary gland

• Associated with pain/ low grade fever/ anorexia/malaise

• Lack of appetite/ metallic taste

• Enlargement peaks in 2-3 days

• Redness and enlargement of SG duct openings

• Diagnosis

• Serology- Mumps specific IgM /4 fold increase in mumps

specific IgG titres• virus can be isolated in cell culture and detected by• hemadsorption. • PCR assay.

• Rx

• Symptomatic, no antiviral therapy available

• MMR vaccine

• Complications

• Epididymo orchitis

• Oophritis

• Meningitis

• Encephalitis

• B. HIV induced SG disease(HIV-SGD)

• AIDS defining condition in children

• Swelling of the salivary glands and/or 

xerostomia in individuals infected with HIV.

• Diagnostic criteria-

• Gradual enlargement of the major salivary glands,

particularly the parotid glands.

• This swelling may be on one side or both sides, may cause

disfigurement and may be painful.

• Xerostomia with no other cause such as a side effect of

medications.

• There may also be xerophthalmia  and arthralgia, similar

to Sjögren syndrome.

• HIV-SGD is more prevalent in HIV positive children than HIV

positive adults,at about 19% and 1% respectively.

•  Incidence of HIV-SGD has increased following the

institution of HAART

• H/P

• Hyperplastic intra-parotid lymph nodes and/or lymphocytic

infiltrates within the salivary gland tissue.

• Long Standing - development of lymphoepithelial cysts.

• Infiltration of CD-8 T cells (Schoidt, 1999).

• Lymphoma results in significant morbidity and mortality

in this group of patients.

• Rx

• Symptomatic

• 4. CMV SialadenitisCauses-Transplacental transmission in infantsimmunosupression generalized infection Infected saliva, transplantation, dialysis CMV hepatitis, myocarditis

C/F- non tender enlargement of the gland - mild feverInfectious- shedding of CMV in saliva

• H/P• Characteristic intracytoplasmic and intranuclear

inclusions – owl eye app• More evident in ductal ep.• PAS+, Gomori methanamine + cytoplasmic inclusions

inclusions• Diagnosis- Serology• Rx• Resolves spontaneously• Antiviral Rx in immunocompromised pts

IV. Autoimmune Disorders• 1. Sjogren’s syndrome

• It is named after Swedish ophthalmologist Henrik C Sjögren

• An autoimmune inflammatory disorder of exocrine glands

mainly affecting salivary, lacrimal glands.

• Common in the middle aged Females. (F:M-10:1)

• Primary SS - Dry eyes (Keratoconjunctivitis/ xerophthalmia) &

dry mouth.

• Secondary SS- Dry eyes, Dry mouth & connective tissue

disorder (RA, SLE, Systemic sclerosis, polymyositis, primary

biliary cirrhosis)

• Etiopathogenesis

• Unknown etiology

• Proposed causes-

• Genetic predisposition- HLA DR3/ HLA B8

• STAT4 polymorphism

• Hormonal changes

• Inflammatory events - Auto antibodies

• Liver dysfunction

• Viral etiology

• A SS type of disease may follow HIV, EBV, HCV, or H pylori

infection, or graft-versus-host disease.

• Autoimmune reaction against alpha fodrin, a cytoskeletal

protein involved in actin binding, with lymphocyte-

mediated destruction of salivary, lacrimal and other

exocrine glands.

• Tumor necrosis factor (TNF), interferon (IFN) and B cell

activating factor (BAFF) are implicated in the

pathogensis.

• A viral etiology, possibly human retrovirus 5 (HRV-5), and

a genetic predisposition may be implicated.

• Rheumatic Diseases associated with Sjogren’s’ syndrome • - RA • - SLE • - Progressive systemic sclerosis • - Dermatomyositis. • - Polyarteritis nodosa. • - Reynaud’s phenomenon.

• Immunologically related diseases associated with SS • - Primary biliary cirrhosis • - Chronic active hepatitis • - Autoimmune thyroid disease • - Pemphigus vulgaris • - Coeliac disease • - Myasthenia gravis • - Graft versus host disease

C/F • Xerostomia, unpleasant taste. • Angular cheilitis • Pus discharge from the ductal orifices. • Unilateral/ Bilateral intermittent enlargement of salivary

glands mainly parotids. • Thick frothy saliva, later stage with loss of saliva pooling. • Glazed, dry mucosa that tend to form wrinkles. • Redness/soreness of the mucosa due to candida

infection. • Lobulated, reddish, partial/complete depapillated tongue

with reduced no of taste buds • Gross accumulation of plaque • Several dental caries esp root caries. • Periodontal diseases

• Recurrent attacks of the acute bacterial sialadenitis: SS is the

most common cause for the acute bacterial sialadenitis.

• Enlarged tender regional lymph nodes.

• Difficulty in eating

• Soreness of the mouth

• dryness of pharynx, larynx

• In Eyes -

• Sensation of dryness, Burning sensation, Redness

• Frequent conjunctival infections, Ulceration.

• CT disorders clinical features also can present in the secondary

SS.

Radiological features

• 1. Multiple sialectasias (snow storm app/ branchless fruit

laden tree/ cherry blossom) in sialogram with atrophy of

ductal system delayed emptying of dye.

• 2. Impaired salivary activity seen in salivary scintiscanning

• H/P

• lymphocytic infiltration of the salivary glands.

• destruction of the acinar units

• focal chronic inflammatory aggregates (50 or more

lymphocytes and plasma cells) .

• These aggregates should be adjacent to normal-appearing

acini and should be found consistently in most of the glands

in the specimen.

• Proliferation of ductal ep. &myoepithelium – epimyoepithelial

islands.

• Sialochemistry• Elevated Ig A• Elevated K+/Na+• Decreased pH• Serology• ANA• SS-A• SS-B• RF• IgG• ESR

For the diagnosis of primary SS:

In patients without any potentially associated disease, primary SS may

be defined as follows:

The presence of any 4 of the 6 items is indicative of primary SS, as

long as either item IV (histopathology) or VI (serology) is positive OR

The presence of any 3 of the 4 objective criteria items (that, is items III,

IV, V, VI)

For the diagnosis of secondary SS:

In patients with a potentially associated disease (for instance, another

well-defined connective tissue disease), the presence of item I or item

II plus any 2 from among items III, IV, and V may be considered as

indicative of secondary SS Fox RI, Saito I. Criteria for diagnosis of Sjogren's syndrome. Rheumatic diseases clinics of North America. 2004 May;20(2):391-407.

• Exclusion criteria: • 1. Past head and neck radiation treatment • 2. Hepatitis C infection • 3. Acquired immunodeficiency disease (AIDS) • 4. Pre-existing lymphoma • 5. Sarcoidosis • 6. Graft versus host disease • 7. Use of anticholinergic drugs

Fox RI, Saito I. Criteria for diagnosis of Sjogren's syndrome. Rheumatic diseases clinics of North America. 2004 May;20(2):391-407.

-

SECONDARY ss

REPEAT LAB TESTS

• Rx

• Most patients are treated with symptomatically

• Oral hygiene improvement

• Management of dry mouth

• Management of dry eyes

• Agents against CD20(B lymphocyte surface antigen) as

curative Rx (experimental)

• Systemic steroids

• 2. Mickulicz disease• Johann von Mikulicz Radecki (1800s)• Also called - benign lymphoepithelial lesion/myoepithelial

sialadenitis• Mikulicz disease- cases associated with benign

Iymphoepithelial lesions • Mikulicz syndrome- benign lymphoepithelial lesions secondary

to disease processes, such as tuberculosis. Sarcoidosis and lymphoma

• C/F• Mean age-50 years.• 60% to 80% of cases occur in women. • 85% occur in the parotid gland.• firm , diffuse swelling of the affected gland. • asymptomatic/ mild pain.

• Histopathologic Features

• heavy lymphocytic infiltrate associated with the destruction of

the salivary acini and persisting ductal ep.

• Germinal centers may or may not be seen.

• ductal cells and surrounding

myoepithelial cells become

hyperplastic, forming

epimyoepitheltal islands

throughout the lymphoid

proliferation.

• Treatment and Prognosis

• Frequently,surgical removal of the involved gland is

necessary.

• The prognosis in most cases is good.

• Individuals with benign Iymphoepithelial lesions have an

increased risk for lymphoma

• a rare malignant counterpart, called a malignant

Iymphoepithelial lesion or Iymphoepithelial carcinoma,

represents a poorly differentiated salivary carcinoma with

a prominent lymphoid stroma

• 3. Chronic sclerosing sialadenitis /Kuttner tumor

• described by H. Kuttner in 1896

• Considered as IgG4RD/ IgG4 related sclerosing disease

(2010)

• C/F

• submandibular gland is frequently involved

• unilateral or bilateral hard masses

• Painless/asymptomatic

• Mimics tumor clinically/ radiographically

Geyer JT, Ferry JA, Harris NL, Stone JH, Zukerberg LR, Lauwers GY, Pilch BZ, Deshpande V. Chronic sclerosing sialadenitis (Küttner tumor) is an IgG4-associated disease. Am J Surg PathoL. 2010 Feb;34(2):202-10

• H/P

• characterized by sclerosis of interlobular septae with resulting

accentuation of the salivary gland lobular architecture and an

interstitial infiltrate of lymphocytes and plasma cells along with

variable degrees of sclerosis.

• The involvement of adjacent salivary lobules may be non-

uniform with focal atrophy and loss of acini in some lobules.

• Reactive lymphoid follicles and collagenous sheaths around

small ducts are frequently seen

Geyer JT, Ferry JA, Harris NL, Stone JH, Zukerberg LR, Lauwers GY, Pilch BZ, Deshpande V. Chronic sclerosing sialadenitis (Küttner tumor) is an IgG4-associated disease. Am J Surg PathoL. 2010 Feb;34(2):202-10

• Diagnosis

• Increase in the absolute number of IgG4+ cells

• increased IgG4+/IgG+ ratio

• Pts may show involvement of lacrimal glands/ gastric

and intestinal glands, pancreas

• Risk of MALT lymphomas

• Rx

• At present- surgical excision

• Targeted immunotherapy ( experimental)

Divatia M, Kim SA, Ro JY. IgG4-related sclerosing disease, an emerging entity: a review of a multi-

system disease. Yonsei medical journal. 2012 Jan 1;53(1):15-34.

V. Functional Disorders• The production of saliva is stimulated both by the

sympathetic nervous system and the parasympathetic

system

• The saliva stimulated by sympathetic innervation is

thicker, and saliva stimulated parasympathetically is

more watery.

• Increased production – sialorrhea (ptyalismus)

• Causes – foreign bodies, new dentures, ulcerations of

the oral cavity, stress, tumors, neurological disorders,

GERD

• C/F-

• Drooling/choking

• Sores, angular cheilitis

• Diagnosis- Salivary flow rate>200ml/hr

• Rx

• Rx of cause, anticholinergics, surgical – ductal relocation

• Decreased production - xerostomia

• Causes-

• Developmental

• Dehydration

• drugs(antidepressants, antihypertensives )

• Physiological (post exercise, mouth breathing)

• autoimmune diseases of SG

• psychogenic (anxiety, depression)

• smoking

• Salivary flow <100ml/hr

• C/F

• Burning sensation

• Thick ropey saliva

• Difficulty in mastication, swallowing

• Leathery tongue

• Dry rough mucosa

• Oral infections, caries

• Rx

• Artificial saliva, hydration, sialogogues, sugarless

gum/candy

VI. Obstructive• 1. Sialolithiasis

• Formation of a sialolith in the SG ducts

• Locations- Intraductal close to orifice (50%)

• intraductal

• intraparenchymatous

• Composed of laminated layers of organic materials covered

with concentric shells of calcified material.

• Mainly hydroxyapatite crystals containing octacalcium

phosphate.

• 85% occur in SMG• Reasons –

• Physiological factors – • Saliva more alkaline • Presence higher conc of Calcium & Phosphate • Higher mucus content • Richness in phosphatase enzyme.• Low content of Co2 Anatomical factors • Longer duct • anti gravity flow(position of the gland) • Smaller orifice than the ductal lumen. • Irregular course of duct.

• C/F• Middle aged people w(M:F-2;1) • Intraglandular s –usually asymptomatic• Meal time swelling• Moderate pain• fever & malaise due to infections• Pus discharge through the orifice • Severe inflammation in the soft tissues.• Overlying mucosa may be ulcerated.• Sialoliths may be palpated if it presents in the extraglandular

portion. • Reduce salivary flow • Enlargement of the glands.

• R/F

• Radiolucent calculi Solitary or Multiple

• Usually oval shape & is cylindrical with multiple layers of

calcifications.

• Sialography -indicated when sialoliths are radiolucent,

ductal dilatation and obstruction .

• Rx

• Near orifice- manually tease out sialolith

• Small sialoliths- sialogogues for Ductal dilatation

• Incision & dissection

• Sialadenectomy-when the gland has fibrosed

VII. Endocrine (Sialosis)

• Non inflammatory enlargement of SG

• Causes-

• endocrine – Diabetes, acromegaly, hypothyroidism,

pregnancy

• Nutritional – malnutrition, alcoholism, anorexia, bulimia

• Dysregulation of autoimmune innervation of acini-

aberrant secretory cycle- excessive accumulation of

secretory granules-enlargement

• C/F

• Slow growing swelling

• Usually painless, bilateral

• Decreased SFR

• Sialography- leafless tree app

• H/P

• Hypertrophy of acinar cells- 2-3 times normal size, nuclei

pushed towards base, cytoplasm engorged with

zymogen granules

• Long standing – acinar atrophy/ lymphocytic infiltration

• Rx- of underlying cause/ sialadenectomy

IX. Miscellaneous• Radiation damage

• Most sensitive is acinar cells followed by vascular endothelium.

• Damage to ductal elements only at high doses

• Serous acini more sensitive than mucous

• Acinar cell damage appear either as focal cytoplasmic

degeneration, resembling large cytolysosomes, or as necrosis

of acinar cells

• Prolonged low dose radiation – In serous acini, basal lipid

vacuoles and less than their normal complement of secretory

granulesStephens LC, Ang KK, Schultheiss TE, King GK, Brock WA, Peters LJ. Target cell and mode of radiation injury in rhesus salivary glands. Radiotherapy and Oncology. 1986 Dec 31;7(2):165-74.

REFERENCES• Marx RE, Stern D. Oral and maxillofacial pathology. Chicago:

Quintessence. 2003.• Rice DH. Neoplastic and Nonneoplastic salivary gland lesions.

Medical Clinics. 1999 Jan 1;83(1):197-218.• Rosen SF. Non neoplastic salivary gland disorders. MD Anderson

Cancer Research Centre. Special issue. Oct 2001. SP 019-024• Neville BW, Chi AC, Damm DD, Allen CM. Oral and maxillofacial

pathology. Elsevier Health Sciences; 2015 May 13.• Rajendran R. Shafer's textbook of oral pathology. Elsevier India;

2009.• Fox RI, Saito I. Criteria for diagnosis of Sjogren's syndrome.

Rheumatic diseases clinics of North America. 2004 May;20(2):391-407.

• Eveson JW, Speight PM. Non-neoplastic lesions of the salivary glands: new entities and diagnostic problems. Current Diagnostic Pathology. 2006 Feb 28;12(1):22-30.

REFERENCES• Geyer JT, Ferry JA, Harris NL, Stone JH, Zukerberg LR, Lauwers

GY, Pilch BZ, Deshpande V. Chronic sclerosing sialadenitis (Küttner tumor) is an IgG4-associated disease. Am J Surg PathoL. 2010 Feb;34(2):202-10

• Divatia M, Kim SA, Ro JY. IgG4-related sclerosing disease, an emerging entity: a review of a multi-system disease. Yonsei medical journal. 2012 Jan 1;53(1):15-34.

• Stephens LC, Ang KK, Schultheiss TE, King GK, Brock WA, Peters LJ. Target cell and mode of radiation injury in rhesus salivary glands. Radiotherapy and Oncology. 1986 Dec 31;7(2):165-74.

Thank You