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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