a dissertation on cytologic spectrum of salivary …

A Dissertation on

CYTOLOGIC SPECTRUM OF SALIVARY GLAND LESIONS

WITH HISTOPATHOLOGICAL CORRELATION

Dissertation submitted to

THE TAMILNADU Dr.M.G.R MEDICAL UNIVERSITY

CHENNAI-600032

In Partial fulfillment of the regulations

Required for the award of

M.D.Degree in PATHOLOGY (BRANCH III)

DEPARTMENT OF PATHOLOGY

COIMBATORE MEDICAL COLLEGE

MAY 2020

UNIVERSITY REGISTRATION NO: 201713251

DECLARATION

I solemnly declare that the dissertation titled “CYTOLOGIC

SPECTRUM OF SALIVARY GLAND LESIONS WITH

HISTOPATHOLOGICAL CORRELATION” was done by me at

Coimbatore Medical College, during the period 2018 -2019 under the

guidance and supervision of Prof.A.DHANALAKSHMI, MD., to be

submitted to The Tamilnadu Dr.M.G.R.Medical University towards the

partial fulfilment of requirements for the award of MD DEGREE in

PATHOLOGY BRANCH –III.

Place : Coimbatore

Date :22.10.2019 Dr.T.ANITHA,

Post Graduate Student, Department of Pathology,

Coimbatore Medical College.

CERTIFICATE I

This to certify that the dissertation entitled “CYTOLOGIC


HISTOPATHOLOGICAL CORRELATION” is a record of bonafide

work done by Dr. T.ANITHA, Post Graduate Student in the Department of

Pathology, Coimbatore Medical College and Hospital, Coimbatore under the

guidance and supervision of Dr.M.KAVITHA, M.D., Senior Assistant

Professor, Department of Pathology, Coimbatore Medical College and

Hospital, Coimbatore in partial fulfillment of the regulations of The

Tamilnadu Dr.M.G.R Medical University, Chennai towards the award of

degree of M.D.PATHOLOGY.

Guide

Dr. M.KAVITHA, M.D., Dr. A.DHANALAKSHMI, M.D.,

Senior Assistant Professor, Professor & Head, Department of Pathology, Department of Pathology, Coimbatore Medical College, Coimbatore Medical College, Coimbatore. Coimbatore.

Dr. B.ASOKAN, M.S, M.Ch.,

Dean, Coimbatore Medical College,

Coimbatore.

CERTIFICATE –II

This is to certify that this dissertation work titled “CYTOLOGIC


HISTOPATHOLOGICAL CORRELATION” of the candidate

Dr.T.ANITHA with registration number 201713251 for the award of

M.D degree in the branch of PATHOLOGY. I personally verified the

urkund.com website for the purpose of plagiarism check I found that the

uploaded thesis file contains from introduction to conclusion pages and

result shows 7 (Seven) percentage of plagiarism in the dissertation.

Guide and Supervisor sign with seal

ACKNOWLEDGEMENT

To begin with I thank the almighty God for bestowing his blessing

on me in this dissertation a successful one.

I wish to thank the dean Dr ASHOKAN, MS., Mch., Coimbatore

Medical College and Hospital, for permitting me to conduct the study.

It’s a great pleasure to express my humble gratitude to the most

respectable teacher Dr .A. Dhanalakshmi MD., Professor and Head of

the Department, Department of Pathology, Coimbatore Medical College,

Coimbatore for her guidance and support.

I express my gratitude and sincere thanks to my guide

Dr.M.Kavitha M.D., Department of Pathology, Coimbatore Medical

College, Coimbatore.

I thank all Assistant Professors and Tutors of Department of

Pathology, Coimbatore Medical College for their opinion and

encouragement.

I thank my parents, my children Srinidhi and Harshan, my friend

Dr.Swathi for their extensive support.

CONTENTS

TABLE OF CONTENTS

S.NO TITLE PAGE.NO

1 INTRODUCTION 1

2 AIM AND OBJECTIVES 4

3 REVIEW OF LITERATURE 5

4 MATERIALS AND METHODS 46

5 OBSERVATION AND RESULTS 49

6 DISCUSSION 71

7 SUMMARY 79

8 CONCLUSION 80

BIBLIOGRAPHY

ANNEXURES

MASTERCHART

LIST OF TABLES S.NO TITLE PAGE.NO

1 Age wise distribution of lesions of salivary gland 49

2 Gender wise distribution of lesions of salivary gland 51

3 Distribution of cases based on clinical diagnosis 52

4 Distribution of cases based on duration of lesion 53

5 Distribution of cases based on size of lesion 55

6 Distribution of cases based on consistency 56

7 Distribution of cases based on location of lesion 57

8 Distribution of neoplastic tumors according to histopathological diagnosis and location 58

9 Distribution of cases based on cellularity 59

10 Cytological diagnosis of salivary gland lesions 60

11 Cytological categorization of lesions 62

12 Histopathological diagnosis of lesion 63

13 Histopathological categorization of lesion 65

14 Cytohistopatholgical correlation 66

15 Diagnostic accuracy in benign neoplastic lesions of salivary gland 67

16 Diagnostic accuracy in malignant neoplastic lesions of salivary gland 68

17 Comparison of consistency –Benign Vs Malignant 69

18 Comparison of site of lesion-Benign Vs Malignant 70

19 Comparison of cellularity – Benign Vs Malignant 70

LIST OF CHARTS

S.NO CHART PAGENO

1 Distribution of cases based on age

groups

50

2 Gender wise distribution of cases 51

3 Distribution of cases based on clinical

diagnosis

52

4 Distribution of case based on duration

of lesions

54

5 Distribution of cases based on size of

lesion

55

6 Distribution of cases based on

consistency

56

7 Distribution of cases based on location

of lesion

57


cellularity

59


Cytologic diagnosis

61


histopathological diagnosis

64

ABBREVIATION

FNAC - Fine needle aspiration cytology

PA – Pleomorphic adenoma

WT – Warthin’s tumor

MEC – Mucoepidermoid Carcinoma

CH SA – Chronic sialadenitis

SD CA – Salivary duct carcinoma

H &E – Hematoxylin and Eosin

MGG – May GrunwaldGiemsa

HPE –Histopathology Examination

WHO - World Health Organisation

INTRODUCTION

1

INTRODUCTION

Salivary glands are exocrine organs that secrete saliva widely

distributed throughout the mouth and oropharynx. There are three pairs of

salivary glands-parotid, submandibular and sublingual glands15.

Minor salivary glands are about 800-100 located throughout the oral

cavity in the buccal, labial lingual mucosa ,the soft palate ,lateral parts of

hard palate and the floor of mouth.

Salivary gland lesions form 2-5 percent of all Head and neck

neoplasms4,6,8. Age incidence varies widely, extending from children to

adults over 80 years of age. These glands are usually not subjected to

incisional or core needle biopsy, because of the possible risk of fistula

formation and tumor seedling18.

Cysts and associated lesions with cystic changes are commonly

encountered in Head and neck region. Pathology of these lesions are

diverse and includes developmental, inflammatory, benign and malignant

tumors which can be primary or metastatic.

FNAC is a useful method for evaluating salivary gland lesions. It is

of particular relevance in the head and neck area because of easy

accessibility of the target site6 minimally invasive procedure, excellent

patient compliance and thereby help to avoid surgery in non-neoplastic,

inflammatory conditions.

2

It is a preferred method due to its low cost, rapid turnaround time,

minimum morbidity. It has a high sensitivity and specificity for

diagnosing neoplastic and non-neoplastic lesions

It is useful to categorize the lesions into inflammatory, reactive,

benign and malignant lesions and thereby useful for appropriate

therapeutic management6,8,10. However, the heterogenecity of many

salivary gland tumors along with overlap of cytomorphological features

presents as a challenging work to conclude with precise diagnosis in some

instances.

The purpose of FNAC is not only to provide a definite specific

diagnosis. But it is also used in conjunction with clinical and radiological

findings to provide the best possible initial assessment from which

management can be planned1,10.

Till date, ultrasonography is acting as bridge between surgery and

pathology.17 Pre-operative assessment of parotid swelling by cytology and

ultrasonography is especially significant in our country where

tuberculosis and metastatic squamous cell carcinoma invading

perisalivary lymph nodes mimic parotid swelling.

Major salivary gland neoplasms usually present with non-specific

clinical symptoms ,requiring high degree of suspicion. FNAC offers an

invaluable and accurate initial diagnostic tool for the management of

these patients even in the era of the Immunohistochemistry.

3

The present study aims to correlate cytomorphological features of

salivary gland lesions in FNAC and the corresponding histopathology in

suspicious malignant cases.

Keeping histopathological diagnosis as gold standard sensitivity,

specificity and diagnostic accuracy of FNAC was calculated. An adequate

and representative sampling is essential for proper cytological evaluation

to reduce the errors in diagnosis.

The diagnostic pitfalls in FNAC were evaluated along with

practical suggestions to improve the diagnostic accuracy especially while

dealing with mucinous lesions. Other varied reasons for diagnostic errors

may be due to uncertainty of the site and tissues aspirated , minimal

material and lack of architectural pattern in the smears as compared to

histological sections.

Relevant clinical data, radiological findings, along with

cooperation between the clinician and cytopathologist10,13 are important

in order to use FNAC to its best advantage.

Thus the present study offers to examine the sensitivity, specificity

and diagnostic accuracy of FNAC of salivary gland lesions with

histopathological correlation and to identify the discrepancies

contributing to pitfalls in diagnosis.

AIM & OBJECTIVES

4

AIMS AND OBJECTIVES

AIM:

To analyse the diagnostic accuracy, sensitivity and specificity of FNAC

in various salivary gland lesions and correlate with the histopathological

findings.

OBJECTIVES:

1. To analyse the clinical, Histological and cytological features of

salivary gland lesions.

2. To correlate the cytological features of salivary gland lesions with

Histological diagnosis.

3. To analyse the reasons for diagnostic pitfalls in cases that have

cytohistological discrepancy.

REVIEW OF LITERATURE

5

REVIEW OF LITERATURE

Over the past three decades, in the work up of salivary gland lesion

fine needle aspiration has been well recognized as the first diagnostic tool.

It is widely accepted as a simple, safe, cost effective a technique in the

evaluation of salivary gland lesions and thereby helps to plan for further

management.

FNAC has an important relevance in head and neck area because of

easy accessibility of the target site, patient compliance, minimally

invasive and thereby helps to avoid surgery in inflammatory lesions and

non-neoplastic lesions.6

The use of aspiration cytology was first reported by Kun in 18479.

The procedure was reintroduced by Martin & Ellis in evaluation of head

and neck lesions in 19305,9. It was further promoted especially in salivary

gland lesions in 1950 and 1960 by Enroth et al9.

Salivary gland tumors constitute about 3-10% of head and neck

tumors4,8,9. When performed and analysed by experienced hands, FNAC

has the advantage of giving valuable diagnostic data in a relatively short

period of time.

6

ANATOMY

Salivary glands are compound tubuloacinar exocrine glands found

in oral cavity that secrete complex fluid called saliva.

There are three pairs of salivary glands involving parotid,

submandibular and sublingual region15.

1.Types of salivary gland based on size:

Major salivary gland

Collection of secretory cells aggregated into large bilaterally paired

extra oral glands with extended duct system through which the gland

secretions reach the mouth. Parotid gland, Submandibular and sublingual.

Minor salivary gland

Collection of secretory cells scattered throughout the mucosa and

submucosa of the oral cavity with short ducts opening directly onto

mucosal surface - serous glands of van ebner.

Anterior lingual glands

Lingual , buccal, labial palatal glands

Glossopalatine and retromolar glands

2 Based on the type of secretory cells

Serous-parotid

Mixed{seromucous}-submandibular

Mucous - minor salivary glands

7

Parotid is the largest salivary gland that constitutes about 60-65%

of total saliva.15 The superficial portion of gland is located subcutaneously

in front of the external ear and the deeper portion lies behind the ramus of

mandible associated with facial nerve.

Stenson’s duct runs forward across masseter muscle, turns inwards

at the anterior border of masseter and opens at just opposite second

maxillary molar crown.19,24

Submandibular gland weighs around 10-15 gm and constitutes for

about 2-30% of total saliva.24 It is located at posterior portion of floor of

mouth, medial aspect of mandible and wrapping around the posterior

border of mylohyoid.

Wharton’s duct opens into the mouth beneath the tongue lateral to

lingual frenulum19.

Sublingual gland constitutes about 2.5% of total saliva. It is located at

anterior part of floor of the mouth, just between mucosa and mylohyoid

muscle. Bartholin’s duct opens with submandibular duct at sublingual

caruncle

.

8

EMBRYOLOGY

Development of salivary gland19

Stage I - Bud formation

Stage II - Formation and growth of epithelial Chord

Stage III - Initiation of branching in parts of epithelial chord

Stage IV - Branching of epithelial chord and Lobule formation

Stage V - Canalization

Stage VI - Cytodifferentiation

Parotid develops around 4 -6 week, submandibular around 6th week

of intrauterine life19.Sublingual and minor salivary gland develops around

8th week of intrauterine life.

9

Secretory component of gland continues to grow postnatally.

Ductal, connective tissue and vascular component decreases upto two

years of age.

HISTOLOGY OF SALIVARY GLAND

Comprises of a series of secretory end piece- acini connected to the

oral cavity by – ductal system

SEROUS CELLS

It is present in demilune formation at the blind ends of mucous

secretory tubules. It is pyramidal in shape, with a spherical nuclei situated

at the basal third of the cell20.

Apical cytoplasm is filled with secretory granules, while basal

cytoplasm contains rough endoplasmic reticulum converging towards the

golgi complex. It also contains cytoskeleton components.

The lumen of serous end piece has small extensions in the form of

intercellular canaliculi.

MUCOUS CELLS:

It forms the secretory cell type of sublingual and most of the minor

salivary glands. It has a tubular or round configuration, larger than serous

cells with a flattened nucleus placed at the base20.Apical cytoplasm is

filled with mucous secretory droplets.

10

Myoepithelial cells-basket cells

These are contractile cells located around the terminal secretory

units, they are stellate like with a flattened nucleus, scant perinuclear

cytoplasm and long branching process which surrounds the secretory

duct cells.

DUCTS

Intercalated ducts:

These are small ducts into which secretory end piece empties24.It is

lined by a single layer of low cuboidal cells and myoepithelial bodies.

Function:

Contributes to the salivary secretion- lysozymes & lactoferrin

11

Undergo proliferation and differentiation to replace damaged or

dying cells in the striated ducts.

Striated ducts:

These are larger duct into which intercalated ducts empty. It is

lined by columnar epithelium15

Function:

Change the salivary secretion-isotonic to hypotonic

Sodium reabsorption &potassium excretion

Terminal excretory ducts:

Main duct leading from the gland to the oral cavity15,24.They are

lined by pseudostratified with columnar cells admixed with small basal

cells and goblet cells.

Function:

Alter the electrolyte concentration of saliva

In the present study the parotid gland was the most frequently

involved followed by submandibular gland and submental gland5,8,9,24.

FNAC has been used for the diagnosis of salivary gland lesions for more

than three decades and was found to be beneficial not only in the diagnosis

of salivary gland lesions , but also in differentiating neoplastic and non-

neoplastic lesions5,6,8.

12

Though the most accurate method of diagnosis is histopathology

yet the role of Fine needle aspiration cytology for the diagnosis of salivary

gland lesions is significant12.

The most common source of diagnostic error is inadequate

sampling because FNAC derives sample only from a small area11.Keeping

into consideration the significance of clinical features in forming the idea

about diagnosis, the role of FNAC in diagnosis of lesion and its accuracy

with histopathology is determined.

Combined with clinical and radiological findings, it can provide a

preliminary assessment on which management decision is based17.

Ultrasound guidance along with immediate assessment of the material by

cytopathologist improves the accuracy of FNAC.

Additionally the degree of differentiation of neoplastic cells can be

determined, which aid in the selection of surgical intervention.9

Categorizing the malignant lesion as low grade or high grade can

determine the extent of surgery example the preservation of facial nerve

and the indication for neck dissection in the case of malignant tumors of

parotid gland .

Assessment of FNAC of suspected salivary gland lesions should

follow step by step approach10. The first aim is to decide whether the

lesion is of salivary gland origin29.The next step is to identify the cells and

13

their morphology to classify them as non-neoplastic and neoplastic

categories.

The majority of salivary gland lesions occur in the superficial lobe

and less often in the deep lobe of parotid gland .Cytopathologist

performing FNAC should be familiar of the basic anatomy of salivary

gland.

A critical aspect of salivary gland FNAC is adequate sampling and

appropriate sample preparation. In FNAC, the adequate cellularity of

target lesion is important for an accurate interpretation5.Specific criteria

for adequacy of salivary gland is yet to be defined.

Many factors including the aspiration technique {manual versus

ultrasound guided}, nature of the lesion {solid versus cystic}sample

collection and preservation method, preparation technique artifacts,

calibre of needle and presence of obscuring blood or other material can

influence the adequacy of salivary gland aspirate.

Advances in technology like ultrasound, sialography, immune

markers are available to aid in the diagnosis, the accelerated use of FNAC

has reduced the expenditure.

The risk of malignancy prior to FNAC varies depending upon its

size and location. 20-25% in the parotid gland,40-50% in the

submandibular gland 80% in the sublingual and minor salivary glands.

14

Kim et al 2018 found a diagnostic accuracy of FNAC to be 92% in

differentiating malignant from benign salivary gland tumors.

Fakhry et al 2012 evaluated the sensitivity and specificity of FNAC

to be 80% and 89.5% respectively.

WHO classification of the Tumors of Head and Neck.25

BENIGN TUMORS

Pleomorphic adenoma

Myoepithelioma

Monomorphic adenoma

Warthin’s tumor

Oncocytoma,

Basal cell and canalicular adenoma

Lymphadenoma

Cystadenoma

Sialadenoma papilleferum

Ductal papilloma

Sebaceous adenoma

NEOPLASTIC LESIONS

Adenoid cystic carcinoma

Mucoepidermoid carcinoma

Acinic cell carcinoma

Polymorphous low-grade adenocarcinoma

15

Epithelial- myoepithelial carcinoma

Carcinoma ex-pleomorphic adenoma

Salivary duct carcinoma

Clear cell carcinoma

Basal cell adenocarcinoma

Intraductal carcinoma

Adenocarcinoma,NOS

Salivary duct carcinoma

Secretory carcinoma

Sebaceous adenocarcinoma

Carcinosarcoma

Poorly differentiated carcinoma

Undifferentiated carcinoma

Large cell neuroendocrine carcinoma

Small cell neuroendocrine carcinoma

Lymphoepithelial carcinoma

Squamous cell carcinoma

Oncocytic carcinoma

Sialoblastoma

Uncertain malignant potential

NON NEOPLASTIC EPITHELIAL LESIONS

Sclerosing polycystic adenosis

16

Nodular oncocytic hyperplasia

Lymphoepithelial sialadenitis

Intercalated duct hyperplasia

BENIGN SOFT TISSUE LESIONS

Hemangioma

Lipoma/sialolipoma

Nodular fasciitis

HAEMOTOLYMPHOID TUMORS

Extranodal marginal zone lymphoma of mucosa associated

lymphoid tissue (MALT LYMPHOMA)

TNM Classification of carcinoma of the major salivary glands25

T - Primary tumor

Tx - Primary tumor cannot be assessed

To - No evidence of primary tumor

T1- Tumor <2 cm in greater dimension, without extra parenchymal

extension.

T2- Tumor >2 cm but <4cm in greater dimension, without extra

parenchymal extension.

T3 – Tumor > 4cm and/or with extra parenchymal extension

T4a- Tumor invades skin, mandible,ear canal or facial nerve.

T4b- Tumor invades base of skull or Pterygoid plates or encases

carotid artery

17

N - Regional lymph nodes – cervical node

Nx – Regional lymph nodes cannot be assessed

N0 – No regional lymph node metastasis

N1 – Metastasis in a single ipsilateral lymph node < 3cm in greater

dimension

N1 – Metastasis in a single ipsilateral lymph node <3cm in greater

dimension.

N2a – Metastasis in a single ipsilateral lymph node,>3cm but < 6cm

in greater dimension.

N2b – Metastasis in multiple ipsilateral lymph nodes, all <6 cm in

greater dimension.

N2c – Metastasis in bilateral or contralateral lymph nodes, all<6 cm

in greater dimension.

N3 – Metastasis in a lymph node >6cm in greater dimension

M - Distant metastasis

M0 – No distant metastasis

M1 – Distant metastasis

STAGE GROUPING

Stage I - T1 N0 M0

Stage II - T2 N0 M0

Stage III - T3 N0 M0

- T1-3 N1 M0

18

Stage IVA - T1-3 N2 M0

- T4a N0-2 M0

Stage IVB - T4b AnyN M0

- AnyT N3 M0

Stage IVC - AnyT AnyN M1

This classification applies to carcinomas of major salivary glands

parotid, submandibular and sublingual glands.

Carcinomas arising in minor salivary glands (mucin secreting

glands in the lining membrane of the upper aerodigestive tract) are not

included in the classification25.

Foschini et al 2008 stated that a non-diagnostic aspirate is one that

for qualitative and quantitative reasons provides insufficient diagnostic

material to provide an informative interpretation.

In the present study,45 cases of major salivary gland lesions were

included irrespective of age and sex.Of the 45cases studied, age range of

15 to 70 years with mean age of 48 years and had male preponderance.

Non –neoplastic lesions constitute 26% and Neoplastic lesions constitute

72% of all the cases9.

Among benign neoplasms, pleomorphic adenoma was more

frequent5. Cytologic smear shows ductal epithelial cells and myoepithelial

cells in varying proportion, extracellular matrix and chondromyxoid

stroma.

19

Among malignant neoplasm, mucoepidermoid carcinoma was

reported in 7 cases5,8. Cytologic smear includes predominantly

intermediate cells resembling squamous metaplastic cell, mucin secreting

cells, infrequently differentiated squamous epithelial cells.

A high accuracy in FNAC is a useful guide for further management

in patients with salivary gland lesions8.

Five group approach in salivary gland cytodiagnosis13.

MYXOID-HYALINE

Benign mixed tumor

Adenoid cystic carcinoma

Carcinoma Ex benign mixed tumor

Polymorphous low grade Adenocarcinoma

BASALOID

Basal cell adenoma

Basal cell carcinoma

Solid variant of Adenoid cystic carcinoma

Polymorphous low grade Adenocarcinoma

Small cell Undifferentiated carcinoma

ONCOCYTOID

Intraglandular lesions

Warthin’s tumor

Oncocytoma

20


Extraglandular lesions

Medullary carcinoma

Hurthle cell carcinoma

LYMPHOID

Chronic sialadenitis

Benign lymphoepithelial lesions

Intra/peri-salivary gland lymph nodes

Warthins tumor

Lymphoepithelial carcinoma

Metastasis to intra/peri parotid lymph nodes

SQUAMOID

Retention cyst

Squamous cell carcinoma

Benign congenital cysts extrinsic to salivary gland

Branchial cleft

Thyroglossal duct

Thymic

Dermoid/epidermal inclusion cyst

21

NON-NEOPLASTIC LESIONS:

SIALADENITIS

Acute and chronic sialadenitis including granulomatous disease are

the most common non-neoplastic lesions8,11.

Acute conditions are localised to the salivary gland or be the

manifestation of systemic infection. Chronic sialadenitis result from

causes that lead to salivary duct obstruction, very often sialolithiasis15.

Granulomatous inflammation of salivary gland includes-obstructive

sialadenopathy -stones, extravasated mucin.24

Specific infections - Mycobacterial, Toxoplasmosis, Tularemia,

Fungal Sarcoidosis. Systemic infections-Wegeners granulomatosis,

crohns disease.

Morphologic criteria - Cytology

Aspirates of the gland involved by sialadenitis show scanty material

of ductal epithelial cells, few acinar cells, variable numbers of

inflammatory cells with fragments of fibrous stroma.14

Histopathology

Microscopic view shows atrophic parenchyma with mixed acute

and chronic inflammatory cells.

22

SIALOLITHIASIS

Formation of ductal calculi is often associated with pain and mimic

a neoplasm. The stones are usually composed of calcium carbonate

,calcium phosphate admixed with other minor components15.

It occurs most commonly in submandibular gland-wharton’s duct

and less often in parotid gland-stenson’s duct24.

Imaging studies are used to detect ductal calculi and corresponding

ductal dilatation.16


Hypocellular aspirate composed of groups of benign ductal cells

and metaplastic squamous , ciliated or mucinous cells, calcification like

stone fragments.13Inflammatory background with mucin.

Histopathology

Dilated ducts with squamous metaplasia or calculi. Variable

chronic inflammation with destruction of acini accompanied by fibrosis.

REACTIVE LYMPH NODE HYPERPLASIA

The etiology of enlargement of intra and peri-parotid lymph nodes

can be non-specific or a response to clinical or subclinical bacterial or

viral infection.

Specific causes – bacterial and fungal lymphadenitis, infectious

mononucleosis, Cat scratch disease, Rosai-dorfmann disease, Sarcoidosis

and kikuchi lymphadenitis.13

23


Aspirates are usually cellular composed of a mixed population of

lymphocytes with predominance of small mature forms. Admixed with

them are tingible body macrophages and lymphohistiocytic aggregates

representing the cytologic correlate of germinal centres16.

Background shows lymphoglandular bodies.

Histopathology

Relative preservation of the lobular outline of gland with

predominance of T lymphocytes. Hyperplasia of ductal basal cells that

lack myoepithelial cells.

LYMPHOEPITHELIAL SIALADENITIS

It is a benign condition characterized by lymphocytic infiltrate

associated with parenchymal atrophy and foci of ductal hyperplasia with

intraepithelial lymphocytes24.

It is more common in women ,and with bilaterality.

Patients with sjogren’s syndrome have increased risk of developing

lymphoma, commonly extra-nodal marginal zone lymphoma.13,24


Aspirate cellular consisting of cohesive sheets of ductal cells, with

squamous metaplastic changes. Mixed population of lymphocytes,

dendritic cells and tingible body macrophages with predominance of

small mature lymphocytes.

Lympho histiocytic aggregates. Acinar cells absent.16

24

Histopathology:

Marked hyperplastic lymphoid infiltrates with loss of salivary

gland acini. Ducts infiltrated by lymphoid cells.

SIALADENOSIS

It is a persistent, non-neoplastic, non-inflammatory enlargement of

salivary gland. It often presents bilaterally involving the parotid gland. It

is associated with systemic conditions: hypothyroidism, diabetes,

malnutrition, obesity, pregnancy, cirrhosis,alcohol abuse, HIV infection16.


Cellular aspirate composed of enlarged hypertrophic acinar cells.

Normal architectural arrangement of acini is maintained. Background

shows stripped acinar cell nuclei and fibroadipose tissue.13

Histopathology:

Grossly the salivary gland is enlarged.

Microscopically, there is an admixture of acinar hypertrophy and

fatty infiltrates. There is no inflammation or fibrosis as compared to

sialadenitis.

BENIGN CATEGORY

The benign tumors comprise almost 60% of all salivary gland

aspirates.29

Patients are managed conservatively with regular clinical and

radiological follow up without surgical intervention.

25

Among the benign lesions, pleomorphic adenoma is the most

common8,11,29 followed in order of frequency are warthins tumors,

oncocytoma, basal cell adenoma and canalicular adenoma.9

PLEOMORPHIC ADENOMA

It occurs approximately 10 times more common in parotid than

submandibular gland24.

Definition

The entity “pleomorphic adenoma” is defined when the aspirate

contains a combination of bland myoepithelial cells and fragments of

chondromyxoid stroma.

In the parotid these tumors arise within the superficial lobe24. It

presents as painless, slow growing discrete mass.


The majority of cells are myoepithelial - round, spindle, clear,

polygonal, plasmacytoid type with bland nuclear features.

Ductal epithelial cells –bland nuclear features.

The aspiration of mucoid paucicellular fluid suggest low grade

mucoepidermoid carcinoma or mucoepidermoid carcinoma arising in

pleomorphic adenoma.29

The chondromyxoid stroma is particularly characteristic in MGG

smears10. Red staining intercellular aggregates is present within

aggregates. Hyaline stromal globules have been noted in some cases.

26

Histopathology:

The dominant histologic feature is the heterogenecity of epithelial

elements and mesenchymal component24.In most of the case there is no

epithelial dysplasia or evident mitotic activity.

It is one of the matrix producing tumors -that includes adenoid

cystic carcinoma, basal cell adenoma/ adenocarcinoma and epithelial-

myoepithelial carcinoma9.

Nanda et al 2014 and cohen et al 2014 documented a higher

incidence of occurrence of pleomorphic adenoma in parotid gland.

Viguer et al199749 stated that sometimes metaplastic cells such as

oncocytic,sebaceous and squamous cells may be seen.

Neha Sikdar et al 20185 also observed plasmacytoid cells and

poorly cohesive clusters of epithelial cells in a fibromyxoid background.

Kotwal et al 2007 observed that smears containing myxoid stroma

was diagnosed as a case of pleomorphic adenoma. Excision of tumor

showed the picture of low grade mucoepidermoid carcinoma. Bland

intermediate cells were misdiagnosed as benign cells of pleomorphic

adenoma.

WARTHIN’S TUMOR

It is found exclusively in parotid gland and periparotid lymph

nodes24. It commonly affects males. It is often multicentric and bilateral.

Smokers have eight times the risk than nonsmokers.7

27

Patients usually present with a doughy painless mass that may

fluctuate in size13.


Aspirate is mucoid or murky fluid14.

There is presence of bland oncocytic cells in cohesive, monolayered

sheets and lymphoid cells in amorphous and granular debris background7.

The aspirate and mucous content stains blue with MGG.

Klijanienko and Vieil et al1997 suggested that mast cells are

commonly associated with oncocytes.

Differential diagnosis of lymphocyte - rich aspirates13

Intrinsic

Non-neoplastic:

Chronic sialadenitis,

Granulomatous sialadenitis

Lymphoepithelial sialadenitis

Lympho-epithelial cyst

Neoplastic:

Warthin’s tumor

Mucoepidermoid carcinoma


Malignant lymphoma

28

Extrinsic:

Non-neoplastic

Reactive lymph node hyperplasia

Neoplastic

Malignant lymphoma of nodal origin

Histopathology

Grossly it appears as lobulated brown mass with a typical

multicystic appearance, fluid filled spaces of dark brown fluid.

Microscopically, lymphoid tissue is prominent24. The lymphoid

stroma is composed of B lymphocytes, but it also contain T lymphocytes,

mast cells.

S-100 protein positive dendritic cells covering the surface of

lymphoid tissue are large epithelial cells with oncocytic features9,24.These

cells are arranged in two layers. The luminal cells are columnar and outer

cells are polygonal.

S V Ramana et al 2017 suggested that warthin’s tumor constitute

4.12% as per cytological diagnosis and 3.09% as per histological

diagnosis.

BASAL CELL ADENOMA

It usually occurs in parotid and within periparotid lymph nodes.

The condition has a slight predilection for females.24

29


Aspirates of the gland shows numerous basaloid epithelial cells,

both single and multi-layered clusters with occasional peripheral

palisading16,24.

Several architectural patterns solid, trabecular, tubular and

membranous are well distinguished in cytologic smears.

Kotwal M et al 2019suggested the distinguishing features between

basal cell adenoma and pleomorphic adenoma. Basal cell adenoma has the

characteristic amorphous ,homogenous stroma ,tightly cohesive cellular

sheets with a background showing naked nuclei.

Hood et al 2008 suggested that adenoid cystic carcinoma is the most

important differential diagnosis. Smears from the trabecular variant of

BCA contain hyaline globules resembling adenoid cystic carcinoma.

Histopathology

Grossly, the tumors are encapsulated and often cystic24.

Microscopically, they are composed of basaloid epithelial cells

arranged in many architectural patterns. Scattered ductular structure filled

with eosinophilic secretions are seen.

ONCOCYTOMA

The majority occur in parotid 24,normal lining cells of the ducts may

be seen.

30


It is characterised by cohesive , multi-layered aggregates of

oncocytic cells with small regular nuclei well defined cytoplasmic

borders with absence of fluid debris and lymphoid cells 13,14.

Nuclear pleomorphism and mitotic figures absent.

Differential diagnosis includes warthins tumor,diffuse oncocytosis

and acinic cell carcinoma13.Immunohistochemistry for DOG-1 and

SOX10 is positive in Acinic cell carcinoma but negative in oncocytoma.

O Dwyer et al 1986 suggested that cells with abundant cytoplasm

from Acinic cell carcinoma can be a differential diagnosis of oncocytoma.

Finfer et al 2007 considered oncocytoma to be cystic and its relationship

to warthin tumor uncertain.

Histopathology:

Monotonous large polygonal cells with well defined cell borders

deeply eosinophilic granular cytoplasm,small round nuclei. Occasionally,

cells undergo clear change as a result of cytoplasmic glycogenation24.

The lumen of glandular spaces contains psammoma bodies or

tyrosine rich crystals.

Cohen et al 2014 suggested that mucin containing cystic spaces is

not a typical feature of oncocytic adenoma and its occasional presence

should raise the suspicion of oncocytic variant of mucoepidermoid

carcinoma.

31

LIPOMA

Uncommon neoplasm of salivary gland representing about 0.5% of

tumors5.Usually present as a soft palpable nodule.


Lace like sheets of cells with single large clear vacuole filling the

cytoplasm small hyperchromatic nuclei displaced to the margin of

the cell.13

Background shows many lipid droplets.

Histopathology:

Mature adipose tissue mixed with acinar, ductal, basal and

myoepithelial cells of normal salivary gland. Also associated with duct

ectasia with fibrosis, prominent lymphoid aggregates with nodular

aggregates in stroma, oncocytic changes and sebaceous differentiation.

SCHWANOMMA


Moderate cellular smear composed of spindle shaped cells in

cohesive groups and clusters.

Individual cells have pale illdefined cytoplasm with small dark

elongated spindled nuclei .Background shows myxoid material.13

The most common differential diagnosis includes pleomorphic

adenoma and myoepithelioma.

32

Histopathology:

Spindle cells with palisading pattern with a thin fibrous capsule.

Residual gland is present in the centre of the tumor.

Immunohistochemistry with S-100 is positive.

LYMPHANGIOMA

Most common in children, presenting as a slowly growing

fluctuant mass.


Hypocellular smears with watery background showing scattered

mature appearing lymphocytes13.Non neoplastic salivary gland acini may

be present in the background at some instances.

Histopathology:

Large lymphatic channels in loose connective tissue stroma.

Disorganised smooth muscle in wall of larger channels. Peripheral

lymphoid aggregates associated with increased mast cells.

Immunohistochemistry with CD31, CD34, D2-40 is positive.

HEMANGIOMA

It is the most common benign mesenchymal tumor of salivary

gland. Juvenile hemangiomas are highly cellular.

33


Aspirates show groups of bland spindle-shaped to polygonal

endothelial cells, which form cord like structures13Background shows

scattered histiocytes.

Histopathology:

Anastomosing thin walled capillaries between the salivary duct and

acini. Variable mitotic figures, epithelioid or kaposiform patterns.Some

cases show microcalcification.

E.D.Rossi et al 2017 suggested that a salivary gland lesion is

classified as suspicious of malignancy when some, but not all criteria for

a specific diagnosis of malignancy are present and yet the overall

cytologic features are suggestive of malignancy.

MALIGNANT NEOPLASMS

MUCOEPIDERMOID CARCINOMA

It is the most common salivary gland malignancy. They represent

about 15% of salivary gland tumors. The MECT1-MAML2 fusion gene

play a key role in the genesis of the tumor24.


Smears of low cellularity in a dirty background of mucus and

debris. Cohesive clusters and sheets of epithelial cells and small streams

of cells within mucus.

34

Predominantly intermediate cells resembling squamous metaplastic

cells, some mucin secreting cells, infrequently differentiated squamous

epithelial cells. Keratinisation is not a feature .

Cohen et al 2014 suggested that cells are relatively bland nuclei,

prominent nucleoli seen in some cells.

Histopathology

Microscopically, mucin –producing, squamous and intermediate.

The intermediate cells are small, cuboidal with minimal eosinophilic

cytoplasm.24 In high grade tumors ,squamous and intermediate

predominate over mucin –producing cells. Morphologic variants include

oncocytic, sclerosing and eosinophilic infiltration.

The most common differential diagnosis of high grade MEC is with

either primary or secondary squamous cell carcinoma. A preceding

history of head and neck cutaneous SCC and the lack of mucin-positive

epithelial cells help in the differential diagnosis.

Neha sikdar et al 2018 suggested that High grade mucoepidermoid

carcinoma containing malignant squamous epithelial cells is difficult to

be distinguished from metastatic squamous cell carcinoma

ACINIC CELL CARCINOMA

It is the second most common salivary gland malignancy

comprising about 1-3% 24. There is a male predominance with a peak

incidence in fifth decade.

35

It most often presents as a mobile, soft to firm, well circumscribed

mass. Fixation to the surrounding tissues and facial nerve involvement are

considered poor prognosis and indicate high –grade transformation.


Smears shows pure population of acinar cells in a clean background

without ductal cells or stroma. Cells are arranged in clusters showing

abundant, fragile, finely vacuolated cytoplasm with rounded medium

sized nuclei. Variably cytoplasmic zymogen granules are seen which are

PAS positive diastase resistant.

Klijanienko and Vielh et al 1997 suggested that mild to moderate

anisokaryosis and bland chromatin can be seen.

S.Mehrotra et al 1998 suggested that Metastatic renal cell

carcinoma can resemble ACC and are differentiated with the help of

immunohistochemistry, clinical history and imaging studies.

Histopathology

Grossly, the tumor presents as encapsulated round mass with a solid

friable, grayish-white cut surface24. Microscopically, the pattern of growth

may be predominantly solid, microcystic, papillary or follicular. The most

characteristic cell acinar, has agranular basophilic cytoplasmic

appearance. When the clear cell predominates the tumor acquires a

hypernephroid appearance24.

36

Skalova et al 2004 reported that Mammary analogue secretory

carcinoma associated with specific translocation has a histologic identity

with acinic cell carcinoma

POLYMORPHOUS LOW GRADE ADENOCARCINOMA

It is an uncommon tumor of low grade malignancy occurring in

minor salivary glands, mainly the palate.


Smears show cells with mildly enlarged pale ovoid homogenous

nuclei arranged in clustered tissue fragments with trabecular pattern.

Hyaline stromal globules are often present.

Frierson et al 2000 reported that small basaloid epithelial cells

resembling ductal epithelium or metaplastic squamous cells are also seen

Histopathology

Grossly, it presents as an exophytic growth, can be ulcerated. It

constitutes a triad of infiltrative growth, multiple architectural growth

patterns cellular uniformity. The patterns may be cribriform, fascicular,

microcystic, mixed and papillary. The cells have only mild atypia with

uniform bland nuclei with prominent perineural invasion.

Gibbons et al 2011 suggested that the tumor exhibits a

morphological overlap with adenoid cystic carcinoma and cellular

pleomorphic adenoma.

37

ADENOID CYSTIC CARCINOMA

It is generally slow growing malignant neoplasm accounting for

about <10 % of salivary gland tumors. It has a female preponderance

presenting as a slow growing ,firm mass which is circumscribed or less

well defined.24

It has a remarkable capacity for recurrence. Grossly, it has a solid

appearance and an infiltrative pattern of growth.


It presents as various configuration –tubular, cribriform and solid

patterns. Smears show small uniform, basaloid cells with coarse

chromatin, round hyperchromatic nuclei. Sometimes show microcystic

sieve like spaces14,16. Hyaline spherical globules with adherent tumor

cells are characteristic. Mitosis and necrosis are uncommon.

Stewart et al 2000 quoted that adenoid cystic carcinoma constitute

about 2.32% of cases.

Histopathology

Microscopically it has a typical cribriform pattern-nests and

column of cells arranged concentrically around gland like spaces filled

with homogenous eosinophilic PAS positive material15,24. Small true

glandular lumina are also formed. These are surrounded by varying

amounts of myoepithelial cells with scant cytoplasm and hyperchromatic,

38

angulated nuclei. The tumor has a remarkable tendency for invasion of

perineural spaces. A majority of the tumors show positivity for CD117.24

Das et al 200459 suggested that pleomorphic adenoma usually is

misdiagnosed as adenoid cystic carcinoma due to the presence of hyaline

stromal globules. But the chondromyxoid stroma and foci of squamous

metaplasia is usually absent.

Postema et al 2004 suggested that polymorphous low grade

carcinoma is an important differential diagnosis, but the nuclei of adenoid

cystic carcinoma tend to be hyperchromatic and angulated rather than

bland and uniform of the former.

Differential diagnosis of hyaline globules:

Basal cell adenoma, Basal cell adenocarcinoma

Polymorphous low grade adenocarcinoma

Epithelial-myoepithelial carcinoma

Basaloid squamous cell carcinoma

EPITHELIAL-MYOEPITHELIAL CARCINOMA

It is a rare entity, low grade tumor with epithelial and myoepithelial

component. Constitutes about 0.5% of tumors. Also known as glycogen

rich adenoma. It is a disease of older individuals in the 6th decade

with no gender predilection. Patients usually present as localized

slow –growing mass.

39


Arrangement of bland cells in pseudopapillary groups, sheets and

3-dimensional groups.Smears show a biphasic population of clustered

small epithelial cells and less cohesive myoepithelial cells with pale

fragile cytoplasm and large vesicular nuclei showing mild to moderate

nuclear enlargement and variation.

Biphasic nature of the tumor is appreciated by immunostaining with

HMW keratin and myoepithelial markers-P63, smooth muscle keratin

and calponin.

Carrilo et al 2009 reported that cell aggregates in trabecular pattern

with strands of fibrous stroma are seen

Differential diagnosis of tumors with basaloid morphology:

Benign

Cellular pleomorphic adenoma, basal cell adenoma

Canalicular adenoma, myoepithelioma

Malignant

Basal cell adenocarcinoma, Epithelial-Myoepithelial carcinoma

Polymorphous low grade carcinoma, Adenoid cystic carcinoma

40

Histopathology

Grossly, well delineated, firm, infiltration into adjacent tissue.

Microscopically, there are ducts or tubules with an outer rim of

myoepithelial cells and inner, dark ductal cells with scant eosinophilic

cytoplasm and round bland nuclei24.Also islands, nests or sheets of spindle

cells, plasmacytoid cells are seen.

Dedifferentiated variant -atypia in >20 % of cells, no myoepithelial

differentiation, elderly age group, aggressive behaviour, extraglandular

and metastatic extension.

Kocjan et al 2006suggested that variable mitotic activity, ancient

changes, sebaceous features and verocay like changes are seen.

CARCINOMA EX PLEOMORPHIC ADENOMA

This is an uncommon event constituting to occur about 3-4% of

pleomorphic adenoma9.The patient usually gives a history of long

standing mass with sudden imcrease in size of tumor24.

Most of the patients have facial nerve palsy or skin involvement .

It is more common in women. Mostly carcinoma ex pleomorphic

adenoma is a salivary duct carcinoma or a poorly differentiated carcinoma

of no specific type.

41


A dual population of malignant epithelial cells and benign cells.

Malignant cluster shows prominent nuclear enlargement and atypia.

Stromal component of pleomorphic adenoma is present.

In addition ,FNAC cannot distinguish between widely invasive and

non-invasive forms and therefore clinical and radiological correlation

is essential.

Postema et al 2004 suggested that an unqualified malignant

diagnosis may lead to unnecessary surgical management and so clinical

correlation is always essential.

Histopathology

Grossly , it appears as an encapsulated ,widely infiltrative tumor

with areas of haemorrhage and necrosis. Microscopically, abrupt

transition from benign tumor (usually pleomorphic adenoma) often

adenocarcinoma, myoepithelial, salivary duct, undifferentiated with

benign stroma.

Extensive infiltration with marked atypia, necrosis, mitotic figures,

perineural and vascular invasion. Benign pleomorphic adenoma may

occasionally show hyalinisation and hypocellularity.

Klijaneiko, El-Naggar and Vielh 1999 found that carcinoma ex

pleomorphic adenoma have the highest false negative rate.

42

Verma and Kapila et al2002 conclude that all cases of carcinoma

ex pleomorphic adenoma in histology was misinterpreted as benign

in histology.

Cohen et al 2014 suggested that it is necessary to obtain more

representative samples from this type of tumor.

SALIVARY DUCT CARCINOMA

It is a high grade malignancy that resembles high grade ductal

carcinoma in situ constituting about 10% of malignant tumors. It is the

most common carcinoma seen in carcinoma ex pleomorphic adenoma24.

It presents as a rapidly growing neck mass associated with facial

pain and weakness. The tumor has poor prognosis.


Smear shows malignant epithelial cells sheets, three dimensional

crowded and cribriform groups. Individual cells are large,with abundant

cytoplasm and pleomorphic hyperchromatic nuclei.13,16

Occasionally squamoid and oncocytic cells are seen. No stromal

component seen. Background shows necrotic debris .Metastasis is

frequent.

S.Mehrotra et al 2007 suggested that high –grade mucoepidermoid

carcinoma, oncocytic carcinoma and metastatic carcinoma from breast,

prostate or lung are the differential diagnosis to the tumor.

43

Histopathology

Tumors typically have ill defined borders but are usually well

circumscribed. Cut surface is heterogenous with evidence of necrosis.

Microscopically, malignant cells arranged in cords,nests and cribriform

glands in desmoplastic stroma. Individual cells are large with ample

eosinophlic cytoplasm and pleomorphic hyperchromatic nuclei. Insitu

component shows central necrosis.

Voker et al 2010 reported that high grade mucoepidermoid

carcinoma is challenging to differentiate from mucinous variant.

HEMATOLYMPHOID TUMORS

Primary salivary gland Non – Hodgkin’s lymphoma constitute 2-

6% of salivary gland neoplasms. Extranodal marginal zone B-cell

lymphoma of MALT type is the most common subtype.24


Cellular aspirate composed of polymorphous population of small to

intermediate size lymphocytes, monocytoid B cells, immunoblasts,

lymphoplasmacytic cells and plasma cells.13 Lymphohistiocytic

aggregates and tingible body macrophages are present16.

In cases of high grade lymphomas, large atypical lymphoid cells >

2 times the size of mature lymphocytes are seen.

44

Cytological distinction between lymphoepithelial sialadenitis and

low grade lymphomas is difficult and hence flow cytometry and other

means of immunophenotypic analysis is necessary16 .

Histopathology:

Monocytoid cells surround ducts-low grade B cells .May have

amyloid deposits, transformation to diffuse large B cell lymphoma.

SECONDARY MALIGNANT TUMORS

Squamous cell carcinoma is the most common tumor metastatic to

salivary gland. The parotid gland,in particular intraparotid and periparotid

lymph nodes is involved 20 times more than submandibular

gland.16Almost 80% of the metastatic tumors are from head and neck

particularly cutaneous carcinomas of face and scalp.


Aspirates are cellular and include atypical squamous cells and

keratin debris in a necrotic background14. Some cases show a cystic

background.

Aspirates of metastatic melanoma show a population of

dyscohesive pleomorphic cells with eccentric nuclei, prominent nucleoli

and granular pigment in the cytoplasm. Intra nuclear inclusions are a

common finding.

45

Histopathology:

Features of squamous cell carcinoma associated with perineural

invasion and clear cell change.Immunohistochemistry with ck 7, ck13,

ck14 and ck19 is positive.

Salivary gland FNAC performance shows a varied range of

sensitivities and specificities depending on a variety of factors including:

quality of cytologic preparations, technical experience of the operator

doing FNAC, morphologic heterogenecity of the lesion, presence of

cystic component and experience of evaluating cytopathologist.

The challenges posted by inherent complexity of salivary gland

FNAC are further complicated by the lack of a standardized, tiered

diagnostic framework by which reporting is performed.

The reporting system should emphasize risk stratification rather

than specific diagnosis, providing the range of management for each risk

category rather than a binary benign or malignant assessment for every

individual case.

MATERIALS & METHODS

46

MATERIALS AND METHODS

All major salivary gland lesions were included in the study. Patients

age, clinical history, ultrasonogram findings were recorded.

STUDY PLACE:

Department of Pathology, Coimbatore Medical College hospital,

Coimbatore.

STUDY DESIGN:

This study includes a total of 45 fine needle aspirates obtained

prospectively from patients who visit our pathology department with

various major salivary gland disorders .

STUDY PERIOD : August 2018-July 2019

Inclusion criteria:

Aspirate from all salivary gland lesions and corresponding

histopathological specimens

Exclusion criteria:

Smears with low cellularity

Hypocellular smear

Smears obscured by blood ,mucus and inflammatory cells.

Inadequate specimen

DATA COLLECTION:

Both male and female patients with clinical and radiological

findings. Informed Consent was obtained from the patient.

47

METHODOLOGY AND TECHNIQUE USED:

FNAC was performed using 23-24gauge needle and 10 ml syringe

applying negative pressure. Smears were either wet fixed or air fixed and

stained by Hematoxylin and Eosin & Giemsa respectively. The

histopathological specimens were fixed overnight in 10 percent formalin

and subjected to gross examination, processing, paraffin embedding ,

section cutting staining by Hematoxylin and eosin ,mounting by DPX.

HEMATOXYLIN AND EOSIN STAINING

1. Fix in isopropyl alcohol – 20 minutes

2. Hematoxylin – 5 minutes

3. Blueing in tap water – 10 minutes

4. Eosin – 3 dips

5. Rinse in tap water

6. Dry, Xylene,Mount with DPX

MAYGRUNWALD GIEMSA STAIN

It is a mixture of two neutral stains .May Grunwald stain is

composed of an acidic stain (eosin) and a basic stain (methylene blue)

Giemsa stain is composed of eosin and metachromatic stain.

PROCEDURE:

1. Smears are air dried

2. May grunwald stain for 2 min

3. Blueing for 5 minutes

48

4. Giemsa stain for 3 minutes

5. Blueing for 5 minutes

6. Dry , xylene, DPX mount

Advantages of MGG staining:

1. Cell morphology is well preserved.

2. Cytoplasmic details are suboptimal.

3. Nuclear characteristic of crisp chromatin is better appreciated.

4. Air-drying artifacts are less compared to wet fixed smears.

5. Overall staining is good.

RESULTS

49

RESULTS AND ANALYSIS

Table 1: Age wise Distribution of lesions of salivary gland

The present study includes the age group from 15– 70 years

.Maximum number of cases are in the age group 41 -50 years.

AGE

(In years)

CASES

NO %

Up to 20 years 1 2.2%

21-30 years 3 6.7%

31-40 years 8 17.8%

41-50 years 14 31.1%

51-60 11 24.4%

>60 8 17.8%

Total 45 100%

Range 15 -70 years

Mean 47.7 years

S.D 11.9 years

50

Fig 1: Distribution of cases based on age groups

1

3

8

14

11

8

2.2

6.7

17.8

31.1

24.4

17.8

0

5

10

15

20

25

30

35

<20 yrs 21-30 31-40 41-50 51-60 >60

No

Percent

No of Cases

Percentage

51

Table 2: Gender wise distribution of lesions of salivary gland

GENDER NO OF CASES PERCENTAGE

MALE 27 60%

FEMALE 18 40%

TOTAL 45 100%

The present study shows a predominance of males constituting

about 60% of the cases.

Fig 2: Gender wise distribution of cases

60%

40%MALE

FEMALE

52

Table 3: Distribution of cases based on clinical diagnosis

Based on clinical findings, clinical diagnosis was made in all 45

cases. Impression obtained was that incidence of non –neoplastic and

benign lesions were higher (98.2%) than malignant (1.8%).

Fig 3: Distribution of cases based on clinical diagnosis

CLINICAL

DIAGNOSIS

Cases

No %

Non –neoplastic lesions 14 31.2%

Pleomorphic adenoma 28 62.2%

Malignant lesions 3 6.6%

Total 45 100%

62%

31%

7%

Pleomorphic adenoma

Non neoplastic

Malignant

53

Table 4: Distribution of cases based on duration of lesion

The present study is consistent with the finding that patients

with malignant neoplasm having long duration .

DURATION

Cases

No %

1 month 9 20.0%

2 months 15 33.3%

3 months 13 28.9%

4 months 2 4.4%

5 months 4 8.9%

6 months 2 4.4%

TOTAL 45 100.0%

54

Fig 4: Distribution of cases based on duration of lesions

20%

33.3%

28.9%

4.4%

8.9%

4.4%

1 months

2 months

3 months

4 months

5 months

6 months

55

Table 5: Distribution of cases based on size of the lesion

The study includes cases with size of the swelling ranging from 3-

6 cm. The most common being 4 cm constituting about 49%.

Fig 5: Distribution of cases based on size of the lesion

49%

24%

23%

4%

4 cm 5 cm 3 cm 6 cm

SIZE OF THE LESION

Cases

No %

3cm 10 22.2 %

4 cm 22 48.9%

5 cm 11 24.4%

6 cm 2 4.4%

TOTAL 45 100.0

56

Table 6: Distribution of cases based on consistency

The lesions were firm in majority of the cases contributing to

78%

Doughy consistency was noted in 8 cases, proved to be

warthin’s tumor in histopathology.

Fig 6: Distribution of cases based on consistency of lesion

20%

78%

2

Doughy

Firm

Hard

CONSISTENCY

Cases

No %

Doughy 8 17.8%

Firm 35 77.8%

Hard 2 4.4%

Total 45 100%

57

Table 7: Distribution of cases based on Location of lesion

The frequency of salivary gland lesions in parotid , submandibular

in the present study was 60% and 40% respectively. Parotid gland is the

most common involved gland which is consistent with other studies too.

Fig 7: Distribution of cases based on location

60%

40%Parotid

Sub mandibular

LOCATION

Cases

No %

Parotid 27 60%

Sub mandibular 18 40.0%

Total 45 100%

58

Table 8: Distribution of neoplastic lesions according to

histopathological diagnosis and site of location

HISTOPATHOLOGY

DIAGNOSIS

Total cases

Parotid Submandibular

No No

PA – Pleomorphic adenoma 17 11 6

WT – Warthin’s tumor

8 8 0

MEC – Mucoepidermoid

Carcinoma

7 5 2

Oncocytoma&

myoepithelioma

3 2 1

SD CA – Salivary Duct

Carcinoma

1 1 0

TOTAL 36 27 9

59

Table 9: Distribution of cases based on Cellularity

CELLULARITY

Cases

No %

Highly Cellular 35 77.8%

Moderately Cellular 10 22.2%

Total 45 100%

The present study showed high cellularity in most of the cases

constituting about 78%.

Fig 8: Distribution of cases based on cellularity

78%

22%

Highly cellular

Moderately cellular

60

Table 10: Cytological diagnosis of salivary gland lesions

Among the benign neoplastic lesions ,pleomorphic adenoma was

the most common constituting about 36%.

Mucoepidermoid carcinoma is the most common malignant

neoplasm constituting about 3%.

CYTOLOGY DIAGNOSIS

Cases

No %


Warthin’s tumor 8 17.8%

Inflammatory Lesion 1 2.2%

Chronic Sialadenitis 8 17.8%

Lymphoepithelial Cyst 4 8.9%

Mucoepidermoid Carcinoma 1 2.2%

Salivary Duct Carcinoma 1 2.2%

Pleomorphic adenoma /

Mucoepidermoid Carcinoma

4 8.9%

Warthin’s tumor / Mucoepidermoid

Carcinoma

2 4.4%

TOTAL 45 100%

61

Fig 9: Distribution of cases based on Cytologic diagnosis

36%

18%2%

18%

9%

2%

2%

9%

4%

PPleomorphic adenoma Warthin’ tumor

Inflammatory Lesion Chronic Sialadenitis

Lymphoepithelial Cyst Mucoepidermoid Carcinoma

Salivary Duct Carcinoma Pleomorphic adenoma / Mucoepidermoid Carcinoma

Warthin’ tumor / Mucoepidermoid Carcinoma

Warthin's tumorPleomorphic adenoma

62

Table 11: Cytological categorization of lesions

In the present study, non –neoplastic lesions constitute about 27%.

Benign neoplasm constitute about 69% of the total cases.

Malignant neoplasm is the least common neoplasm about 4%

CYTOLOGY DIAGNOSIS

Case

No %

Benign 31 68.9%

Malignant 2 4.4%

Non neoplastic lesions 12 26.7%

Total 45 100%

63

Table 12: Histopathological Diagnosis of lesion

In the present study ,pleomorphic adenoma is the most common

benign neoplasm Constituting about about 42%.

Mucoepidermoid carcinoma is the most common malignant

neoplasm constituting about 14%.

HISTOPATHOLOGY

DIAGNOSIS

Cases

No %


Warthin’s tumor 8 17.8%

Myoepithelioma 2 2.2%

Chronic Sialadenitis 8 15.6%

Lymphoepithelial Cyst 1 2.2%

Mucoepidermoid Carcinoma 7 13.3%

Oncocytoma 1 2.2%

Salivary Duct Carcinoma 1 4.4%

TOTAL 45 100%

64

Fig 10: Distribution of cases based on Histopathological diagnosis

42%

18%

2%

16%

2%

13%

2%

5% PA – Pleomorphic adenoma

WT – Warthin’ tumor

INF – Inflammatory Lesion

CH SA – Chronic Sialadenitis

LE CYST – Lymphoepithelial

Cyst

MUCA – Mucoepidermoid

Carcinoma

Oncocytoma

SD CA – Salivary Duct

Carcinoma

Warthin’s tumor

65

Table 13: Histopathological categorization of lesions

In the present study , the non neoplastic lesions constitute about

20%.Most common benign neoplasm constitute about 62%. Malignant

neoplasm are the least common being 18%.

HISTOPATHOLOGY

DIAGNOSIS

Cases

No %

Benign 28 62.2%

Malignant 8 17.8%

Non neoplastic lesions 9 20.0%

Total 45 100%

66

Table 14:Cytohistolopathological correlation

HISTOPATHOLOGICAL DIAGNOSIS

CYTOLOGY

DIAGNOSIS

N0 OF

CASES

Ple

om

orp

hic

ad

en

om

a

Warth

ins

tu

mor

Myoep

ith

eli

om

a

Ch

ron

ic

Sia

lad

en

itis

L

ym

ph

oep

ith

eli

al

Cyst

Mu

coep

iderm

oid

Carcin

om

a

Sali

vary D

uct

Carcin

om

a

On

cocyto

ma

Pleomorphic

adenoma 16 14 2

Warthin’s tumor 8 5 2 1

Inflammatory

Lesion 1 1

Chronic

Sialadenitis 8 3 5

Cystic lesion 4 3 1

Mucoepidermoid

Carcinomo 1 1

Salivary Duct

Carcinoma 1 1

Oncocytoma

Pleomorphic

adenoma /

Mucoepidermoid

Carcinoma

4 4

Warthin’ tumor /

Mucoepidermoid

Carcinoma

2 2

TOTAL 45 17 8 2 8 1 7 1 1

67

Table 15: Diagnostic accuracy in benign neoplastic lesions of

salivary gland

FNAC

HPE

TOTAL

+ -

+ 24 0 24

- 4 8 12

TOTAL 28 8 36

TRUE

POSITIVES

24 SENSITIVITY 85%

FALSE

POSITIVES

0 SPECIFICITY 100%

TRUE

NEGATIVES

4 PPV 100%

FALSE

NEGATIVES

8 NPV 66%

[PPV-Positive predictive value, NPV –Negative predictive value]

The diagnostic accuracy of benign lesions was predicted to be 85%.

68

Table 16: Diagnostic accuracy in malignant neoplastic lesions of

salivary gland

FNAC HPE

TOTAL + -

+ 7 0 7

- 1 28 29

TOTAL 8 28 36

TRUE

POSITIVES 7 SENSITIVITY 87.5%

FALSE

POSITIVES 0 SPECIFICITY 100%

TRUE

NEGATIVES 1 PPV 100%

FALSE

NEGATIVES 28 NPV 96.5%

[PPV-Positive predictive value, NPV –Negative predictive value]

The diagnostic accuracy of malignant lesions was predicted to be

87.5%.

69

PEARSON Chi-square test with 2 x 2 contigency table was used to

calculate p-value to ascertain statistical significance. Probability (p)

values less than 0.05 were considered statistically significant.

Table 17 : COMPARISON OF CONSISTENCY

BENIGN Vs MALIGNANT

The table shows a statistically significant relationship between

consistency of lesion and Benign vs Malignant.

Sex

Benign Malignant

Total P value

No % No %

Doughy 8 0 8

<0.05*(S)

Firm 20 6 26

Hard 0 2 2

Total 28 8 36 100

70

Table 18 : Comparison of site of Lesion Benign vs Malignant

The table shows a statistically significant relationship between

site of lesion and Benign vs Malignant.

Table 19: Comparison of Cellulary – Benign vs Malignant

The table shows a statistically significant relationship between cellularity

of lesion and Benign vs Malignant

Sex

Benign Malignant Total P value

No % No %

<0.05*(S)

Parotid 17 7 24

Submandibular 11 1 12

Total 28 8 36 100

Sex

Benign Malignant Total P value

No % No %

<0.05*

(S)

Moderate 26 0 26

High 02 8 10

Total 28 8 36 100

COLOUR PLATES

FIG 1 : CYTOLOGY - H&E SIALADENOSIS (40X)

FIG 2 : CYTOLOGY - H&E LYMPHOEPITHELIAL CYST (40X)

FIG 3: CYTOLOGY - H&E CHRONIC SIALADENITIS (40X)

FIG 4 : HPE - H&E CHRONIC SIALADENITIS (40X)

FIG 5: CYTOLOGY - MGG PLEOMORPHIC ADENOMA (40X)

FIG 6 : HPE - H&E PLEOMORPHIC ADENOMA (40X)

FIG 7: CYTOLOGY- H&E WARTHIN’S TUMOUR (40X)

FIG 8 : HPE - H&E WARTHIN’S TUMOUR

FIG 9 : CYTOLOGY - MGG MONOMORPHIC ADENOMA (40X)

FIG 10: CYTOLOGY - MGG MUCOEPIDERMOID CARCINOMA (100X)

FIG 11 : HPE - MUCOEPIDERMOID CARCINOMA (40X)

FIG 12 : HPE - ADENOID CYSTIC CARCINOMA (40X)

FIG 13: CYTOLOGY- H&E SALIVARY DUCT CARCINOMA (100X)

DISCUSSION

71

DISCUSSION

Major Salivary gland lesions are common and the associated

histopathology is extremely varied and complex due to the presence of

non neoplastic lesions, epithelial and non-epithelial neoplasms, metastatic

tumors and lymphomas.

Though the typical morphology of most salivary gland lesions are

predictable, many confounding factors make FNAC smears difficult to

interpret. Cytomorphology alone is not sufficient to conclude salivary

gland malignancies. Further, some salivary gland malignancies can only

be differentiated from its benign counterpart by the presence of capsular

invasion which is not possible by FNAC.

Patients referred for FNAC may complain of a palpable mass with

or without pain in the head and neck region, or some cases present with

partial paralysis or paresthesia commonly involving the facial nerve. The

mass may be palpated by a clinician or detected on imaging studies.

Occasionally, the clinician may send the patients who do not have a

palpable or radiologically detectable mass. FNAC should be discouraged

in these instances as there are many chances of false negative diagnosis.

Rapid on site evaluation is recommended wherever possible

because an immediate assessment of adequacy can be made, reducing the

need for repeat FNAC procedures and facilitating the triage of material

for cell blocks, flow cytometry and ancillary studies.

72

Clinical examination should not be ignored in salivary gland

lesions, because the cytological results are useful in both surgical planning

and patient counselling. Preoperative knowledge of the malignant nature

of the tumor may modify the postoperative course.

Prior to the procedure, the cytopathologist should have information

on the clinical features including duration, associated pain , facial

paralysis and cervical lymphadenopathy for accurate interpretation.

Fine needle aspiration have some disadvantages like bleeding,

squamous metaplasia, fibrosis and necrosis in the final histopathological

examination. But, it is accepted that these complications do exist which

usually, do not interfere with the final diagnosis.

FNAC smears are interpreted in five categories:

I. Non-diagnostic: Insufficient acellular or hypocellular material

or elements of peripheral blood.

II. Non-neoplastic lesions

III. Benign neoplastic lesions:

IV. Suspicious for malignancy : Although the result was

suggestive for neoplasm, the accurate differentiation between

benign and malignant disease was not possible.

V. Positive for malignancy: Presence of accurate malignant

findings.

73

I. NON DIAGNOSTIC CATEGORY

Includes cases with< 60 lesional cells

Non-neoplastic normal salivart gland elements in the setting of

clinically or radiologically illdefined mass

Non-mucous cyst fluid without epithelial component

II. NON NEOPLASTIC CATEGORY

Among the non neoplastic category 2 cases of sialadenosis was

reported showing clusters of large vacuolated acinar cells. But clinical

correlation was not available for interpretation.

Christensen et al 2016 suggested that in cases of sialadenosis numerous

acinar cells with architectural arrangement should not be confused with

well differentiated acinic cell carcinoma.

Differential diagnosis of sialadenosis include accessory parotid

gland hamartoma, lipomatosis and sialolithiasis.

Sialadenitis occupies around 20% cases being the most common non-

neoplastic lesion and histopathological correlation is accurate in 50 %

cases. In 4 cases submandibular gland was involved and in 2 cases

parotid gland was involved.

Joshi AR et al35 2017 reported about 21.9 % cases of chronic sialadenitis.

Sharma M et al11 2015 reported around 12.5% of cases of chronic

sialadenitis.

74

In the present study 3 cases reported as chronic sialadenitis was

proved to be warthin’s tumor in histopathology.

W.C.Faquin et al 2015 suggested that the common pitfall in chronic

sialadenitis is the misinterpretation of metaplastic or atrophic ductal cells

as a basaloid neoplasm . In contrast , chronic sialadenitis lacks the three

dimensional epithelial groups and degree of cellularity found in aspirates

of a basaloid neoplasm.

In the present study about 2 cases of lymphoepithelial cyst is reported in

cytology showing a mixed population of lymphocytes and plasma cells.

III. BENIGN CATEGORY:

Among the benign lesions pleomorphic adenoma is the most

common lesion and constitute about 42.2 % of cases. This data is similar

to the observations made by many authors.

Kakoty et al23 2017 reported an incidence of 44% of cases and

Sharma et al11 (2015)reported an incidence of 68.7% of the total cases of

pleomorphic adenoma.

The present study showed a diagnostic accuracy of 84 % for

pleomorphic adenoma and 62 % for warthin’s tumor cases, Which were

significantly better than that observed in the Malaysian J Pathol 20179

reported a diagnostic accuracy of 76% of the total cases.

In the present study about 4 cases given a differential diagnosis of

pleomorphic adenoma / low grade mucoepidermoid carcinoma is proved

75

to be mucoepidermoid in histopathology. The potential pitfall occurs

when the matrix is thin and mucoid along with bland epithelial cells. This

is particularly challenging in the presence of squamous or mucinous

metaplastic cells.

The following points offer a valuable guide line (i) intermediate cell

population is the counterpart and closely resembles myoepithelial cells of

pleomorphic adenoma. (ii)Myxochondroid and fibrillary stroma is absent

in MEC. (iii)Squamous differentiation in pleomorphic adenoma show

keratinisation, which is less evident in MEC. (iv) Plasmacytoid cells,

have not been described in MEC is a good marker for adenoma.

Swati Sahni et al 12017 had an interpretation difficulty in few case of

pleomorphic adenoma harbouring mucin making a potential trap leading

to erroneous diagnosis of mucoepidermoid carcinoma.

Kakoty S et al 201723 suggested that ,the presence of goblet cells or

squamous metaplasia in pleomorphic adenoma should be approached

cautiously as it could be low grade mucoepidermoid carcinoma.

Baloch et al 2014 stated that it is also important to exclude adenoid cystic

carcinoma in the differential diagnosis when faced with matrix producing

tumor.

In the present study 2 cases of pleomorphic adenoma is proved to

be myoepithelioma in histopathology. While myoepithelioma and cellular

adenoma are consistent in the differential diagnosis when myoepithelial

76

cells have clear cytoplasm the diagnostic consideration include

epithelial-myoepithelial carcinoma, sebaceous adenoma, myoepithelial

carcinoma and even metastasis.

In the present study, about 2 cases reported with differential

diagnosis of warthin’stumor /mucoepidermoid carcinoma was proved to

be mucoepidermoid in histopathology.

Swati Sahni et al 12017 reported that predominance of lymphoid cells in

cases of warthin’s tumor may lead to a misdiagnosis of lymphoepithelial

cyst.

Collela et al 2015 reported that other than warthin tumor , acinic cell

carcinoma,which often has a lymphocyte rich stroma, malignant

lymphoma, chronic sialadenitis,lymphoepithelial cyst and benign

lymphoepithelial lesions may result in misdiagnosis.

Another case of warthin’s tumor is proved to be oncocytona in

histopathology. Oncocytomas consists of epithelial cells only and lack the

dirty cystic background.

Oncocytic features can be an accompanying finding in many

salivary gland neoplasms like myoepithelioma,mucoepidermoid

carcinoma and even pleomorphic adenoma.

All cases of warthin’s tumor should be distinguished from intra

parotid lymph nodes ,lymphoepithelial sialadenitis, lymphoepithelial cyst

77

and oncocytoma. Lymphoepithelial sialadenitis lacks the oncocytic

epithelium and dirty cystic debris.

A case of granulomatous lesion involving parotid gland was

reported which showed groups of epithelioid histiocytes, multinucleated

giant cells along with inflammatory cells but histopathological correlation

could not be made.

Mihashi et al 2015 suggested that in case with marked granulomas care

should be taken to avoid the misinterpretation of epithelioid histiocytes

with moderate eosinophilic cytoplasm, curved nuclei as an epithelial

neoplasm.

IV. SUSPICIOUS FOR MALIGNANCY

In 2 cases the FNAC diagnosis was broadly given as cystic lesion

and a possibility of cystic degeneration was suggested.On follow up, the

2 cases were diagnosed as low grade mucoepidermoid carcinoma on

histopathology.

V. MALIGNANCY

Among the malignant lesions, mucoepidermoid was the most

common constituting about 14% of cases. Similar observations were

reported by Sharma M et al 2017, Yogambal et al 20156,Kakoty S et al

201723, S V Ramana et al 42017 . It has a diagnostic accuracy of 66%

which is significantly more than other studies.

78

Overall malignancy was more common in parotid (7 cases) 20% as

compared. with submandibular gland (1case) 3%.

1 case of salivary duct carcinoma on cytology was later confirmed

by histopathology. Tessy PJ et al38 2015 suggested that distinction from

high grade metastasis to salivary gland from primary elsewhere is of

critical importance in these cases.

The present study confirms the increased incidence of benign

neoplastic lesions compared to its malignant counterpart. In the study

there was almost perfect agreement between the cytological and

histological diagnosis and a fairly good accuracy. Some of the common

salivary gland lesions like various cysts, basal cell adenoma, Acinic cell

carcinoma, Adenoid cystic carcinoma, Epithelial-myoepithelial

carcinoma were not encountered in the present study as it had a limitation

period of one year inspite of an effective study population.

SUMMARY

79

SUMMARY

This prospective study was carried over a period of 12 months, in

the Department of pathology, Coimbatore Medical College. The study

included 45 cases of aspirates from major salivary gland lesions.

Among 45 cases, Cytologic distribution were 12 cases (23%) as

non-neoplastic,31 case (68%) as benign lesions and 2 cases (4%) as

malignant lesions.

Among 45 cases, histopathological confirmation showed 9

cases(20%)as non-neoplastic, 28 cases (62%) as benign lesions ,8 cases

(18%) as malignant.

We found a good concordance between FNAC and final histology.

The high sensitivity, specificity and diagnostic accuracy of FNAC

confirms its significant role in association with radiological and clinical

findings to provide the best initial assessment which in turn guide the

management options.

Multiple sampling from various sites helps to avoid

misinterpretation by concluding it by a type specific diagnosis. The most

common lesion in cytology and histology was found to be pleomorphic

adenoma with a high sensitivity and specificity and hence can be used as

a screening of all salivary gland tumors for better therapeutic approach.

In our study there is a statistically significant relationship between

consistency, site and cellularity of lesion for benign and malignant tumors.

CONCLUSION

80

CONCLUSION

The present study confirms the usefulness of FNAC as a safe and

economic procedure in distinguishing benign and malignant salivary

gland lesions which are of utmost value in planning the further

management of the patient. Thus FNAC and Histopathology

complemented each other for the diagnosis to be infalliable and accurate

for further management.

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ANNEXURES

PROFORMA

Name : IP/OP No :

Age : FNAC No :

Sex :

Presenting complaints:

Salivary gland swelling

Duration

Pain

Difficulty in swallowing

Past history:

History of previous surgery \ FNAC

History of any drug intake

Family history :

Personal history:

General Examination:

Pallor ,Lymphadenopathy

Icterus ,Cyanosis

Clubbing ,Oedema

Pulse rate :

Blood pressure :

Respiratory rate:

Systemic examination: RS ,CVS ,Per abdomen

Investigations:

Complete blood count

Ultrasound findings (if available)

Examination of salivary gland:

Clinical diagnosis

Nature of aspirate:

FNAC diagnosis:

ஒப்புதல் படிவம்

எனது உமிழ் நீர் சுரப்பி கட்டியில் சிறு ஊசி பபோட்டு திசு பரிபசோதனன

சசய்து சகோள்ள சம்மதம்

னகசயோப்பம் / னகபரனக

KEY TO MASTER CHART

FNAC - Fine needle aspiration cytology

HPE - Histopathological examination

CLINICAL DIAGNOSIS:

PA - Pleomorphic adenoma

INF - Inflammatory lesions

DURATION:

M - Month

SIZE OF SWELLING :

CM - Centimetre

LOCATION:

P - Parotid

SM - Submandibular

CELLULARITY:

M - Moderate

H - High

FNAC / HPE DIAGNOSIS:

PA – Pleomorphic adenoma

WT – Warthin’ tumor

INF – Inflammatory Lesion

CH SA – Chronic Sialadenitis

LE CYST – Lymphoepithelial Cyst

ME - Myoepthelioma

MUCA – Mucoepidermoid Carcinoma

OC – Oncocytoma

SD CA – Salivary Duct Carcinoma

Sl.No

.N

AM

EA

GE

SEXID

no

.

CLIN

ICA

L

DIA

GN

OSIS

DU

RA

TION

SIZE OF

THE

SWELLIN

GC

ON

SISTENC

YLO

CA

TION

FNA

C N

O

CELLU

LA

RITY

FNA

C D

IAG

NO

SISH

PE N

OH

PE D

IAG

NO

SIS

1M

ani

43M

4321

PA

1M5

CM

FIRM

Paro

tidF5

8/18

MP

A3

42/1

8P

A

2SA

THISH

35M

4842

INF

1M4

CM

FIRM

SMF9

5/18

MC

YSTIC

418

/18

PA

3M

AR

IYA42

F14

3P

A6M

6C

MH

AR

DP

arotid

F10

2/18

HW

T6

58/1

8SD

CA

4V

IJAY

25M

214

PA

2M4

CM

FIRM

SMF3

70/1

8M

PA

827

/18

PA

5SEN

IN45

M65

8P

A1M

5C

MD

OU

GH

YP

arotid

F45

6/18

MW

T1

11

7/18

WT

6R

ATIN

AM

50M

898

INF

1M3

CM

HA

RD

Paro

tidF1

212

/18

HSD

CA

21

36/1

8SD

CA

7K

AR

UP

AN

55M

3411

PA

2M6

CM

DO

UG

HY

Paro

tidF1

407

/18

HW

T2

54

5/18

WT

8P

RA

DEEP

24M

3921

PA

1M3

CM

FIRM

Paro

tidF1

503

/18

MM

A2

56

6/18

CH

SA

9A

RA

THA

L55

F571

2P

A1M

3C

MFIR

MSM

F13

53/1

8M

INF

25

12/1

8C

H SA

10

KA

NA

GA

46F

6450

PA

3M5

CM

FIRM

paro

tidF1

454

/18

HP

A/M

UC

A2

66

8/18

MU

CA

11

BA

NN

AR

I54

M621

0IN

F2M

5C

MD

OU

GH

YP

arotid

F12

56/1

8M

CH

SA2

31

3/18

WT

12

RA

JAN

44M

8430

PA

1M4

CM

FIRM

SMF1

151

/18

MC

YSTIC

23

11/1

8P

A

13

PR

AB

HA

53F

1120

0IN

F1M

3C

MFIR

MP

arotid

F12

83/1

8M

CYSTIC

2

24

2/18

LE CYST

14

PA

RA

MESH

WA

RI

35F

1387

0P

A2M

4C

MFIR

MSM

F20

49/1

8M

PA

35

07/1

8M

E

15

LAK

SHM

I52

F15

600

PA

6M5

CM

FIRM

Paro

tidF2

470

/18

HP

A/M

UC

A4

21

7/18

MU

CA

16

AR

ATH

AL

46F

1765

2P

A2M

4C

MFIR

MSM

F10

55/1

8M

CYSTIC

36

68/1

8P

A

17

LAK

SHM

I54

F17

346

PA

5M5

CM

FIRM

Paro

tidF2

101

/18

HP

A/M

UC

A4

14

6/18

MU

CA

18

KA

MA

LAM

62F

1986

5P

A3M

4C

MFIR

MP

arotid

F94

8/18

MP

A3

42

5/18

PA

19

KA

RU

PA

N64

M21

870

INF

3M4

CM

DO

UG

HY

Paro

tidF9

43/1

8M

CH

SA3

65

2/18

WT

20

NA

GA

RA

J48

M23

410

PA

3M5

CM

DO

UG

HY

Paro

tidF8

32/1

8M

WT

40

31/1

8W

T

21

RA

NI

48F

2876

5P

A2M

4C

MFIR

MP

arotid

F91

0/18

MP

A1

86

0/18

ME

22

RA

VI

24M

2924

0P

A2M

4C

MFIR

MSM

F89

8/18

MM

A1

55

0/18

CH

SA

23

RA

JAM

AN

I50

F30

120

INF

3M4

CM

FIRM

SMF9

19/1

8M

PA

15

62/1

8M

E

24

SAM

Y63

M42

102

INF

4M4

CM

DO

UG

HY

Paro

tidF1

831

/18

MC

H SA

28

13/1

8W

T

25

SAR

ASU

70F

4321

8P

A3M

5C

MFIR

MP

arotid

F18

84/1

8H

WT

21

64/1

8O

C

26

SITHIK

A27

F44

127

PA

3M4

CM

FIRM

SMF2

106

/18

MP

A2

83

0/18

PA

27

PA

LAN

I55

M42

659

PA

5M5

CM

FIRM

SMF2

158

/18

HW

T/MU

CA

28

96/1

8M

UC

A

28

SELVA

RA

J52

M34

875

INF

4M4

CM

DO

UG

HY

Paro

tidF2

245

/18

MW

T2

99

2/18

WT

29

THIN

A46

M46

580

INF

2M3

CM

FIRM

SMF2

387

/18

MC

H SA

31

12/1

8C

H SA

30

MU

NU

SAM

Y64

M48

712

PA

5M5

CM

FIRM

Paro

tidF2

500

/18

HW

T/MU

CA

33

330

/18M

UC

A

31

BA

LA36

M52

198

PA

3M4

CM

FIRM

Paro

tidF2

516

/18

MP

A3

41

8/18

PA

32

PA

LAN

I35

M52

870

INF

2M3

CM

FIRM

SMF1

362

/18

MC

H SA

23

40/1

8C

H SA

33

CH

INN

A65

M54

328

PA

2M3

CM

FIRM

Paro

tidF1

831

/18

MC

H SA

33

22/1

8C

H SA

34

GA

NESA

N60

M867

2IN

F3M

4C

MD

OU

GH

YP

arotid

F73

1/19

MW

T1

49

8/19

WT

35

LAK

SHM

I52

F742

1P

A5M

5C

MFIR

MP

arotid

F58

3/19

HP

A/M

UC

A1

12

8/19

MU

CA

36

REV

ATH

I35

F432

6P

A2M

4C

MFIR

MSM

FII77

/19

MP

A2

18

7/19

PA

37

VEN

KA

TESH45

M389

2P

A3M

4C

MFIR

MP

arotid

F11

56/1

9M

PA

23

44/1

9P

A

38

KA

MA

LAM

60F

3271

INF

2M3

CM

FIRM

SMF1

232

/19

MW

T2

60

3/19

CH

SA

39

CH

ELLAM

65F

1267

INF

1M3

CM

FIRM

SMF9

72/1

9M

CH

SA1

79

1/19

INF

40

SHEELA

20F

437

PA

3M4

CM

FIRM

Paro

tidF4

02/1

9M

PA

10

33/1

9P

A

41

PA

ND

IAN

40M

649

INF

3M4

CM

FIRM

SMF5

73/1

9M

PA

11

82/1

9P

A

42

SAM

SATH

48F

456

PA

3M4

CM

FIRM

Paro

tidF7

60/1

9M

PA

15

55/1

9P

A

43

VA

NN

AN

39M

318

INF

2M3

CM

FIRM

SMF8

08/1

9M

CH

SA1

62

9/19

CH

SA

44

SHA

NK

AR

43M

320

PA

2M4

CM

FIRM

Paro

tidF8

06/1

9M

PA

16

41/1

9P

A

45

SRID

HA

RA

N61

M38

9P

A2M

4C

MFIR

MSM

F47

4/19

MP

A1

36

8/19

PA

a dissertation on cytologic spectrum of salivary …

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