Pathology of Salivary Glands

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PATHOLOGY OF SALIVARY GLANDS

Transcript of Pathology of Salivary Glands

Page 1: Pathology of Salivary Glands

PATHOLOGY OF SALIVARY GLANDS

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MAJOR SALIVARY GLANDS

Parotid: so-called watery serous saliva rich in amylase, proline-rich proteins Stenson’s duct

Submandibular gland: more mucinous Wharton’s duct

Sublingual: viscous saliva ducts of Rivinus; duct of Bartholin

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MINOR SALIVARY GLANDS

Minor salivary glands are not found within gingiva and anterior part of the hard palate

Serous minor glands=von Ebner below the sulci of the circumvallate and folliate papillae of the tongue

Glands of Blandin-Nuhn: ventral tongue Palatine, glossopalatine glands are pure

mucus Weber glands

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Embryology

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• The major salivary glands develop from the 6th-8th weeks of gestation as outpouchings of oral ectoderm into the surrounding mesenchyme.

• The parotid develops first, growing posteriorly as the facial nerve advances anteriorly; eventually, the fully developed parotid surrounds VII.

• However, the Parotid is the last to become encapsulated, after the lymphatics develop, resulting in its unique anatomy with entrapment of lymphatics in the parenchyma of the gland

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Structural elements of the salivary gland unit.

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pleomorphic adenomas originate from the intercalated duct cells and myoepithelial cells

oncocytic tumors originate from the striated duct cells

acinous cell tumors originate from the acinar cells,

Mucoepidermoid tumors and squamous cell carcinomas develop in the excretory duct cells

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• Salivary epithelial cells are often included within these lymph nodes, leading to development of Warthin’s tumors and Lymphoepithelial cysts within the Parotid gland.

• The other major salivary glands do NOT have intraparenchymal lymph nodes.

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Normal Histology

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Mucous cells

Production, storage, and secretion of proteinaceous material; smaller enzymatic component-more carbohydrates-->mucins=more prominent Golgi-less prominent (conspicuous) rough endoplasmic reticulum, mitochondria-less interdigitations

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Serous cells

Seromucus cells=secrete also polysaccharides They have all the features of a cell specialized

for the synthesis, storage, and secretion of protein Rough endoplasmic reticulum (ribosomal sites--

>cisternae) Prominent Golgi-->carbohydrate moieties are added

Secretory granules-->exocytosis

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Serous cells

The secretory process is continuous but cyclic

There are complex foldings of cytoplasmic membrane

The junctional complex consists of: Tight junctions (zonula occludens)--

>fusion of outer cell layer Intermediate junction (zonula

adherens)-->intercellular communication

Desmosomes-->firm adhesion

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Myoepithelial cells

One, two or even three myoepithelial cells in each salivary and piece body

Four to eight processes Desmosomes between

myoepithelial cells and secretory cells

Myofilaments frequently aggregated to form dark bodies along the course of the process

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Myoepithelial cells

The myoepithelial cells of the intercalated ducts are more spindled-shaped and fewer processes

Ultrastructurally very similar to that of smooth muscle cells

Functions of myoepithelial cells Support secretory cells Contract and widen the diameter of the

intercalated ducts Contraction may aid in the rupture of acinar

cells of epithelial origin

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Formation and Secretion of Saliva Primary saliva

Serous and mucous cells Intercalated ducts

Modified saliva Striated and terminal ducts End product is hypotonic

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Macromolecular component

Synthesis of proteins RER, Golgi apparatus Ribosomes RER

posttranslational modification (N- & O-linked glycosylation) Golgi apparatus Secretory granules

Exocytosis Endocytosis of the granule

membrane

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Fluid and Electrolytes

Parasympathetic innervationBinding of acetylcholine to

muscarinic receptors Activation of phospholipase IP3

release of Ca2+ opening of channels K+, Cl- Na+ in

K+ and Cl- in Also another electrolyte transport

mechanism through HCO3-Noepinephrine via alpha-adrenergic

receptors Substance P activates the Ca2+

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Functions

Protection lubricant (glycoprotein) barrier against noxious stimuli; microbial toxins and minor traumas

washing non-adherent and acellular debris

formation of salivary pellicle▪ calcium-binding proteins: tooth protection; plaque

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Functions

Buffering (phosphate ions and bicarbonate) bacteria require specific pH conditions

plaque microorganisms produce acids from sugars

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Functions

Digestion

neutralizes esophageal contents

dilutes gastric chyme forms food bolus brakes starch

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Functions

Tissue repair bleeding time of oral tissues shorter than other tissues

resulting clot less solid than normal

remineralization

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Functions

Taste solubilizing of food substances that can

be sensed by receptors trophic effect on receptors

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Function of Saliva

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At least 8 major functions of saliva have been identified:

1) Moistens oral mucosa. Mucin layer is the most important nonimmune defense mechanism in the oral cavity.

2) Moistens dry food and cools hot food. 3) A medium for dissolved foods to stimulate the taste buds. 4) Buffers oral cavity contents due to high concentration of

bicarbonate ions. 5) Digestion. Alpha-amylase, contained in saliva, breaks 1-4

glycoside bonds, while lingual lipase helps break down fats. 6) Controls bacterial flora of the oral cavity. 7) Mineralization of new teeth and repair of precarious enamel

lesions. Saliva is high in calcium and phosphate. 8) Protects the teeth. This signifies a saliva protein coat on the

teeth which contains antibacterial compounds. Thus, salivary hypofunction results in dental caries.

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The intraoral complications of salivary hypofunction

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• 1) Candidiasis  • 2) Oral Lichen Planus (usually painful)  • 3) Burning Mouth Syndrome (normal appearing

oral mucosa with a subjective sensation of burning) 

• 4) Recurrent aphthous ulcers  • 5) Dental caries. • The best way to evaluate salivary function is to

measure the salivary flow rate in stimulated (e.g., by using a parasympathomimetic as pilocarpine) and unstimulated states. Xerostomia is NOT a reliable indicator of salivary hypofunction. 

• There is a hierarchy of sensory stimuli such that swallow>mastication>taste>smell>sight>thought.

• Stimulation results in an increase in total salivary flow from 0.3 cc/min to >1 cc/min. The salivary response is directly related to a subject’s state of hunger 

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The Parotid Gland

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• The largest salivary gland• Lies wedge-shaped between the mandible and

sternomastoid and over both• Relations: • Above: external auditory meats and temporo-

mandibular joint• Below: post belly digastric• Anteriorly: mandible and masseter• Medially: styloid process and its muscles

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Structures at the Angle of the Mandible

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• Medial relations of the parotid: the styloid process and its muscles separate the gland from the

• internal jugular vein• Internal carotid artery• The last four cranial nerves• Lateral wall of the pharynx

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Relations of the Parotid

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Parotid Bed

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Deep relations of Parotid

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Fascia

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• The parotid is enclosed in a split in the investing fascia

• The parotid lymph nodes lie both on and below the parotid gland

• Antero-inferiorly, the fascia is thickened to form the stylomandibular ligament; the only structure that separates the parotid from the submandibular glands

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The Facial Nerve

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• The parotid gland is divided into superficial and deep lobes by three structures traversing the gland:

• The Facial Nerve• The retromandibular vein (post facial)

formed by the superficial temporal and maxillary

• The external carotid artery dividing at the neck of the mandible into the superficial temporal and maxillary

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Relation of the Facial Nerve and Parotid

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• The parotid develops in the crotch formed by the 2 divisions of the facial nerve

• As it enlarges it overlaps the nerve trunks, the superficial and deep parts fuse and the nerve becomes buried within the gland

• It is not a sandwich

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Facial Nerve

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The Facial Nerve

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• Emerges from the stylomastoid foramen• Winds laterally to the styloid process• Surgical Exposure• In the inverted V between the bony external

auditory meatus and the mastoid process• Just beyond the point the nerve dives into the post

aspect of the parotid and bifurcates almost immediately into its two main divisions

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Branches of the Facial N

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• The nerve then gives rise to 2 divisions: • 1) Temperofacial (upper) • 2) Cervicofacial (lower)

• Followed by 5 terminal branches: • 1) Temporal • 2) Zygomatic • 3) Buccal • 4) Marginal Mandibular • 5) Cervical

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Nerve Injury

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• Clinical examination of the Parotid should include examination of the Facial nerve

• Malignant tumors of the parotid may involve VII and cause facial palsy, while benign tumors never affect VII

• During Superficial Parotidectomy, the nerve is exposed posteriorly in the space bet the bony canal of external auditory meatus and the mastoid process

• It is then traced anteriorly into the gland to excise the gland superficial to nerve branches

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The Parotid Duct

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• Stensen’s duct is 5 cm long.• Arises from the anterior part of the gland and

runs over the masseter one finger below the zygomatic arch to pierce the buccinator and open opposite the second upper molar tooth

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Parotid Duct orifice

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• Clinical examination of the parotid gland should include examination of the duct orifice opposite the upper 2nd molar for signs of inflammation, and palpated for stone

• Parotid Sialogram is performed by injecting a contrast through a canula placed in the orifice of the duct

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Submandibular Gland

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• Large superficial lobe and a small deep lobe, that connect around the mylohyoid

• Superficial lobe lies at the angle of the Jaw, wedged bet the mandible and mylohyoid and overlapping the digastric

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Superficial and Deep Relations

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• Superficially: The skin, the platysma, the capsule (deep fascia), the cervical branch of Facial Nerve, and the Facial Vein

• Deeply: the deep aspect lies against the mylohyoid for the most part. But posteriorly lies on the hyoglossus and comes in contact with the lingual and hypoglossal nerves.

• Both nerves lie on the hyoglossus as they pass forward to the tongue

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The facial Artery

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• Posterior • Arches over its superior aspect to reach

inferior border of the mandible and then ascends on to the face in front of the masseter

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Facial artery52

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The Submandibular Duct

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• Arises from the deep part of the gland, runs forward to open at the side of the frenulum linguae

• Lies beneath the mucosa of the floor of the mouth along the side of the tongue

• Lingual nerve loops around the duct, double-crossing it, by passing from lateral beneath, then medial

• The sublingual salivary gland is also medial to the duct.

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Clinical Applications

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• Submandibular LN are adherent to the gland and partly between it and the mandible

• Differentiating bet submandibular LN and Salivary gland:

• The salivary gland can be palpated bimanually as it extends into the floor of the mouth.

• The Lymph Nodes are only felt below the mandible. • LN may be multiple and a space separates them

from the mandible

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Clinical Applications

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• A stone in the submandibular duct can be felt bimanually in the floor of the mouth and can be seen if large

• The presence of LN adherent to the gland makes removal of the gland part of block neck dissection

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Autonomic Innervations

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• Parasympathetic Stimulation results in abundant, watery saliva with a decrease in [amylase] in saliva and an increase in [amylase] in the serum. Acetylcholine is the active neurotransmitter, binding at muscarinic receptors in the salivary glands. The parasympathetic nervous system is the primary instigator of salivary secretion.

• Parasympathetic Interruption to salivary glands results in atrophy, while sympathetic interruption doesn’t cause a significant change.

• It was once thought that the sympathetic nervous system antagonizes the parasympathetic nervous system, but this is now known not to be true

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Autonomic Innervation

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• In the case of the parotid, parasympathetic fibers originate from CN IX

• In the case of the Submandibular and Sublingual glands, the parasympathetic fibers originate in CN VII

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Sympathetic Innervation

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• Stimulation by the sympathetic nervous system results in a scant, viscous saliva rich in solutes with an increase in [amylase] in the saliva and no change in [amylase] in the serum.

• For all of the salivary glands, these fibers originate in the Superior Cervical ganglion and travel with arteries to reach the glands:

• 1) External Carotid artery for the Parotid • 2) Lingual artery for the Submandibular, and • 3) Facial artery in the case of the Sublingual.

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History• Determine if solitary parotid or moregeneralized salivary gland involvement• Progression of enlargement• Inciting factors for enlargement• Nature and duration of symptoms• Pain: character, severity, frequency

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Associated Symptoms- Head and Neck- Systemic• Review of Systems• Medications• Past Medical History• Social History (eg. alcohol use)• Family History

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Physical Examination• Complete Head and Neck Exam• Inspection / Palpation of Salivary Glands- enlargement (unilateral/bilateral)- consistency- tenderness- mobility• Differentiate diffuse gland enlargement fromdiscrete mass or anatomic anomaly

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BIMANUAL PALPATION OF SUBMANDIBULAR GLAND

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Parotid gland:Inspect the pre- and infra-auricular region, observing for symmetry.Palpate the parotid gland.Lacrimal gland:Have the patient close their eyes and observe the upper and outer aspect of the upper lid.The lid is normally smooth and symmetrical.Gently retract the upper lid and have the patient gaze to the opposite side.The lacrimal gland is located under the lid near the outer angle.Submandibular gland:Observe the submandibular region.Tilt the patient's head forward and gently roll your fingers over the inner surface of the mandible.

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Physical Examination• Oral Cavity-Moisture level-Dentition status-Salivary duct outputamountcharacter-Palpate for sialoliths, masses• Salivary duct probing

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LABORATORY

Chemical analysis of saliva Anti-SS-A, anti-SS-B, and rheumatoid

factor may be present in autoimmune diseases. Saliva may be cultured, which is helpful, and it may be analyzed chemically, which is rarely helpful.

Most laboratories cannot perform useful tests on saliva. Dental researchers had hopes for several decades that analysis of saliva would be of diagnostic importance. Saliva has such wide variations in composition that analysis has produced little of diagnostic value.

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Laboratory Studies• HIV test• Angiotensin converting enzyme (Sarcoid)• Autoantibodies (Sjogren’s)- Rheumatoid factor- Antinuclear antibodies- Anti-SSA, Anti-SSB• Antineutrophil cytoplasmic antibody;ANCA(Wegener’s)• Hormone levels (eg. TSH)

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EXPLORATORI METHODS

1. X-rays without preparation. Plainfilm The views of the salivary glands are

taken full face and profile of the parotid, or the submandibular gland, depending on the pathology. A 3/4 x-ray view of the submandibular gland is preferred.

These different x-rays can show not only radio opaque stones in the salivary glands, but also old calcifications in a lymph node.

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2. Regular occlusal x-rays of the floor of the mouth. These occlusal views are helpful in revealing an opaque stone in the submandibular gland, or in the duct.The procedure entails actually putting film in the mouth to obtain an x-ray image.Regular occlusal X-rays can only be made at the sub-mandibular and sub-lingual glands levels. They either entail the positioning of an occlusal image source in an orthogonal position in relation to the mouth's floor, or scanning the ray to obtain a view of the forward sub-mandibular gland.This results in the visualisation of calcification in the glandular area. These are most frequently stones but may also be calcified lymph node

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(a-d) Transverse CT scans of ductal and glandular calcifications.

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SIALOGRAPHY 3. Sialography Technique A cannula is introduced into the parotid or

submandibular ducts and is used to inject contrast enhancing products (eg Lipiodol) to outline the ramifications of the ductal systems of these glands, showing their patterns and calibers. This examination can be performed on everyone, including children over the age of 4. The injection should be of no more than 0.5 to 1 cc, and injected very slowly. This examination is painless if done smoothly. The only contraindication is an allergic reaction to iodine.It must be know in such cases, pre-medication with corticosteroïds will permit the examination.

Results Basically, sialography is prescribed each time

there is a suspicion of an inflammatory syndrome, especially if there is the possibility of a lithiasis,in order to visualize the exact caliber of the duct and the position of the stone, as opposed to calcification within a lymph node.

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Conventional sialography.

Yousem D M et al. Radiology 2000;216:19-29

©2000 by Radiological Society of North America

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IMAGING

CT scanning and MRI with gadolinium enhancement These studies may be used to

determine the size, shape, and some qualities of neoplasms or swelling within the gland.

Either method reliably differentiates between solid masses, cystic lesions, and diffuse involvement of the gland.

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(a-d) Transverse CT scans of ductal and glandular calcifications.

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Submandibular calculi visualized at MR imaging.

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Simple ranula.

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(a-d) Transverse CT scans of ductal and glandular calcifications.

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Glandular calcifications in a patient with sarcoidosis.

Yousem D M et al. Radiology 2000;216:19-29

©2000 by Radiological Society of North America

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BIOPSY

Incisional biopsy -Under local anesthesia, a biopsy of the tail of the gland may be obtained by an experienced surgeon without injury to the facial nerve. Fine-needle aspiration biopsy frequently is

diagnostic for tumors and may be helpful to identify cell types and to obtain material for cultures when the clinical picture suggests infection. Excisional biopsy of a labial minor salivary gland may be diagnostic when the clinical picture suggests Sjögren syndrome.

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The Most Common Tumors

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• Histologically, salivary gland tumors are the most heterogenous group of tumors of any tissue in the body

• Of salivary gland neoplasms, >50% are benign• Approximately 70% to 80% of all salivary gland

neoplasms originate in the parotid• The palate is the most common site of minor

salivary gland tumors• The frequency of malignant lesions varies by site.

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PLUNGING RANULA

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RANULA

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Pleomorphic Adenoma

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Pleomorphic Adenoma

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Submandibular pleomorphic adenoma.

Yousem D M et al. Radiology 2000;216:19-29

©2000 by Radiological Society of North America

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SUBMAXILLECTOMY

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Warthin's Tumor

Warthin's tumor (benign papillary cystadenoma lymphomatosum)

the second most common benign tumor of the parotid gland

It accounts for 2-10% of all parotid gland tumors

Bilateral in 10% of the cases

may contain mucoid brown fluid in FNA

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Bilateral Warthin tumors.

Yousem D M et al. Radiology 2000;216:19-29

©2000 by Radiological Society of North America

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Monomorphic Adenoma Similar to Pleomorphic Adenoma except no

mesenchymal stromal component Predominantly an epithelial component

More common in minor salivary glands (upper lip)

12% bilateral Rare malignant potential Types:

Basal Cell Adenoma Canicular Adenoma Myoepithelioma Adenoma Clear Cell Adenoma Membranous Adenoma Glycogen-Rich Adenoma

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Malignant Tumors

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• Approximately 20-25% of parotid, 35-40% of submandibular tumors, 50% of palate tumors, and > 90% of sublingual gland tumors are malignant

• The most common benign salivary tumor is pleomorphic adenoma, comprising 50% of all salivary tumors and 65% of parotid gland tumors

• The most common malignant salivary tumor is the mucoepidermoid carcinoma, comprising 10% of all salivary gland neoplasms and 35% of malignant salivary gland neoplasms, occurring most often in the parotid gland.

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Salivary Gland Tumors

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PAROTID CANCER

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Mucoepidermoid Carcinoma

MECs contain two major elements:

mucin-producing cells and epithelial cells of the epidermoid variety

(Epidermoid and Mucinous components).

MEC is divided into low-grade (well differentiated).

High-grade (poorly differentiated).

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Acinic Cell Carcinoma

This lesion is characterized by a benign histomorphologic picture but by occasional malignant behavior.

These lesions are treated by surgical excision

Bilateral involvement occurs in 3% of patients, making acinic cell carcinoma the second-most common neoplasm, after Warthin’s tumor, to exhibit bilateral presentation.

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Adenoid Cystic Carcinoma

Adenoid cystic carcinoma with Swiss cheese pattern.

It is the second-most common malignant tumor of the salivary glands.

ACC is the most common malignant tumor found in the submandibular, sublingual, and minor salivary glands.

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Mucoepidermoid Carcinoma

Mucoepidermoid carcinoma (MEC) is the most common malignant tumor of the parotid gland and the second-most common malignancy (adenoid cystic carcinoma is more common) of the submandibular and minor salivary glands.

Stained +ve by musicarmine. MECs constitute approximately 35%

of salivary gland malignancy, and 80% to 90% of MECs occur in the parotid gland.

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Hodgkin's Lymphoma Hodgkin's

disease involving the parotid gland. 

Note the Reed-Sternberg cell.  (Fine needle aspiration, Pap, 630x)

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PARTIAL PAROTIDECTOMY

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Inflammatory EnlargementAcute Sialadenitis• Viral• Bacterial• Radiation• MedicationChronic Sialadenitis• Obstructive• Granulomatous• Autoimmune• HIV-associated

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Sialadentitis

What is Sialadentitis? Simply inflammation of the salivary

glands Can be due to a number of factors

including: Mumps infection Coxackie Virus Parainfluenza Systemic Disease

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Sialadentitis: Etiology

May be infectious: May be caused by bacterial or viral infections

May be non-infectious: May be caused by systemic disease such as

Sjogren’s or Sarcoidosis or even by radiation therapy

May be Post-Surgical: Called “Surgical Mumps” Pt kept without fluids and given atropine

causes xerostomia predisposing to inflammation

May be Pharmacological: Drugs causing xerostomia

May be architectural: Block of the salivary gland due to a stone

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SIALOLITHIASIS

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Sialolithiasis • Recurrent painful parotid gland swelling• Episodes of acute bacterial sialadenitis• Abscess formation• Chronic sialadenitis• Gland atrophy

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Submandibular calculi visualized at MR imaging.

Yousem D M et al. Radiology 2000;216:19-29

©2000 by Radiological Society of North America

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(a-d) Transverse CT scans of ductal and glandular calcifications.

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Parotitis

Definition: Inflammation of the Parotid Gland

May be infectious or non-infectious Common Causes:

Mumps Sjogren’s Syndrome Bacterial infection of parotid gland

usually Staph. aureus Blocked salivary duct Stone in salivary duct

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Parotitis

Definition: Inflammation of the Parotid Gland

May be infectious or non-infectious Common Causes:

Mumps Sjogren’s Syndrome Bacterial infection of parotid gland

usually Staph. aureus Blocked salivary duct Stone in salivary duct

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Mumps: Clinical Features

Transmitted via airborne droplet Mainly effects the parotid gland Mainly effects children between

the ages of 5-18 Has a 2-3 week incubation period Clinically:

Will see rapid swelling of the parotids bilaterally

Acute pain when salivating

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Mumps (Viral endemic parotitis) Mumps is an acute sialadenitis

which caused by an RNA virus This RNA virus is the

“paramxovirus” Other virus which can cause

salivary infections are: Cytomegalovirus Coxsackieviruses Echovirus

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Mumps (Viral endemic parotitis)TREATMENT: There no effective antiviral therapy

available for the treatment of mumps.

Analgesics and antipyretics are given to control pain and fever

Liquid diet with vitamins should be considered

There should be complete bed rest.

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Bacterial Saladenitis

Bacterial saladinitis usually occurs after surgery most commonly abdominal surgery.

The possible reason may be temporary lack of ductal flow which can develop while atropine sulphate is administered while delivering general anesthesia which allows ascending infections and thus pyogenic bacteria can inhibit the ducts.

Due to this there is pain and swelling . Purulent exudate can be expressed

from the orifice of the duct.

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Clinical Features- continued When looking at the patient:

The ear lobe is elevated due to glandular enlargement

There may be a purulent discharge from the parotid duct but it is clear and unremarkable

Blood Work: As the acini become infected the salivary

amylase leaks into the interstitium and is absorbed in the blood stream raising the serum amylase levels

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Acute right-sided parotitis.

Yousem D M et al. Radiology 2000;216:19-29

©2000 by Radiological Society of North America

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Overall Treatment for Parotitis Acute:

Antibiotics Rehydration stimulating salivary flow Possible IND

Chronic: Eliminate causative agent:

Get rid of salivary stone/ other blockage Warm Compresses Sialogogues Possible surgical resection Ligation of the duct in hopes of atrophy

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Radiation Sialadenitis• Inflammatory process due to radiation effecton gland parenchyma, dose-related injury• Serous glands and acini most susceptible• External beam radiation• Radioactive iodine• Painful, tender glands; swelling; xerostomia• Chronic injury can result• Some benefit with sialendoscopy

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Chronic Sialadenitis• Non-granulomatous chronic inflammatory condition• Etiology may be unclear by history- primary obstruction / secondary infection- primary infection / secondary obstruction• Recurrent painful gland enlargement common- exacerbation with eating• Relief of duct obstruction, sialogogues,glandular massage, warm heat• Gland resection for medical therapy failure

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Sjogren’s Syndrome

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Sjogren’s Syndrome It is a group of autoimmune conditions

with a marked predilection for woman, it has an intense T lymphocyte – mediated autoimmune process in salivary and the lacrimal glands as on of its most prominent component

Sjogren’s syndrome exhibits T cells infiltration and replaces the glandular parenchyma

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Sjogren’s Syndrome

Sjogren’s Syndrome: objective evidence of

keratoconjunctivitis sicca characteristic pathologic features of

the salivary glands 2 out of 3 of:

recurrent chronic idiopathic salivary gland swelling

unexplained xerostomia connective tissue disease

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Sjogren's Syndrome: Age of Onset The frequency distributions of ages at onset of symptoms

& at diagnosis of primary Sjogren's syndrome

0

5

10

15

20

25

30

35

40

45

1-10 11-2021-3031-4041-5051-6061-7071-80

81-90

AGE

% O

F P

AT

IEN

TS

At diagnosisAt diagnosisOnset Onset

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Sjogren’s Syndrome: Clinically Subjective and Objective Findings: Subjective:

Xerostomia Salivary Gland Enlargement

Objective: Stomatitis Oral Ulcers Cracked, “crocodile skin” tongue Carious Teeth Parotid Gland Enlargement Certain Tests can be done

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“Crocodile Skin” Tongue, Carious Teeth

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Tests and Studies: Serology

Autoantibodies % positiveRheumatoid factors (Igs) 80

Cryoglobulins (type II)

30

Ro/SSA 60La/SSB 30a-fodrin 95

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Tests and Studies: Scintigraphy Scintigraphy (Nuclear Medicine) administer

radioactive substance in order to show the physiology and state of the biological process:

Scintigraphy diagnosis

NormalModerate

involvementMarked

involvement

Degree of xerostomia

None Mild Severe

Salivary flow rate (ml/5-min/gland)

1.60 0.42 0.00

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Tests and Studies: Schirmer’s Test A test of whether the eye has enough tears to

keep moist Procedure:

Piece of filter paper inserted for several minutes (usually 5) and moisture recorded

<5 ml in 5 minutes is characteristic of Sjogren’s Syndrome

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Tests and Studies: Salivary Gland Biopsy

A lip biopsy, if positive for Sjogren’s will show lymphocytes clusters and glandular destruction due to inflammation

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Tests and Studies: Salivary Gland Biopsy

A lip biopsy, if positive for Sjogren’s will show lymphocytes clusters and glandular destruction due to inflammation

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Pathophysiology: Continued

Multifactorial disease SS is sometimes called autoimmune

epithelitis in which there is apoptosis of epithelial cells leading to degradation products and leading to antinuclear autoantigens to the immune system

Molecules within the TNF family play a big role in the polyclonal activation of B Cells. This, in turn leads to autoantibodies

There is known inhibition of healthy glands and/or the muscarinic receptors (via antibodies) and also abnormal function of aquaporins leading to poor function of remaining healthy glandular structure

There is prolonged/permanent activation of autoreactive B cells favoring oncogenic activity and possible development of B Lymphoma

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Pathological

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Sjogren’s Syndrome: Systemic Manifestations

Systemic manifestations Frequency (%)

Arthralgia/arthritis 60Raynaud’s phenomenon 30Purpura/Vasculitis 15 (1)Lung involvement(increased liver enzymes)

10 (25)

Kidney involvement(Interstitial Nephritis/Glomerulonephritis)

8 (25)

Liver involvement 5Muscle involvement 1

Skopouli et al., Semin Arthritis Rheum. 2000, 29:296

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Sjogren’s Syndrome: Treatment To Treat Xerostomia:

Glandular Stimulation/Replacement Salivary Substitutes Dx and treatment of candidiasis Meticulous oral hygeine for prevention of

caries To Treat Xerophthalmia:

Stimulation for tears: Cyclosporin A Pilocarpine Cimeviline

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Treatment: Continued

Treatment for Salivary Gland Enlargement: Local moist heat Antibiotic Therapy NSAIDs Rule out a Lymphoma

Treatment for Peripheral Symptoms: Methotrexate Cyclosporin A Infliximab Hydroxychloroquine Corticosteroids

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SARCOIDOSIS –HEERFORD SDR

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Sarcoidosis• Systemic granulomatous disease, unclear etiology• < 1/3 patients - painless salivary gland swelling• Nontender and multinodular glands; xerostomia• ACE elevation (50-80%)• Most patients have pulmonary involvement• CXR- hilar nodes, adenopathy, parenchymalinfiltrates• Noncaseating granulomas on histopathology• Treatment supportive; steroids in select patients

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HIV-Associated Cystic Sialadenitis• Bilateral parotid multicystic enlargement• Lymphocytic (T cell) infiltration of gland• Persistent, nonprogressive• May be mildly painful• Enlarged adenoids, cervical nodes common• Diagnosis largely clinical• Positive HIV test• Must exclude lymphoma or other neoplasm

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Non-Inflammatory EnlargementAcute Enlargement• Neoplasm• Miscellaneous:TraumaPneumoparotitisAnesthesia/EndoscopyChronic Enlargement• Obesity• Sialadenosis- Endocrine- Nutritional- Medication- Idiopathic• Amyloidosis

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Sialadenosis (Sialosis)• Non-inflammatory, non-neoplastic glandparenchyma enlargement• Bilateral parotid enlargement most common• Can be recurrent or persistent• Wide variety of systemic conditions causative• Unifying factor - neuropathic alteration of theautonomic innervation of salivary acini (Batsakis)• Diagnosis primarily clinical, exclusion of others• Complete metabolic and endocrine evaluation

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Sialadenosis - Etiologies• Endocrine Disorders- Diabetes Mellitus (1/4)- Hypothyroidism• Alcoholism (autonomic neuropathy)• Nutritional Disorders- Bulimia (1/3)- Deficiency conditioneg. protein (alcoholism)vitamin (niacin, thiamine, vit. A)

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Sialadenosis - Etiologies• Medications- Direct effect on glandeg. iodine compounds- Drug side-effect (adrenergic, cholinergic)eg. antihypertensives (guanethidine)antiemetics (phenothiazine)antiepileptics (phenobarbital)bronchodilators (isoproterenol)• Idiopathic - diagnosis of exclusion

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SIALADENOSIS - Treatment• Correct underlying disorder

• Pilocarpine - Bulimia• Consider parotidectomy only forunacceptable cosmetic deformityunresponsive to medical therapy

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