Salivary Gland Disease Flashcards

1
Q

What are the salivary gland diseases?

A
  • Mucocele/Ranula
  • Sialolithiasis
  • Acute and Chronic Sialadenitis
  • Xerostomia
  • Benign Lymphoepithelial lesion (BLEL)
  • Sjoren syndrome
  • Necrotizing sialometaplasia
  • Salivary gland Neoplasia
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2
Q

What is a mucocele/Ranula?

A

A ruptured salivary duct in which mucin spills into the surrounding tissues.

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3
Q

What is a common cause of oral swelling?

A

mucocele/ranula

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4
Q

Muccocele/ranula is most often seen in whom?

A

Children and young adults-but all ages

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5
Q

Where in the oral cavity is a mucocele/ranula seen?

A

lower lip, buccal mucosa, ventral tongue floor of mouth

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6
Q

Where is the most common site and how often?

A
  • lower lip near #22,27.

- 82% of the time

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7
Q

What are the clinical features of a mucocele/ranula?

A

-non-tender, soft swelling
-flucuant or firm
-translucent to blue color
-history of repeated swelling and reslolution-superficial
mucocele erupts on own.

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8
Q

Where is a ranula most often located and what is the appearance compared to mucocele?

A

-located on anterior floor of mouth (FOM) right or left to
midline.
-It appears larger than mucocele

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9
Q

Histopathologically, what is its appearance?

A
  • extravasated mucin
  • granulation tissue
  • variable mounts of inflammatory cells
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10
Q

How do you treat a mucocele/ranula?

A
  • microscopic exam to rule out neoplasm
  • some resolve with no tx
  • excision of mucous deposit including involved gland
  • marsupilization-unroofing
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11
Q

What is the prognosis for a mucocele/ranula?

A
  • excellent

- occasionally recur if involved gland not excided

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12
Q

What are Sialolithiasis?

A
  • Salivary duct stone
  • calcified structures that develop within the salivary ductal system
  • Deposition of calcium salts around nidus of debris in lumen
  • Cause unclear,may be promoted by chronic sialadentitis and partial duct obstruction
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13
Q

How do Sialolithiasis appear clinically?

A
  • Hard submucosal mas in soft tissue
  • may or may not have symptoms
  • May have swelling prior or during meals
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14
Q

What is the most common affected gland and how often?

A
  • submandibular gland
  • 80% of the time

-can also be affect the parotid or minor glands

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15
Q

What does sialolithiasis like radiographically?

A

soft tissue appears opaque and lamellated

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16
Q

What is the histological appearance of a sialolithiasis?

A
  • concentric laminations surrounding nidus of amorphous debris
  • if associated duct is removed, often demonstrate squamous metaplasia
  • periductal inflamation
  • acute or chronic sialadenitis of the feeding gland
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17
Q

What is the treatment for sialolithiasis?

A

-gentle message toward orifice
-sialogogues or sour sugarless candies
-moist heat
-“flush”-increase fluid intake
-surgical removal, may include gland if significant
inflammatory damage
-Lithotripsy, sialendoscopy w/basket retrieval (major
gland)

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18
Q

What is the prognosis for sialolithiasis?

A

-Minor glands-good
-Major glands-good, but morbidity if gland needs
removal.

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19
Q

What is Acute/Chronic Sialadenitis?

A

inflammation of the salivary gland

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20
Q

What infectious causes of sialadenitis?

A
  • Bacterial - penicillanase-producing staph

- Viral - mumps

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21
Q

What are non-infectious causes of sialadenitis?

A
  • Ductal obstruction, retograde infection - associated with xerostomia, may follow general anesthesia.
  • Chronic may follow acute sialadenitis due to ductal damage.
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22
Q

What are the clinical features/ symptoms of sialadenitis?

A
  • diffuse, painful and tender, unilateral swelling

- pain, especially around meal times

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23
Q

What gland is usually involved during acute sialadenitis?

A

parotid gland

-purulent exudate expressed from the parotid papilla

24
Q

What gland is usually involved during chronic sialadenitis?

A

submandibular gland

25
Q

Does acute sialadenitis have radiographic or histopathologic features?

A

No

26
Q

What are the radiographic features for chronic sialadenitis?

A

Sialography have “sausage link” appearance due to ductal dilatation.

27
Q

What are the histopathologic features for chronic sialadenitis?

A
  • chronic inflammatory cell infiltrate

- acinar atrophy, ductal dilatation and fibrosis

28
Q

What is the treatment for acute/chronic sialadenitis?

A
  • screening radiograph
  • culture and sensitivity if purulence
  • adjust antibiotic depending on the culture and sensitivity result
  • massage
  • sialogogues w/ hydration
  • ductal stenting
  • sialoendoscopy w/ saline irrigation
  • surgical removal of affected gland may be needed
29
Q

What is the prognosis for sialadenitis?

A

excellent to poor if gland is removed

30
Q

What is xerostomia?

A

“dry mouth”

31
Q

What are the causes of xerostomia?

A
  • glandular aplasia and hypofunction
  • radiation therapy
  • graft vs. host disease-Sjogren syndrome
  • medications (antihistamines,antidepressants,sedatives/anxiolytic agents, anthypertensives)
32
Q

What does Xerostomia predispose you to?

A
  • mucosa susceptible to injury due to lack of lubrication
  • oral candidiasis
  • increased caries, especially cervical
33
Q

How do you treat Xerostomia?

A
  • artificial saliva/lubricants
  • sialogogues, sugar-free lemon drops (Salagen-pilocarpine or Evoxac-cevimeline)
  • 1% neutral sodium fluoride gel or toothpaste nightly
  • antifungal therapy as needed
34
Q

What salivary gland disease may represent an isolated form of or associated with Sjogren syndrome?

A

Benign lymphoepithelial lesion (BLEL)

35
Q

The portion of BLEL that is infiltrated is what?

A

monoclonal and may represent a low-grade lymphoma in situ

36
Q

What group of people get Benign lymphoepithelial lesion (BLEL)?

A

Females,middle aged, and older

37
Q

What are the clinical signs of Benign lymphoepithelial lesion (BLEL)?

A

-Unilateral or bilateral, firm, non-tender swelling of the parotid area.

  • Sialography: “blossoms on a tree”
  • pattern of punctate sialectasis present
38
Q

What are the histopathologic features in Benign lymphoepithelial lesion (BLEL)?

A
  • Destruction of the normal parotid parenchyma with replacement by diffuse lymphocytic infilrate.
  • Remnants of ductal epithelium. “epimyoepithelial islands”
  • Epimyoepithelial islands aslo seen in lymphoma
39
Q

How do you treat Benign lymphoepithelial lesion (BLEL)?

A
  • do nothing
  • Low-dose radiation
  • Corticosteroid therapy
40
Q

What is the prognosis for Benign lymphoepithelial lesion (BLEL)?

A

Good, malignant transformation of lyphoid or epithlial components have been reported.

41
Q

What type of condition is Sjogren syndrome?

A

Autoimmune condition

  • May be continuous of Benign lymphoepithelial lesion (BLEL)
  • primarily in women
  • wax & wane
  • tx steroid condition
42
Q

Sjogren syndrome has 2 conditions. T or F

A

True. Primary (sicca syndrome) and secondary

43
Q

What is Primary (sicca Syndrome) Sjogren syndrome?

A

xerostomia and keratoconjunctivitis (dry eyes)

44
Q

What is Secondary Sjogren syndrome?

A

Sicca syndrome (primary) plus any other autoimmune disease.

-Ex: rheumatoid arthritis, SLE, Hashimoto’s thyroiditis, mixed connective tissue disease

45
Q

What are clinical features of Sjogren syndrome?

A
  • middle age to older adults
  • female predilection 9:1
  • automimmune attackes lacrimal and salivary glands
  • parotid swelling (BLEL)
  • Patients complain of dry gritty feeling in eyes and dry mouth
46
Q

What are oral clinical features of Sjogren syndrome?

A
  • cervical/rampant caries
  • increase prealence of oral candidiasis
  • burning tongue
  • angular cheilitis
  • atrophy of dorsal tongue papillae
47
Q

How do you diagnose Sjogren syndrome?

A

Labaratory: variety of autoantibodies which are characteristic but not specific.
-Nuclear autoantibiodies: Anti-SS-A(anti-Rho) and anti -SS-B (anti-La) may be found in 50% of these patients

Serology: non-specific
-Patients have elevated sedimentation rate, ANA, and polyhypergammaglobulinemia

  • International classification criteria for Sjogren syndrome
  • Diagnosis of autoimmune condition is a long process
  • -Labial salivary gland biopsy
48
Q

What is the Labial salivary gland biopsy technique for sjogren syndrome?

A
  • lower labial mucosa, lateral midline, uninflammedW
  • 1cm incision, parallel to vermilion zone
  • Remove at least 5 minor glands through the incision and place them in routine 10% buffered formalin
  • Exclude lobules of gland exhibiting acinar atrophy and interstitial fibrosis from the assessment, since these are non-specific features related to aging.
49
Q

What are the Histopathologic features of Sjogren syndrome?

A
  • Aggregates (foci) of >50 lymphocytes +/- plasma cells scattered throughout glandular parenchyma
  • > 1 focus/4 mm consistent with the salivary compaonent of Sjogren syndrome
  • (must have 4 foci in thin field of view)
50
Q

What is the treatment for Sjogren Syndrome?

A
  • artificial tears
  • sialogogues-pilocarpine (salagen tablets) or cevimeline (Evoxac)
  • Daily topical fluorides for natural teeth
  • anti-fungal agents for candidiasis, prn
  • For secondary sjogren syndrome, therapy should be given to the other autoimmune process as well
51
Q

what is the prognosis for Sjogren Syndrome?

A

FAIR

-Patients with Sjogren Syndrome have a 44x increase in lymphoma compared to age and sex matched population

52
Q

What causes Necrotizing sialometaplasia?

A

ischemic necrosis from:

  • traumatic injury
  • dental injections
  • ill-fitted dentures
  • eating disorders w/binge-purging
  • URI
  • adjacent tumor
  • previous surgery
53
Q

Who usually get Necrotizing sialometaplasia?

A
  • Adults, rare in children
  • Male predilection
  • Most common in Posterior Hard PALATE/Anterior Soft PALATE
54
Q

What are some clinical features for Necrotizing sialometaplasia?

A
  • swelling +/- pain, paresthesia
  • After 2 weeks patient reports, “a piece of my palate fell out”
  • sharply demarctated ulcer, non-elevated margins
  • minimal peripheral erythema
  • Heals 4-6 weeks
  • “Margins like the cup on a putting green”
55
Q

What are the Histiopathologic features for Necrotizing sialometaplasia?

A
  • mistaken for SCC or Mucoepidermoid carcinoma
  • -Early stages only lobular ischemic necrosis
  • -Pseudoepitheliomatous hyperplasia (PEH) of surface epithelium
  • -Nonspecific reactive hyperplasia of stratified mucocutaneaous epithelia, which stimulates SCC
  • ACINAR NECROSIS, but architecture of involved glands are preserved
  • SQUAMOUS METAPLASIA of the Ductal Epithelium-confined to the normal boundaries of the gland