Oral & Maxillofacial Surgery Fifth Year

1. Salivary Gland
Disorders
Dr. Wael Talaat
Assistant Professor of Oral and
Maxillofacial Surgery
1

2. Salivary Gland Infections



Acute bacterial sialdenitis
Chronic bacterial sialdenitis
Viral infections
2

3. Sialadenitis
Sialadenitis represents inflammation mainly
involving the acinoparenchyma of the gland.
3

4. Sialadenitis
Acute infection more
often affects the
major glands than
the minor glands
4

5. Pathogenesis
1. Retrograde contamination of the salivary ducts
and parenchymal tissues by bacteria inhabiting
the oral cavity.
2. Stasis of salivary flow through the ducts and
parenchyma promotes acute suppurative
infection.
5

6. Acute Suppurative


More common in parotid gland.
The etiologic factor most associated with this
entity is the retrograde infection from the
mouth.
6

7. Predilection for Parotid
Salivary Composition
The composition of parotid secretions
differs from those in other major glands.
Parotid is primarily serous, the others have a
greater proportion of mucinous material.
7

8. Salivary Composition



Mucoid saliva contains elements that protect against
bacterial infection including lysozymes & IgA
antibodies (therefore, parotid has  bacteriostatic activity)
Mucins contain sialic acid which agglutinates bacteria
and prevents its adherence to host tissue.
Specific glycoproteins in mucins bind epithelial cells
competitively inhibiting bacterial attachment to these
cells.
8

9. Parotid Predilection
Anatomic factors

Stensen’s duct lies adjacent to the maxillary
molars and Wharton’s near the tongue.

It is thought that the mobility of the tongue may
prevent salivary stasis in the area of Wharton's that
may reduce the rate of infections in SMG.
9

10. Risk Factors for Sialadenitis


Systemic dehydration (salivary stasis)
Chronic disease and/or immunocompromise
Liver failure
 Renal failure
 Hypothyroid
 Malnutrition
 HIV
 Sjögren’s syndrome

10

11. Risk Factors continued…





Neoplasms (pressure occlusion of duct)
Sialectasis (salivary duct dilation) increases the risk for
retrograde contamination. Is associated with cystic
fibrosis and pneumoparotitis
Extremes of age
Poor oral hygiene
Calculi
11

12. Acute Suppurative Parotitis


Sudden onset of erythematous swelling of the
pre/post auricular areas extend into the angle
of the mandible.
Is bilateral in 20%.
12

13. Bacteriology

Purulent saliva should be sent for culture.
Staphylococcus aureus is most common
 Streptococcus pnemoniae and S.pyogenes
 Haemophilus Influenzae also common

13

14. Treatment of Acute Sialadenitis



Reverse the medical condition that may have
contributed to formation
Warm compresses, give sialogogues (lemon
drops)
External salivary gland massage if tolerated
14

15. Treatment of Acute
Sialadenitis/Parotitis




Antibiotics!
70% of organisms produce B-lactamase or
penicillinase
Need B-lactamase inhibitor like Augmentin or
Unasyn or second generation cephalosporin
Can also consider adding metronidazole or
clindamycin to broaden coverage
15

16. Surgery for Acute Parotitis



When a discrete abscess is identified, surgical
drainage is undertaken
Approach is anteriorly based facial flap with
multiple superficial radial incisions created in the
parotid fascia parallel to the facial nerve
Close over a drain
16

17. Complications of Acute Parotitis

Direct extension



Abscess ruptures into external auditory canal and
TMJ have been reported
Hematogenous spread
Thrombophlebitis of the retromandibular or
facial veins are rare complications
17

18. Complications


Extension of an abscess into the parapharyngeal space
may result in airway obstruction, mediastinitis, internal
jugular thrombosis and carotid artery erosion
Dysfunction of one or more branches of the facial
nerve is rare.
18

19. Chronic Sialadenitis



Causative event is thought to be a lowered
secretion rate with subsequent salivary stasis.
More common in parotid gland.
Damage from bouts of acute sialadenitis over
time leads to progressive acinar destruction
combined with a lymphocyte infiltrate.
19

20. Chronic Sialadenitis

The clinician should look for a treatable
predisposing factor such as a calculus or a
stricture.
20

21. No treatable cause found:


Initial management should be conservative and
includes the use of sialogogues, massage and
antibiotics for acute exacerbations.
Should conservative measures fail, consider
removing the gland.
21

22. Acute viral infection (AVI)


Mumps classically designates a viral parotitis
caused by the paramyxovirus
However, a broad range of viral pathogens have
been identified as causes of AVI of the salivary
glands.
22

23. Viral infection




Mumps is a non-suppurative acute sialadenitis
Is endemic in the community and spread by
airborne droplets
Communicable disease
Enters through upper respiratory tract
23

24. Mumps


2-3 week incubation after exposure (the virus
multiplies in the upper respiratory tract or
parotid gland)
Then localizes to biologically active tissues like
salivary glands, germinal tissues and the CNS.
24

25. Virology


Caused by paramyxovirus, an RNA virus
Others can cause acute viral parotitis:


Coxsackie A & B virus, cytomegalovirus and
adenovirus
HIV involvement of parotid glands is a rare
cause of acute viral parotitis
25

26. Clinical presentation



30% experience prodromal symptoms prior to
development of parotitis
Headache, anorexia, malaise
Onset of salivary gland involvement is
preceeded by earache, gland pain, dysphagia and
trismus
26

27. Physical exam




Glandular swelling (tense, firm) Parotid gland
involved frequently, SMG & SLG can also be
affected.
May displace pinna
75% cases involve bilateral parotids, may not
begin bilaterally (within 1-5 days may become
bilateral)….25% unilateral
Low grade fever
27

28. Treatment



Supportive
Fluid
Anti-inflammatories and analgesics
28

29. Complications





Orchitis, testicular atrophy and sterility in
approximately 20% of young men
Oophoritis in 5% females
Aseptic meningitis in 10%
Pancreatitis in 5%
Hearing loss <5%
Usually permanent
 80% cases are unilateral

29

30. Immunologic Disease
Sjögren’s Syndrome


Most common immunologic disorder
associated with salivary gland disease.
Characterized by a lymphocyte-mediated
destruction of the exocrine glands leading to
xerostomia and keratoconjunctivitis sicca
30

31. Sjögren’s syndrome



90% cases occur in women
Average age of onset is 50y
Published in 1933 by Sjögren, a Swedish
ophthalmologist
31

32. Sjögren’s Syndrome
Two forms:
 Primary: involves the exocrine glands only
 Secondary: associated with a definable
autoimmune disease, usually rheumatoid
arthritis.

80% of primary and 30-40% of secondary involves
unilateral or bilateral salivary glands swelling
32

33. Sjögren’s Syndrome


Salivary gland swelling may be permanent or
intermittent.
Rule out lymphoma
33

34. Sjögren’s Syndrome


Keratoconjuntivitis sicca: diminished tear production
caused by lymphocytic cell replacement of the lacrimal
gland parenchyma.
Evaluate with Schirmer test. Two 5 x 35mm strips of
red litmus paper placed in inferior fornix, left for 5
minutes. A positive finiding is lacrimation of 5mm or
less. Approximately 85% specific & sensitive
34

35. Sjögren’s Lip Biopsy

Biopsy of SG mainly used to aid in the diagnosis
35

36. Sjögren’s Lip Biopsy




Single 1.5 to 2cm horizantal incision labial mucosa.
Not in midline, fewer glands there.
Include 5+ glands for identification
Glands assessed quantitatively to determine the
number of foci of lymphocytes per 4mm2/gland
36

37. Sjögren’s Treatment




Avoid xerostomic meds if possible
Avoid alcohol, tobacco (accentuates xerostomia)
Sugar free gum
Salivary substitutes/sprays
37

38. Sialadenosis




Non-specific term used to describe a noninflammatory non-neoplastic enlargement of a
salivary gland, usually the parotid.
May be called sialosis
The enlargement is generally asymptomatic
Mechanism is unknown in many cases.
38

39. Related to…
a.
b.
Metabolic “endocrine sialendosis”
Nutritional “nutritional mumps”
a.
b.
c.
Obesity: secondary to fatty hypertrophy
Malnutrition: acinar hypertrhophy
Any condition that interferes with the absorption
of nutrients (uremia, chronic pancreatitis)
39

40. Related to…
c.
d.
e.
Alcoholic cirrhosis: likely based on protein
deficiency & resultant acinar hypertrophy
Drug induced: iodine mumps
HIV
40

41. Radiation Injury


Low dose radiation to a salivary gland causes an
acute tender and painful swelling within 24hrs.
Serous cells are especially sensitive and exhibit
marked degranulation and disruption.
41

42. 

Continued irradiation leads to complete
destruction of the serous acini and subsequent
atrophy of the gland.
Similar to the thyroid, salivary neoplasm are
increased in incidence after radiation exposure.
42

43. Granulomatous Disease
Primary Tuberculosis of the salivary glands:
Uncommon, usually unilateral, parotid most
common affected
 Believed to arise from spread of a focus of infection
in tonsils


Secondary TB may also involve the salivary
glands but tends to involve the SMG and is
associated with active pulmonary TB.
43

44. Granulomatous Disease
Sarcoidosis: a systemic disease characterized by
noncaseating granulomas in multiple organ systems

Clinically, SG involvement in 6% cases
44

45. Cysts
True cysts of the parotid account for 2-5% of
all parotid lesions
May be acquired or congenital
Branchial arch cysts are a duplication anomaly
of the membranous external auditory canal
45

46. Cysts
Acquired cysts include:
 Mucus extravasation vs. retention
 Traumatic
 Benign epithelial lesions
 Association with tumors




Pleomorphic adenoma
Adenoid Cystic Carcinoma
Mucoepidermoid Carcinoma
Warthin’s Tumor
46

47. Salivary Gland Neoplasms


Benign Neoplasms
Malignant Neoplasms
47

48. Salivary Gland Neoplasms


Diverse histopathology
Relatively uncommon


2% of head and neck neoplasms
Distribution
Parotid: 80% overall; 80% benign
 Submandibular: 15% overall; 50% benign
 Sublingual/Minor: 5% overall; 40% benign

48

49. Pleomorphic Adenoma

Most common of all salivary gland neoplasms
70% of parotid tumors
 50% of submandibular tumors
 45% of minor salivary gland tumors
 6% of sublingual tumors



4th-6th decades
F:M = 3-4:1
49

50. Pleomorphic Adenoma



Slow-growing, painless mass
Parotid: 90% in superficial lobe, most in tail of
gland
Minor salivary gland: lateral palate
50

51. Pleomorphic Adenoma

Gross pathology





Smooth
Well-demarcated
Solid
Cystic changes
Myxoid stroma
51

52. Pleomorphic Adenoma

Histology





Mixture of epithelial,
myopeithelial and
stromal components
Epithelial cells: nests,
sheets, ducts, trabeculae
Stroma: myxoid,
chrondroid, fibroid,
osteoid
No true capsule
Tumor pseudopods
52

53. Pleomorphic Adenoma
53

54. Pleomorphic Adenoma

Treatment: complete surgical excision
Parotidectomy with facial nerve preservation
 Submandibular gland excision
 Wide local excision of minor salivary gland

54

55. 55

56. 56

57. 57

58. 58

59. Warthin’s Tumor






papillary cystadenoma lymphomatosum
6-10% of parotid neoplasms
Older, Caucasian, males
10% bilateral or multicentric
3% with associated neoplasms
Presentation: slow-growing, painless mass
59

60. Warthin’s Tumor

Gross pathology




Encapsulated
Smooth/lobulated
surface
Cystic spaces of variable
size, with viscous fluid,
shaggy epithelium
Solid areas with white
nodules representing
lymphoid follicles
60

61. Warthin’s Tumor

Histology


Papillary projections
into cystic spaces
surrounded by
lymphoid stroma
Epithelium: double cell
layer



Luminal cells
Basal cells
Stroma: mature
lymphoid follicles with
germinal centers
61

62. Warthin’s Tumor
62

63. Oncocytoma






Rare: 2.3% of benign salivary tumors
6th decade
M:F = 1:1
Parotid: 78%
Submandibular gland: 9%
Minor salivary glands: palate, buccal mucosa,
tongue
63

64. Oncocytoma

Presentation

Enlarging, painless mass
64

65. Oncocytoma

Gross




Encapsulated
Homogeneous, smooth
Orange/rust color
Histology





Cords of uniform cells and
thin fibrous stroma
Large polyhedral cells
Distinct cell membrane
Granular, eosinophilic
cytoplasm
Central, round, vesicular
nucleus
65

66. Monomorphic Adenomas





Basal cell is most common: 1.8% of benign
epithelial salivary gland neoplasms
6th decade
M:F = approximately 1:1
Caucasian > African American
Most common in parotid
66

67. Basal Cell Adenoma
1- Solid




Most common
Solid nests of tumor
cells
Uniform,
hyperchromatic, round
nuclei, indistinct
cytoplasm
Peripheral nuclear
palisading
67

68. Basal Cell Adenoma
2- Trabecular


Cells in elongated
trabecular pattern
Vascular stroma
68

69. Basal Cell Adenoma
3- Tubular



Multiple duct-like
structures
Columnar cell lining
Vascular stroma
69

70. Basal Cell Adenoma
4-
Membranous


Thick eosinophilic hyaline
membranes surrounding
nests of tumor cells
―jigsaw-puzzle‖
appearance
70

71. Monomorphic Adenomas

Canalicular adenoma
7th decade
 F:M – 1.8:1
 Most common in minor salivary glands of the upper
lip (74%)
 Painless submucosal mass

71

72. Canalicular Adenoma

Histology




Well-circumscribed
Multiple foci
Tubular structures line by
columnar or cuboidal
cells
Vascular stroma
72

73. Myoepithelioma





<1% of all salivary neoplasms
3rd-6th decades
F>M
Minor salivary glands > parotid >
submandibular gland
Presentation: asymptomatic mass
73

74. Myoepithelioma

Histology

Spindle cell





More common
Parotid
Uniform, central nuclei
Eosinophilic granular or
fibrillar cytoplasm
Plasmacytoid cell


Polygonal
Eccentric oval nuclei
74

75. Mucoepidermoid Carcinoma







Most common salivary gland malignancy
5-9% of salivary neoplasms
Parotid 45-70% of cases
Palate 18%
3rd-8th decades, peak in 5th decade
F>M
Caucasian > African American
75

76. Mucoepidermoid Carcinoma

Presentation
Low-grade: slow growing, painless mass
 High-grade: rapidly enlarging, +/- pain


**Minor salivary glands: may be mistaken for
benign or inflammatory process
Hemangioma
 Papilloma
 Tori

76

77. Mucoepidermoid Carcinoma

Gross pathology


Well-circumscribed to
partially encapsulated to
unencapsulated
Solid tumor with cystic
spaces
77

78. Mucoepidermoid Carcinoma

Histology—Low-grade



Mucus cell > epidermoid
cells
Prominent cysts
Mature cellular elements
78

79. Mucoepidermoid Carcinoma

Histology—Intermediategrade



Mucus = epidermoid
Fewer and smaller cysts
Increasing pleomorphism
and mitotic figures
79

80. Mucoepidermoid Carcinoma

Histology—High-grade


Epidermoid > mucus
Solid tumor cell
proliferation
80

81. Mucoepidermoid Carcinoma

Treatment
Influenced by site, stage, grade
 Stage I & II



Wide local excision
Stage III & IV
Radical excision
 +/- neck dissection
 +/- postoperative radiation therapy

81

82. Adenoid Cystic Carcinoma





Overall 2nd most common malignancy
Most common in submandibular, sublingual
and minor salivary glands
M=F
5th decade
Presentation
Asymptomatic enlarging mass
 Pain, paresthesias, facial weakness/paralysis

82

83. Adenoid Cystic Carcinoma

Gross pathology



Well-circumscribed
Solid, rarely with cystic
spaces
infiltrative
83

84. Adenoid Cystic Carcinoma

Histology—cribriform
pattern


Most common
―swiss cheese‖
appearance
84

85. Adenoid Cystic Carcinoma

Treatment
Complete local excision
 Tendency for perineural invasion: facial nerve
sacrifice


Prognosis
Local recurrence: 42%
 Distant metastasis: lung
 Indolent course: 5-year survival 75%, 20-year
survival 13%

85

86. Acinic Cell Carcinoma





2nd most common parotid and pediatric
malignancy
5th decade
F>M
Bilateral parotid disease in 3%
Presentation

Solitary, slow-growing, often painless mass
86

87. Acinic Cell Carcinoma

Gross pathology


Well-demarcated
Most often homogeneous
87

88. Acinic Cell Carcinoma

Histology

Solid and microcystic
patterns





Solid sheets
Numerous small cysts
Polyhedral cells
Small, dark, eccentric
nuclei
Basophilic granular
cytoplasm
88

89. Acinic Cell Carcinoma

Treatment


Complete local excision
Prognosis
5-year survival: 82%
 10-year survival: 68%
 25-year survival: 50%

89

90. Adenocarcinoma





Rare
5th to 8th decades
F>M
Parotid and minor
salivary glands
Presentation:
Enlarging mass
 25% with pain or facial weakness

90

91. Adenocarcinoma

Histology


Heterogeneity
Presence of glandular
structures and absence of
epidermoid component
91

92. Adenocarcinoma

Treatment
Complete local excision
 Neck dissection


Prognosis
Local recurrence: 51%
 Regional metastasis: 27%
 Distant metastasis: 26%
 15-year cure rate:




Stage I = 67%
Stage II = 35%
Stage III = 8%
92

93. Malignant Mixed Tumors

Carcinoma ex-pleomorphic adenoma


Carcinosarcoma


Carcinoma developing in the epithelial component of
preexisting pleomorphic adenoma
True malignant mixed tumor—carcinomatous and
sarcomatous components
Metastatic mixed tumor

Metastatic deposits of otherwise typical pleomorphic
adenoma
93

94. Squamous Cell Carcinoma




1.6% of salivary gland neoplasms
7th-8th decades
M:F = 2:1
MUST RULE OUT:
High-grade mucoepidermoid carcinoma
 Metastatic SCCA to intraglandular nodes
 Direct extension of SCCA

94

95. Squamous Cell Carcinoma

Gross pathology



Unencapsulated
Ulcerated
fixed
95

96. Squamous Cell Carcinoma

Histology



Infiltrating
Nests of tumor cells
Well differentiated



Keratinization
Moderately-well
differentiated
Poorly differentiated

No keratinization
96

97. Squamous Cell Carcinoma

Treatment
Radical excision
 Neck dissection


Prognosis
5-year survival: 24%
 10-year survival: 18%

97

98. Thank You
98