Management Of Malignant Salivary Gland Tumors Take note of the peculiarities Management Of Malignant Salivary Gland Tumors Take note of the peculiarities

1. JOS UNIVERSITY TEACHING
HOSPITAL

2. OKOYE C

3. OUTLINE
 Introduction
 Relevant Anatomy/Physiology
 Epidemiology
 Classification
 Etiology
 Malignant Tumours of Salivary Glands
 Investigation
 Staging
 Management
 Complications
 Prognosis
 Conclusion
 References

4. Introduction
• Salivary gland tumours (SGTs) are part and
parcel of Head & Neck tumours.
• Different from other Head & Neck tumours in
several respects.
i. some seen no where else in the body.
ii.SCC,commonest Head & Neck tumours
extremely rare in salivary glands.

5. Introduction
 Can occur at any site where salivary tissue is
found
 Accurate pathologic diagnosis is key to the
management of these lesions
 degree of aggressiveness depends on their
histological profiles

6. Epidemiology
 Global annual incidence for all salivary gland
tumours
 varies from 0.4-13.5 cases per 100,000
population
 represent about 3% of all tumours.
 2.5 per million in Norway; 7.5 in Sweden; 15 in
Caucasians living in the USA.

7. Epidemiology
 Developing nations experience similar
incidence.
 Approximately 80% of salivary gland tumours
are located in the parotid gland
 10% in submandibular gland, and remainder
distributed among sublingual & minor salivary
glands(Snow,1979).

8. Epidemiology
 In Nigeria, reports indicate more malignant than
benign SGTs.
 Our study found the benign to malignant ratio was
1:2.3
 With predominant involvement of major glands.

9. Epidemiology
 Adoga A.S et-al in a 30-month (October 2005 – March
2008) retrospective review of Head and Heck
histopathologically confirmed cancer specimens;
found-
 Thirty-two (41 %)cases confirmed histologically as
malignant Head and Neck tumours out of a total of
seventy-eight histologic specimens
 Twenty three (23) males and 9 females(M:F= 2.6:1).
 Mucoepidermoid carcinoma (6.3%)

10. Epidemiology
 In the USA, salivary gland malignancies accounted for
 6% of Head and Neck cancers,
 and 0.3% of all malignancies
 There is also some geographic variation in the
frequency of tumour types

11. Epidemiology

12. Incidence of benign and malignant salivary neoplasms
according to the site of origin - Memorial Sloan-
Kettering

13. Epidemiology
 There is no obvious gender variation, however there’s a
female preponderance in most tumour types.
 average ages of patients with benign and malignant
tumours are 46 and 47 years, respectively, and
 the peak incidence of most of the specific types is in the
sixth and seventh decades
 Could also occur in children

14. ANATOMY

16. Parotid Gland
 An largely encapsulated gland located
 lateral to the masseter muscle anteriorly and extends
posteriorly over the sternocleidomastoid muscle behind
the angle of the mandible
 Laterally – dermis
 Medially - lateral parapharyngeal space
 Artificially divided into a superficial lobe and a deep
lobe by the branches of the seventh cranial nerve

17. Boundaries
 Superior: External acoustic meatus, condyle of
mandible and zygomatic arch
 Anterior: posterior border of the ramus of the
mandible and the muscles attached to it
 Posterior: Mastoid process, sternocleidomastoid
muscle
 Inferior: Posterior belly of digastric muscle
 Medial: Styloid process

18. Parotid Gland
 Almost purely serous, with an average weight of 25
grams
 Its parenchyma is divided into lobules by fibrous septa
 Has abundant intralobular and extralobular adipose
tissue (increases in relative volume with age)
 Sebaceous glands are commonly seen,
 either individually or in small groups
 Has two layers of draining lymph nodes (range 1 to 20)
 superficial layer lies beneath the capsule, and
 deeper layer lies within the parotid parenchyma

19. Parotid Gland
 Stensen duct:
 courses anteriorly over the masseter muscle
 pierces the buccinator muscle
 enter through the buccal mucosa, usually opposite the
second maxillary molar

20. Submandibular Gland
 Mixed; serous and mucous
 Although the serous element predominates
(~90%).
 In mixed acini the serous cells form caps, or
demilunes, on the periphery of the mucous cells.
 Its intercalated ducts are shorter while the striated
ducts more conspicuous than those of the parotid
gland

21. Submandibular Gland
 The second largest salivary glands, each weighing
approximately 10–15 grams
 Divided into superficial and deep lobes by the
posterior edge of the mylohyoid muscle and
 occupies the submandibular triangle
 Wharton duct
 courses anteriorly above the mylohyoid muscle
 ends in the anterior floor of the mouth

22. Sublingual Gland
 Mixed but predominantly mucous in type.
 The mucous acini form elongated tubules with
peripheral serous demilunes
 They’re paired and located in the submucosa,
superficial to the mylohyoid muscle.
 Each gland is bounded:
 laterally – inner cortex of the mandible and
 medially by the styloglossus muscle; the paired glands
meet in the midline.

23. Sublingual Gland
 Has multiple small or "minor" sublingual ducts,
referred to as the ducts of Rivinus, which open
directly into the oral cavity.
 Some of these ducts unite to form the major ducts of
Bartholin.
 These major ducts can also join the submandibular ducts.
 The lingual nerve
 descends laterally to the anterior end of the sublingual gland
 runs along its inferior border
 anteriorly, the lingual nerve and submandibular duct run
parallel until the lingual nerve ascends into the tongue

25. Minor salivary glands
 Most numerous at the junction of the hard and
soft palate, lips and buccal mucosa and most part
of aerodigestive tract
 In the lateral aspects of the tongue, lips and
buccal mucosa are
 seromucous
 In the ventral tongue, palate, glossopharyngeal
area and retromolar pad
 predominantly mucous.

26. Minor salivary glands
 Those related to the circumvallate papillae
(von Ebner’s glands)
 are serous
 Are not encapsulated,
 Those in the tongue and lip
 can be deeply located in the musculature

27. Functional Unit
 Consist of
 the secretory acinus
 related intercalated, striated and
excretory ducts,
 myoepithelial cells
 Acini may be
 serous, mucous or mixed
 Myoepithelial, or basket cells,
 are contractile
 located between the basement
membrane and the basal plasma
membrane of the acinar cells
 also surround the intercalated ducts

28. Drainage pathway
both serous and mucous
cells are arranged into acini
drained by a series of
ducts—an intercalated duct
drains into a striated duct,
which
empties into an excretory
duct

29. Classification of Salivary Gland Neoplasms
 Armed Forces Institute of Pathology
 Benign Epithelial Neoplasms
 Malignant Epithelial Neoplasms
 Mesenchymal Neoplasms
 Malignant Lymphomas
 Metastatic Tumors
 Nonneoplastic Tumor-like Conditions

30. Classification of Salivary Gland
Neoplasms
 WHO (2017)
 Adenomas
 Carcinomas
 Nonepithelial Tumours
 Malignant lymphomas
 Secondary tumours
 Unclassified tumours
 Tumour-like lesions

32. Physiology
Production of Saliva
 The production of saliva is an active process occurring
in 2 phases:
 1)Primary secretion occurs in the acinar cells. This
results in a product similar in composition and
osmolality to plasma.
 2)Ductal secretion results in a hypotonic salivary fluid.
It also results in decreased sodium and increased
potassium in the end product.

33. Physiology
 Saliva is 99.5% water and otherwise proteins and
electrolytes.
 Humans secrete about a liter of saliva per day.
 Ca2+ concentration is twice as high in the
submandibular gland.
 Gustatory and olfactory stimulation induce
predominantly parotid secretion.
 Submandibular gland secretion has a higher mucin
content and a higher basal flow rate and is the
predominant unstimulated saliva.

34. Etiology
 Not clearly understood but the following risk factors
have been implicated
- exposure to ionizing radiation
- smoking
- genetics; loss of alleles of chromosomes in 12q, 8q
and 17q
- ki-67 and p53

35. Etiology
 Environment and Diet- deficiency of vitamin A,
industrial agents like nickel, cadmium, hair dyes,
silica, preservatives, wood dust
 Infection- mumps, EBV and chronic sialadenitis

36. Theories
 Bicellular reserve cell theory:
 the origin of the various types of salivary neoplasms can be
traced to the basal cells “stem cell” of either the excretory
or the intercalated duct.
 either of these two cells can act as a reserve cell with the
potential for differentiation into a variety of epithelial cells
 Multicellular theory:
 each type of neoplasm is thought to originate from a
distinctive cell type within the salivary gland unit
 supported by the observation that all differentiated salivary
cell types retain the ability to undergo mitosis and
regenerate

37. Bicellular Theory
 Intercalated Ducts
 Pleomorphic adenoma
 Warthin’s tumor
 Oncocytoma
 Acinic cell
 Adenoid cystic
 Excretory Ducts
 Squamous cell
 Mucoepidermoid

38. Multicellular Theory
 Striated duct—oncocytic tumors
 Acinar cells—acinic cell carcinoma
 Excretory Duct—squamous cell and
mucoepidermoid carcinoma
 Intercalated duct and myoepithelial cells—
pleomorphic tumours

39. Malignant Tumours of Salivary
Glands

40. Malignant tumours
 Mucoepidermoid
 Adenoid cystic carcinoma
 Acinic cell carcinoma
 Adenocarcinoma
 Malignant mixed tumour
 Squamous cell carcinoma
 Undifferentiated carcinoma
 Lymphoma
 Sarcoma

41. Mucoepidermoid carcinoma
 It is the most common malignant tumour of the
parotid gland
 Common between 3rd and 8th decades of life( peak in
5th decade)
 More common in female than male
 Commoner in Caucasians

42. Mucoepidermoid carcinoma
 Slow growing tumour but attaining large size
 It could be high grade, intermediate grade or low grade
 High grade is mainly epidermoid, rapidly enlarging,
with or without pain.
 Regional and distant metastasis is common

43. Mucoepidermoid carcinoma
 Low grade contains mucous cells mainly with regional
node spread
 Gross pathology- well circumscribed to partially
encapsulated or unencapsulated, solid tumour with
cystic spaces

45. Adenoid cystic carcinoma
 Rare in parotid gland but overall second most common
malignancy
 It is also called cylindromatous carcinoma
 Equal male: female
 Common in 5th decade

46. Adenoid cystic carcinoma
 It is slow growing but highly malignant
 It has high affinity for perineural spread
 Clinical features may include; pain, paraesthesias,
facial weakness or paralysis
 Spread to lungs, bones and liver
 Histology- cribriform pattern, Swiss cheese
appearance

48. Acinic cell tumour
 Mainly occurs in the parotid glands
 It is a low grade malignant tumour
 It constitute 3% of all salivary gland tumours and 90%
occur in the parotid gland
 Can involve facial nerve or neck nodes
 Metastasis to lungs or vertebrae
 Five year survival is 85%

49. Acinic cell tumour

50. Adenocarcinoma
 Rare
 5thto 8thdecades
 F > M
 Parotid and minor salivary glands
 Presentation:–Enlarging mass–25% with pain or facial
weakness

51. Adenocarcinoma
Histology
 Heterogeneity
 Presence of glandular structures and absence of
epidermoid component
 Grade I–Grade II–GradeIII

53. Malignant mixed tumour
 It has the worst prognosis
 Types :
- carcinoma expleomorphic adenoma; it is the
commonest, most aggressive
- primary malignant mixed tumour
- metastasizing mixed tumour
- extensive infiltration and tissue destruction are
common.

54. Malignant mixed tumour

55. Squamous cell carcinoma
 Rare in the parotid
 High grade tumour
 Common in 6th – 7th decade
 It is rapidly growing tumour associated with pain,
facial nerve palsy, skin fixity and ulceration
 It has poor prognosis
 5-year survival: 24% 10-year survival: 18%
 Treatment is by radical parotidectomy + radiotherapy

56. Lymphoma
 May develop in intraparotid lymph nodes.
 On fine needle aspiration cytology, parotid
lymphomas are frequently confused with Warthin’s
 In many cases, open or core biopsy is necessary to
arrive at the correct diagnosis.

57. Investigations
 General
 Specific

58. General
 FBC
 U/E
 LFT

59. Specific
 Fine needle aspiration cytology
 Ultrasonography
 Computed Tomography
 Magnetic Resonance Imaging
 Frozen Section

60. TNM staging (Union for International
Cancer Control 2017)
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
T1 Tumor 2 cm or less in greatest dimension without gross
extraparenchymal extension
T2 Tumor more than 2 cm but not more than 4 cm in greatest
dimension without gross extraparenchymal extension
T3 Tumor more than 4 cm and/or tumor having gross
extraparenchymal extension
T4a Tumor invades skin, mandible, ear canal, and/or facial nerve
T4b Tumor invades skull base and/or pterygoid plates and/or encases
carotid artery

61. Regional lymph nodes
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest
dimension
N2a Metastasis in a single ipsilateral lymph node, more than 3 cm but
not more than 6 cm in greatest dimension
N2b Metastasis in multiple ipsilateral lymph nodes, none more than 6
cm in greatest dimension
N2c Metastasis in bilateral or contralateral lymph nodes, none more
than 6 cm in greatest dimension
N3 Metastasis in a lymph node more than 6 cm in greatest dimension

62. Distant metastasis
MX Distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis

63. Treatment
 A)Surgery :
- total conservative parotidectomy( T1, T2 and T3)
- radical parotidectomy(t4); both superficial and deep
lobes, facial nerve, soft tissues with skin, mandibular
ramus and masseter muscle
- facial nerve reconstruction; greater auricular nerve/
sural nerve

64. Treatment
 B) Radiotherapy:
- three to six weeks after surgery
- delayed for six weeks if nerve grafting done
- dose- 50- 70 gy( 1.5 – 2 gy in 5 days in 8 weeks)
 C) Chemotherapy:
-5 fluorouracil
- cisplatin
- doxorubicin
- epirubicin

65. Complications
 Hematoma
 Salivary gland fistula
 Flap necrosis
 Paresthesia
 Frey’s syndrome
 Facial nerve palsy
 Recurrence
65

66. Prognosis
 Variables such as histological subtype, grade, stage,
age, gender, pain, skin invasion and facial nerve
dysfunction, resection margins and comorbidity have
been identified as stastically significant prognostic
factors

67. Conclusion
 Parotid gland tumours are the commonest(80%) of all
salivary gland tumours
 They exhibit a diverse range of histological type and
clinical behaviour
 Investigations are essential to help tailor appropriate
treatment and should include fine needle aspiration
cytology reported by an expert pathologist

68.  Majority of these tumours will be treated by surgery,
the extent of which should be tailored to the size,
clinical and histological type of tumour
 Facial nerve conservation should be considered if not
affected
 Adjuvant radiotherapy should be considered in
malignant cases with adverse clinical or histological
features
 Adequate follow up visits is essential for these patients

69. THANK YOU

70. References
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 Kontis TC, Johns Me. Anatomy and Physiology of the
Salivary Glands. Head and Neck Surgery-
Otolaryngology, Second Edition, ed. Byron J. Bailey.
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 Wilson J (ed). Effective Head and Neck Cancer
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