This document provides information on benign and malignant diseases of the salivary glands, including:
1. It discusses the embryology, surgical anatomy, non-neoplastic conditions, benign tumors, and malignant tumors of the major and minor salivary glands.
2. It describes common benign tumors like pleomorphic adenoma and Warthin's tumor, as well as malignant tumors such as mucoepidermoid carcinoma.
3. It provides details on the classification, clinical features, histology, treatment and prognosis of various salivary gland neoplasms.
Introduction
Epidemiology
Etiology
Manifestations
TNM staging
Squamous cell carcinoma is defined as malignant epithelial neoplasm exhibiting squamous differentiation as characterised by the formation of keratin and/or the presence of intercellular bridges.
( Pindborg et al, 1997).
Introduction
Epidemiology
Etiology
Manifestations
TNM staging
Squamous cell carcinoma is defined as malignant epithelial neoplasm exhibiting squamous differentiation as characterised by the formation of keratin and/or the presence of intercellular bridges.
( Pindborg et al, 1997).
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Lymphoid tumors, cavernous hemangiomas, and meningiomas are the most common orbital tumours in adults.
Other tumors include those of the lacrimal gland, tumors from the surrounding sinuses, metastatic tumors such as breast cancer in women, and neural-based tumors
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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4. Embryology
• The parotid anlagen first to develop.
• Parenchymal tissue - proliferation of oral epithelium.
• The stroma (capsule and septae)-from mesenchyme-mesodermal or
neural crest in origin.
• PG first to develop, encapsulate AFTER SMG and SLG.
• The lymphatic system develops after the encapsulation of the SMG
and SLG but BEFORE encapsulation of the parotid
• At around the 7-8th
month in utero, secretory cells (acini) begin to
develop around the ductal system.
• Parotid 4th
wk, SMG 6th
wk, SLG 8th
wk
4
12. Obstructive SG Disorders:
Sialolithiasis
• Sialolithiasis - mechanical obstuction of the
salivary duct
• major cause of unilateral diffuse parotid swelling
• Incidence
• Etiology
• Stone composition and characterstics
• Clinical presentation
• Diagnosis and treatment
12
13. Mucocele
• Mucus is the exclusive secretory product of
the accessory minor salivary glands and the
most prominent product of the sublingual
gland.
• The mechanism for mucus cavity
development is extravasation or retention
• Excision with strict removal of any
projecting peripheral salivary glands
13
14. Ranula
• term used for mucoceles that
occur in the floor of the mouth.
• Source, usually the
sublingual gland
– also arise from the
submandibular duct
– Or minor salivary glands
• Marsupialization fallen into
disfavour due to the excessive
recurrence rate of 60-90%
• Sublingual gland removal via
intraoral approach 14
17. 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 Viral
Infection of the salivary glands.
– HIV associated salivary gland disease
– HCV
– HTLV-I
– EBV/CMV 17
19. Immunologic Disease
Sjögren’s Syndrome
• Most common immunologic disorder
• lymphocyte-mediated destruction of exocrine glands
leading to xerostomia and kerato conjunctivitis sicca
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
19
20. Sjögren’s Treatment
• Avoid xerostomic meds if possible
• Avoid alcohol, tobacco (accentuates xerostomia)
• Sialogogue (eg:pilocarpine) use is limited by other
cholinergic effects like bradycardia & lacrimation
• Sugar free gum or diabetic confectionary
• Salivary substitutes/sprays
20
21. Radiation Injury
• Low dose radiation (1000cGy) to a salivary gland
causes an acute tender and painful swelling within
24hrs.
• Serous cells are especially sensitive and exhibit
marked degranulation and disruption.
• 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. 21
22. Other: Pneumoparotitis
• In the absence of gas-producing bacterial parotitis,
gas in the parotid duct or gland is assumed to be
due to the reflux of pressurized air from the mouth
into Stensen’s duct.
• May occur with episodes of increased intrabuccal
pressure
– Glass blowers, trumpet players
• Aka: pneumosialadenitis, wind parotitis,
pneumatocele glandulae parotis
22
25. Salivary Gland Neoplasms
• There is little to distinguish a benign tumor
from its malignant counterpart
• Pre operative diagnosis by FNAC is
difficult & often inconclusive
• Surgery is challenging and worrying owing
to the relationship with facial nerve
• Recurrence are common
• Malignant transformation of some
recurrent benign tumors is well recognised
& almost impossible to cure.
25
26. Salivary Gland Neoplasms
• Diverse histopathology
• Relatively uncommon
– 3% of head and neck neoplasms : 75% benign
• Distribution
– Parotid: 80% overall; 80% benign;80% pleomorphic
– Submandibular: 15% overall;50% benign;95%
pleomorphic
– Sublingual/Minor: 5% overall; 40% benign
26
27. Etiology
• Exact cause is UNKNOWN
• Probable causes :
Exposure to radiation
Survivors of childhood malignancy
Thyroid CA pts. Treated with Radioactive iodine
Long term effects of high freq. electromagnetic
fields.
Role of PLAG I - pleomorphic adenoma
EBV- lymphoepithelial tumor
27
29. Multicellular Theory
• Each tumour type maps to different cell type
• Acinar cells—acinic cell carcinoma
• Striated duct—oncocytic tumors
• Excretory Duct—squamous cell and
mucoepidermoid carcinoma
• Intercalated duct and myoepithelial cells—
pleomorphic tumors
29
30. Pleomorphic Adenoma
• Most common of all salivary gland neoplasms
• 80% of parotid tumors
• 50% of submandibular tumors
• 45% of minor salivary gland tumors
• 6% of sublingual tumors
• 4th
-6th
decades
• F:M = 1.4:1
30
31. Pleomorphic Adenoma
• Slow growth, Benign course
• Clinical features :
Asymptomatic / Symptomatic
Clinical examination
False capsule-sub capsular clefts
• Prone to recurrence
• Associated with another salivary gland tumor
• Incidence of malignant change 6%
31
36. Warthin’s Tumor
• Papillary cystadenoma lymphomatosum / Adenolymphoma
• 14% of salivary gland neoplasms
• Second most common tumor.
• Exclusively a tumor of Parotid gland.
• Seventh decade; M:F::1.5:1
• Heavily built or obese individuals
• Etiology
• Clinical presentation 10% bilateral
36
37. Warthin’s Tumor
• Most common site
Tail of parotid
• Gross pathology
– Encapsulated
– Smooth/lobulated surface
– Soft, fluctuant, compressible
– Cystic spaces of variable size,
with viscous fluid, shaggy
epithelium
– Solid areas with white nodules
representing lymphoid follicles
37
38. Warthin’s Tumor
• “WHALE”
Warthins Has Abundant Lymphoid and Epithelial
components
• 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
38
39. Warthin’s Tumor
• Second tumor, most commonly
pleomorphic adenoma.
• Almost Never Malignant
• Recurrences very rare
39
42. Malignant Salivary gland tumors
• Relatively UNCOMMON
• Slow growth pattern does not lessen their
malignant nature
• Considerable morbidity & mortality
• INCIDENCE : 1.2 PER 1,00,000 population
• Parotid 58% ; minor salivary glands 23%
• Malignancy is far more frequent in Minor
salivary glands & Sublingual glands
43
44. Cell and molecular biology
• Increased AgNOR clusters
• Immunohistochemical markers of prognostic
interest :
Ki 67 - Adenoid cystic CA
PCNA
Bcl -2
Cytokeratin 14 - SCC
FGF 1 & 2 & FGF R1
45
45. Malignant Salivary gland tumors
• Features suggestive of Malignancy
Induration
Fixed to overlying skin or mucosa
Ulceration of overlying skin or mucosa
Rapid growth; growth spurt
Pain often severe
Facial nerve palsy
Short duration 46
46. MALIGNANT NEOPLASMS
TNM
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
47
47. Stage Grouping
Stage I T1 N0 M0
Stage II T2 N0 M0
Stage III T3 N0 M0
T1 N1 M0
T2 N1 M0
T3 N1 M0
Stage IVA T4a N0 M0
T4a N1 M0
T1 N2 M0
T2 N2 M0
T3 N2 M0
T4a N2 M0
Stage IVB T4b Any N M0
Any T N3 M0
Stage IVC Any T Any N M1 48
48. Mucoepidermoid Carcinoma
• Most common major salivary gland malignancy
• MC salivary gland neoplasm in children
• 5-9% of salivary neoplasms
• Parotid 45-70% of cases
• Palate 41%
• 3rd-8th decades, peak in 5th decade
• M:F 1:1
49
50. Mucoepidermoid Carcinoma
• Gross pathology
– Well-circumscribed ,
partially encapsulated
to unencapsulated
– Solid tumor with cystic
spaces
51
51. Mucoepidermoid Carcinoma
• Histology—
Low-grade
– Mucus cell > epidermoid cells
– 10% tumour cells and 90% intracystic
spaces
– Prominent cysts
– Mature cellular elements
High-grade
– Epidermoid > mucus
– 90% tumour cells,<10% intracystic
spaces.
– Solid tumor cell proliferation
Old classification into
intermediate-dubious and no
prognostic significance 52
52. Mucoepidermoid Carcinoma
• Treatment
– Influenced by site, stage, grade
– Stage I & II
• Wide local excision
– Stage III & IV
• Radical excision
• +/- neck dissection
• +/- postoperative radiation therapy
• low grade-local resection and follow up.
• high grade –Radical resection and RT
53
53. Adenoid Cystic Carcinoma
• 40% of malignant tumors of all salivary sites
• Most common in minor salivary glands
– 25% parotid, 15% submandibular gland, 1% sublingual
gland, 60% minor glands.
• 41% locally advanced, 11% distant metastasis
54
54. Adenoid Cystic Carcinoma
• F > M
• 6th
decade
• Source – intercalated ducts
• Spreads perineural –central and peripheral
• Presentation
– Asymptomatic enlarging mass
– Pain, paresthesias, facial weakness/paralysis
– Nodal spread-8% early and 7% late.
– 7th
nerve palsy – 20%
55
55. Adenoid Cystic Carcinoma
• Gross pathology
– Well-circumscribed
– Solid, rarely with
cystic spaces
– Infiltrative
– hard and fixed
56
63. METASTATIC TUMOURS
• 80% Skin of face, pinna, temple or scalp
• SCC or Melanoma
– Parotidectomy with neck dissection in
continuity with primary lesion
• Lung, breast and kidney.
– Dismal prognosis
64
65. Imaging of Salivary glands
• USG
Distinguish intrinsic from extrinsic tumors
USG guided FNAC
Malignant tumors have low reflectivity with poorly defined borders.
Disadv
Deep lobe parotid masses
Masses with parapharyngeal extension
Bone & dental artefacts
66
66. Imaging of Salivary glands
• CT Scan : CECT / CT Sialography
Differentiate benign from malignant masses
Differentiate superficial from deep lobe tumors
Separate a parapharyngeal mass from deep lobe tumor
Relationship of mass to facial nerve
Considerable insight into probable histology
Malignant tumors : irregular outline
Diffuse border
Nodal metastases
67
67. Imaging of Salivary glands
• MRI :
Superior soft tissue delineation
Multiplanar capabilities
Malignancy :
Infiltration
Bony changes
Perineural enhancement
signal intensity in T2 wt.
images (improved by
gadolinum)
68
68. Fine-Needle Aspiration Biopsy
• Efficacy is well established
– Accuracy = 84-97%: Sensitivity = 54-95%
– Specificity = 86 - 100%
– Safe(controversial– tumor seeding): well tolerated
• Limitations
– offers least possibility of pre op diagnosis
– Missing critical area at tumor border
– Important to distinguish benign vs. malignant nature of
neoplasm
– Preoperative patient counseling
69
69. Sialography
• Watery or oily iodinated contrast
• Multiple radiographs
• Adv-
– Quick
– Widely available
– Depiction of extra and intra glandular ducts
• Disadvantage-
– Invasive
– Complications
– In complete obstruction, not useful
– Interference with TFT 70
70. MANAGEMENT
• TREATMENT
– Surgery
– Radiotherapy
– Chemotherapy
• Factors that influence treatment
• Age
• Metastatic spread
• Facial nerve involvement
• Mandibular / Temporal bone involvement
• Skin
• Site of tumor
• Size, Extent, Grade & stage
71
71. Management
• Parotid masses
– Superficial parotidectomy
Most benign tumors
– Total conservative parotidectomy
-deep to nerve and deep lobe of
gland
– Total Radical parotidectomy
– Extended radical parotidectomy
• Submandibular masses : Total
excision of gland
• Sublingual & Minor salivary
gland tumors : Wide local
excison 72
73. MANAGEMENT
SUB MANDIBULAR GLAND:
• FNAC And Frozen section – malignancy
-complete resection +nerves in close
proximity to tumour + suprahyoid LN
dissection.
MINOR SALIVARY GLAND TUMOUR:
Hard palate –partial maxillectomy
74
74. Role of Radiotherapy
• Deep lobe parotid tumors
• Close or positive histologic surgical margins
• Undifferentiated or high-grade histology
• Recurrent malignancy
• Bone or connective tissue involvement
• Metastatic regional cervical lymph nodes
• Perineural involvement
• Intraoperative tumor spillage or capsular rupture
75
75. ROLE OF CHEMOTHERAPY
• Single or multiple regime – adenoid cystic Ca
• Inoperable disease-distant metastasis
• Cisplatin –slow i.v 50-100mg/m2 every 3-4wks
• Doxorubicin –slow i.v,60-75mg/m2 every 3wks
• 5-fluorouracil –12mg/kg/day for 4 days,6mg/kg
i.v on alternate days
76
76. PROGNOSIS
• Survival time – varies widely
• Depends on :
-age and sex
-grade and stage
-histological type of tumour
-method of diagnosis
-type of treatment administered
• 5 yr survival rate –acinic cell tumour 82%
-mucoepidermoid 70%
-adenoid cystic 62%
malignant mixed tumour 56%
77
Etiology- neoplastic proliferation of ectopic salivary gland ducts within intra or paraparotid lymph node. Absence of lymphoid tissue in other salivary glands explains the exclusive nature to parotid.
CF-slow growing. Soft Painless swelling. Few undergo rapid expansion with pain…may be mistaken for malignancy.