Salivary glands disorders ii

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Oral & Maxillofacial Surgery
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Salivary glands disorders ii

  1. 1. Salivary Gland Disorders Dr. Wael Talaat Assistant Professor of Oral and Maxillofacial Surgery 1
  2. 2. Salivary Gland Infections    Acute bacterial sialdenitis Chronic bacterial sialdenitis Viral infections 2
  3. 3. Sialadenitis Sialadenitis represents inflammation mainly involving the acinoparenchyma of the gland. 3
  4. 4. Sialadenitis Acute infection more often affects the major glands than the minor glands 4
  5. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 20. Chronic Sialadenitis  The clinician should look for a treatable predisposing factor such as a calculus or a stricture. 20
  21. 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. 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. 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. 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. 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. 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. 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. 28. Treatment    Supportive Fluid Anti-inflammatories and analgesics 28
  29. 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. 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. 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. 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. 33. Sjögren’s Syndrome   Salivary gland swelling may be permanent or intermittent. Rule out lymphoma 33
  34. 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. 35. Sjögren’s Lip Biopsy  Biopsy of SG mainly used to aid in the diagnosis 35
  36. 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. 37. Sjögren’s Treatment     Avoid xerostomic meds if possible Avoid alcohol, tobacco (accentuates xerostomia) Sugar free gum Salivary substitutes/sprays 37
  38. 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. 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. 40. Related to… c. d. e. Alcoholic cirrhosis: likely based on protein deficiency & resultant acinar hypertrophy Drug induced: iodine mumps HIV 40
  41. 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. 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. 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. 44. Granulomatous Disease Sarcoidosis: a systemic disease characterized by noncaseating granulomas in multiple organ systems  Clinically, SG involvement in 6% cases 44
  45. 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. 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. 47. Salivary Gland Neoplasms   Benign Neoplasms Malignant Neoplasms 47
  48. 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. 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. 50. Pleomorphic Adenoma    Slow-growing, painless mass Parotid: 90% in superficial lobe, most in tail of gland Minor salivary gland: lateral palate 50
  51. 51. Pleomorphic Adenoma  Gross pathology      Smooth Well-demarcated Solid Cystic changes Myxoid stroma 51
  52. 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. 53. Pleomorphic Adenoma 53
  54. 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. 55
  56. 56. 56
  57. 57. 57
  58. 58. 58
  59. 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. 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. 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. 62. Warthin’s Tumor 62
  63. 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. 64. Oncocytoma  Presentation  Enlarging, painless mass 64
  65. 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. 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. 67. Basal Cell Adenoma 1- Solid     Most common Solid nests of tumor cells Uniform, hyperchromatic, round nuclei, indistinct cytoplasm Peripheral nuclear palisading 67
  68. 68. Basal Cell Adenoma 2- Trabecular   Cells in elongated trabecular pattern Vascular stroma 68
  69. 69. Basal Cell Adenoma 3- Tubular    Multiple duct-like structures Columnar cell lining Vascular stroma 69
  70. 70. Basal Cell Adenoma 4- Membranous   Thick eosinophilic hyaline membranes surrounding nests of tumor cells ―jigsaw-puzzle‖ appearance 70
  71. 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. 72. Canalicular Adenoma  Histology     Well-circumscribed Multiple foci Tubular structures line by columnar or cuboidal cells Vascular stroma 72
  73. 73. Myoepithelioma      <1% of all salivary neoplasms 3rd-6th decades F>M Minor salivary glands > parotid > submandibular gland Presentation: asymptomatic mass 73
  74. 74. Myoepithelioma  Histology  Spindle cell      More common Parotid Uniform, central nuclei Eosinophilic granular or fibrillar cytoplasm Plasmacytoid cell   Polygonal Eccentric oval nuclei 74
  75. 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. 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. 77. Mucoepidermoid Carcinoma  Gross pathology   Well-circumscribed to partially encapsulated to unencapsulated Solid tumor with cystic spaces 77
  78. 78. Mucoepidermoid Carcinoma  Histology—Low-grade    Mucus cell > epidermoid cells Prominent cysts Mature cellular elements 78
  79. 79. Mucoepidermoid Carcinoma  Histology—Intermediategrade    Mucus = epidermoid Fewer and smaller cysts Increasing pleomorphism and mitotic figures 79
  80. 80. Mucoepidermoid Carcinoma  Histology—High-grade   Epidermoid > mucus Solid tumor cell proliferation 80
  81. 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. 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. 83. Adenoid Cystic Carcinoma  Gross pathology    Well-circumscribed Solid, rarely with cystic spaces infiltrative 83
  84. 84. Adenoid Cystic Carcinoma  Histology—cribriform pattern   Most common ―swiss cheese‖ appearance 84
  85. 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. 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. 87. Acinic Cell Carcinoma  Gross pathology   Well-demarcated Most often homogeneous 87
  88. 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. 89. Acinic Cell Carcinoma  Treatment   Complete local excision Prognosis 5-year survival: 82%  10-year survival: 68%  25-year survival: 50%  89
  90. 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. 91. Adenocarcinoma  Histology   Heterogeneity Presence of glandular structures and absence of epidermoid component 91
  92. 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. 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. 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. 95. Squamous Cell Carcinoma  Gross pathology    Unencapsulated Ulcerated fixed 95
  96. 96. Squamous Cell Carcinoma  Histology    Infiltrating Nests of tumor cells Well differentiated    Keratinization Moderately-well differentiated Poorly differentiated  No keratinization 96
  97. 97. Squamous Cell Carcinoma  Treatment Radical excision  Neck dissection   Prognosis 5-year survival: 24%  10-year survival: 18%  97
  98. 98. Thank You 98

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