Salivary glands


Published on

Published in: Health & Medicine, Technology
1 Comment
No Downloads
Total Views
On Slideshare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Salivary glands

  1. 1. Mohammad Akheel OMFS PG
  3. 3. INTRODUCTION Any changes producing pain and swelling of salivary glands leads to Salivary Gland Disorders.
  4. 4. Embryology The parotid anlagen are the first to develop, followed by the submandibular gland, and finally the sublingual gland. Parenchymal tissue (secretory) of the glands arises from the proliferation of oral epithelium.
  5. 5. Embryology The stroma (capsule and septae) of the glands originates from mesenchyme that may be mesodermal or neural crest in origin.
  9. 9. STAGE 4 ( LOBULE STAGE )
  12. 12. Parotid development Although the parotid anlagen are the first to develop, they become encapsulated after the SMG and SLG. This delayed encapsulation is critical because after the encapsulation of the SMG and SLG but before encapsulation of the parotid, the lymphatic system develops.
  13. 13. Parotid development Therefore, there are intraglandular lymph nodes and lymphatic channels entrapped within the parotid gland (PG). PG is also unique because its epithelial buds grow, branch and extend around the divisions of the facial nerve.
  14. 14. Embryology The epithelial buds of each gland enlarge, elongate and branch initially forming solid structures. Branching of the glandular mass produces arborization. Each branch terminates in one or two solid end bulbs.
  15. 15. Embryology Elongation of the end bulb follows and lumina appears in their centers, transforming the end bulbs into terminal tubules. These tubules join the canalizing ducts to the peripheral acini.
  16. 16. Microanatomy The Secretory Unit Acinus (serous, mucous, mixed) Myoepithelial cells Intercalated duct Striated duct Excretory duct
  17. 17.  Striated & Intercalated ducts well developed in serous, than in mucous glands Striated duct: HCO3 taken in , Cl taken out from lumen Intercalated duct: K into lumen, Na from lumen, producing hypotonic fluid Excretory ducts do NOT modify saliva
  18. 18. Duct Canalization Canalization results from mitotic activity of the outer layers of the cord outpacing that of the inner cell layers Canalization is complete by 6th month post conception.
  19. 19. Acinar cells At around the 7-8th month in utero, secretory cells (acini) begin to develop around the ductal system.
  20. 20. Acinar cells of Salivary Glands Classified as either:  Serous cells: produce a thin watery secretion  Mucous cells: produce a more viscous secretion
  21. 21. Major glands/Secretions Major SG are paired structures and include the parotid, submandibular and sublingual Parotid: serous Submandibular: mucous & serous Sublingual: mucous
  22. 22. Anatomy: Parotid Gland  Nearly 80% of the parotid gland (PG) is found below the level of the external auditory canal, between the mandible and the SCM.  Superficial to the posterior aspect of the masseter .
  23. 23. Anatomy:Parotid Gland Extensions of PG project to mastoid process Down the anterior aspect of the SCM for a short distance Around the posterior border of the mandible. Superiorly to the to inferior margin of the zygomatic arch
  24. 24. Anatomy:Parotid Gland  CN VII branches roughly divide the PG into superficial (lateral) and deep lobes while coursing anteriorly from the stylomastoid foramen to the muscles of facial expression.
  25. 25. Anatomy: Deep Lobe The remaining 20% extends medially through the stylomandibular tunnel, which is formed ventrally by the posterior edge of the ramus dorsally by the anterior border of the SCM & posterior digastric muscle deeply and dorsally by the stylomandibular ligament.
  26. 26. Parotid : Deep lobe lies on... V: internal jugular vein A: external and internal carotid arteries N: glossopharyngeal N vagus N spinal accesory N hypoglossal N S: styloid process styloglossus m stylohyloid m
  27. 27. Anatomy: Parotid Duct Small ducts coalesce at the anterosuperior aspect of the PG to form Stensen’s duct. Runs anteriorly from the gland and lies superficial to the masseter muscle Follows a line from the EAM to a point just above the commissure. Is inferior to the transverse facial artery It is 1-3 mm in diameter 6cm in length
  28. 28. Anatomy: Parotid Duct At the anterior edge of the masseter muscle, Stensen’s duct turns sharply medial and passes through the buccinator muscle, buccal mucosa and into the oral cavity opposite the maxillary second molar.
  29. 29. Anatomy: Parotid Fascia Gland encapsulated by a fascial layer that is continuous w/the deep cervical fascia (DCF). The stylomandibular ligament (portion of the DCF) separates the parotid and submandibular gland.
  30. 30. Anatomy: Parotid Lymphatics Lymphatic drainage is to the superficial and deep cervical nodes Preauricular lymph nodes (LN) in the superficial fascia drain the temporal scalp, upper face, anterior pinna LN within the gland drain the parotid gland, nasopharynx, palate, middle ear and external auditory meatus
  31. 31. Parotid: ParasympatheticInnervation  Preganglionic parasympathetic (from CN9) arrives at otic ganglion via lesser petrosal n.  Postganglionic parasympathetic leaves the otic ganglion and distributes to the parotid gland via the auriculotemporal nerve.
  32. 32. Parotid: SympatheticInnervation Postganglionic innervation is provided by the superior cervical ganglion and distributes with the arterial system
  33. 33. Parotid Anatomy: Great AuricularNerve (C2,C3)  Emerges from the posterior border of the SCM at Erb’s point. It crosses the mid-portion of the SCM about 6.5cm beneath the EAM.  Passes parallel and superior to the external jugular vein to supply the ear and pre-auricular region.
  34. 34. Parotid Anatomy:Auriculotemporal Nerve  Branch of V3  Traverses the upper part of the parotid gland and emerges from the superior surface with the superficial temporal vessels.  It carries sensory fibers from the trigeminal and post-ganglionic parasympathetic (secretory)fibers.
  35. 35. Parotid Anatomy: FacialNerve Emerges at the level of the digastric muscle, through the stylomastoid foramen. Main trunk divides at the pes anserinus (intraparotid plexus of CN7) into the upper temporofacial and lower cervicofacial divisions. Before it enters gland, gives off 3 branches: Posterior auricular, posterior digastric, stylohyoid
  36. 36. Parotid Anatomy: Vessels Retromandibular Vein: located within the substance of the gland External carotid : at the inferior level of the gland, the external carotid divides into the superficial temporal and internal maxillary artery.
  37. 37. Anatomy:Submandibular gland Located in the submandibular triangle of the neck, inferior & lateral to mylohyoid muscle. The posterior-superior portion of the gland curves up around the posterior border of the mylohyoid and gives rise to Wharton’s duct.
  38. 38. Anatomy: SubmandibularLymphatics Submandibular gland drains into submandibular nodes.
  39. 39. Anatomy: Submandibular Duct  Wharton’s duct passes forward along the superior surface of the mylohyoid adjacent to the lingual nerve.  The nerve winds around the duct, first being lateral, then inferior, and finally medial.
  40. 40. Anatomy: Submandibular duct 2-4mm in diameter & about 5cm in length. It opens into the floor of the mouth through a punctum. The punctum is a constricted portion of the duct to limit retrograde flow of bacteria-laden oral fluids.
  41. 41. Anatomy: Sublingual glands Lie on the superior surface of the mylohyoid muscle and are separated from the oral cavity by a thin layer of mucosa.
  42. 42. Anatomy: Sublingual glands  The ducts of the sublingual glands are called Bartholin’s ducts.  In most cases, Bartholin’s ducts consists of 8-20 smaller ducts of Rivinus. These ducts are short and small in diameter.
  43. 43. Anatomy: Sublingual glands The ducts of Rivinis either open… individually into the FOM near the punctum of Wharton’s duct on a crest of sublingual mucosa called the plica sublingualis open directly into Wharton’s duct
  44. 44. Function of Saliva Moistens oral mucosa Moistens & cool food Medium for dissolved food Mineralization Buffer (HCO3) Protective Pellicle Digestion (Amylase, Lipase) Antibacterial (Lysozyme, IgA, Peroxidase,
  45. 45. Salivary hypofunction Candidiasis Lichen Planus Burning Mouth Aphthous ulcers Dental caries Xerostomia
  46. 46. Autonomic Innervation Parasympathetic Abundant, watery saliva Amylase down Sympathetic Scant, viscous saliva Amylase up
  48. 48. CLASSIFICATION Congenital Agenesis Hypoplasia Acquired Inflammatory Infection  bacterial  viral  fungal
  49. 49. CLASSIFICATION ○ Autoimmune  Sjogrens  Sicca Syndromes ○ Idiopathic  necrotizing sialometaplasia  sarcoidosis Traumatic ○ Mucocele ○ Ranula ○ Salivary fistula ○ Radiotherapy induced xerostomia
  50. 50. CLASSIFICATION Obstructive Calculus disease Ductal stenosis Ductal atresia Benign Adenomas ○ Pleomorpic adenoma ○ Basal cell adenoma ○ Adenolymphoma ○ Cystadenoma
  51. 51. Classification Non epithelial ○ Angioma ○ Lipoma ○ Neural Malignant Acinic cell carcinoma Mucoepidermoid carcinoma Polymorphous low grade adenocarcinoma Squamous cell carcinoma Squamous cell ex Pleomorphic Carcinoma Adenoid cystic carcinoma Lymphomas
  52. 52. Classification Tumor like lesions Sialadenosis Necrotising sialometaplasia Benign lymphoepithelial lesions Salivary gland cysts Cystic lymphoid hyperplasia (HIV)
  54. 54. Clinical presentation  Painful swelling (60%)  Painless swelling (30%)  Pain only (12%) Sometimes described as recurrent salivary colic and spasmodic pains upon eating
  55. 55. Clinical History History of swellings / change over time? Trismus? Pain? Variation with meals? Bilateral? Dry mouth? Dry eyes? Recent exposure to sick contacts (mumps)? Radiation history? Current medications?
  56. 56. Exam: Inspection Asymmetry (glands, face, neck) Diffuse or focal enlargement Erythema extra-orally Trismus Medial displacement of structures intraorally? Examine external auditory canal (EAC)
  57. 57. Exam: Palpation Palpate for cervical lymphadenopathy Bimanual palpation of floor of mouth in a posterior to anterior direction Have patient close mouth slightly & relax oral musculature to aid in detection Examine for duct purulence Bimanual palpation of the gland (firm or spongy/elastic).
  59. 59. ObstructiveSalivary Gland Disorders Sialolithiasis Mucous retention/extravasation
  60. 60. Sialolithiasis  Sialolithiasis results in a mechanical obstuction of the salivary duct  Is the major cause of unilateral diffuse parotid or submandibular gland swelling
  61. 61. Sialolithiasis Incidence Escudier & McGurk 1:15-20 000 Marchal & Dulgurerov 1:10-20 000 Sialolithiasis remains the most frequent reason for submandibular gland resection
  62. 62. Sialolithiasis  The exact pathogenesis of sialolithiasis remains unknown.  Thought to form via…. an initial organic nidus that progressively grows by deposition of layers of inorganic and organic substances.  May eventually obstruct flow of saliva from the gland to the oral cavity.
  63. 63. Sialolithiasis Acute ductal obstruction may occur at meal time when saliva producing is at its maximum, the resultant swelling is sudden and can be painful. MEAL TIME SYNDROME
  64. 64. Gradually reduction of the swelling can result but it recurs repeatedly when flow is stimulated. This process may continue until complete obstruction and/or infection occurs.
  65. 65. Etiology Hypercalcemia… Xerostomic meds Tobacco smoking Smoking has an increased cytotoxic effect on saliva, decreases PMN phagocytic ability and reduces salivary proteins
  66. 66. Etiology Gout is the only systemic disease known to cause salivary calculi and these are composed of uric acid.
  67. 67. Stone Composition Organic; often predominate in the center Glycoproteins Mucopolysaccarides Bacteria Cellular debris Inorganic; often in the periphery Calcium carbonates & calcium phosphates in the form of hydroxyapatite
  68. 68. Parotid (PG) vs. SubmandibularGland (SMG)…. Obstructive phenomemnon such as mucous plugs and sialoliths are most commonly found in the SMG Parotid glands are not most commonly affected
  69. 69. Reasons sialolithiasis may occurmore often in the SMG  Saliva more alkaline  Higher concentration of calcium and phosphate in the saliva  Higher mucus content  Longer duct  Anti-gravity flow
  70. 70. Other characteristics: Despite a similar chemical make-up, 80-90% of SMG calculi are radio- opaque 50-80% of parotid calculi are radiolucent 30% of SMG stones are multiple 60% of Parotid stones are multiple
  71. 71. Diagnostics: Plain occlusal film  Effective for intraductal stones, while….  intraglandular, radiolucent or small stones may be missed.
  72. 72. Diagnostic approachesCT Scan: large stones or small CT slices done also used for inflammatory disordersUltrasound: operator dependent, can detect small stones (>2mm), inexpensive, non- invasive
  73. 73. Diagnostic approaches:Sialography Consists of opacification of the ducts by a retrograde injection of a water-soluble or oil based dye. Provides image of stones and duct morphological structure May be therapeutic, but success of therapeutic sialography never documented
  74. 74. Sialography Disadvantages: irradiation dose  pain with procedure infection dye reaction push stone further contraindicated in active infection
  75. 75. Diagnostic approach:Radionuclide Studies Useful to image the parenchyma T99 is an artificial radioactive element (atomic #43, atomic weight 99) that is used as a tracer in imaging studies. T99 is a radioisotope that decays and emits a gamma ray. Half life of 6 hours.
  76. 76. Diagnostic Approaches:Radionuclide Studies Some authors say T99 is useful preoperatively to determine if gland is functional. However, no evidence to suggest gland won’t recover function after stone removed. Not advised for pre-op decision making.
  77. 77. Diagnostic approach:Diagnostic Sialendoscopy  Allows complete exploration of the ductal system, direct visualization of duct pathology  Success rate of >95%  Disadvantage: technically challenging, trauma could result in stenosis, perforation
  79. 79. Sialolithiasis Treatment  None: antibiotics and anti-inflammatories, hoping for spontaneous stone passage.  Stone excision: Lithotripsy Interventional sialendoscopy Simple removal (20% recurrence)7  Gland excision
  80. 80. Sialolithiasis Treatment If patients donot undergo treatment, they need to know: Stones will likely enlarge over time Seek treatment early if infection develops Salivary gland massage and hyper- hydration when symptoms develop.
  81. 81. Calculi excision External lithotripsy Stones are fragmented and expected to pass spontaneously The remaining stone may be the ideal nidus for recurrence Interventional Sialendoscopy Can retrieve stones, may also use laser to fragment stones and retrieve.
  82. 82. Transoral vs. Extraoral Removal Some authors say: if a stone can be palpated through the mouth, it can be removed trans-orally . Or if it can be visualized on a true central occlusal radiograph, it can be removed Trans orally . Finally, if it is no further than 2cm from the punctum, it can be removed Trans orally.
  83. 83. Posterior Stones Deeper submandibular stones (~15-20% of stones) may best be removed via sialadenectomy or excision of the gland has to be done . Floor of mouth (FOM) opened opposite the first premolar, duct dissected out, lingual nerve identified. Duct opened & stone removed, FOM approximated.
  84. 84. Submandibular Sialoliths:Transoral Advantages Preserves a functional gland Avoids neck scar Possibly less time from work Avoids risk to CN 7 & 12
  85. 85. Gland excision After SMG excision, 3% cases have recurrence via: Retention of stones in intraductal portion or new formation in residual Whartons duct
  86. 86. Gland excision Indications Very posterior stones Intra-glandular stones Significantly symptomatic patients Failed transoral approach
  87. 87. ObstructiveSalivary Gland Disorders  Sialolithiasis Mucous retention/extravasation
  88. 88. 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
  89. 89. Mucocele Mucoceles, exclusive of the irritation fibroma, are most common of the benign soft tissue masses in the oral cavity. Muco: mucus , coele: cavity. When in the oral floor, they are called ranula.
  90. 90. MucoceleExtravasation is the leakage of fluid from the ducts or acini into the surrounding tissue. Extra: outside, vasa: vesselRetention: narrowed ductal opening that cannot adequately accommodate the exit of saliva produced, leading to ductal dilation and surface swelling. Less common phenomenon
  91. 91. Mucocele Consist of a circumscribed cavity in the connective tissue and submucosa producing an obvious elevation in the mucosa
  92. 92. Mucocele The majority of the mucoceles result from an extravasation of fluid into the surrounding tissue after traumatic break in the continuity of their ducts. Lacks a true epithelial lining.
  93. 93. Ranula Is a term used for mucoceles that occur in the floor of the mouth. The name is derived form the word rana, because the swelling may resemble the translucent underbelly of the frog.
  94. 94. Ranula  Although the source is usually the sublingual gland, may also arise from the submandibular duct or possibly the minor salivary glands in the floor of the mouth.
  95. 95. Ranula Presents as a blue dome shaped swelling in the floor of mouth (FOM). They tend to be larger than mucoceles & can fill the FOM & elevate tongue. Located lateral to the midline, helping to distinguish it from a midline dermoid cyst.
  96. 96. Plunging or Cervical Ranula Occurs when spilled mucin dissects through the mylohyoid muscle and produces swelling in the neck. Concomitant FOM swelling may or may not be visible.
  97. 97. Treatment of Mucocelesin Lip or Buccal mucosa Excision with strict removal of any projecting peripheral salivary glands Avoid injury to other glands during primary wound closure
  98. 98. Ranula Treatment Sublingual gland removal via intraoral approach
  99. 99. Salivary Gland Infections  Acute bacterial sialdenitis  Chronic bacterial sialdenitis  Viral infections
  100. 100. Sialadenitis Sialadenitis represents inflammation mainly involving the acinoparenchyma of the gland.
  101. 101. Sialadenitis Awareness of salivary gland infections was increased in 1881 when President Garfield died from acute parotitis following abdominal surgery and associated systemic dehydration.
  102. 102. Sialadenitis Acute infection more often affects the major glands than the minor glands
  103. 103. Pathogenesis1. 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.
  104. 104. Acute Suppurative More common in parotid gland. Suppurative parotitis, surgical parotitis, post-operative parotitis, surgical mumps, and pyogenic parotitis. The etiologic factor most associated with this entity is the retrograde infection from the mouth. 20% cases are bilateral
  105. 105. Predilection for ParotidSalivary 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.
  106. 106. Parotid PredilectionAnatomic factors Minor role in formation of infections 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 Whartons that may reduce the rate of infections in SMG.
  107. 107. Risk Factors for Sialadenitis Systemic dehydration (salivary stasis) Chronic disease and/or immunocompromise Liver failure Renal failure DM, hypothyroid Malnutrition HIV Sjögren’s syndrome
  108. 108. Risk Factors Neoplasms Sialectasis (salivary duct dilation) increases the risk for retrograde contamination. Is associated with cystic fibrosis and pneumoparotitis Extremes of age Poor oral hygiene Calculi, duct stricture NPO status (stimulatory effect of mastication on salivary production is lost)
  109. 109. Complex picture Sialolithiasis can produce mechanical obstruction of the duct resulting in salivary stasis and subsequent gland infection. Calculus formation is more likely to occur in SMG duct (85-90% of salivary calculi are in the SMG duct) However, the parotid gland remains the Main site of acute suppurative infection
  110. 110. Acute Suppurative Parotitis -History  Sudden onset of erythematous swelling of the pre/post auricular areas extend into the angle of the mandible.  Is bilateral in 20%.
  111. 111. Bacteriology Purulent saliva should be sent for culture. Staphylococcus aureus is most common Streptococcus pnemoniae and S.pyogenes Haemophilus Influenzae also common
  112. 112. Lab Testing Parotitis is generally a clinical diagnosis However, in critically ill patients further diagnostic evaluation may be required Elevated white blood cell count Serum amylase generally within normal If no response to antibiotics in 48 hrs can perform MRI, CT or ultrasound to exclude abscess formation Can perform needle aspiration of abscess
  113. 113. Treatment of AcuteSialadenitis Reverse the medical condition that may have contributed to formation Discontinue anti-sialogogues if possible Warm compresses, give sialogogues (lemon drops) External salivary gland massage if tolerated
  114. 114. Treatment of AcuteSialadenitis/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
  115. 115. Failure to respond After 48 hours the patient should respond Consider adding a third generation ceph Possibly add an aminoglycoside The preponderance of MRSA in nursing homes and nosocomial environments has prompted the recommendation of vancomycin in these groups
  116. 116. Surgery for Acute Parotitis Limited role for surgery 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
  117. 117. Complications of AcuteParotitis Direct extension Abscess ruptures into external auditory canal and TMJ . Hematogenous spread Thrombophlebitis of the retromandibular or facial veins are rare complications
  118. 118. Complications Fascial capsule around parotid displays weakness on the deep surface of the gland adjacent to the loose areolar tissues of the lateral pharyngeal wall (Achilles’heel of parotid) Extension of an abscess into the parapharyngeal space may result in airway obstruction, mediastinitis, internal jugular thrombosis and carotid artery erosion
  119. 119. Complications Dysfunction of one or more branches of the facial nerve is rare. Occurs secondary to perineuritis or direct neural compression ; but resolves with adequate treatment of the parotitis. These patients need to be followed to ensure resolution….must rule out TUMOR.
  120. 120. 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 sialectasis, ductal ectasia and progressive acinar destruction combined with a lymphocyte infiltrate.
  121. 121. Chronic Sialadenitis Workup… The clinician should look for a treatable predisposing factor such as a calculus or a stricture.
  122. 122. 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.
  123. 123. 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.
  124. 124. Acute Viral infection Derived from the Danish word “mompen” Means mumbling, the name given to describe the characteristic muffled speech that patients demonstrate because of glandular inflammation and trismus.
  125. 125. Viral Infections As opposed to bacterial sialadenitis, viral infections of the salivary glands are SYSTEMIC from the onset!
  126. 126. 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
  127. 127. Mumps 2-3 week incubation after exposure (the virus multiplies in the URI or parotid gland) Then localizes to biologically active tissues like salivary glands, germinal tissues and the CNS.
  128. 128. Epidemiology Occurs world wide and is highly contagious Prior to the widespread use of the Jeryl Lynn vaccine (live attenuated), cases were clustered in epidemic fashion Sporadic cases are observed today likely resulting from non-paramyxoviral infection, failure of immunity or lack of vaccination
  129. 129. Virology Classic mumps syndrome is caused by paramyxovirus, an RNA virus Others can cause acute viral parotitis: Coxsackie A & B, ECHO virus, cytomegalovirus and adenovirus HIV involvement of parotid glands is a rare cause of acute viral parotitis, is more commonly associated with chronic cystic disease.
  130. 130. Clinical presentation 30% experience prodromal symptoms prior to development of parotitis Headache, myalgias, anorexia, malaise Onset of salivary gland involvement is heralded by earache, gland pain, dysphagia and trismus
  131. 131. Physical exam Glandular swelling (tense, firm) Parotid gland involved frequently, SMG & SLG can also be affected. May displace ispilateral pinna 75% cases involve bilateral parotids, may not begin bilaterally (within 1-5 days may become bilateral) 25% unilateral Low grade fever
  132. 132. Diagnostic Evaluation Leukocytopenia, with relative lymphocytosis Increased serum amylase (normal by 2- 3 week of disease) Viral serology essential to confirm: Complement fixing antibodies appear following exposure to the virus
  133. 133. Serology “S” or soluble antibodies directed against the nucleoprotein core of the virus appear within the first week of infection, peak in 2 weeks. Disappear in 8-9 months and are therefore associated with active or recent infection
  134. 134. Serology “V”, or viral antibodies directed against the outer surface hemagglutinin, appear several weeks after the S antibodies and persist at low levels for about 5 years following exposure. V antibodies are associated with past infection, prior vaccination and the late stages of active infection
  135. 135. Serology If the initial serology is noncontributory, then a non-paramyxovirus may be responsible for the infection. Blood HIV tests should also be obtained The mumps skin test is not useful in diagnosis an acute infection because dermal hypersensitivity does not develop until 3 or 4 weeks following exposure.
  136. 136. Treatment  Supportive  Fluid  Anti-inflammatories and analgesics
  137. 137. Prevention The live attenuated vaccine became available in 1967 Commonly combined with the measles and rubella vaccines, the mumps vaccine is administered in a single subcutaneous dose after 12 months of age. Booster at 4-6yr
  138. 138. 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
  139. 139. 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
  140. 140. Sjögren’s syndrome 90% cases occur in women Average age of onset is 50y Classic monograph on the disease published in 1933 by Sjögren, a Swedish ophthalmologist
  141. 141. Sjögren’s SyndromeTwo 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
  142. 142. Sjögren’s Syndrome  Unilateral or bilateral salivary gland swelling occurs, may be permanent or intermittent.  Rule out lymphoma
  143. 143. 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
  144. 144. Sjögren’s Lip Biopsy Biopsy of SG mainly used to aid in the diagnosis Can also be helpful to confirm sarcoidosis
  145. 145. 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 semi-quantitatively to determine the number of foci of lymphocytes per 4mm2/gland
  146. 146. 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
  147. 147. Sialadenosis Non-specific term used to describe a non-inflammatory 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.
  148. 148. Related to…a. Metabolic “endocrine sialendosis”b. Nutritional “nutritional mumps” a. Obesity: secondary to fatty hypertrophy b. Malnutrition: acinar hypertrhophy c. Any condition that interferes with the absorption of nutrients (celiac dz, uremia, chronic pancreatitis, etc)
  149. 149. Related to…a. Alcoholic cirrhosis: likely based on protein deficiency & resultant acinar hypertrophyb. Drug induced: iodine mumpse. HIV
  150. 150. 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.
  151. 151.  Continued irradiation leads to complete destruction of the serous acini and subsequent atrophy of the gland7. Similar to the thyroid, salivary neoplasm are increased in incidence after radiation exposure7.
  152. 152. Granulomatous DiseasePrimary 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.
  153. 153. Granulomatous DiseaseSarcoidosis: a systemic disease characterized by noncaseating granulomas in multiple organ systems Clinically, SG involvement in 6% cases Heerfordts’s disease is a particular form of sarcoid characterized by uveitis, parotid enlargement and facial paralysis. Usually seen in 20-30’s. Facial paralysis transient.
  154. 154. Granulomatous DiseasesCat Scratch Disease: Does not involve the salivary glands directly, but involves the periparotid and submandibular triangle lymph nodes May involve SG by contiguous spread. Bacteria is Bartonella Henselae(G-R) Also, toxoplasmosis and actinomycosis.
  155. 155. CystsTrue cysts of the parotid account for 2-5% of all parotid lesionsMay be acquired or congenitalType 1 Branchial arch cysts are a duplication anomaly of the membranous external auditory canal (EAC)Type 2 cysts are a duplication anomaly of the membranous and cartilaginous EAC
  156. 156. CystsAcquired cysts include: Mucus extravasation vs. retention Traumatic Benign epithelial lesions Association with tumors Pleomorphic adenoma Adenoid Cystic Carcinoma Mucoepidermoid Carcinoma Warthin’s Tumor
  157. 157. 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
  158. 158. Pneumoparotitis Crepitation, on palpation of the gland Swelling may resolve in minutes to hours, in some cases, days. US and CT show air in the duct and gland Consider antibiotics to prevent superimposed infection
  159. 159. Other: NecrotizingSialometaplasia Cryptogenic origin, possibly a reaction to ischemia or injury Manifests as mucosal ulceration, most commonly found on hard palate. May have prodrome of swelling or feeling of “fullness” in some. Pain is not a common complaint
  160. 160. Necrotizing Sialometaplasia Self limiting lesion, heals by secondary intention over 6-8 weeks Histologically may be mistaken for SCC
  162. 162. 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
  163. 163. Pleomorphic Adenoma Slow-growing, painless mass Parotid: 90% in superficial lobe, most in tail of gland Minor salivary gland: lateral palate, submucosal mass Solitary vs. synchronous/metachronous neoplasms
  164. 164. Pleomorphic Adenoma Gross pathology Smooth Well-demarcated Solid Cystic changes Myxoid stroma
  165. 165. 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
  166. 166. Pleomorphic Adenoma Treatment: complete surgical excision Parotidectomy with facial nerve preservation Submandibular gland excision Wide local excision of minor salivary gland Avoid enucleation and tumor spill
  167. 167. 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
  168. 168. 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
  169. 169. 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
  170. 170. 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
  171. 171. Oncocytoma Presentation Enlarging, painless mass Technetium-99m pertechnetate scintigraphy Mitochondrial hyperplasia
  172. 172. 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
  173. 173. Oncocytoma Electron microscopy: Mitochondrial hyperplasia 60% of cell volume
  174. 174. Monomorphic Adenomas  Basal cell, canalicular, sebaceous, glycogen-rich, clear cell  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
  175. 175. 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
  176. 176. Basal Cell Adenoma Solid Most common Solid nests of tumor cells Uniform, hyperchromatic, round nuclei, indistinct cytoplasm Peripheral nuclear palisading Scant stroma
  177. 177. Basal Cell Adenoma Trabecular Cells in elongated trabecular pattern Vascular stroma
  178. 178. Basal Cell Adenoma Tubular Multiple duct-like structures Columnar cell lining Vascular stroma
  179. 179. Basal Cell Adenoma Membranous Thick eosinophilic hyaline membranes surrounding nests of tumor cells “jigsaw-puzzle” appearance
  180. 180. Myoepithelioma <1% of all salivary neoplasms 3rd-6th decades F>M Minor salivary glands > parotid > submandibular gland Presentation: asymptomatic mass
  181. 181. Myoepithelioma Histology Spindle cell ○ More common ○ Parotid ○ Uniform, central nuclei ○ Eosinophilic granular or fibrillar cytoplasm Plasmacytoid cell ○ Polygonal ○ Eccentric oval nuclei
  182. 182. 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
  183. 183. 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
  184. 184. Mucoepidermoid Carcinoma Gross pathology Well-circumscribed to partially encapsulated to unencapsulated Solid tumor with cystic spaces
  185. 185. Mucoepidermoid Carcinoma Histology—Low- grade Mucus cell > epidermoid cells Prominent cysts Mature cellular elements
  186. 186. Mucoepidermoid Carcinoma Histology— Intermediate- grade Mucus = epidermoid Fewer and smaller cysts Increasing pleomorphism and mitotic figures
  187. 187. Mucoepidermoid Carcinoma Histology—High- grade Epidermoid > mucus Solid tumor cell proliferation Mistaken for SCCA ○ Mucin staining
  188. 188. Mucoepidermoid Carcinoma Treatment Influenced by site, stage, grade Stage I & II ○ Wide local excision Stage III & IV ○ Radical excision ○ +/- neck dissection ○ +/- postoperative radiation therapy
  189. 189. 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
  190. 190. Adenoid Cystic Carcinoma Gross pathology Well-circumscribed Solid, rarely with cystic spaces infiltrative
  191. 191. Adenoid Cystic Carcinoma Histology— cribriform pattern Most common “swiss cheese” appearance
  192. 192. Adenoid Cystic Carcinoma Histology—tubular  Histology—solid pattern pattern  Layered cells forming  Solid nests of cells duct-like structures without cystic or  Basophilic mucinous tubular spaces substance
  193. 193. Adenoid Cystic Carcinoma  Treatment Complete local excision Tendency for perineural invasion: facial nerve sacrifice Postoperative XRT  Prognosis Local recurrence: 42% Distant metastasis: lung Indolent course: 5-year survival 75%, 20-year survival 13%
  194. 194. 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
  195. 195. Acinic Cell Carcinoma Gross pathology Well-demarcated Most often homogeneous
  196. 196. Acinic Cell Carcinoma Histology Solid and microcystic patterns ○ Most common ○ Solid sheets ○ Numerous small cysts Polyhedral cells Small, dark, eccentric nuclei Basophilic granular cytoplasm
  197. 197. Acinic Cell Carcinoma Treatment Complete local excision +/- postoperative XRT Prognosis 5-year survival: 82% 10-year survival: 68% 25-year survival: 50%
  198. 198. Adenocarcinoma  Rare  5th to 8th decades  F>M  Parotid and minor salivary glands  Presentation: Enlarging mass 25% with pain or facial weakness
  199. 199. Adenocarcinoma Histology Heterogeneity Presence of glandular structures and absence of epidermoid component Grade I Grade II Grade III
  200. 200. Adenocarcinoma  Treatment Complete local excision Neck dissection Postoperative XRT  Prognosis Local recurrence: 51% Regional metastasis: 27% Distant metastasis: 26% 15-year cure rate:  Stage I = 67%  Stage II = 35%  Stage III = 8%
  201. 201. Malignant Mixed Tumors  Carcinoma ex-pleomorphic adenoma ○ Carcinoma developing in the epithelial component of preexisting pleomorphic adenoma  Carcinosarcoma ○ True malignant mixed tumor—carcinomatous and sarcomatous components  Metastatic mixed tumor ○ Metastatic deposits of otherwise typical pleomorphic adenoma
  202. 202. Carcinoma Ex-PleomorphicAdenoma  2-4% of all salivary gland neoplasms  4-6% of mixed tumors  6th-8th decades  Parotid > submandibular > palate  Risk of malignant degeneration ○ 1.5% in first 5 years ○ 9.5% after 15 years  Presentation ○ Longstanding painless mass that undergoes sudden enlargement
  203. 203. Carcinoma Ex-PleomorphicAdenoma Gross pathology Poorly circumscribed Infiltrative Hemorrhage and necrosis
  204. 204. Carcinoma Ex-Pleomorphic Adenoma Histology Malignant cellular change adjacent to typical pleomorphic adenoma Carcinomatous component ○ Adenocarcinoma ○ Undifferentiated
  205. 205. Carcinoma Ex-PleomorphicAdenoma Treatment Radical excision Neck dissection (25% with lymph node involvement at presentation) Postoperative XRT Prognosis Dependent upon stage and histology
  206. 206. Carcinosarcoma  Rare: <.05% of salivary gland neoplasms  6th decade  M=F  Parotid  History of previously excised pleomorphic adenoma, recurrent pleomorphic adenoma or recurring pleomorphic treated with XRT  Presentation
  207. 207. Carcinosarcoma Gross pathology Poorly circumscribed Infiltrative Cystic areas Hemorrhage, necrosis Calcification
  208. 208. Carcinosarcoma Histology Biphasic appearance Sarcomatous component ○ Dominant ○ chondrosarcoma Carinomatous component ○ Moderately to poorly differentiated ductal carcinoma ○ Undifferentiated
  209. 209. Carcinosarcoma  Treatment Radical excision Neck dissection Postoperative XRT Chemotherapy (distant metastasis to lung, liver, bone, brain)  Prognosis Poor, average survival less than 2 ½ years
  210. 210. 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
  211. 211. Squamous Cell Carcinoma Gross pathology Unencapsulated Ulcerated fixed
  212. 212. Squamous Cell Carcinoma Histology Infiltrating Nests of tumor cells Well differentiated ○ Keratinization Moderately-well differentiated Poorly differentiated ○ No keratinization
  213. 213. Squamous Cell Carcinoma Treatment Radical excision Neck dissection Postoperative XRT Prognosis 5-year survival: 24% 10-year survival: 18%
  214. 214. Polymorphous Low-Grade Adenocarcinoma 2nd most common malignancy in minor salivary glands 7th decade F>M Painless, submucosal mass Morphologic diversity ○ Solid, glandular, cribriform, ductular, tubular, trabecular, cystic
  215. 215. Polymorphous Low-GradeAdenocarcinoma Histology Isomorphic cells, indistinct borders, uniform nuclei Peripheral “Indian- file” pattern Treatment Complete yet conservative excision
  216. 216. Clear Cell Carcinoma AKA glycogen-rich Palate and parotid 6th-8th decade M=F Histology ○ Uniform, round or polygonal cells ○ Peripheral dark nuclei ○ Clear cytoplasm Treatment ○ Complete local excision
  217. 217. Epithelial-Myoepithelial Carcinoma < 1% of salivary neoplasms 6th-7th decades, F > M, parotid ? Increased risk for 2nd primary Histology ○ Tumor cell nests ○ Two cell types ○ Thickened basement membrane Treatment
  218. 218. INCISIONS
  220. 220. REFERENCESOral anatomy & histology – K . AveryOral pathology – ShaffersOral medicine – BurkitGrays anatomy – GraysHead and neck otolaryngologyLore and Medina AtlasDental Clinics of north americaTextbook of HuppInternet
  1. A particular slide catching your eye?

    Clipping is a handy way to collect important slides you want to go back to later.