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Salivary glands /certified fixed orthodontic courses by Indian dental academy


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Salivary glands /certified fixed orthodontic courses by Indian dental academy

  1. 1. Salivary Glands & Disease INDIAN DENTAL ACADEMY Leader in continuing dental education
  2. 2. 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.
  3. 3. Embryology • The stroma (capsule and septae) of the glands originates from mesenchyme that may be mesodermal or neural crest in origin.
  4. 4. Parotid development13 • 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.
  5. 5. Parotid development13 • 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.
  6. 6. 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.
  7. 7. 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.
  8. 8. 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.
  9. 9. Acinar cells • At around the 7-8th month in utero, secretory cells (acini) begin to develop around the ductal system.
  10. 10. Acinar cells of Salivary Glands Classified as either: • Serous cells: produce a thin watery secretion • Mucous cells: produce a more viscous secretion
  11. 11. Salivary gland secretory unit12 • Composed of terminal acini • Intercalated, striated and excretory ducts • Myoepithelial cells
  12. 12. Major glands/Secretions • Major SG are paired structures and include the parotid, submandibular and sublingual • Parotid: serous • Submandibular: mucous & serous • Sublingual: mucous
  13. 13. Salivary Function12 • Aid is mastication, deglutination • Salivary lysozyme, IgA and other antibacterial substances protect against caries and oral cavity infections • Saliva also aids in speech
  14. 14. Anatomy: Parotid Gland12,13 • 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 mm
  15. 15. Anatomy:Parotid Gland12 • 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
  16. 16. Anatomy:Parotid Gland • CN VII branches roughly divide the PG into superficial and deep lobes while coursing anteriorly from the stylomastoid foramen to the muscles of facial expression.
  17. 17. Anatomy: Deep Lobe13 • 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.
  18. 18. 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
  19. 19. 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.
  20. 20. Anatomy: Parotid Fascia12 • 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.
  21. 21. Anatomy: Parotid Lymphatics12 • 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
  22. 22. Parotid: Parasympathetic Innervation • 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.
  23. 23. Parotid: Sympathetic Innervation • Postganglionic innervation is provided by the superior cervical ganglion and distributes with the arterial system
  24. 24. Parotid Anatomy: Great Auricular Nerve (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 preauricular region.
  25. 25. 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.
  26. 26. Parotid Anatomy: Facial Nerve • 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
  27. 27. 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.
  28. 28. Parotid Bed: Deep lobe lies on...14 • V: internal jugular vein • A: external and internal carotid arteries • N: glossopharyngeal N vagus N spinal accesory N hypoglossal N • S: styloid process styloglossus mm stylohyloid mm
  29. 29. 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.
  30. 30. Anatomy: Submandibular Lymphatics Submandibular gland drains into submandibular nodes.
  31. 31. Anatomy: Submandibular Duct13 • 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.
  32. 32. Anatomy: Submandibular duct • 2-4mm in diameter & about 5cm in length. • It opens into the floor of the mouth thru a punctum. • The punctum is a constricted portion of the duct to limit retrograde flow of bacterialaden oral fluids.
  33. 33. 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.
  34. 34. 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.
  35. 35. 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
  36. 36. Physiology13 • Physiologic control of the SG is almost entirely by the autonomic nervous system; parasympathetic effects predominate. • If parasympathetic innervation is interrupted, glandular atrophy occurs. • Normal saliva is 99.5% water • Normal daily production is 1-1.5L
  37. 37. Obstructive Salivary Gland Disorders • Sialolithiasis • Mucous retention/extravasation
  38. 38. Obstructive SG Disorders: Sialolithiasis • Sialolithiasis results in a mechanical obstuction of the salivary duct • Is the major cause of unilateral diffuse parotid or submandibular gland swelling 2
  39. 39. Sialolithiasis Incidence2 • Escudier & McGurk 1:15-20 0003 • Marchal & Dulgurerov 1:10-20 0002 Sialolithiasis remains the most frequent reason for submandibular gland resection 5
  40. 40. 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.
  41. 41. 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.
  42. 42. 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.
  43. 43. Etiology2 • • • • • Water hardness ↑likelihood? …Maybe…. Hypercalcemia…in rats only Xerostomic meds Tobacco smoking, positive correlation Smoking has an increased cytotoxic effect on saliva, decreases PMN phagocytic ability and reduces salivary proteins
  44. 44. Etiology7 Gout is the only systemic disease known to cause salivary calculi and these are composed of uric acid.
  45. 45. Stone Composition2 • 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
  46. 46. Parotid (PG) vs. Submandibular Gland (SMG)…. • Most authorities agree obstructive phenomemnon such as mucous plugs and sialoliths are most commonly found in the SMG – Escudier et al3 – Lustmann et al4 – Rice7 • Others note that parotid glands are most commonly affected2
  47. 47. Reasons sialolithiasis may occur 7 more often in the SMG • Saliva more alkaline • Higher concentration of calcium and phosphate in the saliva • Higher mucus content • Longer duct • Anti-gravity flow
  48. 48. Other characteristics: • Despite a similar chemical make-up, 80-90% of SMG calculi are radio-opaque 7 50-80% of parotid calculi are radiolucent 7 • 30% of SMG stones are multiple 60% of Parotid stones are multiple
  49. 49. Clinical presentation10 • Painful swelling (60%) • Painless swelling (30%) • Pain only (12%) – Sometimes described as recurrent salivary colic and spasmodic pains upon eating
  50. 50. 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?
  51. 51. Exam: Inspection12 • • • • • • • Asymmetry (glands, face, neck) Diffuse or focal enlargement Erythema extra-orally Trismus Medial displacement of structures intraorally? Examine external auditory canal (EAC) Cranial nerve testing
  52. 52. 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).
  53. 53. Diagnostics: Plain occlusal film • Effective for intraductal stones, while…. • intraglandular, radiolucent or small stones may be missed.
  54. 54. Diagnostic approaches2 CT Scan: • large stones or small CT slices done also used for inflammatory disorders Ultrasound: • operator dependent, can detect small stones (>2mm), inexpensive, non-invasive
  55. 55. Diagnostic approaches: 2 Sialography • Consists of opacification of the ducts by a retrograde injection of a water-soluble dye. • Provides image of stones and duct morphological structure • May be therapeutic, but success of therapeutic sialography never documented
  56. 56. Sialography continued… • Disadvantages: – – – – – – irradiation dose pain with procedure poss.perforation infection dye reaction push stone further contraindicated in active infection.
  57. 57. 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. • Helman & Fox 1987, found that Technitium-99 shares the Na-K-Cl transport system on the basement membrane of the parotid acinar cells
  58. 58. Diagnostic Approaches: 11 Radionuclide Studies • Some 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!
  59. 59. Diagnostic Approach: 2 MR Sialography • T2 weighted fast spin echo slides in sagittal and axial planes. Volumetric reconstruction allows visualization of ducts • ADV: No dye, no irradiation, no pain • DIS: Cost, possible artifact
  60. 60. Diagnostic approach: 2 Diagnostic Sialendoscopy • Allows complete exploration of the ductal system, direct visualization of duct pathology • Success rate of >95%2 • Disadvantage: technically challenging, trauma could result in stenosis, perforation
  61. 61. Sialolithiasis Treatment2 • None: antibiotics and anti-inflammatories, hoping for spontaneous stone passage. • Stone excision: – Lithotripsy – Interventional sialendoscopy – Simple removal (20% recurrence)7 • Gland excision
  62. 62. Sialolithiasis Treatment11 • If patients DO defer treatment, they need to know: • Stones will likely enlarge over time • Seek treatment early if infection develops • Salivary gland massage and hyperhydration when symptoms develop.
  63. 63. Stone excision2 • 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.
  64. 64. Transoral vs. Extraoral 11 Removal • Some say: – if a stone can be palpated thru the mouth, it can be removed trans-orally (TO) – Or if it can be visualized on a true central occlusal radiograph, it can be removed TO. – Finally, if it is no further than 2cm from the punctum, it can be removed TO.
  65. 65. Posterior Stones11 • Deeper submandibular stones (~15-20% of stones) may best be removed via sialadenectomy. • Some surgeons say can still remove transorally, but should be done via general anesthetic. • Floor of mouth (FOM) opened opposite the first premolar, duct dissected out, lingual nerve identified. • Duct opened & stone removed, FOM approximated.
  66. 66. Submandibular Sialoliths: Transoral Advantages • • • • • Preserves a functional gland Avoids neck scar Possibly less time from work No overnight stay in hospital Avoids risk to CN 7 & 12
  67. 67. Gland excision11 • After SMG excision, 3% cases have recurrence via: – Retention of stones in intraductal portion or new formation in residual Wharton's duct • No data regarding recurrence after parotidectomy
  68. 68. Gland excision indicated11 • • • • Very posterior stones Intra-glandular stones Significantly symptomatic patients Failed transoral approach
  69. 69. Gland excision 6 • While some believe that a gland with sialolithiasis is no longer functional, a recent study on SMGs removed due to sialolithiasis found there was no correlation between the degree of gland alteration and the number of infectious episodes. • 50% of the glands were histopathologically normal or close to normal • A conservative approach to the gland/stone seems to be justified
  70. 70. Obstructive Salivary Gland Disorders • Sialolithiasis • Mucous retention/extravasation
  71. 71. Mucocele9 • 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
  72. 72. Mucocele 9 • 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.
  73. 73. Mucocele9 Extravasation is the leakage of fluid from the ducts or acini into the surrounding tissue. Extra: outside, vasa: vessel Retention: narrowed ductal opening that cannot adequately accommodate the exit of saliva produced, leading to ductal dilation and surface swelling. Less common phenomenon
  74. 74. Mucocele • Consist of a circumscribed cavity in the connective tissue and submucosa producing an obvious elevation in the mucosa
  75. 75. 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.
  76. 76. Ranula9 • 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.
  77. 77. Ranula9 • 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.
  78. 78. 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.
  79. 79. 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.
  80. 80. Treatment of Mucoceles9 in Lip or Buccal mucosa • Excision with strict removal of any projecting peripheral salivary glands • Avoid injury to other glands during primary wound closure
  81. 81. Ranula Treatment9 • Marsupialization has fallen into disfavor due to the excessive recurrence rate of 6090% • Sublingual gland removal via intraoral approach
  82. 82. Salivary Gland Infections • Acute bacterial sialdenitis • Chronic bacterial sialdenitis • Viral infections
  83. 83. Sialadenitis Sialadenitis represents inflammation mainly involving the acinoparenchyma of the gland.
  84. 84. Sialadenitis1 Awareness of salivary gland infections was increased in 1881 when President Garfield died from acute parotitis following abdominal surgery and associated systemic dehydration.
  85. 85. Sialadenitis Acute infection more often affects the major glands than the minor glands1
  86. 86. Pathogenesis1 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.
  87. 87. Acute Suppurative1 • 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 bilateral7
  88. 88. Predilection for Parotid 1 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.
  89. 89. Salivary Composition1 • 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.
  90. 90. Parotid Predilection Anatomic factors 1 • Minor role in formation of infections • Stensen’s duct lies adjacent to the maxillary mandibular 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.
  91. 91. Risk Factors for Sialadenitis1 • Systemic dehydration (salivary stasis) • Chronic disease and/or immunocompromise – – – – – – Liver failure Renal failure DM, hypothyroid Malnutrition HIV Sjögren’s syndrome
  92. 92. 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, duct stricture • NPO status (stimulatory effect of mastication on salivary production is lost)
  93. 93. Complex picture1 • There must be other factors at work….. • 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 MC site of acute suppurative infection!
  94. 94. Differential Diagnosis of Parotid Gland Enlargement • • • • • • Lymphoma Actinomycoses Cat-scratch disease Sjogren’s syndrome Wegener’s granulomatosis Viral infection
  95. 95. 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%.
  96. 96. Bacteriology1 • Purulent saliva should be sent for culture. – Staphylococcus aureus is most common – Streptococcus pnemoniae and S.pyogenes – Haemophilus Influenzae also common
  97. 97. Lab Testing1 • 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
  98. 98. Treatment of Acute Sialadenitis1 • Reverse the medical condition that may have contributed to formation • Discontinue anti-sialogogues if possible • Warm compresses, maximize OH, give sialogogues (lemon drops) • External salivary gland massage if tolerated
  99. 99. Treatment of Acute 1 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
  100. 100. Failure to respond1 • • • • 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
  101. 101. Surgery for Acute Parotitis1 • 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
  102. 102. Complications of Acute Parotitis1 • 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
  103. 103. Complications1 • 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
  104. 104. Complications1 • 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.
  105. 105. Chronic Sialadenitis7 • 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.
  106. 106. Chronic Sialadenitis7 • Of importance in the workup… • The clinician should look for a treatable predisposing factor such as a calculus or a stricture.
  107. 107. No treatable cause found7: • 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.
  108. 108. Acute viral infection (AVI)1 • 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.
  109. 109. AVI1 • 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.
  110. 110. Viral Infections1 As opposed to bacterial sialadenitis, viral infections of the salivary glands are SYSTEMIC from the onset!
  111. 111. Viral infection1 • Mumps is a non-suppurative acute sialadenitis • Is endemic in the community and spread by airborne droplets • Communicable disease • Enters through upper respiratory tract
  112. 112. Mumps1 • 2-3 week incubation after exposure (the virus multiplies in the URI or parotid gland) • 3-5day viremia • Then localizes to biologically active tissues like salivary glands, germinal tissues and the CNS.
  113. 113. Epidemiology1 • 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
  114. 114. Virology1 • 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 dz
  115. 115. Clinical presentation1 • 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
  116. 116. Physical exam1 • 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
  117. 117. Diagnostic Evaluation1 • 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
  118. 118. Serology1 • “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
  119. 119. Serology1 • “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
  120. 120. Serology1 • 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.
  121. 121. Treatment • Supportive • Fluid • Anti-inflammatories and analgesics
  122. 122. Prevention1 • 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
  123. 123. Complications1 • Orchitis, testicular atrophy and sterility in approximately 20% of young men • Oophoritis in 5% females • Aseptic meningitis in 10% • Pancreatitis in 5% • Sensorineural hearing loss <5% – Usually permanent – 80% cases are unilateral
  124. 124. Immunologic Disease 7 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
  125. 125. Sjögren’s syndrome7 • 90% cases occur in women • Average age of onset is 50y • Classic monograph on thediease published in 1933 by Sjögren, a Swedish ophthalmologist
  126. 126. Sjögren’s Syndrome7 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
  127. 127. Sjögren’s Syndrome • Unilateral or bilateral salivary gland swelling occurs, may be permanent or intermittent. • Rule out lymphoma
  128. 128. Sjögren’s Syndrome15 • 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
  129. 129. Sjögren’s Lip Biopsy15 • Biopsy of SG mainly used to aid in the diagnosis • Can also be helpful to confirm sarcoidosis
  130. 130. Sjögren’s Lip Biopsy15 • 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
  131. 131. Sjögren’s Treatment15 • 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
  132. 132. Sialadenosis7 • 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.
  133. 133. Related to7… 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)
  134. 134. Related to7… a. Alcoholic cirrhosis: likely based on protein deficiency & resultant acinar hypertrophy b. Drug induced: iodine mumps e. HIV
  135. 135. Radiation Injury7 • 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.
  136. 136. • 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.
  137. 137. Granulomatous Disease7 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.
  138. 138. Granulomatous Disease7 Sarcoidosis: 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.
  139. 139. Granulomatous Disease7 Cat 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.
  140. 140. Cysts7 True cysts of the parotid account for 2-5% of all parotid lesions May be acquired or congenital Type 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
  141. 141. Cysts7 Acquired cysts include: • Mucus extravasation vs. retention • Traumatic • Benign epithelial lesions • Association with tumors – – – – Pleomorphic adenoma Adenoid Cystic Carcinoma Mucoepidermoid Carcinoma Warthin’s Tumor
  142. 142. Other: Pneumoparotitis7,8 • 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
  143. 143. Pneumoparotitis8 • 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
  144. 144. Other: Necrotizing 7 Sialometaplasia • 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
  145. 145. Necrotizing Sialometaplasia15 • Self limiting lesion, heals by secondary intention over 6-8 weeks • Histologically may be mistaken for SCC
  146. 146. References 1. 2. 3. 4. 5. McQuone, SJ: Acute viral and bacterial infections of the salivary glands. Oto Clinics North America, 32:793,1999 Marchal F, Dulguerov P. Sialolithiasis Management. Arch Oto, 129:951, 2003 Escudier MP, McGurk M. Symptomatic sialodenitiis and sialolithiasis in the english population:an estimate of the cost of hospital treatment. Br Dent J. 1999;186:463 Lustmann J, Regev E, Melamed Y. Sialolithiasis: a survey on 245 patients and a review of the literature. Int J Oral Maxillofacial. 1990; 19, 135 Crabtree GM, Yartington CT. Submandibular gland excision. Laryngoscope. 1988;98:1044
  147. 147. References 6. Marchal F, Kurt AM, Dulgeurov P, Becker M et al. Histopathology of submandibular glands removed for sialolithiasis. Ann Oto Rhinol.2001;110, 464 7. Rice DH. Salivary Gland Disorders. Med Clin North Am. 1999; vol 83, 197. 8. Kirsh CM, Shinn J, Porzio R et al. Chest. 1999, vol 116, 1476 9. Baurmash HD. Mucoceles and Ranulas. J Oral Maxillo Surg. 2003, vol 61, 369 10. Ellies M, Laskawi R, Arglebe C, et al. Surgical management of nonneooplastic disease of the submandibular gland. Int J Oral Maxillofac Surg. 25:1996, 285 11. Williams MF. Salivary gland diseases: sialolithiasis. Oto Clin North America. Vol 32, 819, 1999
  148. 148. References • 12: Krause GE, Meyers AD. Management of parotid swelling. Comprehensive Therapy. 1996, 22:256. • 13. Silvers AR, Som PM. Head and Neck Imaging: the Salivary Glands. 1998, 36:941 • 14. Carlson GW. The salivary glands. Surgical Clin North America. 2000, 80:261 • 15. Feinberg SE. Diagnosis and management of salivary gland disorders. Ch.34
  149. 149. Thank you For more details please visit