Salivary Glands Disease

1. Salivary Glands& Disease

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. Embryology The stroma (capsule and septae) of the glands originates from mesenchyme that may be mesodermal or neural crest in origin.

4. 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.

5. 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.

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. 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. 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. Acinar cells At around the 7-8th month in utero, secretory cells (acini) begin to develop around the ductal system.

10. Acinar cells of Salivary Glands Classified as either: Serous cells: produce a thin watery secretion Mucous cells: produce a more viscous secretion

11. Salivary gland secretory unit Composed of terminal acini Intercalated, striated and excretory ducts Myoepithelial cells

12. 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 muscle.

13. 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

14. 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.

15. 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.

16. 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

17. 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.

18. 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.

19. 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

20. 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.

21. Parotid: SympatheticInnervation Postganglionic innervation is provided by the superior cervical ganglion and distributes with the arterial system

22. 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 pre-auricular region.

23. 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.

24. 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

25. 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.

26. 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

27. 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.

28. Anatomy: Submandibular Lymphatics Submandibular gland drains into submandibular nodes.

29. 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.

30. 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 bacteria-laden oral fluids.

31. 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.

32. 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.

33. 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

34. Diseases of Salivary Glands

35. Physiology 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

36. Major glands/Secretions Major SG are paired structures and include the parotid, submandibular and sublingual Parotid: serous Submandibular: mucous & serous Sublingual: mucous

37. Salivary Function Aid is mastication, deglutination Salivary lysozyme, IgA and other antibacterial substances protect against caries and oral cavity infections Saliva also aids in speech

38. ObstructiveSalivary Gland Disorders Sialolithiasis Mucous retention/extravasation �

39. 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

40. Sialolithiasis Incidence Escudier & McGurk 1:15-20 000 Marchal & Dulgurerov 1:10-20 000 Sialolithiasis remains the most frequent reason for submandibular gland resection

41. 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.

42. 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.

43. 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.

44. Etiology 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

45. Etiology Gout is the only systemic disease known to cause salivary calculi and these are composed of uric acid.

46. 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

47. 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 al Lustmann et al Rice

48. Reasons sialolithiasis may occur 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

49. 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

50. Clinical presentation Painful swelling (60%) Painless swelling (30%) Pain only (12%) Sometimes described as recurrent salivary colic and spasmodic pains upon eating

51. 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?

52. Exam: Inspection 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 ( Facial Nerve )

53. 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).

54. Diagnostics: Plain occlusal film Effective for intraductal stones. intraglandular, radiolucent or small stones may be missed.

55. Diagnostic approaches 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

56. Diagnostic approaches: 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

57. Sialography Disadvantages: irradiation dose pain with procedure Possible perforation infection dye reaction push stone further contraindicated in active infection.

58. 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

59. Diagnostic Approaches: 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!

60. Diagnostic Approach: 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

61. 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

62. Sialolithiasis Treatment None: antibiotics and anti-inflammatories, hoping for spontaneous stone passage. Stone excision: Lithotripsy Interventional sialendoscopy Simple removal (20% recurrence) Gland excision

63. Sialolithiasis Treatment 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 hyper-hydration when symptoms develop.

64. Stone 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.

65. Transoral vs. Extraoral 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.

66. Posterior Stones 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.

67. 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

68. Gland excision 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

69. Gland excision indicated Very posterior stones Intra-glandular stones Significantly symptomatic patients Failed transoral approach

70. Gland excision 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

71. ObstructiveSalivary Gland Disorders� Sialolithiasis Mucous retention/extravasation

72. 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

73. 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.

74. Mucocele 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

75. Mucocele Consist of a circumscribed cavity in the connective tissue and submucosa producing an obvious elevation in the mucosa

76. 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.

77. 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.

78. 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.

79. 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.

80. 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.

81. 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

82. Ranula Treatment Marsupialization has fallen into disfavor due to the excessive recurrence rate of 60-90% Sublingual gland removal via intraoral approach

83. Salivary Gland Infections Acute bacterial sialdenitis Chronic bacterial sialdenitis Viral infections

84. Sialadenitis Sialadenitis represents inflammation mainly involving the acinoparenchyma of the gland.

85. Sialadenitis Awareness of salivary gland infections was increased in 1881 when President Garfield died from acute parotitis following abdominal surgery and associated systemic dehydration.

86. Sialadenitis Acute infection more often affects the major glands than the minor glands

87. 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.

88. 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

89. 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.

90. 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.

91. Parotid PredilectionAnatomic factors 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.

92. Risk Factors for Sialadenitis Systemic dehydration (salivary stasis) Chronic disease and/or immunocompromise Liver failure Renal failure DM hypothyroid Malnutrition HIV Sj�gren�s syndrome

93. Risk Factors continued� Neoplasms (pressure occlusion of duct) Sialectasis (salivary duct dilation) increases the risk for retrograde contamination. cystic fibrosis and pneumoparotitis Extremes of age Poor oral hygiene Calculi, duct stricture NPO status (stimulatory effect of mastication on salivary production is lost)

94. Complex picture 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 site of acute suppurative infection!

95. Differential Diagnosis of Parotid Gland Enlargement Lymphoma Actinomycoses Cat-scratch disease Sjogren�s syndrome Wegener�s granulomatosis Viral infection

96. 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%.

97. Bacteriology Purulent saliva should be sent for culture. Staphylococcus aureus is most common Streptococcus pnemoniae S.pyogenes Haemophilus Influenzae also common

98. 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

99. Treatment of Acute Sialadenitis 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

100. 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

101. Failure to respond After 48 hours the patient should respond Consider adding a third generation cephalosporin Possibly add an aminoglycoside The preponderance of MRSA in nursing homes and nosocomial environments has prompted the recommendation of vancomycin in these groups

102. 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

103. 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

104. 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

105. 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.

106. 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.

107. Chronic Sialadenitis Of importance in the workup� The clinician should look for a treatable predisposing factor such as a calculus or a stricture.

108. 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. Dilatations & Irrigation

109. 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.

110. AVI 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.

111. Viral Infections As opposed to bacterial sialadenitis, viral infections of the salivary glands are SYSTEMIC from the onset!

112. 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

113. Mumps 2-3 week incubation after exposure 3-5 day viremia Then localizes to biologically active tissues like salivary glands, germinal tissues and the CNS.

114. 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

115. 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

116. 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

117. 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

118. 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

119. 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

120. 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

121. 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.

122. Treatment Supportive Fluid Anti-inflammatories and analgesics

123. 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

124. Complications 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

125. Immunologic Disease Sj�gren�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

126. Sj�gren�s syndrome 90% cases occur in women Average age of onset is 50y Classic monograph on the diease published in 1933 by Sj�gren, a Swedish ophthalmologist

127. Sj�gren�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

128. Sj�gren�s Syndrome Unilateral or bilateral salivary gland swelling occurs, may be permanent or intermittent. Rule out lymphoma

129. Sj�gren�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

130. Sj�gren�s Lip Biopsy Biopsy of SG mainly used to aid in the diagnosis Can also be helpful to confirm sarcoidosis

131. Sj�gren�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

132. Sj�gren�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

133. 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.

134. Related to� Metabolic �endocrine sialendosis� Nutritional �nutritional mumps� Obesity: secondary to fatty hypertrophy Malnutrition: acinar hypertrhophy Any condition that interferes with the absorption of nutrients (celiac dz, uremia, chronic pancreatitis, etc)

135. Related to� Alcoholic cirrhosis: likely based on protein deficiency & resultant acinar hypertrophy Drug induced: iodine mumps e. HIV

136. 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.

137. 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.

138. 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.

139. Granulomatous Disease 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.

140. Granulomatous Disease 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.

141. Cysts 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

142. 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

143. 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

144. 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

145. Other: Necrotizing 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

146. Necrotizing Sialometaplasia Self limiting lesion, heals by secondary intention over 6-8 weeks Histologically may be mistaken for SCC

147. Neoplasms Benign: - Pleaomorphic Adenoma: Commonest (2/3 of all salivary tumors) 85% in Parotid Gland. ? Capsulated with Psudopods 30% recurrence rate

148. Neoplasms Benign: - Warthins Tumor: 2nd most common almost exclusive to tail of parotid Well encapsulated Bil in 10%

149. Neoplasms Benign: - Monomorphic Adenoma - Oncocytomas - Hemangiomas

150. Neoplasms Malignant: make up a relatively small percentage of all cancer occurring in the head and neck region. Radiation exposure is one known risk factor Pain is present in 10 to 29% of patients with cancer in the parotid gland. Facial paralysis is detected in 10 to 15% of parotid gland malignancies

151. Neoplasms Malignant: - Mucoepidermoid Carcinoma most common (1/2 in Parotid ) High Grade & Low Grade.

152. Neoplasms Malignant: - Adenoid Cystic Carcinoma 2nd most common most common in submandibular & minors perineural invasion is hallmark High grade & low grade.

153. Neoplasms Malignant: - Polymorphus low grade Adenocarcinoma - Acinic Cell Carcinoma - Malignant Mixed Tumors - Sqaumous Cell Carcinoma

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