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Salivary glands Salivary glands Presentation Transcript

  • Mohammad Akheel OMFS PG
  • CONTENTS INTRODUCTION EMBRYOLOGY ANATOMY FUNCTIONS OF SALIVA CLASSIFICATION SALIVARY GLAND DISORDERS
  • INTRODUCTION Any changes producing pain and swelling of salivary glands leads to Salivary Gland Disorders.
  • 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.
  • Embryology The stroma (capsule and septae) of the glands originates from mesenchyme that may be mesodermal or neural crest in origin.
  • STAGES OF DEVELOPMENTSTAGE 1BUD STAGE
  • STAGE 2 CORD STAGE
  • STAGE 3 (TERMINAL BULB)
  • STAGE 4 ( LOBULE STAGE )
  • STAGE 5 ( DUCTCANALISATION)
  • STAGE 6 ( CYTODIFFERENTIATION)
  • 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.
  • 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.
  • 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.
  • 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.
  • Microanatomy The Secretory Unit Acinus (serous, mucous, mixed) Myoepithelial cells Intercalated duct Striated duct Excretory duct
  •  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
  • 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.
  • Acinar cells At around the 7-8th month in utero, secretory cells (acini) begin to develop around the ductal system.
  • Acinar cells of Salivary Glands Classified as either:  Serous cells: produce a thin watery secretion  Mucous cells: produce a more viscous secretion
  • Major glands/Secretions Major SG are paired structures and include the parotid, submandibular and sublingual Parotid: serous Submandibular: mucous & serous Sublingual: mucous
  • 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 .
  • 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
  • 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.
  • 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.
  • 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
  • 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
  • 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.
  • 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.
  • 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
  • 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.
  • Parotid: SympatheticInnervation Postganglionic innervation is provided by the superior cervical ganglion and distributes with the arterial system
  • 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.
  • 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.
  • 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
  • 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.
  • 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.
  • Anatomy: SubmandibularLymphatics Submandibular gland drains into submandibular nodes.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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
  • 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,
  • Salivary hypofunction Candidiasis Lichen Planus Burning Mouth Aphthous ulcers Dental caries Xerostomia
  • Autonomic Innervation Parasympathetic Abundant, watery saliva Amylase down Sympathetic Scant, viscous saliva Amylase up
  • CLASSIFICATION OF SALIVARY GLAND DISORDERS
  • CLASSIFICATION Congenital Agenesis Hypoplasia Acquired Inflammatory Infection  bacterial  viral  fungal
  • CLASSIFICATION ○ Autoimmune  Sjogrens  Sicca Syndromes ○ Idiopathic  necrotizing sialometaplasia  sarcoidosis Traumatic ○ Mucocele ○ Ranula ○ Salivary fistula ○ Radiotherapy induced xerostomia
  • CLASSIFICATION Obstructive Calculus disease Ductal stenosis Ductal atresia Benign Adenomas ○ Pleomorpic adenoma ○ Basal cell adenoma ○ Adenolymphoma ○ Cystadenoma
  • 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
  • Classification Tumor like lesions Sialadenosis Necrotising sialometaplasia Benign lymphoepithelial lesions Salivary gland cysts Cystic lymphoid hyperplasia (HIV)
  • EXAMINATION OF SALIVARY GLANDS
  • Clinical presentation  Painful swelling (60%)  Painless swelling (30%)  Pain only (12%) Sometimes described as recurrent salivary colic and spasmodic pains upon eating
  • 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?
  • Exam: Inspection Asymmetry (glands, face, neck) Diffuse or focal enlargement Erythema extra-orally Trismus Medial displacement of structures intraorally? Examine external auditory canal (EAC)
  • 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).
  • SALIVARY GLAND DISORDERS.
  • ObstructiveSalivary Gland Disorders Sialolithiasis Mucous retention/extravasation
  • Sialolithiasis  Sialolithiasis results in a mechanical obstuction of the salivary duct  Is the major cause of unilateral diffuse parotid or submandibular gland swelling
  • Sialolithiasis Incidence Escudier & McGurk 1:15-20 000 Marchal & Dulgurerov 1:10-20 000 Sialolithiasis remains the most frequent reason for submandibular gland resection
  • 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.
  • 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
  • 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.
  • Etiology Hypercalcemia… Xerostomic meds Tobacco smoking Smoking has an increased cytotoxic effect on saliva, decreases PMN phagocytic ability and reduces salivary proteins
  • Etiology Gout is the only systemic disease known to cause salivary calculi and these are composed of uric acid.
  • 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
  • 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
  • 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
  • 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
  • Diagnostics: Plain occlusal film  Effective for intraductal stones, while….  intraglandular, radiolucent or small stones may be missed.
  • 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
  • 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
  • Sialography Disadvantages: irradiation dose  pain with procedure infection dye reaction push stone further contraindicated in active infection
  • 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.
  • 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.
  • 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
  • SIALOENDOSCOPY
  • Sialolithiasis Treatment  None: antibiotics and anti-inflammatories, hoping for spontaneous stone passage.  Stone excision: Lithotripsy Interventional sialendoscopy Simple removal (20% recurrence)7  Gland excision
  • 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.
  • 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.
  • 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.
  • 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.
  • Submandibular Sialoliths:Transoral Advantages Preserves a functional gland Avoids neck scar Possibly less time from work Avoids risk to CN 7 & 12
  • Gland excision After SMG excision, 3% cases have recurrence via: Retention of stones in intraductal portion or new formation in residual Whartons duct
  • Gland excision Indications Very posterior stones Intra-glandular stones Significantly symptomatic patients Failed transoral approach
  • ObstructiveSalivary Gland Disorders  Sialolithiasis Mucous retention/extravasation
  • 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
  • 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.
  • 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
  • Mucocele Consist of a circumscribed cavity in the connective tissue and submucosa producing an obvious elevation in the mucosa
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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
  • Ranula Treatment Sublingual gland removal via intraoral approach
  • Salivary Gland Infections  Acute bacterial sialdenitis  Chronic bacterial sialdenitis  Viral infections
  • Sialadenitis Sialadenitis represents inflammation mainly involving the acinoparenchyma of the gland.
  • Sialadenitis Awareness of salivary gland infections was increased in 1881 when President Garfield died from acute parotitis following abdominal surgery and associated systemic dehydration.
  • Sialadenitis Acute infection more often affects the major glands than the minor glands
  • 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.
  • 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
  • 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.
  • 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.
  • Risk Factors for Sialadenitis Systemic dehydration (salivary stasis) Chronic disease and/or immunocompromise Liver failure Renal failure DM, hypothyroid Malnutrition HIV Sjögren’s syndrome
  • 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)
  • 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
  • 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%.
  • Bacteriology Purulent saliva should be sent for culture. Staphylococcus aureus is most common Streptococcus pnemoniae and S.pyogenes Haemophilus Influenzae also common
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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.
  • 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.
  • Chronic Sialadenitis Workup… The clinician should look for a treatable predisposing factor such as a calculus or a stricture.
  • 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.
  • 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.
  • 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.
  • Viral Infections As opposed to bacterial sialadenitis, viral infections of the salivary glands are SYSTEMIC from the onset!
  • 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
  • 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.
  • 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
  • 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.
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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.
  • Treatment  Supportive  Fluid  Anti-inflammatories and analgesics
  • 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
  • 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
  • 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
  • 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
  • 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
  • Sjögren’s Syndrome  Unilateral or bilateral salivary gland swelling occurs, may be permanent or intermittent.  Rule out lymphoma
  • 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
  • Sjögren’s Lip Biopsy Biopsy of SG mainly used to aid in the diagnosis Can also be helpful to confirm sarcoidosis
  • 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
  • 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
  • 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.
  • 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)
  • Related to…a. Alcoholic cirrhosis: likely based on protein deficiency & resultant acinar hypertrophyb. Drug induced: iodine mumpse. HIV
  • Radiation Injury Low dose radiation (1000cGy) to a salivary gland causes an acute tender and painful swelling within 24hrs. Serous cells are especially sensitive and exhibit marked degranulation and disruption.
  •  Continued irradiation leads to complete destruction of the serous acini and subsequent atrophy of the gland7. Similar to the thyroid, salivary neoplasm are increased in incidence after radiation exposure7.
  • 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.
  • 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.
  • 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.
  • 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
  • CystsAcquired cysts include: Mucus extravasation vs. retention Traumatic Benign epithelial lesions Association with tumors Pleomorphic adenoma Adenoid Cystic Carcinoma Mucoepidermoid Carcinoma Warthin’s Tumor
  • 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
  • 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
  • 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
  • Necrotizing Sialometaplasia Self limiting lesion, heals by secondary intention over 6-8 weeks Histologically may be mistaken for SCC
  • SALIVARY GLANDNEOPLASMS
  • 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
  • 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
  • Pleomorphic Adenoma Gross pathology Smooth Well-demarcated Solid Cystic changes Myxoid stroma
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • Oncocytoma Presentation Enlarging, painless mass Technetium-99m pertechnetate scintigraphy Mitochondrial hyperplasia
  • 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
  • Oncocytoma Electron microscopy: Mitochondrial hyperplasia 60% of cell volume
  • 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
  • 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
  • Basal Cell Adenoma Solid Most common Solid nests of tumor cells Uniform, hyperchromatic, round nuclei, indistinct cytoplasm Peripheral nuclear palisading Scant stroma
  • Basal Cell Adenoma Trabecular Cells in elongated trabecular pattern Vascular stroma
  • Basal Cell Adenoma Tubular Multiple duct-like structures Columnar cell lining Vascular stroma
  • Basal Cell Adenoma Membranous Thick eosinophilic hyaline membranes surrounding nests of tumor cells “jigsaw-puzzle” appearance
  • Myoepithelioma <1% of all salivary neoplasms 3rd-6th decades F>M Minor salivary glands > parotid > submandibular gland Presentation: asymptomatic mass
  • Myoepithelioma Histology Spindle cell ○ More common ○ Parotid ○ Uniform, central nuclei ○ Eosinophilic granular or fibrillar cytoplasm Plasmacytoid cell ○ Polygonal ○ Eccentric oval nuclei
  • 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
  • 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
  • Mucoepidermoid Carcinoma Gross pathology Well-circumscribed to partially encapsulated to unencapsulated Solid tumor with cystic spaces
  • Mucoepidermoid Carcinoma Histology—Low- grade Mucus cell > epidermoid cells Prominent cysts Mature cellular elements
  • Mucoepidermoid Carcinoma Histology— Intermediate- grade Mucus = epidermoid Fewer and smaller cysts Increasing pleomorphism and mitotic figures
  • Mucoepidermoid Carcinoma Histology—High- grade Epidermoid > mucus Solid tumor cell proliferation Mistaken for SCCA ○ Mucin staining
  • Mucoepidermoid Carcinoma Treatment Influenced by site, stage, grade Stage I & II ○ Wide local excision Stage III & IV ○ Radical excision ○ +/- neck dissection ○ +/- postoperative radiation therapy
  • 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
  • Adenoid Cystic Carcinoma Gross pathology Well-circumscribed Solid, rarely with cystic spaces infiltrative
  • Adenoid Cystic Carcinoma Histology— cribriform pattern Most common “swiss cheese” appearance
  • 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
  • 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%
  • 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
  • Acinic Cell Carcinoma Gross pathology Well-demarcated Most often homogeneous
  • Acinic Cell Carcinoma Histology Solid and microcystic patterns ○ Most common ○ Solid sheets ○ Numerous small cysts Polyhedral cells Small, dark, eccentric nuclei Basophilic granular cytoplasm
  • Acinic Cell Carcinoma Treatment Complete local excision +/- postoperative XRT Prognosis 5-year survival: 82% 10-year survival: 68% 25-year survival: 50%
  • Adenocarcinoma  Rare  5th to 8th decades  F>M  Parotid and minor salivary glands  Presentation: Enlarging mass 25% with pain or facial weakness
  • Adenocarcinoma Histology Heterogeneity Presence of glandular structures and absence of epidermoid component Grade I Grade II Grade III
  • 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%
  • 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
  • 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
  • Carcinoma Ex-PleomorphicAdenoma Gross pathology Poorly circumscribed Infiltrative Hemorrhage and necrosis
  • Carcinoma Ex-Pleomorphic Adenoma Histology Malignant cellular change adjacent to typical pleomorphic adenoma Carcinomatous component ○ Adenocarcinoma ○ Undifferentiated
  • Carcinoma Ex-PleomorphicAdenoma Treatment Radical excision Neck dissection (25% with lymph node involvement at presentation) Postoperative XRT Prognosis Dependent upon stage and histology
  • 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
  • Carcinosarcoma Gross pathology Poorly circumscribed Infiltrative Cystic areas Hemorrhage, necrosis Calcification
  • Carcinosarcoma Histology Biphasic appearance Sarcomatous component ○ Dominant ○ chondrosarcoma Carinomatous component ○ Moderately to poorly differentiated ductal carcinoma ○ Undifferentiated
  • 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
  • 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
  • Squamous Cell Carcinoma Gross pathology Unencapsulated Ulcerated fixed
  • Squamous Cell Carcinoma Histology Infiltrating Nests of tumor cells Well differentiated ○ Keratinization Moderately-well differentiated Poorly differentiated ○ No keratinization
  • Squamous Cell Carcinoma Treatment Radical excision Neck dissection Postoperative XRT Prognosis 5-year survival: 24% 10-year survival: 18%
  • 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
  • Polymorphous Low-GradeAdenocarcinoma Histology Isomorphic cells, indistinct borders, uniform nuclei Peripheral “Indian- file” pattern Treatment Complete yet conservative excision
  • 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
  • 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
  • INCISIONS
  • FACE LIFT INCISION
  • REFERENCESOral anatomy & histology – K . AveryOral pathology – ShaffersOral medicine – BurkitGrays anatomy – GraysHead and neck otolaryngologyLore and Medina AtlasDental Clinics of north americaTextbook of HuppInternet