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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
Salivary Gland Pathology: Diagnosis and Management, Second Edition, updates the landmark text in this important discipline within oral and maxillofacial surgery, otolaryngology/head and neck surgery, and general surgery. Written by well-established clinicians, educators, and researchers in oral and maxillofacial surgery, this book brings together information on the etiology, diagnosis, and treatment of all types of salivary gland pathology. Clear and comprehensive, Salivary Gland Pathology: Diagnosis and Management offers complete explanation of all points, supported by a wealth of clinical and surgical illustrations to allow the reader to gain insight into every facet of each pathologic entity and its diagnosis and treatment. Salivary Gland Pathology: Diagnosis and Management offers comprehensive coverage of all aspects of this topic. Beginning with the embryology, anatomy and physiology of the salivary glands, the first section of the book discusses radiographic imaging, infections, cystic conditions, sialoadenitis and sialolithiasis, and systemic diseases. The second section of the book is devoted to the classification of salivary gland tumors and devotes individual chapters to the discussion of each type. Additions for this section of the second edition include molecular biology of salivary gland neoplasia, radiation therapy, and chemotherapy and targeted therapy for salivary gland malignancies. The book closes with a discussion of pediatric salivary gland pathology, traumatic injuries of the salivary glands and miscellaneous pathologic processes of the salivary glands and ducts, including a section on saliva as a diagnostic fluid. The book is intended for a very diverse audience, including academic oral and maxillofacial surgeons, otolaryngologists / head and neck surgeons, general surgeons, as well as residents in these disciplines. Private practitioners will want to place this publication on the bookshelves of their offices so as to consult the textbook when evaluating a patient with salivary gland pathology.
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Veröffentlichungsjahr: 2015
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Table of Contents
Cover
Title Page
Copyright
Contributors
Foreword First Edition
Foreword Second Edition
Preface First Edition
Preface Second Edition
Acknowledgments
Chapter 1: Surgical Anatomy, Embryology, and Physiology of the Salivary Glands
Introduction
The Parotid Gland
The Submandibular Gland
The Sublingual Gland
Minor Salivary Glands
Histology of the Salivary Glands
Control of Salivation
Summary
References
Chapter 2: Diagnostic Imaging of Salivary Gland Pathology
Introduction
Imaging Modalities
Diagnostic Imaging Anatomy
Pathology of the Salivary Glands
Summary
References
Chapter 3: Infections of the Salivary Glands
Introduction
General Considerations
Bacterial Salivary Gland Infections
Viral Salivary Gland Infections
Collagen Sialadenitis
Summary
References
Chapter 4: Cysts and Cyst-like Lesions of the Salivary Glands
Introduction
Mucous Escape Reaction
Mucous Retention Cysts
Parotid Cysts Associated with Human Immunodeficiency Virus Infection
Branchial Cleft Cysts
Summary
References
Chapter 5: Sialolithiasis
Introduction
Pathophysiology of Sialolithiasis
Clinical Features of Sialolithiasis
Differential Diagnosis and Diagnosis of Sialolithiasis
Treatment of Sialolithiasis
Miscellaneous Sialolithiasis
Summary
References
Chapter 6: Systemic Diseases Affecting the Salivary Glands
Introduction
Sjogren Syndrome
Sarcoidosis
Sialosis
Summary
References
Chapter 7: Classification, Grading, and Staging of Salivary Gland Tumors
Introduction
Classification Systems for Salivary Gland Neoplasms
Grading and Staging of Salivary Gland Tumors
Staging of Salivary Gland Tumors
Summary
References
Chapter 8: The Molecular Biology of Benign and Malignant Salivary Gland Tumors
Introduction: The Puzzle and the Promise
Salivary Gland Tumor Cell Biology
Molecular Biology of Salivary Gland Neoplasms
Summary and Clinical Applications
Summary
References
Chapter 9: Tumors of the Parotid Gland
Introduction
Etiology and Epidemiology
Diagnosis
Surgical Management
Summary
References
Chapter 10: Tumors of the Submandibular and Sublingual Glands
Introduction
Epidemiology and Etiology
Diagnosis
Management
Summary
References
Chapter 11: Minor Salivary Gland Tumors
Introduction
Etiology of Minor Salivary Gland Tumors
Diagnosis of Minor Salivary Gland Tumors
Treatment of Minor Salivary Gland Tumors
Summary
References
Chapter 12: Radiation Therapy for Salivary Gland Tumors
Introduction
Low Risk Salivary Gland Malignancies
Moderate Risk Salivary Gland Malignancies
High Risk Salivary Gland Malignancies
Evolution of Radiation Techniques in Salivary Gland Malignancies
Radiation Technique for Low and Moderate Risk Salivary Gland Tumors
Radiation Technique for High Risk Salivary Gland Tumors
Advanced Radiation Therapy Techniques: Fast Neutron and Proton Therapy
Summary
References
Chapter 13: Systemic Therapy for Salivary Gland Cancer
Introduction
Epidemiology and Risk Factors
Molecular Biology of Salivary Gland Tumors
Clinical Presentation
Treatment
Summary
References
Chapter 14: Non-salivary Tumors of the Salivary Glands
Introduction
Mesenchymal Tumors
Epithelial Non-salivary Tumors
Tumors of Salivary Gland Lymph Nodes
Miscellaneous
Summary
References
Chapter 15: Pediatric Salivary Gland Pathology
Introduction
Non-Neoplastic Salivary Gland Lesions
Neoplastic Salivary Gland Disease
Summary
References
Chapter 16: Trauma and Injuries to the Salivary Glands
Introduction
Penetrating Injuries
Radiation Injury
Barotrauma
Summary
References
Chapter 17: Miscellaneous Pathologic Processes of the Salivary Glands
Introduction
Hereditary and Congenital Conditions
Saliva
Ischemic/degenerative Changes
Küttner Tumor
Summary
References
Index
End User License Agreement
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Guide
Cover
Table of Contents
Foreword First Edition
Preface First Edition
Begin Reading
List of Illustrations
Chapter 1: Surgical Anatomy, Embryology, and Physiology of the Salivary Glands
Figure 1.1 A lateral view of the skull showing some of the bony features related to the bed of the parotid gland. 1: Mandibular fossa; 2: Articular eminence; 3: Tympanic plate; 4: Mandibular condyle; 5: Styloid process; 6: Ramus of mandible; 7: Angle of mandible; 8: Mastoid process; 9: External acoustic meatus. Source:
Surgical Management of the Infratemporal Fossa
. (J. Langdon, B. Berkovitz & B. Moxham). ISBN 9781899066797. Reproduced with permission of Taylor & Francis Books UK.
Figure 1.2 The parotid gland and associated structures. 1: Auriculotemporal nerve; 2: Superficial temporal vessels; 3: Temporal branch of facial nerve; 4: Zygomatic branch of facial nerve; 5: Buccal branch of facial nerve; 6: Mandibular branch of facial nerve; 7: Cervical branch of facial nerve; 8: Parotid duct; 9: Parotid gland; 10: Masseter muscle; 11: Facial vessels; 12: Platysma muscle; 13: External jugular vein; 14: Sternocleidomastoid muscle; 15: Great auricular nerve. Source:
Surgical Management of the Infratemporal Fossa
. (J. Langdon, B. Berkovitz & B. Moxham). ISBN 9781899066797. Reproduced with permission of Taylor & Francis Books UK.
Figure 1.3 The mandibulostylohyoid ligament and surrounding anatomy.
Figure 1.4 Anatomical landmarks of the extratemporal facial nerve.
Figure 1.5 Clinical photograph of dissected facial nerve following superficial parotidectomy.
Figure 1.6 The branching patterns of the facial nerve.
Figure 1.7 The facial nerve and its relationship to the retromandibular vein within the parotid gland. Source:
Surgical Management of the Infratemporal Fossa
. (J. Langdon, B. Berkovitz & B. Moxham). ISBN 9781899066797. Reproduced with permission of Taylor & Francis Books UK.
Figure 1.8 The surface markings for the parotid duct.
Figure 1.9 The parasympathetic innervations of the salivary glands. The parasympathetic fibers are shown as blue lines.
Figure 1.10 The relationship of the superficial and deep lobes of the submandibular gland. (a) cross-sectional anatomy. (b) The superficial lobe from outside. (c) The relationship of the deep and superficial lobes to the mylohyoid muscle.
Figure 1.11 Superficial dissection of the left submandibular gland. The investing layer of the deep cervical fascia is elevated off of the submandibular gland and the facial vein is identified.
Figure 1.12 Deep dissection of the left submandibular gland. With the submandibular gland retracted, the facial artery is identified in proximity to the facial vein.
Figure 1.13 Clinical photograph showing the relationship of the lingual nerve to the submandibular gland.
Figure 1.14 Diagram showing the histology of the major components of the salivary glands.
Chapter 2: Diagnostic Imaging of Salivary Gland Pathology
Figure 2.1 Axial CT of the neck in soft tissue window without contrast demonstrating poor definition between soft tissue structures. The blood vessels are unopacified and cannot be easily distinguished from lymph nodes. Note the sialolith (arrow) in the hilum of the left submandibular gland.
Figure 2.2 Axial CT of the neck in soft tissue window with IV contrast demonstrates improved visualization of structures with enhancement of tissues and vasculature. Note the small lipoma (arrow) anterior to the left submandibular gland, which distorts the anterior aspect of the gland with slight posterior displacement.
Figure 2.3 Axial CT of the skull base reconstructed in a sharp algorithm and in bone window and level display demonstrating sharp bone detail. Note the sharply defined normal right stylomastoid foramen (arrow).
Figure 2.4 Axial CT of the neck at the thoracic inlet in lung windows demonstrating lung parenchyma (a). Axial image of dedicated CT of chest demonstrating cannon ball lesions in a patient previously treated for adenoid cystic carcinoma of the palate (b). These lesions are representative of diffuse metastatic disease of the lungs, but not pathognomonic of adenoid cystic carcinoma.
Figure 2.5 Coronal CT reformation of the neck in soft tissue window at the level of the submandibular glands. Orthogonal images with MDCT offer very good soft tissue detail in virtually any plane of interest in order to assess anatomic and pathologic relationships.
Figure 2.6 Sagittal CT reformation of the neck in soft tissue window at the level of the parotid gland. Note the accessory parotid gland (black arrow) sitting atop the parotid (Stensen) duct (thin white arrow). Also note the retromandibular vein (large white arrow) and external auditory canal.
Figure 2.7 CT angiogram (CTA) of the neck at the level of the parotid gland demonstrating the retromandibular vein and adjacent external carotid artery (large white arrow). Note the right cervical lymphangioma (thin white arrow) associated with the tail of the right parotid gland.
Figure 2.8 Axial MRI T1 weighted image at level of the skull base and brainstem without contrast demonstrating high signal in the subcutaneous fat, intermediate signal of the brain and low signal of the CSF and mucosa. Note dilated right parotid duct (arrow).
Figure 2.9 Axial MRI FSE T2 weighted image demonstrating the high signal of CSF and subcutaneous fat, intermediate signal of the brain and mucosa, and the low signal in the arteries.
Figure 2.10 Axial MRI GRE image.
Figure 2.11 Axial MRI STIR image at the skull base demonstrating the high signal of CSF but suppression of subcutaneous fat signal.
Figure 2.12 Sagittal MRI STIR image at the level of the parotid gland demonstrating the deep lobe seen through the stylomandibular tunnel (arrows). Note the parotid gland extending superiorly to the skull base.
Figure 2.13 Coronal MRI T1 post-contrast fat saturated image of the skull base demonstrating a mass in the left parotid gland extending to the stylomastoid foramen (arrow). Note the mild vascular enhancement and suppression of fat high signal on T1 weighted image.
Figure 2.14 Axial MRI FLAIR image at the skull base demonstrating CSF flow related artifactual increased signal in the right prepontine cistern.
Figure 2.15 Axial MRI DWI image at the skull base demonstrating susceptibility artifact adjacent to the left temporal bone (arrow).
Figure 2.16 Ultrasound of the submandibular gland (black arrow) adjacent to the mylohyoid muscle (white arrow).
Figure 2.17 Ultrasound of the parotid gland demonstrating a normal intraparotid lymph node on a hyperechoic background. The lymph node is round and has a hypoechoic rim but demonstrates a fatty hyperechoic hilum (arrow).
Figure 2.18 Ultrasound of the parotid gland in longitudinal orientation demonstrating the Doppler signal of the external carotid artery.
Figure 2.19 Ultrasound of the parotid gland in longitudinal orientation demonstrating the Doppler signal of the retromandibular vein.
Figure 2.20 Submandibular sialogram (a). Note the continuity defect that represents a sialolith (arrow). The corresponding submandibular CT (b) demonstrates a partially calcified stone that is less impressive compared to the sialogram.
Figure 2.21 Parotid sialogram. Note the numerous areas of duct dilatation and stenosis. These features are diagnostic of obstructive disease.
Figure 2.22 Submandibular sialogram: Note the “soft” non-calcified stone filling the duct.
Figure 2.23 Parotid sialogram. Note the punctate filling areas without ductal involvement. These findings are seen predominately in Sjogren syndrome patients.
Figure 2.24 Parotid sialo-CT. Although the main duct is opacified, it is impossible to determine areas of stenosis and/or dilatation.
Figure 2.25 CT (a), PET (b), and fused PET/CT (c) images in axial plane, and an anterior maximum intensity projection (MIP) image (d) demonstrating skeletal muscle uptake in the sternocleidomastoid muscle and biceps muscle (arrows). Also note the intense uptake in the abdominal, psoas, and intercostal muscles on the MIP image. The very high focal uptake in the middle of the image is myocardial activity.
Figure 2.26 PET image (a), corresponding CT image (b), and a fused PET/CT image (c) in the axial plane demonstrating Brown adipose tissue (BAT) uptake in the supraclavicular regions bilaterally which could mimic lymphadenopathy (see arrows on a and b). Direct correlation enabled by the PET/CT prevents a false positive finding. Note the similar uptake on the MIP image (arrow) (d) including paraspinal BAT uptake.
Figure 2.27 CT (a) and PET (b) images in axial plane demonstrating normal parotid gland activity (arrow).
Figure 2.28 CT (a) and PET (b) images in axial plane demonstrating normal submandibular (long, thin arrow) and sublingual gland (medium arrow) activity. Note the abnormal uptake higher than and anterior to the submandibular glands (short, fat arrow). Metastatic lymphadenopathy was diagnosed at the time of surgery.
Figure 2.29 Axial CT of the neck demonstrates the intermediate to low density of the parotid gland.
Figure 2.30 Reformatted coronal CT of the neck at the level of the parotid gland demonstrating its relationship to adjacent structures. Note the distinct soft tissue anatomy below the skull base.
Figure 2.31 Reformatted sagittal CT of the neck at the level of the parotid gland demonstrating its relationship to adjacent structures including the external auditory canal. Note the slightly denser soft tissue density in the parotid tail, the so-called “earring lesion” of the parotid gland. Cervical lymphadenopathy (arrow) was diagnosed at surgery.
Figure 2.32 Axial T1 MRI image at the level of the parotid gland demonstrating the slightly higher signal as compared to skeletal muscle but less than subcutaneous fat.
Figure 2.33 Coronal STIR MRI image at the level of the parotid gland demonstrating the nulling of the subcutaneous fat signal on STIR images and low signal from the partially fatty parotid gland.
Figure 2.34 Sagittal fat suppressed T1 MRI image of the parotid gland demonstrating mild enhancement and lack of subcutaneous fat signal in the upper neck but incomplete fat suppression at the base of the neck.
Figure 2.35 Axial CT scan (a) and corresponding PET scan (b) at the level of the parotid gland. Note the asymmetric slightly higher uptake on the right corresponding to partially resected parotid gland on the left, confirmed by CT.
Figure 2.36 Axial CT at the level of the submandibular gland demonstrating density higher than skeletal muscle.
Figure 2.37 Reformatted coronal CT at the level of the submandibular gland demonstrating its relationship to the mylohyoid muscle and floor of mouth.
Figure 2.38 Reformatted sagittal CT at the level of the submandibular gland demonstrating its relationship to the floor of mouth. Note the slight notch at the hilum of the gland. Majority of the gland “hangs” below the mylohyoid muscle.
Figure 2.39 Axial T1 MRI of the submandibular gland demonstrating slight hyperintensity to muscle. Note the bright subcutaneous fat.
Figure 2.40 Coronal fat saturated T2 MRI of the submandibular gland. Note the slightly incomplete fat suppression and the engorged and edematous mucosa of the nasal cavity and turbinates.
Figure 2.41 Sagittal T1 fat saturated MRI of the submandibular gland demonstrating the well-defined appearance on a fat suppressed background. Note the slight notch at the hilum. Also note the entire internal jugular vein is visualized.
Figure 2.42 Axial CT (a) and corresponding PET (b) of the submandibular gland demonstrating slight normal uptake. Note the strong asymmetry of uptake on the PET corresponds to the absent submandibular gland on the right confirmed by the CT.
Figure 2.43 Axial CT of the neck at the level of the sublingual gland demonstrating mild normal enhancement along the lateral floor of mouth.
Figure 2.44 Axial contrast enhanced T1 MRI of the sublingual gland demonstrating enhancement (a). Note the deep lobe of the submandibular glands seen at the posterior margin of the sublingual glands. Coronal T2 weighted image demonstrating the sublingual gland “cradled” between the mandible laterally, the genioglossus muscle medially, the geniohyoid muscle inferomedially, and the combined mylohyoid and digastric muscles inferiorly (b).
Figure 2.45 Axial PET of the sublingual gland demonstrating the intense uptake seen in the sublingual glands bilaterally medial to the mandible (photopenic linear regions).
Figure 2.46 Axial contrast enhanced CT of the neck at the level of the submandibular glands demonstrating a low density structure on the right of approximately fluid density (compare to the CSF in the spinal canal), which is intermediate in density relative to the muscles and subcutaneous fat. A large lymphangioma associated with the right submandibular gland was diagnosed.
Figure 2.47 Coronal STIR MRI of the face of a different patient with a very large lymphangioma with large septations. Note the lymphangioma fluid is brighter than the CSF and there is fat suppression of the subcutaneous fat.
Figure 2.48 Direct coronal CT displayed in bone window demonstrating smooth erosion of the hard palate on the right lateral aspect, along with a dense calcification consistent with a phlebolith (arrow). A hemangioma is presumed based on this CT scan.
Figure 2.49 Coronal fat suppressed contrast enhanced T1 MRI image corresponding to the same level as Figure 2.48, demonstrating a sharply marginated homogenously enhancing mass (arrow).
Figure 2.50 Coronal fat saturated T2 MRI image demonstrating a well demarcated hyperintense mass with a focal signal void centrally. A hemangioma containing a phlebolith (arrow) was presumed based on this MRI.
Figure 2.51 Axial CT with contrast at the level of the masseter muscles demonstrating a left accessory parotid gland abscess.
Figure 2.52 Axial contrast enhanced fat saturated T1 MRI demonstrating heterogenous enhancement consistent with abscess of the left accessory parotid gland.
Figure 2.53 Reformatted coronal CT demonstrating enlargement and enhancement of the submandibular glands consistent with viral sialadenitis.
Figure 2.54 Axial CT demonstrating a large cystic lesion in the right parotid gland and multiple small lesions in the left parotid diagnosed as lymphoepithelial cysts.
Figure 2.55 Reformatted coronal contrast enhanced CT of the submandibular gland demonstrating a sialolith in the hilum of the right submandibular gland.
Figure 2.56 Axial contrast enhanced CT of the parotid gland demonstrating a small left parotid sialolith (black arrow).
Figure 2.57 Axial contrast enhanced CT at the level of the submandibular glands with a very large left hilum sialolith (black arrow).
Figure 2.58 Axial contrast enhanced CT (a) of the head with a cystic mass at the level of the left external auditory canal and sagittal T2 MRI of a different patient (b) consistent with a type 1 branchial cleft cyst.
Figure 2.59 Axial contrast enhanced CT of the maxillofacial soft tissues with a cystic mass interposed between the left submandibular gland and sternocleidomastoid muscle, consistent with a type 2 branchial cleft cyst.
Figure 2.60 Axial contrast enhanced CT of the parotid gland with a heterogenous mass with cystic changes. A pleomorphic adenoma (arrow) was diagnosed at surgery.
Figure 2.61 Axial PET/CT fused image demonstrating intense FDG uptake in a parotid mass. Pleomorphic adenoma was diagnosed at surgery.
Figure 2.62 Axial contrast enhanced CT of a heterogenous parotid mass at the tail of the gland, with multiplicity and cystic or necrotic changes, diagnosed as a Warthin tumor (arrow).
Figure 2.63 Axial contrast enhanced CT demonstrating an ill-defined mass diagnosed as a mucoepidermoid carcinoma (arrow).
Figure 2.64 Axial contrast enhanced CT demonstrating large bulky cervical lymphadenopathy with ill-defined borders, diagnosed as a mucoepidermoid carcinoma.
Figure 2.65 Reformatted coronal contrast enhanced CT demonstrating an ill-defined heterogenous density mass diagnosed as a mucoepidermoid carcinoma (arrow).
Figure 2.66 Coronal contrast enhanced MRI of the skull base demonstrating a mass extending through the skull base via the left foramen ovale (arrow), diagnosed as an adenoid cystic carcinoma originating from a minor salivary gland of the pharyngeal mucosa.
Figure 2.67 Axial CT in bone window demonstrating a mass eroding through the left side of the hard palate and extending into the maxillary sinus (arrow) diagnosed as adenoid cystic carcinoma.
Figure 2.68 Coronal CT corresponding to the case illustrated in Figure 2.67 with a mass eroding the hard palate and extending into the left maxillary sinus (arrow).
Figure 2.69 Reformatted contrast enhanced coronal CT with a mass in the right submandibular gland (arrow) diagnosed as an adenoid cystic carcinoma.
Figure 2.70 Reformatted sagittal contrast enhanced CT corresponding to the case illustrated in Figure 2.64.
Figure 2.71 Axial contrasted enhanced CT of the head with a fat density mass at the level of the parotid gland and extending to the submandibular gland, diagnosed as a lipoma.
Figure 2.72 Axial contrast enhanced CT through the submandibular gland with fat density mass partially surrounding the gland. A lipoma was diagnosed.
Figure 2.73 Coronal T1 contrast enhanced MRI demonstrating a mass in the left parotid gland with smooth margins. The mass extends superiorly into the skull base at the stylomastoid foramen (arrow). A benign schwannoma was diagnosed.
Figure 2.74 Coronal T2 MRI corresponding to the case illustrated in Figure 2.73.
Figure 2.75 Axial CT at the skull base displayed in bone window showing dilatation of the stylomastoid foramen with soft tissue mass (arrow). A benign schwannoma was diagnosed.
Figure 2.76 Coronal T1 contrast image showing a very ill defined mass with heterogenous enhancement in the parotid gland with skull base extension via the stylomastoid foramen. A malignant schwannoma was diagnosed.
Figure 2.77 Axial T2 MRI image corresponding to the case illustrated in Figure 2.76.
Figure 2.78 Axial CT scan with contrast at the level of the parotid tail demonstrating an ill-defined heterogeneously enhancing mass adjacent to or exophytic from the parotid tail medially (arrow). Lymphoma in cervical lymphadenopathy was diagnosed at surgery.
Figure 2.79 Axial PET scan image corresponding to the case in Figure 2.78. A large mass of the left parotid gland (arrow) is noted.
Figure 2.80 Fused axial PET/CT image corresponding to the case illustrated in Figure 2.78.
Figure 2.81 Axial CT of a mass (arrow) in the right parotid gland with homogenous enhancement. The patient had a history of right facial melanoma. Metastatic melanoma was diagnosed at surgery.
Figure 2.82 Axial PET scan corresponding to the case illustrated in Figure 2.81. The mass in the right parotid gland (arrow) is hypermetabolic. Also note two foci of intense uptake corresponding to inflammatory changes in the tonsils.
Figure 2.83 Axial contrast enhanced CT scan through the parotid glands demonstrating a large mass of heterogenous density and enhancement partially exophytic from the gland. Metastatic squamous cell carcinoma from the scalp was diagnosed.
Chapter 3: Infections of the Salivary Glands
Figure 3.1 A 55-year-old woman (a and b) with a one week history of pain and swelling in the left parotid gland. No pus was present at the Stensen duct. The diagnosis was community acquired acute bacterial parotitis (APB). Conservative measures were instituted including the use of oral antibiotics, warm compresses to the left face, sialogogues, and digital massage. Two weeks later, she was asymptomatic, and physical examination revealed resolution of her swelling (c and d).
Figure 3.2 A 45-year-old man (a) with a 6-month history of left submandibular pain and swelling. A clinical diagnosis of chronic submandibular sialadenitis was made. A screening panoramic radiograph is obtained in a similar patient that revealed the presence of a large sialolith in the gland (b). As such, the obstruction of salivary outflow by the sialolith was responsible for the chronic sialadenitis. This case underscores the importance of obtaining a screening panoramic radiograph in a patient with a clinical diagnosis of sialadenitis, as it permitted expedient diagnosis of sialolithiasis.
Figure 3.3 A severe case of hospital acquired parotitis related to insufficient rehydration of this patient.
Figure 3.4 A mild case of community acquired parotitis is noted by the expression of pus at the left Stensen duct.
Figure 3.5 Lacrimal probes are utilized to probe the salivary ducts. The four shown in this Figure incrementally increase in size. Cannulation of salivary ducts begins with the smallest probe and proceeds sequentially to the largest so as to properly dilate the duct. It is recommended that patients initiate a course of antibiotics prior to probing salivary ducts so as to not exacerbate the sialadenitis by introducing oral bacteria into the gland.
Figure 3.6 Axial (a) and coronal (b) CT scans of a patient with a hospital acquired parotitis. The degree of swelling led to the acquisition of these scans so as to rule out intra-parotid abscess.
Figure 3.7 The algorithm for diagnosis and treatment of a unilateral or bilateral parotid swelling.
Figure 3.8 A 65-year-old man with a two week history of left parotid/neck swelling and pain (a and b). Computerized tomograms (c) revealed an abscess within the tail of the left parotid gland. The patient underwent incision and drainage in the operating room for a diagnosis of community acquired APB with abscess formation (d). Methicillin resistant staph aureus species were cultured. At two months postoperatively (e and f) he showed resolution of his disease.
Figure 3.9 Algorithm for the management of chronic recurrent bacterial parotitis.
Figure 3.10 The miniature endoscope for diagnostic and interventional sialoendoscopic procedures (a – Karl Storz Endoscopy, Germany). The instrumentation seen here is utilized for diagnostic procedures only. The endoscope may be connected to an operating sheath for interventional procedures (see Chapter 5). A series of duct dilators (b) are inserted in the Stensen duct prior to placing the sialoendoscope (c). A representative image is noted in (d) that demonstrates normal findings in a patient with chronic parotid pain. The sialoendoscopy procedure, including dilatation and irrigation of the duct, resulted in resolution of symptoms. A 76-year-old-man (e) with a chronic history of right parotid swelling. His symptom of right facial swelling waxed and waned (f and g) and he was noted to have the forced expression of pus from the right Stensen duct (h). He underwent imaging studies (i and j) due to the chronicity of his diagnosis of chronic parotitis. A sialoendoscopy was performed (k) that identified thick mucus in his main Stensen duct (l) and strictures in his distal ductwork within the gland (m).
Figure 3.11 A 35-year-old man with a 2-year history of left parotid pain and swelling (a and b). Computerized tomograms (c) showed sclerosis of the parotid parenchyma as well as a suspected abscess. The patient underwent left superficial parotidectomy with a clinical and radiographic diagnosis of chronic bacterial parotitis with abscess formation. The superficial parotidectomy was accessed with a standard incision (d). A nerve sparing approach was followed (e) that allowed for delivery of the specimen (f). Histopathology showed chronic sialadenitis with abscess formation (g). At 3 years postoperatively (h and i) he displays resolution of his disease.
Figure 3.12 The CT scan (a) of a 73-year-old man with a one year history of right submandibular swelling. Physical examination of the neck identified a mass with a differential diagnosis of submandibular gland mass versus enlarged lymph node in the submandibular region. This CT scan was obtained due to the equivocal nature of the finding on physical examination. Fine needle aspiration biopsy of this mass led to a diagnosis of low-grade lymphoma. By distinction, a 24-year-old woman with right submandibular swelling and pain who underwent a CT scan that identified intense uptake of intravenous contrast of the right submandibular gland indicative of acute bacterial submandibular sialadenitis (b). Fat stranding in the left neck indicative of inflammation is also noted.
Figure 3.13 Algorithm for diagnosis and management of acute bacterial submandibular sialadenitis (ABSS).
Figure 3.14 A 52-year-old man (a) with a 1-year history of vague discomfort in the left upper neck. Screening panoramic radiograph (b) showed no evidence of a sialolith. His diagnosis was chronic submandibular sialadenitis and he was prepared for left submandibular gland excision (c). The surgery was carried through anatomic planes, including the investing layer of the deep cervical fascia (d). The dissection is carried deep to this layer since a cancer surgery is not being performed that would require a dissection superficial to the investing fascia. Exposure of the gland demonstrates a small submandibular gland due to scar contracture (e). Inferior retraction of the gland allows for identification and preservation of the lingual nerve (f). The specimen (g) is bivalved (h) which allows for the appreciation of scar within the gland. The resultant tissue bed (i) shows the hypoglossal nerve which is routinely preserved in excision of the submandibular gland. Histopathology shows a sclerosing sialadenitis (j). The patient's symptoms were eliminated postoperatively, and he healed uneventfully, as noted at 1 year following the surgery (k).
Figure 3.15 A 23-year-old woman (a) with a 2-week history of left submandibular pain and swelling. A history of animal scratch was provided. Computerized tomograms (b) revealed a mass of the left submandibular gland. The patient was taken to the operating room where excision of the submandibular gland and mass was performed. Wide access was afforded (c) and the mass was exposed (d). The specimen is noted in (e). Histopathology showed a stellate abscess (f). A Steiner stain (g) showed
Bartonella
(gram negative bacillus). Her disease resolved without long term antibiotics as seen in five year postoperative images (h and i).
Figure 3.16 A 9-year-old girl with a left parotid swelling with overlying erythema of skin but no signs of acute infection (a). The patient underwent left superficial parotidectomy and excision of a submandibular lymph node. Histopathology showed non-caseating granulomas (b), and cultures showed mycobacterium avium intracellulare. Two months following the parotidectomy, a left submandibular lymph node became enlarged (c) and was treated with medical therapy.
Figure 3.17 Axial (a) and coronal (b) CT images demonstrating contrast enhancement of bilateral submandibular and parotid glands in a patient with a clinical viral prodrome.
Figure 3.18 A 6-year-old African female with AIDS showing involvement of the right parotid gland by diffuse infiltrative lymphocytosis syndrome (DILS).
Chapter 4: Cysts and Cyst-like Lesions of the Salivary Glands
Figure 4.1 The typical appearance of a ranula of the floor of mouth. The characteristically raised nature of the lesion, as well as its blue hue, is appreciated.
Figure 4.2 This ranula has resulted in significant pain experienced by the patient. The size of the ranula has resulted in obstruction of the sublingual gland.
Figure 4.3 The classic appearance of a mucocele of the lower lip. Similar to a ranula of the floor of mouth, it shows an elevated blue lesion.
Figure 4.4 A ranula of the left floor of mouth. While the lesion is clearly elevated, only subtle signs exist of its blue color.
Figure 4.5 A ranula of the right floor of mouth. Classic signs of elevation and the blue discoloration are present.
Figure 4.6 An 8-year-old girl with obvious right submandibular swelling (a) as well as simultaneous clinical evidence of a ranula in the right floor of mouth (b).
Figure 4.7 This elderly woman shows left submandibular swelling (a). Her history includes numerous aspirations of fluid within a ranula of the left floor of mouth. Computerized tomograms of the neck show a fluid filled lesion of the submandibular region (b). A diagnosis of plunging ranula was made and the patient underwent left sublingual gland excision (c). Examination of the left floor of mouth did not show signs of ranula in this region. Scar tissue formation from her previous aspirations resulted in the development of a plunging ranula.
Figure 4.8 The excision of the sublingual gland and associated ranula from Figure 4.1. An incision is designed over the prominence of the sublingual gland and ranula, and lateral to the Wharton duct (a). Careful dissection allows for separation of the mucosa from the underlying pseudocystic membrane (b). The dissection continues to separate the sublingual gland from surrounding tissues, including the underlying Wharton duct and the lingual nerve beneath the Wharton duct (c). The specimen and ranula are able to be delivered en bloc (d). If the pseudocyst bursts intraoperatively, no compromise in cure exists as long as the sublingual gland is completely excised. The histopathology shows the non-epithelial lining (e) and the intimate association of the sublingual gland and mucus escape reaction (f). The remaining tissue bed shows the anatomic relationship of the preserved superficial Wharton duct and underlying lingual nerve (g). Wharton duct originates posteriorly in a medial position to the lingual nerve and terminates in a position lateral to the nerve. The sublingual vein can be visualized in the tissue bed lateral to the anterior aspect of Wharton duct (g). Healing is uneventful as noted in the one month postoperative image (h).
Figure 4.9 The specimen from the excision of the mucocele seen in Figure 4.3. The minor salivary gland tissue remains attached to the mucus escape reaction.
Figure 4.10 The patient seen in Figure 4.7 underwent excision of her left sublingual gland for her plunging ranula. The specimen (a) includes the sublingual gland and associated mucus escape reaction. Her 2-year postoperative examination shows no mass in the submandibular region (b) and a normal oral examination without recurrence of the ranula (c).
Figure 4.11 A 48-year-old man with a swelling of the right submandibular region (a). Palpation of this swelling revealed a ballotable mass. A CT scan revealed a fluid filled lesion intimately associated with the right submandibular gland (b). A clinical diagnosis of submandibular gland mucocele was made and the patient underwent excision of his right sublingual gland and submandibular gland/mucocele (c). The presence of a submandibular gland mucocele was confirmed by histopathology (d). Hematoxylin and eosin, original magnification ×100.
Figure 4.12 A cyst of Blandin and Nuhn of the ventral surface of the tongue. Simple excision of the cyst and associated minor salivary gland tissue is curative for this mucus escape phenomenon.
Figure 4.13 A mucous retention cyst of the parotid gland as noted on MRI (T1 images – a; T2 images – b). The patient underwent a superficial parotidectomy due to the concern for a cystic neoplasm. Histopathology showed a parotid cyst lined by columnar epithelium in one section of the cyst (c) and squamoid epithelium in another section (d).
Figure 4.14 A 50-year-old HIV positive male presented in 1994 with obvious right parotid swelling (a,b). This time period pre-dated the development of HAART. Examination of the bilateral parotid gland regions revealed a large mass of the right parotid gland, and a smaller mass of the left parotid gland. Computerized tomograms (c) confirmed the findings of the physical examination. A clinical diagnosis of bilateral lymphoepithelial cysts was made. The patient requested removal of these cysts. A standard incision was made (d). This permitted unroofing of the large cyst in the right parotid gland (e) and the smaller cysts in the left parotid gland (f). The specimen from the right parotid gland (g) and the left parotid gland (h) showed typical gross signs of lymphoepithelial cysts. The resultant right parotid tissue bed is noted (i). Six months postoperatively, the patient showed well healed surgical sites without signs of recurrent lymphoepithelial cysts (Figure j, k, l, and m).
Figure 4.15 A 35-year-old HIV positive man presented in 2005 with a complaint of bilateral parotid swellings. He admitted to non-compliance with his HAART. His CD4/CD8 was 0.69 at the time of initial consultation. Physical examination revealed an obvious right parotid swelling and a subtle mass of the left parotid gland (a and b). Computerized tomograms (c and d) confirmed these findings. A fine needle aspiration biopsy was performed that yielded thick white fluid. A diagnosis of lymphoepithelial cysts was made. The patient resumed his HAART and was the cysts regressed as noted on an examination 4 months later (e and f). His CD4/CD8 was 1.12 at this time.
Chapter 5: Sialolithiasis
Figure 5.1 A single sialolith noted within the right submandibular gland. Isolated stones are most common in the submandibular system.
Figure 5.2 This panoramic radiograph close-up shows two sialoliths within the left submandibular gland.
Figure 5.3 This lateral cephalometric radiograph shows a single stone located within the Stensen duct.
Figure 5.4 This panoramic radiograph shows an oval sialolith of the left submandibular gland.
Figure 5.5 This very large sialolith is associated with the right submandibular gland as seen on panoramic radiograph (a). Due to its size, it might be confused with an osteoma of the mandible such that computerized tomograms help to identify its presence within the submandibular gland (b).
Figure 5.6 This axial section of computerized tomograms show the presence of bilateral sialoliths of the submandibular glands.
Figure 5.7 A close-up of a panoramic radiograph obtained in a patient with a chief complaint of right submandibular pain (a). The calcifications noted on this radiograph are located in the retromandibular region as well as the submandibular gland area. Exploration of the neck showed indurated lymph nodes present in association with the right submandibular gland, but clearly not sialoliths (b). The lymph nodes were removed (c) and bisected, showing macroscopic (d) and microscopic evidence of caseous necrosis (e). A diagnosis of tuberculous adenitis was therefore established. The patient was subjected to a purified protein derivative (PPD) skin test that was positive.
Figure 5.8 A panoramic radiograph demonstrating calcifications within the left submandibular region (a). At first glance of the radiograph, submandibular sialolithiasis is a reasonable consideration. Close examination of the radiograph reveals multicentric lamellated calcifications in the submandibular and preauricular regions, as well as a calcification superimposed on the left mandibular second molar roots. A complete physical examination revealed signs consistent with a hemangioma associated with the left mandibular gingiva (b). As such, the calcifications are presumed to represent phleboliths, and are not removed. It is important, therefore, to diagnose sialolithiasis based on a review of a radiograph as well as a physical examination.
Figure 5.9 This panoramic radiographic close-up shows an irregular mass associated with the left submandibular region (a). Computerized tomograms were not obtained preoperatively, and a differential diagnosis of submandibular sialolithiasis was established. The calcification, however, does not show typical radiographic signs of a sialolith, including its irregular borders. The patient underwent exploration of the left submandibular region, whereupon the calcified mass was identified as a distinct entity from the left submandibular gland (b). The mass was removed (c) and the left submandibular gland remained in the tissue bed (d). A histopathologic diagnosis of osteoma was made. A subsequent diagnosis of Gardner syndrome was made, and the patient underwent colectomy when a diagnosis of adenocarcinoma of the colon was established.
Figure 5.10 Algorithm for submandibular sialolithiasis.
Figure 5.11 A sialolith is noted at the opening of the right Wharton duct (a). Since this stone was able to be palpated on oral examination, it was removed transorally without necessitating the removal of the right submandibular gland. The main stone was removed (b), after which time exploration of the proximal duct revealed two additional stones that were also removed (c). A sialodochoplasty was performed to widen and shorten the right Wharton duct (d). A sialodochoplasty performed near the papilla of the Wharton duct is termed a papillotomy.
Figure 5.12 The clinical appearance of a man with pain and left submandibular swelling (a). His panoramic radiographic (b) shows a sialolith in the left submandibular gland. A standard transcutaneous approach was followed to submandibular gland excision (c). A subfascial dissection of the gland was performed. Inferior retraction on the gland allowed for preservation of the marginal mandibular branch of the facial nerve (d). Superior and anterior retraction of the gland allowed for identification of the sialolith that was located at the hilum of the gland (e). The excised gland (f) was bisected (g) and demonstrated significant scar tissue formation.
Figure 5.13 Interventional sialoendoscopic instrumentation for retrieval of salivary calculus, including the operating sheaths (a) that accept the miniature endoscope in the
telescope
channel (b). The grasping forceps (c), are placed within the
working
channel of the operating sheaths (d), and are able to retrieve stones that may be identified on diagnostic sialoendoscopy (e). Figure 5.13(e) Source: Maria Troulis, Boston, Massachusetts.
Figure 5.14 Algorithm for parotid sialolithiasis.
Figure 5.15 Management of an extraglandular parotid duct sialolith. The panoramic radiograph demonstrates a small sialolith in the right Stensen duct (a). The approach for this transoral sialolithotomy involved a mucosal incision anterior to the Stensen papilla (b). A mucosal flap was developed that included the Stensen duct such that the dissection occurred lateral to the duct (c). Continued dissection allowed for palpation of the sialolith within the duct. The duct was longitudinally incised over the sialolith (d), such that the stone was able to be removed (e). The mucosal flap was sutured without reapproximating the incision in the Stensen duct (f). Patent salivary flow was re-established as noted two months postoperatively (g). No further treatment of the gland was required.
Figure 5.16 Axial CT scan demonstrating a parotid sialolith at the hilum with proximal dilatation of the duct due to obstruction of salivary flow (a). A parotidectomy approach to stone retrieval was performed without parotidectomy (b).
Figure 5.17 A lateral oblique plain film demonstrating two sialoliths of the Stenson duct (a). An incision through skin was placed in a resting tension line of the cheek (b). A finger was inserted in the oral cavity to created better access to the duct, thereby permitting stone retrieval (c). A primary closure was obtained (d). Source: Ord RA: Salivary gland disease. In: Fonseca R (ed.),
Oral and Maxillofacial Surgery, Volume 5, Surgical Pathology
. Philadelphia, W.B. Saunders Co., pp. 273–293. Reproduced with permission of Elsevier.
Figure 5.18 A 72-year-old man with pain and swelling of one month's duration in the right submandibular gland (a). Physical examination was significant for a tender right submandibular gland but no symptoms associated with the left submandibular gland (b). The patient underwent CT scanning that demonstrated an enlarged right submandibular gland with the presence of a single intraglandular sialolith (c and d). Thorough evaluation of the CT scans also identified five extraglandular right submandibular stones and two extraglandular left submandibular stones (e, and f). The patient underwent right submandibular gland excision in a standard fashion (g and h) with exploration of bilateral Wharton ducts so as to remove five right extraglandular stones and two left extraglandular stones (i). A left Wharton sialodochoplasty was performed.
Figure 5.19 Floor of mouth swelling present in a 55-year-old woman (a). A diffuse mass is noted beneath the surface mucosa that is smooth and of normal color. A presumptive diagnosis of ranula versus neoplasm was established. A left sublingual gland excision was performed in the standard fashion (b). The specimen (c) exhibited mild induration without signs of ranula, such that a neoplastic process was favored while the possibility of a mucous escape reaction was discarded. Final histopathology showed a sialolith (d) in the background of sialadenitis (e). The tissue bed is noted (f), particularly the lingual nerve (retracted with the vessel loop) and the Wharton duct. A 6-month postoperative evaluation showed acceptable healing (g).
Chapter 6: Systemic Diseases Affecting the Salivary Glands
Figure 6.1 The association between the lymphoepithelial lesion, Sjogren syndrome, and lymphoma.
Figure 6.2 A 36-year-old woman with a known history of Sjogren syndrome associated with rheumatoid arthritis. She described a recent history of painful swelling of the right parotid gland such that an incisional parotid biopsy was recommended.
Figure 6.3 A 75-year-old woman (a, b) with a left parotid mass. Fine needle aspiration biopsy suggested lymphoma, leading to superficial parotidectomy. Histopathology identified benign lymphoepithelial lesion.
Figure 6.4 A 45-year-old woman diagnosed with Sjogren syndrome with bilateral parotid lesions shown on axial (a) and coronal images (b).
Figure 6.5 A 55-year-old woman (a) with a 10-year history of a progressively enlarging mass of the left cheek that is able to be visualized inferior to her left zygomatic buttress when she opens her mouth. She reported a history of Sjogren syndrome and rheumatoid arthritis of the hands (b). Computerized tomograms (c) identified a heterogenous mass of the left buccal region, associated with minor salivary gland tissue versus an accessory parotid gland. A salivary gland neoplasm was favored based on clinical and radiographic information. Excision was accomplished with a Weber–Ferguson incision (d) so as to provide access and minimize trauma to the Stenson duct and the buccal branch of the facial nerve. An incision in the buccal mucosa (e) was also utilized, which permitted effective dissection of the tissue bed (f). The specimen was able to be removed without difficulty (g) and was diagnosed as a lymphoepithelial lesion (h, Hematoxylin and eosin, original magnification ×200). She healed well and without recurrence of her lymphoepithelial lesion as noted at 5 years postoperatively (i).
Figure 6.6 A 32-year-old woman with the recent development of dry eyes and mouth, possibly suggestive of Sjogren syndrome (a). No swelling of the parotid glands was appreciated on physical examination. An incisional biopsy of the lower lip and right parotid gland were performed. The histopathology showed a normal lower lip biopsy (b – hematoxylin and eosin, original magnification ×100) and signs consistent with Sjogren syndrome on parotid biopsy (c – hematoxylin and eosin, original magnification ×200).
Figure 6.7 An incisional parotid biopsy was performed on the patient seen in Figure 6.1. The incision is placed behind the right ear, which enables the surgeon to procure sufficient parotid tissue to establish a diagnosis, while also providing a cosmetic scar (a). The dissection proceeds through skin and subcutaneous tissue after which time the parotid capsule is noted. This is incised and a 1 cm
2
specimen of parotid gland is removed (b). The closure requires a reapproximation of the parotid capsule so as to avoid a salivary fistula postoperatively.
Figure 6.8 The histopathology of the incisional parotid biopsy of the patient in Figure 6.1 (a, b). Signs consistent with Sjogren syndrome were noted including an intense lymphocytic infiltrate and destruction of acinar tissue. (a = hematoxylin and eosin, original magnification ×200. b = hematoxylin and eosin, original magnification ×40).
Figure 6.9 Posterior-anterior (a) and lateral (b) chest radiographs of a patient with type II sarcoidosis. This patient presented with severe shortness of breath.
Figure 6.10 Severe nasal cartilage involvement by sarcoidosis in this elderly woman. Source: Image courtesy of Dr. James Sciubba.
Figure 6.11 A 64-year-old woman with parotid swelling of 2 months' duration. The patient had been clinically diagnosed with Sjogren syndrome yet serology was negative. A fine needle aspiration biopsy of the left parotid gland swelling had been performed that suggested a Warthin tumor. Physical examination identified tender swellings of the bilateral parotid glands, with the left being larger than the right (a, b, c). CT examination identified diffuse enlargement of the parotid glands (d) and multiple enlarged lymph nodes in the left submandibular region (e). Her chest radiograph identified bilateral interstitial prominence (f). With an equivocal diagnosis of her left parotid swelling, the patient underwent left superficial parotidectomy and removal of left submandibular lymph nodes in a standard fashion (g, h, i). Final histopathology (j – hematoxylin and eosin, original magnification ×100) demonstrated non-caseating granulomas consistent with a diagnosis of sarcoidosis. The excised submandibular lymph nodes showed identical histopathology. The patient was treated with a 54-week course of prednisone and methotrexate for her diagnosis of pulmonary and extrapulmonary sarcoidosis, and showed a favorable response. She was doing well at her 5-year postoperative evaluation (k, l).
Figure 6.12 A 55-year-old man with bilateral submandibular gland swellings (a, b), as well as lower lip lesions (c). Excision of the left submandibular gland and biopsy of the lower lip swelling identified non-caseating granulomas. Additional workup identified signs consistent with sarcoidosis.
Figure 6.13 Histopathology of sarcoidosis (hematoxylin and eosin, original magnification ×200). Source: Image courtesy of Dr. Joseph A. Regezi.
Figure 6.14 A 32-year-old man with a chronic history of bilateral parotid swellings. He gave a history of achalasia. The history suggested that the parotid swellings were consistent with a diagnosis of sialosis. There were no physical or historical findings suggestive of another diagnosis.
Figure 6.15 The fluoroscopic images of the barium swallow performed in the patient in Figure 6.14. The characteristic “bird's beak” deformity is noted, reflective of failure of the lower esophageal sphincter to relax. This is diagnostic of achalasia.
Figure 6.16 The histopathology of the incisional parotid biopsy performed on the patient in Figure 6.14 (hematoxylin and eosin, original magnification ×200). Acinar hypertrophy is noted. The physical, radiographic, and histologic information confirms a diagnosis of achalasia. He was treated with surgical myotomy of the lower esophageal sphincter.
Chapter 7: Classification, Grading, and Staging of Salivary Gland Tumors
Figure 7.1 (a) Pleomorphic adenoma containing tubular and solid structures composed of round to basaloid cells. Foci of squamous, myxoid, and chondroid metaplasia are seen as well. (Lower left panel.) H&E staining, 200×. (b) Composite Figure of a pleomorphic adenoma demonstrating myxoid components (upper right), spindle-cell components (lower right), clear ductal cells surrounded by hyaline stroma (upper left), and tubular elements surrounded by a loose basophilic stroma (lower left). H&E staining, 400×.
Figure 7.2 Warthin tumor with well- developed fibrous capsule delineating the lesion from normal parotid gland. The tumor is characterized by bilayered oncocytic epithelium lining cystic spaces closely associated with lymphoid tissue. Lower right panel depicting the oncocytic epithelium in close proximity to a lymphoid aggregate. H&E staining, 200×/400×. Source: Courtesy of Dr. Mark Bernstein.
Figure 7.3 Basal cell adenoma consisting of monotonous sheets of basaloid cells lacking any myxochondroid tissues, spindled or plasmacytoid cells observed in pleomorphic adenomas. Lower right panel depicting palisaded basaloid cells surrounding a tumor cell nest. H&E staining, 200×. Source: Courtesy of Dr. Mark Bernstein.
Figure 7.4 Canalicular adenoma demonstrating columns of columnar cells lining canaliculi forming interconnecting tubules and microcysts. Lower right panel higher magnification detail. H&E staining, 100×/200×. Source: Courtesy of Dr. Mark Bernstein.
Figure 7.5 Oncocytoma characterized by eosinophilic, granular cytoplasm, with stippled nuclei. H&E staining, 400×.
Figure 7.6 Sebaceous adenoma demonstrating numerous islands of tumor cells exhibiting both squamous and sebaceous differentiation. H&E staining, 200×.
Figure 7.7 One morphologic pattern of myoepithelioma demonstrating a monotonous population of myoepithelial cells with uniform nuclei. H&E staining, 200×.
Figure 7.8 Cystadenoma characterized by tortuous cystic spaces cystic spaces lined by cuboidal epithelium. H&E staining, 100×.
Figure 7.9 Sialadenoma papilliferum demonstrating papillary stalks composed of uniform cuboidal epithelium. H&E staining, 200×.
Figure 7.10 Polycystic sclerosing adenosis composed of numerous tubuloacinar structures within a dense sclerotic stroma. H&E staining, 200×.
Figure 7.11 Mucoepidermoid carcinoma exhibiting large cystic spaces containing mucin and solid tumor elements. Lower right panel depicting epidermoid, intermediate and mucous cells. H&E staining, 100×/200×. Source: Courtesy of Dr. Mark Bernstein.
Figure 7.12 Intermediate grade mucoepidermoid carcinoma with mostly solid features and few mucous cells. H&E staining, 200×.
Figure 7.13 Intermediate grade mucoepidermoid carcinoma from Figure 7.12 demonstrating numerous areas of mucin production/deposition. Mucicarmine stain, 200×.
Figure 7.14 Adenoid cystic carcinoma manifesting cribriform and tubular patterns, right panel and lower left panel. Solid pattern of growth shown in upper left panel. H&E staining, 200×/400×. Source: Courtesy of Dr. Mark Bernstein.
Figure 7.15 Adenoid cystic carcinoma demonstrating classic nerve invasion pattern. H&E staining, 400×.
Figure 7.16 Acinic cell carcinoma of the microcystic pattern type. H&E staining, 200×.
Figure 7.17 Acinic cell carcinoma composed predominately of acinar cells. H&E staining, 200×.
Figure 7.18 Polymorphous low grade adenocarcinoma comprised of both small and intermediate size tumor cells. H&E staining, 100×.
Figure 7.19 Polymorphous low grade adenocarcinoma arranged in a concentric pattern. Near the center is peripheral nerve infiltration. H&E staining, 200×.
Figure 7.20 Adenocarcinoma, NOS: Infiltrative growth of neoplastic epithelium forming islands, cords and dense cell sheets invading a peripheral nerve. H&E staining, 200×/400×.
Figure 7.21 Basal cell adenocarcinoma arranged much like a basal cell adenoma but with atypical cellular features. H&E staining, 200×.
Figure 7.22 Primary clear cell carcinoma arising within the parotid gland. H&E staining, 100×.
Figure 7.23 A clear cell variant of a mucoepidermoid carcinoma. H&E staining, 200×.
Figure 7.24 The classic clear cell variant of a renal cell carcinoma metastatic to the parotid gland. H&E staining, 200×.
Figure 7.25 Low-grade cribriform cystadenocarcinoma, also known as the low-grade salivary duct carcinoma, is easily confused with an acinic cell carcinoma. H&E staining, 200×.
Figure 7.26 Sebaceous adenocarcinoma is characterized by sebaceous differentiation within islands of squamoid cells. H&E staining, 400×.
Figure 7.27 Oncocytic carcinoma demonstrating the atypical features of the oncocytes. H&E staining, 200×.
Figure 7.28 Salivary duct carcinoma containing comedonecrosis centrally within a tumor nodule surrounded by a prominent hyalinized fibrous connective tissue. H&E staining, 400×. Source: Courtesy of Dr. Mark Bernstein.
Figure 7.29 Nodules of salivary duct carcinoma embedded within a dense connective tissue stroma. H&E staining, 400×.
Figure 7.30 Carcinoma ex. pleomorphic adenoma demonstrating an adenoid cystic carcinoma on the right arising within a basal cell adenoma on the left. H&E staining, 100×.
Figure 7.31 Carcinoma ex. pleomorphic adenoma exhibiting nuclear abnormalities, including pleomorphism, hyperchromatism, and large nucleoli with variations in cellularity within a pleomorphic adenoma. H&E staining, 400×. Source: Courtesy of Dr. Mark Bernstein.
Figure 7.32 Primary squamous cell carcinoma arising within a parotid gland. Note the large amount of keratin production in this moderately differentiated tumor. H&E staining, 200×.
Figure 7.33 Closer view of case Figure 7.32 exhibiting atypical nuclear features. H&E staining, 400×.
Figure 7.34 Myoepithelial carcinoma of salivary gland. Note the larger clear cells as well as the smaller epithelial cells. Each group of cells is surrounded by a dense fibrous stroma. H&E staining, 200×.
Figure 7.35 Anaplastic small cell carcinoma arranged in groups. Note the lack of cellular organization. H&E staining, 200×.
Figure 7.36 Same anaplastic small cell carcinoma as in Figure 7.35. This immunostain demonstrates the positive neuroendocrine features of these cells. Chromogranin immunostain, 200×.
Figure 7.37 Small cell undifferentiated carcinoma of minor salivary gland. Note the complete lack of cell orientation. The cells are slightly larger than mature lymphocytes. H&E staining, 200×.
Figure 7.38 Large cell undifferentiated carcinoma of the submandibular gland. The entire tumor is composed of large, pleomorphic cells with no specific orientation. H&E staining, 200×.
Figure 7.39 Lymphoepithelial carcinoma is composed of large malignant cells imbedded within a lymphoid stroma. Often times it is difficult to microscopically discern the malignant cells in this dense stroma. H&E staining, 100×.
Figure 7.40 Immunohistochemistry is a great help in determining the exact tumor type in the same lesion as Figure 7.39. Note the ease with which stain depicts these large malignant cells. Pan cytokeratin (pan CK) immunostain, 100×.
Figure 7.41 Sjogren syndrome: Lymphoid aggregate in mucous minor salivary gland in Sjogren syndrome. H&E staining, 100×. Source: Courtesy of Dr. Mark Bernstein.
Figure 7.42 Benign lymphoepithelial lesion of the submandibular gland taken from a patient with Sjogren syndrome. Note the obliteration of normal glandular architecture by the lymphocytes. H&E staining, 100×.
Figure 7.43 Small B-cell lymphoma arising within a Warthin tumor of major salivary gland. Note the diffuse lymphocyte pattern without germinal centers. H&E staining, 200×.
Figure 7.44 Hodgkin lymphoma within an intraparotid node. Note the classic Reed Sternberg cell in the middle of the field. H&E staining, 200×.
Figure 7.45 Benign spindle cell tumor of the parotid gland. After immunostaining, this lesion was determined to be an aggressive fibromatosis. H&E staining, 400×.
Figure 7.46 Another spindle cell tumor of the parotid gland, which was determined to represent a hemangiopericytoma. Note the high degree of cellularity. H&E staining, 200×.
Chapter 8: The Molecular Biology of Benign and Malignant Salivary Gland Tumors
Figure 8.1
Why are salivary gland tumors so hard to study?
Among the most important characteristics that make salivary gland tumors extremely difficult to study at the molecular level is the heterogeneity of the cellular and extracellular matrix composition and distribution. For example, pleomorphic adenoma, the most common benign salivary gland tumor, shows a wide array of normal and neoplastic cell types, as will a variety of cell products. In this view, the tumor is composed of a proliferation of glandular epithelium and myoepithelial cells (black arrows) within a variably hyalinized and myxoid stroma. Discrete ductal elements cuffed by myoepithelial cells are appreciated throughout (yellow arrows). Focal squamous differentiation/cystic degeneration is also appreciated (red arrow). Understanding the role and interactions of each cell type in the biology of the developing tumor is a complex task. (
Source
: Courtesy of Dr. Vikki Noonan, Division of Oral Pathology, Boston University Henry M. Goldman School of Dental Medicine, Boston, MA.)
Figure 8.2
Histogenetic versus morphogenetic classification: How do salivary gland tumors arise?
(a) Based on related histology between normal salivary gland development and salivary gland tumors, histogenetic classification proposes that heterogeneity is dependent on the location of the stem/progenitor cells. (b) Morphogenetic classification is based on (i) cell type (luminal cells, myoepithelial-like cells, basal-like cells), (ii) type and distribution of extracellular material, and (iii) pattern of cellular organization. Both schemes are important attempts at understanding the biology of salivary gland tumor development to better identify and predict the behavior of this heterogeneous group of neoplasms.
Figure 8.3
Paradigms in tumor biology: What are the cellular and molecular alterations of a cancer cell?
(a) Neoplastic cells acquire several phenotypes that provide a selective advantage to their normal counterparts. These important characteristics include enhanced proliferation (due to overactive growth promoters and inactivated/suppressed growth inhibitors), failure to undergo apoptosis, immortalization, neovascularization (allowing tumors to increase in size and spread), and invasion/metastasis (allowing malignant cells to grow at sites remote from the primary tumor). These phenotypes are regulated by networks of signal transduction pathways. (b) Deregulation of these cell traits can occur through alterations in the fundamental molecular mechanisms governing normal cell behavior. Elements of signal transduction pathways include protein ligands (cytokines, growth factors, matrix molecules), cell surface ligand receptors, cytoplasmic secondary messengers, and nuclear transcription factors (
left panel
). In neoplastic salivary gland cells, large scale and small scale damage to chromosomal DNA (as well as epigenetic alterations) can lead to quantitative or qualitative changes in messenger RNA which carries the blueprint of the signal transduction proteins for production. Synthesis of quantitatively or qualitatively altered regulatory proteins can, in turn, lead to the phenotypes observed in tumor cells (
right panels
).
Figure 8.4
Enhanced cellular proliferation: How does protein deregulation lead to salivary gland tumor cell behavior?
(
Left panel
) Important signal transduction pathways that regulate cellular proliferation are abrogated in salivary gland tumors. In normal cells, extracellular ligands bind to cell surface receptors. Ligand-receptor binding activates secondary messengers that regulate several functions, including the production of response proteins via nuclear transcription factors. (
Right Panel
) Qualitative or quantitative alteration of signal transduction proteins leads to a release from pathway regulation. (A) In adenoid cystic carcinoma, the epidermal growth factor receptor (EGFR) is overexpressed, leading to hypersensitivity of the cell to the many ligands that bind to EGFR. (B) The secondary messenger H-ras is constituently active (or activated independent of upstream stimuli) in mucoepidermoid carcinomas. (C) The cell cycle regulator pRb is downregulated in acinic cell carcinoma. Without pRb, the transcription factor E2F proceeds unhindered, thereby enhancing cellular proliferation programs. While there are many regulators within each signal transduction pathway, only one element needs to be altered to potentially change a phenotype like enhanced proliferation. However, networks of other pathways may limit some alterations from causing an overall cellular change.
Figure 8.5
How chromosomal alterations lead to phenotypes in salivary gland tumors
. The MYB-NFIB gene fusion is a molecular hallmark of adenoid cystic carcinoma. (a) A translocation of genetic material occurs between chromosomes 6 and 9 (t(6;9)(q22–23;p23–24). (b) The fusion of genetic material leads to a modification of both genes. This fused gene is then transcribed into modified mRNA that is later translated into a highly overexpressed fusion protein that leads to the deregulation of several signal pathways involved in cell proliferation, apoptosis and differentiation, including BCL2, KIT, CD34 BIRC3, MYC, and MAD1L1.
Figure 8.6
How can biomarkers aid in salivary gland tumor diagnosis?
Biomarkers of neoplasia are already being explored to augment the current diagnostic work-up of salivary gland tumor patients. (a) In addition to utilizing biopsy and fine needle aspiration samples, investigators are testing biomarker availability in saliva and the bloodstream. Diagnostic targets may be DNA, mRNA or proteins. The purpose of these targets would be to better understand patient risk/predisposition, identify/classify disease earlier, guide treatment choice and improve patient monitoring. (b) Tumor biomarkers can target specific neoplastic phenotypes (middle circle) or individual molecular events (outer circle).
Figure 8.7
How can an understanding of salivary gland tumor biology lead to targeted therapeutic options?
At present, several biologically-based tumor therapies are in clinical trials. (a) The cellular phenotypes that salivary gland tumors share with other forms of neoplasia are potential targets. (b) The HER cell surface receptors are deregulated in several tumors, including salivary gland tumors. After binding a ligand, these receptors dimerize and activate secondary messengers, which support cellular proliferation (middle). Aberrant activity of HER-1/EGFR secondary messenging can be blocked using the small molecule inhibitor Lapatinab (
left
). Dimerization of HER-2/NEU can be blocked using the monoclonal antibody Trastuzumab, thereby preventing any downstream signaling.
Chapter 9: Tumors of the Parotid Gland
Figure 9.1 (a) A woman with a Warthin Tumor in the right parotid tail presenting as a neck mass.(b) CT scan confirms the mass to be present in the parotid tail. (c) Surgical specimen following partial parotidectomy of parotid tail with tumor (see also Figure 9.11). (d) and (e) Low and high-power microscopic views of the specimen that identified a Warthin tumor.
