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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4518_Библиотеки_им_академика_М_И_Перельмана
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12 Head andNeck Pathology
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Fig. 12.51 Ceruminous adenoma: myoepithelial layer (solid arrow) surrounding cells with apo-
crine “snouting” (open arrow forms)
Squamous Cell Carcinoma (Fig.12.52)
Denition
• Malignant epithelial neoplasm of the pinna external auditory canal (EAC) exhibiting squamous differentiation
• Cutaneous SCC:
– Similar to other solar exposed areas, SCC can occur on pinna.
– Histomorphology essentially identical to keratinizing SCC in other sites.
– Precursor lesions (actinic keratosis, carcinoma in situ) in adjacent sun-
exposed epithelium.
• EAC: SCC localized to EAC rare, exclude extensions from adjacent primary
sites (nasopharynx, etc.)
• Middle ear: SCC very rare as a primary site
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Fig. 12.52 (a) Squamous cell carcinoma of the ear: (a) cutaneous exophytic and endophytic proliferation on sun damaged skin. (b) Squamous cell carcinoma of external auditory canal (arrow).
(c) Middle ear squamous cell carcinoma (middle ear epithelium = arrows, carcinoma = arrowheads)
Basal Cell Carcinoma (Fig.12.53)
• Carcinoma originating from basal cells of epidermis
• Sun-exposed skin, over 60% located on the head, only occasionally within EAC
• Clinical: varies somewhat with BCC-subtype, but classically described feature is
pearly papules or shiny plaque, traversed by microvasculature
• Subtypes: nodular, micronodular, supercial, inltrating, and morpheaform,
among others
• Epithelial cells: peripheral palisading, hyperchromatic and basaloid (very little
cytoplasm and large nuclei imparts basaloid appearance), mitoses+
• Stroma: Often myxoid or mucinous. Cleft or separation often develops between
stroma and neoplastic epithelial island interface
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Fig. 12.53 Basal cell carcinoma: Peripheral palisading (double arrows), tumor-stromal clefting
(arrowhead), stromal mucin (single arrow)
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Cutaneous Melanoma (Fig.12.54)
• Malignant melanocytes within epithelial layer (pagetoid spread); but importantly, invasion of connective tissue is seen.
• Melanin may be seen, pigmented cells.
• Spindle, round, polygonal epithelioid cells with large “cherry red” or “stop sign”
nucleolus.
• IHC: S100 +, HMB45.
Cholesterol Granuloma (Fig.12.55)
• Cholesterol clefts result from degrading red blood cells, which form crystals that
dissolve upon processing.
• Appear as clear, “needle-like” spaces microscopically.
• Foreign body multinucleated giant cells often present alongside granulation tissue.
• Foamy and hemosiderin-laden macrophages present as focal hemorrhage
resolves.
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Fig. 12.54 Cutaneous melanoma: Invasive melanocytic proliferation
C. J. Fan et al.
Fig. 12.55 Cholesterol granuloma: needle-like spaces of cholesterol clefts
Cholesteatoma (Fig.12.56)
• Destructive and expansive non-neoplastic growth in the middle ear and/or mastoid
• Can be congenital or acquired
• Clinical: keratinous debris, cheesy/white
• Three components for diagnosis
– Epithelium (matrix): keratinizing squamous epithelium with granular layer,
non-dysplastic
– Keratinaceous debris (cystic contents): akes, laminated scales, desqua-
mated keratin
– Stromal tissue (perimatrix): Granulation tissue, often chronically inamed
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Fig. 12.56 Cholesteatoma: benign squamous epithelium, laminated keratin debris, and inamed
stromal tissue
• Can occur with foci of multinucleated giant cells and formation of cholesterol
clefts and/or with cholesterol granuloma
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Langerhans Cell Histiocytosis (LCH) (Fig.12.57)
• Clonal proliferation of myeloid dendritic cells expressing a Langerhans cell
phenotype
• Neoplastic cells exhibit pale eosinophilic cytoplasm and enlarged, irregular,
often grooved nuclei (reniform), inconspicuous nucleoli
• Admixed eosinophils, multinucleated giant cells, neutrophils, lymphocytes,
plasma cells
• IHC: S100+, CD1a+, CD207 (Langerin), CD68
• Electron microscopy: Birbeck granules (appear like zippers or tennis rackets)
Middle Ear Neuroendocrine Tumor (Fig.12.58)
• Formerly middle ear adenoma
• Epithelial neoplasm of middle ear with neuroendocrine differentiation
• Unencapsulated neoplasm capable of multiple patterns: sheet-like, glandular,
trabecular, ribbon-like proliferation
• IHC: keratins+, neuroendocrine markers (synaptophysin, chromogranin, INSM1)+
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Fig. 12.57 Langerhans cell histiocytosis: Neoplastic cells (arrows) and associated eosinophils
(arrowheads)
C. J. Fan et al.
Fig. 12.58 Middle ear neuroendocrine tumor: cords of neoplastic cells with plasmacytoid appearance, with focal ductal formation evident
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Otosclerosis
• Inherited and localized bone dysplasia affecting the bones of the ear.
• Active areas (otospongiotic bone) show immature bone with osteoblasts and cellular connective tissue, lytic phase.
– Non-specic blue accentuation of otospongiotic bone changes known as blue
mantles of Manasse
• Otosclerotic bone is inactive and is sharply demarcated from normal lamellar bone.
Paraganglioma (Fig.12.59)
Paraganglioma is non-epithelial neoplasm derived from paraganglion cells
• Hereditary predisposition in ~40% of patients
• Tumors located at carotid body >> middle ear > vagal nerve among other
sites in HN
• Classically organized into zellballen pattern
• Zellballen composed of two cell types: chief cells and sustentacular cells
– Chief cells:
Abundant, eosinophilic, vaguely granular cytoplasm. Eccentric nucleus,
+/− hyperchromatic nuclei, +/− nuclear polymorphism
Special stain: positive for tyrosine hydroxylase
Fig. 12.59 Paraganglioma: Zellballen formation of neuroendocrine cells with ample pink
cytoplasm
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– Sustentacular cells:
Form a delicate, inconspicuous peripheral framework around chief cells
IHC: S100+, SOX10+, glial brillary acidic protein+
Vestibular Schwannoma (Fig.12.60)
• Benign peripheral nerve neoplasm derived from Schwann cells
• Associated with 8th cranial nerve, internal auditory canal
• Acoustic neuroma acceptable terminology, but remains a misnomer
• Most common cerebellopontine angle tumor (80–90%)
• Clinical: in setting of bilateral tumors, must exclude neurobromatosis-2
• Encapsulated neural tumor showing spindle cells with buckled or fusiform nuclei
• Two coexisting histologic patterns present (Antoni A and Antoni B) with areas of
characteristic perivascular hyalinization
• Antoni A:
– Hypercellular and compact, with nuclear palisading (Verocay bodies)
– Palisading nuclei, pink cells
• Antoni B:
– Microcystic degeneration: hypocellular, myxoid areas, pale, pattern-less
– IHC: Strong, diffuse S100+, SOX10+
Fig. 12.60 Vestibular schwannoma: Antoni A tissue with Verocay body formation and small focus
of Antoni B (arrows)
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Endolymphatic Sac Tumor (ELST) (Fig.12.61)
• Epithelial neoplasm associated with the endolymphatic sac/duct.
• Formerly aggressive papillary adenoma; low-grade papillary adenomatous tumor
of temporal bone; low-grade papillary adenocarcinoma; endolymphatic sac
carcinoma.
• Bilateral tumors show association with von Hippel-Lindau (VHL) syndrome;
current recommendation however is to evaluate all patients with ELST for VHL.
• Single layer of low cuboidal epithelial cells with clear cytoplasm and hyperchromatic nuclei arranged into papillary fronds.
Endocrine
Thyroid Tissue (Fig.12.62)
• Delicate connective tissue septae divide gland into lobules.
• Thyroid follicles lined by single layer of cells.
• Normal lumen contents: colloid (pink/eosinophilic), can also see calcium oxalate
crystals.
• Follicles vary in diameter.
Fig. 12.61 Endolymphatic sac tumor. Papillary projections composed of a single layer of low
cuboidal tumor cells (arrows)
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Fig. 12.62 Normal thyroid: Low magnication of thyroid follicles
C. J. Fan et al.
Fig. 12.63 Thyroglossal duct cyst: thyroid tissue within wall of cyst (arrows) This cyst shows a
respiratory epithelium
Thyroglossal Duct Cyst (Fig.12.63)
• Persistence of tract in midline neck through which thyroid descends during
embryogenesis.
• Most common midline mass in children.
• Majority located at or below level of hyoid bone and move vertically during
swallow.
• Treatment of choice: Sistrunk procedure.
• Cyst contents may be mucoid or purulent.
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