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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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Neuroendocrine Tumors (Fig. 12.13)
• Classication of head and neck neuroendocrine neoplasms has moved away
from terms such as carcinoid, atypical carcinoid, etc.
• Nomenclature now mirrors the consensus classication framework provided by
the International Agency for Research on Cancer and the World Health
Organization.
– Well-differentiated neuroendocrine tumor
Grade 1: equivalent to former typical carcinoid
Grade 2: equivalent to former atypical carcinoid
– Small-cell neuroendocrine carcinoma (SCNEC) (See next section.)
– Large-cell neuroendocrine carcinoma (LCNEC) (See next section.)
• Affects 6th–7th decades, male predominance.
• Small nests, cords, or trabeculae of tumor cells.
• Abundant cytoplasm and characteristic “salt-and-pepper” nuclei, limited
pleomorphism.
Small-Cell Neuroendocrine Carcinoma (SCNEC) (Fig.12.14)
• Poorly differentiated (high-grade) neuroendocrine carcinoma
• In H&N, supraglottic larynx most common site
• Affects 6th–7th decades, male predominance
• Sheet-like growth of tumor; cords, rosettes, trabeculae possible
Fig. 12.13 Well-differentiated neuroendocrine tumor (Grade1): Organoid and trabeculae growth
of uniform cells with abundant eosinophilic cytoplasm
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Fig. 12.14 Small-cell neuroendocrine carcinoma. Scant cytoplasm, hyperchromatic nuclei, small
cell size
C. J. Fan et al.
Fig. 12.15 Large-cell neuroendocrine carcinoma: large cells with prominent nucleoli, abundant
cytoplasm, comedonecrosis
• Abundant cytoplasm and characteristic “salt-and-pepper” nuclei, limited
pleomorphism
• Necrosis, >10 mitoses per 2mm2; Ki67 proliferation index easily >20%
• Small cell size, scant cytoplasm, hyperchromatic nuclei, inconspicuous nucleoli
(Fig.12.15)
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Fig. 12.16 Necrotizing sialometaplasia: coagulative necrosis of salivary gland acini (arrow-
heads), metaplastic salivary ducts (arrows), and inammation
• Organoid and trabecular growth
• Tumor cells large with ample cytoplasm and coarse chromatin
• Comedo-type necrosis common, rosettes and peripheral palisading possible
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Salivary Gland
Necrotizing Sialometaplasia (Fig.12.16)
• Ischemic necrosis of salivary glands, most commonly affecting the hard palate
• Intact or ulcerated surface epithelium
• Submucosal, lobular coagulative necrosis of acini
• Acinus-sized pools of mucin with lobular architecture as a result of coagulative
necrosis
• Squamous metaplasia of residual salivary ductal elements
• Bland squamous epithelium of ductal elements with uniform nuclei, unlike SCC
• Preservation of lobular pattern at low magnication unlike mucoepidermoid
carcinoma
Lymphoepithelial Cyst (Fig.12.17)
• Epithelial-lined cystic lesion with dense lymphoid stroma in cyst wall.
• Can occur in parotid gland and oor of the mouth.
• Bilateral involvement of parotid gland classically described in HIV-related cases.
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Fig. 12.17 Lymphoepithelial cyst: Stratied squamous epithelial cyst lining present. Germinal
center formation within cyst wall
C. J. Fan et al.
Fig. 12.18 Pleomorphic adenoma: (a) Well-circumscribed, encapsulated (arrow) neoplasm in the
parotid gland at low magnication; (b) chondroid-like matrix (star), epithelial cells (long arrow),
and myoepithelial cells (short arrow) are present
• Multiple cystic lesions of parotid can also occur in Sjogren syndrome.
• Benign squamous epithelial lining borders cystic space.
Pleomorphic Adenoma (Fig.12.18)
• Most common benign salivary gland neoplasm.
• Over 70% arise in the parotid gland.
• Recurrent pleomorphic adenoma most often multinodular growth pattern.
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Fig. 12.19 Warthin tumor. Eosinophilic epithelial cells forming papillary and cystic structures and
surrounded by lymphoid cells
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• In oral cavity, palate most commonly affected.
• Major gland tumors: well-delineated or show well-circumscribed brous capsule.
• Minor gland tumors or any myxoid-variant tumors: unencapsulated (pushing
borders).
• Ductal epithelial cells and myoepithelial cells present in stroma rich in chondro-
myxoid (cartilage-like) tissue with cytomorphological and architectural diversity.
• Rate of malignant transformation difcult to estimate, likely less than 5%.
Warthin Tumor (Fig.12.19)
• Benign salivary gland tumor with lymphoid component and papillary oncocytic
epithelium.
• Second most common salivary gland tumor.
• Tumors composed of papillary epithelial architecture, cystic spaces, and dense
lymphoid stroma.
– Epithelial component:
“Double lines” or double-layered tram-track appearance of oncocytic,
eosinophilic (pink) epithelium
Epithelial cytoplasmic granularity due to increased number of mitochondria
Papillary epithelium projects into cystic spaces
Interspersed mucous cells in epithelium; note: with extensive mucinous
differentiation, must exclude Warthin-type mucoepidermoid carcinoma
– Dense lymphoid stroma (deep blue appearance) with germinal center forma-
tion present
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Fig. 12.20 Oncocytoma: Encapsulated eosinophilic salivary gland neoplasm in parotid gland.
Composed of large polygonal cells with eosinophilic granular cytoplasm
C. J. Fan et al.
Oncocytoma (Fig.12.20)
• Uncommon benign salivary neoplasm with large, polygonal oncocytic epithe-
lial cells.
• Oncocytic cells = granular pink cytoplasm due to abnormal accumulation of
mitochondria.
• Encapsulated tumor.
• Nuclei uniform, small and with prominent single nuclei.
• Occasional clear cells present, rarely clear cell predominant.
• Oncocytoma most common in major glands (parotid >> submandibular).
• Tumor cells present in sheets, separated by a thin brovascular stroma.
Mucoepidermoid Carcinoma (MEC) (Fig.12.21)
• Malignant salivary gland neoplasm with cystic and solid growth
• Composed of mucous cells, intermediate cells, and epidermoid (squamoid) cells
• Most common salivary gland malignancy in adults and children
• MEC graded as low, intermediate, or high by pathologist
– Various grading scales exist.
– Low- and intermediate-grade MECs have similar clinical outcomes.
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Fig. 12.21 Mucoepidermoid carcinoma: tumor islands composed of epidermoid cells (open
arrow), intermediate cells (solid arrow), and mucous cells (arrowhead)
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• Diagnostic pitfalls:
– High-grade MEC may be misdiagnosed as conventional SCC.
– Salivary duct carcinoma may be misdiagnosed as high-grade MEC.
– MEC variant with dense lymphoid component (Warthin-like MEC) may be
misdiagnosed as Warthin tumor on FNA or even at surgical resection.
– Largely cystic tumors may be diagnostically problematic by FNA.
– Intraosseous MEC most common in the mandible and may be misdiagnosed
as cyst.
Acinic Cell Carcinoma (ACC) (Fig.12.22)
• Malignant salivary gland neoplasm with serous acinar differentiation.
• Most common in parotid gland 90–95%, average age 45–55 years.
• Cells are arranged into a variety of growth patterns:
– Solid/classic: deep purple granular cytoplasm (zymogen granules). May be
misdiagnosed as “salivary parenchyma” on FNA if very well differentiated.
– Microcystic: “holes” or circular clearing among syncytium of basophilic cells.
– Papillary: more eosinophilic papillary growth.
– Pitfall: a subset of papillary tumors and microcystic tumors diagnosed as
ACC may actually represent Secretory carcinoma (SC) of the salivary gland
prior to description of SC as a distinct salivary gland entity.
• Acinic cell carcinoma is not currently graded.
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Fig. 12.22 Acinic cell carcinoma: Trabeculae of large, basophilic, slightly granular-appearing
tumor cells. Eccentric position of the nucleus within cells
C. J. Fan et al.
c
Fig. 12.23 Adenoid cystic carcinoma: (a) Cribriform pattern of growth. (b) Solid pattern. (c)
Tubular pattern
Adenoid Cystic Carcinoma (AdCC) (Fig.12.23)
• Malignant biphasic salivary gland neoplasm composed of neoplastic epithelial
cells and myoepithelial cells arranged in tubular, cribriform, and solid growth
patterns.
• t(6;9) or t(8;9) translocations → MYB-NFIB and MYBL1-NFIB fusions,
respectively.
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Fig. 12.24 (a) Polymorphous adenocarcinoma, conventional: Slender cords of uniform cells with
scant cytoplasm inltrate regional salivary tissue. (b) Polymorphous adenocarcinoma, cribriform:
Papillary and glomeruloid growth and optical chromatin clearing in tumor nuclei
• AdCC is the most common submandibular salivary gland malignancy and the
most common tracheal salivary gland-type malignancy.
• Myoepithelial cells are hyperchromatic and with angulated nuclei.
• Ductal (epithelial) cells are cuboidal cells with eosinophilic cytoplasm.
• Perineural invasion is the hallmark of AdCC.
• Growth patterns:
– Tubular growth: Elongated simple duct-like arrays of epithelial cells and
myoepithelial cells
– Cribriform: “Swiss-cheese” or “rotary-telephone” biphasic pattern
– Solid: cellular, basaloid (blue) nests lacking ductal or pseudocystic spaces
Generally >30% of solid component is thought to be more aggressive.
Recent studies emphasize notation of any solid tumor component.
Polymorphous Adenocarcinoma (PAC) (Fig.12.24)
• Malignant salivary gland tumor consisting of two subtypes, conventional and
cribriform
– PAC, conventional:
Formerly polymorphous low-grade adenocarcinoma (lobular carcinoma)
Morphological diversity and inltrative growth
Perineural invasion, often in a targetoid “eye-of-the-storm” pattern
Uniform tumor cells with scant cytoplasm and bland, oval nuclei
Most commonly occurring at hard-soft palate or lip
– PAC, cribriform:
Formerly cribriform adenocarcinoma of tongue and minor salivary gland
Papillary and glomeruloid growth pattern, with “cleared-out” nuclei
Most commonly occurring at tongue base
Higher risk of nodal metastasis
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C. J. Fan et al.
Carcinoma Ex-pleomorphic Adenoma (CEPA) (Fig.12.25)
• An epithelial and/or myoepithelial predominant salivary gland malignancy arising in association with a primary or recurrent pleomorphic adenoma (PA).
• Most common in parotid > submandibular gland.
• Clinical history may reveal long-standing mass with recent clinical change.
• With report on the histologic classication of the malignant component of
the tumor
– Salivary duct carcinoma, most common type of carcinoma arising ex-PA
– Myoepithelial carcinoma, second most common
– Adenocarcinoma, NOS
Sinus
Infectious/Inammatory
Rhinosinusitis
• Inammation of nasal cavity mucosa—usually due to infection/allergies
• Submucosal inammation and edema—lymphocytes, plasma cells, macrophages, eosinophils (allergic), neutrophils (bacterial)
• Can develop epithelial inammation, metaplasia, and reactive papillary
hyperplasia
Fig. 12.25 Salivary duct carcinoma ex-pleomorphic adenoma: myxoid nodule representing residuum of PA (open arrow) with high-grade salivary duct carcinoma (solid arrows) admixed and
inltrating into adjacent tissues
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