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143Chapter 10 Pathology of Sinonasal Lesions
A
Figs. 10.6A and B: Adenoid cystic carcinoma: (A) Tumor cells are arranged in cribriform
pattern (arrow) which means complex tubular pattern with intermittent cystic spaces lled
with thin basophilic material (asterisk) (B).
A
Figs. 10.7A and B: Nasopharyngeal angiobroma shows an admixture of stellate shaped
blood vessels (V) of varying thickness and brous to cellular stroma (S).
B
B
MALIGNANT NEOPLASTIC LESIONS
Carcinomas
Keratinizing Squamous Cell Carcinoma and Non-keratinizing
Squamous Cell Carcinoma (Figs. 10.8 and 10.9)
■ ese tumors arise from the surface epithelium lining the nasal cavity
and paranasal sinuses. In 30–50% cases of non-keratinizing squamous
cell carcinoma (NKSCC), high risk HPV association is seen.
■ e newly recognized HPV related carcinoma with adenoid cysticlike features shows surface dysplasia and underlying carcinoma with
morphology similar to high grade adenoid cystic carcinomas. High risk
HPV association is seen.
2,3
Sarcomatoid (Spindle Cell) Squamous Cell Carcinoma
Variant of squamous cell carcinoma with predominant spindle cell
morphology.
Lymphoepithelial carcinoma:
■ More than 90% cases harbor Epstein-Barr virus (EBV)
■ Mostly seen in Asian countries where EBV is endemic.
Section 3 Tumor and Tumor-like Conditions144
B
Fig. 10.8: Keratinizing squamous cell carcinoma: inltrating islands of malignant
squamous cells (dashed arrow and inset) with keratin pearls (thick arrow).
A
Figs. 10.9A and B: Non-keratinizing squamous cell carcinoma: inltrating islands of
malignant squamous cells (arrows) without intra- or extracellular keratin.
B
Sinonasal undierentiated carcinoma (SNUC): No squamous/glandular
dierentiation
■ No viral (EBV/HPV) association
NUT Midline carcinoma:
■ Poorly dierentiated carcinoma with squamous dierentiation.4
■ Denite diagnosis is made by detection of NUT gene rearrangement
t(15;19) by either uorescence in situ hybridization (FISH) or immunohistochemistry (IHC) (Figs. 10.10A and B).
■ No viral association.
■ Very poor prognosis.
SMARCB1 (INI1)-decient Sinonasal Carcinoma
■ SMARCB1 gene is known as SWI/SNF related, matrix associated, actindependent regulator of chromatin, subfamily B, member 1.
■ Inactivation of tumor suppressor gene INI1 has been implicated in the
pathogenesis of this tumor. Only few cases are available in the literature.
It remains unclear if it represents a distinct tumor entity.
■ Diagnosis is conrmed by INI1 loss on IHC or in-situ hybridization.
A B
Figs. 10.10A and B: A case of NUT midline carcinoma shows poorly differentiated tumor
cells admixed with neutrophils. Tumor cells are positive for NUT immunohistochemistry (IHC).
145Chapter 10 Pathology of Sinonasal Lesions
Fig. 10.11: Intestinal adenocarcinoma: malignant glands (arrow) oating in large areas or
pools of mucin (asterisk).
Intestinal and Non-intestinal Type
Adenocarcinomas (Figs. 10.11 and 10.12)
Intestinal adenocarcinomas are morphologically similar to intestinal tumors
(Fig. 10.11) whereas non-intestinal types do not show intestinal phenotypes
(Fig. 10.12).
MALIGNANT SOFT TISSUE TUMORS
Biphenotypic Sinonasal Sarcoma
Malignant low-grade spindle cell sarcoma with neural (S100 IHC positive)
and myogenic (smooth muscle actin IHC positive) dierentiation.
Sinonasal Glomangiopericytoma
■ A tumor of perivascular myoid cells.
■ Microscopically a patternless architecture with dilated blood vessels
(Fig. 10.13).
Section 3 Tumor and Tumor-like Conditions146
Fig. 10.12: Non-intestinal adenocarcinoma: inltrating cords and glands of tumor (arrow).
The tumor cells show abundant cytoplasm and low-grade nuclei.
Fig. 10.13: Glomangiopericytoma: a tumor beneath normal respiratory lining epithelium
(asterisk). Tumor is composed of large gaping vessels (arrows). Tumor cells are spindle to
oval with mild nuclear atypia (Inset).
■ Immunohistochemically positive for smooth muscle actin, beta-catenin
and cyclin D1.
TERATOCARCINOSARCOMA
Combination of teratoma and admixture of epithelial, mesenchymal and
neuroepithelial elements.
HEMATOLYMPHOID TUMORS
■ Nearly all hematolymphoid tumors in sinonasal region are non-Hodgkin’s
lymphomas (NHL) and extramedullary plasmacytomas.
■ Sinonasal lymphomas are third most common malignancy after
squamous cell carcinoma and adenocarcinoma. Among NHL, extranodal
NK/T cell lymphomas (ENKTL) and diuse large B cell lymphomas are
two most common types in nasal cavity and paranasal sinuses.
■ ENKTL commonly occurs in East Asians and has a strong association
with EBV.
■ Histologically, these show angioinvasive growth pattern lead on to
geographic areas of necrosis (Fig. 10.14).
■ Immunohistochemistry shows positivity for CD3, granzyme, perforin,
and CD56.
Fig. 10.14: NK-T cell lymphoma: non-Hodgkin’s lymphoma shows atypical large lymphoid
cells (thin arrows) with high apoptosis (thick arrow).
OLFACTORY NEUROBLASTOMA
■ Malignant neuroectodermal tumor with neuroblastic dierentiation
localized in the superior nasal cavity conned to cribriform plate.
■ Histologically low- and high-grade based on tumor architecture, mitotic
activity, nuclear pleomorphism, presence of brillary matrix, rosettes,
and necrosis (Fig. 10.15).
■ Immunohistochemistry positive for neuroendocrine markers.
An algorithmic approach to the malignant sinonasal tumors on IHC is
detailed in Flowchart 10.1.
147Chapter 10 Pathology of Sinonasal Lesions
Fig. 10.15: Olfactory neuroblastoma: photomicrograph shows malignant round blue cell
tumor with rosettes (R and arrow). The cells are small to intermediate in size, have high
nuclear cytoplasmic ratio and hyperchromatic nuclei.
Section 3 Tumor and Tumor-like Conditions148
Flowchart 10.1: Algorithmic immunohistochemistry approach for sinonasal malignant tumors
(ADC: Adenocarcinoma; H: High; HPV: Human papilloma virus; NEC: Neuroendocrine carcinoma; NB: Neuroblastoma; SCC: Squamous cell carcinoma).
REFERENCES
1. Slootweg PJ, Chan JKC, Stelow EB, et al. Tumors of the nasal cavity, paranasal
sinuses and skull base. In: El-Naggar AK, Chan JKC, Grandis JR, Takata T,
Slootweg PJ (Eds). WHO Classication of Head and Neck Tumors, fourth edition.
IARC Lyon; 2017. pp. 14-61.
2. Stelow EB, Bishop JA. Update from the 4th Edition of the World Health
Organization Classication of Head and Neck Tumours: Tumors of the Nasal
Cavity, Paranasal Sinuses and Skull Base. Head Neck Pathol. 2017;1:3-15.
3. Bishop JA, Guo TW, Smith DF, et al. Human papillomavirus-related carcinomas
of thesinonasal tract. Am J Surg Pathol. 2013;37:185-92.
4. Bishop JA, Westra WH. NUT midline carcinomas of the sinonasal tract. Am J Surg
Pathol. 2012;36:1216-21.
149Chapter 10 Pathology of Sinonasal Lesions
11
CHAPTER
Pathology of Bony/Cartilaginous
Sinonasal Tumors
Asit R Mridha, Adarsh W Barwad
• Introduction
• Benign Tumors/Tumor-Like
Conditions
– Central Giant Cell Granuloma
– Osteoma
– Ossifying Fibroma
– Fibrous Dysplasia
▪ Histopathologic Patterns on
Biopsy
– Aneurysmal Bone Cyst
• Malignant Tumors
– Chondrosarcoma
– Plasmacytoma
INTRODUCTION
■ World Health Organization (WHO) classication of sinonasal tumors
have been discussed in detail in Chapter 11.
■ Common benign and malignant bony/cartilaginous tumors will be
discussed here (Table 11.1).
Table 11.1: Common osseous/cartilaginous sinonasal tumors.
Benign tumor/tumor-like lesions Malignant
Central giant cell granuloma Chondrosarcoma
Chondroma Plasmacytoma
Osteoma Osteosarcoma
Ossifying broma Chordoma
Fibrous dysplasia
Chondroblastoma
Chondromyxoid broma
Osteochondroma
Osteoid osteoma
Osteoblastoma
Ameloblastoma
Aneurysmal bone cyst
BENIGN TUMORS/TUMOR-LIKE CONDITIONS
Central Giant Cell Granuloma (Fig. 11.1)
■ Central giant cell granulomas (CGCGs) are intraosseous nonproliferative
lesions with obscure etiology and occur almost exclusively in the
mandible and maxilla. CGCG is also known as reparative giant cell
granuloma.
■ ere are lot of morphological similarities between giant cell tumor and
CGCL and the distinction between jaw bone and extragnathic lesions
is dicult on histomorphology. Only comparison between the two is
the more number of nuclei present in the giant cells in giant-cell tumor
(GCT) of bone. Some authors consider that the GCT and CGCG represent
dierent spectra of same lesion.
■ Microscopically, CGCL is characterized by dense proliferation of oval and
spindle-shaped mesenchymal cells, a varying number of multinucleated
giant cells in small aggregates and dispersed in the brous stroma.
■ Giant cells are often present in a perivascular location or adjacent areas
of hemorrhage and usually contain 4–20 nuclei. ese are often small
and irregular with few nuclei or large and round containing more nuclei.
■ e lesion can also show round macrophages, deposition of hemosiderin,
extravasated erythrocytes, foci of osteoid matrix, bony trabeculae and
dystrophic calcication.
■ e mesenchymal and multinucleated giant cells are strongly
immunoreactive to anti-CD68 antibody, which suggesting that they
belong to the macrophage lineage.
■ An expression of osteoclastogenic nuclear factor of activated T cells
(NFATc1) has been seen in giant cells from CGCL, cherubism and brown
tumor of hyperparathyroidism.
151Chapter 11 Pathology of Bony/Cartilaginous Sinonasal Tumors
Fig. 11.1: Central giant cell granuloma (CGCG): Histology showing dense proliferation
of oval and spindle-shaped mesenchymal cells (blue arrow) along with osteoclastic
multinucleated giant cells (green arrow).
Section 3 Tumor and Tumor-like Conditions152
Fig. 11.2: Osteoma: Histological photomicrograph showing dense, compact bone and broad
trabeculae of mature bone.
Osteoma (Fig. 11.2)
■ Osteoma is characterized by compact cortical bone with scanty
intervening brovascular stroma. In some cases, there is a peripheral rim
of dense sclerotic lamellar bone surrounding trabeculae of lamellar or
occasionally woven bone.
■ It is usually classied into three histologic types according to bone
formation: (1) eburneous type (hard laminated), (2) cancellous type
(spongy), and (3) mixed type (combining features of the eburneous and
cancellous type).
■ Ivory type lesions contain compact, usually lamellar bone, with scant or
no intertrabecular spaces.
■ In the cancellous type, the ratio of bone volume to intertrabecular space
decreases and the morphology becomes similar to normal trabecular
bone tissue.
■ No signicant practical dierences are found between these forms of
morphology when diagnostic techniques, treatment and prognosis are
considered.
Ossifying Fibroma
Depending on the pattern of mineralization, four entities have been
described: (1) Juvenile psammomatous ossifying broma (JPOF), (2) Juvenile
trabecular ossifying broma (JTOF), (3) Gigantiform cementoma (GC), and
(4) Cemento-ossifying broma (COF) and ossifying broma-not otherwise
specied (NOS).
Histopathologic Patterns on Biopsy
Ossifying broma NOS—shows three histologic or a mixture of these patterns
(Table 11.2; Figs. 11.3 and 11.4).
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