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Pleomorphic Adenoma (Mixed Tumor)

With more than 100 cases reported in the literature (Compagno and Wong 1977; Freeman et al.

Nasal Septal Mass

Fig. 8.45a-d. Myofibroblasts inflammatory tumor. TSE T2 (a) and enhanced T1 (b) on coronal plane. a On left side, the ethmoid is occupied by an hypointense mass (asterisk) abutting the adjacent lamina papyracea. Extensive thickening of the nasal septum due to spread of lesion is demonstrated (arrows). Retained secretions within frontal sinus are characterized by bright signal. b Posteriorly, the mass shows intermediate signal intensity (white arrows), it causes blockage of left maxillary sinus. On the opposite side, the maxillary sinus is partially filled by signal intensity consistent with lesion (1). Thickening of anterior infraorbital canal is present (2). c Same level as (a) after Gd-DTPA: non-homogeneous enhancement of the left ethmoid (asterisk) and septal lesions is shown. Effacement of intraorbital fat is also present (arrows). d Same level as (b) after Gd-DTPA: enhancement of the lesion extending into right maxillary sinus is demonstrated (1). Compared to the left side (3), the right infraorbital nerve presents perineural thickening and enhancement (2). Focal interruption of hypointense periosteal/bony layer (arrowhead) of the left fovea is associated with enhanced thickened dura (4)

Fig. 8.45a-d. Myofibroblasts inflammatory tumor. TSE T2 (a) and enhanced T1 (b) on coronal plane. a On left side, the ethmoid is occupied by an hypointense mass (asterisk) abutting the adjacent lamina papyracea. Extensive thickening of the nasal septum due to spread of lesion is demonstrated (arrows). Retained secretions within frontal sinus are characterized by bright signal. b Posteriorly, the mass shows intermediate signal intensity (white arrows), it causes blockage of left maxillary sinus. On the opposite side, the maxillary sinus is partially filled by signal intensity consistent with lesion (1). Thickening of anterior infraorbital canal is present (2). c Same level as (a) after Gd-DTPA: non-homogeneous enhancement of the left ethmoid (asterisk) and septal lesions is shown. Effacement of intraorbital fat is also present (arrows). d Same level as (b) after Gd-DTPA: enhancement of the lesion extending into right maxillary sinus is demonstrated (1). Compared to the left side (3), the right infraorbital nerve presents perineural thickening and enhancement (2). Focal interruption of hypointense periosteal/bony layer (arrowhead) of the left fovea is associated with enhanced thickened dura (4)

1990; Prager et al. 1991; Liao and Chong 1993; Wakami et al. 1996; Goiz et al. 1997; Jassar et al. 1999; Makeieff et al. 1999; Facon et al. 2002), pleo-morphic adenoma is the most common benign tumor of the sinonasal tract after osteoma and inverted papilloma. Histologically, the neoplasm displays a pleomorphic architecture, being made up of lumi-

nal-type ductal epithelial cells, myoepithelial cells and tissue of mucoid, myxoid, or chondroid appearance (Shanmugaratnam 1991). Most pleomorphic adenomas take origin from major salivary glands, whereas only about 10% affect minor salivary glands, more commonly of the hard and soft palate (PrageR et al. 1991; Liao and Chong 1993). The tumor may rarely occur in other sites such as the lacrimal gland, larynx, pharynx, sinonasal tract, and trachea. Data from two major reviews of patients with pleomor-phic adenoma of the sinonasal area (Compagno and Wong 1977; Wakami et al. 1996) clearly identify the nasal septum as the most frequently affected site, followed by the maxillary sinus. Pleomorphic adenoma usually affects patients in the fifth decade of life, with a slight female predominance. At present, no one of the histogenetic hypotheses (i.e., misplaced embryo-genic ectodermal epithelial cells, residual of the vomeronasal organ, fully developed salivary gland tissue) postulated to explain the origin of the lesion from the nasal septum is fully accepted (Stevenson 1932; Matthew et al. 1944; Evans and CruickshanK 1970). Strangely enough, fewer minor salivary glands are present in the septal submucosa than in other sinonasal anatomic areas (Wallace et al. 1990).

A recurrence rate of 10% after surgical treatment has been specifically reported for sinonasal localizations by Compagno and Wong (1977). According to the authors, this low recurrence rate might be related to the histologic profile of sinonasal pleomorphic adenoma, which presents more cells and less myxoid stroma than the major salivary gland counterpart. Distant metastases and malignant degeneration have been rarely observed (Freeman et al. 1990; Cho et al. 1995).

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