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Imaging to Assess the Patterns of Growth of Maxillary Sinus Neoplasms

Progressive growth of maxillary sinus malignant neoplasms leads to extra-sinusal spread through the invasion of one or more of its five bony walls: medial, anterior, postero-lateral, inferior (alveolar recess), and roof (Fig. 9.2). According to the direction of tumor growth, different implications regarding treatment and prognosis will result.

Invasion of the medial wall is certainly the less critical pathway of spread as it leads to intra-nasal extent where the lesion has to grow further prior to involve critical structures, usually via ethmoid sinus invasion. Nonetheless, once the tumor reaches the choana and spreads along its lateral surface, there is the risk of nasopharyngeal wall invasion with pos

Fig Scan Showing The Nasopharynx

Fig. 9.2a,b. Squamous cell carcinoma of left maxillary sinus. On post-contrast CT images the lesion shows slight heterogeneous enhancement. On the axial plane (a) the tumor is shown to invade the anterior (white arrows), the postero-lateral (arrowheads), and the medial sinusal walls. Invasion of the pterygopalatine fossa is present (black arrows). On the coronal plane (b) intraorbital invasion with involvement of the inferior rectus muscle is detected (arrowheads). Marked sclerosis of the alveolar process (black arrows) suggests reactive changes or intramedullary spread

Fig. 9.2a,b. Squamous cell carcinoma of left maxillary sinus. On post-contrast CT images the lesion shows slight heterogeneous enhancement. On the axial plane (a) the tumor is shown to invade the anterior (white arrows), the postero-lateral (arrowheads), and the medial sinusal walls. Invasion of the pterygopalatine fossa is present (black arrows). On the coronal plane (b) intraorbital invasion with involvement of the inferior rectus muscle is detected (arrowheads). Marked sclerosis of the alveolar process (black arrows) suggests reactive changes or intramedullary spread

Fig Scan Showing The Nasopharynx

Fig. 9.3a,b. Squamous cell carcinoma of left maxillary sinus. On post-contrast CT in the axial plane (a), extensive involvement of the masticator space (black arrows) with a residual bone fragment of the pterygoid laminae (black arrowheads) is demonstrated. In addition, tumor invades the left nasopharyngeal wall and the pre-styloid compartment of the parapharyngeal space (white arrowheads). Invasion of the pterygoid process with both erosion and sclerotic changes is shown (black arrows) in the coronal plane (b). The left pterygoid canal is not detectable. Downward extent is associated with remodeling and lateral displacement of the lateral pterygoid lamina (white arrows)

Fig. 9.3a,b. Squamous cell carcinoma of left maxillary sinus. On post-contrast CT in the axial plane (a), extensive involvement of the masticator space (black arrows) with a residual bone fragment of the pterygoid laminae (black arrowheads) is demonstrated. In addition, tumor invades the left nasopharyngeal wall and the pre-styloid compartment of the parapharyngeal space (white arrowheads). Invasion of the pterygoid process with both erosion and sclerotic changes is shown (black arrows) in the coronal plane (b). The left pterygoid canal is not detectable. Downward extent is associated with remodeling and lateral displacement of the lateral pterygoid lamina (white arrows)

sible involvement of the opening of the Eustachian tube (Fig. 9.3)

Because in the area of posterior fontanellae (behind natural sinusal ostium) the medial wall is thin and very often dehiscent, in some cases its neoplas-tic invasion can be suggested on CT by the extent of the mass into the nasal cavity, rather than by bone destruction. Conversely, invasion of the anterior portion of the medial wall may be directly demonstrated by bone erosion, eventually extended to the horizontal portion of the uncinate process and to the inferior concha. Particular attention has to be placed to the lacrimal pathways because their involvement - like the invasion of pre-antral soft tissues through the anterior wall - contraindicates the surgical approach with midfacial degloving.

Tumor extent toward the alveolar process and into the hard palate should be evaluated by means of coronal (or sagittal) images (Fig. 9.2b, 9.4). A critical pathway of spread may be observed when the posterior portion of the alveolar process is invaded, as the neoplasm may involve the buccinator muscle and/or the maxillary tuberosity, from which it may access the pterygomandibular raphe.

Certainly, the two most critical bony boundaries are the postero-lateral wall, a pathway to spread into the masticator space and pterygopalatine fossa, and the maxillary sinus roof - i.e., the orbital floor - because its involvement leads to orbital invasion. In both settings, the main goal of imaging is to as sess the integrity of the bony-periosteal barrier (Fig. 9.2b, 9.4).

As most malignant maxillary sinus tumors are squamous cell carcinomas, this histotype is used to describe the expected MR signal intensity of neoplasms in this site. Because of its highly cellular composition, squamous cell carcinoma has usually homogeneous intermediate-to-low signal intensity on T2 sequences and moderate-to-relevant enhancement after contrast agent administration (Som et al. 1989) (Fig. 9.5).

The first step in the assessment of neoplastic extent is the evaluation of the relationship of maxillary sinus tumor with the sinusal walls. The sinusal walls contacting the neoplasm may present various signal patterns on imaging studies, ranging from inflammatory changes to abnormalities indicating neoplastic invasion.

On CT, chronic inflammatory abnormalities of the bony walls may be either due to long standing mucus drainage impairment or represent reactive changes induced by tumor contact. They appear as asymmetric thickening of sinusal walls. On MR, both T2 and T1 sequences show thicker hypointense sinusal walls, even though focal areas of signal hyperintensity may be observed (Maroldi et al. 1996) (Fig. 9.5b). The presence of a double shape, due to a hypointense line parallel to the outer surface of the wall, represents periosteal thickening. Inflammatory changes of the sinusal mucosa are frequently associated. They usu

Fig. 9.4a,b. Squamous cell carcinoma of left maxillary sinus, post-contrast coronal multislice CT (a) and VIBE (b). Both techniques demonstrate the sub-periosteal and sub-mucosal spread of tumor, which is covered by residual mucosa both in the maxillary sinus (black arrows) and in the left nasal fossa floor. The precise extent of submucosal spread into the hard palate is clearly defined by MR (short white arrows). Both CT and MR show invasion of the bony nasal septum (black arrowhead). Whereas on CT the medial left maxillary sinus wall appears undetectable, as the mineralized component is reabsorbed, its residual bony framework is still detectable on MR (white arrowheads). On CT, enlargement of the infraorbital foramen is shown (white arrow on a). At this level, MR shows regular and smooth thickening of the periorbita (long white arrows on b)

Fig. 9.4a,b. Squamous cell carcinoma of left maxillary sinus, post-contrast coronal multislice CT (a) and VIBE (b). Both techniques demonstrate the sub-periosteal and sub-mucosal spread of tumor, which is covered by residual mucosa both in the maxillary sinus (black arrows) and in the left nasal fossa floor. The precise extent of submucosal spread into the hard palate is clearly defined by MR (short white arrows). Both CT and MR show invasion of the bony nasal septum (black arrowhead). Whereas on CT the medial left maxillary sinus wall appears undetectable, as the mineralized component is reabsorbed, its residual bony framework is still detectable on MR (white arrowheads). On CT, enlargement of the infraorbital foramen is shown (white arrow on a). At this level, MR shows regular and smooth thickening of the periorbita (long white arrows on b)

Sinus Squamous Cell Carcinoma

Fig. 9.5a,b. Squamous cell carcinoma of right maxillary sinus. a On TSE T2 the tumor (T) has heterogeneous hypointense intensity signal, lower than fluid and mucosa within the sinus. Apart for the invasion of pterygopalatine fossa and pterygoid process (arrows), the path of neoplastic spread progresses posteriorly (b) with involvement of masticator space (white arrowheads) where tumor abuts the mandibular nerve (black thick arrows). While part of the lesion is still confined by the posterolateral wall (black arrowheads), invasion of the choana with spread into the lateral nasopharyngeal wall is present (white thick arrows). Thickening of left maxillary sinus walls is particularly evident along the postero-lateral wall (white thin arrows), where focal hyperintense areas are also present (black thin arrows)

Fig. 9.5a,b. Squamous cell carcinoma of right maxillary sinus. a On TSE T2 the tumor (T) has heterogeneous hypointense intensity signal, lower than fluid and mucosa within the sinus. Apart for the invasion of pterygopalatine fossa and pterygoid process (arrows), the path of neoplastic spread progresses posteriorly (b) with involvement of masticator space (white arrowheads) where tumor abuts the mandibular nerve (black thick arrows). While part of the lesion is still confined by the posterolateral wall (black arrowheads), invasion of the choana with spread into the lateral nasopharyngeal wall is present (white thick arrows). Thickening of left maxillary sinus walls is particularly evident along the postero-lateral wall (white thin arrows), where focal hyperintense areas are also present (black thin arrows)

ally appear as diffuse and lobulated thickening, hy-podense on CT, homogeneously hyperintense on T2 sequences, hypointense on plain T1. After contrast agent administration, the thin superficial mucosal layer enhances - a finding more easily demonstrated on MR - whereas the liquid content within the sub-mucosa does not (Som et al. 1988).

Among the different patterns of bone changes due maxillary sinus neoplasms, remodeling may be observed, even though less frequently than cortical destruction, permeative bone invasion with subperiosteal and submucosal spread (Fig. 9.4), which may be more thoroughly mapped by MR (see Chapter 4).

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