Tumours of the nasal cavity and paranasal sinuses Introduction

L. Barnes M. Brandwein-Gensler

J.L. Hunt P. Boffetta

Anatomy

The nasal cavities are separated in the midline by the nasal septum. Each cavity is wide caudally, and narrow cranially. The roof of the nasal cavity is formed by the thin (0.5 mm) cribriform plate. The floor is the hard palate, formed by the palatine processes of the maxillae and the horizontal portions of the palatine bones. The lateral nasal wall contains the maxillary and ethmoid ostia, plus three or four turbinates. These turbinates are delicate scroll-like projections of bone and vascular soft tissue that become smaller as they ascend in the nasal cavity. They attach to the lateral nasal wall anteriorly, and have a free edge posteriorly. The turbinates are covered with a thick mucous membrane and contain a dense, thick-walled venous plexus. The upper margins of the nasal fossa are bound laterally by the superior nasal turbinate and adjacent lateral nasal wall, and medially by the nasal septum. This region is the olfactory recess and it has a yellowish epithelium, the olfactory mucosa (OM). This mucosa contains bipolar olfactory nerve fibers that cross through the cribriform plate. The terminal axons of the olfactory nerves extend to the free surface of the epithelium, where they expand into knob-like protrusions bearing cilia (olfactory cilia). Bowman's glands, or olfactory glands, within the lamina propria appear similar to serous minor salivary glands. The nasal cavity and paranasal sinuses are lined by Schneiderian mucosa, consisting of pseudostratified columnar ciliated epithelium with interspersed goblet cells. The lamina propria within the paranasal sinuses, especially the maxillary antrum, is loose and well vascular-ized, with seromucinous glands, and can easily become polypoid as a result of edema. The goblet cell component of the mucosal surface and seromucinous glands is variable. In chronic sinusitis, goblet cell hyperplasia can result in a papillary mucosal lesion. The major portion of the nasal septum is formed by the perpendicular plate of the ethmoid bone posteriorly and the septal cartilage anteriorly. The vomer completes the posteroinferior portion of the septum. The septum is lined by relatively thin, ciliated respiratory mucosa, which may regularly undergo squamous metaplasia. The underlying thin lamina propria, although containing seromucinous glands, is tethered to the septal cartilage, restricting reactive polyp formation.

The frontal sinus

These paired sinuses reside between the internal and external cranial tables and drain either via a nasofrontal duct into the frontal recess or more directly into the anterior infundibulum, or less often, into the anterior ethmoid cells, which in turn will open into the infundibulum of the bulla ethmoidalis.

Ethmoid complex

This paired complex of sinuses contains 3-18 cells that are grouped as anterior, middle, or posterior, according to the location of their ostia. There is an inverse relationship between the number and size of the cells. Generally, the posterior cells are both larger and fewer than the anterior cells. Each ethmoid labyrinth lies between the orbit and the upper nasal fossa. The left and right groups of ethmoid cells are connected in the midline by the cribriform plate (nasal roof) of the ethmoid bone. The cribriform plate is an important landmark in evaluation of

Fig. 1.1 Normal coronal T1 WI shows foramen rotundum (white arrow) and entrance to the Vidian canal (black arrow).

sinonasal tumour stage - violation of the cribriform plate signifies direct extension of the tumour into the anterior cranial fossa. The crista galli is a distinctive pointed bony landmark that extends from the midline of the cribriform plate upward into the floor of the anterior cranial fossa. The perpendicular plate of the ethmoid bone extends downward from the cribriform plate to contribute to the nasal septum. The medial wall of each ethmoid labyrinth is formed by a thin lamella of bone from which arise the middle, superior, and supreme turbinates. The lateral ethmoid wall is formed by the thin lamina papyracea, which separates the ethmoid cells from the orbit. This is yet another important landmark for tumour staging. Tumour violation of the lamina papyracea may necessitate including the orbit and globe with the surgical resection. This area should be sampled in a maxillecto-my specimen a) if the globe has not been removed (as the lamina papyracea represents the lateral orbital margin), or b) if orbital exenteration has been performed. The roof of the ethmoid complex is formed by a medial extension of the orbital plate of the frontal bone, which projects to articulate with the cribriform plate. This is often referred to as the fovea ethmoidalis.

Sphenoid sinus

The average adult sphenoid sinus measures 20 mm high, 23 mm long, and 17 mm wide. The relationship of the posterior extension of the sphenoid in relation to the sella turcica is variable. The sphenoid sinus septum is usually in the mid-line, and anteriorly aligned with the nasal septum. However, it can also deviate far to one side creating two unequal sinus cavities. With the exception of the sinus roof, the other sinus walls are of variable thickness depending on the degree of pneumatization. The sphenoid roof is thin, often measuring only 1 mm. (planum sphenoidale), and is vulnerable to perforation during surgery. The sinus roof relates to the floor of the anterior cranial fossa, anteriorly; the optic chiasm and the sella turcica, posteriorly. The lateral sphenoid wall is related to the orbital apex, the optic canal, the optic nerve, and the cavernous sinus, containing the internal carotid artery. The sinus floor is the roof of the nasopharynx, and the anterior sinus wall is the back of the nasal fossa.

Maxillary sinus

The maxillary sinus lies within the body of the maxillary bone. Behind the orbital rims, each sinus roof/orbital floor slants obliquely upward so that the highest point of the sinus is in the posteromedial portion, lying directly beneath the orbital apex. The medial antral wall is the inferior lateral wall of the nasal cavity ("party wall"). The curved posterolateral wall separates the sinus from the infratemporal fossa. The anterior sinus wall is the facial surface of the maxilla that is perforated by the infraorbital foramen below the orbital rim. The floor of the sinus is lowest near the second premolar and first molar teeth and usually lies 3-5 mm below the nasal floor. The lower expansion of the antrum is intimately related to dentition. The location of the maxillary sinus ostia, is high on the medial wall. They drain through the ethmoidal infundibulum and then the nasal fossa. This pattern of drainage in the erect position is accomplished by intact ciliary action. The maxillary hiatus is a bony window leading to the interior of the maxillary sinus. The hiatus is normally partially covered by portions of four bones: the perpendicular plate of the palatine bone, posteriorly; the lacrimal bone, anterosu-periorly; the inferior turbinate, inferiorly, and above the turbinate attachment, the uncinate process of the ethmoid bone.

Epidemiology

Carcinomas of the nasal cavity and paranasal sinuses account for 0.2-0.8% of all malignant neoplasms and 3% of those occurring in the head and neck {169,2378}. Sixty percent of sinonasal tumours originate in the maxillary sinus, 20-30% in the nasal cavity, 10-15% in the ethmoid sinus, and 1% in the sphenoid and frontal sinuses {1493,2186}. When considering the paranasal sinuses alone, 77% of malignant tumours arise in the maxillary sinus, 22% in the ethmoid sinus and 1% in the sphenoid and frontal

Frontal Sinus Malignancy

Fig. 1.2 Malignancy of ethmoid and nasal cavity. Coronal CT with contrast. The tumour erodes the cribriform plate and fovea ethmoidalis (white arrowhead). The lamina papyracea is eroded (black arrowhead) but the fat (white arrow) medial to the medial rectus (MR) is normal. The orbital fat is not invaded. The margin (black arrow) of the tumour in the maxillary sinus is separable from the obstructed secretions because of different densities.

Fig. 1.2 Malignancy of ethmoid and nasal cavity. Coronal CT with contrast. The tumour erodes the cribriform plate and fovea ethmoidalis (white arrowhead). The lamina papyracea is eroded (black arrowhead) but the fat (white arrow) medial to the medial rectus (MR) is normal. The orbital fat is not invaded. The margin (black arrow) of the tumour in the maxillary sinus is separable from the obstructed secretions because of different densities.

Fig. 1.3 Malignancy of upper nasal cavity invading orbital fat and extending intracranially. The tumour (white arrow) extends through the roof of the ethmoid and along the roof of the orbit (white arrowhead). The tumour bulges (black arrow) the periorbita near the medial rectus but breaks through into the orbital fat more superiorly (black arrowhead). Note that the tumour enhances intermediately and less intensely than the mucosa.

sinuses {2378}. Malignant neoplasms of this region may lead to significant morbidity and disfigurement. The incidence of cancer of the nasal cavity and paranasal sinuses (sinonasal cancer) is low in most populations (<1.5/100,000 in men and <1.0/100,000 in women). Higher rates are recorded in Japan and certain parts of China and India. Squamous cell carcinomas are the commonest. Time trends have shown in most populations a stable incidence or a small decline in recent decades.

Etiology

Occupational exposure to wood dust, in particular to dust of hard woods such as beech and oak, is the main known risk factor for sinonasal cancer. The increase in risk (in the order of 5-50 fold) is strongest for adenocarcinomas and for cancers originating from the sinuses. The effect is present after 40 or more years since first exposure and persists after cessation of exposure. An increased risk of sinonasal cancer has been shown among workers in nickel refining and chromate pigment manufacture, but not among workers exposed to these metals in other processes, such as plating and welding. Among other suspected occupational carcinogens are formaldehyde, diisopropyl sulfate and dichloroethyl sulfide.

A relatively weak (relative risks in the range 2-5) but consistent association has been shown between tobacco smoking and sinonasal cancer, in particular squa-mous cell carcinoma. Exposure to Thorotrast, a radioactive contrast agent, represents an additional risk factor.

Imaging

Modern imaging plays a key role in the evaluation of sinonasal tumours {2423}. The anatomy of the lesion can be defined with the exact margins clearly delineated in almost every case. Imaging is a dominant factor in determining surgical approach and is an integral part of radiation therapy planning. Computed tomography (CT) and magnetic resonance imaging (MRI) provide significant information about the texture, the margins, the effect on bone and even the vascularity. In addition, some findings are typical for a particular diagnosis, and although biopsy is still required for ascertaining the nature of the lesion, the imaging appearance may help limit the list of differential diagnoses.

Staging and surgical planning

The spread of a sinonasal tumour intracranially or into the orbit and the relationship of tumour to the optic nerve and carotid artery are important features that can be delineated with imaging. Tumour can invade the orbit through the lamina papyracea or the roof of the maxillary sinus. Even if the bony wall is apparently destroyed, orbital fat may not be invaded {515}. A smooth bowing of the soft tissue interface with the orbital fat

Fig. 1.4 Sinonasal polyps with multiple obstructed sinuses. A Axial T1 WI after intravenous gadolinium. The enhancing mucosa (arrowheads) lines the obstructed sphenoid sinus (S). The sinus was also dark on T2WI indicating high protein and long standing obstruction. B Coronal T1WI shows cascading polyps filling the nasal cavity. The secretions in the maxillary sinus (S) are dark and the lining mucosa (white arrowhead) is visible. The nasal septum (black arrow) is intact. Hard palate - (black arrowhead), minor salivary glands at roof of mouth (G), olfactory bulb (white arrow).

Fig. 1.4 Sinonasal polyps with multiple obstructed sinuses. A Axial T1 WI after intravenous gadolinium. The enhancing mucosa (arrowheads) lines the obstructed sphenoid sinus (S). The sinus was also dark on T2WI indicating high protein and long standing obstruction. B Coronal T1WI shows cascading polyps filling the nasal cavity. The secretions in the maxillary sinus (S) are dark and the lining mucosa (white arrowhead) is visible. The nasal septum (black arrow) is intact. Hard palate - (black arrowhead), minor salivary glands at roof of mouth (G), olfactory bulb (white arrow).

suggests that the lesion is contained by periorbital fascia. Infiltration or irregularity of this margin suggests extension into the fat or true orbital invasion. The thin line of fat between the medial rectus muscle and the lamina papyracea is a key landmark in the evaluation of orbital extension of ethmoid neoplasms. The key landmarks for the assessment of intracranial extension of tumour are the roof of the ethmoid, the cribriform plate and the crista galli. Elevation or frank invasion of the dura may be evaluated using MRI.

A tumour in the maxillary sinus region may extend posteriorly and laterally through the bony wall into the ptery-gopalatine fossa and the infratemporal fossa. Tumour can invade the ptery-gopalatine fossa area either by direct extension or by following the nerves. From there, perineural extension of tumour in the foramen rotundum and Vidian canal may result in intracranial spread {516}.

Tumour may spread from the sphenoid sinus region, laterally into the cavernous sinus through the very thin layer of bone separating these two structures. If the bone is intact, the tumour is likely contained within the sinus.

Radiographic signs

Bone changes can give an indication of the aggressiveness of a tumour {2038}. In general, slowly growing lesions, such as Schneiderian papillomas, appear to push bone as they slowly remodel the osseous structure. More aggressive lesions, such as squamous cell carcinoma, can aggressively destroy bony walls leaving only a few remaining fragments {2425}. Occasionally, however, malignant lesions can cause bowing rather than infiltrating destruction of bone {2424}. The integrity of the thin plates of bone in the ethmoid sinus as well as the bony walls of the sphenoid sinus and the bony nasal septum also suggests that malignancy is unlikely.

Mineralization can be seen in several tumours, such as ring-like calcifications in cartilage lesions as well as calcifications in olfactory neuroblastomas {2130}. Meningioma can cause hyperostosis and can also calcify.

Tumour location plays a significant role in differential diagnosis. Tumours in the region of the cribriform plate and upper nasal cavity suggest diagnoses such as olfactory neuroblastoma or meningioma. Inverted Schneiderian papilloma occurs predominantly along the lateral wall of

Fig. 1.5 Sinonasal polyps. Coronal T2WI. The secretions in the sinus (S) are dark indicating high protein desiccated secretions. Compare to high signal of the edematous mucosa. Intact nasal septum (black arrow), crista galli (white arrow).

Fig. 1.5 Sinonasal polyps. Coronal T2WI. The secretions in the sinus (S) are dark indicating high protein desiccated secretions. Compare to high signal of the edematous mucosa. Intact nasal septum (black arrow), crista galli (white arrow).

the nasal cavity or the medial maxillary sinus {534}. In the lower maxilla, odontogenic lesions should be considered. Such lesions arise in the bone of the alveolar process and as they grow elevate the floor of the maxillary sinus. Fibro-osseous lesions enter the differential diagnosis when a radiodense lesion arises from or follows the contour of bone. Correlation of imaging studies with histo-logic appearance is crucial in the evaluation of bony lesions.

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