Masticator space anatomy and pathologic conditions are illustrated examples from computed tomography and magnetic resonance imaging. Characteristic imaging features of various disease processes are presented to aid the otolaryngologist (head and neck surgeon) in diagnosis. The article describes infection, primary neoplasm, metastatic disease, Osteonecrosis, and vascular anomalies.
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Differential diagnosis for disease of the masticator space depends largely on consideration of the structures that normally occupy the space, with the exception of infection, which tends to be from odontogenic causes.
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Noninfectious pathologic conditions may commonly involve neural structures, such as with schwannoma or perineural tumor spread.
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Neoplastic disease of the masticator space may arise from the musculoskeletal elements, such as sarcoma or non-Hodgkin lymphoma.
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Metastatic disease may affect the masticator space.
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Vascular disease is typified by vasoformative anomalies such as venous malformation, which has a propensity…such as lymphatic malformation or arteriovenous malformation.
| AVM | Arteriovenous malformation |
| LM | Lymphatic malformation |
| MPNST | Malignant peripheral nerve sheath tumor |
| MS | Masticator space |
| NF1 | Neurofibromatosis type I |
| NHL | Non-Hodgkin lymphoma |
| NPCA | Nasopharyngeal carcinoma |
| ONJ | Osteonecrosis of the jaw |
| PNS | Perineural spread of tumor |
| PPS | Parapharyngeal space |
| VM | Venous malformation |
Introduction
With the exception of infection, which tends to have odontogenic causes, the differential diagnosis for disease of the masticator space (MS) depends largely on consideration of the structures that normally occupy the space. Therefore, noninfectious pathologic conditions may commonly involve neural structures, with schwannoma or perineural tumor spread as representative examples. In addition to perineural tumor spread, neoplastic disease of the MS may arise from the musculoskeletal elements, such as sarcoma or non-Hodgkin lymphoma (NHL). Metastatic disease may also affect the MS. Vascular disease is typified by vasoformative anomalies such as venous malformations (VM), which have a propensity for the masticator muscles, and related entities such as lymphatic or arteriovenous malformations (AVM).
Pseudolesions
There are several conditions that may simulate the presence of a mass lesion on cross-sectional imaging, and some of these may also represent diagnostic pitfalls on physical examination. The most common entities to be considered in this category are accessory parotid tissue, asymmetry of the pterygoid plexus, denervation of the muscles of mastication, and unilateral masseter hypertrophy.
At imaging, these entities are usually easily distinguishable from true pathologic entities owing to their characteristic appearances. Accessory parotid tissue appears identical to orthotopic parotid tissue and lies along the lateral aspect of the masseter. Similarly a hypertrophied masseter, as in the setting of bruxism, will otherwise resemble the normal contralateral muscle. Asymmetry of the pterygoid venous plexus is common, and easily recognized once the physician is aware of its existence.
In the acute setting, denervation may result in transient enlargement and enhancement of the affected muscles, which may mimic an acute inflammatory or neoplastic process. The finding of an associated lesion affecting the mandibular or trigeminal nerves should allow correct diagnosis ( Fig. 1 ).
Infection
Odontogenic Infection
The teeth are considered to be a component of the oral cavity, rather than the MS. However, odontogenic infection is the most common pathologic condition to affect the MS. The classic presentation of a patient with an MS infection is facial swelling, pain, and trismus. The infection most commonly arises from the mandibular third molar (wisdom) tooth, followed in frequency by the more anterior molars and bicuspids. The propensity of the third molar to become impacted may be related to its higher frequency of infection (as in the setting of pericoronitis). The lingual cortex of the mandible is thinner than the buccal cortex at this location, leading to more frequent involvement of the medial pterygoid muscle compared with the masseter muscle.
The MS encompasses a portion of the posterior mandibular alveolar ridge. Infection may easily extend posteriorly along the alveolar ridge, tracking along the bone and/or periosteum and breaching the lingual cortex at the attachment of the medial pterygoid muscle. Alternatively, odontogenic infection may access the MS by tracking along the posterior alveolar ridge to the retromolar trigone, from which it may cross the fat space between the mandible and the medial pterygoid muscle. This pathway of disease spread via the retromolar trigone has also been described in the setting of carcinoma of the mandibular gingiva.
An infectious process in the MS may also traverse the parapharyngeal space (PPS) to involve the lateral oropharynx, potentially resulting in airway compromise ( Fig. 2 ). Patients with PPS involvement may present with dyspnea or dysphagia, in addition to the more classic presenting symptoms previously described.
Osteomyelitis of the mandible
Osteomyelitis of the mandible is an infectious process that involves the cancellous and cortical portions of the bone. Osteomyelitis of the mandible has been described as both a precursor to and a result of soft tissue infection in the MS. Historically, the disease process has been divided into acute (<1 month duration) or chronic (>1 month) forms. Chronic osteomyelitis may further be characterized as primary, with an insidious course that does not present with a typical acute phase, or secondary, which follows an acute episode. The term subacute osteomyelitis refers to a transitional stage between acute and chronic.
Mandibular osteomyelitis, either acute or chronic, may be a component of infection in the MS. Chronic mandibular osteomyelitis will typically manifest as abnormal sclerosis and cortical/periosteal thickening, which are best depicted on CT ( Fig. 3 ). There may be associated myositis of the muscles of mastication. Classically, acute osteomyelitis will demonstrate CT findings of cortical thinning or erosion. There may be progression to periosteal reaction, with thickening of the periosteum that may eventually sequester the diseased bone. Mandibular osteomyelitis may require subperiosteal drainage for effective treatment.
Infection arising from neighboring spaces
Infection of the spaces that border on the MS may secondarily involve the muscles of mastication. This is most commonly seen in the setting of parotitis. The inflammatory process in the parotid gland may be due to viral or bacterial infection. Parotitis may also be secondary to obstruction of the parotid duct by sialolithiasis, in which case there may be secondary inflammation of the masseter due to sialodochitis in the buccal space, immediately anterior to the muscle ( Fig. 4 ). If there is accessory parotid tissue, the process may mimic an inflammatory process arising in the underlying masseter muscle.
Although the oropharynx is technically not a direct neighbor of the MS, it is common for infection of the lateral oropharyngeal wall (as in the setting of peritonsillar abscess) to cross the intervening PPS and involve the muscles of mastication ( Fig. 5 ). The clinical finding of trismus is the classic sign of MS involvement. This lateral extension of the infection may have implications for surgery, possibly requiring a percutaneous approach, instead of transoral. As with any infectious process, the severity of the infectious process at the time of imaging is variable. The progression is from edema to phlegmon and, finally, to mature abscess with liquefied content and a well-defined enhancing wall.
Otitis externa may occasionally involve the MS, with the classic symptom of trismus. The temporomandibular joint or parotid gland may become secondarily infected. The process may then spread anteriorly to the muscles of mastication, involving the intervening parotid tissue. This pattern of infection is more common in diabetic or immunocompromised patients.
Neoplasm
As elsewhere in the body, neoplasms arising in the MS may be categorized as benign or malignant, and the differential diagnosis will reflect the array of tissues normally found in this location. Benign lesions include nerve sheath tumors such as schwannoma or neurofibroma. Primary neoplasms of the muscles of mastication are rare; NHL may arise in the muscles, although it more commonly affects the mandible. Benign or malignant osseous tumors of the mandible may arise within the MS. Soft tissue sarcomas may also arise in this space.
Schwannoma of the trigeminal nerve
Schwannoma is a benign nerve sheath tumor that may affect the cranial nerves as an isolated finding or in the setting of neurofibromatosis type II (NFII). When schwannoma affects the trigeminal nerve, the patient may present with facial paresthesia (less commonly pain) or difficulty chewing owing to related weakness of the ipsilateral muscles of mastication. Trigeminal schwannoma, also known as neurinoma, accounts for approximately 0.2% of intracranial tumors.
The middle cranial fossa component of trigeminal schwannoma is considered interdural, maintaining the location between the layers of the lateral cavernous sinus wall that the ophthalmic and maxillary divisions normally occupy. When present, the posterior fossa component also remains enveloped by dura, presumably stretching from the cavernous sinus or petrous apex, and may be considered subdural. This relationship to the dural layers may allow the surgeon, through a basal temporal surgical approach, to access the intracranial components without exposing the carotid artery or the venous space of the cavernous sinus. For tumors with a large infratemporal component, a transmandibular or zygomatic infratemporal approach may be considered.
Schwannoma typically has T2-signal hyperintensity and enhance briskly with intravenous contrast. As schwannomas enlarge, they may begin to show areas of cystic degeneration and more heterogeneous enhancement. The finding of trigeminal schwannoma should prompt careful search for other intracranial tumors that may signify underlying NFII ( Fig. 6 ).
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