Imaging of Jaw Lesions

Mandibular and maxillary lesions are common imaging findings, which pose a unique diagnostic challenge as dental pathology overlaps that of the remainder of the oral cavity. This review will guide radiologists in the interpretation of benign and malignant odontogenic and non odontogenic neoplasms.

Key points

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Jaw lesion imaging characteristics can help identify benign versus malignant disease.
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The location of a lesion with respect to the dentition is an important consideration.
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Systemic diseases can affect the jaw.

Abbreviations

AC	ameloblastic carcinoma
AF	ameloblastic fibroma
AFS	ameloblastic fibrosarcoma
AOT	adenomatoid odontogenic tumor
BOCs	botyroid odontogenic cysts
CCOC	clear cell odontogenic cyst
CEOT	calcifying epithelial odontogenic tumor
DCs	dentigerous cysts
GCOC	ghost cell odontogenic cyst
GOCs	glandular odontogenic cysts
LCH	langerhans cell histiocytosis
LPCs	lateral periodontal cysts
OKC	odontogenic keratocysts
OS	odontogenic sarcomas
POTs	primordial odontogenic tumors
RC	radicular cyst
SOC	sclerosing odontogenic carcinoma

Introduction

Mandibular and maxillary lesions are common imaging findings, which pose a unique diagnostic challenge as dental pathology overlaps with that of the remainder of the oral cavity. Differentiating incidental lesions from those which cause significant morbidity and even mortality can be difficult. This article will provide a classification framework for jaw lesions and help the interpreting radiologist guide patient management. Identifying lesions that are of odontogenic origin based on lesion descriptors and location is a good first step in approaching the differential.

The main components of the teeth are enamel, dentin, pulp, and cementum, anchored to the alveolus by the periodontal ligament. Dental enamel is derived from the oral ectoderm during odontogenesis, formed by ameloblasts within the epithelium. The dentin and cementum, derived from the neural crest, are formed by odontoblasts and cementoblasts respectively. The more complex dental pulp and periodontal ligament are associated with odontoblasts, fibroblasts, osteoblasts, and endothelial cells. Both proliferation and inflammation of these dental components and the epithelial and mesenchymal cells that form them play a role in the formation of odontogenic lesions. The cystic, solid and/or nonmass-like sclerotic appearance of the lesions, their infiltrative, erosive and/or expansile nature, and location with respect to the erupted versus unerupted tooth can help narrow the odontogenic differential considerations.

Nonodontogenic maxillary and mandibular lesions have a broader differential, including mucosal space, salivary gland rest, and osseous and systemic pathologies. Systemic disease, the global bone marrow appearance, and involvement of adjacent structures such as the periosteum, mucosal space, hard palate, cranial nerve branches, and deep cervical soft tissues factor into the differential diagnosis of nonodontogenic lesions.

The location of mass-like lesion with respect to the adjacent dentition and alveolus is a critical factor. Like osseous lesions outside of the jaw, the zone of transition and ability to delineate the lesion from adjacent normal appearing structures can help identify lesion location. The more benign or chronic process have descriptors such as osseous remodeling, tooth displacement and chronic appearing periosteal new bone formation. In contrast, the inflammatory, infiltrative and/or malignant processes exhibit osseous erosion, soft tissue invasion and more aggressive periosteal reaction resulting in a sunburst or triangular configuration of new bone. Mass-like lesions can be described as cystic, solid or mixed, with or without peripheral versus central enhancement, internal mineralization, and/or fluid-fluid levels.

Using these descriptors and lesion location with respect to the dentition in combination with known systemic disease can significantly improve the ability to confidently narrow differential considerations before recommending tissue diagnosis.

Well circumscribed cystic lesions

Most jaw lesions will present as hypoattenuating-radiolucent lesions or cystic masses. The first step in formulating the differential diagnosis is to distinguish inflammatory lesions associated with the dentition from cystic masses in tooth bearing versus nontooth bearing areas of the alveolus. Hypoattenuating-radiolucent odontogenic lesions are most commonly inflammatory and the relationship of a cystic mass to the dentition is essential in differentiating among odontogenic cysts and neoplasms.

Apical rarefying osteitis, synonymous with apical periodontitis, appears as a circumscribed lytic area at the root with egress of inflammation from pulpal necrosis. Chronic Apical Rarefying Osteitis may develop an epithelial lining and form a cyst, called a Radicular Cyst (RC), the most common cystic odontogenic lesion. ^,^, RCs can expand or erode through the cortex when large, mimicking other cystic odontogenic neoplasms ( Fig. 1 A–C ).

Three axial T 2 SPACE scans show cystic lesions near the maxillary region with smooth boundaries and well-defined margins. — Fig. 1

Dentigerous Cysts (DCs), the most common noninflammatory odontogenic cyst, arise from fluid accumulation in the follicle surrounding an unerupted or impacted tooth. ^,^,^, DCs are typically solitary and circumscribed, surrounding the crown of an unerupted or impacted tooth, most commonly involving the mandibular third molars ( Fig. 2 A, B ). The apex of the cyst will be at the cementoenamel junction (see Fig. 2 ). Large DCs will expand the alveolus, displace adjacent teeth, and envelop the involved tooth. The cyst wall is thin and corticated on computed tomography (CT), though chronic hydrostatic pressure or superimposed inflammation may result in wall thickening or dehiscence with mild peripheral enhancement. The nonenhancing central cystic contents will be hypoattenuating in the absence of proteinaceous debris or cholesterol granules, with a corresponding appearance on MR imaging ( Fig. 3 A–C ). Lack of diffusion restriction is important in differentiating DCs from other benign or malignant odontogenic and nonodontogenic lesions. The presence of multiple DCs is rare, typically syndromic, and can be associated with odontogenic keratocyst syndromes.

Two axial bone Computed Tomography views capturing a unilocular expansile lesion involving the mandibular third molar. — Fig. 2

Three M R I scans show hyperintense lesions near impacted molars with well-defined boundaries and cystic characteristics. — Fig. 3

Tooth involvement is one of the key features which distinguishes a large expansile DC from an OKC. OKCs can displace, partially resorb, or engulf a tooth, although the cyst wall is not directly associated with the cementoenamel junction. As opposed to the follicle of an unerupted tooth, odontogenic keratocysts (OKCs) develop from the dental lamina and are most common in the posterior mandible (up to 80%) of young males in their second-third decade of life. OKC typically presents as an expansile unilocular cystic lesion with well-defined sclerotic borders that can become scalloped as the lesion grows ^, ( Fig. 4 A–C ). The mandibular ramus is often involved in larger lesions, necessitating scrutinous evaluation for an associated pathologic fracture. It is important to assess for extraosseous extension as these lesions are notoriously difficult to surgically resect from soft tissue ( Fig. 5 A ). OKCs can have a heterogenous central appearance on precontrast MR imaging secondary to the presence of parakeratin, although they should only demonstrate peripheral enhancement ( Fig. 5 B, C). Small lesions are often found incidentally. Pain and trismus can develop as the lesion grows, with associated cellulitis and drainage in the setting of superinfection. OKCs can grow rapidly and have a high recurrence rate after surgical treatment. The amount of enhancement can increase in the setting of recurrence. OKCs can also be multilocular, septate, and multifocal. More complex multilocular and septate OKCs can be difficult to confidently delineate from an ameloblastoma, for which postcontrast MR imaging or CT imaging can be helpful to identify central nodular enhancement of ameloblastoma. Multifocal disease should raise suspicion for syndromic etiologies such as basal cell nevus syndrome ( Fig. 6 A–C ), Gardener’s syndrome, clediocranial dysplasia or mucopolysacchroidosis VI. Multifocal expansile lucent jaw lesions can also be seen in the setting of cherubism, with improvement as patients grow beyond puberty.

Three computed tomography views show a mandibular lesion with confirmed odontogenic keratocyst pathology around an unerupted third molar. — Fig. 4

Three computed tomography scans show a cystic lesion with central low intensity content in the mandible with preserved surrounding bone structure. — Fig. 5

Three images show computed tomography scans of jaw cysts and a photograph of a scalp lesion in a patient with basal cell nevus syndrome. — Fig. 6

An ameloblastoma is a benign odontogenic neoplasm of epithelial origin, which occurs in the tooth bearing portions of the mandible and maxilla. Ameloblastomas can arise from the epithelium of the tooth germ, enamel organ or odontogenic cyst lining, and occur in the posterior mandible approximately 80% of the time. ^, In contrast to OKCs, ameloblastomas typically have a more complex appearance, presenting as a cystic and solid expansile mass with scalloped margins and enhancing soft tissue components ( Figs. 7 A–G and 8 A, B ). ^, They can be unicystic or multicystic, with the number of cystic components increasing with the age at presentation. MR imaging can be useful to define the soft tissue components and their margins, with specific attention to the mandibular canal, adjacent deep spaces of the suprahyoid neck, and, in the case of maxillary lesions, the maxillary sinuses, nasal cavity, and orbit. Ameloblastomas can be divided into histopathologic subtypes, with the follicular subtype having the highest recurrence rate ^, and mixed acanthomatous or desmoplastic lesions demonstrating aggressive local invasion due to matrix metalloproteinases ( Fig. 9 A–E ). En bloc surgical resection with osseous margins is the treatment of choice, demonstrating a significantly improved recurrence rate compared to more conservative management often reserved for younger patients and unicentric disease.

Six computed tomography scans show mandibular symphysis lesions with mural nodules in cystic structures demonstrating enhanced soft tissue components. — Fig. 7

Two computed tomography scans show a mixed solid and cystic lesion in the mandible with heterogeneous internal content and lobulated margins. — Fig. 8

Five medical imaging scans show a dense mandibular mass with restricted diffusion and high cellularity, suggesting malignant odontogenic tumor pathology. — Fig. 9

Less common cystic appearing odontogenic lesions include lateral periodontal cysts (LPCs), botyroid odontogenic cysts (BOCs), glandular odontogenic cysts (GOCs), and primordial odontogenic tumors (POTs). LPCs are noninflammatory developmental cysts typically measuring less than 1 cm along the lateral margin of a vital tooth root. LPCs often present incidentally as thin walled hypoattenuating lesions within the premolar mandible of adults in their fifth-seventh decades. ^, While the morphology is like that of dentigerous and gingival cysts, LPCs are intraosseous and associated with erupted teeth along the periodontal ligament space. BOCs are noninflammatory developmental cysts that are also most common in the premolar mandible; some believe they may arise from or are subsets of LPCs. In contrast to LPCs, BOCs can be multiloculated and tend to be larger at presentation, measuring up to 4.5 cm with mandibular expansion, pain, and possibly paresthesia. GOCs are developmental cysts that present in the fourth-fifth decade and are most common in the anterior mandible near or crossing the symphysis. ^, GOCs can be unilocular or multilocular and demonstrate slow growth over time but are locally aggressive with a propensity to recur, especially those treated with curettage or enucleation, versus resection with reconstruction. While the radiographic features can overlap ( Fig. 10 A, B ), GOCs can be differentiated from LPCs, BOCs, and Ameloblastomas histologically, demonstrating cilia, ducts, and mucous cells, true to their suspected salivary origin. ^, POTs also have a well-circumscribed lucent radiographic appearance despite central fibromyxoid tissue, which sets them apart from the fibrous tissue of ameloblastoma. POTs typically present in the first or second decade of life along the crown of an unerupted posterior tooth, often with tooth displacement and root resorption.

Two computed tomography scans show a mandibular cyst with internal soft tissue mass demonstrating patchy enhancement and irregular morphology. — Fig. 10

Osteolytic, erosive, and infiltrative cystic lesions

Osteoradionecrosis and medication related osteonecrosis can result in trabecular irregularity with mixed lytic and sclerotic changes, cortical irregularity, sequestrum, and bone exposure. A history of radiation and offending medical therapy such as bisphosphonates, bevacizumab, and tyrosine kinase inhibitors are key to making the diagnosis. The mandible is more prone to osteonecrosis. Superimposed infection and subsequent osteomyelitis are more common in osteoradionecrosis. Cellulitis, abscesses, and draining sinus tracts can develop in the setting of osteomyelitis. Careful inspection for solid enhancement suggestive of recurrent disease is important in the setting of prior oral cavity-directed radiation therapy.

Langerhans cell histiocytosis (LCH) can also result in an osteolytic appearance of the jaw and can be molecularly classified as an inflammatory neoplasm. Imaging characteristics range from benign to aggressive, including ill-defined infiltrative borders with cortical destruction, periosteal new bone formation, sclerosis, soft tissue inflammation and lymph node involvement ( Fig. 11 A, B ). Symptoms include swelling, pain, bleeding with gingival ulceration, floating teeth, and pathologic fractures. Age at presentation, lack of infectious markers, and additional systemic lesions can be helpful to imply the diagnosis and prompt biopsy to exclude malignancy. Additional mandibular and maxillary neoplasms include those derived from salivary gland rests, the adjacent oral cavity, systemic disease and malignant transformation or variants of odontogenic lesions.