Skull Patterns

Chapter 16

Skull Patterns

Dennis M. Marchiori

SK1. Basilar Invagination

SK2. Button Sequestration of the Skull

SK3. Cystic Lesions of the Mandible

SK4. Diffuse Demineralization

SK5. Enlargement or Destruction of the Sella Turcica

SK6. Increased Radiodensity of the Calvarium

SK7. Intracranial Calcifications

SK8. Mass in the Paranasal Sinuses

SK9. Multiple Wormian Bones

SK10. Osteolytic Defects of the Skull

SK11. Radiodense Mandible Lesions


SK1 Basilar Invagination

Basilar invagination (or basilar impression) occurs where there is upward migration of the base of the skull. Platybasia is an anthropologic term describing flattening of the skull base and should not be used synonymously with basilar invagination; in platybasia, the mean height of the odontoid over the palatine line is elevated above normal. The major causes of basilar invagination are reflected in the mnemonic COOP (congenital, osteogenesis imperfecta, osteomalacia, and Paget disease).

McGregor line is a widely used roentgenometric method for detecting basilar invagination. It involves drawing a line from the posterior aspect of the hard palate to the inferior margin of the skull on a lateral radiograph. Basilar invagination is probable if the tip of the odontoid process is more than 8 mm above the line segment in men or more than 10 mm in women.

The diagnosis of basilar invagination is made using conventional radiography and is supplemented by computed tomography (CT) and magnetic resonance imaging (MRI). MRI is particularly helpful for assessing possible concurrent neurologic involvement.

Disease Comments
More Common
Bone-softening disorders (Fig. 16-1) Alterations of the skull base secondary to bone-softening diseases: osteogenesis imperfecta, rickets, osteomalacia, and Paget disease
Less Common
Congenital anomalies Alterations of the skull base associated with atlantooccipital fusion (occipitalization or assimilation), Klippel-Feil syndrome, and stenosis of the foramen magnum
Achondroplasia (p. 425) Rhizomelic dysplasia resulting from a congenital defect of enchondral bone formation; characteristics include rounded lumbar “bullet-nosed” vertebrae, lumbar spine kyphosis, posterior vertebral body scalloping, increased intervertebral disc height, flattened vertebral bodies, narrowed spinal canal, and alterations of the skull base; the pelvis may appear hypoplastic; milder expressions of the disease may occur
Arnold-Chiari malformation (p. 1417) Malformation of the skull base with caudal displacement of the cerebellomedullary region; several levels of inferior displacement are recognized
Cleidocranial dysplasia (p. 429) Defect of intramembranous bone formation manifesting as osseous defects of the calvarium, clavicles, and pelvis; associated with persistence of metopic suture
Trauma Posttraumatic deformity from a skull fracture


FIG 16-1 Basilar invagination secondary to bone softening from Paget disease of the skull (arrow). Courtesy Joseph W. Howe, Sylmar, CA.

SK2 Button Sequestration of the Skull

A button sequestration is a small solitary osteolytic bone lesion that contains a central focus of calcification. Often this change represents a normal variant, particularly if it is surrounded by an osteosclerotic margin (“donut lesion”); however, aggressive pathologies should be considered.

Disease Comments
More Common
Eosinophilic granulomas (Fig. 16-2) (p. 954) Common cause of osteolytic skull defects; the inner and outer skull tables are affected; however, the defects in the skull tables do not completely superimpose, leaving an appearance of a beveled margin
Infection Osteolytic defects may occur secondary to Staphylococcus, syphilis, or tuberculosis infections; often result from contiguous spread of scalp infection
Bone metastasis (p. 904) Primary carcinomas from the lung, breast, prostate, and colon commonly metastasize to the skull
Normal variant Radiolucent defects with central calcification and surrounding sclerosis, possibly representing normal variants; these defects are differentiated from true button sequestrations by the absence of reported pain and disability; these variants usually are discovered incidentally and are not clinically significant
Less Common
Necrosis Osteonecrosis resulting from irradiation, electric shock therapy, or electric burns; often a latent period of several years elapses before osteolytic lesion becomes apparent
Postsurgical Burr hole or shunt placement
Primary neoplasm Epidermoid, dermoid cyst, meningioma, and hemangiomas may cause radiolucent skull lesions


FIG 16-2 A, Lateral skull projection and, B, close-up view of eosinophilic granuloma, producing an osteolytic defect of the skull (arrowheads) with a central radiodense sequestrum (button sequestration) (arrow). Courtesy Stan Higgins, Davenport, IA.

SK3 Cystic Lesions of the Mandible

Cystic lesions of the mandible may be caused by pathologies producing cystic lesions elsewhere in the skeleton, with a variety of causes that are seen only in the mandible. Most pathologies comprising the latter group are related to pathologic conditions of the teeth.

Disease Comments
More Common
Dentigerous (follicular) cyst (Fig. 16-3) Well-circumscribed mandibular cyst that characteristically contains the crown of an unerupted tooth; this cyst is usually found in children
Periodontal cyst Common cyst of the jaw associated with chronic infection; it appears as a well-defined radiolucent cyst in the periapical location and is contained within osteosclerotic margins
Periapical granulomas Well-circumscribed cyst in a periapical location, which may develop into periodontal cyst
Less Common
Ameloblastoma (adamantinoma) (Figs. 16-4 and 16-5) (p. 904) Multilocular radiolucent lesion with coarse inner trabeculation; it may grow very large, distorting the symmetry of the face; the condition usually is noted in patients older than 30 years of age
Aneurysmal bone cyst/osteoblastomas/hemangiomas (Fig. 16-6) Benign nonodontogenic tumors, including aneurysmal bone cysts, osteoblastomas, and hemangiomas, all producing osteolytic, expansile lesion of the mandible; each is much more common in other skeletal locations
Cherubism Bilateral, symmetric enlargement of the mandible, histologically similar to fibrous dysplasia, although the former has a familial incidence and is limited to the jaw
Fibrous dysplasia (p. 861) Unilateral, expansile, usually osteolytic, well-circumscribed lesions appearing locally or in association with other skeletal lesions. The osteosclerotic form of the disease is more typical of the maxilla. The craniofacial form (leontiasis ossea) of the disease is limited to the calvarium and face.
Giant cell reparative granuloma (p. 896) Expansile osteolytic lesion of the mandible and maxilla with thin overlying cortex; this lesion is believed to represent a nontumorous reparative process
Histiocytosis X (eosinophilic granuloma) (Fig. 16-7) (p. 954) Common in the mandible; the destruction may be so advanced that the teeth appear to “float” without surrounding osseous support; Ewing tumor, metastatic neuroblastoma, and non-Hodgkin lymphoma may produce similar appearances of “floating teeth”
Hyperparathyroidism (p. 928) Single or multiple osteolytic lesions representing brown tumors; the lamina dura thins, as is also noted in fibrous dysplasia, Paget disease, and osteomalacia
Infection Infections of the mandible and maxilla may develop from hematogenous seeding or via direct extension from dental or sinus infection; they appear as irregular osteolytic lesions, often with accompanying sequestration; trauma and local carcinoma also have been implicated
Metastasis Osteolytic lesions similar to those of other skeletal sites; metastasis may appear secondary to hematogenous seeding or direct extension from general nasal, oral, cutaneous, or salivary gland primary lesions
Multiple myeloma (p. 834) Multiple osteolytic lesions that appear well defined and of uniform size; concomitant skull changes are nearly always present
Paget disease (p. 967) Diffuse osteolytic, osteosclerotic, or mixed pattern of bone disease with bilateral enlargement; concomitant skull changes nearly always occur
Solitary bone cyst (hemorrhagic bone cyst) (p. 900) Poorly defined irregular cyst of the mandible; this condition is seen in children; usually accompanied by a history of trauma


FIG 16-3 Dentigerous cyst of the right ramus of the mandible (A and B) appearing as a radiolucency with a central radiodense unerupted tooth (arrows). C, A second case of dentigerous cyst appearing as a markedly expansile lesion with a tooth in the lower right margin of the defect (arrow). Courtesy Steven P. Brownstein, MD, Springfield, NJ.
FIG 16-4 Ameloblastoma. Oblique view of mandible reveals a large cystic lesion in body and ramus of mandible with attenuation and loss of bone superiorly. The lesion has broken through the upper part of the mandible. From Som PM, Curtin HD: Head and neck imaging, ed 4, St. Louis, 2003, Mosby.
FIG 16-5 Panoramic view of the mandible shows an expansile, multilocular, radiolucent mass in the reading left mandibular ramus (arrow) consistent with ameloblastoma.
FIG 16-6 Aneurysmal bone cyst, presenting as a cystic expansile lesion of the mandible (arrow). Courtesy William E. Litterer, Elizabeth, NJ.
FIG 16-7 Eosinophilic granuloma in the right mandible. Panorex view of mandible reveals a lucent, irregular area that is well defined in the body of the mandible between the second molar tooth and first premolar tooth. Some loss of lamina dura has occurred in the lower second molar tooth. From Som PM, Curtin HD: Head and neck imaging, ed 4, St. Louis, 2003, Mosby.

SK4 Diffuse Demineralization

Diffuse demineralization of the skull typically is related to senile osteoporosis; however, many other conditions have classic presentations in the skull. Hyperparathyroidism mimics the radiographic appearance of osteoporosis; both appear with pure patterns of diffuse demineralization. Most of the other conditions listed in the following table produce patterns of diffuse demineralization occurring in combination with larger osteolytic lesions. For example, hemolytic anemias, leukemia, and metastatic neuroblastoma may produce a classic “hair-on-end” appearance in addition to diffuse demineralization.

Disease Comments
More Common
Osteoporosis (p. 916) Appears with diffuse demineralization and is typically related to aging; less commonly, osteoporosis develops from steroid supplementation or endocrinopathy
Less Common
Anemias Possible diffuse osteoporosis related to marrow hyperplasia caused by sickle-cell anemia and thalassemia; other findings include a “hair-on-end” appearance involving the outer table of the calvarium
Hyperparathyroidism (Fig. 16-8) (p. 928) Granular, or “salt-and-pepper,” appearance of the skull as a result of diffuse demineralization; rarely, larger focal osteolytic lesions develop
Infection (p. 789) Diffuse presentation of infection is uncommon; in general, infections of the skull are less common in the United States than in underdeveloped countries
Metastatic bone disease (p. 904) Typically noted with multiple, ill-defined osteolytic lesions; this disease infrequently results in a diffuse demineralization pattern; breast, lung, and prostate origins are common in adults; in children, neuroblastoma and leukemia are more likely
Multiple myeloma (p. 834) Characterized by diffuse demineralization with focal “punched-out” lesions
Paget disease (p. 967) Diffuse demineralization that may accompany the more classic presentation of large osteolytic areas of bone destruction (osteoporosis circumscripta); demineralization occurs most often in the outer table of the skull during the lytic phase of the disease
FIG 16-8 Hyperparathyroidism. Granular deossification appearance of the calvarium, resulting in a salt-and-pepper appearance to skull. From Deltoff MN, Kogon PL: The portable skeletal x-ray library, St. Louis, 1998, Mosby.


SK5 Enlargement or Destruction of the Sella Turcica

Although variations exist, the sella turcica generally should not exceed an anteroposterior dimension of 16 mm or a vertical depth of 12 mm on a lateral skull radiograph. Also, the floor of the sella turcica is normally well defined by a single cortical line. The appearance of two cortical lines is known as a “double-floor” sign, suggesting osseous erosion of the floor by an expansile mass. Hurler disease is associated with elongation of the posterior aspect of the sella, creating a J-shaped configuration.

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Disease Comments
More Common
Aneurysm of internal carotid vessel Enlarged sella resulting from expanded cavernous segment of the carotid artery; linear vascular calcification often is present, projecting over the enlarged sella on a lateral radiograph
Craniopharyngioma Seen in children and young adults, this tumor may produce bone destruction of the sella; most lesions calcify; gliomas of the optic chiasm may cause similar changes
Empty sella syndrome (Fig. 16-9) (p. 1418) Appears as an enlarged sella without bone destruction or considerable deformity; the syndrome is believed to result from a congenital or acquired defect of the diaphragm sellae, which allows an intrasellar extension of the suprasellar arachnoid space; pulsations of the cerebrospinal fluid are thought to cause the sellar enlargement; the pituitary function typically is normal
Pituitary tumors (Fig. 16-10)
Feb 16, 2016 | Posted by in RESPIRATORY IMAGING | Comments Off on Skull Patterns
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