Altered vertebral shape typically results from congenital conditions. Although a vertebra’s appearance may be altered in many ways, the following table lists the more commonly encountered alterations. Vertebral collapse and vertebral expansion are larger topics and are discussed separately in this chapter.

SP1a Beaked or Hooked Vertebrae

Disease	Comments
More Common
Achondroplasia (p. 425)	Congenital defect of endochondral bone formation, producing characteristic rounded lumbar “bullet-nosed” vertebrae, lumbar kyphosis, posterior scalloping of the vertebrae, increased intervertebral disc height, flattened vertebral bodies, and narrowed spinal canal; the pelvis may appear hypoplastic; milder forms of the disease may occur
Mucopolysaccharidoses (p. 451)	A group of lysosomal storage diseases marked by a common disorder in mucopolysaccharide metabolism evidenced by various mucopolysaccharides excreted in the urine; these substances collect in connective tissue, resulting in bone, cartilage, and connective tissue defects; characteristics are platyspondyly with dwarfism, kyphosis, and alterations in the appearance of the vertebrae; mucopolysaccharidosis I (Hurler syndrome) is associated with oval, posteriorly scalloped, anterior-inferiorly beaked vertebrae; mucopolysaccharidosis IV (Morquio syndrome) is associated with flattened, anterior centrally beaked vertebrae
Normal variant	Slightly beaked vertebrae, most often occurring in the thoracic spine; the vertebral defect usually appears more wedged than beaked; the vertebral body may appear anteriorly beaked before ossification of the ring epiphyses; these step-like defects contain the cartilage growth centers of the vertebral endplate; as ossification proceeds, a focus of bone fills the radiolucent defect (6–12 years of age), fusing to the vertebral body at 20 to 25 years of age
Less Common
Diastrophic dysplasia (p. 434)	Autosomal, recessive, rhizomelic dwarfism secondary to a cartilage disorder; characterized by multiple skeletal disorders, including progressive kyphoscoliosis, anteriorly deformed vertebrae, hypoplastic first metacarpal, clubfoot, and deformed flattened epiphyses
Neurofibromatosis (von Recklinghausen disease) (p. 961)	Congenital disturbance of mesodermal and neuroectodermal tissue development, appearing clinically with cutaneous markings, bone deformity, and neurofibromas; spinal changes include posterior vertebral scalloping, enlarged intervertebral foramina, kyphoscoliosis, and anteriorly beaked or wedged vertebrae
Cretinism (p. 934)	Congenital hypothyroidism with delayed appearance of ossification centers, skeletal underdevelopment, wormian bones, and poorly developed sinuses; sail-like or tongue-like vertebrae and kyphosis at the thoracolumbar junction are common; changes may regress in adulthood

SP1b Biconcave Vertebrae

Disease	Comments
More Common
Metastatic bone disease (p. 904)	Metastatic bone deposition and subsequent tumor growth may weaken the vertebrae, promoting endplate impaction, producing a biconcave deformity; metastasis typically occurs in patients older than the age of 40 years and is common in those with a personal history of primary malignancy
Notochordal persistence (Fig. 17-1)	Nonfocal, congenital, smooth, inward deformity of all or part of the superior, inferior, or both vertebral endplates; this type of deformity is less focal and involves more of the endplate than Schmorl nodes
Osteopenia (metabolic disorders)	Deformity from decreased bone mass secondary to rickets, osteomalacia, steroid therapy, hyperparathyroidism, malnutrition, senile osteoporosis, immobilization, or postmenopausal bone alterations
Schmorl nodes (p. 464)	Prolapse of the nucleus pulposus into the vertebrae, producing abrupt, inward deformities of a focal area of the endplate; both endplates and multiple vertebrae may be involved
Gaucher disease (p. 952)	Genetic deficiency of glucocerebroside, with clinical findings of hepatosplenomegaly, osteopenia, osteonecrosis, focal osteolytic bone changes; biconcave vertebrae is a less common feature of the disease
Homocystinuria (Fig. 17-2) (p. 1013)	Genetic disorder causing defect in collagen metabolism; its presentation is similar to Marfan disease; vertebrae appear osteopenic and biconcave or flattened
Renal osteodystrophy (Fig. 14-39)	Secondary to renal glomerular disease; vertebral changes present with osteosclerosis (“rugger jersey”) and, less commonly, a biconcave appearance
Sickle-cell anemia (Fig. 17-3) (p. 784)	Genetic abnormality in which red blood cells assume a sickled configuration in low oxygen tension; the sickled cells may occlude small vessels with resulting ischemia; skeletal changes include osteopenia, coarse trabeculae, biconcave (more precisely, step-like or H-shaped) vertebrae, and dactylitis

FIG 17-1 Biconcave appearance of, A, the cervical and, B, lumbar vertebrae in different patients’ notochordal persistency (or nuclear impression).

FIG 17-2 Homocystinuria presenting with osteoporosis and biconcave vertebrae *(arrows)*. Courtesy Steven P. Brownstein, MD, Springfield, NJ.

FIG 17-3 A and B, Sickle-cell anemia causing biconcave deformity of the lumbar vertebrae secondary to underperfusion of the center of the vertebrae in two patients *(arrows)*.

SP1c Blocked Vertebrae

Disease	Comments
Congenital
Isolated anomalies (Fig. 17-4)	Congenital failure of segmentation; presentation varies from slight hypoplasia of intervertebral disc space to complete fusion of adjacent vertebral bodies and neural arches; interbody fusion and neural arch fusion are most common in the lumbar spine but frequently occur in the thoracic and cervical regions as well; the sagittal diameter of the vertebrae is decreased with an inward concavity of the anterior body margins at the site of segmentation failure; fusion of posterior elements and under development of the intervertebral disc space is common and used to differentiate congenital from acquired etiology
Klippel-Feil syndrome (Figs. 17-5 and 17-6) (p. 444)	Congenital failure of segmentation occurring at multiple levels; associated radiographic findings may include Sprengel deformity (elevation and medial rotation of the scapula), syndactyly, platybasia, and renal anomalies; patients usually demonstrate a clinical triad of a short neck, restricted cervical motion, and a low posterior hairline
Acquired
Ankylosing spondylitis (p. 505)	Acquired interbody fusion, seronegative spondyloarthropathy characterized by involvement in the sacroiliac joints and spine; the vertebrae appear square with ossification of the annulus fibrosus; disc height maintained; the disease has a strong male predominance and always involves the sacroiliac joints
Infections	Acquired interbody fusion secondary to pyogenic (e.g., Staphylococcus) or tuberculosis infections; disc height usually is decreased or absent
Rheumatoid arthritis (p. 480)	Chronic inflammatory arthritide that may demonstrate acquired interbody fusion; occurs more commonly with juvenile than adult rheumatoid presentations; the spinous processes do not fuse, but the remaining vertebral arches may fuse, particularly in the juvenile form
Surgical fusion	Acquired interbody fusion resulting from surgery; multiple levels may be involved; posterior joints typically are spared, intervertebral disc spaces are not visible; vertebral bodies may have a thick, square appearance, resulting from surgically placed paraspinal layers of bone as part of the fusion surgery
Trauma	Acquired interbody fusion from bone remodeling after severe trauma

FIG 17-4 **A and B** Cervical; C, lumbar; and D, congenital blocked vertebrae. All four patients exhibit hypoplasia of the intervertebral disc *(arrows)*.

FIG 17-5 Klippel-Feil syndrome characterized by the multiple blocked segments in the cervical spine. The occipitoatlantal space is nonexistent because of occipitalization of atlas, and the C2 and C3 levels are fused across the vertebral bodies and neural arches *(arrow)*. Courtesy Joseph W. Howe, Sylmar, CA.

FIG 17-6 Multiple congenital blocked segments of Klippel-Feil syndrome. Fusion is noted across the disc spaces and the vertebral arches. Courtesy Joseph W. Howe, Sylmar, CA.

SP1d Wide Enlarged Vertebrae

Disease	Comments
Acromegaly (p. 925)	Pituitary eosinophilic adenoma that produces excess somatotropin, leading to increased levels of growth hormone; the disorder is marked by progressive enlargement of the hands, feet, head, jaw, and abdominal organs; vertebrae are enlarged with posterior body scalloping; patients may have diabetes mellitus
Expansile bone lesions (Figs. 17-7 to 17-9)	Examples of expansile lesions known to develop in the vertebrae: giant cell tumor, hemangioma, aneurysmal bone cyst, osteoblastoma, Paget disease, hydatid cyst, eosinophilic granuloma, fibrous dysplasia, chordoma, metastasis, osteosarcoma, chondrosarcoma, and angiosarcoma
Paget disease (Fig. 17-10) (p. 967)	A generalized skeletal disease in which bone formation and resorption are both increased, leading to abnormally thick and soft bones with disorganized “mosaic” trabeculae; skull, pelvis, and vertebrae are common sites of involvement; vertebrae appear enlarged with thick cortices (“picture-framed” vertebrae)

FIG 17-7 Fibrous dysplasia causing expansile lesions of C2 and C3.

FIG 17-8 A and B, Giant cell tumor appearing as a cystic expansile lesion of L3. Courtesy Joseph W. Howe, Sylmar, CA.

FIG 17-9 Hemangioma of L4 presenting as an expansile body lesion. Courtesy Joseph W. Howe, Sylmar, CA.

FIG 17-10 Marked enlargement of the L3 vertebra secondary to Paget disease.

SP1e Tall Enlarged Vertebrae

Disease	Comments
Blocked vertebrae (p. 444)	Associated with congenital or acquired etiologies, may appear as a single “tall” vertebra; a congenital etiology is indicated when the posterior arches are fused
Gibbus formation	A gibbus formation, often developed from tuberculosis discitis in a child, may be associated with altered compressive forces on the vertebra, causing the lower segment of the gibbus to appear with increased vertical height along its posterior margin
Marfan syndrome (arachnodactyly) (p. 448)	Congenital disturbance of collagen formation primarily expressed as defects of the skeleton and heart valves; skeletal changes include “tall” vertebrae, posterior vertebral scalloping, wide spinal canal, scoliosis, and a long, slender appearance of the metatarsals, metacarpals, phalanges, and long narrow bones (dolichostenomelia)

SP1f Anterior Scalloped Vertebrae

Disease	Comments
Aortic aneurysms (Figs. 17-11 and 17-12) (p. 1178)	Because of proximity, may cause erosions along the anterior left side of the vertebrae, which are sometimes termed Oppenheimer erosions; although not always present, a majority of cases also demonstrate calcification of the dilated vessel walls; the intervertebral disc is not involved
Lymphadenopathy	Enlarged lymph nodes resulting from lymphoma, inflammatory lymphadenopathy, or metastatic lymphadenopathy may cause pressure erosions on the anterior surfaces of the vertebrae, primarily the lumbar vertebrae
Normal variant	Mild in concavity; multiple levels are common; variants are most often seen in the lower thoracic and upper lumbar spine
Tuberculosis (p. 1198)	Common to find infectious erosions of the vertebral margins with paraspinal masses and involvement of the intervertebral disc

FIG 17-11 Lateral lumbar radiograph with an increased anterior concavity of the upper lumbar vertebrae *(arrows)*, which represents pressure erosions from an aneurysm later diagnosed in this patient. Courtesy Joseph W. Howe, Sylmar, CA.

FIG 17-12 Lateral lumbar radiographs with, A, vascular calcification in the posterior wall of the abdominal aorta and, B, poor visualization of the anterior wall. There is an exaggerated anterior concavity of the L2 vertebral body, suspicious for erosion secondary to the aneurysm *(crossed arrow).* The contrast-enhanced computed tomography scan demonstrates an aneurysm of the abdominal aorta *(arrows)*. The central, more radiodense region (where the *arrowheads* are pointing) corresponds to the region of blood flow; the less radiodense outer region (space where the *arrowheads* are located) denotes lack of contrast corresponding to clotted blood.

SP1g Posterior Scalloped Vertebrae

Disease	Comments
Achondroplasia (p. 425)	Congenital defect of endochondral bone formation resulting in the following spinal changes: posterior scalloping of the vertebrae, increased intervertebral disc height, flattened vertebral bodies, narrow spinal canal, lumbar kyphosis, and “bullet-shaped” lumbar vertebrae; the pelvis may appear hypoplastic; milder forms of the disease may occur
Acromegaly (p. 925)	Excess levels of growth hormone resulting from a pituitary eosinophilic adenoma overproducing somatotropin; the disorder is marked by progressive enlargement of the hands, feet, head, jaw, and abdominal organs; vertebrae are enlarged with posterior scalloping; patients may have diabetes mellitus
Congenital syndromes (Figs. 17-13 and 17-14)	Arachnodactyly (see previous discussion on enlarged vertebrae), mucopolysaccharidosis syndromes (e.g., Hurler, Hunter, Morquio), Marfan syndrome, Ehlers-Danlos syndrome, and others
Increased intraspinal pressure	Increased intraspinal pressure from an ependymoma or communicating hydrocephalus may cause adjacent bone erosions
Neurofibromatosis (von Recklinghausen disease) (p. 961)	Congenital disturbance of mesodermal and neuroectodermal tissues, appearing clinically with cutaneous markings, bone deformity, and neurofibromas; selected skeletal changes include kyphoscoliosis, enlarged intervertebral foramina, posterior vertebral body scalloping from dural ectasia or neurofibroma, and bowing deformity of the lower extremities
Tumors	Bone erosion from adjacent spinal canal tumors (e.g., meningioma, ependymoma, lipoma, neurofibroma)

FIG 17-13 Posterior body scalloping secondary to dural ectasia of unknown etiology *(arrows)*. Courtesy Joseph W. Howe, Sylmar, CA.

FIG 17-14 Marfan syndrome with prominent scalloping of the posterior vertebral bodies *(arrows)*.

SP1h Square Vertebrae

Disease	Comments
Inflammatory arthropathies (Fig. 17-15)	Square vertebrae is one of the earliest findings of ankylosing spondylitis; square vertebrae also may be a feature of psoriatic arthritis, Reiter syndrome, and rheumatoid arthritis (usually juvenile); the seronegative inflammatory arthropathies usually involve the sacroiliac joints
Paget disease (p. 967)	A generalized skeletal disease in which bone formation and resorption are both increased, leading to abnormally thick, soft bones with disorganized “mosaic” trabeculae; the skull, pelvis, and vertebrae are common sites of involvement; vertebrae usually appear enlarged and square with thick cortices (“picture-framed” vertebrae)

FIG 17-15 A to C, Three cases of ankylosing spondylitis presenting with square lumbar vertebrae resulting from corner erosion and proliferation *(arrows)*. A and B, Courtesy Joseph W. Howe, Sylmar, CA.

SP1i Wedged Vertebrae

Disease	Comments
Congenital syndromes	Possible causes of wedged congenital vertebrae and other characteristic alterations; syndromes include achondroplasia, hypothyroidism, and mucopolysaccharidoses; usually multiple levels are involved
Hemivertebrae (Fig. 17-16)	Focal vertebral hypoplasia, resulting in a lateral, anterior, or posterior wedged hemivertebra at one or multiple levels; lateral hemivertebrae produce scoliosis; posterior hemivertebrae are commonly posteriorly displaced up to 3 mm and produce a kyphosis
Infections (Fig. 17-17)	Tuberculosis and pyogenic infections (e.g., Staphylococcus); clues to an infection include involvement of intervertebral disc space, paraspinal masses and calcifications, cortical demineralization, and angular kyphosis
Normal variant	Slightly wedged vertebrae may occur as normal variants, usually in the thoracolumbar region.
Scheuermann disease (p. 464)	Posttraumatic defect of vertebral endplate maturation presenting during adolescence with three or more levels of wedged vertebrae, narrowed anterior disc space, multiple Schmorl nodes, and vertebral endplate irregularity; the disease usually develops in the middle and lower thoracic spine
Trauma (Figs. 17-18 and 17-19)	Compression fracture leading to wedged configuration; endplate defects, cortical offset of anterior body margin (“step defect”), horizontal zone of bone impaction within vertebrae (zone of condensation), and history of trauma are clues to traumatic etiology

FIG 17-16 A, Lateral cervical, B, dorsal, and C, thoracic hemivertebrae *(arrows)*. A Courtesy Ian McLean, Le Claire, IA; B, Courtesy Joseph W. Howe, Sylmar, CA.

FIG 17-17 Infection leading to the trapezoidal shape of a middle thoracic vertebra with destructive endplate changes and narrowing of the intervertebral disc space *(arrow)*. Courtesy Joseph W. Howe, Sylmar, CA.

FIG 17-18 Compression fracture in the upper lumbar spine *(arrow)* and multiple levels of costal cartilage calcification *(arrowheads).* Courtesy Steven P. Brownstein, MD, Springfield, NJ.

FIG 17-19 Compression fracture and resulting wedged vertebral configuration. In addition, a grade I degenerative spondylolisthesis of L4 to L5 is present with degenerative vacuum phenomena at L4. Calcification of the abdominal aorta anterior to the spine also can be seen.

SP2 Atlantoaxial Subluxation

The normal measurement of the atlantodental interval (ADI) is less than or equal to 5 mm in children and 3 mm in adults. A measurement beyond these limits suggests instability of the atlantoaxial articulation. Instability results from compromise of the transverse atlantal ligament or C2 odontoid process. Because the joint is most stressed during flexion, forward flexion radiographs provide a more specific measure of ADI enlargement than neutral lateral radiographs. If the anterior tubercle or odontoid process does not represent fixed, clearly defined points of mensuration, atlantoaxial instability can be assessed by choosing another point on the atlas and axis, such as the distance between the posterior surface of the odontoid and the anterior surface of the posterior tubercle of the atlas (this space is known as the posterior atlantodental interval).

Disease	Comments
Congenital conditions	Occipitalization of atlas, Down syndrome (20% of cases), Morquio syndrome, and spondyloepiphyseal dysplasia; these are associated with atlantoaxial subluxation secondary to absence or attenuation of the transverse atlantal ligament, occurring as an isolated anomaly or in association with other defects
Inflammatory spondyloarthropathy (Fig. 17-20)	Condition that includes rheumatoid (adult and juvenile types) arthritis, ankylosing spondylitis, psoriatic arthritis, Reiter syndrome, and systemic lupus erythematosus; these are associated with synovitis, ligament attenuation, and odontoid erosions, which may lead to instability of the atlantoaxial articulation; rheumatoid arthritis is the most common inflammatory arthropathy to involve the atlantodental joint
Marfan syndrome (p. 448)	Genetic disorder of connective development that leads to ocular, cardiovascular, and musculoskeletal abnormalities; joint instability follows ligamentous laxity
Odontoid anomalies (p. 331)	Aplasia, hypoplasia, or malunion of the odontoid process may lead to instability
Regional infections	Include retropharyngeal abscesses, otitis media, mastoiditis, cervical adenitis, parotitis, and alveolar abscesses
Trauma	Instability resulting from fracture or torn ligaments

FIG 17-20 A through C, Three patients, each with rheumatoid arthritis and an increased atlantodental space *(arrows)*. Courtesy Joseph W. Howe, Sylmar, CA.

SP3 Bony Outgrowths of the Spine

Most bony outgrowths of the spine represent osteophytes related to degenerative arthropathy of the intervertebral disc spaces or posterior joints. An appearance of multilevel, flowing, thick, mostly anterior paravertebral outgrowths is characteristic of diffuse idiopathic skeletal hyperostosis (DISH). Large, coarse, incompletely bridging paravertebral outgrowths are associated with Reiter syndrome and psoriatic arthropathy. In contrast, delicate, thin, completely bridging outgrowths (marginal syndesmophytes) are characteristic of ankylosing spondylitis. As the terms are generally used, osteophytes suggest a degenerative etiology and syndesmophytes an inflammatory etiology. Because the condition is classified as idiopathic, the bony outgrowths of DISH are neither osteophytes nor syndesmophytes; rather, exostasis or another generic term is used to describe the changes.

Disease	Comments
More Common
Ankylosing spondylitis (Fig. 17-21) (p. 505)	Seronegative spondyloarthropathy characterized by arthritis targeted to the sacroiliac joints and spine; bilateral, symmetric, thin intervertebral connections, known as syndesmophytes, are prominent features, representing ossification of the outermost lamellae of the annulus fibrosis; posterior joint fusion is common; collectively, multiple levels produce a “bamboo spine” appearance; in addition, the anterior body margins appear straight or square
Diffuse idiopathic skeletal hyperostosis (Fig. 17-22) (p. 601)	Idiopathic disease marked by thick, flowing anterior longitudinal ligament ossifications along the anterior and lateral body margins; DISH is most common in the thoracolumbar region
Reiter syndrome and psoriatic arthropathy (Figs. 17-23 and 17-24) (p. 525)	Inflammatory arthropathies associated with paravertebral ossifications incompletely bridging the intervertebral disc spaces; usual to the thoracolumbar spine; the paravertebral ossifications are typically thick but may at times appear thin; the latter appearance is identical to that of ankylosing spondylitis
Spondylosis deformans (degenerative disc disease) (Fig. 17-25) (p. 544)	Degenerative disease involving principally the outer portions of the intervertebral disc, appearing as curved (“claw”) or horizontal (“traction”) vertebral osteophytes with or without other findings of degenerative disc disease (e.g., endplate osteosclerosis and irregularity, narrowed disc space, misalignment); osteophytes form in response to increased tension at the Sharpey fibers, anchoring the outer annulus into the cortical bone of the adjacent endplate; degenerative osteophytes are moderately thick (thicker than ankylosing spondylitis, thinner than DISH) and typically do not fully bridge the intervertebral disc space
Less Common
Acromegaly (p. 925)	Excess levels of growth hormone resulting from a pituitary eosinophilic adenoma overproducing somatotropin; the disorder is marked by progressive enlargement of the hands, feet, head, jaw, and abdominal organs; vertebrae are enlarged with posterior scalloping and new bone growth along the anterior body margins
Fluorosis	Chronic fluoride intoxication associated with osteophytosis and vertebral hyperostosis with calcification of the paraspinal ligaments; vertebrae have increased radiodensity; fluorosis is most marked in the innominates and lumbar spine
Hypoparathyroidism (p. 931)	Inadequate parathormone from undersecretion or surgical removal of the gland; skeletal changes include increased or decreased radiodensity, thickened calvarium, premature fusion of ossification centers, and ossification of the paraspinal ligaments
Neuropathic spine (p. 606)	Primarily caused by diabetes mellitus, syringomyelia, and tabes dorsalis; the radiographic appearance is marked by loss of intervertebral disc height, increased bone radiodensity, misalignment, fragmentation, and prominent osteophytosis
Ochronosis	Inherited disorder of excessive homogentisic acid production and subsequent accumulation within connective tissues; the spine is affected by multiple levels of intervertebral disc calcification and massive osteophytosis and ankylosis, especially in elderly adults
Trauma	May cause bony outgrowths from degenerative joint changes or dystrophic tissue calcifications