DOI: 10.1148/radiol.2302020388
(Radiology 2004;230:491-492.)
© RSNA, 2004
The Rugger Jersey Spine Sign1
Aaron Wittenberg, MD
1 From the Department of Radiology, MetroHealth Medical Center, 2500 MetroHealth Dr, Cleveland, OH 44109. Received April 1, 2002; revision requested June 13; revision received October 2; accepted December 19. Address correspondence to the author (e-mail: aaronwittenberg@yahoo.com).
Index terms: Bones, renal osteodystrophy, 321.573, 331.573 • Bones, sclerosis, 321.573, 331.573 • Signs in Imaging • Spine, radiography, 321.11, 331.11
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APPEARANCE
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At radiography, sclerotic bands along the superior and inferior thoracic and lumbar vertebral body endplates give a striped appearance to the vertebral bodies, with a relative band of lucency at the center of each vertebral body. The alternating parallel sclerotic and lucent bands are analogous to the stripes on an English rugby sweater, from which arises the name "rugger jersey spine" (1) (Figure).
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Lateral radiograph of the thoracic spine in a 69-year-old woman with chronic renal failure. The image shows bandlike regions of increased opacity at the superior and inferior margins of the vertebral bodies, which is typical of the rugger jersey spine sign.
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EXPLANATION
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The opaque sclerotic bands seen on the inferior and superior endplates of vertebral bodies represent accumulations of excess osteoid. Although they are deficiently mineralized, the areas of osteoid appear opaque at radiography because of their increased volume in comparison with that of normal bone (2). The spinal canal and intervertebral disk spaces are normal.
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DISCUSSION
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The rugger jersey spine sign is said to be almost diagnostic of the osteosclerosis associated with secondary hyperparathyroidism of chronic renal failure. The major skeletal components of renal osteodystrophy that can be seen on radiographs include osteomalacia, osteosclerosis, and soft-tissue calcification. Osteomalacia is defined as bone that contains insufficient or delayed mineralization of osteoid tissue. In children, osteomalacia secondary to renal disease may manifest as rickets. In adults, osteomalacia as a result of renal osteodystrophy may manifest as osteopenia, a decrease in bone density (3). Renal osteodystrophy may manifest radiographically as subperiosteal resorption of bone in the radial aspect of the middle phalanges of the hand. This process later manifests radiographically as areas of resorption in concave areas such as the proximal tibia and femoral neck (4). In contrast, osteosclerosis due to renal osteodystrophy tends to predominate in the axial skeleton, most commonly manifesting in the pelvis, ribs, and spine. Osteosclerosis occurs in about 20% of patients with chronic uremia and renal osteodystrophy (5).
The physiology of osteosclerosis due to renal failure is complex. Prolonged renal failure causes phosphate retention and subsequent hyperplasia of parathyroid gland chief cells, which results in a decrease in serum calcium and an increase in serum parathyroid hormone. Increased serum phosphate causes a decrease in 1,25(OH)2D synthesis, which decreases calcium absorption. The increased parathyroid hormone acts on the kidneys and on bone to normalize serum calcium. The direct results are (a) stimulation of vitamin D metabolism, which increases intestinal resorption of calcium, thereby antagonizing the effects of phosphate on 1,25(OH)2D synthesis; (b) increased resorption of calcium from the kidneys, with increased excretion of phosphate in the kidneys; and (c) increased osteoclast activity, which causes the release of calcium from bone (6). Osteoblasts form an increased amount of osteoid in response to bone resorption and a subsequent loss of bone mass. This excess osteoid does not contain hydroxyapatite but appears opaque on radiographs, thus producing the rugger jersey spine appearance.
Renal transplantation paradoxically worsens osteodystrophy, and steroids necessary to prevent transplant rejection accentuate osteoporosis and can cause ischemic necrosis of the femoral heads. In addition, secondary hyperparathyroidism can continue after renal transplantation. Tertiary hyperparathyroidism may develop, an entity in which the parathyroid glands develop autonomous control, which results in persistent bone resorption and hypercalcemia.
Other disease processes may mimic the rugger jersey spine sign. Paget disease, osteoporosis, metastatic lesions, or osteomalacia are the diseases that have radiographic appearances that are commonly confused with the rugger jersey spine (7).
One factor to keep in mind when differentiating spinal dystrophic findings is that the rugger jersey spine sign is multisegmental, as it affects multiple vertebral bodies. The bands of increased opacity along the superior and inferior aspect of the vertebral bodies differ from the uniformly increased opacity seen in Paget disease, skeletal metastasis, or lymphoma. Skeletal metastasis and lymphoma produce the so-called ivory vertebral body, and these diseases may affect a solitary vertebral body (7).
The rugger jersery spine sign can be differentiated from the "picture frame" vertebral body seen with Paget disease. The cortex of the vertebral body is thickened in a patient with Paget disease. This is a result of disorganized new cortical bone formation after excessive osteoclastic activity causes the resorption of normal bone (8). At radiography, this results in increased opacity of the cortex on all sides of the vertebral body, whereas the characteristic sclerosis of the rugger jersey spine is seen only at the superior and inferior endplates.
The appearance of osteoporotic vertebral bodies can vary and at times may mimic that of osteosclerosis. Osteoporosis most frequently results in wedging and compression of the vertebral bodies. Osteoporosis can result in concavity of the superior and inferior endplates. These appearances are caused by diffuse weakening of the bone and occur most commonly in the thoracic and lumbar spine. Trabecular thinning, which is usually seen in the middle to upper thoracic spine, leads to relative radiographic opacity of the superior and inferior endplates.
Other generalized disease processes that seemingly imitate the rugger jersey spine sign include fluorosis and myelofibrosis. Fluorosis and myelofibrosis involve the axial skeleton and result in increased opacity of the vertebral bodies, pelvis, and bones of the thorax. Diffuse findings such as ligamentous calcification, periostitis, and vertebral osteophytosis differentiate fluorosis from renal osteodystrophy (9). Myelofibrosis is associated with splenomegaly and cortical thinning of long bones. A complete skeletal survey, in addition to pertinent clinical and laboratory data, aids in distinguishing these disorders (5).
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FOOTNOTES
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A trainee (resident or fellow) wishing to submit a manuscript for Signs in Imaging should first write to the Editor for approval of the sign to be prepared, to avoid duplicate preparation of the same sign.
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REFERENCES
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- Karani S. Secondary hyperparathyroidism: primary renal failure. Proc R Soc Med 1955; 48:527-530.[Medline]
- Pitt MJ. Rickets and osteomalacia. In: Resnick D, eds. Diagnosis of bone and joint disorders. 3rd ed. Philadelphia, Pa: Saunders, 1995; 1904.
- Pitt MJ. Osteomalacia. In: Resnick D, eds. Diagnosis of bone and joint disorders. 3rd ed. Philadelphia, Pa: Saunders, 1995; 491-524.
- Resnick D, Niwayama G. Parathyroid disorders and renal osteodystrophy. In: Resnick D, eds. Diagnosis of bone and joint disorders. 3rd ed. Philadelphia, Pa: Saunders, 1995; 2014-2015.
- Kakarla S. Rugger jersey spine. N Y State J Med 1980; 80:1724-1725.[Medline]
- Koeppen B, Stanton B. Renal physiology. In: Berne R, Levy M, eds. Principles of physiology. 2nd ed. St Louis, Mo: Mosby, 1996; 633-639.
- Resnick D. The "rugger jersey" vertebral body. Arthritis Rheum 1981; 24:1191-1193.[Medline]
- Frame B, Marel GM. Paget disease: a review of current knowledge. Radiology 1981; 141:21-24.[Abstract/Free Full Text]
- Wang Y, Yin Y, Gilula LA, et al. Endemic fluorosis of the skeleton. AJR Am J Roentgenol 1994; 162:93-98.[Abstract/Free Full Text]
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