The Rugger Jersey Spine Sign


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”.


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.

Previous SectionNext Section


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.
Previous SectionNext Section


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. 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. 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.

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

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.

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. 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. 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.
Previous SectionNext Section

Popular posts from this blog

PG Doctors of India must work not more than 48 Hr/week: SC

Why DNB exam tougher than MS/MD exam?