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We evaluated the pattern of osteoporosis after spinal cord injury, determined the time-frame of the changes, and elucidated the relationship among parathyroid hormone levels, biochemical markers of bone formation, and the pattern of bone mass loss. We included 176 subjects with spinal cord injury and 62 subjects without spinal cord injury as controls in the study. Bone mineral density of the spine and the proximal femur was measured. The participants' age, level of injury, and length of time since injury were compared with the nonspinal cord-injured controls and with each other. Serum levels of calcium, calcitonin, biochemical markers of bone formation, and parathyroid hormone were determined. Our results revealed that bone mineral density of the proximal femur declined and reached fracture threshold at one to five years after injury. The decline was detected at 12 months after injury in all age groups. Spinal bone mineral density neither declined significantly nor reached fracture threshold. Parathyroid hormone levels declined before the end of the first year postinjury and increased at one to nine years postinjury in the 20- to 39-year age group. The increase correlated with the initial decline of bone mineral density of the proximal femur. Our studies in spinal cord-injured subjects revealed a pattern of osteoporosis similar to age and parathyroid dysfunction-related osteoporosis. No other correlation was detected between indexes of bone metabolism and bone mineral density measurements.

Bone Gla protein (BGP) was measured in the plasma by radioimmunoassay (RIA) during treatment of 59 patients with bone diseases including Paget's disease (N = 9), primary hyperparathyroidism (N = 25), chronic renal failure (N = 20), and cancer involving bone (N = 5). Plasma BGP was increased above normal in all patients. BGP decreased in the patients with Paget's disease following the acute and chronic administration of salmon calcitonin. Plasma BGP was higher in women then in men with primary hyperparathyroidism. Following parathyroidectomy, BGP decreased in both sexes but the decrease was significant in women only. Plasma BGP was increased in patients with renal osteodystrophy and did not change after hemodialysis. In the patients with bone cancer, plasma BGP decreased during treatment of the attendant hypercalcemia with salmon calcitonin. Although plasma BGP and serum alkaline phosphatase (AP) levels were generally correlated in these studies, there were examples of dissociation between the two. The measurement of plasma BGP appears to provide a specific index of bone metabolism that may in some circumstances be more sensitive than serum alkaline phosphatase measurement. However, further studies are necessary to establish the clinical value of plasma BGP measurement by RIA in the management of patients with bone diseases.

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