The following is Part II of a series of columns on the topic of osteoporosis in people with disabilities. This month's column is focusing on people with spinal cord injury.

Jennifer Rowland, Ph.D.

Because of the great amount of available material investigating osteoporosis risk for people with different types of disabilities, I'll be dedicating several months of columns to this issue, which has generated a large volume of reader comments and questions. Thank you to those who have responded to the first column on osteoporosis which was published in the May 2006 NCHPAD newsletter, and can be accessed through the newsletter archives at www.ncpad.org. In future columns I will address each of the issues raised by readers as a way of sharing information that may be helpful to others experiencing similar circumstances. This month's installment will focus on osteoporosis risk in people with spinal cord injury.

Osteoporosis Risk in People with Spinal Cord Injury

Physical mobility and weight bearing limitations for some people with disabilities make them more likely to experience osteoporosis than the general population. Osteoporosis is a major complication in people with spinal cord injury (SCI; Biering-Sorensen et al., 1998), and this population experiences lower limb bone loss and increased fracture susceptibility (Bauman et al., 2006; Biering-Sorensen, Bohr, & Schaadt, 1998; Garland et al., 1992). Factors influencing bone mass for people with SCI include: severity of injury, muscle spasticity, age, gender, and duration after injury (Jiang, Dai, & Jiang, 2006). An identical twin study comparing bone mineral density for one twin with SCI and the other without SCI found that over time there was an increasing loss of bone mineral content and density in the lower limbs and pelvis of the twin with SCI (Bauman et al., 1999). There is also evidence that women with spinal cord injuries have rapid bone loss of 25-50% in the lower extremities within the first few years following their injury.

Within the first months post-injury, weight-bearing bone structures including the distal femur and proximal tibia are primarily affected by demineralization (Nance et al., 1999). The imbalance between bone formation and bone resorption, beginning immediately after injury and peaking within 3-5 months post-injury, is responsible for bone loss for people with SCI. It is thought that approximately 2 years post-injury, a new steady state level of bone resorption and formation is established which alters bone structure and microstructure. This restructuring is believed to contribute to fracture risk (Jiang et al., 2006).

Although mobility limitations and disuse affecting mechanical force applied to bone (Zerwekh et al., 1998) are thought to be primary contributors to osteoporosis for people with SCI, some researchers postulate that neural factors may impair calcium and phosphate metabolism (Jiang et al., 2006). Associated hormonal deficiences (Bauman et al., 1994) and bone circulation problems linked to the injury may also be contributors to increased osteoporosis risk for this population (Chantraine et al., 1979). Little is known about the exact cause of osteoporosis in this population, and future research and treatments will need to focus on this issue.

Next month, I'll discuss two primary therapeutic approaches tested in experimental and clinical studies on the SCI population that involve application of mechanical stimulus to bone tissue and determination of the effects of antiresorptive drugs.

Continuing next month, this series of osteoporosis columns will provide information on osteoporosis risk for people with other types of physical and cognitive disabilities in addition to prevention recommendations, examination of intervention research focusing on prevention and treatment efforts, and an overview of medical treatment options.

Questions from Column Readers

Thank you for your questions and comments relating to last month's Part I column discussing osteoporosis as a secondary condition. Several people wrote to me asking for information about the effects of Fosomax on jaw bone health. I am in the process of gathering information about this issue and will answer this question in addition to the many thoughtful responses from other readers. Your feedback is important and stimulates dialogue which can be part of an effort to provide information and resources to decrease secondary conditions for people with disabilities.

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I encourage you to write to me with suggestions for future column topics or to comment on the information provided in this column. You can reach me, Dr. Jennifer L. Rowland, by e-mail at jenrow@uic.edu or (312) 413-1850.