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Nicholas U. Ahn, MD, Darien, IL, USA; Uri M. Ahn, MD, Bedford, NH, USA; Leelakrishna Nailamshetty, BS, Philadelphia, PA, USA; Jacob M. Buchowski, MS, Baltimore, MD, USA; Peter S. Rose, BS, Bethesda, MD, USA; Paul D. Sponseller, MD, Baltimore, MD, USA
Introduction: A great deal of attention has been directed toward the hypothesis that low back pain is caused by vascular insult to the intervertebral discs or joints of the lumbar spine. More specifically, numerous authors have suggested that atherosclerotic occlusion of the lumbar vessels is a primary cause of low back pain and lumbar spondylosis. A previous study examined the relationship between lumbar spine disease and single atherosclerotic risk factors. It was found that smoking, hypertension and hypercholesterolemia were associated with the development of lumbar spondylosis. Smoking and hypertension were associated with the development of chronic low back pain. It is well known that the presence of multiple risk factors dramatically increases the risk of atherosclerotic occlusion of the coronary arteries and small arteries of the extremities. This leads to a nearly exponential increase in risk of heart disease and peripheral vascular disease as the number of risk factors increases. It would thus follow, if atherosclerosis of the lumbar vessels is a cause of lumbar spine disease, that increasing the number of atherosclerotic risk factors in an individual would increase his or her odds of developing low back pain or lumbar spondylosis.
This is the only study that investigates the effect of multiple atherosclerotic risk factors on the development of lumbar spine disease. Furthermore, we have been able to study this relationship using a prospective, long-term (53-year) cohort. Should the increase in number of risk factors lead to an increase in the odds of developing lumbar spine pathology, this would provide further evidence that the vascular hypothesis is valid.
Materials and methods: Graduates from the medical school classes from 1948 to 1964 at our institution were asked to participate in a longitudinal study that was started in 1949; 1,337 physicians consented to this study. All volunteers had medical records and questionnaires sent in each year, and all data were stored and recorded. Numerous risk factors for atherosclerosis were identified: smoking history, diabetes mellitus, hypertension, hypercholesterolemia, obesity, family history and peripheral vascular disease. The subsequent development of lumbar spine pathology, including chronic low back pain, lumbar herniated nucleus propolsus and lumbar spondylosis, was determined. Logistic regression analyses were used to examine the relationship between the number of risk factors and the development of lumbar spine disease. Because this is a prospective cohort, only those risk factors that existed before the development of the lumbar spine disease were considered in the analyses.
Results: The odds of developing chronic low back pain increased significantly as the number of risk factors increased only in those patients who had a smoking history (p=.02) or a history of hypertension (p=.04). The odds of developing lumbar spondylosis increased significantly as the number of risk factors increased in all patients (p=.03). The odds of developing lumbar herniated nucleus propolsus were not significantly associated with an increase in the number of risk factors.
Conclusion: An increase in the number of atherosclerotic risk factors was found to significantly increase the odds of developing chronic low back pain and lumbar spondylosis in this prospective, long-term cohort. This suggests that atherosclerosis of the segmental arteris is a cause of lumbar spine disease and that the vascular hypothesis to the cause of low back pain and lumbar spine degeneration is valid.
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© 2002 Published by Elsevier Inc.