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Abstract
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.