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LUMBAR SPINE DEGENERATION
AND ATHEROSCLEROTIC RISK FACTORS (A 52YEAR PROSPECTIVE STUDY OF 1337
PATIENTS)
Nicholas U. Ahn, MD,
Uri M. Ahn, MD,
Paul Sponseller, MD,
L. Nallamshetty, BS,
Porama K. Thanaporn, BS,
Peter Rose, BS,
Mesfin Lemma, MD,
J. Buchowski, MS,
John P. Kostuik, MD
Johns Hopkins Hospital Department of Orthopaedic Surgery,
Baltimore, Maryland, USA
INTRODUCTION:
A great deal of attention has been directed towards the hypothesis that
lumbar spine deterioration is caused by vascular insult to the intervertebral
disks 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 spine pathology, such as spondylosis
and degenerative spondylolisthesis. However, no prospective studies exist
which link atherosclerotic risk factors such as smoking to lumbar spine
pathology. Such knowledge would give further insight into the etiology
of lumbar spine degeneration and hopefully lead investigators in the correct
direction when searching for a solution to this costly and ubiquitous
problem.
MATERIALS AND METHODS:
Graduates from the medical school classes from 19481964 at our institution
were asked to participate in a longitudinal study which was started in
1949; 1337 physicians consented to this study. All volunteers had medical
records and questionnaires sent in each year; all data were stored and
recorded. Risk factors for athersoclerosis were identified: smoking history,
diabetes mellitus, hypertension, hypercholesterolemia, hyperlipidemia,
CAD, peripheral vascular disease, and obesity. The subsequent development
of lumbar spine pathology including low back pain, lumbar spondylosis,
degenerative spondylolisthesis, HNP, and spinal stenosis was determined.
A stepwise logistic regression was utilized to determine whether or not
development of each lumbar spine process was associated with different
atherosclerotic risk factors. The contributions of age and sex were corrected
for.
RESULTS:
Development of back pain was significantly associated with prior positive
smoking history (p=0.02), hypertension (p=0.03), and CAD (p=0.04). Also,
a positive association existed between pack years smoked and back pain
(p=0.04), and a negative association existed between number of years quit
and back pain (p=0.05). Development of degenerative spondylosis and spondylolisthesis
were significantly associated with prior positive smoking history (p <0.05),
hypertension (p=0.03), coronary artery disease (p=0.01), and hypercholesterolemia
(p=0.03). CONCLUSION: Smoking, hypertension, and CAD are all associated
with development of low back pain. These same factors, as well as hypercholesterolemia,
are associated with development of degenerative lumbar spondylosis and
spondylolisthesis. This suggests that the vascular hypothesis to the etiology
of low back pain is valid.
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