Does long-term compressive loading on the intervertebral disc cause degeneration?

Coil springs were stretched and attached to produce a compressive force across the lumbar intervertebral discs of dogs for up to 53 weeks. To test the hypothesis that compressive forces applied to the intervertebral disc for a long period of time cause disc degeneration in vivo in a dog model. It is...

Full description

Saved in:
Bibliographic Details
Published in:Spine (Philadelphia, Pa. 1976) Pa. 1976), 2000-12, Vol.25 (23), p.2993-3004
Main Authors: HUTTON, William C, GANEY, Timothy M, ELMER, William A, KOZLOWSKA, Eva, UGBO, John L, DOH, Eun-Sig, WHITESIDES, Thomas E
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Collagen - analysis
Compressive Strength
Dogs
Enzyme-Linked Immunosorbent Assay
Intervertebral Disc - chemistry
Intervertebral Disc - physiopathology
Intervertebral Disc Displacement - etiology
Lumbar Vertebrae - physiopathology
Male
Medical sciences
Orthopedic surgery
Proteoglycans - analysis
Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases
Time Factors
Weight-Bearing
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Coil springs were stretched and attached to produce a compressive force across the lumbar intervertebral discs of dogs for up to 53 weeks. To test the hypothesis that compressive forces applied to the intervertebral disc for a long period of time cause disc degeneration in vivo in a dog model. It is a commonly held belief that high forces applied to the intervertebral disc, and to joints in general, play a role in causing degeneration. Coil springs were stretched and attached to produce a compressive force across the lumbar intervertebral discs (L3/L4) of 12 dogs. After up to a year, the dogs were killed, and their lumbar spines were removed and radiographed. The L3/L4 disc and the controls (T13/L1 and L4/L5) were excised and examined for visible signs of degeneration. The discs then were assessed using immunohistochemical analysis and enzyme-linked immunosorbent assay. Disc chondrocytes also were assayed for apoptosis. No obvious signs of degeneration in the discs (L3/L4) that had been under compression for up to a year could be observed. There was no disc bulging, anular fissures, or disc space narrowing. Some changes were observed at the microscopic level, although no thickening of the endplate was apparent. The enzyme-linked immunosorbent assay analysis provided significant data for all three regions of the disc (nucleus, inner anulus, and outer anulus). When comparing the compressed disc (L3/L4) with either of the control discs (T13/L1 and L4/L5), in the compressed disc: 1) the nucleus contained less proteoglycan and more collagen I and II; 2) the inner anulus contained less proteoglycan and collagen I; and 3) the outer anulus contained more proteoglycan and less collagen I. The collagen II differences for the inner and outer anulus were not significant. Compression applied to the lumbar intervertebral discs of dogs for up to a year does not produce degeneration in any visible form. It does produce microscopic changes and numerical changes, however, in the amounts of proteoglycan and collagen in the nucleus, inner anulus, and outer anulus. The present results add no credence to the commonly held belief that high compressive forces play a causative role in disc degeneration.
ISSN:0362-2436
1528-1159
DOI:10.1097/00007632-200012010-00006