Intervertebral disc degeneration causes substantial back pain and associated pain that shoots down the legs (radiculopathy). Back issues associated with bad intervertebral discs are a leading cause of disability. Such disability costs employers millions of dollars of lost man and woman power and employees extensive loss of wages. Chronic back pain can also seriously compromise the quality of life and presents a large societal burden.
To date, surgery is the only effective treatment option, but surgical interventions sometimes leave patients worse off than before. Thus there is presently no effective intervention for this disease.
However, in a recent paper, Victor Y.L. Leung and his colleagues from the University of Hong Kong and several other institutions as well have used human mesenchymal stem cells from bone marrow to treat damaged intervertebral discs in rabbits. The results, published in the journal Stem Cells, are quite hopeful
Leung and others discovered that by puncturing the intervertebral discs of rabbits with a syringe needle, they could induce damage to the disc that mimics disc degeneration in humans.
Next, they implanted human bone marrow-derived mesenchymal stem cells (MSCs) into the damaged discs. Such implantations prevented scarring of the disc in the center of the disc. The center of the disc, the nucleus pulposus, is more gel-like than the surrounding annulus fibrosus. Scarring of the nucleus pulposus stiffens it and prevents it from moving with stress. An inability to bend with stress causes the disc to become brittle with time and herniate. However, implantation of mesenchymal stem cells preserved the mechanical properties of the disc and benefitted overall spinal function.
By looking more deeply at the mechanism by which mesenchymal stem cells preserve disc function, Leung and others showed that MSCs suppress abnormal deposition of collagen I in the nucleus pulposus. Since collagen is made during scarring, suppression of collagen I synthesis suppressed scarring. Secondly, implanted MSCs decreased the expression of two molecules that promote the synthesis of collagen I. By suppressing the expression of MMP12 and HSP47, the implanted MSCs also reduced collagen aggregation and maintained the microarchitecture of the disc and its mechanical properties.
This study supports the ability of MSCs to stimulate resident stem cell activities and disc healing. The implanted MSCs seem to do so by means of down-regulating collagen fibril formation. This provides the basis for the MSC‐based disc therapies.