Transplanted mesenchymal stem cells with pure fibrinous gelatin-transforming growth factor-β1 decrease rabbit intervertebral disc degeneration

BACKGROUND CONTEXT: Disc degeneration is a major reason for low back pain and can be caused by apoptosis. The prevention of apoptosis using mesenchymal stem cells (MSCs) may lead to new treatments for low back pain. Previous studies have reported that transplanted MSCs can proliferate and differentiate into cells expressing some of the major phenotypic qualities of nucleus pulposus cells. However, the effects of MSC transplantation on the disc height index (DHI) and apoptosis inhibition have not yet been thoroughly investigated. PURPOSE: The present study evaluates the effects of MSC transplantation on DHI and its potential to inhibit apoptosis. STUDY DESIGN/SETTING: Random, controlled, animal experiment study. METHODS: The annulus fibrosus of 54 white New Zealand rabbits was punctured with a 21-gauge needle, and the nucleus pulposus tissue from the intervertebral discs was aspirated. The degenerative disc model was produced in each rabbit, which were then randomly divided into three groups: degenerative model group; pure fibrinous gelatin-transforming growth factor-beta 1 (PFG-TGF-beta 1) transplanted group; and MSC-PFG-TGF-beta 1 transplanted group. Computed radiography imaging, magnetic resonance imaging, and histological examinations were performed at Weeks 4, 8, and 12. RESULTS: The transplanted MSCs inhibited apoptosis and slowed the rate of decrease in DHI. Magnetic resonance imaging results showed that the MSC-PFG-TGF-beta 1 group had less degeneration and a slower decrease in DHI compared with both the degenerative model and PFG-TGF-beta 1 groups. An increased quantity of nucleus pulposus and type II collagen content and a decrease in the rate of cell apoptosis were noted in the MSC-PFG-TGF-beta 1 group. CONCLUSIONS: Mesenchymal stem cells can slow the rate at which the DHI decreases. This effect may be because of the inhibition of apoptosis by MSCs. Published by Elsevier Inc.