Abstract

Intervertebral disc (IVD) degeneration is a multifactorial process that is influenced by contributions from genetic predisposition, the aging phenomenon, lifestyle conditions, biomechanical loading and activities, and other health factors (such as diabetes). Attempts to decelerate disc degeneration using various techniques have been reported. However, to date, there has been no proven technique effective for broad clinical application. Granulocyte colony-stimulating factor (GCSF) is a growth factor cytokine that has been shown to enhance the availability of circulating hematopoietic stem cells to the brain and heart as well as their capacity for mobilization of mesenchymal bone marrow stem cells. GCSF also exerts significant increases in circulating neutrophils as well as potent anti-inflammatory effects. In our study, we hypothesize that GCSF can induce bone marrow stem cells differentiation and mobilization to regenerate the degenerated IVD. We found that GCSF had no contribution in disc regeneration or maintenance; however, there were cell proliferation within end plates. The effects of GCSF treatment on end plates might deserve further investigation.

Highlights

  • The pathophysiology of disc degeneration is still unknown [1, 2]

  • We found chondroitinase ABC (ChABC) injection resulted in no significant change at 3 weeks after injection; some early osteophyte formation with decrease in disc height index (DHI) was disclosed at 6 weeks after injection (Figure 1)

  • There were no significant changes of nucleus pulposus (NP) after Granulocyte colony-stimulating factor (GCSF) treatment than sham-operated treatment on the Safranin O staining

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Summary

Introduction

The pathophysiology of disc degeneration is still unknown [1, 2]. Disc degeneration can be considered as a loss of proper stability and mobility [3, 4]. And histopathologically, disc degeneration can be characterized as a decrease in water content associated with proteoglycan reduction of the nucleus pulposus and inner annulus. This effect brings on destruction of annular structure and flattening of the disc [5,6,7]. Disc tissues have a limited ability to regenerate, since they are avascular and nutritionally supported only by passive diffusion at the end plates [2, 8, 9]. Once the degenerative process is activated, it is difficult to decelerate and is considered to be an irreversible condition [2]

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