Abstract
Low back pain (LBP), commonly induced by intervertebral disc degeneration, is a lumbar disease with worldwide prevalence. However, the mechanism of degeneration remains unclear. The intervertebral disc is a nonvascular organ consisting of three components: Nucleus pulposus, annulus fibrosus, and endplate cartilages. The disc is structured to support our body motion and endure persistent external mechanical pressure. Thus, there is a close connection between force and intervertebral discs in LBP. It is well established that with aging, disordered mechanical stress profoundly influences the fate of nucleus pulposus and the alignment of collagen fibers in the annulus fibrosus. These support a new understanding that disordered mechanical stress plays an important role in the degeneration of the intervertebral discs. Tissue-engineered regenerative and reparative therapies are being developed for relieving disc degeneration and symptoms of lower back pain. In this paper, we will review the current literature available on the role of disordered mechanical stress in intervertebral disc degeneration, and evaluate the existing tissue engineering treatment strategies of the current therapies.
Highlights
Low back pain (LBP) is the most common reason for disability in developed countries accounting for 10.7% of the total population of disabled people [1]
Intervertebral disc degeneration (IDD) is a chronic disease that slowly degrades the content of intervertebral disc (IVD) and leads to unstable IVD, which limits the mobility of the spinal cord [3]
We investigated the role of disordered mechanical stress in Nucleus pulposus (NP), Annulus fibrosus (AF), and angiogenesis in IDD, and current trends in tissue engineering therapies in IDD (Figure 4)
Summary
Low back pain (LBP) is the most common reason for disability in developed countries accounting for 10.7% of the total population of disabled people [1]. Depending on the stage of degeneration, current clinical strategies are divided into conservative and surgical therapies These strategies are restricted to relieving the pain and symptoms without eliminating the disease itself due to an incomplete understanding of the pathobiology of IDD [11,12,13,14,15]. We work [35] raise high risk lumbar disc degeneration While hypomobility, such as sedentary define these aberrant alteredthe biomechanics as disordered mechanical stress. NPasconsists of notochordal (NCs), which gradually define these aberrant biomechanics disordered mechanical cells stress. The embryonic stage, NP consists of notochordal have that disordered mechanical stress can result in a loss of NCs, subsequently leadinghave to intoshown chondrocyte-like cells (CLCs) post-embryonic and adult states [37]. We expect that this review will support a new direction to an understanding of IDD mechanism and therapy application
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