Abstract
Low back pain (LBP) has been among the leading causes of disability for the past 30 years. This highlights the need for improvement in LBP management. Many clinical trials focus on developing treatments against degenerative disc disease (DDD). The multifactorial etiology of DDD and associated risk factors lead to a heterogeneous patient population. It comes as no surprise that the outcomes of clinical trials on intradiscal mesenchymal stem cell (MSC) injections for patients with DDD are inconsistent. Intradiscal MSC injections have demonstrated substantial pain relief and significant disability-related improvements, yet they have failed to regenerate the intervertebral disc (IVD). Increasing evidence suggests that the positive outcomes in clinical trials might be attributed to the immunomodulatory potential of MSCs rather than to their regenerative properties. Therefore, patient stratification for inflammatory DDD phenotypes may (i) better serve the mechanisms of action of MSCs and (ii) increase the treatment effect. Modic type 1 changes—pathologic inflammatory, fibrotic changes in the vertebral bone marrow—are frequently observed adjacent to degenerated IVDs in chronic LBP patients and represent a clinically distinct subpopulation of patients with DDD. This review discusses whether degenerated IVDs of patients with Modic type 1 changes should be treated with an intradiscal MSC injection.
Highlights
A fundamental challenge for improving the lives of chronic low back pain (CLBP)patients is the lack of effective targeted treatments
Multiple clinical trials investigating the efficacy of antibiotics or intradiscal steroid injections for the treatment of CLBP patients with Modic changes (MC) were not listed in the ClinicalTrials.gov database
We review the impact of the harsh intervertebral disc (IVD) microenvironment on IVD cells (IVDCs) and mesenchymal stem cell (MSC) and discuss its relevance in MC
Summary
Patients is the lack of effective targeted treatments. The development of novel targeted therapies for CLBP patients is hampered in part by the heterogeneity of the CLBP population. Endplate defects enhance the fluid flow between the disc and the bone marrow [23,24] and may provide a physical explanation for the inflammatory and pro-fibrotic cross-talk between the disc and the bone marrow observed in MC [25]. This cross-talk likely promotes MC development, representing an interesting treatment target. 1; RUNX2, transcription factor the inflammatory and pro-fibrotic cross-talk between the disc and the bon Despite an increasing understanding of the molecular and cellular changes in MC bone served in MC. A pro-fibrotic [46], possibly due to the pro-fibrotic and pro-inflammatory cross-talk with the ‘MC1 disc’
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