A multitude of studies has indicated the potential of cell therapy as a method for intervertebral disc (IVD) regeneration. Transplantation of a variety of cells has been assessed and shown capable of deterring the rate of degeneration in animal models and in human clinical trials. In this study, a novel approach using human discogenic nucleus pulposus cells directly from their cryopreserved state was assessed. In an established canine disc degeneration model, the degeneration process was evaluated in IVDs receiving precultured discogenic cells, thawedonly discogenic cells, and a saline sham injection after induction of degeneration. Degeneration progression was followed over time by the evaluation of the disc height index (DHI). Finally, after 12 weeks, the manipulated and control discs were explanted, histologically stained, and of the estimated 632 million low back pain patients globally will advance to a chronic condition. 1,2 Together, these compelling numbers engender a critical social-economic burden on society. For example, within the USA, 100 billion USD is spent annually on low back pain associated costs. 3,4 Currently, treatment options are limited and fail to restore or halt further advancement of the underlying pathology. 5 Degeneration of the intervertebral disc (IVD) is widely considered to be a predominant cause of low back pain. IVD degeneration is hallmarked by a dysregulation in extracellular matrix (ECM) homeostasis. 6,7 The exact origin of IVD degeneration remains to be elucidated; however, the nucleus pulposus (NP) is believed to be the place of onset. 8,9 Progression of IVD degeneration is characterized by a decline in proteoglycan production, an increase in matrix degenerative proteins, and a switch from type II collagen to type I collagen production. 6,7 Moreover, NP cells undergo senescence and dedifferentiation toward a more fibrotic phenotype. 10 The NP disorganization and height loss causes incorrect loading of adhering tendons promoting reorganization of tendon ECM to thicker and stiffer structures, further disrupting the mechanical features along the spine.