Discogenic pain, or back pain from intervertebral disc (IVD) degeneration, involves not only IVDs, but also the peripheral and central nervous systems. While the inflammatory environment of degenerated IVDs is thought to sensitize peripheral sensory neurons, this interaction’s mechanism is not fully understood. Further, back pain is the leading cause of global disability, but is more prevalent in women than men, so sex-specific pathology is likely. However, most preclinical back pain research uses only one sex of animals, and chronic pain research has a pronounced male bias. Thus, there is a need to examine both how involved tissues interact, and how discogenic low back pain pathogenesis may differ by sex. In particular, using an animal model allows analysis of sex differences without gender confounds seen in human populations. This thesis generated knowledge evaluating possible sex differences in low back pain by measuring sex differences in IVD degeneration after injury, relationships between structural and functional IVD degeneration and pain, and dorsal root ganglion (DRG) gene expression in two pain transduction pathways. Within degenerated IVDs, sex differences were strongest in measures of the outer annulus fibrosus (AF), and suggested greater fibrotic healing in males, a sex difference seen in fibrosis of other tissues. Due to the sex differences in IVD degeneration, sex-specific relationships between structural and functional IVD degeneration and behavioral and molecular nociception measurements were assessed with correlation network analysis. Injury correlated with structural but not functional degeneration in both females and males. Pain measurements correlated with injury only in males, suggesting a more linear relationship between IVD degeneration and pain in males. Lastly, gene expression in DRGs from sinuvertebral nerve and rami communicans pathways six weeks after IVD injury was measured by RNAseq. Gene expression changes were limited, but there were sex and DRG level differences in gene set enrichment, indicating that DRGs may respond differently to IVD degeneration in females and males, and that the IVD innervation pathways may play different roles in pain pathogenesis. This work demonstrates complex interactions between tissues and sex differences in pain pathogenesis, which informs both future preclinical study design and potential sexspecific therapies.