Animal models provide important clues to the pathomechanisms of human intervertebral disc degeneration. Previous reviews on this topic have highlighted the fact that loss of nuclear volume (and, consequently, pressure) is a common trigger for tissue-remodeling and anatomic change consistent with degeneration in humans. Unfortunately, a large gap still exists in the medical knowledge base that serves to distinguish symptomatic from asymptomatic degeneration. Because disc degeneration per se is not a basis for clinical intervention, identification of specific features underlying discogenic pain is of the utmost importance to advance the current level of care and identify novel therapeutic targets. This article presents animal-model evidence that pathologic, or painful, degeneration is characterized by ineffective injury-healing of peripheral tissue. Because the disc is only vascularized at the vertebral end plate and the outer part of the anulus, these are the likely sites for focal damage, inflammation, neoinnervation, and nociceptor sensitization. Consequently, while nuclear insufficiency is likely the root of degenerative change, the end plate and peripheral part of the anulus are more likely the source of patient discomfort.