Cervical facet joint injury is an accepted mechanism of neck pain from whiplash. Nearly half of whiplash injuries become chronic, with staggering costs associated with these injuries and their related syndromes. Little is known about the specific biomechanical mechanisms producing chronic pain, and the physiologic mechanisms responsible for its persistence. During whiplash, the cervical facet joint stretches the capsular ligament beyond its physiologic range. The capsule is innervated by nociceptive afferents that can activate under tension, suggesting certain capsule loading scenarios as initiating transmission of nociceptive signals. Persistent pain from mechanical facet injury may be due to combined peripheral and spinal cascades that are initiated and/or sustained by a mechanical insult. This thesis defines the relationship between cervical facet joint distraction and behavioral hypersensitivity (pain symptoms) in the rat. The microstructural response of the collagen fibers in the joint capsule and associated spinal neuronal activation are defined for painful facet distraction to identify potential structural and spinal mechanisms for generating pain. The neuropeptide substance P (SP) and its receptor, neurokinin-1 (NKlr), modulate pain, but their contribution to facet-mediated pain is undefined. Accordingly, SP and NKlr mRNA and protein are quantified in the dorsal root ganglion and the spinal cord following facet loading to define one potential mechanism for producing facetmediated pain. Additional studies selectively ablated NKlr-bearing cells in the joint using injections of a neurotoxin conjugated to substance P to begin to evaluate the role of those cells in contributing to pain. A finite element model is developed to extend these in vivo studies to dynamic scenarios by predicting the force across the capsule that is necessary to generate pain for high-rate loading. That predicted force is imposed in vivo and allodynia monitored to define if the hypothesized target force actually produces pain when imposed across the joint in the rat at a high-rate of distraction. Collectively, these studies establish relationships between facet loading and pain symptoms, suggest that joint distraction magnitude may be associated with pain outcomes and neuropeptide responses, and help focus future investigations into additional mechanisms underlying the transduction of mechanical facet joint injury into pain.