Chronic neck pain is a common condition and a primary clinical symptom of whiplash and other spinal injuries. Loading-induced neck injuries produce abnormal kinematics between the vertebrae, with the potential to injure facet joints and the afferent fibers that innervate the specific joint tissues, including the capsular ligament. Mechanoreceptive and nociceptive afferents that innervate the facet have their peripheral terminals in the capsule, cell bodies in the dorsal root ganglia, and terminal processes in the spinal cord. As such, biomechanical loading of these afferents can initiate nociceptive signaling in the peripheral and central nervous systems. Their activation depends on the local mechanical environment of the joint and encodes the neural processes that initiate pain and lead to its persistence. This commentary reviews the complex anatomical, biomechanical, and physiological consequences of facet-mediated whiplash injury and pain. The clinical presentation of facet-mediated pain is complex in its sensory and emotional components. Yet, human studies are limited in their ability to elucidate the physiological mechanisms by which abnormal facet loading leads to pain. Over the past decade, however, in vivo models of cervical facet injury that reproduce clinical pain symptoms have been developed and used to define the complicated and multifaceted electrophysiological, inflammatory, and nociceptive signaling cascades that are involved in the pathophysiology of whiplash facet pain. Integrating the whiplash-like mechanics in vivo and in vitro allows transmission of pathophysiological mechanisms across scales, with the hope of informing clinical management. Yet, despite these advances, many challenges remain. This commentary further describes and highlights such challenges.