Idiopathic low back pain has confounded health care practitioners for decades. Although there has been much advance in the understanding of the biomechanics of the lumbar spine over the past 25 years, the cellular and neural mechanisms that lead to facet pain are not well understood. An extensive series of experiments was undertaken to help elucidate these mechanisms and gain a better understanding of lumbar facet pain. Biomechanic and neuroanatomic studies were performed in human cadaveric facet joints and neurophysiologic studies were performed in New Zealand White rabbits. These studies provide the following evidence to help explain the mechanisms of lumbar facet pain: (1) The facet joint can carry a significant amount of the total compressive load on the spine when the human spine is hyperextended. (2) Extensive stretch of the human facet joint capsule occurs when the spine is in the physiologic range of extreme extension. (3) An extensive distribution of small nerve fibers and free and encapsulated nerve endings exists in the lumbar facet joint capsule, including nerves containing substance P, a putative neuromodulator of pain. (4) Low and high threshold mechanoreceptors fire when the facet joint capsule is stretched or is subject to localized compressive forces. (5) Sensitization and excitation of nerves in facet joint and surrounding muscle occur when the joint is inflamed or exposed to certain chemicals that are released during injury and inflammation. (6) Marked reduction in nerve activity occurs in facet tissue injected with hydrocortisone and lidocaine. Thus, the facet joint is a heavily innervated area that is subject to high stress and strain. The resulting tissue damage or inflammation is likely to cause release of chemicals irritating to the nerve endings in these joints, resulting in low back pain.