Curr Rev Musculoskelet Med (2009) 2:15–24 associated with pathology. However, Grogan et al. [33] examined 104 cadaveric facet joints for severity of carti- lage degeneration and found no association with facet tropism. They reported that the factors associated with sclerosis and cartilage degeneration of the facet joint were not facet tropism, but rather advanced age, spinal level, and increasingly coronal joint angles. However, other studies have linked degenerative spondylolisthesis to facet joints that have an increased sagittal orientation [34, 35]. Facet joints may also serve important proprioceptive functions. This is based on the presence of low threshold, mechanoreceptors lining the facet capsule. These receptors are similar to mechanosensitive neurons involved in pro- prioception of other peripheral joints [36, 37]. Radiographically, the facet joint may be visualized more clearly with oblique views. With this radiographic angle, the classic ‘‘Scotty dog’’ is visualized, allowing for easier recognition of anatomic landmarks. To review, the nose is formed by the transverse process; the eye formed by the pedicle, the neck is the pars interarticularis, the ear is formed by the superior articular process and the front leg formed by the inferior articular process (Fig. 2). The facet joint as a pain mediator In 1963, Hirsch et al. [38] injected 11% hypertonic saline in the region of the facet joints and provoked low back and thigh pain. Subsequently, facet joint-mediated pain was conﬁrmed with more speciﬁc studies involving direct intra- articular injections of hypertonic saline [39, 40]. In the study conducted by Mooney and colleagues, the intra- articular injection of saline was followed by the injection of local anesthetic. This obliterated the discomfort in all subjects tested [39]. Similar results were obtained with subsequent experiments that utilized intra-articular injec- tion of contrast to provoke pain through distention of the Fig. 2 Oblique view of the lumbar spine. SAP superior articular process, IAP inferior articular process, P pedicle 17 facet joint capsule [41]. The results of these earlier studies have been reproduced through experiments involving stimulation of not only facet joints but also the medial branches [42]. The development of facet joint-mediated pain involves both biomechanical and inﬂammatory components. Multi- ple factors can destabilize the facet joint and its capsule. Biomechanical model Intervertebral disc degeneration has been reported to be a source of low back pain in adults [43]. Studies have linked pathological changes in facet joints with preceding disc degeneration [44–46]. The intervertebral discs support most of the weight during ﬂexed postures but the facet joints bear an increasingly greater burden as the lumbar spine is ranged into extension. In addition to stabilizing the spine and guiding segmental motion, facet joints function as weight-bearing structures that support axial loading along with the intervertebral discs. Studies have shown that the facet joints can carry up to 33% of the dynamic axial load [47–49]. Disc degeneration with associated narrowing of the disc space alters the mechanical load distribution and may result in a degenerative cascade with increased mechanical stress on the facet joint and joint capsule. Within the active range of the lumbar spine, the paraspinal muscles act as the principal contributors to vertebral sta- bility. However, both cyclic and sustained ﬂexion movements decrease the reﬂexive muscle activity of the paraspinal muscles such as the multiﬁdus muscle [50–57]. In theory, this may result in increased laxity across the facet joint leading to both decreased stability and increased stress on the facet joint capsule [55]. The role of the facet joint capsule in stabilizing the motion characteristics of these joints cannot be understated. Studies have suggested that disc degeneration results in