Low back pain (LBP) remains a common musculoskeletal complaint, with a reported lifetime incidence of 60-90%. Various structures have been incriminated as possible sources of chronic LBP, including the posterior longitudinal ligament, dorsal root ganglia, dura, annular fibers, muscles of the lumbar spine, and facet joints. 
In 1911, Goldwaith first implicated the facet joints as a source of LBP. In 1933, Ghormley described the facet syndrome, and in 1941, Badgley endorsed the idea of the facets as the cause of LBP, based on pathomorphologic studies of the joint. [2, 3] Rees in 1972 and Shealy in 1974 accepted the notion and developed techniques in which the joint allegedly could be denervated to stop pain stemming from the facet joints. [4, 5]
In 1963, Hirsch and colleagues injected normal saline into facet joints, demonstrating that facet joints can produce LBP.  Systematic studies began in 1976, when Mooney and Robertson used fluoroscopy to confirm this location of intra-articular lumbar facet joint injections of normal saline in asymptomatic volunteers.  (Three years later, McCall and colleagues did the same.  ) These injections of normal saline caused back and lower extremity pain. In addition, Mooney and Roberts documented relief of low back and lower extremity pain in these patients after injection of local anesthetic into the provoked facet joints. A 1989 study by Marks demonstrated similar findings in patients with chronic LBP. 
In 1991, Kuslich and colleagues probed facet joint capsules in patients undergoing lumbar decompression surgeries and found that pain could be induced.  Many investigators developed techniques to diagnose facet joint pain using intra-articular joint blocks and medial branch nerve blocks, as well as ways to treat such pain with intra-articular steroids, surgical ablation, or radiofrequency (RF) denervation. Controversy continues regarding the true prevalence, most accurate diagnostic methods, and most efficacious treatment of symptomatic lumbar facet joints. 
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Bones of the spine articulate anteriorly by intervertebral disks and posteriorly by paired joints. The latter, formally known as zygapophyseal joints (but commonly termed facet joints), are true synovial joints, with a joint space, hyaline cartilage surfaces, a synovial membrane, and a fibrous capsule. Two medial branches of the dorsal rami innervate the facet joints. Medial branches of the lumbar dorsal rami issue from their respective intervertebral foramina, cross the superior border of the transverse process, and then run medially around the base of the facet joint before innervating the joints.
In studies, autonomic nerves and nociceptive, substance P–immunoreactive nerve fibers have been identified in the lumbar facet joint capsule and synovial folds. Douglas and colleagues identified substance P–immunoreactive nerve fibers in erosion channels that extended through the subchondral bone and calcified cartilage into the articular cartilage. Giles and Harvey identified them in the inferior recess capsule and synovial folds, whereas Ashton and coauthors found them running freely in the facet capsule stroma. [12, 13] Grönblad and colleagues demonstrated sparsely distributed substance P–immunoreactive nerve fibers in facet joint plical tissue. 
The presence of nociceptive nerve fibers in the various tissue structures of facet joints, as well as the existence of autonomic nerves there, suggests that these structures may cause pain under increased or abnormal loads. Substance P is a well-known inflammatory mediator that may sensitize nociceptors to them and other mediators, resulting in chronic pain.
Like other joints, the facet joints consist of bone, cartilage, synovial tissue, and menisci that are rudimentary invaginations of the joint capsule. In the synovial fluid of patients with rheumatoid arthritis, osteoarthritis, or traumatic joint disease, increased levels of prostaglandins have been measured and are implicated as an important cause of pain. Prostaglandin, a known inflammatory mediator, also is released from facet joints.
A study by Netzer et al indicated that in patients with facet joint osteoarthritis associated with lumbar spinal stenosis, the subchondral bone in the osteoarthritic facet joints is characterized by the infiltration of macrophage-rich tissues into the marrow and by enhanced de novo bone formation. 
Biomechanically, facet joints assume a prominent role in resisting stress, and their importance is well established. A cadaveric study by Adams and Hutton demonstrated that the facet joints resist most of the intervertebral shear force and share in resisting the intervertebral compressive force, albeit only in lordotic postures.  In the rotation of the spine, the facet capsular ligaments are the spinal ligaments that undergo by far the most strain. They protect the intervertebral disks by preventing excessive movement. 
The prevalence of facet joint pain in the general population or in persons with acute back pain has not been investigated. The reported rate of facet joint pain for patients with chronic low back pain (LBP) ranges from 4-75%. The reported prevalence seems to be a function of the size of the sample studied and the conviction of the authors.
Three studies report the prevalence of lumbar facet joint pain among chronic LBP patients based on 100% relief of pain using less than 2 mL of intra-articular diagnostic injection. In 1988, Jackson and colleagues reported that 7.7% of 454 patients with chronic LBP had 100% relief with diagnostic injection.  In 1991, Carette and coauthors reported that 11 (5.8%) of 190 patients experienced complete relief of symptoms with a single lidocaine injection.  In 1994, Schwarzer and colleagues reported that 7 (4%) of 176 patients reported 100% relief. [20, 21] This last study was the most stringent of the 3 because the authors performed a second confirmatory block with bupivacaine, documenting longer relief of pain commensurate with the longer half-life of the local anesthetic.
When less stringent criteria are used, higher prevalences of lumbar facet joint pain are reported. In 1988, Moran and colleagues reported relief in 9 (16.7%) of 45 patients using 1.5 mL of bupivacaine.  Pain provocation followed by pain relief with local anesthetic was used as the diagnostic criterion. In 1992, Schwarzer and co-investigators reported relief in 9 (9.8%) of 92 patients, using a 50% reduction of pain as the criterion and employing double-block screening with lidocaine and confirmatory bupivacaine block.  In a separate investigation, Schwarzer and colleagues reported a prevalence of 26 (15%) of 176 patients, using the same diagnostic criterion. [20, 21]
In another study, Schwarzer and coauthors reported that 23 (40.3%) of 57 patients obtained pain relief of 50% or more pain with bupivacaine but experienced no relief with saline control injection.  A 2004 study by Manchikanti and colleagues reported a 27% prevalence rate of lumbar facet pain, using controlled, comparative local anesthetic blocks of the dorsal medial nerves. 
Higher prevalence rates are reported when control blocks are not used. In 1984, Raymond and Dumas—using a strict intracapsular technique but no control block—reported a 16% prevalence rate.  In 1992, Revel and coauthors reported that 22 (55%) of 40 subjects had pain relief of 75% or more and that 17 (42.5%) of 40 patients had greater than 90% relief of their pain with a single intra-articular lidocaine injection. 
As seen from these data, reports of prevalence are a function of the investigators' choice of selection criteria. Studies requiring the most stringent criteria (100% relief of symptoms after a diagnostic block) report a 4-7.7% prevalence rate of facet joint pain among chronic LBP patients. Investigations using double blocks and requiring 50% relief report prevalence rates of about 10-15%. Numerous other studies using a single diagnostic block report prevalence rates of 16-75%.
In a sample of 472 South Korean adults, aged 20-84 years, Ko et al found the prevalence of lumbar facet osteoarthritis, as derived through multidetector computed tomography (MDCT) scanning, to be 17.58%. The prevalence increased with age. 
See also Frequency/United States.
No studies specifically address the mortality and morbidity of chronic back pain from facet joint – mediated pain. The mortality and morbidity of chronic low back pain, however, have been extensively addressed.
No studies have specifically addressed the correlation between the prevalence of facet-mediated chronic low back pain and race.
No studies have specifically addressed the male-to-female prevalence ratio of chronic, facet-mediated low back pain.
A higher prevalence among the older population would be expected if the etiology of facet joint–mediated back pain arose from degenerative changes of the joint, similar to the way it does in other osteoarthritic joint damage. One small study by Revel and colleagues and a larger investigation by Jackson and coauthors noted that older patients responded more commonly to diagnostic injections. [18, 27] The 1995 study by Schwarzer and colleagues involving 57 patients reported higher positive response rates in older patients (40%), even with the use of saline control injections.  They noted that the average age of patients was 59 years, which was higher than the average age in studies reporting much lower prevalence rates.
A 2008 report by Manchikanti et al looked at the rate of facet joint–related chronic low back pain in 424 patients, separated into 6 age groups.  According to their retrospective analysis, the prevalence ranged from 18% (in individuals aged 31-40 years) to 44% (in persons aged 51-60 years).
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