Key Points
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Pathologic changes seen in facet joint degeneration include fibrillation, joint space narrowing, articular cartilage thinning, subchondral bone sclerosis, osteophytosis, and development of juxta-facet cysts.
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Risk factors for facet joint degeneration include lower spinal level, increasing age, sagittal orientation, and intervertebral disc degeneration.
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Facet tropism, gender, increasing body mass index, and ligamentum flavum abnormalities may also be risk factors for facet joint degeneration.
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Pathologic and imaging grading systems exist for grading facet joint degeneration, with moderate agreement between the different classifications.
Introduction
The facet joints, also known as zygapophysial or apophyseal joints, are synovial joints located in the posterior aspect of the vertebral column. The paired facet joints, along with the intervertebral disc (IVD) (see Chapter 1, Chapter 6 ) of the same vertebral level, comprise an entity that is called a spinal motion segment. Functioning in concert with the IVDs, the facet joints participate in the articulation of adjacent vertebrae, spinal load transmission, execution of physiological spinal motions, and stabilization of the vertebral column. The facet joints also play a protective role, in that they provide resistance against deleterious motions such as forward translation, and extreme flexion or extension. Over time, facet joints may undergo degenerative change as seen in other synovial joints, but there is no conclusive evidence of these pathophysiological changes in the facet joints are similar to in other joints. What matters is that these degenerative changes can significantly impact the biomechanical functions of the spine and lead to various spine pathologies such as scoliosis and spondylolisthesis (see Chapter 2, Chapter 3 ).
Anatomy
The lumbar facet joints are mesenchyme-derived, paired, diarthrodial sliding synovial joints that develop from the posterior vertebral arch and form the posterior aspect of the intervertebral foramina along with the ligamentum flavum (see Chapter 1 ) [ , ]. The facet joints are “true” synovial joints in that they are lined with articulating cartilage and are surrounded by a complete, ligamentous capsule. These joints contain two opposing articulating surfaces: a dorsomedially located concave superior facet and a dorsolaterally located convex inferior facet [ ].
Each facet joint is innervated by a medial descending branch from the dorsal ramus of the same spinal level, as well as a medial branch from the dorsal ramus of the vertebral level above [ , ]. The facet joints receive their blood supply from arterial branches of the lumbar segmental artery, which pass through the intervertebral foramina [ ]. Facet joints, along with their capsules, are extensively covered by nociceptors, free and encapsulated nerves, and substance-P carrying nerves [ ]. The rich innervation of the lumbar facet joints makes them a potential source of back pain [ ].
Multiple types of intraarticular inclusions called “meniscoids” or facet folds have been described in facet joints [ ]. Of the most commonly reported types of meniscoids found in facet joints, the first type constitutes fibrous invaginations of the dorsal and ventral portions of the facet joints, and the second type constitutes fat-filled synovial reflections arising from the superior and inferior poles of the facet joints [ ]. These structures, which have been hypothesized to function in covering areas within the facet joint not covered with articular cartilage and protecting the articular processes during flexion and extension, tend to be more fibrous in younger persons, and more of a fatty nature in older patients [ , ].
Biomechanical function of facet joints
As stated, the spinal facet joints and the IVDs are part of an entity called the spinal motion segment, the three-joint complex [ ], or the articular triad [ ]. Functioning together, the structures in the spinal motion segments allow for the execution of physiological spinal motions while protecting the spine by preventing activities that can be injurious. While the IVD is more involved in weight transmission and shock absorption, the spinal facet joints’ function is to aid in the stabilization of the motion segment through the prevention of forward translation and the restriction of rotation and flexion, spinal motion control, and protection of the neurovascular structures that are conveyed through the intervertebral foramina [ ].
Loads applied to the spine are transferred to the IVD anteriorly and the facet joints posteriorly, which transfer them through the spinal column. Greater loads are applied to the facet joints during spinal extension and axial rotation than during spinal flexion, with reports that facet joints can sustain approximately 33% of dynamic compressive loads [ ]. When the spine is in a normal erect position, the load applied to the lumbar spine is transmitted to, and is shared between the IVDs and facet joints.
Facet joint degeneration
As with other synovial joints, the facet joints undergo degenerative change over time. Such change seen in facet joints has been attributed to a variety of causes such as increasing age, repetitive stress, low-grade trauma, IVD degeneration, and extensive motion and loading conditions (see Chapter 2, Chapter 6 ). The degeneration of the lumbar facet joints can lead to spinal instability, which can result in spinal pathologies such as spondylosis, spondylolisthesis, and scoliosis, among others, and thus may be associated with low back pain (LBP).
Pathological changes associated with facet joint degeneration include fibrillation, joint space narrowing, articular cartilage thinning, subchondral bone sclerosis, hypertrophy of articular processes, vacuum jet phenomenon, osteophytosis, juxtafacet cysts, and joint capsule calcifications [ ]. Lewin et al. [ ] found that before the age of 45, minor articular cartilage changes were commonly seen. However, past that time point, more advanced changes in the articular cartilage, subchondral sclerosis, and osteophytosis were prevalent [ , ].
Some of the earliest degenerative changes that can be seen in facet joints are seen within the articular cartilage [ ] initially determined as a loss of facet joint space width. Over time, the organization of the collagen fibril network within the hyaline cartilage is lost, contributing to the early articular changes seen in facet joint degeneration, a phenomenon known as fibrillation [ ]. Fibrillation, which occurs secondary to the loss of matrix proteoglycan, leads to disruption and degradation of the collagen fibril structures [ ]. It starts more superficially and spreads to deeper levels with increasing erosion of the articulating cartilage [ ]. Microscopically, the fibrillated cartilage shows clefts or fissures that begin in the superficial layers and deepen as the cartilage is lost from the surface by tangential flaking, pitting, and grooving ( Fig. 14.1 ) [ , ].
Over time, the avascular articulating cartilage decreases, and the subchondral bone is exposed. Changes in the subchondral bone associated with cartilage and facet joint degeneration include hypervascularization, sclerosis, and eburnation [ , , ]. Using a novel validated MR-based technique, Duan et al. [ ] found that subchondral bone thickness increased caudally in the lumbar spine, and that superior facet subchondral bone was consistently thicker than inferior facet subchondral bone. In addition to subchondral bone changes, erosion of articulating cartilage can also lead to narrowing of the facet joint space width, which is a key measure of degradation in other synovial joints. Simon et al. found that in a cohort of healthy subjects ( n = 62) and LBP patients ( n = 34), the joint space width was smaller among the patients, with specific narrowing around the periphery of the facet joints [ ]. This study highlighted the fact that lumbar facet joint space narrowing was dependent on the spinal level and began in the third decade of life. A recent comparison between computed tomography (CT) and ultrasound confirmed that increasing age is associated with decreasing gap width [ ].
Osteophyte formation, bony projections that can grow from the margins of bone, can occur late in the process of facet joint degeneration [ , ], can greatly limit the range of motion, and have been implicated in back pain [ ]. Osteophytes occur commonly in the facet joints of older patients with facet joint degeneration [ , , , , ] but are less common than cartilage defects. Twomey and Taylor [ ] suggested that osteophyte formation may occur as a result of degenerating facet joints’ attempt to increase the load-bearing area to deal with the greater loads they experience over time. Otsuka et al. [ ] found that facet joint surface area increased with age and also credited this increase to larger load-bearing in the lower lumbar segments and facet joint degeneration. One study found that osteophyte formation of the lumbar facet joint typically occurred in areas with increased stress secondary to high axial lumbar rotation [ ]. This increased stress may lead to fibrous metaplasia of the dorsal capsule and subsequent osteophyte formation [ ].
The formation of juxtafacet cysts, which are extradural lesions, is also associated with facet joint degeneration. Juxtafacet cysts can occur at any spinal level; however, they are most prevalent at L4/L5 [ ]. Depending on their location, juxtafacet cysts have been identified as possible causes of LBP and radiculopathy [ ]. One study found that juxtafacet cysts were more frequently associated with coronally oriented and arthritic facet joints [ ]. The exact etiology of juxtafacet cyst formation is unknown; however, multiple mechanisms have been proposed. Some proposed mechanisms include synovial fluid extrusion from the joint capsule, latent growth of developmental rest, and myxoid degeneration [ ]. Juxtafacet cysts can arise when the synovium out-pouches through defects in the facet joint capsule or from mucinous degeneration of periarticular connective tissue [ ].
Factors that influence facet joint degeneration
Several factors, such as age, gender, body mass index (BMI), spinal level, tropism, orientation, IVD degeneration, and ligamentum flavum abnormalities have been associated with degenerative change in facet joints.
Spinal level
Facet joint degeneration has most frequently been reported at L4/L5 and L5/S1 [ ]. One hypothesis as to why this occurs is based on the differences in the orientation between the facet joints at the L4/L5 and L5/S1 vertebral levels. The L4/L5 level has a more sagittal orientation than L5/S1, which has a more stable, coronal orientation [ ]. Other factors adding to the increased stability of the L5/S1 facet joints include a greater angle [ ] between the pedicle and facet joint at this level, and increased support from the transverse processes and iliolumbar ligaments (see Chapter 12 ) [ , ].
Body mass index
The association between BMI and facet joint degeneration has not been very well characterized. The few existing studies looking at this association have yielded mixed results. One study, comparing the prevalence of facet joint degeneration in patients with and without spinal stenosis (see Chapter 13 ), found that facet joint arthrosis (i.e., osteoarthritis [OA]) was not related to BMI [ ]. Kalichman et al. [ ], using CT data from the Framingham study to evaluate intervertebral disc narrowing, facet joint OA, spondylolysis, spondylolisthesis, and spinal stenosis, found a significant association between obesity and facet joint OA, which was most pronounced at the L4-L5 level.
A more recent study looked at the association between obesity, using outer abdominal fat measurements with CT as a proxy for obesity, and facet joint OA on CT ( n = 620) [ ]. Results from this report indicated a significant association ( P = .01) between increasing amounts of outer abdominal fat and higher degrees of facet joint degeneration from L2 to S1 [ ]. Due to the mixed results of past studies and the paucity of longitudinal studies regarding BMI and facet joint degeneration, the relationship between facet joint degeneration and BMI remains unclear.
Tropism
Facet tropism is defined as the asymmetry of the left and right facet joint angles with respect to the sagittal plane, usually with one joint exhibiting a more sagittal orientation than the other ( Fig. 14.3 ). Researchers have used various methods to define facet tropism in past studies: some methods base their definition on bilateral angle difference (i.e., angle difference greater than 5 degrees [ , ], 8 degrees [ ], or 10 degrees [ , ]), some use standard deviation [ ], percentile of asymmetry [ ], and yet others use variation in intraobserver errors [ ]. This lack of consensus on the definition of tropism makes the comparison between studies rather a challenge.
However defined, numerically or structurally, facet joint tropism can alter the biomechanical function of the spinal motion segment, and accelerate the degeneration of spinal components. Like other factors that have been associated with facet joint degeneration, there are mixed data regarding the association between facet tropism and facet degeneration. While multiple studies have reported that there is no association between facet joint OA and tropism, other studies have yielded slightly different results [ ]. For example, one study in which 900 spinal motion segments from 300 subjects were analyzed showed that facet tropism was associated with the presence of high-grade facet joint degeneration at L4/L5 [ ]. Another study found that there was a significant association between asymmetric facet joint OA and facet tropism [ ]. Yet another study found that facet tropism was associated with a higher rate of progressive facet degeneration following total IVD replacement surgery [ ]. Some hypothesize that facet tropism is associated with higher rates of facet joint degeneration because asymmetry can lead to an imbalance in load transmission and subsequent degeneration of the components within the spinal motion segment. A recent study seeking association between degenerative spondylolisthesis and tropism found that in a large, multinational cohort in the Asia–Pacific region, tropism was present in 47%, 51%, and 31% of L3/L4, L4/L5, and L5/S1 levels, respectively, in patients with degenerative spondylolisthesis, with the nonspondylotic adjacent levels having also tropism in 33% and 50% of the cases [ ]. This initial report highlighted the need to evaluate the entire lumbar spine to detect early degenerative changes in the spine and gave rise to the concept of a developmental origin of facet joint tropism as well as the Samartzis et al. [ ] classification scheme for facet joint tropism.
Orientation
Normal facet joint orientation can vary depending on the spinal level of the facet joint. In the lumbar spine, the upper facet joints have more sagittal orientation that provides resistance against axial rotation. In the lower lumbar spine, the facet joints assume a more coronal orientation, which permits axial rotation while providing greater resistance against extreme flexion and shearing force. Studies conducted among various ethnicities found that sagittal facet orientation is significantly associated with facet joint OA [ , , ] and age [ ]. Due to the lack of longitudinal studies related to facet orientation and facet osteoarthritis, it has not been determined with certainty whether the sagittal orientation of the facet joint is a precursor for the development of facet joint OA or a result of pathological processes associated with facet joint OA. No gender differences in facet orientation have been reported [ ]. Depending on their location, a more sagittal or coronal orientation of the facet joint reduces the provision of resistance against spinal motion and forces encountered at any given spinal level, which over time may increase their susceptibility to degenerative change [ , ]. For example, if the facet joints of the upper lumbar spine are more coronally oriented, they are more prone to degenerative changes because, unlike more sagittal oriented facet joints, their ability to provide resistance against axial rotation is reduced. Conversely, if facet joints are oriented more sagittally than usual, this may be a potential mechanism to predispose the spine to the anterior–posterior displacement characteristically seen in spondylolisthesis, by allowing the superior vertebra to slip forward by an “overriding mechanism” over the inferior vertebra with a given disc level ( Fig. 14.2 ) [ , ].
The etiology of facet joint tropism has not been well studied. To address the lack of information regarding the development of facet tropism, Masharawi et al. [ ] investigated 544 thoracic and lumbar vertebrae from 32 individuals aged from 4 to 17 years from T1 to L5. For each vertebra, they measured intrafacet lateral height, superior facet concavity, inferior facet convexity, facet length, facet width, and transverse and sagittal facet angles using a coordinate measuring machine [ ]. The main findings from this study were that first, they did not find facet asymmetry in the lumbar regions; second, facet asymmetry was independent of age, and third, compared to right superior facets, the left superior facets in the thoracic region tended to be significantly more narrow, and have significantly smaller superior transverse and sagittal angles [ ]. One question that the researchers considered in this study was whether facet tropism was congenital or acquired. The researchers were unable to make a definitive statement due to the shortage of data for individuals younger than 4 years [ ] and it was not a longitudinal study. They hypothesized that facet joint tropism in the thoracic region occurred secondary to two types of forces: flexion forces experienced in utero when the fetus is forced into a flexed position due to space limitations, and rotational forces that originate from asymmetric upper extremity movement as children develop their hand preference [ ].
Ligamentum flavum abnormalities
The ligamenta flava are spinal ligaments that connect adjacent vertebrae by their laminae and function in maintaining an upright posture. Thickening and ossification of the ligamentum flavum may occur with increasing age. Increasingly researchers have been examining the association between ligamentum flavum hypertrophy and facet joint degeneration. One study looked at 2000 facet joints and 2000 ligamenta flava from 200 patients (100 males and 100 females) and found a strong positive association between ligamentum flavum thickness and facet joint degeneration [ ]. These results were corroborated by results from another study in which researchers also identified a close relationship between ligamentum flavum size and the presence and severity of degeneration of the facet joints and other posterior elements [ ]. Another study found that in patients with facet tropism the increased thickness of the ligamentum flavum was closely associated with more advanced degenerative facet joint change [ ].
Currently, it is difficult to determine whether facet joint degeneration is a direct result of ligamentum flavum hypertrophy or not. Munns et al. [ ] recently found an association between ligamentum flavum thickening, older age, lower lumbar level, and increased severity in disc degeneration. All of the abovementioned factors have also been associated with facet joint degeneration. Thus, longitudinal studies looking at ligamentum flavum thickening and facet joint degeneration will help to establish the true temporal relationship between the two pathological processes.
Gender
Data regarding whether there are gender-related associations with degenerative facet joint changes have been conflicting so far. In the past, some studies found that there was no significant association between sex and facet joint degeneration [ , ]. However, a cadaveric investigation reported a significant association between male gender and facet joint OA [ ]. Further studies found a significant association between female gender and facet joint degeneration [ , , ].
One hypothesis proposed for gender prevalence of facet joint OA may be related to the fact that facet cartilage is an estrogen-responsive tissue. In an immunochemical study of the lumbar facet joint tissues, Ha et al. [ ] found that there were estrogen receptors in the facet joint tissues, and increased estrogen receptor expression was associated with more severe facet joint degeneration. Another study that looked at cadaveric specimens of male and female lumbar spinal motion segments found that motion segments in females displayed greater degrees of extension, flexion, and lateral bending [ ]. As facet joints carry higher dynamic loads, the increased motion in female spinal segments may predispose females to degenerative changes of the facet joints.
Age
Many studies have confirmed a significant association between increasing age and degenerative facet joints [ , , , , , , , , ], as seen in other forms of joint degeneration. Lewin [ ] reported that degenerative changes were fairly rare before the fourth decade of life; however, multiple studies report that facet joint degeneration can be seen as early as the second decade of life [ , , ]. In a cadaveric study, Eubanks et al. [ ] found that 57% of the cadavers of persons aged 20–29 displayed facet joint degeneration. Tischer et al. [ ] also found significant degenerative changes in the articular cartilage in facet joints in persons under the age of 30. These findings were also corroborated by Gries et al. [ ], who found varying levels of cartilage destruction in individuals under the age of 40.
Disc degeneration
The IVD and paired facet joints that make up the spinal motion segment work together to accommodate spinal loads. Failure, injury, or degeneration of any one of the components of the spinal motion segment can lead to excessive load transmission to the other components and subsequent degeneration of those structures as well. Several studies have found that degenerative change in facet joints generally occurred after disc degeneration, and that facet joint degeneration was often seen at the levels of the degenerative discs [ , , ]. Disc degeneration leads to disc-space narrowing, which in turn greatly increases load transmission and forces sustained by the facet joints [ ]. In cases with a high degree of disc space narrowing, the facet joints may bear up to 70% of the axial load [ ].
Despite the previously mentioned and generally accepted evidence for IVD degeneration preceding facet joint degeneration, there have been studies with opposing results. For example, Videman et al. [ ] found that facet joint degeneration preceded degeneration of the IVD in 20% of male participants. On the other hand, Eubanks and coworkers [ ] found that while disc degeneration preceded facet joint degeneration in older patients, the opposite appeared to be true in younger patients.
Grading of facet joint degeneration
Over time, many different systems have been introduced to grade degenerative change in the facet joint. Kellgren et al. [ ] were one of the first to develop a system for grading degenerative changes in cervical facet joints using lateral radiographs. Initially, Kellgren et al. [ ] grading system was a four-item grading scale in which grade 1 indicated doubtful osteophytes on the margin of the articular facets, grade 2 definite detection of osteophytes and some subchondral sclerosis, grade 3 the presence of moderate-size osteophytes, subchondral sclerosis, and some irregularity of the articular facet, while grade 4 indicated the presence of many large osteophytes, severe subchondral sclerosis, and irregularity of apophysial joints. A few decades later, Cote et al. [ ] used a modified version of Kellgren’s grading system in which they added grade 0 to indicate the absence of facet joint degeneration. Although Kellgren’s grading system was seen as adequate for epidemiological research, they felt this system was not reliable for use in clinical outcomes research [ ]. However, a more recent study found that the modified Kellgren scale may be able to compensate for shortcomings of plain radiographs for detecting facet joint degeneration providing acceptable reliability [ ].
In 2006, Kettler and Wilke [ ] reviewed and analyzed existing grading for cervical and lumbar facet joint degeneration. In this review, researchers looked at 12 grading systems created to detect degenerative changes in lumbar facet joints using techniques such as macroscopic anatomy, histology, plain radiography, conventional tomography, computed tomography, and magnetic resonance imaging (MRI) (see Chapter 5 ). They reviewed four gradings to detect a degenerative change in cervical facet joints that were based on macroscopic anatomy and plain radiography findings. Out of 16 grading systems reviewed, four were recommended for use as they had kappa measures or intraclass correlation coefficient for interobserver reliability greater than 0.40 [ ]. These gradings will be discussed in the following paragraphs.
Pathria et al. [ ] system was developed from a 1987 study in which two radiologists graded facet joints from the L3/L4, L4/L5, and L5/S1 levels using a 4-point scale on oblique radiographs, as well as CT scans. On this 4-point scale, a score of 0 indicated a normal facet joint, a score of 1 indicated narrowing of the facet joint (mild degeneration), a score of 2 indicated that there was narrowing of the facet joint and sclerosis or hypertrophy (moderate degeneration), and a score of 3 indicated that there was severe OA of the facet joint with narrowing, sclerosis and osteophyte formation [ ]. After each radiologist graded the facet joint radiographs and CT scans, interobserver and kappa values were calculated independently for both imaging methods. One conclusion of this study was that oblique radiographs were insufficient to identify mild or early degeneration of the facet joints; however, their sensitivity increased with more severe degeneration [ ].
Fujiwara et al. [ ] are credited with developing the standard MRI-based classification system for lumbar facet joint OA. The authors studied 14 consecutive patients with disc degeneration who were candidates for lumbar spine surgery. Spin-echo T1-weighted axial images and bone window CT images ( Fig. 14.4 ) were scored as in Pathria’s study [ ]. In contrast to the previous facet grading studies that used radiologists as the primary clinical raters, Fujiwara used two orthopedic surgeons to grade the MRI images. There was substantial interobserver agreement in 76% of the 82 joints studied with a calculated kappa value of 0.64 [ ].
