Severity Of Facet Joint Osteoarthritis Research Articles

Rates and risk factors of intrapedicular accuracy and cranial facet joint violation among robot-assisted, fluoroscopy-guided percutaneous, and freehand techniques in pedicle screw fixation of thoracolumbar fractures: a comparative cohort study

BackgroundRobot-assisted (RA) technique has been increasingly applied in clinical practice, providing promising outcomes of inserting accuracy and cranial facet joint protection. However, studies comparing this novel method with other assisted methods are rare, and the controversy of the superiority between the insertion techniques remains. Thus, we compare the rates and risk factors of intrapedicular accuracy and cranial facet joint violation (FJV) of RA, fluoroscopy-guided percutaneous (FP), and freehand (FH) techniques in the treatment of thoracolumbar fractures.MethodsA total of 74 patients with thoracolumbar fractures requiring pedicle screw instruments were retrospectively included and divided into RA, FP, and FH groups from June 2016 to May 2020. The primary outcomes were the intrapedicular accuracy and cranial FJV. The factors that affected the intrapedicular accuracy and cranial FJV were assessed using multivariate analyses.ResultsThe optimal intrapedicular accuracy of pedicle screw placement (Grade A) in the RA, FP, and FH groups was 94.3%, 78.2%, and 88.7%, respectively. This finding indicates no significant differences of RA over FH technique (P = 0.062) and FP technique (P = 0.025), but significantly higher accuracies of RA over FP (P < 0.001). In addition, the rates of proximal FJV in RA, FP, and FH groups were 13.9%, 30.8%, and 22.7%, respectively. RA had a significantly greater proportion of intact facet joints than the FP (P = 0.002). However, FP and FH (P = 0.157), as well as RA and FH (P = 0.035) showed significantly similar outcomes with respect to the proximal FJV. The logistic regression analysis showed that FP technique (OR = 3.056) was independently associated with insertion accuracy. Meanwhile, the age (OR = 0.974), pedicle angle (OR = 0.921), moderate facet joint osteoarthritis (OR = 5.584), and severe facet joint osteoarthritis (OR = 11.956) were independently associated with cranial FJV.ConclusionRA technique showed a higher rate of intrapedicular accuracy and a lower rate of cranial FJV than FP technique, and similar outcomes to FH technique in terms of intrapedicular accuracy and cranial FJV. RA technique might be a safe method for pedicle screw placement in thoracolumbar surgery.Level of evidence3

Characterization of spontaneous facet joint osteoarthritis

Purpose: Although rodent models of traumatically or chemically induced spinal facet joint osteoarthritis (FJOA) were previously described, animal models of typical spontaneous FJOA haven’t been documented. This study aimed to identify the characteristics of murine spontaneous FJOA and its molecular mechanisms. Methods: The lumbar facet joints of mice bearing mutant NFAT1 alleles and of wild-type (WT, control) mice were examined by histopathology, quantitative gene expression, immunohistochemistry, and histomorphometry using a novel FJOA scoring system at 2, 6, 12, and 18 months of age. The reproducibility of the FJOA scoring system was confirmed by inter-observer and intra-observer variability tests. Tissue-specific histomorphometric and gene expression changes were statistically analyzed. Results: NFAT1-mutant facet joints displayed dysfunction of articular chondrocytes and synovial cells with aberrant gene and protein expression in cartilage and synovium as early as 2 months. osteoarthritic structural changes such as articular surface destruction and chondro-osteophyte formation became evident in NFAT1-mutant facet joints at 6 months. Severe FJOA changes including deeper cartilage loss, synovial thickening, separation of cartilage from thickened subchondral bone, as well as tissue-specific molecular and cellular alterations were evident in NFAT1-mutant mice at 12 and 18 months. OA-like structural changes were not detected in WT facet joints at any ages, though aging-related cartilage degeneration was observed at 18 months. Conclusions: This study characterized a novel murine model of spontaneous FJOA and developed the first FJOA scoring system. The age- and tissue-specific molecular and cellular characteristics in the NFAT1-mutant facet joints have provided new insights into the pathogenetic mechanisms for initiation and progression of spontaneous FJOA.

Transcription factor NFAT1 deficiency causes lumbar facet joint osteoarthritis in mice

Purpose: Facet joint osteoarthritis (FJOA) is widely prevalent in middle-aged and older populations and is thought to be a common cause of back pain. The etiopathogenesis of FJ OA remains unclear. NFAT1 (NFATc2) is a member of the family of nuclear factor of activated T cells (NFAT/Nfat) transcription factors. Previous studies revealed that mice with a global deletion of the Nfat1 gene displayed osteoarthritic changes in appendicular synovial joints. However, whether NFAT1 deficiency affects synovial joints of the spine remains unknown. This study aimed to test our hypothesis that NFAT1 deficiency causes FJOA in mice because NFAT1 is essential for maintaining homeostasis of articular cartilage and synovium of the facet joints. Methods: Lumbar spine tissue samples were harvested from Nfat1 knockout (Nfat1-/-) mice and wild-type (WT) mice as negative controls at the age of 2, 6, and 12 months for histopathological and molecular biological analyses. L3-S1 lumbar spine samples were fixed in 2% paraformaldehyde. Tissue sections prepared with decalcification and embedded in paraffin were used for safranin-O and fast green staining to identify cartilage cells and matrices. Hematoxylin and Eosin (H&E) staining was performed for structural/cellular analysis of bone and soft tissues. Total RNA isolated from articular cartilage and synovium (with a thin layer of fibrous capsular tissue) of L3-S1 facet joints were reverse-transcribed for gene expression analysis using quantitative real-time RT-PCR (qPCR). All animal procedures were approved by the Institutional Animal Care and Use Committee. Statistical analyses were performed with the Student t-test and ANOVA. Results: At 2 months of age, the intensity of safranin-O staining (for proteoglycans) in articular cartilage of the lumbar facet joints was substantially reduced in Nfat1-/- mice, compared to that of the WT mice. OA-like structural changes (e.g. articular surface fibrillations/clefts and osteophyte formation) were not evident. At 6 months, mild to moderate OA structural changes occurred in the lumbar facet joints of Nfat1-/- mice, but not in WT mice. At 12 months, severe OA structural changes were observed in the lumbar facet joints of Nfat1-/- mice, but not in WT mice. Subchondral bone changes were not remarkable in the Nfat1-/- facet joints at any time points. qPCR gene expression analysis demonstrated significantly decreased expression of mRNA for aggrecan (Acan) with significantly increased expression of mRNA for interleukin-1β (Il1b) in the Nfat1-/- facet joint cartilage at 2 months. Significantly decreased expression of mRNA for collagen-II (Col2a1) and significantly increased expression of mRNAs for collagen-10, matrix metalloproteinase-3 (Mmp3), a disintegrin and metalloproteinase with thrombospondin motifs-5 (Adamts5), Il1b, and β-catenin (Ctnnb1) was detected in the Nfat1-/- facet joint cartilage at 6 and 12 months. Gene expression analysis of the synovial-capsular tissues revealed significantly increased Tnfa mRNA at 2 months and significantly increased Mmp3 and Adamts5 at 6 and 12 months. No sex differences were identified in the histological or gene expression analyses. Conclusions: The present study demonstrated for the first time that NFAT1 deficiency causes severe FJOA in mice. FJOA in the Nfat1-deficient mouse model initiates with increased expression of proinflammatory cytokines in articular cartilage and synovium, suggesting that inflammation may play an important role in the initiation stage of NFAT1 deficiency-induced FJOA in mice. These results support our hypothesis that NFAT1 deficiency causes FJOA through dysfunction of both articular chondrocytes and synovial cells.

Association between lumbar disc herniation and facet joint osteoarthritis

BackgroundThis study was performed to investigate the association between lumbar disc herniation (LDH) and facet joint osteoarthritis (FJOA) using magnetic resonance imaging (MRI).MethodsBetween March 2012 and September 2018, a total of 441 segments from 394 patients with LDH were included in the study. LDH was classified according to the Michigan State University (MSU) classification, in which the degree of LDH is divided into 3 levels (expressed as 1, 2, and 3) and the location of LDH is divided into 4 zones (described as A, AB, B, and C). Bilateral FJOA was graded from 0 to 3 using the criteria introduced by Weishaupt et al., and bilateral facet orientations were measured on axial MRI slices. A mixed-effects ordinal logistic regression model was utilized to determine the potential factors that may be associated with FJOA, including sex, age, body mass index (BMI), segment, facet orientation and tropism, and the degree and location of LDH.ResultsIn general, the prevalence of FJOA (grade ≥ 2) was 66.2% in LDH segments. For both the left and right sides, the degree of LDH was associated with the severity of FJOA (p < 0.01). Age and BMI were also associated with the severity of left and right FJOA (p = 0.002 and p < 0.001 for age, p < 0.001 and p = 0.003 for BMI, respectively), while segment, facet orientation, and facet tropism were not (p > 0.05 for all). Notably, MSU-B LDH was associated with greater odds of having more severe FJOA on the herniation side (left: p < 0.001, odds ratio (OR) = 2.714, 95% confidence interval (CI) = 1.583~4.650; right: p = 0.003, OR = 2.615, 95% CI = 1.405~4.870). However, other locations of LDH were not associated with the severity of FJOA (p > 0.05 for all).ConclusionsBoth the degree of LDH and MSU-B LDH are associated with the severity of FJOA. The association between LDH and FJOA highlights the complexity of the etiology of FJOA.

Outcome of intra-articular lumbar facet joint corticosteroid injection according to the severity of facet joint arthritis.

Lumbar facet joint osteoarthritis (FJOA) caused by degenerative change(s) is considered to be the main cause of facet joint-origin low back pain (LBP). Intra-articular lumbar facet joint (IA LFJ) corticosteroid injection is widely used for controlling pain induced by FJOA. In the current study, the outcomes of IA LFJ corticosteroid injection were evaluated according to the severity of FJOA. A total of 50 patients who received IA LFJ corticosteroid injections for the treatment of LFJ pain were recruited. Patients were classified into three groups according to the severity of FJOA, which was indicated during a lumbar axial MRI. A total of 10 patients were assigned to group A (patients with mild FJOA), 27 to group B (patients with moderate FJOA) and 13 to group C (patients with severe FJOA). Pain intensity was evaluated using a numerical rating scale (NRS) prior to treatment and at 1, 2 and 3 months after treatment. A total of 26 (52%) patients experienced successful treatment outcomes (defined as >50% reduction in NRS score at 3 months). Patients in all groups demonstrated a significant decrease in NRS scores at 1, 2 and 3 months after IA LFJ corticosteroid injection compared with the pre-treatment score (P<0.001). However, the effect of IA LFJ corticosteroid injection was not significantly different among the three groups (P=0.889). The results demonstrated that facet joint-origin LBP was significantly reduced after IA LFJ corticosteroid injection, regardless of the severity of FJOA. The results of the current study indicated that IA LFJ corticosteroid injection is a beneficial clinical option for managing LBP caused by FJOA.

Identification of microRNA-181A-5P and microRNA-4454 as mediators of facet cartilage degeneration through the activation of zinc finger protein 440 mediated NF-KB signaling pathway and potential circulating biomarkers for detecting the severity of facet joint osteoarthritis in blood

Purpose: Osteoarthritis (OA) of the spine (facet joints, FJ) is one of the major causes of severe low back pain and disability worldwide. However, specific mechanisms associated with facet cartilage degeneration during FJ OA are largely unknown. For the first time, in this study we aimed to investigate the role of microRNAs (miRNAs) in the pathophysiology of facet cartilage degeneration during FJ OA and the potential as biomarkers for detecting and determining the severity of FJ OA in human blood plasma. Methods: Based on MRI grading (by Weishaupt et al) and histopathology, we first established and validated a patient cohort (n = 203) (Group 1 patients [control group]: normal or mild facet cartilage degeneration and Group 2 patients [FJ OA group]: moderate to severe facet cartilage degeneration). Using this large and unique cohort, we screened 2,100 miRNAs using miRNA-array and differentially regulated the expressions of miRNAs in facet cartilage. miRNAs were further tested by qPCR analysis and their correlation with FJ OA severities were evaluated based on MRI grading score (grade 0; normal, grade 1; mild, grade 2; moderate and grade 3; severe). Human FJ OA chondrocytes were cultured and transfected with miRNA enhancers/inhibitors (or control enhancer/inhibitor) with/without interleukin (IL)-1β to determine the effect of miRNA enhancement/inhibition on the expression of catabolic (MMP13)/inflammatory (IL6, MCP1, TNFA)/anabolic (COL2A1)/cell death (PARP p85) markers by qPCR and western blot analysis. Target genes and signaling pathways modulated by miRNAs were also identified using mirDIP/pathDIP. Furthermore, we injected the miR-181a-5p in-vivo mimic (enhancer) into FJs of rats to see the effect of the overexpression in animal FJ cartilage. Finally, we tested the expression of two miRNAs in human blood plasma obtained from patients with various FJ OA severities (from grade 0 to grade 3) using qPCR analysis to identify any correlations between the circulating levels of two miRNAs in human blood plasma and FJ OA severity based on MRI grading. Results: Out of 2,100 miRNAs, we specifically identified 2 miRNAs (miR-181a-5p and miR-4454) whose expression were markedly up-regulated in FJ OA cartilage compared to control facet cartilage. Our data from patients with varying degrees of FJ OA disease severity showed that the expression levels of miR-181a-5p and miR-4454 in human facet cartilage were markedly elevated with increased degeneration and exhibited significant correlation with clinical disease severity based on MRI grading. We then treated FJ OA chondrocytes with miR-181a-5p or miR-4454 enhancer/inhibitor and showed that treatment with miR-181a-5p or miR-4454 enhancer significantly elevated the expression of inflammatory (IL6, MCP1, TNFA)/catabolic (MMP13)/cell death (PARP p85) markers and reduced expression of type II collagen (COL2A1). Inhibition of these two miRNAs was able to reverse these destructive effects compared to control enhancer/inhibitor in facet chondrocytes treated with IL-1β. Our study using mirDIP/pathDIP also identified that in facet cartilage both miR-181a-5p and miR-4454 signal zinc finger protein 440 (ZNF440) via modulation of the NF-κB pathway. Induction of NF-κB signaling using IL-1β treatment elevated miR-181a-5p and miR-4454 expression, which mediated a feedback loop to sustain NF-κB signaling through ZNF440 expression. FJ OA chondrocytes co-transfected with miR-181a-5p or miR-4454 mimic (or control mimic) and ZNF440 siRNA (or control siRNA) regulated phosphorylation of Ser536 NF-κB-p65 and reduction of IκB expression compared to control. Furthermore, by injecting miR-181a-5p in vivo-mimic (enhancer) in rat FJs, we observed a FJ OA phenotype in facet cartilage associated with enhanced catabolic activity and chondrocyte apoptosis in vivo. Finally, we determined that circulating forms of miR-181a-5p and miR-4454 in human blood plasma were sufficiently detectable and elevated in patient blood plasma with increased degree of FJ OA severity based on MRI grading. Conclusions: Using clinical, in vitro functional and in vivo studies, we have uniquely identified miR-181a-5p and miR-4454 as active players of facet cartilage degeneration during FJ OA through the activation of ZNF440-mediated NF-κB signaling pathway and potential circulating biomarkers in human blood plasma for detecting and determining the severity of FJ OA.

Identification of microrna-181a-5p and microrna-4454 as mediators of facet cartilage degeneration through the activation of zinc finger protein 440 mediated nf-kb signaling pathway and potential circulating biomarkers for detecting the severity of facet joint osteoarthritis in blood

Identification of microrna-181a-5p and microrna-4454 as mediators of facet cartilage degeneration through the activation of zinc finger protein 440 mediated nf-kb signaling pathway and potential circulating biomarkers for detecting the severity of facet joint osteoarthritis in blood

Asymmetric Facet Joint Osteoarthritis and Its Relationships to Facet Orientation, Facet Tropism, and Ligamentum Flavum Thickening

The degrees of osteoarthritis of the left and right facet joints were evaluated by using computerized tomography among elderly patients with low back or leg pain. To reveal the phenomenon of asymmetry regarding facet joint osteoarthritis (FJOA) in old patients and establish its relationships to spinal level, facet orientation, facet tropism and ligamentum flavum (LF) thickening. There were few reports regarding left-right asymmetry among severity of FJOA and its relationships to spinal level, facet orientation, facet tropism, and LF thickening remained unclear. The grade of bilateral FJOA was evaluated using 4-grade scale on computerized tomography images at the L3-4, L4-5, and L5-S1 levels of patients with age ranging from 60 to 80 years. All subjects were divided into 2 groups: symmetric FJOA group (FJOA I-II on both sides or FJOA III-IV on both sides) and asymmetric FJOA group (FJOA I-II on one side and FJOA III-IV on the other side). The relationships of FJOA to spinal level, facet orientation, facet tropism, and LF hypertrophy were evaluated. No association between asymmetric FJOA and spinal level was noted (P>0.05). In asymmetric FJOA group, significant difference in facet orientation between 2 sides was observed at the L4-5 (P=0.018) and L5-S1 levels (P=0.033). Compared with symmetric FJOA, asymmetric FJOA showed significant difference in prevalence of facet tropism at the L5-S1 level (P<0.001). The LF showed significantly thicker on the side of FJOA III-IV than the side of FJOA I-II at each level in asymmetric FJOA group (P<0.05). However, no difference was found in thickness between 2 sides in symmetric FJOA group (P>0.05). Asymmetric FJOA is associated with facet orientation and tropism, but not with spinal level. There is a close relationship between severity of FJOA and LF thickness.

Histopathological Features of Facet Osteoarthritis in Patients with Lumbar Spinal Stenosis

Introduction Lumbar spinal stenosis (LSS) is a degenerative, age-related narrowing of the lower spinal canal that causes pressure on the nerves, leading to pain and reduced mobility. Hypertrophy of ligament flava and facet joints combined with disc protrusions are a causative for LSS. Osteoarthritic changes to the facet joint, including joint space narrowing, subchondral cysts and osteophyte formation are commonly detected using magnetic resonance imaging (MRI) and computed tomography (CT) scanning. However, the pathomechanisms of facet joint osteoarthritis (OA) at a cellular and molecular level are poorly understood and have been scarcely studied. In this study we sought to investigate the histological features and to uncover cellular pathomechanisms of facet joint OA. Material and Methods Fifteen patients undergoing surgical decompression due to degenerative LSS were included in this study (9 female/6 male, median age 66, range 49–85). Routine preoperative X-ray and MRI scanning of the lumbar spine was performed in all subjects. Severity of facet joint OA was assessed in MRI images using the Weishaupt grading system for the lumbar spine. The medial portion of facet joints was collected during surgical decompression of the spinal canal and processed for tissue histology. Tissue morphology was evaluated using haematoxylin and eosin (HE), Safranin-O and van Gieson's stains. The presence of macrophages, blood vessels and nerve fibers was investigated using immunohistological staining for their respective markers CD68, CD34 and PGP9.5. Functional osteoclasts were visualized using tartrate-resistant acid phosphatase (TRAP) staining. Subchondral bone area fraction (B.Ar/T.Ar) was determined using the ImageJ-plugin BoneJ. Results OA was evident in MRI images characterized by joint space narrowing, bone edema and cysts and hypertrophy of articular processes. The severe OA phenotype in facet joints from LSS patients was confirmed at a histological level by complete loss of proteoglycan staining, CD34+ vessel penetration, and fissuring of cartilage tissue. Subchondral B.Ar/T.Ar ranged between 0.6 and 0.8. In all samples, subchondral marrow spaces contained CD34+ blood vessels and CD68+ mononuclear macrophages. CD68+ multinucleated osteoclasts were detected in resorption pits at the bone surface in 80 percent of the patients. Functionality of osteoclasts was confirmed by positive staining of multinucleated bone cells for TRAP in serial sections. Osteoblast activity was demonstrated in 60 percent of the patients and predominantly characterized by large areas of intramembranous bone formation near the osteochondral junction. Formation of an osteoclast-rich pannus-like tissue was seen in one sample. Innervation of subchondral marrow spaces by PGP9.5-positive nerve fibers was scarce and exclusively found in the vicinity of arterioles. Conclusion Facet joints in LSS patients display radiological and histopathological features of OA. Two major OA phenotypes can be distinguished based upon cellular pathomechanisms in subchondral bone tissue: 1) osteoblast-rich intramembranous bone formation and 2) osteoclast/macrophage rich remodeling. Osteoimmunological mechanisms, specifically the interaction of CD68+ macrophages with bone-resident cells, play a – previously unknown – role in regulating subchondral bone sclerosis in progressive osteoarthritis. Targeting osteoimmunology might hold potential as a disease-modifying treatment for osteoarthritis.

Analysis of the Relationship between Ligamentum Flavum Thickening and Lumbar Segmental Instability, Disc Degeneration, and Facet Joint Osteoarthritis in Lumbar Spinal Stenosis.

Study DesignCross-sectional study.PurposeTo investigate the relationship between ligamentum flavum (LF) thickening and lumbar segmental instability and disc degeneration and facet joint osteoarthritis.Overview of LiteraturePosterior spinal structures, including LF thickness, play a major role in lumbar spinal canal stenosis pathogenesis. The cause of LF thickening is multifactorial and includes activity level, age, and mechanical stress. LF thickening pathogenesis is unknown.MethodsWe examined 419 patients who underwent computed tomography (CT) myelography and magnetic resonance imaging after complaints of clinical symptoms. To investigate LF hypertrophy, 57 patients whose lumbar vertebra had normal disc heights at L4–5 were selected to exclude LF buckling as a hypertrophy component. LF thickness, disc space widening angulation in flexion, segmental angulation, presence of a vacuum phenomenon, and lumbar lordosis at T12–S1 were investigated. Disc and facet degeneration were also evaluated. Facet joint orientation was measured via an axial CT scan.ResultsThe mean LF thickness in all patients was 4.4±1.0 mm at L4–5. There was a significant correlation between LF thickness and disc degeneration; LF thickness significantly increased with severe disc degeneration and facet joint osteoarthritis. There was a tendency toward increased LF thickness in more sagittalized facet joints than in coronalized facet joints. Logistic regression analysis showed that LF thickening was influenced by segmental angulation and facet joint osteoarthritis. Patient age was associated with LF thickening.ConclusionsLF hypertrophy development was associated with segmental instability and severe disc degeneration, severe facet joint osteoarthritis, and a sagittalized facet joint orientation.

Preliminary Results of Minimally Invasive Decompression, TLIF and Percutaneous Pedicle Screw Insertion in Stenotic Spondylolisthesis with Severe Facet Joint Osteoarthritis

Object: Minimally invasive spine (MIS) procedures are increasingly being recognized as equivalent to open procedures with regard to clinical and radiographic outcomes. These techniques are also believed to result in less pain and disability in the immediate postoperative period. There are, however, little data to assess whether these procedures in combination with minimally invasive transforaminal interbody fusion (MI-TLIF) and percutaneous pedicle screw insertion are effective in complex cases of stenotic degenerative spondylolisthesis with severe facet joint osteoarthritis (FJO). Methods: This study retrospectively reviewed all patients who underwent lumbar instrumentation, fusion and decompression for degenerative spondylolisthesis with severe stenosis and facet joint osteoarthritis (FJO) between June 2010 and June 2011. Blood loss, operative time and intraoperative complications were assessed in all surgically treated patients who were treated with MIS decompression, MI-TLIF and percutaneous transpedicular instrumentation. Clinical outcome was measured using the Oswestry Disability Index (ODI) and Visual Analogue Scale (VAS) for back pain, leg pain, and activity level. Satisfaction was assessed with VAS for satisfaction. Radiological follow-up includes x-ray films, computed tomography and in some cases magnetic tomography scan. Results: Twenty four cases with severe stenotic changes accompanied by severe FJO were treated with minimally invasive procedure. The minimum follow-up was 6 months with a mean of 8 months. The mean preoperative ODI score was 46.8, decreasing to a mean of 23 postoperatively. The mean VAS leg and back pain scores were 67.5 improving to means of 25.8. Twenty one out of 24 cases experienced a clinical benefit according to VAS for satisfaction and ODI. Complications included wound healing disturbance (4%), CSF fistula (4%) and contralateral radiculopathy due to articular bone spurs (8%). The accuracy of pedicle screws was high and only one revision surgery was performed. Conclusion: MIS for severe stenotic spondylolisthesis leads to adequate and safe decompression of lumbar stenosis and results in a highly significant reduction of symptoms and disability. MIS-TLIF and percutaneous pedicle screw insertion constitute a promising treatment alternative for patients with severe stenosis and facet joint osteoarthritis.

Association between disc degeneration and degenerative spondylolisthesis? Pilot study

The aim of this pilot study was to test the generally believed hypothesis that intervertebral disc degeneration is a prerequisite for degenerative spondylolisthesis (DS). This cross-sectional study was an ancillary project to the Framingham Study. A sample of 3529 participants aged 40-80 years had a CT scan performed to assess aortic calcification. 188 individuals were randomly enrolled in this study. The prevalence of intervertebral disc narrowing, facet joint osteoarthritis (FJOA) and DS were evaluated. We used the multiple logistic regressions to evaluate the association between DS as a dependent variable and FJOA, disc narrowing, age, sex and BMI as independent variables. There were 23 individuals (24 spinal segments) affected by DS (15 female, 8 male), mean age 62.0 +/- 6.8 years. In segments with DS, FJOA was observed and rated "severe" at 20 (83.3%) segments, "moderate" at 3 (12.5%) levels, and "mild" at 1 (4.2%) level. Intervertebral disc height was normal in 6 (25.0%), slightly decreased in 6 (25.0%), moderately decreased in 5 (20.8%) and severely decreased in 7 (29.2%) of the segments. Three (12.5%) segments with DS had severe FJOA but no apparent disc degeneration. In 9 (37.5%) segments with DS we found no or mild disc degeneration and severe FJOA. In a multiple regression analysis age, sex and FJOA, but not disc narrowing, showed significant associations with DS. The results of our study did not support the theory that disc degeneration necessarily precedes vertebral subluxation in DS.

Synovial cysts of the lumbar facet joints in a symptomatic population: prevalence on magnetic resonance imaging.

A retrospective review of 303 MRI scans of the lumbar spine was conducted. To determine the prevalence of lumbar facet joint synovial cysts arising from the joints anteriorly and posteriorly. To examine the association of these cysts with facet joint osteoarthritis and degenerative disc disease. Sporadic reports of such cysts exist as do limited studies describing the prevalence of symptomatic anterior facet joint synovial cysts. However, the overall prevalence of lumbar facet joint synovial cysts has not been formally studied, and the mechanism of formation of these cysts is not fully understood. One observer undertook a review of MRI of the lumbar spine from one facility in a series of 303 patients referred mostly for back pain or radiculopathy. The presence of lumbar facet joint synovial cysts, their relationship to the facet joint, the degree of associated facet joint osteoarthritis, the presence of spondylolisthesis, and the degree of associated disc degeneration were recorded. Seven anterior cysts (prevalence = 2.3%) were identified, only two of which did not clearly cause nerve root compression. Twenty-three posterior cysts in 22 patients (prevalence = 7.3%) were identified. Statistically significant associations with increased frequency and severity of facet joint osteoarthritis and with spondylolisthesis were demonstrated compared to patients without cysts. Both anterior and posterior lumbar facet joint synovial cysts are rare. Posterior cysts are more common than anterior cysts. Both types of cysts are related to facet joint osteoarthritis but not to disc disease.

Orientation and Osteoarthritis of the Lumbar Facet Joint

Several studies have shown an association between sagittal orientation of the facet joint and degenerative spondylolisthesis. There is currently no information available on the association between orientation of the facet joint and osteoarthritis. This study examined the association between orientation and osteoarthritis of the lumbar facet joints. One hundred eleven consecutive patients underwent plain radiography and magnetic resonance imaging. These patients were divided into two groups: No Degenerative Spondylolisthesis Group (98 patients) and Degenerative Spondylolisthesis Group (13 patients). In the No Degenerative Spondylolisthesis Group, segments with higher grades of osteoarthritis showed more sagittal orientation of the facetjoints at the L3-L4 and L4-L5 levels. The facet joint was oriented significantly more sagittally in the Degenerative Spondylolisthesis Group than in the No Degenerative Spondylolisthesis Group at the L4-L5 and L5-S1 levels. The severity of facet joint osteoarthritis was significantly higher in the Degenerative Spondylolisthesis Group than in the No Degenerative Spondylolisthesis Group at the L3-L4, L4-L5, and L5-S1 levels. A significant association was found between sagittal orientation and osteoarthritis of the lumbar facet joints, even in patients without degenerative spondylolisthesis. Facet joint osteoarthritis, rather than spondylolisthesis, is the pathoanatomic feature that is associated with sagittal orientation of the facet joints in patients with degenerative spondylolisthesis.

The relationship between facet joint osteoarthritis and disc degeneration of the lumbar spine: an MRI study.

The role of MRI in assessing facet joint osteoarthritis is unclear. By developing a grading system for severity of facet joint osteoarthritis on MRI, the relationship between disc degeneration and facet joint osteoarthritis was determined. The accuracy of MRI in assessing facet joint osteoarthritis against CT was 94%. Under 40 years of age, the degree of disc degeneration varied among individuals. Over the age of 60, most of the discs were markedly degenerated. Under 40 years of age osteoarthritic changes in facet joints were minimal. Over the age of 60, variable degrees of facet joint osteoarthritis were observed but some facets did not show osteoarthritis. No facet joint osteoarthritis was found in the absence of disc degeneration and most facet joint osteoarthritis appeared at the intervertebral levels with advanced disc degeneration. Disc degeneration is more closely associated with aging than with facet joint osteoarthritis. The present study supports the hypothesis that "disc degeneration precedes facet joint osteoarthritis", and also supports the concept that it may take 20 or more years to develop facet joint osteoarthritis following the onset of disc degeneration.