An array of different MRI (magnetic resonance imaging) based grading systems is used to measure disc degeneration (DD) in the lumbar spine. It is currently unclear which grading systems are most commonly used to assess lumbar DD and how these grading systems are applied and reported.
The aim of this scoping review was to describe different MRI-based grading systems for DD in the lumbar spine and report which grading systems have been assessed for measurement properties such as reliability, validity, and sensitivity to change.
Scoping review.
A search was conducted in EMBASE, Medline, and CINAHL for studies related to MRI-based grading systems for DD in the lumbar spine, conducted in living humans. Data were extracted from each study, including the description of the grading system, which levels of the lumbar spine were graded, who graded the degeneration, how the degeneration was scored for analysis, and whether measurement properties such as reliability, validity, and sensitivity to change were assessed.
The search identified 569 studies that graded DD. Ninety-three different grading systems were identified, including 63 subjective systems, 25 quantitative systems, and 5 that were unspecified. The Pfirrmann method was used in over 50% of all reports. A range of grading components was used to measure DD, with disc signal intensity (DSI), disc height (DH), and the assessment of the distinctiveness between the annulus and nucleus being most common. Sensitivity to change was rarely assessed.
A large number of DD grading systems were identified in this review, many of which were infrequently used. Variability in methods of assessing DD on MRI and how the MRI data is synthesized may influence reported associations between DD and low back pain (LBP).
Accurately evaluating the radiological features of facet joint osteoarthritis (FJOA) may help to elucidate its relationship with pain. Multitask deep learning (DL) models have emerged as promising tools for this purpose.
This retrospective study employed a dataset of 13 223 axial CT facet joint (FJ) patches cropped from 1 360 patients across two hospitals. At the image level, the dataset was categorized as training dataset (n = 7430), validation dataset (n = 2000), internal test dataset (n = 1890), and external test dataset (n = 1903). The radiologic features of FJOA were qualitatively assessed using a multitask DL model based on ResNet-18 according to the FJOA grading guidelines proposed by Weishaupt. Two batches of images from each of the internal and external test datasets were used to test the change in readers' assessment accuracy with and without DL assistance, as measured using a paired t test.
In this study, the accuracy of the model on the internal and external test datasets was 89.8% and 76.6% for joint space narrowing (JSN), 79.6% and 80.2% for osteophytes, 65.5% and 56% for hypertrophy, 88% and 89.6% for subchondral bone erosions, and 82.8% and 89.8% for subchondral cysts. The model's Gwet κ values reach 0.88. When junior readers used the DL model for assistance, the accuracy was significantly improved (p value ranged from < 0.001 to 0.043).
A multitask DL model is a viable method for assessing the severity of radiological features in FJOA, offering support to readers during image evaluation.
Spine kinematics assessment is crucial for understanding intervertebral joint motion, particularly in conditions like spinal deformity, which alters and reduces spinal motion. Estimating spine kinematics in vivo usually relies on kinematic constraints to reduce the degrees of freedom in musculoskeletal models, but they lack standardization and fail to generalize across populations. This study proposes a novel method utilizing coordinate optimization instead of kinematic constraints, aiming to improve the generalizability and accuracy of spine kinematics estimation across different populations and marker protocols.
This study used two retrospective datasets: 13 subjects with spinal deformities and 11 healthy individuals. Spine kinematics were estimated by minimizing errors between simulated and experimental marker positions and penalizing large intervertebral joint angles. 3D orientation and position errors against image-based ground truth vertebral orientations and positions and experimental marker positions were calculated and compared for eight different weight settings. The accuracy was further assessed using standard error of measurements (SEM) compared to kinematic constraint methods.
The best-performing optimization settings resulted in average vertebral orientation errors of 5.1°, 3.2°, and 3.2° for axial rotation, lateral bending, and flexion-extension, respectively, and 3D position errors of 7.7 mm. These values reflect the average of vertebra-specific errors within each subject, further averaged across all subjects in the deformity dataset. Similarly, in the healthy dataset, average 3D marker errors remained below 1 cm, and SEM values remained below 1.3°.
The coordinate optimization method showed robust performance, achieving high accuracy in vertebral orientation and position (deformity) and marker tracking (healthy). This method consistently matched or surpassed state-of-the-art kinematic constraints methods while introducing generalizability across different populations and marker protocols.
Preclinical animal models are indispensable for the development of new therapeutic strategies and the study of the pathological mechanisms of intervertebral disc (IVD) degeneration (IVDD). This study aims to develop a reliable and reproducible rat model of IVDD by injecting advanced glycation end products (AGEs) into the IVD of ovariectomized rats.
Twenty-eight female Sprague–Dawley rats were allocated into the 31G needle group, vehicle group, 0.5 μg AGEs group, 1 μg AGEs group, 2 μg AGEs group, 4 μg AGEs group, and non-ovariectomy group (n = 4). The coccygeal discs of the 31G needle group were punctured only, while the coccygeal discs of the vehicle group were injected with 1 μL PBS. The coccygeal discs of the AGEs groups underwent injection of AGEs at 0.5, 1, 2, and 4 μg, respectively. The coccygeal discs of the non-ovariectomy group were injected with 2 μg AGEs. Rats in all groups, except for the non-ovariectomy group, underwent bilateral ovariectomy. Two weeks later, the rat caudal models were evaluated using radiological examination, histological staining, and immunohistochemistry (IHC).
No signs of IVDD were found by radiological imaging, histology, or IHC in the 31G needle group or the vehicle group. By contrast, in the 0.5, 1, 2, and 4 μg AGEs groups, caudal IVDD was successfully established and the IVDD severity is increasing in a dose-dependent manner. Compared with the 2 μg AGEs group, rats in the non-ovariectomized group showed less IVDD, indicating the protective effect of endogenous estrogen on degenerative IVD.
A single injection of AGEs to caudal discs can cause reliable and reproducible IVDD in ovariectomized female rats. Additionally, the endogenous estrogen might have a protective effect on the IVD to mitigate the degeneration.
Intervertebral disc degeneration (IDD) is a prevalent spinal condition frequently associated with pain and motor impairment, imposing a substantial burden on quality of life. Despite extensive investigations into the genetic predisposition to IDD, the precise pathogenic genes and molecular pathways involved remain inadequately characterized, underscoring the need for continued research to clarify its genetic underpinnings.
This study leveraged IDD data from the FinnGen R12 cohort and integrated expression quantitative trait loci data across 49 tissues from the Genotype-Tissue Expression version 8 database to perform a cross-tissue transcriptome-wide association study (TWAS). The analytical framework incorporated functional summary-based imputation (FUSION), unified test for molecular signatures (UTMOST), and gene-level analysis via multi-marker genome annotation (MAGMA). To substantiate the findings, Mendelian randomization (MR) and colocalization analyses were subsequently conducted.
Through TWAS and MAGMA analyses, 33 susceptibility genes associated with IDD were identified. Subsequent MR and colocalization analyses refined this list to six candidate genes—ADD1, GFPT1, MAPRE3, MSANTD1, SLC30A6, and XBP1—which may contribute to the initiation and progression of IDD by modulating pathways implicated in the endoplasmic reticulum stress response.
Six susceptibility genes associated with the risk of IDD were identified in this study, offering novel insights into the genetic architecture and potential pathogenic pathways underpinning the development of IDD.
Ossification of the posterior longitudinal ligament (OPLL) is a pathological condition characterized by ectopic ossification of spinal ligaments, primarily driven by abnormal osteogenic differentiation of ligament fibroblasts with stem cell-like properties. The SOX transcription factor family is crucial in regulating cell stemness and differentiation. Among them, SOX8 is known to influence osteoblast differentiation, but its role in OPLL remains unclear.
SOX8 expression was analyzed in non-OPLL and OPLL ligament tissues and cells. Its role in osteogenic differentiation was assessed using ALP/Alizarin Red staining, qPCR, Western blotting, and subcutaneous ectopic ossification models in nude mice. Mass spectrometry and co-immunoprecipitation identified SOX8-interacting E3 ubiquitin ligases, with ubiquitination assays assessing their effects on SOX8 stability. RNA-seq, GTRD analysis, and dual-luciferase reporter assays revealed SOX8 target genes. Functional recovery experiments were conducted to explore the role of these interactions in the osteogenic differentiation of ligament fibroblasts.
SOX8 expression was downregulated in OPLL ligament tissues and cells. Functional analyses showed that SOX8 inhibits osteogenic differentiation of ligament fibroblasts both in vitro and in vivo. Mechanistically, TRIM25, an E3 ubiquitin ligase, was found to interact with SOX8, promoting its ubiquitination and degradation. Rescue experiments showed that SOX8 knockdown or overexpression reversed the osteogenic effects of TRIM25 knockdown or overexpression in ligament fibroblasts. Additionally, OSR2 was identified as a transcriptional target of SOX8, with SOX8 promoting OSR2 transcription. OSR2 knockdown negated the inhibitory effects of SOX8 overexpression on osteogenic differentiation.
SOX8 serves as a critical negative regulator of osteogenic differentiation in ligament fibroblasts. TRIM25 promotes ectopic ossification in OPLL by enhancing SOX8 ubiquitination and degradation, while SOX8 inhibits osteogenic differentiation through transcriptional activation of OSR2. These findings highlight the TRIM25/SOX8/OSR2 axis as a key regulator in OPLL ectopic ossification, suggesting it to be a potential target for non-surgical treatment.
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