An exploratory study of different definitions and thresholds for lumbar disc degeneration assessed by MRI and their associations with low back pain using data from a cohort study of a general population

Abstract

Background: Lumbar disc degeneration seen on magnetic resonance imaging (MRI) is defined as loss of signal intensity and/or disc height, alone or in combination with other MRI findings. The MRI findings and thresholds used to define disc degeneration vary in the literature, and their associations with low back pain (LBP) remain uncertain. Objective: To explore how various thresholds of lumbar disc degeneration alter the association between disc degeneration and self-reported LBP. Methods: An exploratory, cross-sectional cohort study of a general population. Participants in the cohort 'Backs-on-Funen' had MRI scans and completed questionnaires about LBP at ages 41, 45 and 49 years. The MRI variables, signal intensity (Grades 0-3) and disc height (Grades 0-3), were dichotomised at different thresholds. Logistic regression analyses were used to determine associations. Arbitrarily, a difference in odds ratio (OR) of > 0.5 between thresholds was considered clinically relevant. Receiver Operating Characteristic curves were used to investigate differences between diagnostic values at each threshold. Results: At age 41, the difference in ORs between signal loss and LBP exceeded 0.5 between the thresholds of ≥2 (OR = 2.02) and = 3 (OR = 2.57). Difference in area under the curves (AUC) was statistically significant (p = 0.02). At ages 45 and 49, the difference in ORs exceeded 0.5 between the thresholds of ≥2 and = 3, but the differences between AUC were not statistically significant. At age 41, the difference in ORs between disc height loss and LBP at the thresholds of ≥1 (OR = 1.44) and ≥ 2 (OR = 2.53) exceeded 0.5. Differences in AUC were statistically significant (p = 0.004). At age 49, differences in ORs exceeded 0.5 (OR = 2.49 at the ≥1 threshold, 1.84 at ≥2 and 0.89 at =3). Differences between AUC were not statistically significant.

1,25(OH)2D3 Mitigates Oxidative Stress-Induced Damage to Nucleus Pulposus-Derived Mesenchymal Stem Cells through PI3K/Akt Pathway

“…LBP has become the most common cause of disability in adults worldwide in the past 30 years, and IVDD is an important cause of LBP in middle-aged and elderly patients. As a result, the treatment cost places a substantial burden on the family and society [ 2 , 3 ]. Much effort has been expended in the development of medicines and surgical treatments for IVDD, but they mainly relieve symptoms and cannot effectively alleviate or reverse the process of IVDD [ 34 , 35 ].…”

“…The prevalence of low back pain (LBP) is 11.9%, as reported in the Lancet , and the peak prevalence ranges from 28% to 42% in people of middle- to old-age (40~69 years) [ 1 ]. Intervertebral disc degeneration (IVDD) is a usual cause of LBP in aging people and increases the socioeconomic burden [ 2 , 3 ]. Regrettably, conventional treatments mainly relieve symptoms instead of repairing or regenerating the structure and function of the degenerative intervertebral disc (IVD) [ 4 ].…”

Probable lumbar acute noncompressive nucleus pulposus extrusion: a case report of acute pain caused by a hydrated nucleus pulposus and review of the literature

“…[3] The diagnosis of LDD on MRIis based on one or a combination of abnormal findings (eg, loss of signal intensity alone or a combination of loss of signal intensity, loss of disc height, inhomogeneous structure of the disc, and reduced distinction between the nucleus and annulus in the disc). [4] Degenerative changes or damage forces might contribute to the NP to herniate through the annulus fibrosis or even the posterior longitudinal ligament.…”

“…The catabolic process of the disc is accompanied by loss of the hydrophilic glycosaminoglycan (GAG) primary structure within the nucleus pulposus (NP), resulting in reduced water content in the disc, which can be seen on MRI as a decreased T2-weighted signal (hypointense) [3] . The diagnosis of LDD on MRIis based on one or a combination of abnormal findings (eg, loss of signal intensity alone or a combination of loss of signal intensity, loss of disc height, inhomogeneous structure of the disc, and reduced distinction between the nucleus and annulus in the disc) [4] . Degenerative changes or damage forces might contribute to the NP to herniate through the annulus fibrosis or even the posterior longitudinal ligament.…”

Protocol for disease-oriented Russian disc degeneration study (RuDDS) biobank facilitating functional omics studies of lumbar disc degeneration

“…Biology of intervertebral DD is actively studied from different points of view. Besides various studies of degenerative disc morphology [18][19][20][21][22] and molecular biology [16,[23][24][25] there is an increasing number of genetic [26,27], transcriptomic [28][29][30] and proteomic [31][32][33] studies of intervertebral DD. Thus, nowadays based on candidate-gene [34] and genome-wide associated studies (GWAS) [35,36] over 160 genes were considered as potentially involved in intervertebral disc degeneration, although less than ten of them provide strong evidence for the association [34].…”