Abstract
Introduction
Low back pain (LBP) is the world's most disabling condition and a global burden. Although many etiological factors have been associated with LBP, lumbar disc degeneration on magnetic resonance imaging (MRI) is certainly one of them. Moderate/severe degrees of global disc degeneration are significantly associated with LBP compared with less degenerative stages. However, the association of LBP with disc degeneration remains controversial as there are individuals with very degenerative spines who are asymptomatic and, conversely, there are individuals with nondegenerated discs that have LBP. The following large-scale population-based study addressed the role of determinants such as various MRI findings, lifestyle/environmental and cardiovascular factors, and family history of LBP in extreme stages of lumbar disc degeneration (i.e., nondegenerated [normal] vs. moderate/severe disc degeneration) and the occurrence of LBP.
Materials and Methods
This was a cross-sectional study of the Hong Kong Disc Degeneration-Cardiovascular Cohort, currently composed of approximately 1,800 Southern Chinese volunteers. The current study was composed of two groups: Group 1 (n = 229) was composed of individuals with nondegenerated discs (i.e., degenerative disc disease [DDD] score = 0) and Group 2 (n = 335) entailed individuals with moderate/severe global disc degeneration (i.e., DDD score ≥ 5). Serum lipid profile, glucose, erythrocyte sedimentation rate (ESR), high-sensitivity C-reactive protein (hs-CRP), and other blood parameters were assessed. Anthropomorphic and lifestyle/environmental (e.g., smoking, exercise, occupation) measurements as well as LBP profiles were obtained of all subjects. Oswestry disability index (ODI) questionnaire was administered to each subject, with a total score ≥ 20/100 representing an abnormal profile. Each subject had undergone T2-weighted MRI of the lumbar spine from L1-S1. Schneiderman et al classification was used to grade disc degeneration of each lumbar disc, whereby patterns of regional degeneration were also assessed. DDD score was obtained by summating the grades of all the levels. Additional spinal imaging phenotypes (e.g., Modic changes, Schmorl nodes, etc.) were also noted. A family history of LBP was also assessed for all subjects.
Results
In Group 1 (Table 1), 30.6 and 69.4% of individuals had LBP or no-LBP, respectively. The mean age was 49.6 years (standard deviation [SD]: ± 6.0; range: 29.0-65.0 years) and 68% were females. Multivariate regression modeling noted that a family history of LBP (odds ratio [OR]: 3.80; 95% confidence interval [CI]: 1.43-10.04; p = 0.007), younger age (OR: 0.92; 95% CI: 0.89-1.01; p = 0.069), and elevated hs-CRP (OR: 1.26; 95% CI: 0.91-1.73; p = 0.17) were related to the presentation of LBP. Similarly, family history of LBP (OR: 10.62; 95% CI: 1.28-88.27; p = 0.029), younger age (OR: 0.83; 95% CI: 0.68-1.03; p = 0.086), and elevated hs-CRP (OR: 1.97; 95% CI: 1.17-3.33; p = 0.011) were significantly associated with abnormal ODI values for Group 1. Regarding Group 2 (Table 2), 61.5 and 35.5% of individuals had LBP or no-LBP, respectively. The mean age was 54.6 years (SD: ±6.7; range: 39-89 years) and 56% were females. In a multivariate regression model, male gender (OR: 14.84; 95% CI: 1.30-169.70; p = 0.030), younger age (OR: 0.80; 95% CI: 0.68-0.96; p = 0.014), and elevated ESR (OR: 1.11; 95% CI: 1.01-1.23; p = 0.032) were significantly associated with LBP. In a similar multivariate analysis, female gender (OR: 3.68; 95% CI: 1.15-11.71; p = 0.028) and family history of LBP (OR: 5.28; 95% CI: 1.56-17.85; p = 0.007) were significantly related to abnormal ODI values in Group 2.
Conclusion
Based on one of the largest population-based studies addressing risk factors of disc degeneration and LBP, this study has illustrated for the first time that a “family history of LBP” is one of the most significant risk factors that may account for the variation between imaging findings of spine degeneration on MRI and pain/functional profiles. This study raises awareness that family up-bringing/values or a genetic predisposition to pain may exist that may broaden our understanding as to why certain individuals develop LBP, irrespective of MRI findings. Although a deeper understanding of the phenotype of disc degeneration may be needed to help “image pain,” the current study gives further credence to a more “personalized” approach toward understanding the development of LBP.
None declared