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BACKGROUND CONTEXT: Imaging signs of disc degeneration (DD) are common in both symptomatic and asymptomatic individuals and increase with age. In adults, DD progression typically peaks before age 50 and is strongly influenced by genetic factors at younger ages. However, longitudinal data describing DD progression from childhood through adulthood remain limited. PURPOSE: To characterize individual DD progression and examine the relationship between DD and lifetime low back pain (LBP) in a cohort of healthy volunteers followed from childhood into adulthood. STUDY DESIGN: Prospective longitudinal cohort study. PATIENT SAMPLE: Healthy children originally examined at ages 8 (n=94), 11(n=81) and 19 (n=71), with long-term follow-up at age 34 (n=48). The present analysis included 40 individuals with complete data (structured interview, clinical examination, lumbar spine MRI) at all 4 time points. OUTCOME MEASURES: Annual rate of DD progression, level-specific disc changes, and the association between DD and self-reported lifetime LBP. METHODS: Mid-sagittal T2-weighted MR images (L1/L2 to L5/S1) were graded using the 5-level Pfirrmann classification. A Pfirrmann Summary Score (PSS; range 5-25) was calculated as the sum of all lumbar disc grades. DD progression was defined as an increase in PSS compared with the previous assessment. Lifetime LBP unrelated to trauma was assessed through standardized interviews. Generalized Estimating Equation (GEE) models estimated annual changes in PSS. Participants were further categorized according to the presence or absence of at least one lumbar disc graded Pfirrmann ≥ 3 or according to lifetime LBP at age 34. Covariates included sex, BMI, smoking, and physical activity when appropriate. RESULTS: Forty participants completed all 4 assessments. The proportion of participants with at least one disc graded Pfirrmann ≥ 3 increased from 5% at age 8 to 12% at age 11, 48% at age 19 and 72% at age 34. PSS increased significantly over time in all participants. The annual increase in PSS was significantly greater between ages 11 and 19 (0.55; 95% CI: 0.48 to 0.63) than between ages 19 and 34 (0.08; 95% CI: 0.05 to 0.11). Participants reporting lifetime LBP at age 34 had more widespread or severe disc changes at age 19 compared to their asymptomatic peers, independent of covariates. CONCLUSIONS: DD progression appears strongly age-dependent, with the pubertal growth spurt representing a period of accelerated structural change. Progression slowed substantially after age 19. In this cohort, more widespread or severe degeneration at age 19 was associated with lifetime LBP at age 34. These findings highlight adolescence as a potentially critical period in the natural history of DD.
Lund et al. (Sun,) studied this question.