Cross-Sectional and Longitudinal Association Between Biological Aging Acceleration and the Risk of Osteoarthritis: A Cohort Study From UK Biobank.

OBJECTIVE

To evaluate the relationship between biological ages and the prevalence and incidence of osteoarthritis (OA).

METHODS

332 261 participants from UK Biobank were analyzed. Biological aging was measured using phenotypic age (PhenoAge) and Klemera-Doubal (KDMAge). KDMAge was derived from nine clinical biomarkers to gauge system integrity decline, while PhenoAge was computed from chronological age and nine clinical biomarkers to gauge mortality risk. Biological aging accelerations were computed as residuals from regressing KDMAge and PhenoAge against chronological age. The associations between biological aging and prevalence and incidence of OA were analyzed using logistic and Cox regression models.

RESULTS

At baseline, 55.4% of included individuals had younger PhenoAge aging acceleration. In cross-sectional analyses, individuals with accelerated aging had higher odds of OA compared to those with non-accelerated aging (odds ratios [OR]: 1.12 [95% CI: 1.09-1.14] for PhenoAge acceleration and 1.05 [1.03-1.08] for KDMAge acceleration). In the longitudinal analyses, increased PhenoAge acceleration was associated with a higher risk of incident OA (hazard ratios [HR]: 1.12 [1.10-1.15]). However, the association between KDMAge acceleration and the incidence of OA was not statistically significant (HR: 0.99 [0.97-1.01]). Accelerated biological aging showed a more pronounced association with OA among individuals > 60 years. No additive or multiplicative interactions were found between OA polygenic risk score (PRS) and biological aging.

CONCLUSION

Advanced biological aging may increase the risk of OA, independent of OA genetic risk, particularly in individuals aged over 60 years. The two biological aging indicators hold potential as novel composite clinical biomarkers, directing prevention and intervention strategies for high-risk populations for OA.