Research Paper Volume 8, Issue 9 pp 2222—2231
Specific premature epigenetic aging of cartilage in osteoarthritis
- 1 Laboratorio Investigacion 10 and Rheumatology Unit, Instituto Investigacion Sanitaria, Hospital Clinico Universitario de Santiago, Travesia Choupana, sn. 15706- Santiago de Compostela, Spain
- 2 Grupo de Reumatología, Instituto de Investigación Biomédica de A Coruña. Complexo Hospitalario Universitario de A Coruña, Universidade da Coruña. As Xubias, sn. 15006- A Coruña, Spain
- 3 Department of Human Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA
- 4 Discipline of Genetics, Faculty of Medicine, Memorial University of Newfoundland, A1B- St. John's, NL, Canada
- 5 Department of Internal Medicine, Hospital U. M. Valdecilla-IDIVAL, University of Cantabria, Cardenal Herrera Oria, 39011, Santander, Spain
Received: June 14, 2016 Accepted: September 14, 2016 Published: September 28, 2016
https://doi.org/10.18632/aging.101053How to Cite
Abstract
Osteoarthritis (OA) is a disease affecting multiple tissues of the joints in the elderly, but most notably articular cartilage. Premature biological aging has been described in this tissue and in blood cells, suggesting a systemic component of premature aging in the pathogenesis of OA. Here, we have explored epigenetic aging in OA at the local (cartilage and bone) and systemic (blood) levels. Two DNA methylation age-measures (DmAM) were used: the multi-tissue age estimator for cartilage and bone; and a blood-specific biomarker for blood. Differences in DmAM between OA patients and controls showed an accelerated aging of 3.7 years in articular cartilage (95% CI = 1.1 to 6.3, P = 0.008) of OA patients. By contrast, no difference in epigenetic aging was observed in bone (0.04 years; 95% CI = -1.8 to 1.9, P = 0.3) and in blood (-0.6 years; 95% CI = -1.5 to 0.3, P = 0.2) between OA patients and controls. Therefore, premature epigenetic aging according to DNA methylation changes was specific of OA cartilage, adding further evidence and insight on premature aging of cartilage as a component of OA pathogenesis that reflects damage and vulnerability.