Mitochondrial dysfunction is an acute response of articular chondrocytes to mechanical injury

Delco ML, Bonnevie ED, Bonassar LJ, Fortier LA · Journal of Orthopaedic Research

Impact caused mitochondrial depolarization and impaired respiratory function within 2 hours of injury — basal oxygen consumption fell 20–32% and maximal respiration 26–44% in the higher impact groups, with more proton leak and less ATP turnover — before widespread cell death, which rose above 7 MPa peak stress; the non-weight-bearing patellofemoral groove depolarised and died at impacts the condyle tolerated. Identifies mitochondrial dysfunction as one of the earliest measurable chondrocyte responses to cartilage trauma.

Population

Cartilage explants from the medial femoral condyle and patellofemoral groove of 10 neonatal (1–3 day old) calves

Intervention

Single rapid impact injury (5-17 MPa, 5-34 GPa/s)

Comparator

Non-impacted explants

Limitations

Neonatal bovine explants at 21% oxygen; no treatment tested — characterizes the injury response that SS-31 is later aimed at. NIH, Weill Cornell and Zweig Fund grants, no Stealth involvement.