Injury Causes Altered Metabolism including O₂ Consumption in Bovine and Human Chondrocytes.

Authors

Aidan J Gregory, Molly E Piazza, Priyanka P Brahmachary, Samuel Battles, William S Rockwell, Erik Myers, Mark Greenwood, Ross P Carlson, Ronald K June

Published in

Osteoarthritis and cartilage. Oct 02, 2026. Epub Oct 02, 2026.

Abstract

Traumatic joint injuries both disrupt chondrocyte metabolism and increase the risk for post-traumatic osteoarthritis. Yet the relationships between trauma, altered metabolism, and cartilage degradation remain unclear. This study compares the metabolic responses of bovine (normal) and osteoarthritic (OA) chondrocytes to physiological and injurious mechanical stimuli under normoxic (20% O₂) and hypoxic (5% O₂) conditions.
Primary chondrocytes were encapsulated in agarose and subjected to physiological and injurious mechanical stimulation in normoxic and hypoxic conditions. Samples were analyzed for O₂ saturation and metabolomic profiles of central carbon metabolites using LC-MS.
We find that healthy bovine chondrocytes exhibit robust, time-dependent adaptation to mechanical stimuli, whereas OA chondrocytes display a blunted response, particularly under injury conditions. Injurious mechanical stimuli led to altered O₂ consumption and glutamine accumulation, suggesting disrupted respiration and reduced protein synthesis hypothesized to be a result of altered mitochondrial metabolism in OA cells.
These findings underscore the role of mechanical cues in chondrocyte metabolism and inform future studies aimed at identifying metabolic targets relevant to post-traumatic osteoarthritis progression.

PMID:
42826895
Bibliographic data and abstract were imported from PubMed on 03 Oct 2026.

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