PAR2 deletion in the osteoblast lineage affords long-term cartilage protection in experimental osteoarthritis

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The study investigates the long-term effects of PAR2 deletion on cartilage protection in osteoarthritis.
Utilized a destabilization of the medial meniscus OA model in mice.
Conducted in vivo and in vitro assessments over 12 months post-OA induction.
Analyzed global and tissue-specific PAR2 knockout mice (osteoblast and chondrocyte) to determine the role of PAR2.
Wild-type mice showed increasing cartilage damage over time, consistent with OA progression.
PAR2 knockout mice had significantly reduced cartilage pathology (MD 4.35, 95%CI 2.55 to 6.16).
Absence of PAR2 in osteoblasts led to reduced cartilage damage (MD 2.6, 95%CI 0.5 to 4.6), unlike its absence in chondrocytes (MD 0.61, 95%CI -1.4 to 2.6).
The findings suggest PAR2 in osteoblasts influences joint deterioration during advanced OA stages.

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Experimentally deleting PAR2 from osteoblasts reduces cartilage damage in a mouse model of osteoarthritis, suggesting therapeutic potential.

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Huesa et al. (2026) studied this question.

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