This 2016 study compared body clock genes in cartilage cells (chondrocytes) from osteoarthritic and healthy human cartilage. Osteoarthritic cells had higher PER2 and lower BMAL1. When the researchers turned BMAL1 down in healthy cells, the cells multiplied more and made more MMP13, two features of the osteoarthritic cartilage cell.
The team reset the internal clocks of human chondrocytes with a serum shock, then measured the clock genes PER2 and BMAL1 in cells from osteoarthritic cartilage and from healthy cartilage. They then used RNA interference, a lab tool that silences a chosen gene, to knock down BMAL1 in healthy cells and watched how the cells changed.
After the serum shock, PER2 expression was significantly higher and BMAL1 expression significantly lower in osteoarthritic chondrocytes. Knocking down BMAL1 in healthy chondrocytes went with more cell proliferation and more MMP13 expression, both features of osteoarthritic chondrocytes. The authors suggest that clock disruption inside the cartilage cell may be a critical early step in the disease.
This is a short abstract that does not give the number of donors. The experiments were done on cells in a dish, where clocks are reset artificially. Silencing a gene in the lab is a much stronger change than anything daily life produces, so the study does not show that sleep patterns or shift work affect MMP13 in a person's joint.
It adds a less obvious trigger to the list of things that can raise MMP13. Cartilage cells run their own 24-hour clock, separate from the brain's, and when one of its genes is turned down, MMP13 goes up. The same research group later showed that inflammation, oxidative stress and crystals can upset that clock.
In human cartilage cells, MMP13 rose in response to inflammatory messengers such as IL-1, oxidative stress, calcium phosphate crystals, a disrupted cell body clock...
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