This 2005 study took cartilage cells (chondrocytes) from human donors of different ages and provoked them with fibronectin fragments or interleukin-1 beta. Cells from older donors made significantly more MMP13. Blocking NF-kB stopped the fragment-driven rise, and unprovoked cells from older donors also made more IL-1 beta.
Researchers isolated chondrocytes from human articular cartilage from donors across a range of ages. They stimulated the cells with fibronectin fragments, pieces of a matrix protein that appear when cartilage is damaged, or with interleukin-1 beta, an inflammatory signal, and measured MMP13 production as a sign of a breakdown response. They also used an inhibitor of NF-kB, a switch inside the cell that turns on inflammatory genes.
MMP13 production in response to the stimuli rose significantly with donor age. The NF-kB inhibitor blocked the effect of fibronectin fragments on MMP13. Unstimulated cells from older donors also made more interleukin-1 beta, a cytokine NF-kB controls. The authors describe this as an age-related increase in how strongly chondrocytes respond to breakdown signals, which could contribute to joint disease in older adults.
The abstract gives neither the number of donors nor their exact ages. The cells were studied in a dish after being taken out of the cartilage, which changes how chondrocytes behave. The study shows a stronger response in older cells. It does not show that this response causes cartilage loss in a living older joint, or how often such triggers occur.
Read with Aurich's 2002 finding that healthy ageing cartilage keeps its collagen in balance, this paper gives a more precise picture. Age does not simply switch MMP13 on, but older cells over-react when something provokes them. Part of that reaction runs through NF-kB, the same switch several plant compounds have been studied against.
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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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