Researchers here link age-related issues with the body clock to the development of osteoarthritis, a degenerative condition of joints. The body clock controls changes in cell and organ activities according to the time of day. This overall system has its reflections in the biochemistry of all types of cells, and, as for many other aspects of cellular biology, the mechanisms involved in clock-related regulation become disarrayed with age. The proximate causes of this disarray are only partially cataloged and explored, long lists of changing protein levels and relationships mapped one by one. The root cause is most likely the well-known forms of cell and tissue damage that cause aging, but - as ever - drawing a line between that damage, through largely unmapped, complicated chains of cause and consequence, to link up with any one specific end result of aging is a challenging, expensive, and time-consuming process. It would be faster to fix the damage and see what happens, a path that would also provide a much greater chance of meaningful therapies resulting from research work.
Researchers have for the first time established that the painful and debilitating symptoms endured by osteoarthritis sufferers are intrinsically linked to the human body clock. Body clocks within cartilage cells - or chondrocytes - control thousands of genes which segregate different biological activities at different times of the day. The body clock, researchers realised, controls the equilibrium between when chondrocyte cells are repaired during rest and when they are worn down through activity. But the research revealed that as we age, our cartilage cell body clocks deteriorate, making the repair function insufficient, which could contribute to osteoarthritis.
The team examined three types of human cartilage under the microscope : normal, mildly affected by osteoarthritis and severely affected. As the osteoarthritis became more severe, the number of cells that express BMAL1 - a protein which controls the body clock - became less and less. And in terms of aging, he found similar reduction of BMAL1 in chondrocytes, which coincided with the reduced 'amplitude' of the body clock (up to 40% weaker in older mice), supporting the theory that aging, at least partially through dysregulation of the chondrocyte clocks, is a major risk factor for osteoarthritis.