Recently, Delaissé and his colleagues looked for a link between senescent chondrocytes and cartilage damage. Cells in this sleep-like state have been linked to a chromosomal change in which telomeres (pronounced TEAL-oh-meres), which form caps at the ends of chromosomes, like the hard tips on shoelaces, become shortened. Telomere shortening occurs as cells divide over and over again, or as cells are submitted to stress.

Researchers have already shown that very short telomeres can push cells into senescence. Delaissé wanted to find out whether chondrocytes with short telomeres were linked to cartilage damage. His team used a new assay (laboratory test) that can detect shortening of individual telomeres – previous assays could only detect average telomeres length – but a few recent studies have shown that only a few shortened temeres (and perhaps even one shortened telomere) can push cells into senescence.  With that in mind, Delaissé’s team used cartilage tissue left over from knee replacement surgery and studied cartilage in four different places, from the worst cartilage lesion to farthest away.

The results, published in January 2012 in Arthritis Research & Therapy, showed that telomeres closest to the most damaged cartilage tissue were shortest in length, perhaps indicating that stress from damaged tissue prevents cartilage repair.  

“We hope to extend this research to more patients and to other joints,” says Delaisse. “Targeting telomere shortening may help us produce a therapy that prevents articular cartilage [the cartilage in joints] from breaking down.”

Another way to study genetic changes that may lead to OA is to screen a large number of people to uncover any genes – even those not previously suspected – that might harbor such changes. A team of researchers in the United Kingdom published a study in the American Journal of Human Genetics in September 2011, using a systemic method to screen a large group of people with hip or knee OA. They compared 3,177 people who needed total joint replacement to 4,894 people who probably did not have osteoarthritis. The search uncovered a variation in a gene called MCF2L, which directs nerve growth.