Ultra-short telomeres may cause osteoarthritis

Danish researchers have found a link between ultra-short telomeres and osteoarthritis, according a recently published study. The shorted telomeres in arthritic knees increased in closer proximity to damaged regions in joints.

“We see both a reduced mean telomere length and an increase in the number of cells with ultra-short telomeres associated with increased severity of [osteoarthritis (OA)], proximity to the most damaged section of the joint and with senescence,” lead researcher Maria Harbo said in a news release. “Senescence can be most simply explained as biological aging and senescent cartilage within joints is unable to repair itself properly.”

Harbo and her team used the universal single telomere length assay to examine samples from osteoarthritic knees at two different distances from central lesion sites. They looked at ultra-short single telomeres associated with cellular senescence, according to the study abstract. The team found the load of ultra-short telomeres and their length were related to how close the telomeres were to the lesions, the severity of the OA, and the level of senescence.

“The telomere story shows that that there are, in theory, two processes going on in OA,” Harbo said. “Age-related shortening of telomeres, which leads to the inability of cells to continue dividing and so to cell senescence, and ultra-short telomeres, probably caused by compression stress during use, which lead to senescence and failure of the joint to repair itself. We believe the second situation to be the most important in OA. The damaged cartilage could add to the mechanical stress within the joint and so cause a feedback cycle driving the progression of the disease.”

Reference:

Harbo M, Bendix L, Bay-Jensen, et al. The distribution pattern of critically short telomeres in human osteoarthritic knees. Arthritis Res Ther. Published online ahead of print Jan. 18, 2012;14(1):R12. doi: 10.1186/ar3687.

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