Osteoarthritis (OA) is often associated with aging. As bodies age, so do cells and, over time, neither bodies nor cells can perform as well as they did when they were young and fit. Within the world of OA, chondrocytes become less effective at keeping cartilage healthy, resulting in a breakdown of tissue and symptoms of OA.
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An important aspect of cell aging and senescence is telomere shortening. To this end, investigators have measured chondrocyte telomere length and suggested that it might play a role in the natural aging of cartilage, as well as the development and progression of OA. Previous studies have also noted the presence of subpopulations of cells other than chondrocytes throughout the osteoarthritic cartilage, and speculated as to their role in the aging joint.
Maria Harbo, PhD, in the department of clinical genetics at Lillebaelt Hospital in Vejle, Denmark, and colleagues published research in the journal Mechanisms of Ageing and Development that confirms the role of short telomeres in the aging of articular cartilage and the development of OA. Their work also suggests that progenitor-like cells that possess long telomeres may be recruited to damaged areas within the cartilage.
Dr. Harbo and team made their contribution by measuring the distribution pattern of telomere length across 23 human femoral heads from patients with and without OA. They divided the femoral heads into four zones and determined the relative mean telomere length within each zone.
The authors scored the tissues for cartilage degradation (Mankin score) and found significantly higher Mankin scores in OA samples compared to non-OA samples. The mean telomere length was slightly negatively correlated with Mankin scores in the OA samples (p < 0.05) but not in non-OA samples.
The investigators also calculated the load of ultra-short telomeres in four representative femoral heads from OA patients and six representative femoral heads from non-OA patients. They focused on the ultra-short telomeres on the assumption that ultra-short telomere length is an important indicator of cell senescence. The investigators found that the ultra-short telomere load correlated with cartilage degradation in samples from patients with OA, as well as patients without OA. They also found that the load of ultra-short telomeres increased in the weight-bearing areas of the femoral head.
While mean telomere length decreased with decreased distance from the central weight-bearing area, mean telomere length increased in the most central weight-bearing zone. The increase in mean telomere length in the weight-bearing zone was associated with the presence of cells that were not chondrocytes. Using immunohistochemistry, the authors characterized these cells as progenitor-like cells.
“Our results are not surprising when looking at OA in the broad context of aging. However, the modern discovery technologies—e.g., gene expression profiling and gene polymorphism—do not take telomere alterations into consideration, and the standard assay for measuring telomere length misses the ultra-short telomeres we identified with our new assay, and which we found systematically associated with OA. Thus, our findings may be a surprise for the OA researchers using the classical leading edge discovery technologies,” explained Dr. Harbo in an e-mail to The Rheumatologist.
Dr. Pullen is a medical writer based in the Chicago area.