A new study published in the American Journal of Sports Medicine shows that apoptosis is a part of the disease process in tendinosis. This finding may explain why degenerative changes may exist without inflammation.
This study was a cooperation between Oslo Sports Trauma Research Center, Kristiansund Hospital, Oslo University Hospital and the University of British Colombia, and was conducted by Øystein Lian with co-workers Alex Scott, Lars Engebretsen, Vincent Duronio, Roald Bahr and Karim Khan.
The pathogenesis of tendon overuse injuries is poorly understood. The histopathology underlying tendinopathy at various anatomical locations is similar and may reflect a common pathologic process. The objective of this case-control study was to investigate the role of apoptosis in patellar tendinosis.
We compared biopsies from the patellar tendon in patients with patellar tendinopathy diagnosed clinically and with typical MRI findings with biopsies from a control group without any previous or current knee complaints to suggest patellar tendinopathy. The presence of apoptosis was examined with immunohistochemical methods using a polyclonal antibody recognizing active caspase-3, confirmed by labeling DNA strand breaks (F7-26 antibody) and nuclear morphology.
The number of apoptotic cells per unit area (4.5 mm2) was 0.91 ±0.81 (SD) in tendinopathic samples and 0.21±0.21 in controls (P=.026). Although the tendinopathic samples displayed increased cellularity (average 52.0 nuclei/mm2 vs 31.46 nuclei/mm2), the apoptotic index was higher (0.42% vs 0.17%, P=.014).
Apoptosis is a feature of tendinosis. This suggests that tenocyte death may either limit the ability of injured tendon to recover from chronic injury, or may be involved in the ongoing repair and remodeling of the chronically injured tendon.
Read the article here.