Abstract
The effects of mechanical stress on cells and their extracellular matrix, especially in gliding sections of tendon, are still poorly understood. This study sought to compare the effects of uniaxial stretching on both gliding and traction areas in the same tendon. Flexor digitorum longus muscle tendons explanted from rats were subjected to stretching in a bioreactor for 6, 24, or 48 h, respectively, at 1 Hz and an amplitude of 2.5%. After stimulation, marker expression was quantified by histological and immunohistochemical staining in both gliding and traction areas. We observed a heightened intensity of scleraxis after 6 and 24 h of stimulation in both tendon types, though it had declined again 48 h after stimulation. We observed induced matrix metalloproteinase-1 and -13 protein expression in both tendon types. The bioreactor produced an increase in the mechanical structural strength of the tendon during the first half of the loading time and a decrease during the latter half. Uniaxial stretching of flexor tendon in our set-up can serve as an overloading model. A combination of mechanical and histological data allows us to improve the conditions for cultivating tendon tissues.
Highlights
The bioreactor employed in the present study enabled a thorough assessment of uniaxial stretching of elastic scaffolds seeded with tendon tissue or tenocytes
We have considered the effect of stretching at different cycles and time point in both the intrasynovial gliding part as well as the extrasynovial traction part of the flexor tendon
We observed a heightened intensity of scleraxis up to 24 h of stimulation in both tendon types, whereas matrix metalloproteinases (MMPs) level were increased in both types
Summary
Tendons consist of hypovascularized and hypocellular tissue with low regeneration potential. Tendon disorders due to overuse or age-related degeneration are a common clinical problem in orthopedic medicine [1,2]. Tendon rupture is generally categorized either as spontaneous, traumatic, or open-incision. Spontaneous rupture results from overstretching and is accompanied by pathological changes in the tissue [3,4]. Treating a ruptured tendon is a lengthy process. The formation of new fibrovascular tissue with reduced stability (and reduced mechanical performance) results in a high risk of re-rupture of the tendon. Most tendon ruptures are localized in either the intrasynovial area of flexor tendons, where the blood supply to the fibrocartilaginous area is diminished within an enthesis, or where the tendon changes its tension direction (called a gliding tendon) [5,6]
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