The effect of low- and high-velocity tendon excursion on the mechanical properties of human cadaver subsynovial connective tissue.

The effect of low- and high-velocity tendon excursion on the mechanical properties of human cadaver subsynovial connective tissue.
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DOI:
10.1002/jor.22489
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发表时间:
2014-01
影响因子:
2.8
通讯作者:
Amadio, Peter C.
Amadio, Peter C.
中科院分区:
医学3区
文献类型:
--
作者:
Filius, Anika;Thoreson, Andrew R.;Yang, Tai-Hua;Vanhees, Matthias;An, Kai-Nan;Zhao, Chunfeng;Amadio, Peter C.

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腕管滑膜下结缔组织(SSCT)纤维化是腕管综合征(CTS)最常见的组织学表现。纤维化可能由受损的SSCT引起。以前的研究发现,在低速(2 mm/s)下,肌腱偏移会不可逆地损伤SSCT。我们研究了肌腱偏移速度在SSCT损伤产生中的作用。使用了9具人类尸体的手腕。进行三个重复循环的斜坡拉伸测试,模拟40%、60%、90%和120%的中指浅屈肌腱生理偏移,偏移速度为60 mm/s。计算能量和力,并通过每个偏移水平的第一个循环中获得的值进行归一化。将数据与低速偏移数据进行比较。对于高速偏移,在60%生理偏移的偏移水平下首次观察到偏移能量比的显著下降(P<0.024),而对于低速偏移,在90%生理偏移的偏移水平下首次观察到偏移能量比的显著下降(P<0.038)。此外,高流速时能量比较低,为60%(P≤0.039)。增加速度会降低SSCT损伤阈值。这一发现可能与理解SSCT纤维化的发病机制有关,例如伴随CTS,以及与职业因素的关系。
Fibrosis of the subsynovial connective tissue (SSCT) in the carpal tunnel is the most common histological finding in carpal tunnel syndrome (CTS). Fibrosis may result from damaged SSCT. Previous studies found that with low-velocity (2 mm/s), tendon excursions can irreversibly damage the SSCT. We investigated the effect of tendon excursion velocity in the generation of SSCT damage. Nine human cadaver wrists were used. Three repeated cycles of ramp-stretch testing were performed simulating 40, 60, 90 and 120% of the middle finger flexor tendon superficialis physiological excursion with an excursion velocity of 60 mm/s. Energy and force were calculated and normalized by values obtained in the first cycle for each excursion level. Data were compared with low-velocity excursion data. For high-velocity excursions, a significant drop in the excursion energy ratio was first observed at an excursion level of 60% physiological excursion (P<0.024) and that for low-velocity excursions was first observed at 90% physiological excursion (P<0.038). Furthermore, the energy ratio was lower at 60% for high velocities (P≤0.039). Increasing velocity lowers the SSCT damage threshold. This finding may be relevant for understanding the pathogenesis of SSCT fibrosis, such as that accompanying CTS, and a relationship with occupational factors.
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