McKay Orthopaedic Research Laboratory, University of Pennsylvania, Stemmler Hall, 3450 Hamilton Walk, Philadelphia, PA 19104-6081.
J Biomech Eng. 2020 Nov 1;142(11). doi: 10.1115/1.4047629.
Pregnant women experience weight gain, gait changes, and biochemical fluctuations that impair joint function and alter the maternal skeleton. Hormonal changes increase pelvic ligament laxity in preparation for childbirth and affect peripheral joint laxity. Calcium demands also rise during pregnancy and lactation, resulting in reduced bone mineral density (BMD) and maternal bone loss. Altered tendon properties and bone loss during pregnancy and lactation may impact tendon insertion sites, such as rotator cuff tendons where insertion site ruptures are common. However, the effects of pregnancy and lactation at the tendon-to-bone interface have not been investigated. Therefore, the objective of this study was to evaluate supraspinatus tendon mechanical properties and insertion site microstructure during pregnancy, lactation, and postweaning recovery in female rats. We hypothesized that pregnancy and lactation would compromise supraspinatus tendon mechanical properties and subchondral bone microstructure. Female rats were divided into virgin, pregnancy, lactation, and recovery groups, and supraspinatus tendons were mechanically evaluated. Surprisingly, tendon mechanics was unaffected by pregnancy and lactation. However, tendon modulus decreased two-weeks postweaning. Additionally, tendons failed by bony avulsion at the insertion site, and the lactation group exhibited reduced failure properties corresponding to decreased subchondral bone mineralization. Lactation also resulted in dramatic bone loss at the epiphysis, but trabecular bone microarchitecture recovered postweaning. In conclusion, lactation following pregnancy impaired trabecular bone microstructure and subchondral bone mineralization, leading to reduced supraspinatus tendon-to-bone insertion site failure properties. These findings will contribute toward understanding the pathogenesis of tendon-to-bone disorders.
孕妇会经历体重增加、步态改变和生化波动，这些会损害关节功能并改变母体骨骼。激素变化会增加骨盆韧带的松弛度，为分娩做准备，并影响外周关节的松弛度。怀孕期间和哺乳期的钙需求也会增加，导致骨密度（BMD）降低和母体骨质流失。怀孕期间和哺乳期的肌腱特性和骨质流失可能会影响肌腱插入部位，例如旋转袖肌腱，其插入部位的撕裂很常见。然而，妊娠和哺乳对肌腱-骨界面的影响尚未得到研究。因此，本研究的目的是评估雌性大鼠在妊娠、哺乳和断奶后恢复期间的冈上肌腱机械性能和插入部位微观结构。我们假设妊娠和哺乳会损害冈上肌腱的机械性能和软骨下骨的微观结构。雌性大鼠分为处女、妊娠、哺乳和恢复组，并对冈上肌腱进行了机械评估。令人惊讶的是，妊娠和哺乳并未影响肌腱力学性能。然而，两周断奶后肌腱模量降低。此外，肌腱在插入部位发生骨性撕脱，哺乳期组表现出与软骨下骨矿化减少相对应的较低失效特性。哺乳期还导致骨骺处的骨量明显减少，但小梁骨微结构在断奶后恢复。总之，妊娠后哺乳会损害小梁骨微观结构和软骨下骨矿化，导致冈上肌腱-骨插入部位失效特性降低。这些发现将有助于了解肌腱-骨疾病的发病机制。
