Pregnancy and Lactation Impair Subchondral Bone Leading to Reduced Rat Supraspinatus Tendon-to-Bone Insertion Site Failure Properties
Pregnancy and Lactation Impair Subchondral Bone Leading to Reduced Rat Supraspinatus Tendon-to-Bone Insertion Site Failure Properties
复制标题
怀孕和哺乳期损伤软骨下骨，导致大鼠冈上肌腱-骨插入部位失效特性降低
DOI：
10.1115/1.4047629
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发表时间：
2020
期刊：
影响因子：
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通讯作者：
Soslowsky, Louis J.
中科院分区：
文献类型：
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作者：
Fung, Ashley K.;Shetye, Snehal S.;Li, Yihan;Zhou, Yilu;Sherry Liu, X.;Soslowsky, Louis J.
孕妇会经历体重增加、步态变化和生化波动，这些都会损害关节功能，改变母亲的骨骼。激素变化会增加准备分娩时骨盆韧带的松弛，并影响周围关节松弛。在怀孕和哺乳期间，钙的需求量也会增加，导致骨密度(BMD)降低和母亲骨丢失。妊娠和哺乳期间肌腱特性的改变和骨丢失可能会影响肌腱插入部位，如常有插入部位断裂的肩袖肌腱。然而，在肌腱-骨界面处怀孕和哺乳的影响还没有被研究。因此，本研究的目的是评估雌性大鼠在妊娠、哺乳和断奶后恢复过程中冈上肌腱的力学性能和起止点的微结构。我们假设怀孕和哺乳会损害冈上肌腱的力学性能和软骨下骨的微结构。将雌性大鼠分为处女组、妊娠组、哺乳组和恢复组，对冈上肌腱进行力学评估。令人惊讶的是，肌腱力学没有受到怀孕和哺乳的影响。然而，在断奶后两周，肌腱弹性系数下降。此外，肌腱在止点处因骨质撕脱而失效，而哺乳组的失效特性与软骨下骨矿化的减少相对应。哺乳期也导致了骨骺的剧烈骨质丢失，但在断奶后骨小梁微结构恢复。总而言之，妊娠后哺乳损害了松质骨微结构和软骨下骨矿化，导致冈上肌腱-骨植入部位失效特性减少。这些发现将有助于理解肌腱到骨的疾病的发病机制。
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.