A Simulation Analysis of Maternal Pelvic Floor Muscle

Pelvic floor disorder (PFD) is a common disease affecting the quality of life of middle-aged and elderly women. Pelvic floor muscle (PFM) damage is related to delivery mode, fetal size, and parity. Spontaneous vaginal delivery causes especially great damage to PFM. The purpose of this study was to summarize the characteristics of PFM action during the second stage of labor by collecting female pelvic MRI (magnetic resonance imaging) data and, further, to try to investigate the potential pathogenetic mechanism of PFD. A three-dimensional model was established to study the influence factors and characteristics of PFM strength. In the second stage of labor, the mechanical responses, possible damage, and the key parts of postpartum lesions of PFM due to the different fetal biparietal diameter (BPD) sizes were analyzed by finite element simulations. The research results showed that the peak stress and strain of PFM appeared at one-half of the delivery period and at the attachment point of the pubococcygeus to the skeleton. In addition, during the simulation process, the pubococcygeus was stretched by about 1.2 times and the levator ani muscle was stretched by more than two-fold. There was also greater stress and strain in the middle area of the levator ani muscle and pubococcygeus. According to the statistics, either being too young or in old maternal age will increase the probability of postpartum PFM injury. During delivery, the entire PFM underwent the huge deformation, in which the levator ani muscle and the pubococcygeus were seriously stretched and the attachment point between the pubococcygeus and the skeleton were the places with the highest probability of postpartum lesions.

Transperineal ultrasound shear-wave elastography is a reliable tool for assessment of the elastic properties of the levator ani muscle in women

Our main objective was to assess the intraoperator intersession reproducibility of transperineal ultrasound Shear Wave Elastography (SWE) to measure the levator ani muscle (LAM) elastic properties. Secondary objective was to compare reproducibility when considering the mean of three consecutives measurements versus one. In this prospective study involving non-pregnant nulliparous women, two visits were planned, with a measurement of the shear modulus (SM) on the right LAM at rest, during Valsalva maneuver and maximal contraction. Assessments were done with a transperineal approach, using an AIXPLORER device with a linear SL 18–5 (5-18 MHz) probe. For each condition, 3 consecutive measures were performed at each visit. The mean of the three measures, then the first one, were considered for the reproducibility by calculating intraclass correlation coefficient (ICC), and coefficient of variation (CV). Twenty women were included. Reproducibility was excellent when considering the mean of the 3 measures at rest (ICC = 0.90; CV = 15.7%) and Valsalva maneuver (ICC = 0.94; CV = 10.6%), or the first of the three measures at rest (ICC = 0.87; CV = 18.6%) and Valsalva maneuver (ICC = 0.84; CV = 19.9%). Reproducibility was fair for measurement during contraction. Transperineal ultrasound SWE is a reliable tool to investigate LAM elastic properties at rest and during Valsalva maneuver.

Exosomes Secreted by M1-type Macrophages Improve Stress Urinary Incontinence by Promoting the Repair of the Levator ani Muscle Injury in Mice

Background: Macrophages are involved in the regeneration of skeletal muscle injury and the exosomes secreted by a variety of cells promote the regeneration of tissues after injury. However, the potential effect of exosomes secreted by polarized macrophages on the repair of skeletal muscle after injury remains unclear. This study explored the effect of exosomes derived from M1 macrophages (M1-Exo) on the repair of levator ani muscle in mice after Vaginal Dilation (VD) modeling and the viability of C2C12 myoblasts after mechanical injury.Methods: Differential ultracentrifugation was used to separate M1-Exo from 200 ng/mL lipopolysaccharide-induced polarization of M1 type macrophages culture medium. Nanoparticle tracking analysis, transmission electron microscopy, and western blotting of CD9 and Tsg101 proteins were employed to identify M1-Exo. In vivo experiment involving the vaginal balloon expansion method was used to simulate the trauma to the pelvic floor of the mouse during delivery. M1-Exo was injected into the levator ani muscle and its surroundings to detect the abdominal leak point pressure (ALPP) and the maximum bladder volume (MBV) of the VD mice at 3, 7, and 14 days. Then the levator ani muscle was taken for hematoxylin and eosin (H&E) staining to observe the muscle damage and repair. To evaluate the functional and anatomical recovery of M1-Exo on stress urinary incontinence (SUI) mice caused by VD model delivery trauma. Subsequently, an in vitro C2C12 myoblasts cyclic mechanical strain injury model was constructed to determine the best mechanical injury parameters. In the next step, through a series of in vitro functional tests, the effect of M1-Exo on the proliferation, senescence, and apoptosis of C2C12 myoblasts injured by cyclic mechanical strain was assessed. The effect of M1-Exo on the prevention and treatment of SUI caused by injury to the levator ani muscle after delivery was evaluated using animal experiments and cell-level studies.Results: Powerlab software test results showed that the injection of M1-Exo into the levator ani muscle of SUI mice and its surroundings can significantly increase the mouse's ALPP, and MBV. H&E staining results revealed that M1-Exo can prevent secondary necrosis of broken muscle fibers, reduce nuclear migration of muscle fibers, maintain the shape of the muscle bundles, and promote normal muscle regeneration. CCK-8 proliferation reagent, senescence-associated β-galactosidase (SA-β-Gal) staining, and flow cytometry (PE/7-AAD staining) were used to determine the best in vitro simulation of the C212 myoblasts. The best damage parameters of the C2C12 myoblast injury model occurred at 5333 μ strain for a duration of 8 hours at 1 Hz. Subsequently, the test results of the CCK-8 proliferation reagent and EdU cell proliferation reagent suggested that M1-Exo promoted the proliferation of C2C12 myoblasts subjected to mechanically induced damage. SA-β-Gal staining results indicated that M1-Exo delayed the senescence of C2C12 myoblasts subjected to mechanically induced injury. Hoechst 33258 staining reagent and flow cytometry (PE/7-AAD staining) revealed that M1-Exo inhibited mechanically induced apoptosis of the C2C12 myoblasts.Conclusions: Our experimental results established that M1-Exo helps in the functional and anatomical recovery of SUI mice caused by labor trauma. Furthermore, the findings imply that M1-Exo has a protective effect on C2C12 myoblasts after cyclic mechanical strain damage, promotes their proliferation, delays aging, and inhibits apoptosis.