Abstract
Postpartum stress urinary incontinence (SUI) is associated with chronic SUI in later life, which is 240% more likely to occur in women who deliver vaginally than those who did not. The etiology of SUI is multifactoral and has been associated with defects in both neuromuscular and structural components of continence. Specifically, clinical studies have demonstrated that pudendal nerve damage occurs during vaginal delivery, supporting the concept that neuromuscular damage to the continence mechanism can result in postpartum SUI. Urethral hypermobility and the loss of pelvic floor support, such as that involved in pelvic organ prolapse, have also been associated with SUI. Animal models provide an opportunity to investigate these injuries, individually and in combination, enabling researchers to gain further insight into their relative contributions to the development of SUI and the effectiveness of potential therapies for it. This article discusses the use of animal models of postpartum SUI in addition to the broad insights into treatment efficacy they provide.
Financial & competing interests disclosure
This work was supported in part by NIH grant R01HD38679 and the Rehabilitation Research and Development Service of the Department of Veterans’ Affairs. Courtenay Moore is a consultant for Pfizer. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.