Cesarean scar defects (CSDs) represent a growing concern in gynecology due to the global rise in cesarean section (CS) rates. CSD is defined by the International Niche Taskforce as “an indentation at the site of the cesarean scar with a depth of at least 2 mm” at transvaginal ultrasound [1]. While CSD prevalence varies widely, studies suggest that up to 80% of women may develop these defects after CS [2]. CSDs are characterized by myometrial thinning or dehiscence at the site of the cesarean incision and may be the causative factor for several gynecological and obstetrical disorders [1, 2, 3, 4]. They are associated with pelvic pain in up to 50% of cases and abnormal uterine bleeding in up to two-thirds of cases [5]. CSD also seems to increase the risk of obstetric complications, including scar pregnancies, placenta accreta spectrum disorders, and uterine rupture, which has been reported in up to 5% of cases and appears to correlate with the severity of the defect [4, 5, 6].

Surgical approaches to CSD repair, including hysteroscopic, vaginal, and laparoscopic techniques—both conventional and robot-assisted—aim to alleviate symptoms, improve reproductive outcomes, and reduce risks during future pregnancies [2,7]. Preoperative assessment of CSD is essential for determining the most appropriate surgical approach. Two- or three-dimensional transvaginal ultrasound and magnetic resonance imaging are the preferred diagnostic modalities, as they accurately evaluate CSD morphology, dimensions, and residual myometrial thickness (RMT) [1,5,8,9]. Additionally, saline infusion sonohysterography can enhance the diagnosis and characterization of CSD, particularly in cases where intracavitary fluid is absent [5]. In contrast, while hysteroscopy is valuable for confirming the presence of a CSD, it does not appear to be a reliable method for preoperative planning due to its inability to assess RMT accurately [10].

While hysteroscopic treatment may be appropriate for symptomatic patients with limited-depth CSDs, full-thickness uterine wall repairs via vaginal or laparoscopic approaches are indicated in the case of no or minimal RMT [2]. Although no precise consensus exists, an RMT <2–3 mm is commonly proposed as a cutoff to contraindicate hysteroscopic intervention due to the risk of uterine perforation and injury to surrounding organs [1,2,11,12]. Instead, full-thickness repair via vaginal or laparoscopic approaches is recommended for managing symptomatic severe CSD or for addressing severe CSD in patients planning future pregnancies to reduce the risk of uterine rupture and other obstetric complications [2,12].

First described by Jacobson et al. in 2003, laparoscopic repair has gained traction, offering precise excision of fibrotic tissue and secure uterine sutures​ [13, 14, 15]. Studies have demonstrated significant short- and mid-term improvements in RMT, symptom resolution, and fertility outcomes following laparoscopic repair ​[2,14]. However, data on long-term outcomes are scarce, leaving a critical gap in understanding their durability over time.

This study aims to fill the gap in understanding the long-term anatomical effectiveness of laparoscopic CSD repair, particularly given the complex histopathological and inflammatory processes associated with these defects. Chronic inflammation, fibrosis, vascular abnormalities, and adenomyosis have been frequently observed in CSD lesions and may increase the risk of recurrence over time [14,16, 17, 18]. These processes, along with scar remodeling, could lead to progressive changes in the myometrium and endometrium, potentially compromising the durability of surgical repair. By evaluating long-term anatomical and clinical outcomes, this study seeks to determine whether laparoscopic repair can effectively address these challenges and minimize the risk of recurrence over extended follow-up periods.