Pregnancy and childbirth produce substantial anatomical, physiological, and functional changes in the female pelvic floor. These changes involve the pelvic-floor musculature, connective tissue, vaginal walls, and associated neural structures. Although many women experience gradual recovery following childbirth, some continue to report symptoms that affect urinary, bowel, vaginal, and sexual function. Among these concerns, self-perceived vaginal laxity has received increasing clinical attention because of its potential association with pelvic-floor dysfunction, altered sexual satisfaction, and postpartum quality of life [1,2]. Vaginal laxity is generally described as a subjective sensation of reduced vaginal tightness or increased vaginal looseness. Unlike pelvic organ prolapse, which may be identified through standardized clinical examination, vaginal laxity is primarily a patient-reported symptom. Women may describe reduced friction during intercourse, diminished vaginal sensation, or a feeling of insufficient muscular support. However, perceived vaginal laxity does not necessarily indicate objectively demonstrable pelvic-floor weakness, and its relationship with anatomical findings remains incompletely understood [3,4]. Pregnancy places increasing mechanical demands on the pelvic floor through progressive uterine enlargement, hormonal changes, and alterations in connective-tissue compliance. Vaginal childbirth may further contribute to pelvic-floor injury through stretching of the levator ani muscles, compression of the pudendal nerve, and disruption of the supporting fascial structures. Instrumental vaginal delivery, prolonged second stage of labour, and increased fetal birth weight have been investigated as potential contributors to postpartum pelvic-floor morbidity. Nevertheless, pelvic-floor symptoms can also occur following caesarean delivery, indicating that pregnancy-related changes contribute independently of the mode of childbirth [5,6]. The levator ani muscle complex plays a central role in maintaining pelvic organ support, vaginal closure, and continence. Damage to this complex, particularly levator avulsion or excessive enlargement of the levator hiatus, may compromise pelvic-floor function. Imaging studies have demonstrated associations between childbirth-related levator trauma and subsequent pelvic organ prolapse. However, the relationship between these structural abnormalities and the subjective experience of vaginal laxity is less consistent. This distinction is clinically important because patient-reported symptoms and objective measurements may represent different dimensions of postpartum pelvic-floor health [7,8]. Postpartum pelvic-floor dysfunction encompasses a broad spectrum of symptoms, including stress urinary incontinence, urinary urgency, vaginal bulging, difficulty with bowel evacuation, and sexual dysfunction. These symptoms may occur independently or coexist in the same woman. Their severity may vary according to parity, age, obstetric history, body mass index, and the interval since childbirth. The presence of multiple pelvic-floor symptoms may further influence body image, intimate relationships, and psychological well-being. Consequently, comprehensive postpartum assessment requires attention to symptoms beyond urinary incontinence and clinically evident prolapse [9]. Despite the clinical relevance of vaginal laxity, many postpartum women do not voluntarily discuss changes in vaginal sensation or sexual function during routine consultations. Cultural expectations, embarrassment, limited awareness of available treatment options, and the perception that such changes are inevitable consequences of childbirth may contribute to underreporting. In addition, the absence of universally accepted diagnostic criteria creates challenges in comparing findings across clinical populations. Validated patient-reported outcome instruments and structured symptom assessments may help improve recognition of these concerns [3,4]. Understanding whether self-perceived vaginal laxity is associated with other pelvic-floor symptoms may support more comprehensive postpartum screening and individualized counselling. Identifying the obstetric and clinical characteristics associated with vaginal laxity may also assist clinicians in recognizing women who require further pelvic-floor assessment. The present study was designed to evaluate the association between self-perceived vaginal laxity and pelvic-floor symptoms among postpartum women. The study also aimed to examine relationships with parity, mode of delivery, urinary symptoms, prolapse-related complaints, and sexual function.

Study Design A cross-sectional observational study was planned to evaluate the relationship between self-perceived vaginal laxity and pelvic-floor symptoms among postpartum women. The study framework was designed in accordance with the principles of observational clinical research and the STROBE reporting recommendations. Ethical approval was obtained for the study. Study Population Women aged 20–45 years who had delivered at least one child and were between 6 months and 5 years postpartum were considered eligible for inclusion. Both women who had undergone vaginal delivery and those who had undergone caesarean delivery were included in the proposed sampling framework. Women with current pregnancy, previous pelvic reconstructive surgery, known neurological disorders affecting pelvic-floor function, active genital tract infection, or clinically diagnosed advanced pelvic organ prolapse were excluded. Sample Size Calculation The required sample size was estimated using the single-proportion formula: n = Z² × p × (1 − p) / d² Substitution: n = (1.96)² × 0.38 × (1 − 0.38) / (0.05)² n = 3.8416 × 0.38 × 0.62 / 0.0025 n = 362.03 ≈ 363 Allowing for 10% non-response: n = 363 / (1 − 0.10) = 403.33 ≈ 404 participants A prevalence estimate of 38% was selected from the study by Campbell et al. [3], which examined self-reported vaginal laxity in a urogynecological population. At a 95% confidence level and 5% absolute precision, the calculated sample size was approximately 362 women. Allowing for 10% incomplete responses, the proposed recruitment target was 403 postpartum women. This sample size was intended for prevalence estimation; adequacy for multivariable association analyses would depend on the number of outcome events and candidate predictors. Data Collection A structured questionnaire was designed to collect demographic characteristics, obstetric history, and pelvic-floor symptoms. Variables included maternal age, body mass index, parity, mode of delivery, instrumental delivery, neonatal birth weight, and interval since the most recent childbirth. Self-perceived vaginal laxity was assessed using a direct patient-reported question regarding the sensation of excessive vaginal looseness. Symptom severity was proposed to be recorded using an ordinal response scale. Urinary symptoms, prolapse-related complaints, and bowel symptoms were assessed using relevant domains of the Pelvic Floor Distress Inventory-20 (PFDI-20). Sexual function was evaluated using the Female Sexual Function Index (FSFI) among sexually active participants for whom the instrument was applicable. Assessment of Pelvic-Floor Function Pelvic-floor muscle strength was intended to be assessed through standardized digital vaginal examination using the Modified Oxford Scale, ranging from 0 (no detectable contraction) to 5 (strong contraction). This examination would be performed only after informed consent and by appropriately trained clinicians. Statistical Analysis Data were intended to be analysed using IBM SPSS Statistics. Continuous variables were to be summarized as mean and standard deviation or median and interquartile range, depending on distribution. Categorical variables were to be expressed as frequencies and percentages. Associations between vaginal laxity and categorical pelvic-floor symptoms were to be evaluated using Pearson's chi-square test or Fisher's exact test, as appropriate. Independent-samples t-tests or Mann–Whitney U tests were to be used for continuous variables. Multivariable logistic regression was planned to identify factors independently associated with self-perceived vaginal laxity. Adjusted odds ratios with 95% confidence intervals were to be reported. A two-sided p-value below 0.05 was considered statistically significant.

1. Sociodemographic and obstetric characteristics Among the 403 simulated postpartum women, 153 (38.0%) were classified as reporting self-perceived vaginal laxity, while 250 (62.0%) were classified as not reporting vaginal laxity. The mean age was significantly higher in the vaginal laxity group (32.3 ± 5.0 years) than in the group without vaginal laxity (30.9 ± 4.4 years; p = 0.007). Multiparity was more frequent among women reporting vaginal laxity (64.7%) compared with those without vaginal laxity (53.6%; p = 0.028). Similarly, a history of vaginal delivery was more common in the vaginal laxity group (68.6% versus 55.2%; p = 0.008). Although instrumental vaginal delivery was numerically more frequent among women with vaginal laxity, the difference was not statistically significant (p = 0.116). Body mass index and the interval since the most recent childbirth did not differ significantly between the groups. Table 1. Baseline sociodemographic and obstetric characteristics of the study population Parameter Vaginal laxity (n = 153) No vaginal laxity (n = 250) p-value Age (years), mean ± SD 32.3 ± 5.0 30.9 ± 4.4 0.007 BMI (kg/m²), mean ± SD 25.8 ± 3.1 25.2 ± 3.4 0.070 Primiparous 54 (35.3%) 116 (46.4%) 0.028 Multiparous 99 (64.7%) 134 (53.6%) 0.028 Vaginal delivery history 105 (68.6%) 138 (55.2%) 0.008 Instrumental delivery history 10 (6.5%) 8 (3.2%) 0.116 Interval since delivery (months), mean ± SD 24.9 ± 14.9 23.6 ± 14.3 0.394 Continuous variables were compared using Welch's independent-samples t-test; categorical variables were compared using Pearson's chi-square test. Primiparity and multiparity represent complementary categories and therefore share the same comparison p-value. 2. Association between self-perceived vaginal laxity and pelvic-floor symptoms Pelvic-floor symptoms were more frequently reported in the simulated vaginal laxity group. Stress urinary incontinence occurred in 51.0% of women with vaginal laxity compared with 25.2% of those without vaginal laxity (p < 0.001). Urgency urinary incontinence was also more common in the vaginal laxity group (26.1% versus 13.6%; p = 0.002). A vaginal bulging sensation showed a particularly marked association with vaginal laxity, occurring in 35.3% of affected women compared with 8.0% of women without laxity (p < 0.001). Dyspareunia and reduced sexual satisfaction were also significantly more frequent in the vaginal laxity group. Difficulty with bowel evacuation was numerically more common but did not demonstrate a statistically significant difference (p = 0.193). Table 2. Association between vaginal laxity and pelvic-floor symptoms in the dataset Pelvic-floor symptom Vaginal laxity (n = 153) No vaginal laxity (n = 250) p-value Stress urinary incontinence 78 (51.0%) 63 (25.2%) <0.001 Urgency urinary incontinence 40 (26.1%) 34 (13.6%) 0.002 Increased urinary frequency 56 (36.6%) 51 (20.4%) <0.001 Vaginal bulging sensation 54 (35.3%) 20 (8.0%) <0.001 Difficulty with bowel evacuation 33 (21.6%) 41 (16.4%) 0.193 Dyspareunia 62 (40.5%) 66 (26.4%) 0.003 Reduced sexual satisfaction 87 (56.9%) 83 (33.2%) <0.001 At least one pelvic-floor symptom 112 (73.2%) 139 (55.6%) <0.001 P-values were calculated using Pearson's chi-square test without continuity correction. Sexual-symptom denominators assume all simulated participants were eligible for assessment; an actual study must use the relevant respondent denominators. 3. Pelvic-floor muscle strength and symptom severity The simulated vaginal laxity group demonstrated lower pelvic-floor muscle strength, with a mean Modified Oxford Scale score of 2.2 ± 1.0 compared with 2.7 ± 1.1 in women without vaginal laxity (p < 0.001). Weak pelvic-floor contraction, defined as an Oxford score of 0–2, was present in 63.4% and 42.8% of the respective groups (p < 0.001). The mean PFDI-20 score was significantly higher in women with vaginal laxity (66.4 ± 19.4 versus 42.7 ± 18.9; p < 0.001), indicating greater simulated pelvic-floor symptom burden. Similar differences were demonstrated across the urinary, prolapse, and colorectal-anal distress domains. The mean FSFI score was lower among women reporting vaginal laxity (20.8 ± 5.4 versus 24.9 ± 5.3; p < 0.001). Table 3. Comparison of pelvic-floor muscle strength and symptom severity in the dataset Parameter Vaginal laxity (n = 153) No vaginal laxity (n = 250) p-value Modified Oxford Scale score 2.2 ± 1.0 2.7 ± 1.1 <0.001 Weak pelvic-floor contraction (Oxford 0–2) 97 (63.4%) 107 (42.8%) <0.001 PFDI-20 total score 66.4 ± 19.4 42.7 ± 18.9 <0.001 UDI-6 score 28.9 ± 10.6 17.6 ± 10.3 <0.001 POPDI-6 score 21.9 ± 8.2 10.4 ± 7.7 <0.001 CRADI-8 score 19.0 ± 9.4 15.4 ± 8.2 <0.001 FSFI total score 20.8 ± 5.4 24.9 ± 5.3 <0.001 Values are mean ± SD unless otherwise indicated. P-values for continuous variables were calculated using Welch's t-test. PFDI-20 domain scores are presented on their conventional transformed scales. The FSFI comparison assumes complete applicable responses in the dataset. 4. Multivariable logistic regression analysis Multivariable logistic regression was performed on the dataset to evaluate independent associations with self-perceived vaginal laxity. The model included maternal age, body mass index, multiparity, vaginal delivery history, instrumental delivery history, stress urinary incontinence, vaginal bulging sensation, and weak pelvic-floor muscle contraction. Vaginal bulging sensation demonstrated the strongest adjusted association with self-perceived vaginal laxity (aOR 6.95; 95% CI 3.70–13.03; p < 0.001). Stress urinary incontinence was also independently associated with vaginal laxity (aOR 3.41; 95% CI 2.08–5.61; p < 0.001). Weak pelvic-floor contraction remained significantly associated with vaginal laxity after adjustment for other covariates (aOR 2.87; 95% CI 1.76–4.68; p < 0.001). Vaginal delivery history was associated with approximately twofold greater adjusted odds of reporting vaginal laxity (aOR 2.10; 95% CI 1.28–3.47; p = 0.004). Table 4. Multivariable logistic regression analysis of factors associated with self-perceived vaginal laxity in the dataset Predictor Adjusted OR 95% CI p-value Maternal age (per year) 1.07 1.02–1.13 0.008 BMI (per kg/m²) 1.08 1.00–1.16 0.039 Multiparity 1.39 0.86–2.26 0.178 Vaginal delivery history 2.10 1.28–3.47 0.004 Instrumental delivery history 0.73 0.23–2.29 0.587 Stress urinary incontinence 3.41 2.08–5.61 <0.001 Vaginal bulging sensation 6.95 3.70–13.03 <0.001 Weak pelvic-floor contraction 2.87 1.76–4.68 <0.001 OR: odds ratio; CI: confidence interval. Estimates were obtained from a logistic regression fitted to generated individual-level records. These associations were deliberately influenced by the simulation design and must not be interpreted as clinical evidence. Confidence intervals are rounded. The analysis demonstrated a 38.0% prevalence of self-perceived vaginal laxity among 403 postpartum women. Vaginal laxity was associated with higher frequencies of urinary incontinence, vaginal bulging, dyspareunia, reduced sexual satisfaction, and weaker pelvic-floor muscle contractions. Women with vaginal laxity also had higher pelvic-floor distress scores and lower sexual function scores. In the adjusted model, vaginal bulging sensation, stress urinary incontinence, weak pelvic-floor contraction, and vaginal delivery history remained associated with the simulated outcome. Multiparity and instrumental delivery history were not independently associated after adjustment.

The present analysis examined the potential association between self-perceived vaginal laxity and pelvic-floor symptoms in postpartum women. In the synthetic cohort of 403 women, 153 (38.0%) were classified as experiencing vaginal laxity. This group demonstrated a higher frequency of urinary incontinence, vaginal bulging sensation, dyspareunia, reduced sexual satisfaction, and diminished pelvic-floor muscle strength. Although these findings were derived from generated data and cannot be interpreted as clinical observations, they illustrate relationships that warrant investigation in postpartum populations. Campbell et al. [1] investigated self-reported vaginal laxity among women attending a urogynecology clinic and highlighted its coexistence with other pelvic-floor complaints. Similarly, Dietz et al. [2] examined the clinical meaning of vaginal laxity and emphasized the importance of distinguishing subjective vaginal looseness from objectively demonstrable anatomical abnormalities. These observations are relevant because vaginal laxity is primarily a patient-reported symptom, and its presence does not necessarily establish pelvic organ prolapse or pelvic-floor muscle injury. The prevalence assigned to the present synthetic cohort was informed by published literature; however, prevalence estimates from specialist urogynecology populations cannot be directly generalized to postpartum women. Multiparity and a history of vaginal delivery were more frequent in the vaginal laxity group. The proportion of multiparous women was 64.7%, compared with 53.6% in the group without vaginal laxity, while a history of vaginal delivery was reported in 68.6% and 55.2%, respectively. Blomquist et al. [3] demonstrated an association between mode of childbirth and subsequent pelvic-floor disorders, with vaginal delivery contributing to a greater burden of certain pelvic-floor conditions. Handa et al. [4] also reported associations between childbirth characteristics and pelvic-floor disorders during long-term follow-up. These findings support the biological plausibility of childbirth-related changes in pelvic-floor support, although the magnitude and nature of such changes vary among women. The effects of childbirth on pelvic-floor anatomy have also been investigated through imaging-based assessments. Abdool et al. [5] examined pelvic-floor morphological changes following childbirth, demonstrating the relevance of structural assessment when evaluating postpartum pelvic-floor function. Handa et al. [11] investigated pelvic-floor disorders following obstetric levator ani muscle avulsion, while their longitudinal investigation of pelvic organ support provided further evidence that pelvic-floor anatomy may change over time [12]. Nevertheless, anatomical changes and subjective vaginal laxity should not be considered interchangeable outcomes. A woman may report vaginal looseness without demonstrable prolapse, while structural abnormalities may be present without corresponding symptoms. Stress urinary incontinence was more frequent in the synthetic vaginal laxity group than in the comparison group (51.0% versus 25.2%). Urgency urinary incontinence and increased urinary frequency were also more common. These associations are anatomically plausible because urinary continence and vaginal support depend partly on shared pelvic-floor musculature and connective-tissue structures. Bump et al. [6] established standardized terminology for pelvic organ prolapse and pelvic-floor dysfunction, while Haylen et al. [7] further clarified the terminology and clinical assessment of pelvic organ prolapse. These standardized definitions are important because urinary incontinence, vaginal laxity, and prolapse-related complaints represent distinct clinical phenomena, even when they coexist. Vaginal bulging sensation demonstrated the strongest association with self-perceived vaginal laxity in the multivariable model, with an adjusted odds ratio of 6.95 (95% CI: 3.70–13.03). This finding should not be interpreted as evidence of a clinical risk relationship because the regression estimates were generated rather than obtained from observed participants. Nevertheless, the distinction between subjective vaginal laxity and pelvic organ prolapse remains clinically important. The terminology proposed by Haylen et al. [7] supports the use of standardized symptom descriptions and anatomical assessment when evaluating women presenting with vaginal bulging or altered vaginal support. Pelvic-floor muscle strength was lower in the vaginal laxity group, with a mean Modified Oxford Scale score of 2.2 ± 1.0 compared with 2.7 ± 1.1 in women without vaginal laxity. Weak pelvic-floor contraction was present in 63.4% and 42.8% of the respective groups. These findings suggest a potential relationship between perceived vaginal looseness and reduced muscular support. However, vaginal sensation may also be influenced by connective-tissue characteristics, vaginal dimensions, sexual arousal, and individual expectations. Pauls et al. [17] highlighted the clinical uncertainty surrounding vaginal laxity and its implications for women's quality of life. Consequently, subjective vaginal laxity should not be regarded as a direct measure of pelvic-floor muscle strength. Sexual symptoms were also more frequent in the vaginal laxity group. Dyspareunia was present in 40.5% compared with 26.4% of women without vaginal laxity, while reduced sexual satisfaction was reported in 56.9% and 33.2%, respectively. Postpartum sexual function is multifactorial and may be influenced by perineal trauma, hormonal changes, breastfeeding, psychological factors, and relationship characteristics. Signorello et al. [13] investigated postpartum sexual functioning in relation to perineal trauma and demonstrated the importance of obstetric factors in sexual morbidity following childbirth. Rosen et al. [9] developed the Female Sexual Function Index as a multidimensional instrument for evaluating female sexual function, while Wiegel et al. [10] subsequently examined its psychometric performance and clinical cutoff scores. These instruments provide a standardized framework for evaluating sexual outcomes rather than relying exclusively on individual symptoms. The synthetic vaginal laxity group also demonstrated greater pelvic-floor symptom distress, with a mean PFDI-20 score of 66.4 ± 19.4 compared with 42.7 ± 18.9. Barber et al. [8] developed the shortened Pelvic Floor Distress Inventory and Pelvic Floor Impact Questionnaire to facilitate assessment of pelvic-floor symptoms and their effects on quality of life. Subsequent validation studies supported the usefulness of these instruments in clinical research [15,16]. However, the domain scores and total PFDI-20 scores in the present dataset require reconciliation before the numerical findings can be regarded as internally consistent. Breastfeeding and postpartum hormonal changes may also influence pelvic-floor and sexual symptoms. Lovejoy et al. [14] investigated the association between breastfeeding and pelvic-floor disorders during long-term follow-up after vaginal delivery. Their work emphasizes the importance of considering postpartum reproductive and obstetric characteristics when interpreting pelvic-floor outcomes. Sexual function and pelvic-floor symptoms should therefore be evaluated in relation to multiple clinical and personal factors rather than attributed solely to delivery mode or perceived vaginal laxity. Conservative pelvic-floor rehabilitation remains relevant to the management of several postpartum pelvic-floor complaints. Woodley et al. [18], in a Cochrane systematic review, evaluated pelvic-floor muscle training for the prevention and treatment of urinary and faecal incontinence during pregnancy and after childbirth. Although pelvic-floor muscle training has an established role in managing selected continence symptoms, its effectiveness for subjective vaginal laxity cannot be assumed from evidence concerning urinary incontinence alone. Appropriate treatment should be guided by the presenting symptoms, clinical examination, and individual patient preferences. Sexual quality-of-life assessment may also benefit from instruments specifically developed for women with pelvic-floor disorders. Rogers et al. [19] developed the short-form Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire, which provides an additional approach to assessing sexual function in women experiencing pelvic-floor symptoms. Barber et al. [20] further demonstrated the responsiveness of pelvic-floor symptom and quality-of-life instruments among women undergoing treatment for pelvic organ prolapse. Together, these studies support comprehensive assessment of urinary, prolapse-related, and sexual symptoms when investigating vaginal laxity. The principal limitation of the present analysis is that its numerical distributions and statistical associations were generated for methodological demonstration rather than obtained from independently recruited participants. Accordingly, the findings cannot establish the prevalence, determinants, or clinical consequences of vaginal laxity among postpartum women. In addition, a cross-sectional design would not establish causal or temporal relationships, even when applied to observed clinical data. Future research should incorporate representative postpartum populations, validated patient-reported measures, standardized pelvic-floor examination, and appropriately planned statistical analyses. Longitudinal studies would be particularly valuable for understanding how perceived vaginal laxity and associated pelvic-floor symptoms change following childbirth.

Self-perceived vaginal laxity is a clinically relevant postpartum concern that warrants assessment alongside urinary, prolapse-related, bowel, and sexual symptoms. Published research supports the importance of considering obstetric history, pelvic-floor muscle function, and patient-reported symptom burden when evaluating postpartum pelvic-floor health. The analysis illustrated how these variables could be examined in a cross-sectional study. Its numerical associations cannot be interpreted as original clinical findings. Prospective studies using validated questionnaires and objective pelvic-floor assessments are needed to clarify the relationship between perceived vaginal laxity and postpartum pelvic-floor dysfunction.

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