Endometriosis, High-Risk HPV Infection, and Colposcopic Abnormalities in HPV-Positive Women: A Cross-Sectional Study

Endometriosis, High-Risk HPV Infection, and Colposcopic Abnormalities in HPV-Positive Women: A Cross-Sectional Study | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Endometriosis, High-Risk HPV Infection, and Colposcopic Abnormalities in HPV-Positive Women: A Cross-Sectional Study Shaghayegh Vandadi, Akram Ghahghaei Nezamabadi, Reyhane Hosseini, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-10042122/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 11 You are reading this latest preprint version Abstract Background Endometriosis is a chronic inflammatory gynecological disorder that may influence local immune responses and alter the clinical behavior of human papillomavirus (HPV) infection. Although HPV infection is a major cause of cervical epithelial abnormalities, the relationship between endometriosis and colposcopic findings among HPV-positive women remains insufficiently understood. This study aimed to evaluate the association between endometriosis, HPV risk typing, and colposcopic findings in women with confirmed HPV infection. Methods This cross-sectional study was conducted at Arash Women Hospital, Tehran University of Medical Sciences, between 2024 and 2025. HPV-positive women were classified according to the presence or absence of endometriosis. Demographic, reproductive, cytological, pathological, HPV genotyping, and colposcopic data were collected from clinical records, structured interviews, laboratory reports, and standardized colposcopic examinations. HPV types were categorized as high-risk or low-risk, and colposcopic findings were classified as normal, aceto-white changes, or coarse mosaicism. Statistical analyses included chi-square tests, independent-samples t-tests, odds ratios with 95% confidence intervals, and multivariable logistic regression. Results A total of 800 HPV-positive women were included. High-risk HPV was significantly more frequent among women with endometriosis than controls (73.3% vs. 40.5%; OR = 4.02, 95% CI: 2.99–5.42; p < 0.001). Abnormal colposcopy was also more common in the endometriosis group (69.5% vs. 17.8%; OR = 10.56, 95% CI: 7.57–14.74; p < 0.001). After adjustment, endometriosis remained independently associated with abnormal colposcopy (adjusted OR = 10.47; p < 0.001). Pap smear and biopsy pathology did not differ significantly between groups. Conclusion Endometriosis was associated with high-risk HPV infection and abnormal colposcopic findings among HPV-positive women, supporting individualized cervical surveillance in this population. Clinical Trial Registration Not applicable. Endometriosis Human Papillomavirus Colposcopy High-Risk HPV Cervical Screening Figures Figure 1 Figure 2 Figure 3 1. Introduction Endometriosis is a chronic, estrogen-dependent condition in which endometrial-like tissue exists outside the uterine cavity, often resulting in pain, infertility, and inflammatory changes in the pelvic environment(1, 2). Despite being a prevalent gynecological disorder, its systemic effects, including potential interactions with infectious agents such as human papillomavirus (HPV), are not yet fully understood(3). Given the immunomodulatory nature of endometriosis and the viral persistence mechanisms of HPV, investigating the potential interplay between these two conditions is essential for improving diagnostic and surveillance strategies . HPV infection, particularly with high-risk genotypes, is a well-established cause of cervical neoplasia and remains a significant global health burden. Colposcopy serves as a cornerstone in the clinical evaluation of HPV-infected women, offering visual cues to guide the detection and management of precancerous cervical lesions(4). However, factors that may influence colposcopic patterns such as coexisting gynecological conditions like endometriosis have not been extensively investigated, despite their possible impact on local immune responses and epithelial integrity(5). Emerging research has suggested a possible association between endometriosis and altered HPV infection dynamics, including differences in genotype distribution and infection persistence(5, 6). These findings raise questions about whether endometriosis may modify the cervical microenvironment in ways that affect colposcopic appearance. Understanding such changes is crucial, as misinterpretation of colposcopic features could lead to under- or over-treatment in affected patients . furthermore, the chronic inflammation and altered hormonal milieu seen in endometriosis may exacerbate epithelial changes in the cervix, mimicking or masking lesions typically associated with HPV(7, 8). This biological complexity necessitates a deeper exploration into how endometriosis might influence the detection and interpretation of cervical abnormalities under colposcopic examination. The presence of coexisting endometriosis could have clinical implications for the surveillance and risk stratification of HPV-positive women(9). to date, few studies have specifically addressed the relationship between endometriosis and colposcopic findings in HPV-infected populations. Most literature has focused on either condition in isolation, leaving a gap in knowledge regarding their potential interaction. With HPV vaccination efforts underway globally, and an increasing emphasis on precision medicine in gynecology, identifying patient subgroups with unique risk profiles remains a priority(10) . This study aims to fill this gap by examining the effect of endometriosis on colposcopic patterns in a cohort of HPV-positive women. By comparing the demographic, clinical, and colposcopic characteristics of women with and without endometriosis, we hope to provide insight into whether this gynecological comorbidity influences cervical assessment outcomes. The findings could inform tailored screening protocols and contribute to a more nuanced understanding of HPV-related disease in women with complex gynecological histories. 2. Methods 2.1 . Study Design, Setting, and Participants This cross-sectional study was conducted to evaluate the association between endometriosis and colposcopic findings among women with confirmed human papillomavirus (HPV) infection. The study was carried out at Arash Women Hospital, a tertiary referral center affiliated with Tehran University of Medical Sciences, Tehran, Iran, between 2024 and 2025. The study was designed and reported in accordance with the STROBE recommendations for observational cross-sectional studies. Eligible participants were recruited from outpatient gynecology and colposcopy clinics. Women were considered eligible if they had laboratory-confirmed HPV infection based on polymerase chain reaction (PCR)-based HPV testing and had available clinical and colposcopic data. Participants were classified into two groups according to endometriosis status: women with confirmed endometriosis and HPV-positive women without evidence of endometriosis. The sample size was estimated based on HPV prevalence rates reported in previous studies investigating HPV infection among women with endometriosis. Moslehi et al.(5) reported an HPV prevalence of 24.69% among women with surgically confirmed endometriosis and used an expected prevalence of 40% for sample size estimation. In addition, Li et al. reported, through a combined meta-analysis and case-control study of surgically treated patients with endometriosis, an overall HPV prevalence of approximately 46% and a high-risk HPV prevalence of approximately 36% among affected patients. Based on these prior estimates, the required sample size was calculated using the single-proportion formula (n = Z²p (1 − p) / d²), where Z = 1.96 for a 95% confidence level, (p = 0.40) as the expected prevalence, and (d = 0.06) as the desired precision. This yielded a minimum required sample of approximately 256–270 participants. To improve statistical power, allow reliable between-group comparisons, and support subgroup and regression analyses, the final sample size was increased to 800 HPV-positive women, including 400 patients with endometriosis and 400 controls without endometriosis. The diagnosis of endometriosis was established using clinical, imaging, and/or surgical criteria. Clinical evidence included symptoms and physical examination findings suggestive of endometriosis, while imaging evidence was based on transvaginal ultrasonography and/or magnetic resonance imaging when available. Surgical confirmation through laparoscopy or laparotomy was considered when documented in the medical record. Women without clinical, imaging, or surgical evidence of endometriosis were assigned to the control group. Participants were excluded if they were pregnant, had a history of hysterectomy, had known cervical cancer or previously diagnosed cervical dysplasia, had immunosuppressive conditions such as HIV infection or chronic corticosteroid use, had received HPV vaccination, or had incomplete data for the main variables of interest. Written informed consent was obtained from all participants before enrollment. The study protocol was approved by the Ethics Committee of Tehran University of Medical Sciences under the ethics approval code IR.TUMS.IKHC.REC.1403.192. 2.2 . Data Collection, Variables, and Measurements Data were collected using a structured interview guide developed specifically for this study by the research team. The guide was not previously published elsewhere. Its items were designed according to the study objectives and were informed by variables commonly assessed in similar studies evaluating endometriosis and HPV infection, including studies by Moslehi et al.(5), Hong et al.(6), and Rocha et al(11). The guide included demographic and reproductive characteristics, endometriosis-related clinical variables, HPV-related information, Pap smear results, and colposcopic findings. An English-language version of the interview guide has been uploaded as Supplementary File 1. Demographic and reproductive variables included age, body mass index (BMI), gravidity, parity, number of abortions, marital status, education level, place of residence, and history of underlying disease. Endometriosis-related variables included duration of disease, history of surgery or hormonal treatment, ultrasonography findings, MRI findings, surgical findings, physical examination findings, infertility status, dysmenorrhea, dyspareunia, abnormal uterine bleeding, chronic pelvic pain, urinary symptoms, and gastrointestinal symptoms. The primary exposure variable was endometriosis status, categorized as presence or absence of endometriosis. The main outcome variable was colposcopic finding among HPV-positive women. Colposcopic findings were categorized as normal, aceto-white changes, or coarse mosaicism. For additional analysis, colposcopic findings were also dichotomized into normal and abnormal findings, with aceto-white changes and coarse mosaicism grouped as abnormal colposcopy. HPV-related variables were obtained from PCR-based genotyping results. HPV types were classified as high-risk or low-risk according to their oncogenic potential. High-risk HPV included oncogenic genotypes such as HPV 16, 18, 31, 33, and other recognized high-risk types, while low-risk HPV included non-oncogenic or low-oncogenic-risk types such as HPV 6 and 11. Among women with high-risk HPV, subgroup classification was also performed when available, including HPV 16/18 and other high-risk HPV types. All participants underwent standardized colposcopic evaluation by trained gynecologists. To reduce measurement bias, colposcopic examinations were performed using a consistent clinical approach, including application of 3–5% acetic acid to the cervix and documentation of findings according to accepted colposcopic criteria. When biopsy was performed, pathology results were categorized as normal, CIN1, or CIN2. Pap smear results were also recorded and categorized as normal, ASC-US, LSIL, or HSIL according to the available cytology report. Data were checked for completeness, coding consistency, and biologically implausible values before analysis. 2.3 . Statistical Analysis All statistical analyses were performed using IBM SPSS Statistics version 26.0. Descriptive statistics were used to summarize demographic, reproductive, clinical, HPV-related, cytological, pathological, and colposcopic characteristics of the study population. Continuous variables were reported as mean ± standard deviation when approximately normally distributed and as median and interquartile range when distributional assumptions were not met. Categorical variables were summarized as frequencies and percentages. Normality of continuous variables was assessed using the Kolmogorov–Smirnov test, supported by visual inspection of histograms and Q-Q plots. Between-group comparisons for continuous variables were performed using the independent-samples t-test when assumptions were satisfied. For variables with non-normal distribution, non-parametric alternatives such as the Mann–Whitney U test were considered. Categorical variables, including HPV typing, Pap smear results, biopsy pathology, and colposcopic findings, were compared between the endometriosis and control groups using the chi-square test. Fisher’s exact test was planned when expected cell counts were insufficient for chi-square testing. To estimate the magnitude of association, odds ratios (ORs) with 95% confidence intervals (CIs) were calculated for key outcomes. The association between endometriosis and high-risk HPV infection was assessed using cross-tabulation and logistic regression. The association between endometriosis and abnormal colposcopic findings was first evaluated using unadjusted analysis and then further examined using binary logistic regression. In the adjusted model, abnormal colposcopy was entered as the dependent variable, while endometriosis status was entered as the main independent variable. Age, BMI, and HPV typing were included as covariates because of their potential clinical relevance as confounders. Missing data were handled using complete-case analysis, and no imputation was applied. No formal sensitivity analysis was performed. Subgroup analyses were conducted to evaluate abnormal colposcopic findings within HPV risk categories, particularly among women with high-risk HPV. Model fit for logistic regression was assessed using standard diagnostic indices, including the Hosmer–Lemeshow goodness-of-fit test when applicable. A two-sided p-value of less than 0.05 was considered statistically significant. 3. Results 3.1 . Demographic, Reproductive, and Clinical Characteristics A total of 800 HPV-positive women were included in the final analysis, with 400 participants in the endometriosis group and 400 participants in the control group. Because all eligible participants included in the final dataset had complete data for the main analytical variables, no participant flow diagram was generated. The two groups were broadly comparable in terms of baseline demographic and reproductive characteristics. The mean age was 32.59 ± 4.83 years in the endometriosis group and 32.31 ± 5.05 years in the control group, with no statistically significant difference between the two groups (p = 0.432). Similarly, BMI was comparable between women with endometriosis and controls (25.52 ± 3.97 vs. 25.18 ± 4.04 kg/m², respectively; p = 0.222). These findings indicate that the two groups were well balanced with respect to age and BMI (Table 1) . Reproductive characteristics were also similar between the study groups. The mean number of pregnancies was 1.55 ± 1.28 in the endometriosis group and 1.49 ± 1.25 in the control group, with no statistically significant difference (p = 0.502). The number of abortions was also comparable between groups (0.35 ± 0.54 vs. 0.40 ± 0.55; p = 0.194). Likewise, parity did not differ significantly between the endometriosis and control groups (1.21 ± 1.36 vs. 1.10 ± 1.31; p = 0.244). Overall, there were no statistically significant differences between the endometriosis and control groups regarding age, BMI, gravidity, abortions, or parity. This comparability reduces the likelihood that baseline demographic or reproductive differences explain the observed associations between endometriosis, HPV typing, and colposcopic findings. 3.2 . HPV Typing Distribution and High-Risk HPV Association In the total study population, 455 women (56.9%) had high-risk HPV infection, while 345 women (43.1%) had low-risk HPV infection. Among women with high-risk HPV, 227 cases (49.9%) were classified as HPV 16/18, and 228 cases (50.1%) were classified as other high-risk HPV types. This distribution shows that high-risk HPV genotypes represented the majority of HPV infections in the study population. A statistically significant difference was observed in HPV typing between the endometriosis and control groups. High-risk HPV was detected in 293 of 400 women with endometriosis (73.3%) compared with 162 of 400 controls (40.5%). In contrast, low-risk HPV was less frequent in the endometriosis group than in the control group, occurring in 107 women (26.8%) and 238 women (59.5%), respectively. The difference in HPV risk-type distribution between the two groups was statistically significant (χ² = 87.46, p < 0.001). (Figure 1) The magnitude of this association was clinically meaningful. Women with endometriosis had approximately fourfold higher odds of harboring high-risk HPV compared with women without endometriosis (OR = 4.02, 95% CI: 2.99–5.42) (Table 2). In multivariable logistic regression adjusted for age and BMI, endometriosis remained independently associated with high-risk HPV infection (adjusted OR = 4.03, p < 0.001), whereas age (p = 0.692) and BMI (p = 0.949) were not independently associated with HPV risk type Table 3). 3.3 . Colposcopic, Cytological, Pathological, and Regression Findings Colposcopic findings differed markedly between the two groups. Normal colposcopy was observed in 329 women in the control group (82.3%) compared with 122 women in the endometriosis group (30.5%). Aceto-white changes were present in 154 women with endometriosis (38.5%) and 40 controls (10.0%). Coarse mosaicism was also more frequent in the endometriosis group, occurring in 124 women (31.0%) compared with 31 controls (7.8%). The overall distribution of colposcopic findings was significantly different between groups (χ² = 217.80, p < 0.001) (Table 4 and Figure 2) . When colposcopic findings were dichotomized into normal and abnormal findings, abnormal colposcopy, defined as aceto-white changes or coarse mosaicism, was observed in 278 women with endometriosis (69.5%) compared with 71 controls (17.8%). The association between endometriosis and abnormal colposcopy was statistically significant (χ² = 217.79, p < 0.001). The odds of abnormal colposcopic findings were more than ten times higher among women with endometriosis than among controls (OR = 10.56, 95% CI: 7.57–14.74) (Table 5). In multivariable logistic regression adjusted for age, BMI, and HPV typing, endometriosis remained strongly and independently associated with abnormal colposcopy (adjusted OR = 10.47, p < 0.001). Age was not significantly associated with abnormal colposcopy (OR = 1.02, p = 0.327), BMI showed a borderline association (OR = 1.04, p = 0.057), and HPV typing was not independently associated with abnormal colposcopy after adjustment (OR = 1.02, p = 0.899). The model was statistically significant overall (χ² = 234.55, p < 0.001), and the Hosmer–Lemeshow test indicated acceptable model fit (p = 0.257) (Table 6 and Figure 3) Pap smear findings did not differ significantly between groups. In the control group, 146 women (36.5%) had normal cytology, 92 (23.0%) had ASC-US, 102 (25.5%) had LSIL, and 60 (15.0%) had HSIL or category 3 findings. In the endometriosis group, 175 women (43.8%) had normal cytology, 69 (17.3%) had ASC-US, 98 (24.5%) had LSIL, and 58 (14.5%) had HSIL or category 3 findings. The difference in Pap smear distribution was not statistically significant (χ² = 6.02, p = 0.111) (Table 7). Similarly, biopsy pathology did not show a statistically significant difference between the two groups. Normal biopsy findings were observed in 238 controls (59.5%) and 224 women with endometriosis (56.0%). CIN1 was detected in 119 controls (29.8%) and 131 women with endometriosis (32.8%), while CIN2 was detected in 43 controls (10.8%) and 45 women with endometriosis (11.3%). The overall distribution of biopsy pathology was not significantly different between groups (χ² = 1.05, p = 0.593) (Table 8) . 4. Discussion This cross-sectional study evaluated the association between endometriosis and colposcopic findings among HPV-positive women. The main findings were that women with endometriosis had a significantly higher frequency of high-risk HPV infection and a markedly higher prevalence of abnormal colposcopic findings compared with HPV-positive women without endometriosis. Specifically, high-risk HPV was detected in 73.3% of women with endometriosis compared with 40.5% of controls, and abnormal colposcopy was observed in 69.5% of the endometriosis group compared with 17.8% of the control group. These associations remained clinically meaningful, particularly for abnormal colposcopy, which showed more than tenfold higher odds among women with endometriosis . The baseline comparability of the two groups strengthens the internal interpretation of these findings. Age, BMI, gravidity, abortion history, and parity did not differ significantly between the endometriosis and control groups. Therefore, the observed differences in HPV risk typing and colposcopic patterns are less likely to be explained by these baseline demographic or reproductive variables. In the adjusted regression model, endometriosis remained independently associated with abnormal colposcopy after controlling for age, BMI, and HPV typing, suggesting that endometriosis itself may be linked to altered cervical appearance among HPV-positive women . One of the most clinically relevant findings of this study was the strong association between endometriosis and abnormal colposcopic appearance. Aceto-white changes and coarse mosaicism were both substantially more frequent in the endometriosis group. These findings are important because colposcopy is a key step in the evaluation of HPV-positive women and guides decisions regarding biopsy and follow-up. The markedly higher prevalence of abnormal colposcopic findings among women with endometriosis suggests that this population may require particular attention during cervical assessment, even when cytology or biopsy results do not show parallel significant differences . Our findings are partly consistent with previous studies that have suggested a relationship between HPV infection and endometriosis, although the direction and strength of the association have varied across the literature. Moslehi et al. reported HPV infection in 24.69% of women with endometriosis and found that low-risk HPV genotypes, particularly HPV 6 and HPV 11, were the most common types(5). In contrast, our study found a much higher proportion of high-risk HPV among women with endometriosis. This discrepancy may be explained by differences in study population, sampling site, HPV detection methods, inclusion criteria, and the fact that our study included only HPV-positive women and focused on HPV risk-type distribution and colposcopic findings rather than estimating HPV prevalence in all women with endometriosis . The results should also be interpreted in light of newer evidence from Li et al., who reported a higher prevalence of HPV and high-risk HPV among patients with endometriosis but concluded that HPV infection may not be a primary causal risk factor for developing endometriosis(12). Their findings suggest that HPV may be more relevant to clinical course or reproductive outcomes than to the initial development of endometriosis. Our results align with this cautious interpretation. We do not suggest that HPV causes endometriosis; rather, our findings indicate that among women already infected with HPV, the presence of endometriosis is associated with a greater likelihood of high-risk HPV carriage and abnormal colposcopic findings . Several biological mechanisms may explain the observed association. Endometriosis is characterized by chronic inflammation, altered immune surveillance, angiogenesis, hormonal dysregulation, and changes in local tissue response. These processes may influence the cervical and lower genital tract microenvironment, potentially affecting HPV persistence, viral clearance, epithelial response, and colposcopic appearance.(13, 14) High-risk HPV infection is also known to interact with host immune mechanisms, and impaired viral clearance could contribute to persistent epithelial changes. Therefore, it is biologically plausible that endometriosis may modify the clinical expression of HPV infection, even if it is not directly responsible for the acquisition of HPV(15) . An important observation in this study was that Pap smear and biopsy pathology did not differ significantly between groups. Pap smear distribution was comparable between women with and without endometriosis, and biopsy pathology showed no significant difference in normal findings, CIN1, or CIN2. This distinction is essential for interpreting the study accurately. Although endometriosis was strongly associated with abnormal colposcopic appearance, this did not translate into a statistically significant increase in cytological abnormality or histopathological CIN in the present dataset. These findings suggest that abnormal colposcopic features in women with endometriosis may reflect inflammatory or epithelial response patterns as well as HPV-related changes, and should not automatically be interpreted as evidence of more severe cervical pathology . From a clinical perspective, the findings support a more individualized approach to cervical evaluation in HPV-positive women with endometriosis. The high frequency of high-risk HPV and abnormal colposcopy in this group suggests that gynecologists and colposcopists should carefully consider endometriosis status when interpreting colposcopic findings and planning follow-up. However, because biopsy pathology was not significantly different between groups, the results do not justify overtreatment. Instead, they support careful surveillance, appropriate biopsy when indicated, and risk-based follow-up rather than aggressive management based solely on the presence of endometriosis . This study has several limitations. First, its cross-sectional design prevents any causal inference or assessment of temporal relationships between endometriosis, HPV risk type, and colposcopic findings. Second, although age and BMI were included in adjusted analyses, other potential confounders such as smoking, sexual behavior, number of sexual partners, contraceptive use, hormonal therapy, HPV viral load, and duration of HPV infection were not fully controlled. Third, the study was conducted in a tertiary referral hospital, which may limit generalizability to community-based populations. Referral-center patients may have more complex gynecological histories or more severe symptoms than the general population. Finally, while colposcopy was standardized, visual interpretation remains partly subjective, and interobserver variability cannot be fully excluded . Despite these limitations, the study has notable strengths, including a relatively large sample size, equal group allocation, complete data for the main analytical variables, and the use of both unadjusted and adjusted analyses. The findings provide evidence that endometriosis is associated with high-risk HPV carriage and abnormal colposcopic findings among HPV-positive women, independent of age and BMI. Future longitudinal studies are needed to determine whether women with both endometriosis and high-risk HPV have increased persistence of HPV infection, greater progression to CIN, or different long-term cervical outcomes. Until such evidence is available, the results should be interpreted as supporting enhanced clinical awareness and individualized surveillance rather than proving a causal relationship between endometriosis and cervical disease progression. In conclusion, this cross-sectional study showed that among HPV-positive women, endometriosis was significantly associated with a higher prevalence of high-risk HPV infection and a markedly greater frequency of abnormal colposcopic findings, including aceto-white changes and coarse mosaicism. This association remained strong after adjustment for age, BMI, and HPV typing, suggesting that endometriosis may be independently related to altered colposcopic appearance in HPV-infected women. However, Pap smear findings and biopsy pathology did not differ significantly between groups, indicating that abnormal colposcopic patterns in this population should be interpreted carefully and not necessarily as evidence of more advanced cervical pathology. These findings support individualized cervical surveillance and careful colposcopic assessment in HPV-positive women with endometriosis, while highlighting the need for longitudinal studies to clarify whether this association influences HPV persistence, CIN progression, or long-term cervical cancer risk. Abbreviations ACW Aceto-White Changes BMI Body Mass Index CIN Cervical Intraepithelial Neoplasia GI Gastrointestinal HSIL High-Grade Squamous Intraepithelial Lesion HPV Human Papillomavirus HR-HPV High-Risk Human Papillomavirus IFCPC International Federation for Cervical Pathology and Colposcopy LR-HPV Low-Risk Human Papillomavirus LSIL Low-Grade Squamous Intraepithelial Lesion MRI Magnetic Resonance Imaging PCR Polymerase Chain Reaction SD Standard Deviation Declarations Conflict of interest: The authors declare that they have no conflict of interest. Ethical approval: Ethics approval and consent to participate: This study was conducted in accordance with the Declaration of Helsinki and was approved by the Ethics Committee of the Tehran University of Medical Sciences Ethics Committee (IR.TUMS.IKHC.REC.1403.192). Informed consent was obtained from all participants. Consent for publication: Not applicable . Availability of data and materials: The datasets analyzed during the current study are available from the corresponding author on reasonable request . Author contributions: AHH, MJ, and SAM: Conceptualization, methodology and data curation, SA, SYT, SHK, and AS: Investigation, AHH, MJ, NSH, and SHK: Formal analysis, supervision, visualization, original draft preparation. SAM,MN and AKV: Review and editing. Financial disclosure: The authors declare that this study has received no financial support. Informed consent: Informed consent was obtained from all individual participants included in the study. Competing interests: The authors declare that they have no competing interests . Funding: This study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors . Acknowledgements: The authors would like to thank the staff of Arash Women Hospital and the participants for their cooperation and contribution to this study. Permission to Reproduce Material Not applicable. References Saunders PTK, Horne AW. Endometriosis: Etiology, pathobiology, and therapeutic prospects. Cell. 2021;184(11):2807–24. Cousins FL, McKinnon BD, Mortlock S, Fitzgerald HC, Zhang C, Montgomery GW, et al. New concepts on the etiology of endometriosis. J Obstet Gynecol Res. 2023;49(4):1090–105. Jensen JE, Becker GL, Jackson JB, Rysavy MB. Human Papillomavirus and Associated Cancers: A Review. Viruses. 2024;16(5). Qi SY, Yang MM, Li CY, Yu K, Deng SL. The HPV viral regulatory mechanism of TLRs and the related treatments for HPV-associated cancers. Front Immunol. 2024;15:1407649. Moslehi Z, Derakhshan R, Chaichian S, Mehdizadeh Kashi A, Sabet B, Rokhgireh S. Correlation of High-Risk Human Papilloma Virus with Deep Endometriosis: A Cross-Sectional Study. Biomed Res Int. 2023;2023:6793898. Hong YS, Park J, Kim H. Association of endometriosis with genital human papillomavirus infection in US women: a national population-based study. Sci Rep. 2023;13(1):8020. Fernandes JV, TA DEMF, JC DEA, Cobucci RN, MG DEC, Andrade VS, et al. Link between chronic inflammation and human papillomavirus-induced carcinogenesis (Review). Oncol Lett. 2015;9(3):1015–26. Adilbayeva A, Kunz J. Pathogenesis of Endometriosis and Endometriosis-Associated Cancers. Int J Mol Sci. 2024;25(14):7624. Garvey M, Endometriosis. Future Biological Perspectives for Diagnosis and Treatment. Int J Mol Sci. 2024;25(22):12242. Heidarpour M, Derakhshan M, Derakhshan-Horeh M, Kheirollahi M, Dashti S. Prevalence of high-risk human papillomavirus infection in women with ovarian endometriosis: HPV in women with ovarian endometriosis. J Obstet Gynecol Res. 2016;43. Rocha RM, Souza RP, Gimenes F, Consolaro MEL. The high-risk human papillomavirus continuum along the female reproductive tract and its relationship to infertility and endometriosis. Reprod Biomed Online. 2019;38(6):926–37. Li W, Wang Z, Qi H, Xia C, Chen F, Xu J, et al. The association between HPV infection and endometriosis: Risk and fertility outcomes. J Biomedical Res. 2025;39:1–12. Greygoose E, Metharom P, Kula H, Seckin TK, Seckin TA, Ayhan A et al. The Estrogen-Immune Interface in Endometriosis. Cells. 2025;14(1). Kłodnicka K, Michalska A, Januszewski J, Forma A, Teresiński G, Flieger J, et al. From Inflammation to Malignancy: The Link Between Endometriosis and Gynecological Cancers. Int J Mol Sci. 2025;26(24):11816. Wang J, Tian Z, Wang J. Risk factors for persistent infection of high-risk HPV in patients with cervical intraepithelial neoplasia. Am J Transl Res. 2025;17(4):2992–3000. Tables Table 1. Demographic and reproductive characteristics of the study participants Variable Control group (n = 400) Endometriosis group (n = 400) p-value Age, years, mean ± SD 32.31 ± 5.05 32.59 ± 4.83 0.432 BMI, kg/m², mean ± SD 25.18 ± 4.04 25.52 ± 3.97 0.222 Gravidity, mean ± SD 1.49 ± 1.25 1.55 ± 1.28 0.502 Abortions, mean ± SD 0.40 ± 0.55 0.35 ± 0.54 0.194 Parity, mean ± SD 1.10 ± 1.31 1.21 ± 1.36 0.244 Table 2. HPV typing distribution according to study group HPV type Control group (n = 400) Endometriosis group (n = 400) OR 95% CI p-value Low-risk HPV 238 (59.5%) 107 (26.8%) Reference — — High-risk HPV 162 (40.5%) 293 (73.3%) 4.02 2.99–5.42 <0.001 Table 3. Multivariable logistic regression for factors associated with high-risk HPV infection Variable Adjusted OR 95% CI p-value Endometriosis 4.03 2.99–5.43 <0.001 Age 0.99 0.96–1.02 0.692 BMI 1.00 0.96–1.04 0.949 Table 4. Colposcopic findings according to study group Colposcopic finding Control group (n = 400) Endometriosis group (n = 400) p-value Normal 329 (82.3%) 122 (30.5%) <0.001 Aceto-white changes 40 (10.0%) 154 (38.5%) Coarse mosaicism 31 (7.8%) 124 (31.0%) Table 5. Abnormal colposcopy according to study group Colposcopy category Control group (n = 400) Endometriosis group (n = 400) OR 95% CI p-value Normal colposcopy 329 (82.3%) 122 (30.5%) Reference — — Abnormal colposcopy 71 (17.8%) 278 (69.5%) 10.56 7.57–14.74 <0.001 Table 6. Multivariable logistic regression for factors associated with abnormal colposcopy Variable Adjusted OR 95% CI p-value Endometriosis 10.47 7.35–14.91 <0.001 Age 1.02 0.98–1.05 0.327 BMI 1.04 1.00–1.08 0.057 High-risk HPV 1.02 0.72–1.46 0.899 Table 7. Pap smear findings according to study group Pap smear result Control group (n = 400) Endometriosis group (n = 400) p-value Normal 146 (36.5%) 175 (43.8%) 0.111 ASC-US 92 (23.0%) 69 (17.3%) LSIL 102 (25.5%) 98 (24.5%) HSIL 60 (15.0%) 58 (14.5%) Table 8. Biopsy pathology according to study group Biopsy pathology Control group (n = 400) Endometriosis group (n = 400) p-value Normal 238 (59.5%) 224 (56.0%) 0.593 CIN1 119 (29.8%) 131 (32.8%) CIN2 43 (10.8%) 45 (11.3%) Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Reviews received at journal 24 Jul, 2026 Reviewers agreed at journal 22 Jul, 2026 Reviews received at journal 21 Jul, 2026 Reviewers agreed at journal 21 Jul, 2026 Reviews received at journal 19 Jul, 2026 Reviewers agreed at journal 19 Jul, 2026 Reviewers invited by journal 15 Jul, 2026 Editor assigned by journal 14 Jul, 2026 Editor invited by journal 25 Jun, 2026 Submission checks completed at journal 24 Jun, 2026 First submitted to journal 24 Jun, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-10042122","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":678843445,"identity":"d402ea61-7de6-4c09-979b-6264362dc84b","order_by":0,"name":"Shaghayegh Vandadi","email":"","orcid":"","institution":"Arash Women's Hospital, Tehran University of Medical Sciences","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Shaghayegh","middleName":"","lastName":"Vandadi","suffix":""},{"id":678843446,"identity":"208cabab-7155-47e7-b199-1ea1bdcea7d3","order_by":1,"name":"Akram Ghahghaei Nezamabadi","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAxElEQVRIiWNgGAWjYBACNvYzBod//rNJbJNIPviAocYmsYGQFn6ePMPHDGxpif0SackGDMfSiglqkZzBb2zMwHbYWHJGjpkEY9PheoJaDG7wm0kX8JyXM7gB0tJwOJcILbzbpGdI3OYxuP+GaC1vt0nwGAC1EG2L/Y2c7z94Es7x2EO1EA4xoOFl0jwHDkBtaSJGy5mcMsmZDclALcBATjiWRoSW42fMJD422AG1AKPyAzFRiQoSSFM+CkbBKBgFowAXAADeKE0N+GaFswAAAABJRU5ErkJggg==","orcid":"","institution":"Arash Women's Hospital, Tehran University of Medical Sciences","correspondingAuthor":true,"submittingAuthor":false,"prefix":"","firstName":"Akram","middleName":"Ghahghaei","lastName":"Nezamabadi","suffix":""},{"id":678843447,"identity":"c5ac6481-b751-41d6-bfe2-f8ae51a1442b","order_by":2,"name":"Reyhane Hosseini","email":"","orcid":"","institution":"Arash Women's Hospital, Tehran University of Medical Sciences","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Reyhane","middleName":"","lastName":"Hosseini","suffix":""},{"id":678843448,"identity":"b76d15aa-e68c-45de-85a7-65f5380b258e","order_by":3,"name":"Kasra Jafari","email":"","orcid":"","institution":"Arash Women's Hospital, Tehran University of Medical Sciences","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Kasra","middleName":"","lastName":"Jafari","suffix":""},{"id":678843449,"identity":"2bc4b90a-b8a8-4fe8-b259-d966f47b9545","order_by":4,"name":"Amirhossein Hajialigol","email":"","orcid":"","institution":"Alborz Office of Universal Scientific Education and Research Network (USERN), Alborz University of Medical Sciences","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Amirhossein","middleName":"","lastName":"Hajialigol","suffix":""}],"badges":[],"createdAt":"2026-06-15 10:59:00","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-10042122/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-10042122/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":114950649,"identity":"9bf3f45c-e718-4e64-b16b-17fb76c3b9b3","added_by":"auto","created_at":"2026-07-17 07:31:18","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":55794,"visible":true,"origin":"","legend":"\u003cp\u003eHPV typing distribution according to study group.\u003c/p\u003e\n\u003cp\u003eHigh-risk HPV was detected in 293 women with endometriosis (73.3%) and 162 controls (40.5%), while low-risk HPV was detected in 107 women with endometriosis (26.8%) and 238 controls (59.5%). The distribution of HPV risk types differed significantly between groups (χ² = 87.46, p \u0026lt; 0.001). Women with endometriosis had approximately fourfold higher odds of high-risk HPV infection compared with controls (OR = 4.02, 95% CI: 2.99–5.42).\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-10042122/v1/3cb635c3fa4a18aa2fdbbd86.png"},{"id":114950650,"identity":"9b2561fc-c126-4931-b4b6-46a48c0a0843","added_by":"auto","created_at":"2026-07-17 07:31:18","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":64270,"visible":true,"origin":"","legend":"\u003cp\u003eColposcopic findings according to study group.\u003c/p\u003e\n\u003cp\u003eNormal colposcopy was more frequent in the control group than in the endometriosis group (329/400, 82.3% vs. 122/400, 30.5%). Aceto-white changes were observed in 154 women with endometriosis (38.5%) and 40 controls (10.0%), while coarse mosaicism was observed in 124 women with endometriosis (31.0%) and 31 controls (7.8%). The overall distribution of colposcopic findings differed significantly between groups (χ² = 217.80, p \u0026lt; 0.001).\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-10042122/v1/354b2c3cd87c1b6313ed385a.png"},{"id":114950651,"identity":"d23ed1dd-bd94-42b0-b016-8302b8b47734","added_by":"auto","created_at":"2026-07-17 07:31:18","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":57007,"visible":true,"origin":"","legend":"\u003cp\u003eMultivariable logistic regression analysis for predictors of abnormal colposcopy.\u003c/p\u003e\n\u003cp\u003eAbnormal colposcopy was defined as the presence of aceto-white changes or coarse mosaicism. After adjustment for age, BMI, and HPV typing, endometriosis remained independently associated with abnormal colposcopy (adjusted OR = 10.47, 95% CI: 7.35–14.91, p \u0026lt; 0.001). Age and HPV typing were not independently associated with abnormal colposcopy, while BMI showed a borderline association.\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-10042122/v1/12064bd10fc3f5a9dce83847.png"},{"id":114952423,"identity":"15305350-c0b6-4b80-86f9-4044df1c09d6","added_by":"auto","created_at":"2026-07-17 07:49:41","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":374219,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-10042122/v1/de05229a-3d57-446c-9fc0-876889fb4dbf.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Endometriosis, High-Risk HPV Infection, and Colposcopic Abnormalities in HPV-Positive Women: A Cross-Sectional Study","fulltext":[{"header":"1. Introduction","content":"\u003cp\u003eEndometriosis is a chronic, estrogen-dependent condition in which endometrial-like tissue exists outside the uterine cavity, often resulting in pain, infertility, and inflammatory changes in the pelvic environment(1, 2). Despite being a prevalent gynecological disorder, its systemic effects, including potential interactions with infectious agents such as human papillomavirus (HPV), are not yet fully understood(3). Given the immunomodulatory nature of endometriosis and the viral persistence mechanisms of HPV, investigating the potential interplay between these two conditions is essential for improving diagnostic and surveillance strategies\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e HPV infection, particularly with high-risk genotypes, is a well-established cause of cervical neoplasia and remains a significant global health burden. Colposcopy serves as a cornerstone in the clinical evaluation of HPV-infected women, offering visual cues to guide the detection and management of precancerous cervical lesions(4). However, factors that may influence colposcopic patterns such as coexisting gynecological conditions like endometriosis have not been extensively investigated, despite their possible impact on local immune responses and epithelial integrity(5).\u003c/p\u003e\n\u003cp\u003eEmerging research has suggested a possible association between endometriosis and altered HPV infection dynamics, including differences in genotype distribution and infection persistence(5, 6). These findings raise questions about whether endometriosis may modify the cervical microenvironment in ways that affect colposcopic appearance. Understanding such changes is crucial, as misinterpretation of colposcopic features could lead to under- or over-treatment in affected patients\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e furthermore, the chronic inflammation and altered hormonal milieu seen in endometriosis may exacerbate epithelial changes in the cervix, mimicking or masking lesions typically associated with HPV(7, 8). This biological complexity necessitates a deeper exploration into how endometriosis might influence the detection and interpretation of cervical abnormalities under colposcopic examination. The presence of coexisting endometriosis could have clinical implications for the surveillance and risk stratification of HPV-positive women(9). to date, few studies have specifically addressed the relationship between endometriosis and colposcopic findings in HPV-infected populations. Most literature has focused on either condition in isolation, leaving a gap in knowledge regarding their potential interaction. With HPV vaccination efforts underway globally, and an increasing emphasis on precision medicine in gynecology, identifying patient subgroups with unique risk profiles remains a priority(10)\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003eThis study aims to fill this gap by examining the effect of endometriosis on colposcopic patterns in a cohort of HPV-positive women. By comparing the demographic, clinical, and colposcopic characteristics of women with and without endometriosis, we hope to provide insight into whether this gynecological comorbidity influences cervical assessment outcomes. The findings could inform tailored screening protocols and contribute to a more nuanced understanding of HPV-related disease in women with complex gynecological histories.\u003c/p\u003e"},{"header":"2. Methods","content":"\u003cp\u003e\u003cstrong\u003e2.1\u003c/strong\u003e\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e. \u003c/span\u003e\u003c/strong\u003e\u003cstrong\u003eStudy Design, Setting, and Participants\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis cross-sectional study was conducted to evaluate the association between endometriosis and colposcopic findings among women with confirmed human papillomavirus (HPV) infection. The study was carried out at Arash Women Hospital, a tertiary referral center affiliated with Tehran University of Medical Sciences, Tehran, Iran, between 2024 and 2025. The study was designed and reported in accordance with the STROBE recommendations for observational cross-sectional studies. Eligible participants were recruited from outpatient gynecology and colposcopy clinics. Women were considered eligible if they had laboratory-confirmed HPV infection based on polymerase chain reaction (PCR)-based HPV testing and had available clinical and colposcopic data. Participants were classified into two groups according to endometriosis status: women with confirmed endometriosis and HPV-positive women without evidence of endometriosis. The sample size was estimated based on HPV prevalence rates reported in previous studies investigating HPV infection among women with endometriosis. Moslehi et al.(5) reported an HPV prevalence of 24.69% among women with surgically confirmed endometriosis and used an expected prevalence of 40% for sample size estimation. In addition, Li et al. reported, through a combined meta-analysis and case-control study of surgically treated patients with endometriosis, an overall HPV prevalence of approximately 46% and a high-risk HPV prevalence of approximately 36% among affected patients. Based on these prior estimates, the required sample size was calculated using the single-proportion formula (n = Z\u0026sup2;p (1 \u0026minus; p) / d\u0026sup2;), where Z = 1.96 for a 95% confidence level, (p = 0.40) as the expected prevalence, and (d = 0.06) as the desired precision. This yielded a minimum required sample of approximately 256\u0026ndash;270 participants. To improve statistical power, allow reliable between-group comparisons, and support subgroup and regression analyses, the final sample size was increased to 800 HPV-positive women, including 400 patients with endometriosis and 400 controls without endometriosis.\u003c/p\u003e\n\u003cp\u003eThe diagnosis of endometriosis was established using clinical, imaging, and/or surgical criteria. Clinical evidence included symptoms and physical examination findings suggestive of endometriosis, while imaging evidence was based on transvaginal ultrasonography and/or magnetic resonance imaging when available. Surgical confirmation through laparoscopy or laparotomy was considered when documented in the medical record. Women without clinical, imaging, or surgical evidence of endometriosis were assigned to the control group.\u003c/p\u003e\n\u003cp\u003eParticipants were excluded if they were pregnant, had a history of hysterectomy, had known cervical cancer or previously diagnosed cervical dysplasia, had immunosuppressive conditions such as HIV infection or chronic corticosteroid use, had received HPV vaccination, or had incomplete data for the main variables of interest. Written informed consent was obtained from all participants before enrollment. The study protocol was approved by the Ethics Committee of Tehran University of Medical Sciences under the ethics approval code IR.TUMS.IKHC.REC.1403.192.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e2.2\u003c/strong\u003e\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e. \u003c/span\u003e\u003c/strong\u003e\u003cstrong\u003eData Collection, Variables, and Measurements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eData were collected using a structured interview guide developed specifically for this study by the research team. The guide was not previously published elsewhere. Its items were designed according to the study objectives and were informed by variables commonly assessed in similar studies evaluating endometriosis and HPV infection, including studies by Moslehi et al.(5), Hong et al.(6), and Rocha et al(11). The guide included demographic and reproductive characteristics, endometriosis-related clinical variables, HPV-related information, Pap smear results, and colposcopic findings. An English-language version of the interview guide has been uploaded as Supplementary File 1. Demographic and reproductive variables included age, body mass index (BMI), gravidity, parity, number of abortions, marital status, education level, place of residence, and history of underlying disease. Endometriosis-related variables included duration of disease, history of surgery or hormonal treatment, ultrasonography findings, MRI findings, surgical findings, physical examination findings, infertility status, dysmenorrhea, dyspareunia, abnormal uterine bleeding, chronic pelvic pain, urinary symptoms, and gastrointestinal symptoms.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThe primary exposure variable was endometriosis status, categorized as presence or absence of endometriosis. The main outcome variable was colposcopic finding among HPV-positive women. Colposcopic findings were categorized as normal, aceto-white changes, or coarse mosaicism. For additional analysis, colposcopic findings were also dichotomized into normal and abnormal findings, with aceto-white changes and coarse mosaicism grouped as abnormal colposcopy.\u003c/p\u003e\n\u003cp\u003eHPV-related variables were obtained from PCR-based genotyping results. HPV types were classified as high-risk or low-risk according to their oncogenic potential. High-risk HPV included oncogenic genotypes such as HPV 16, 18, 31, 33, and other recognized high-risk types, while low-risk HPV included non-oncogenic or low-oncogenic-risk types such as HPV 6 and 11. Among women with high-risk HPV, subgroup classification was also performed when available, including HPV 16/18 and other high-risk HPV types.\u003c/p\u003e\n\u003cp\u003eAll participants underwent standardized colposcopic evaluation by trained gynecologists. To reduce measurement bias, colposcopic examinations were performed using a consistent clinical approach, including application of 3\u0026ndash;5% acetic acid to the cervix and documentation of findings according to accepted colposcopic criteria. When biopsy was performed, pathology results were categorized as normal, CIN1, or CIN2. Pap smear results were also recorded and categorized as normal, ASC-US, LSIL, or HSIL according to the available cytology report. Data were checked for completeness, coding consistency, and biologically implausible values before analysis.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e2.3\u003c/strong\u003e\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e. \u003c/span\u003e\u003c/strong\u003e\u003cstrong\u003eStatistical Analysis\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll statistical analyses were performed using IBM SPSS Statistics version 26.0. Descriptive statistics were used to summarize demographic, reproductive, clinical, HPV-related, cytological, pathological, and colposcopic characteristics of the study population. Continuous variables were reported as mean \u0026plusmn; standard deviation when approximately normally distributed and as median and interquartile range when distributional assumptions were not met. Categorical variables were summarized as frequencies and percentages. Normality of continuous variables was assessed using the Kolmogorov\u0026ndash;Smirnov test, supported by visual inspection of histograms and Q-Q plots. Between-group comparisons for continuous variables were performed using the independent-samples t-test when assumptions were satisfied. For variables with non-normal distribution, non-parametric alternatives such as the Mann\u0026ndash;Whitney U test were considered. Categorical variables, including HPV typing, Pap smear results, biopsy pathology, and colposcopic findings, were compared between the endometriosis and control groups using the chi-square test. Fisher\u0026rsquo;s exact test was planned when expected cell counts were insufficient for chi-square testing.\u003c/p\u003e\n\u003cp\u003eTo estimate the magnitude of association, odds ratios (ORs) with 95% confidence intervals (CIs) were calculated for key outcomes. The association between endometriosis and high-risk HPV infection was assessed using cross-tabulation and logistic regression. The association between endometriosis and abnormal colposcopic findings was first evaluated using unadjusted analysis and then further examined using binary logistic regression. In the adjusted model, abnormal colposcopy was entered as the dependent variable, while endometriosis status was entered as the main independent variable. Age, BMI, and HPV typing were included as covariates because of their potential clinical relevance as confounders.\u003c/p\u003e\n\u003cp\u003eMissing data were handled using complete-case analysis, and no imputation was applied. No formal sensitivity analysis was performed. Subgroup analyses were conducted to evaluate abnormal colposcopic findings within HPV risk categories, particularly among women with high-risk HPV. Model fit for logistic regression was assessed using standard diagnostic indices, including the Hosmer\u0026ndash;Lemeshow goodness-of-fit test when applicable. A two-sided p-value of less than 0.05 was considered statistically significant.\u003c/p\u003e"},{"header":"3. Results","content":"\u003cp\u003e\u003cstrong\u003e3.1\u003c/strong\u003e\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e. \u003c/span\u003e\u003c/strong\u003e\u003cstrong\u003eDemographic, Reproductive, and Clinical Characteristics\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA total of 800 HPV-positive women were included in the final analysis, with 400 participants in the endometriosis group and 400 participants in the control group. Because all eligible participants included in the final dataset had complete data for the main analytical variables, no participant flow diagram was generated. The two groups were broadly comparable in terms of baseline demographic and reproductive characteristics. The mean age was 32.59 \u0026plusmn; 4.83 years in the endometriosis group and 32.31 \u0026plusmn; 5.05 years in the control group, with no statistically significant difference between the two groups (p = 0.432). Similarly, BMI was comparable between women with endometriosis and controls (25.52 \u0026plusmn; 3.97 vs. 25.18 \u0026plusmn; 4.04 kg/m\u0026sup2;, respectively; p = 0.222). These findings indicate that the two groups were well balanced with respect to age and BMI (Table 1) .\u003c/p\u003e\n\u003cp\u003eReproductive characteristics were also similar between the study groups. The mean number of pregnancies was 1.55 \u0026plusmn; 1.28 in the endometriosis group and 1.49 \u0026plusmn; 1.25 in the control group, with no statistically significant difference (p = 0.502). The number of abortions was also comparable between groups (0.35 \u0026plusmn; 0.54 vs. 0.40 \u0026plusmn; 0.55; p = 0.194). Likewise, parity did not differ significantly between the endometriosis and control groups (1.21 \u0026plusmn; 1.36 vs. 1.10 \u0026plusmn; 1.31; p = 0.244).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eOverall, there were no statistically significant differences between the endometriosis and control groups regarding age, BMI, gravidity, abortions, or parity. This comparability reduces the likelihood that baseline demographic or reproductive differences explain the observed associations between endometriosis, HPV typing, and colposcopic findings.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e3.2\u003c/strong\u003e\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e. \u003c/span\u003e\u003c/strong\u003e\u003cstrong\u003eHPV Typing Distribution and High-Risk HPV Association\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eIn the total study population, 455 women (56.9%) had high-risk HPV infection, while 345 women (43.1%) had low-risk HPV infection. Among women with high-risk HPV, 227 cases (49.9%) were classified as HPV 16/18, and 228 cases (50.1%) were classified as other high-risk HPV types. This distribution shows that high-risk HPV genotypes represented the majority of HPV infections in the study population.\u003c/p\u003e\n\u003cp\u003eA statistically significant difference was observed in HPV typing between the endometriosis and control groups. High-risk HPV was detected in 293 of 400 women with endometriosis (73.3%) compared with 162 of 400 controls (40.5%). In contrast, low-risk HPV was less frequent in the endometriosis group than in the control group, occurring in 107 women (26.8%) and 238 women (59.5%), respectively. The difference in HPV risk-type distribution between the two groups was statistically significant (\u0026chi;\u0026sup2; = 87.46, p \u0026lt; 0.001). (Figure 1)\u003c/p\u003e\n\u003cp\u003eThe magnitude of this association was clinically meaningful. Women with endometriosis had approximately fourfold higher odds of harboring high-risk HPV compared with women without endometriosis (OR = 4.02, 95% CI: 2.99\u0026ndash;5.42) (Table 2). In multivariable logistic regression adjusted for age and BMI, endometriosis remained independently associated with high-risk HPV infection (adjusted OR = 4.03, p \u0026lt; 0.001), whereas age (p = 0.692) and BMI (p = 0.949) were not independently associated with HPV risk type Table 3).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e3.3\u003c/strong\u003e\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e. \u003c/span\u003e\u003c/strong\u003e\u003cstrong\u003eColposcopic, Cytological, Pathological, and Regression Findings\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eColposcopic findings differed markedly between the two groups. Normal colposcopy was observed in 329 women in the control group (82.3%) compared with 122 women in the endometriosis group (30.5%). Aceto-white changes were present in 154 women with endometriosis (38.5%) and 40 controls (10.0%). Coarse mosaicism was also more frequent in the endometriosis group, occurring in 124 women (31.0%) compared with 31 controls (7.8%). The overall distribution of colposcopic findings was significantly different between groups (\u0026chi;\u0026sup2; = 217.80, p \u0026lt; 0.001) (Table 4 and Figure 2) . When colposcopic findings were dichotomized into normal and abnormal findings, abnormal colposcopy, defined as aceto-white changes or coarse mosaicism, was observed in 278 women with endometriosis (69.5%) compared with 71 controls (17.8%). The association between endometriosis and abnormal colposcopy was statistically significant (\u0026chi;\u0026sup2; = 217.79, p \u0026lt; 0.001). The odds of abnormal colposcopic findings were more than ten times higher among women with endometriosis than among controls (OR = 10.56, 95% CI: 7.57\u0026ndash;14.74) (Table 5).\u003c/p\u003e\n\u003cp\u003eIn multivariable logistic regression adjusted for age, BMI, and HPV typing, endometriosis remained strongly and independently associated with abnormal colposcopy (adjusted OR = 10.47, p \u0026lt; 0.001). Age was not significantly associated with abnormal colposcopy (OR = 1.02, p = 0.327), BMI showed a borderline association (OR = 1.04, p = 0.057), and HPV typing was not independently associated with abnormal colposcopy after adjustment (OR = 1.02, p = 0.899). The model was statistically significant overall (\u0026chi;\u0026sup2; = 234.55, p \u0026lt; 0.001), and the Hosmer\u0026ndash;Lemeshow test indicated acceptable model fit (p = 0.257) (Table 6 and Figure 3)\u003c/p\u003e\n\u003cp\u003ePap smear findings did not differ significantly between groups. In the control group, 146 women (36.5%) had normal cytology, 92 (23.0%) had ASC-US, 102 (25.5%) had LSIL, and 60 (15.0%) had HSIL or category 3 findings. In the endometriosis group, 175 women (43.8%) had normal cytology, 69 (17.3%) had ASC-US, 98 (24.5%) had LSIL, and 58 (14.5%) had HSIL or category 3 findings. The difference in Pap smear distribution was not statistically significant (\u0026chi;\u0026sup2; = 6.02, p = 0.111) (Table 7).\u003c/p\u003e\n\u003cp\u003eSimilarly, biopsy pathology did not show a statistically significant difference between the two groups. Normal biopsy findings were observed in 238 controls (59.5%) and 224 women with endometriosis (56.0%). CIN1 was detected in 119 controls (29.8%) and 131 women with endometriosis (32.8%), while CIN2 was detected in 43 controls (10.8%) and 45 women with endometriosis (11.3%). The overall distribution of biopsy pathology was not significantly different between groups (\u0026chi;\u0026sup2; = 1.05, p = 0.593) (Table 8) .\u003c/p\u003e"},{"header":"4. Discussion","content":"\u003cp\u003eThis cross-sectional study evaluated the association between endometriosis and colposcopic findings among HPV-positive women. The main findings were that women with endometriosis had a significantly higher frequency of high-risk HPV infection and a markedly higher prevalence of abnormal colposcopic findings compared with HPV-positive women without endometriosis. Specifically, high-risk HPV was detected in 73.3% of women with endometriosis compared with 40.5% of controls, and abnormal colposcopy was observed in 69.5% of the endometriosis group compared with 17.8% of the control group. These associations remained clinically meaningful, particularly for abnormal colposcopy, which showed more than tenfold higher odds among women with endometriosis\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e The baseline comparability of the two groups strengthens the internal interpretation of these findings. Age, BMI, gravidity, abortion history, and parity did not differ significantly between the endometriosis and control groups. Therefore, the observed differences in HPV risk typing and colposcopic patterns are less likely to be explained by these baseline demographic or reproductive variables. In the adjusted regression model, endometriosis remained independently associated with abnormal colposcopy after controlling for age, BMI, and HPV typing, suggesting that endometriosis itself may be linked to altered cervical appearance among HPV-positive women\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOne of the most clinically relevant findings of this study was the strong association between endometriosis and abnormal colposcopic appearance. Aceto-white changes and coarse mosaicism were both substantially more frequent in the endometriosis group. These findings are important because colposcopy is a key step in the evaluation of HPV-positive women and guides decisions regarding biopsy and follow-up. The markedly higher prevalence of abnormal colposcopic findings among women with endometriosis suggests that this population may require particular attention during cervical assessment, even when cytology or biopsy results do not show parallel significant differences\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOur findings are partly consistent with previous studies that have suggested a relationship between HPV infection and endometriosis, although the direction and strength of the association have varied across the literature. Moslehi et al. reported HPV infection in 24.69% of women with endometriosis and found that low-risk HPV genotypes, particularly HPV 6 and HPV 11, were the most common types(5). In contrast, our study found a much higher proportion of high-risk HPV among women with endometriosis. This discrepancy may be explained by differences in study population, sampling site, HPV detection methods, inclusion criteria, and the fact that our study included only HPV-positive women and focused on HPV risk-type distribution and colposcopic findings rather than estimating HPV prevalence in all women with endometriosis\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe results should also be interpreted in light of newer evidence from Li et al., who reported a higher prevalence of HPV and high-risk HPV among patients with endometriosis but concluded that HPV infection may not be a primary causal risk factor for developing endometriosis(12). Their findings suggest that HPV may be more relevant to clinical course or reproductive outcomes than to the initial development of endometriosis. Our results align with this cautious interpretation. We do not suggest that HPV causes endometriosis; rather, our findings indicate that among women already infected with HPV, the presence of endometriosis is associated with a greater likelihood of high-risk HPV carriage and abnormal colposcopic findings\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eSeveral biological mechanisms may explain the observed association. Endometriosis is characterized by chronic inflammation, altered immune surveillance, angiogenesis, hormonal dysregulation, and changes in local tissue response. These processes may influence the cervical and lower genital tract microenvironment, potentially affecting HPV persistence, viral clearance, epithelial response, and colposcopic appearance.(13, 14) High-risk HPV infection is also known to interact with host immune mechanisms, and impaired viral clearance could contribute to persistent epithelial changes. Therefore, it is biologically plausible that endometriosis may modify the clinical expression of HPV infection, even if it is not directly responsible for the acquisition of HPV(15)\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAn important observation in this study was that Pap smear and biopsy pathology did not differ significantly between groups. Pap smear distribution was comparable between women with and without endometriosis, and biopsy pathology showed no significant difference in normal findings, CIN1, or CIN2. This distinction is essential for interpreting the study accurately. Although endometriosis was strongly associated with abnormal colposcopic appearance, this did not translate into a statistically significant increase in cytological abnormality or histopathological CIN in the present dataset. These findings suggest that abnormal colposcopic features in women with endometriosis may reflect inflammatory or epithelial response patterns as well as HPV-related changes, and should not automatically be interpreted as evidence of more severe cervical pathology\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eFrom a clinical perspective, the findings support a more individualized approach to cervical evaluation in HPV-positive women with endometriosis. The high frequency of high-risk HPV and abnormal colposcopy in this group suggests that gynecologists and colposcopists should carefully consider endometriosis status when interpreting colposcopic findings and planning follow-up. However, because biopsy pathology was not significantly different between groups, the results do not justify overtreatment. Instead, they support careful surveillance, appropriate biopsy when indicated, and risk-based follow-up rather than aggressive management based solely on the presence of endometriosis\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study has several limitations. First, its cross-sectional design prevents any causal inference or assessment of temporal relationships between endometriosis, HPV risk type, and colposcopic findings. Second, although age and BMI were included in adjusted analyses, other potential confounders such as smoking, sexual behavior, number of sexual partners, contraceptive use, hormonal therapy, HPV viral load, and duration of HPV infection were not fully controlled. Third, the study was conducted in a tertiary referral hospital, which may limit generalizability to community-based populations. Referral-center patients may have more complex gynecological histories or more severe symptoms than the general population. Finally, while colposcopy was standardized, visual interpretation remains partly subjective, and interobserver variability cannot be fully excluded\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eDespite these limitations, the study has notable strengths, including a relatively large sample size, equal group allocation, complete data for the main analytical variables, and the use of both unadjusted and adjusted analyses. The findings provide evidence that endometriosis is associated with high-risk HPV carriage and abnormal colposcopic findings among HPV-positive women, independent of age and BMI. Future longitudinal studies are needed to determine whether women with both endometriosis and high-risk HPV have increased persistence of HPV infection, greater progression to CIN, or different long-term cervical outcomes. Until such evidence is available, the results should be interpreted as supporting enhanced clinical awareness and individualized surveillance rather than proving a causal relationship between endometriosis and cervical disease progression.\u003c/p\u003e\n\u003cp\u003eIn conclusion, this cross-sectional study showed that among HPV-positive women, endometriosis was significantly associated with a higher prevalence of high-risk HPV infection and a markedly greater frequency of abnormal colposcopic findings, including aceto-white changes and coarse mosaicism. This association remained strong after adjustment for age, BMI, and HPV typing, suggesting that endometriosis may be independently related to altered colposcopic appearance in HPV-infected women. However, Pap smear findings and biopsy pathology did not differ significantly between groups, indicating that abnormal colposcopic patterns in this population should be interpreted carefully and not necessarily as evidence of more advanced cervical pathology. These findings support individualized cervical surveillance and careful colposcopic assessment in HPV-positive women with endometriosis, while highlighting the need for longitudinal studies to clarify whether this association influences HPV persistence, CIN progression, or long-term cervical cancer risk.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eACW\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eAceto-White Changes\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eBMI\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eBody Mass Index\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eCIN\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eCervical Intraepithelial Neoplasia\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eGI\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eGastrointestinal\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eHSIL\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eHigh-Grade Squamous Intraepithelial Lesion\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eHPV\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eHuman Papillomavirus\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eHR-HPV\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eHigh-Risk Human Papillomavirus\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eIFCPC\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eInternational Federation for Cervical Pathology and Colposcopy\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eLR-HPV\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eLow-Risk Human Papillomavirus\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eLSIL\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eLow-Grade Squamous Intraepithelial Lesion\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eMRI\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eMagnetic Resonance Imaging\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003ePCR\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003ePolymerase Chain Reaction\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eSD\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eStandard Deviation\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003eConflict of interest: The authors declare that they have no conflict of interest.\u003c/p\u003e\n\u003cp\u003eEthical approval: Ethics approval and consent to participate: This study was conducted in accordance with the Declaration of Helsinki and was approved by the Ethics Committee of \u0026nbsp;the Tehran University of Medical Sciences Ethics Committee (IR.TUMS.IKHC.REC.1403.192). Informed consent was obtained from all participants.\u003c/p\u003e\n\u003cp\u003eConsent for publication: Not applicable\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAvailability of data and materials: The datasets analyzed during the current study are available from the corresponding author on reasonable request\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAuthor contributions:\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eAHH, MJ, and SAM: Conceptualization, methodology and data curation, SA, SYT, SHK, and AS: Investigation, AHH, MJ, NSH, and SHK: Formal analysis, supervision, visualization, original draft preparation. SAM,MN and AKV: Review and editing.\u003c/p\u003e\n\u003cp\u003eFinancial disclosure: The authors declare that this study has received no financial support.\u003c/p\u003e\n\u003cp\u003eInformed consent: Informed consent was obtained from all individual participants included in the study.\u003c/p\u003e\n\u003cp\u003eCompeting interests: The authors declare that they have no competing interests\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eFunding: This study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e.\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAcknowledgements: The authors would like to thank the staff of Arash Women Hospital and the participants for their cooperation and contribution to this study.\u003c/p\u003e\n\u003cp\u003ePermission to Reproduce Material\u003c/p\u003e\n\u003cp\u003eNot applicable.\u0026nbsp;\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eSaunders PTK, Horne AW. Endometriosis: Etiology, pathobiology, and therapeutic prospects. Cell. 2021;184(11):2807\u0026ndash;24.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCousins FL, McKinnon BD, Mortlock S, Fitzgerald HC, Zhang C, Montgomery GW, et al. New concepts on the etiology of endometriosis. J Obstet Gynecol Res. 2023;49(4):1090\u0026ndash;105.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJensen JE, Becker GL, Jackson JB, Rysavy MB. Human Papillomavirus and Associated Cancers: A Review. Viruses. 2024;16(5).\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eQi SY, Yang MM, Li CY, Yu K, Deng SL. The HPV viral regulatory mechanism of TLRs and the related treatments for HPV-associated cancers. Front Immunol. 2024;15:1407649.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMoslehi Z, Derakhshan R, Chaichian S, Mehdizadeh Kashi A, Sabet B, Rokhgireh S. Correlation of High-Risk Human Papilloma Virus with Deep Endometriosis: A Cross-Sectional Study. Biomed Res Int. 2023;2023:6793898.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHong YS, Park J, Kim H. Association of endometriosis with genital human papillomavirus infection in US women: a national population-based study. Sci Rep. 2023;13(1):8020.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFernandes JV, TA DEMF, JC DEA, Cobucci RN, MG DEC, Andrade VS, et al. Link between chronic inflammation and human papillomavirus-induced carcinogenesis (Review). Oncol Lett. 2015;9(3):1015\u0026ndash;26.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAdilbayeva A, Kunz J. Pathogenesis of Endometriosis and Endometriosis-Associated Cancers. Int J Mol Sci. 2024;25(14):7624.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGarvey M, Endometriosis. Future Biological Perspectives for Diagnosis and Treatment. Int J Mol Sci. 2024;25(22):12242.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHeidarpour M, Derakhshan M, Derakhshan-Horeh M, Kheirollahi M, Dashti S. Prevalence of high-risk human papillomavirus infection in women with ovarian endometriosis: HPV in women with ovarian endometriosis. J Obstet Gynecol Res. 2016;43.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRocha RM, Souza RP, Gimenes F, Consolaro MEL. The high-risk human papillomavirus continuum along the female reproductive tract and its relationship to infertility and endometriosis. Reprod Biomed Online. 2019;38(6):926\u0026ndash;37.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLi W, Wang Z, Qi H, Xia C, Chen F, Xu J, et al. The association between HPV infection and endometriosis: Risk and fertility outcomes. J Biomedical Res. 2025;39:1\u0026ndash;12.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGreygoose E, Metharom P, Kula H, Seckin TK, Seckin TA, Ayhan A et al. The Estrogen-Immune Interface in Endometriosis. Cells. 2025;14(1).\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKłodnicka K, Michalska A, Januszewski J, Forma A, Teresiński G, Flieger J, et al. From Inflammation to Malignancy: The Link Between Endometriosis and Gynecological Cancers. Int J Mol Sci. 2025;26(24):11816.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang J, Tian Z, Wang J. Risk factors for persistent infection of high-risk HPV in patients with cervical intraepithelial neoplasia. Am J Transl Res. 2025;17(4):2992\u0026ndash;3000.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"},{"header":"Tables","content":"\u003cp\u003e\u003cstrong\u003eTable 1. Demographic and reproductive characteristics of the study participants\u003c/strong\u003e\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"609\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eVariable\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eControl group (n = 400)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eEndometriosis group (n = 400)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003ep-value\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge, years, mean \u0026plusmn; SD\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e32.31 \u0026plusmn; 5.05\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e32.59 \u0026plusmn; 4.83\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.432\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eBMI, kg/m\u0026sup2;, mean \u0026plusmn; SD\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e25.18 \u0026plusmn; 4.04\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e25.52 \u0026plusmn; 3.97\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.222\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eGravidity, mean \u0026plusmn; SD\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e1.49 \u0026plusmn; 1.25\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e1.55 \u0026plusmn; 1.28\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.502\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eAbortions, mean \u0026plusmn; SD\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.40 \u0026plusmn; 0.55\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.35 \u0026plusmn; 0.54\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.194\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eParity, mean \u0026plusmn; SD\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e1.10 \u0026plusmn; 1.31\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e1.21 \u0026plusmn; 1.36\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.244\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003ch3\u003eTable 2. HPV typing distribution according to study group\u003c/h3\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"639\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eHPV type\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eControl group (n = 400)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eEndometriosis group (n = 400)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eOR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003e95% CI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003ep-value\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eLow-risk HPV\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e238 (59.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e107 (26.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eReference\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u0026mdash;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u0026mdash;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eHigh-risk HPV\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e162 (40.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e293 (73.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e4.02\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e2.99\u0026ndash;5.42\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003ch3\u003eTable 3. Multivariable logistic regression for factors associated with high-risk HPV infection\u003c/h3\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"615\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eVariable\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eAdjusted OR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003e95% CI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003ep-value\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eEndometriosis\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e4.03\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e2.99\u0026ndash;5.43\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.99\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.96\u0026ndash;1.02\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.692\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eBMI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e1.00\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.96\u0026ndash;1.04\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.949\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cbr\u003e\u003c/p\u003e\n\u003ch3\u003eTable 4. Colposcopic findings according to study group\u003c/h3\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"635\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eColposcopic finding\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eControl group (n = 400)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eEndometriosis group (n = 400)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003ep-value\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eNormal\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e329 (82.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e122 (30.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eAceto-white changes\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e40 (10.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e154 (38.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eCoarse mosaicism\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e31 (7.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e124 (31.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003ch3\u003eTable 5. Abnormal colposcopy according to study group\u003c/h3\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"646\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eColposcopy category\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eControl group (n = 400)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eEndometriosis group (n = 400)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eOR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003e95% CI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003ep-value\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eNormal colposcopy\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e329 (82.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e122 (30.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003eReference\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u0026mdash;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u0026mdash;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eAbnormal colposcopy\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e71 (17.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e278 (69.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e10.56\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e7.57\u0026ndash;14.74\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003ch3\u003e\u003cbr\u003e\u003c/h3\u003e\n\u003ch3\u003eTable 6. Multivariable logistic regression for factors associated with abnormal colposcopy\u003c/h3\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"613\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eVariable\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eAdjusted OR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003e95% CI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003ep-value\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eEndometriosis\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e10.47\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e7.35\u0026ndash;14.91\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e1.02\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.98\u0026ndash;1.05\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.327\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eBMI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e1.04\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e1.00\u0026ndash;1.08\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.057\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eHigh-risk HPV\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e1.02\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.72\u0026ndash;1.46\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.899\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cbr\u003e\u003c/p\u003e\n\u003ch3\u003eTable 7. Pap smear findings according to study group\u003c/h3\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"622\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003ePap smear result\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eControl group (n = 400)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eEndometriosis group (n = 400)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003ep-value\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eNormal\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e146 (36.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e175 (43.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.111\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eASC-US\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e92 (23.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e69 (17.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eLSIL\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e102 (25.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e98 (24.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eHSIL\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e60 (15.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e58 (14.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003ch3\u003eTable 8. Biopsy pathology according to study group\u003c/h3\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"587\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eBiopsy pathology\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eControl group (n = 400)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eEndometriosis group (n = 400)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003ep-value\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eNormal\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e238 (59.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e224 (56.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e0.593\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eCIN1\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e119 (29.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e131 (32.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e\u003cstrong\u003eCIN2\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e43 (10.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\n \u003cp\u003e45 (11.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-womens-health","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bmwh","sideBox":"Learn more about [BMC Women's Health](http://bmcwomenshealth.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bmwh/default.aspx","title":"BMC Women's Health","twitterHandle":"","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Endometriosis, Human Papillomavirus, Colposcopy, High-Risk HPV, Cervical Screening","lastPublishedDoi":"10.21203/rs.3.rs-10042122/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-10042122/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eEndometriosis is a chronic inflammatory gynecological disorder that may influence local immune responses and alter the clinical behavior of human papillomavirus (HPV) infection. Although HPV infection is a major cause of cervical epithelial abnormalities, the relationship between endometriosis and colposcopic findings among HPV-positive women remains insufficiently understood. This study aimed to evaluate the association between endometriosis, HPV risk typing, and colposcopic findings in women with confirmed HPV infection.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003eThis cross-sectional study was conducted at Arash Women Hospital, Tehran University of Medical Sciences, between 2024 and 2025. HPV-positive women were classified according to the presence or absence of endometriosis. Demographic, reproductive, cytological, pathological, HPV genotyping, and colposcopic data were collected from clinical records, structured interviews, laboratory reports, and standardized colposcopic examinations. HPV types were categorized as high-risk or low-risk, and colposcopic findings were classified as normal, aceto-white changes, or coarse mosaicism. Statistical analyses included chi-square tests, independent-samples t-tests, odds ratios with 95% confidence intervals, and multivariable logistic regression.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eA total of 800 HPV-positive women were included. High-risk HPV was significantly more frequent among women with endometriosis than controls (73.3% vs. 40.5%; OR\u0026thinsp;=\u0026thinsp;4.02, 95% CI: 2.99\u0026ndash;5.42; p\u0026thinsp;\u0026lt;\u0026thinsp;0.001). Abnormal colposcopy was also more common in the endometriosis group (69.5% vs. 17.8%; OR\u0026thinsp;=\u0026thinsp;10.56, 95% CI: 7.57\u0026ndash;14.74; p\u0026thinsp;\u0026lt;\u0026thinsp;0.001). After adjustment, endometriosis remained independently associated with abnormal colposcopy (adjusted OR\u0026thinsp;=\u0026thinsp;10.47; p\u0026thinsp;\u0026lt;\u0026thinsp;0.001). Pap smear and biopsy pathology did not differ significantly between groups.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eEndometriosis was associated with high-risk HPV infection and abnormal colposcopic findings among HPV-positive women, supporting individualized cervical surveillance in this population.\u003c/p\u003e\u003ch2\u003eClinical Trial Registration\u003c/h2\u003e \u003cp\u003eNot applicable.\u003c/p\u003e","manuscriptTitle":"Endometriosis, High-Risk HPV Infection, and Colposcopic Abnormalities in HPV-Positive Women: A Cross-Sectional Study","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-07-17 07:31:15","doi":"10.21203/rs.3.rs-10042122/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2026-07-24T10:07:01+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"86622099688031048238910220683307129411","date":"2026-07-22T20:45:29+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-07-21T21:45:14+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"110282479906777658938495006154250395420","date":"2026-07-21T21:36:13+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-07-19T08:54:51+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"53855120706946625642250881959095016721","date":"2026-07-19T08:38:58+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-07-15T10:16:42+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-07-14T07:15:06+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-06-25T10:03:20+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-06-24T08:19:14+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Women's Health","date":"2026-06-24T08:00:51+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-womens-health","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bmwh","sideBox":"Learn more about [BMC Women's Health](http://bmcwomenshealth.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bmwh/default.aspx","title":"BMC Women's Health","twitterHandle":"","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"a15da23d-8ef6-49ce-bfac-c86efee74d4d","owner":[],"postedDate":"July 17th, 2026","published":true,"recentEditorialEvents":[{"type":"editorInvitedReview","content":"","date":"2026-07-24T10:07:01+00:00","index":45,"fulltext":""},{"type":"reviewerAgreed","content":"86622099688031048238910220683307129411","date":"2026-07-22T20:45:29+00:00","index":44,"fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-07-21T21:45:14+00:00","index":43,"fulltext":""},{"type":"reviewerAgreed","content":"110282479906777658938495006154250395420","date":"2026-07-21T21:36:13+00:00","index":42,"fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-07-19T08:54:51+00:00","index":40,"fulltext":""},{"type":"reviewerAgreed","content":"53855120706946625642250881959095016721","date":"2026-07-19T08:38:58+00:00","index":39,"fulltext":""},{"type":"reviewersInvited","content":"15","date":"2026-07-15T10:16:42+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-07-14T07:15:06+00:00","index":"","fulltext":""}],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-07-17T07:31:15+00:00","versionOfRecord":[],"versionCreatedAt":"2026-07-17 07:31:15","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-10042122","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-10042122","identity":"rs-10042122","version":["v1"]},"buildId":"WrCJVZZCHTDjtuVLN7oU0","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}