{"paper_id":"dc6a52d6-7a2d-47ec-8a36-0db95956e9d5","body_text":"Vol.:(0123456789)\nInternational Urogynecology Journal \nhttps://doi.org/10.1007/s00192-026-06957-1\nREVIEW ARTICLE\nPathophysiological Mechanisms and Clinical Implications of Lower \nUrinary Tract Symptoms in Patients with Deep Endometriosis: \nA Narrative Review\nRok Šumak 1  · Tamara Serdinšek1\nReceived: 5 August 2026 / Accepted: 6 October 2026 \n© The Author(s) 2026\nAbstract\nIntroduction and Hypothesis Endometriosis is a chronic inflammatory condition characterized by endometrium-like tissue \noutside the uterus. Deep endometriosis (DE) frequently involves the posterior pelvic compartment and can affect the uri-\nnary tract directly or indirectly, leading to a wide spectrum of lower urinary tract symptoms (LUTS). This narrative review \naimed to synthesize current evidence on the mechanisms underlying LUTS in women with deep endometriosis, including \ndirect urinary tract involvement, extra-urinary mechanisms, and postoperative dysfunction, and to discuss their diagnostic \nand therapeutic implications.\nMethods A structured, non-systematic literature search was conducted using PubMed/MEDLINE for English-language \npublications from 2000 to July 2026. Four thematic domains were considered: (1) prevalence and pathophysiological mecha-\nnisms of LUTS in endometriosis; (2) LUTS due to direct urinary tract involvement; (3) LUTS without direct urinary tract \ninvolvement; and (4) de novo LUTS after surgery for deep endometriosis.\nResults In women with DE undergoing preoperative urodynamic assessment, pooled estimates indicated voiding dysfunction \nin 21% and detrusor overactivity in 15%, with substantial heterogeneity. LUTS may reflect direct urinary tract involvement, \nneural dysfunction, inflammation, or surgical injury. Evidence for proposed neuroinflammatory and nociplastic mechanisms \nremains largely indirect or experimental.\nConclusions Multiple pathophysiological mechanisms may contribute to LUTS in DE. Clinicians should be aware of the \nassociation between these two conditions and address treatment of both, which often requires a multidisciplinary approach. \nWhere surgery is indicated, nerve-sparing techniques should be considered when technically feasible to reduce the risk of \npostoperative urinary dysfunction. Emerging mechanistic and phenotype-based approaches require further validation.\nKeywords Deep endometriosis · Endometriosis · Lower urinary tract symptoms · Voiding dysfunction\nIntroduction\nEndometriosis is a chronic disease defined by the presence \nof endometrial-like tissue outside the uterine cavity, affect-\ning approximately 10% of reproductive-aged women [1 ]. It \npresents in several forms—superficial peritoneal lesions, \novarian endometriomas, and deep endometriosis (DE), with \nDE being the most symptomatic and anatomically disruptive \nsubtype [2 ]. Commonly affected sites include the uterosa-\ncral ligaments, retrocervical region, rectovaginal septum, \nand rectosigmoid colon; urinary tract involvement is also \nrelatively frequent in women with deep endometriosis [3 , \n4]. Lower urinary tract symptoms (LUTS) are also common \nin the general female population, although estimates depend \nstrongly on age and symptom definitions. In the population-\nbased EpiLUTS survey of adults aged 40 years and older, \nprevalence among women ranged from 52.5% using a higher \nsymptom-frequency threshold to 76.3% using a lower thresh-\nold [5].\nHandling Editor: Kaven Baessler\nEditor in Chief: Kaven Baessler\n * Rok Šumak \n rok.sumak@ukc-mb.si\n1 Department of General Gynecology and Gynecologic \nUrology, Clinic for Gynecology and Perinatology, University \nMedical Centre Maribor, Ljubljanska Ulica 5, 2000 Maribor, \nSlovenia\n\n International Urogynecology Journal\nLUTS such as urgency, frequency, nocturia, dysuria, \nsuprapubic pain, and incomplete bladder emptying are \nreported in a substantial proportion of women with endo-\nmetriosis, particularly those with DE and/or bladder involve-\nment [6 ]. Although LUTS in deep endometriosis have \ntraditionally been attributed to direct bladder or ureteral \ninvolvement, accumulating evidence indicates that they may \nalso reflect pelvic neural involvement, pelvic-floor muscle \ndysfunction, viscero-visceral cross-sensitization, and periph-\neral and central neuroimmune sensitization—even without \novert urinary tract endometriosis [7 , 8].\nEpidemiological studies demonstrate that women with \nsurgically confirmed endometriosis experience LUTS more \nfrequently than healthy controls, independent of disease \nstage or lesion location [6 ]. Endometriosis also frequently \ncoexists with other chronic pain syndromes, supporting a \nbroader concept of centrally mediated pain modulation. \nNeuropathic-like pain was identified in 36% of women in \na cohort with DE and chronic pelvic pain. Features con-\nsistent with central sensitization and nociplastic pain have \nalso been reported in endometriosis, although assessment \nmethods vary and their diagnostic validity requires fur -\nther evaluation [9 , 10]. These pain-related mechanisms \nmay help explain persistent symptom amplification after \nlesion excision, although their specific contribution to DE-\nassociated LUTS remains incompletely established [11].\nDE may also involve the urinary tract directly, particu-\nlarly the bladder and ureters [12]. Ureteral endometriosis \nmay remain asymptomatic until hydronephrosis devel-\nops, highlighting the importance of assessing the upper \nurinary tract when ureteral involvement is suspected on \nthe basis of disease location, symptoms, or imaging find-\nings. Furthermore, surgical excision of DE carries a risk \nof autonomic nerve injury, which may result in de novo \nLUTS, sometimes becoming apparent after surgery [13]. \nRecent research has also highlighted emerging neuro-\ninflammatory pathways, including mast-cell activation \nand the Janus kinase/signal transducer and activator of \ntranscription (JAK–STAT) signaling, which may con-\ntribute to neural sensitization and neuroangiogenesis in \nendometriosis. Their specific relevance to LUTS remains \nhypothetical and requires further investigation [14]. Given \nthe multifactorial origins of LUTS in DE, an integrated \nand multidisciplinary approach to diagnosis and manage-\nment is important. The aim of this narrative review was \nto synthesize current evidence on the pathophysiological \nmechanisms associated with LUTS in DE and to discuss \ntheir diagnostic and therapeutic implications, while dis-\ntinguishing established clinical evidence from emerging \nor hypothesis-generating mechanisms.\nMethods\nA structured, non-systematic literature search was con-\nducted using the PubMed/MEDLINE database to identify \nclinically relevant and mechanistic literature concerning \nlower urinary tract symptoms in endometriosis, with par -\nticular emphasis on deep endometriosis. PubMed/MED-\nLINE was selected as the principal database because of \nits broad coverage of biomedical and clinically oriented \nliterature relevant to endometriosis and lower urinary tract \ndysfunction. As this was a narrative review based exclu-\nsively on previously published literature, ethical approval \nwas not required.\nLiterature Search and Selection\nThe principal search combined terms related to endome-\ntriosis with terms related to lower urinary tract symp-\ntoms and urinary dysfunction: (endometriosis OR “deep \nendometriosis” OR “deep infiltrating endometriosis” OR \nendometrioma) AND (“lower urinary tract symptoms” \nOR dysuria OR “voiding dysfunction” OR “urinary reten-\ntion” OR hematuria OR “urinary frequency” OR “uri-\nnary incontinence” OR “urinary urgency” OR “overactive \nbladder”). Searches were focused on English-language \npublications from 2000 to July 2026; earlier seminal pub-\nlications were included when relevant for historical or \nconceptual context.\nBecause the review also aimed to discuss potential bio-\nlogical mechanisms underlying LUTS, targeted searches \nand reference-list screening were additionally used to \nidentify relevant literature on pelvic-floor dysfunction, \nautonomic innervation, peripheral and central sensitiza -\ntion, nociplastic and neuropathic pain, mast-cell activa-\ntion, neuroangiogenesis, and JAK/STAT signaling.\nPriority was given to clinical studies, systematic \nreviews, meta-analyses, clinical guidelines, and larger \nobservational studies directly addressing LUTS, urinary \ntract endometriosis, urodynamic findings, or postopera-\ntive urinary dysfunction. Mechanistic, anatomical, histo-\nlogical, and pain-related studies were included selectively \nwhen they provided relevant biological context for pro-\nposed pathways linking endometriosis with LUTS. Com-\nmentaries, case reports, case series, and meeting abstracts \nwere generally not included. Both authors participated in \nthe selection of relevant publications and in the thematic \ninterpretation of the evidence. Differences in the perceived \nrelevance or interpretation of individual publications were \nresolved by discussion and consensus.\n\nInternational Urogynecology Journal \nEvidence directly examining LUTS in women with DE \nwas distinguished from indirect evidence derived from \nstudies of endometriosis-associated pain, OAB, IC/BPS, \npelvic-floor dysfunction, or experimental mechanisms. \nSuch indirect evidence was used to provide biological con-\ntext and generate hypotheses, rather than as direct proof of \ncausation or treatment efficacy for DE-associated LUTS. A \nflowchart of literature search and selection is presented in \nFig.  1. Because this was a narrative rather than a system-\natic review, formal PRISMA or SWiM methodology and \nrisk-of-bias assessment were not applied. The use of Pub-\nMed/MEDLINE as the principal bibliographic database \nand the non-systematic nature of study selection may have \nresulted in incomplete literature retrieval and introduced \nselection bias; but these limitations are inherent to the \nnarrative-review design.\nNarrative Synthesis\nThe identified literature was organized into four thematic \ndomains:\n(1) prevalence and pathophysiological mechanisms of \nLUTS in endometriosis\n(2) LUTS due to direct urinary tract involvement\n(3) LUTS without direct urinary tract involvement\n(4) de novo LUTS after surgery for deep endometriosis.\nPrevalence and Pathophysiological Mechanisms \nof LUTS in Endometriosis\nBoth endometriosis and LUTS are prevalent in the general \nfemale population, and patients with DE often experience \nLUTS [15]. A systematic review from 2024 showed that \n15% of patients with DE had detrusor overactivity, 21% had \npreoperative voiding dysfunction, and 39% had an abnormal \nbladder sensation. On urodynamic evaluation, 18% had low \nmaximum cystometric capacity, 35% low preoperative blad-\nder compliance, and 37% painful preoperative bladder filling \n[16]. In women with parametrial endometriosis, LUTS are \npresent in 27% and dysuria in 15%, with rare reporting of \nvoiding dysfunction before surgery [17]. Overactive bladder \n(OAB) and non-urinary tract endometriosis may co-occur in \n20.5% of patients [11].\nThe mechanisms underlying LUTS in endometriosis are \ncomplex and multifactorial (Table 1). Endometriotic lesions \nmay infiltrate the bladder, ureters, or other components of \nthe urinary tract, resulting in structural and functional abnor-\nmalities. However, LUTS can also occur in the absence of \ndirect urinary tract involvement, suggesting that altered \ninnervation or inflammatory mechanisms may contribute \nto bladder dysfunction [11]. Additionally, LUTS may arise \npostoperatively as a consequence of nerve injury, fibrosis, \nor altered pelvic anatomy following excision of deep lesions \n[18].\nDespite the high prevalence of LUTS in women with \nendometriosis, they are often unrecognized or untreated. \nNotably, endometriosis commonly coexists with chronic \npain syndromes such as migraine, interstitial cystitis/bladder \npain syndrome (IC/BPS), and irritable bowel syndrome [19]. \nWomen with endometriosis and dysmenorrhea are more \nlikely to report dysuria and urgency, and LUTS are present \nin approximately 40% of patients with endometriosis [ 6]. \nThese symptoms are strongly associated with diminished \nquality of life, daily functioning, and productivity. Similar \nto endometriosis itself, LUTS independently contribute to \nimpaired physical and emotional well-being.\nNeuropathic and nociplastic mechanisms: indirect \nevidence from endometriosis‑associated pain\nAn imbalance between sympathetic and sensory innerva-\ntion has been identified in peritoneal endometriosis, with \na predominance of sensory nerve fibers promoting a pro-\nnociceptive environment. This neuroanatomical alteration \nmay contribute to persistent pelvic pain and provides a \nbiologically plausible basis for altered sensory processing \ninvolving adjacent pelvic organs. However, direct evidence \nlinking these changes specifically to LUTS in women with \nDE remains limited [20]. Pelvic pain may improve or per -\nsist after excision of peritoneal lesions because of ongo -\ning abnormal nerve activity, neurogenic inflammation, and \nperipheral sensitization in surrounding pelvic tissues [21, \n22].\nIn addition to classical nociceptive and inflammatory \npathways, recent work has highlighted a substantial neu-\nropathic component in women with DE and chronic pelvic \npain (CPP). In an observational study from 2025, which \nincluded 149 women with DE and CPP, neuropathic-like \npain (defined by a positive Douleur Neuropathique 4 score) \nwas identified in 36% of patients and was associated with \nsignificantly higher pain intensity, greater catastrophizing, \nand worse quality of life [9 ]. Although this cohort did not \nspecifically evaluate urinary tract involvement or LUTS, it \nsupports the presence of a neuropathic-like pain phenotype \nin a subset of women with DE. Whether this phenotype con-\ntributes directly to urinary symptoms remains uncertain.\nFeatures consistent with nociplastic pain, including wide-\nspread hypersensitivity, fatigue, and coexisting pain condi-\ntions, have been described in women with endometriosis, \neven when lesion burden is limited [23]. In this context, \npersistent urgency, frequency, or suprapubic pain after \ntechnically successful excision could potentially be influ-\nenced by central sensitization, although direct evidence \ndemonstrating this mechanism in DE-associated LUTS is \nlacking. Brain imaging studies in women with CPP and \n\n International Urogynecology Journal\nFig. 1  Literature-search framework and thematic organization of the narrative review\n\nInternational Urogynecology Journal \nendometriosis demonstrate altered structure and connectiv -\nity in pain-modulating regions such as the periaqueductal \ngray and anterior insula, supporting a central contribution \nto pain amplification; these findings provide indirect rather \nthan LUTS-specific evidence [24].\nThe potential therapeutic implications of these pain \nphenotypes for DE-associated LUTS remain uncertain. \nNeuromodulatory agents such as gabapentinoids or seroto-\nnin–noradrenaline reuptake inhibitors, as well as multidisci-\nplinary approaches, including pain neuroscience education, \ncognitive-behavioral therapy, and pelvic-floor rehabilitation, \nare used in selected chronic pain populations [25, 26]. How-\never, their efficacy for LUTS specifically associated with DE \nhas not been established. Assessment of neuropathic-like \nor nociplastic features may therefore be useful for charac-\nterizing the broader pain phenotype, but its role in guiding \nLUTS-specific treatment requires prospective validation.\nEmerging and Experimental Mechanisms: JAK–STAT \nSignaling, Mast Cells, and Neuroangiogenesis\nAn emerging conceptual advance in endometriosis pain biol-\nogy is the recognition of the JAK/STAT pathway as a central \nhub linking inflammation, angiogenesis, and neurogenesis. \nEvidence for this pathway derives primarily from mecha-\nnistic and endometriosis-pain research, and direct clinical \nevidence linking JAK/STAT signaling specifically to LUTS \nin women with DE is currently lacking. Neuroinflamma-\ntion in endometriosis lesions, including activation of dorsal \nroot ganglia and lesion-associated nerve fibers, converges on \nJAK/STAT signaling, with mast cells acting as key effector \ncells in this network [14]. Mast cells, via mediators such \nas tryptase, histamine, and nerve growth factor (NGF), can \npromote growth and sensitization of afferent fibers; in deep \nlesions involving the bladder wall or ureter, this provides \na plausible but unproven mechanistic link to LUTS via \nincreased activity of vesical afferents (Fig.  2).\nCytokines and growth factors associated with JAK/STAT-\nrelated pathways, including IL-6-family mediators, PDGF, \nand VEGF, have also been implicated in angiogenic and neu-\nroinflammatory processes in endometriosis [14, 27].\nFrom a translational perspective, JAK inhibitors and \nmast-cell-stabilizing agents have been proposed as potential \ntargets for future investigation in endometriosis-associated \nneuroinflammation [14]. However, no clinical trials have \nevaluated these agents for urinary tract endometriosis or DE-\nassociated LUTS, and their relevance to urinary symptom \nmanagement remains speculative. These pathways should \ntherefore be regarded as hypothesis-generating targets for \nfuture mechanistic and clinical research rather than estab-\nlished therapeutic options.\nUrinary Tract Endometriosis: Bladder \nSymptoms and Ureteral Involvement\nUrinary tract endometriosis has been reported in approxi-\nmately 20–50% of women with DE, although estimates vary \nconsiderably according to referral setting, disease definition, \nand diagnostic method [12]. Among urinary tract sites, the \nbladder is most frequently involved, followed by the ure -\nters; renal and urethral involvement are rare [28]. Bladder \nendometriosis may present with suprapubic pain, dysuria, \nhematuria, urgency, frequency, incomplete emptying, or \nrecurrent urinary tract symptoms, often with a cyclical pat-\ntern. In contrast, ureteral endometriosis frequently causes no \nLUTS and may remain clinically silent until hydronephro-\nsis or impaired renal function develops [28, 29]. Because \nureteral endometriosis may be clinically silent, assessment \nfor ureteral involvement and upper urinary tract obstruction \nshould be considered when disease location, imaging find-\nings, or clinical suspicion suggest urinary tract involvement.\nEndometriotic lesions involving the bladder may be \nsuperficial, remaining confined to the peritoneal surface \noverlying the bladder, or deep, infiltrating the detrusor \nTable 1  Proposed pathophysiological mechanisms underlying LUTS in endometriosis\nMechanism Description Clinical consequences\nMechanical Caused by infiltration of endometriotic lesions into the \nbladder, ureters, and other components of the urinary \ntract, or adhesions and fibrosis, leading to structural and \nfunctional abnormalities\nObstruction, reduced bladder compliance, LUTS, hematu-\nria, suprapubic pain, dysuria\nNeural and nociplastic Altered afferent signaling from pelvic organs, possible \ncentral sensitization, and viscero-visceral cross-talk\nPotential contribution to persistent urgency, frequency, and \nbladder pain\nChronic inflammation Potentially involving JAK/STAT signaling, mast cells, \nIL-1, IL-6, and NGF, which may promote growth and \nsensitization of afferent fibers\nPotential afferent sensitization and contribution to LUTS\nIatrogenic Consequence of nerve injury, fibrosis, or altered pelvic \nanatomy following excision of DE\nde novo LUTS after surgery, detrusor underactivity, urinary \nretention\n\n International Urogynecology Journal\nmuscle and, rarely, the urothelium. Transvaginal ultrasound \nis the first-line imaging modality, with MRI providing com-\nplementary evaluation when required. Cystoscopy may help \ndetermine whether the lesion involves the bladder mucosa \nand assess its relationship with the ureteric orifices. Hor -\nmonal therapy may be considered for symptomatic bladder \nendometriosis, whereas surgery is appropriate when medical \ntreatment is ineffective or unsuitable. Ureteral obstruction or \nhydronephrosis generally requires surgical treatment regard-\nless of symptoms because of the risk of irreversible loss of \nrenal function [4, 30].\nHistological studies have identified nerve fibers and neu-\nroinflammatory mediators in endometriotic lesions. How -\never, nerve bundle density and NGF and IL-1β expression \nvary substantially between lesions and anatomical subtypes \nwithin the same patient, without a uniform increase with \nlesion depth [31]. When lesions involve densely innervated \nregions such as the trigone, their proximity to intrinsic \nganglia and sensory afferent pathways provides a plausible \nanatomical basis for urgency, frequency, and bladder pain, \nalthough direct clinical evidence linking lesion location to \nspecific LUTS remains limited [32].\nTransurethral resection of bladder endometriotic lesions \nis generally inadequate, as lesions typically invade from \nthe outside inward and full excision via this approach is \nrarely achievable. When opting for surgical excision, the \ngoal should be complete resection of the lesion, which may \ninvolve partial or full-thickness resection of the bladder \nwall depending on the depth of invasion [4 , 12].\nUreteral endometriosis may cause progressive ureteral \nobstruction, hydronephrosis, and potentially irreversible \nloss of renal function. Preoperative identification is there-\nfore important for surgical planning, and management \nshould involve interdisciplinary collaboration between \ngynecologic and urologic surgeons. Depending on the \ntype, location, and extent of ureteral involvement, surgical \noptions include ureterolysis, segmental ureterectomy with \nend-to-end ureteroureterostomy, or ureteroneocystostomy. \nPatients should be counseled regarding the planned pro-\ncedure, its potential complications and outcomes, and the \npossible need for ureteral stenting or, in cases of severe \nobstruction, nephrostomy [30].\nDiagnostic evaluation is tailored to the suspected site \nof disease and may include transvaginal ultrasonography, \nrenal tract ultrasonography, pelvic MRI, and, when ure-\nteral obstruction requires further characterization, CT \nurography. While surgery remains the cornerstone of treat-\nment in symptomatic cases, hormonal suppression therapy \nFig. 2  Hypothesized role of JAK/STAT signaling in DE-associated \nLUTS. The diagram illustrates proposed links between local inflam-\nmation, JAK/STAT activation, mast-cell activity, angiogenesis, neu-\nrogenesis, and altered bladder afferent signaling. These pathways are \nsupported mainly by indirect or experimental evidence; their specific \ncontribution to LUTS in women with DE remains unproven. DE deep \nendometriosis; LUTS lower urinary tract symptoms; JAK/STAT  Janus \nkinase/signal transducer and activator of transcription; NGF nerve \ngrowth factor\n\nInternational Urogynecology Journal \nwith gonadotropin-releasing hormone (GnRH) analogs or \nprogestins may help control symptoms and reduce recur -\nrence risk following lesion excision [4 , 12].\nRecent outcome studies indicate that urinary symptom \ntrajectories after surgery for bladder or ureteral endome-\ntriosis are heterogeneous. Although dysuria and cyclical \nhematuria often improve after complete lesion excision, \nOAB-like symptoms or bladder pain may persist in some \npatients [4]. Persistent symptoms after technically successful \nsurgery may reflect mechanisms beyond residual structural \ndisease, including pelvic-floor dysfunction or altered sen-\nsory processing; however, the relative contribution of these \nmechanisms remains uncertain.\nLUTS Without Direct Involvement \nof the Urinary Tract\nIn most cases of DE, the urinary tract is not directly affected \nby endometriotic lesions. Nevertheless, many patients expe-\nrience LUTS even in the absence of identifiable urinary tract \ninfiltration. These symptoms appear to be independent of \ndisease extent [4, 6].\nIC/BPS is defined as chronic pelvic pain with discomfort \nperceived to originate in the bladder, accompanied by at \nleast one symptom of urinary urgency or frequency in the \nabsence of infection or other identifiable pathology. The co-\noccurrence of endometriosis and IC/BPS has been described \nas the “evil twin syndrome,” due to their overlapping clini-\ncal features and pathophysiological similarities. Studies of \nselected populations with chronic pelvic pain have reported \nsubstantial overlap between endometriosis and IC/BPS [33]. \nThe reported prevalence of their coexistence ranges from \n15.5% to 78.3% across chronic pelvic pain cohorts, with sub-\nstantial variation in patient selection, diagnostic criteria, and \nassessment instruments [34]. Differences include whether \nvalidated symptom questionnaires were used and whether \nassessment relied on clinical symptoms, cystoscopy with \nhydrodistension, or combinations of these approaches. These \nestimates should not be interpreted as the prevalence of IC/\nBPS among all women with endometriosis.\nAlthough the precise relationship between endometrio-\nsis and IC/BPS remains unclear, shared inflammatory and \nsensory mechanisms have been proposed. In IC/BPS, dis -\nruption of the urothelial barrier, including alterations of the \nglycosaminoglycan layer, may increase bladder permeabil-\nity and facilitate exposure of underlying tissues to urinary \nirritants, thereby contributing to pain and urinary symp-\ntoms [35]. Whether endometriosis-associated inflamma-\ntory mediators directly promote such urothelial dysfunction \nremains uncertain. Because of the substantial symptomatic \noverlap between the two conditions, IC/BPS may be under-\nrecognized in women with endometriosis. When IC/BPS \nis suspected as a coexisting condition, management should \nfollow established IC/BPS principles rather than being inter-\npreted as treatment of DE itself. Management may include \nlifestyle and dietary modification, pain-directed therapy, \npelvic-floor management, and selected bladder-directed \ntreatments according to applicable IC/BPS guidelines [36]. \nPersistent or recurrent bladder-related pain or urinary symp-\ntoms after adequate endometriosis treatment should there-\nfore prompt consideration of coexisting IC/BPS.\nPelvic floor dysfunction, including muscle hypertonic-\nity and myofascial pain, has been frequently observed in \nwomen with endometriosis, potentially exacerbating LUTS \nthrough non-neurogenic mechanisms. Assessment of pelvic \nfloor muscle abnormalities may therefore be appropriate in \nwomen with endometriosis and LUTS, particularly when \npelvic-floor hypertonicity or myofascial pain is present [37].\nRecent evidence indicates that oxidative stress plays a role \nin the pathogenesis of endometriosis, contributing to both \nthe establishment and progression of the disease. Elevated \nlevels of reactive oxygen species (ROS) in the peritoneal \nfluid of affected women may disrupt cellular homeostasis, \npromote inflammation and sensitize peripheral nerves. These \nmechanisms may contribute to peripheral sensitization and \npain generation in endometriosis; however, a direct role of \noxidative stress in the development of LUTS has not been \nestablished [38].\nUrodynamic studies suggest that functional bladder \nabnormalities may occur even in the absence of direct blad-\nder wall involvement, although the relative contributions of \nautonomic dysfunction and inflammation remain uncertain \n[39].\nPeripheral innervation of the bladder can be affected \ndirectly by endometriotic lesions or indirectly via pro-\ninflammatory mediators. Lesions involving the posterior \npelvic compartment, particularly the uterosacral ligaments, \nfrequently contribute to LUTS. In up to 50% of such cases, \nthese ligaments undergo fibrotic retraction. The cardinal \nand uterosacral ligaments contain autonomic nerve fibers, \nincluding sympathetic fibers in the hypogastric nerve and \nparasympathetic fibers via the pelvic splanchnic nerves, \nwhich converge in the inferior hypogastric plexus [40]. His-\ntological studies have confirmed the presence of autonomic \nand sensory (C and Aδ) nerve fibers within resected endo-\nmetriotic lesions from these ligaments [41]. These lesions \npromote a pro-inflammatory microenvironment rich in \ncytokines and neurotransmitters, leading to peripheral nerve \nsensitization, altered synaptic transmission, and potentially \ncentral sensitization.\nCentral sensitization refers to the heightened respon-\nsiveness of central neurons to nociceptive stimuli, result-\ning in exaggerated and persistent pain responses to ther -\nmal, mechanical, or chemical stimuli [42]. Chronic \nnociceptive input from endometriotic lesions can lead to \n\n International Urogynecology Journal\nhyperexcitability of spinal cord neurons, which relay signals \nto the thalamus and cortex. Over time, stimuli of constant \nintensity may be perceived as increasingly painful. Build-\ning on the concept of central sensitization, recent work has \nproposed distinct pain phenotypes in endometriosis: (i) a \npredominantly nociceptive/inflammatory phenotype, (ii) a \nneuropathic-like phenotype, and (iii) a nociplastic phenotype \ncharacterized by widespread pain and sensory amplification \n[23]. These pain phenotypes may also influence the clinical \nexpression of LUTS. Pelvic-floor hypertonicity may contrib-\nute to dysuria and obstructive voiding symptoms, whereas \nneuropathic-like pain may include burning or electric-shock-\nlike sensations. Nociplastic mechanisms could contribute \nto persistent or fluctuating urgency and frequency that are \ndisproportionate to identifiable pelvic pathology. However, \ndirect evidence linking specific pain phenotypes to distinct \nLUTS patterns in endometriosis remains limited. Recogniz-\ning these overlapping mechanisms may nevertheless help \nguide individualized therapeutic priorities [43].\nMoreover, cross-sensitization between pelvic organs may \noccur—a phenomenon known as viscero-visceral hyperal-\ngesia—where pain originating from one organ (e.g., uterus) \nsensitizes sensory pathways shared with adjacent organs \n(e.g., bladder), thereby generating LUTS even in the absence \nof direct pathology [42].\nManagement of LUTS without direct urinary tract \ninvolvement is individualized based on symptom severity. \nFirst-line therapies include lifestyle modification, bladder \nretraining, pelvic floor relaxation techniques, and dietary \nadjustments to minimize bladder irritation. Pharmacologic \ntreatments such as antimuscarinics and β3-adrenergic ago-\nnists are used for overactive bladder symptoms. In refrac -\ntory cases, intravesical botulinum toxin injections and neuro-\nmodulatory techniques—including sacral nerve stimulation \n(SNS) and percutaneous tibial nerve stimulation (PTNS)—\nmay be beneficial [44]. A proposed, phenotype-based frame-\nwork could stratify women with DE-related LUTS into:\n(1) inflammatory/nociceptive-dominant phenotype, in \nwhom treatment may primarily target endometriosis \nitself when clinically indicated;\n(2) neuropathic-like phenotype, in whom treatment of \ncoexisting neuropathic pain may be considered accord-\ning to established chronic-pain principles; and\n(3) central sensitization/nociplastic-dominant phenotype, \nin whom multidisciplinary pain management and pel-\nvic-floor assessment may be appropriate.\nThese categories are conceptual and hypothesis-generat-\ning and have not been prospectively validated as treatment \npathways for DE-associated LUTS. Pelvic-floor physiother-\napy may be considered in women with documented pelvic-\nfloor dysfunction or hypertonicity. However, evidence for \nimprovement of urinary symptoms specifically in women \nwith DE remains limited; in the randomized trial by Del \nForno et al., pelvic-floor physiotherapy did not significantly \nimprove urinary-function outcomes [45]. The principal clini-\ncal presentations, associated mechanisms, and established \nversus proposed management considerations are summa-\nrized in Table  2.\nDe Novo LUTS After Surgery for Deep \nEndometriosis\nSurgical treatment of deep endometriosis (DE) is indicated \nfor patients with severe symptoms, visible lesions and failure \nof conservative management. However, owing to the pres-\nence of adhesions and proximity of lesions to critical pel-\nvic structures, these procedures carry a substantial risk of \ncomplications. Among them, LUTS that arise de novo after \nsurgery are frequently overlooked. Although some patients \nexperience symptomatic improvement in LUTS after DE \nsurgery, others experience deterioration of LUTS [ 46–48], \nparticularly those with extensive parametrial and pelvic \nnerve involvement [47]. Postoperative lower urinary tract \ndysfunction may therefore represent true de novo dysfunc-\ntion related to surgical injury, persistence or worsening of \npre-existing dysfunction, or unmasking of previously sub-\nclinical abnormalities.\nEndometriotic lesions may directly involve autonomic \nnerves responsible for urinary tract function. In cases where \nlesions infiltrate the hypogastric nerve, inferior hypogastric \nplexus, or pelvic splanchnic nerves, their resection may \nresult in neural injury. These autonomic pathways provide \nsympathetic and parasympathetic innervation to the bladder \nand contribute to visceral afferent signaling involved in blad-\nder sensation and voiding. Postoperative lower urinary tract \ndysfunction has been reported after surgery for DE, particu-\nlarly when extensive dissection involves the parametrium, \nuterosacral ligaments, or pelvic autonomic nerves. Reported \nrates vary according to the extent of disease, surgical tech-\nnique, and definition of postoperative dysfunction [51, 52].\nExcision of endometriotic lesions from the rectovaginal \nseptum, uterosacral ligaments, or parametria may damage \nautonomic innervation of the bladder. The inferior hypogas-\ntric plexus comprises parasympathetic fibers via pelvic \nsplanchnic nerves and sympathetic fibers via the hypogastric \nnerve. Surgical disruption of this plexus can have segment-\nspecific consequences. The functional consequences of \ninjury depend on the location and extent of neural damage \nand may include impaired bladder sensation, reduced detru-\nsor contractility, and postoperative urinary retention [50].\nParasympathetic fibers are located a few centimeters \nbelow the cul-de-sac (Douglas pouch) and are at risk during \nresection of the rectovaginal septum or rectosigmoid colon. \n\nInternational Urogynecology Journal \nTable 2  Clinical presentations, relevant mechanisms, and established versus proposed management considerations for lower urinary tract symptoms in deep endometriosis\nUrinary symptom/clinical phenotype Relevant mechanism Established/standard approach Hypothetical/proposed approach Supporting references\nDysuria, hematuria, urgency or fre-\nquency with bladder endometriosis\nDirect bladder-wall involvement; local \ninflammation and fibrosis\nImaging according to suspected disease \nextent; hormonal or surgical treatment \naccording to symptoms and lesion \ncharacteristics\nPersistent LUTS after treatment may \nalso involve pelvic-floor or sensory \nmechanisms\n[4, 12, 28, 31, 32]\nUreteral obstruction/hydronephrosis Direct ureteral infiltration and/or fibrosis \ncausing obstruction\nAssessment of the upper urinary tract \nwhen ureteral involvement is sus-\npected; surgical treatment when clini-\ncally significant obstruction is present\n/ [28–30]\nOAB-like symptoms without direct \nurinary tract involvement\nFunctional bladder abnormalities; possi-\nble altered autonomic or inflammatory \nsignaling\nManagement according to established \nOAB principles\nAn endometriosis-specific neuroinflam-\nmatory contribution remains unproven\n[11, 39, 44]\nBladder pain with coexisting IC/BPS Urothelial and sensory dysfunction \nrelated to IC/BPS\nManagement according to established \nIC/BPS principles\nA direct contribution of endometriosis-\nassociated inflammation to IC/BPS \nremains uncertain\n[19, 33–36]\nLUTS with pelvic-floor hypertonicity or \nmyofascial pain\nPelvic-floor dysfunction and altered \npelvic-floor coordination\nPelvic-floor assessment when dysfunc-\ntion is suspected\nPelvic-floor physiotherapy may be \nconsidered when dysfunction is docu-\nmented, but improvement of urinary \nsymptoms specifically in DE has not \nbeen established\n[37, 45]\nLUTS with neuropathic-like or nociplas-\ntic pain features\nPossible peripheral and central sensitiza-\ntion; evidence is largely indirect\nTreatment of coexisting chronic pain \naccording to established chronic-pain/\nendometriosis principles\nWhether pain phenotyping can guide \nLUTS-specific therapy remains \nunvalidated\n[9, 10, 20–26, 43]\nPostoperative voiding dysfunction/uri-\nnary retention\nPelvic autonomic nerve injury, impaired \nbladder sensation and/or reduced detru-\nsor contractility\nPostvoid residual assessment, intermit-\ntent self-catheterization when indi-\ncated, and nerve-sparing surgery when \ntechnically feasible\nSacral neuromodulation may be consid-\nered in selected persistent cases\n[13, 18, 46–57]\nExperimental neuroinflammatory \nmechanisms\nJAK/STAT signaling, mast-cell activa-\ntion and neuroangiogenesis\nNo established LUTS-specific treatment JAK/STAT- or mast-cell-directed thera-\npies remain experimental and require \nclinical validation\n[14, 27, 31]\n\n International Urogynecology Journal\n\n\nInternational Urogynecology Journal \nDamage to afferent sensory fibers in the distal hypogastric \nnerve—typically during uterosacral ligament excision—may \ninitially be asymptomatic but later result in progressive blad-\nder dysfunction [58].\nProspective and retrospective studies confirm that lower \nurinary tract dysfunction (LUTD) after DE surgery is not \nrare, particularly when resection involves the uterosacral \nligaments, parametrium or rectovaginal septum. In a cohort \nof 198 women undergoing surgery for posterior compart-\nment DE, 41% initially had postoperative voiding dysfunc-\ntion, defined as a postvoid residual volume > 100 mL at the \nsecond bladder scan. This proportion decreased to 11% at \nhospital discharge [52]. Seventeen women required self-\ncatheterization after discharge, with a median duration of \n41 days before recovery. In the same study, ENZIAN com-\npartment B involvement, particularly lesions > 3 cm, was \nassociated with postoperative voiding dysfunction. Benoit \net al. reported that combined resection of the torus uterinus, \nuterosacral ligaments, parametrium, and vagina was associ-\nated with postoperative voiding dysfunction compared with \nuterosacral ligament resection alone (adjusted odds ratio \n37.3, 95% confidence interval 6.8–203.1) [53]. The wide \nconfidence interval indicates substantial imprecision, and \nresidual confounding by disease severity and surgical com-\nplexity may partly explain the magnitude of the association. \nAdditionally, colorectal surgery for endometriosis is asso-\nciated with postoperative voiding dysfunction despite the \nuse of nerve-sparing techniques. The incidence is highest in \nsegmental colorectal resection and lower in discoid excision \nand rectal shaving [54, 55]. According to the meta-analysis \nby Vesale et al., self-catheterization was mainly required \nafter segmental colorectal resection [54].\nBladder afferent signaling is mediated principally by \nmyelinated Aδ fibers and unmyelinated C fibers traveling \nthrough pelvic and hypogastric pathways. Aδ fibers are pri-\nmarily involved in physiological bladder-filling sensation, \nwhereas C fibers are relatively quiescent under normal con-\nditions and become increasingly active during inflammation, \nchemical irritation, or other noxious stimuli [59]. Surgical \ninjury to pelvic autonomic pathways may impair bladder \nsensation and detrusor function, leading to prolonged void-\ning intervals, increased bladder capacity, incomplete empty-\ning, and, in severe cases, urinary retention [50].\nMore recent prospective work using pre- and post-\noperative multichannel urodynamics in women treated \nfor DE reported both pre-existing and de novo detrusor \nunderactivity or acontractile bladder in a substantial \nminority, highlighting that lower urinary tract dysfunction \nmay already be present before surgery and that surgery \nmay unmask or exacerbate pre-existing abnormalities [18].\nThese observations reinforce the importance of system-\natic preoperative counseling regarding the risk of LUTD, \nespecially in women requiring extensive dissection near \nthe inferior hypogastric plexus, ureteric tunnels or bladder \nbase. They also support the use of selective nerve-sparing \ntechniques and careful intraoperative identification of \nneural structures wherever feasible. Early postoperative \nscreening with bladder scanning and, in selected cases, \nformal urodynamics allows prompt initiation of appropri-\nate management, including intermittent catheterization \nwhen clinically indicated. Where technically feasible, \nnerve-sparing approaches are associated with a lower risk \nof postoperative urinary retention compared with non-\nnerve-sparing techniques [18, 58].\nDelayed bladder dysfunction has been described after \nextensive pelvic nerve injury, and patients with persistent \nvoiding symptoms may require longitudinal assessment \nof postvoid residual volume. When clinically significant \nincomplete bladder emptying is present, clean intermit-\ntent self-catheterization may be required to prevent chronic \nbladder overdistension and secondary detrusor deterioration. \nIncreased urethral outlet resistance following autonomic \ndenervation has also been proposed as an additional con-\ntributor to postoperative urinary retention [50]. Postopera-\ntive voiding dysfunction may result from injury to pelvic \nautonomic pathways, leading to impaired bladder sensa-\ntion, reduced detrusor contractility, and incomplete bladder \nemptying. Functional outlet obstruction due to inadequate \nrelaxation of the pelvic floor or urethral sphincter may also \ncontribute in some patients. Management should be indi-\nvidualized according to the underlying dysfunction. Early \npostoperative assessment of spontaneous voiding and post-\nvoid residual volume is important, with clean intermittent \nself-catheterization when clinically indicated. Subsequent \nmanagement may include bladder rehabilitation, pelvic-floor \nphysiotherapy and, in selected persistent cases, sacral neu-\nromodulation [56]. In a retrospective cohort of 61 women \ndischarged with intermittent self-catheterization after DE \nsurgery, Boulus et al. reported that 43 (70.5%) discontin-\nued catheterization during a median follow-up of 25 weeks \n(range 7–223 weeks). The estimated probability of recovery \nsufficient to discontinue self-catheterization reached 77% at \n78 weeks [57]. Preoperative bladder dysfunction was the \nonly statistically significant independent predictor of cath-\neterization cessation in the multivariable model and was \nassociated with a lower recovery hazard (hazard ratio 0.36, \n95% confidence interval 0.15–0.83). These findings support \nassessment of baseline voiding function and counseling \nabout the possibility of prolonged postoperative dysfunction.\nFig. 3  Proposed pathophysiological mechanisms of lower urinary \ntract symptoms in deep endometriosis. Neuroinflammatory and noci-\nplastic pathways represent proposed mechanisms whose specific con-\ntribution to DE-associated LUTS remains incompletely established. \nDE deep endometriosis; LUTS  lower urinary tract symptoms; IL \ninterleukin; NGF nerve growth factor; JAK/STAT  Janus kinase/signal \ntransducer and activator of transcription\n◂\n\n International Urogynecology Journal\nConclusion\nEndometriosis, particularly DE, may be associated with \nLUTS through both direct urinary tract involvement and \nextra-urinary mechanisms. Multiple pathophysiological \nmechanisms may contribute to LUTS in these patients, \nincluding direct infiltration of urinary organs, neuroin-\nflammatory processes, autonomic nerve involvement, and \npostoperative complications (Fig.  3). Symptoms may range \nfrom urinary urgency and frequency to pain, voiding dys-\nfunction, and retention.\nEffective management of LUTS in endometriosis \nrequires a multidisciplinary approach, involving gynecolo-\ngists, urologists, physiotherapists, and clinical psycholo-\ngists. Treatment strategies must be individualized and \nmay include conservative measures, pelvic floor rehabili-\ntation, pharmacotherapy, pain management, and surgical \nintervention when indicated. Where surgery is indicated, \nnerve-sparing techniques should be considered when tech-\nnically feasible to reduce the risk of postoperative urinary \ndysfunction. Reconstructive procedures, such as uretero -\nneocystostomy or bladder reconstruction, may be required \nin selected cases of extensive urinary tract involvement. \nImportantly, delayed urinary dysfunction may occur after \nextensive pelvic nerve injury, initially presenting with \nprolonged voiding intervals and later increased postvoid \nresidual volumes. Early recognition and timely interven-\ntion are critical to preventing irreversible detrusor damage. \nUltimately, the goal of treating deep pelvic endometriosis \nis to improve patients’ quality of life—an objective that \nincludes the proactive identification and management of \nLUTS both before and after treatment.\nFuture Directions\nLooking ahead, three areas appear particularly promising \nfor improving outcomes in women with deep pelvic endo-\nmetriosis and LUTS. First, pain phenotyping—distinguish-\ning nociceptive, neuropathic-like, and nociplastic profiles \nusing validated questionnaires and clinical assessment—\nmay warrant further evaluation in prospective studies [9 ]. \nIf validated, this approach could support personalized \ntreatment plans combining lesion-directed surgery or hor -\nmonal therapy with neuromodulators and multidisciplinary \nrehabilitation for patients with prominent neuropathic or \ncentrally mediated features.\nSecond, advanced imaging biomarkers may help clar -\nify relationships between lesion characteristics and LUTS \nphenotypes. Prospective studies correlating standardized \nultrasound and MRI findings with urinary symptom pro-\nfiles could improve understanding of clinically relevant \ndisease patterns. Third, molecular biomarkers and neu-\nroinflammatory pathways, including JAK/STAT signal -\ning and mast-cell activation, warrant further investigation \n[14]. These approaches remain experimental and require \nmechanistic and clinical validation before their relevance \nto DE-associated LUTS management can be established.\nAuthor Contributions RS conceived the review, performed the litera-\nture search, synthesized the evidence, prepared the figures, and drafted \nthe manuscript. TS contributed to the conceptualization of the review, \ncritically revised the manuscript for important intellectual content, and \napproved the final version. Both authors read and approved the final \nmanuscript.\nFunding This work was supported by the Slovenian Research and Inno-\nvation Agency (ARIS), with project number P3-0327.\nData Availability No datasets were generated or analyzed during the \ncurrent study. All information discussed in this narrative review is \nderived from previously published literature cited in the reference list.\nDeclarations \nEthical Approval Ethical approval was not required because this study \nis a narrative review based exclusively on previously published litera-\nture and did not involve human participants, animals, or identifiable \npatient data.\nConflicts of Interest None.\nOpen Access This article is licensed under a Creative Commons Attri-\nbution 4.0 International License, which permits use, sharing, adapta-\ntion, distribution and reproduction in any medium or format, as long \nas you give appropriate credit to the original author(s) and the source, \nprovide a link to the Creative Commons licence, and indicate if changes \nwere made. The images or other third party material in this article are \nincluded in the article’s Creative Commons licence, unless indicated \notherwise in a credit line to the material. 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