Pathophysiological Mechanisms and Clinical Implications of Lower Urinary Tract Symptoms in Patients with Deep Endometriosis: A Narrative Review

Introduction and Hypothesis Endometriosis is a chronic inflammatory condition characterized by endometrium-like tissue outside the uterus. Deep endometriosis (DE) frequently involves the posterior pelvic compartment and can affect the uri- nary tract directly or indirectly, leading to a wide spectrum of lower urinary tract symptoms (LUTS). This narrative review aimed to synthesize current evidence on the mechanisms underlying LUTS in women with deep endometriosis, including direct urinary tract involvement, extra-urinary mechanisms, and postoperative dysfunction, and to discuss their diagnostic and therapeutic implications.

A structured, non-systematic literature search was conducted using PubMed/MEDLINE for English-language publications from 2000 to July 2026. Four thematic domains were considered: (1) prevalence and pathophysiological mecha- nisms of LUTS in endometriosis; (2) LUTS due to direct urinary tract involvement; (3) LUTS without direct urinary tract involvement; and (4) de novo LUTS after surgery for deep endometriosis.

In women with DE undergoing preoperative urodynamic assessment, pooled estimates indicated voiding dysfunction in 21% and detrusor overactivity in 15%, with substantial heterogeneity. LUTS may reflect direct urinary tract involvement, neural dysfunction, inflammation, or surgical injury. Evidence for proposed neuroinflammatory and nociplastic mechanisms remains largely indirect or experimental.

Multiple pathophysiological mechanisms may contribute to LUTS in DE. Clinicians should be aware of the association between these two conditions and address treatment of both, which often requires a multidisciplinary approach. Where surgery is indicated, nerve-sparing techniques should be considered when technically feasible to reduce the risk of postoperative urinary dysfunction. Emerging mechanistic and phenotype-based approaches require further validation.

Deep endometriosis · Endometriosis · Lower urinary tract symptoms · Voiding dysfunction

Endometriosis is a chronic disease defined by the presence of endometrial-like tissue outside the uterine cavity, affect- ing approximately 10% of reproductive-aged women [1 ]. It presents in several forms—superficial peritoneal lesions, ovarian endometriomas, and deep endometriosis (DE), with DE being the most symptomatic and anatomically disruptive subtype [2 ]. Commonly affected sites include the uterosa- cral ligaments, retrocervical region, rectovaginal septum, and rectosigmoid colon; urinary tract involvement is also relatively frequent in women with deep endometriosis [3 , 4]. Lower urinary tract symptoms (LUTS) are also common in the general female population, although estimates depend strongly on age and symptom definitions. In the population- based EpiLUTS survey of adults aged 40 years and older, prevalence among women ranged from 52.5% using a higher symptom-frequency threshold to 76.3% using a lower thresh- old [5]. Handling Editor: Kaven Baessler Editor in Chief: Kaven Baessler * Rok Šumak [email protected] 1 Department of General Gynecology and Gynecologic Urology, Clinic for Gynecology and Perinatology, University Medical Centre Maribor, Ljubljanska Ulica 5, 2000 Maribor, Slovenia International Urogynecology Journal LUTS such as urgency, frequency, nocturia, dysuria, suprapubic pain, and incomplete bladder emptying are reported in a substantial proportion of women with endo- metriosis, particularly those with DE and/or bladder involve- ment [6 ]. Although LUTS in deep endometriosis have traditionally been attributed to direct bladder or ureteral involvement, accumulating evidence indicates that they may also reflect pelvic neural involvement, pelvic-floor muscle dysfunction, viscero-visceral cross-sensitization, and periph- eral and central neuroimmune sensitization—even without overt urinary tract endometriosis [7 , 8]. Epidemiological studies demonstrate that women with surgically confirmed endometriosis experience LUTS more frequently than healthy controls, independent of disease stage or lesion location [6 ]. Endometriosis also frequently coexists with other chronic pain syndromes, supporting a broader concept of centrally mediated pain modulation. Neuropathic-like pain was identified in 36% of women in a cohort with DE and chronic pelvic pain. Features con- sistent with central sensitization and nociplastic pain have also been reported in endometriosis, although assessment

vary and their diagnostic validity requires fur - ther evaluation [9 , 10]. These pain-related mechanisms may help explain persistent symptom amplification after lesion excision, although their specific contribution to DE- associated LUTS remains incompletely established [11]. DE may also involve the urinary tract directly, particu- larly the bladder and ureters [12]. Ureteral endometriosis may remain asymptomatic until hydronephrosis devel- ops, highlighting the importance of assessing the upper urinary tract when ureteral involvement is suspected on the basis of disease location, symptoms, or imaging find- ings. Furthermore, surgical excision of DE carries a risk of autonomic nerve injury, which may result in de novo LUTS, sometimes becoming apparent after surgery [13]. Recent research has also highlighted emerging neuro- inflammatory pathways, including mast-cell activation and the Janus kinase/signal transducer and activator of transcription (JAK–STAT) signaling, which may con- tribute to neural sensitization and neuroangiogenesis in endometriosis. Their specific relevance to LUTS remains hypothetical and requires further investigation [14]. Given the multifactorial origins of LUTS in DE, an integrated and multidisciplinary approach to diagnosis and manage- ment is important. The aim of this narrative review was to synthesize current evidence on the pathophysiological mechanisms associated with LUTS in DE and to discuss their diagnostic and therapeutic implications, while dis- tinguishing established clinical evidence from emerging or hypothesis-generating mechanisms.

A structured, non-systematic literature search was con- ducted using the PubMed/MEDLINE database to identify clinically relevant and mechanistic literature concerning lower urinary tract symptoms in endometriosis, with par - ticular emphasis on deep endometriosis. PubMed/MED- LINE was selected as the principal database because of its broad coverage of biomedical and clinically oriented literature relevant to endometriosis and lower urinary tract dysfunction. As this was a narrative review based exclu- sively on previously published literature, ethical approval was not required. Literature Search and Selection The principal search combined terms related to endome- triosis with terms related to lower urinary tract symp- toms and urinary dysfunction: (endometriosis OR “deep endometriosis” OR “deep infiltrating endometriosis” OR endometrioma) AND (“lower urinary tract symptoms” OR dysuria OR “voiding dysfunction” OR “urinary reten- tion” OR hematuria OR “urinary frequency” OR “uri- nary incontinence” OR “urinary urgency” OR “overactive bladder”). Searches were focused on English-language publications from 2000 to July 2026; earlier seminal pub- lications were included when relevant for historical or conceptual context. Because the review also aimed to discuss potential bio- logical mechanisms underlying LUTS, targeted searches and reference-list screening were additionally used to identify relevant literature on pelvic-floor dysfunction, autonomic innervation, peripheral and central sensitiza - tion, nociplastic and neuropathic pain, mast-cell activa- tion, neuroangiogenesis, and JAK/STAT signaling. Priority was given to clinical studies, systematic reviews, meta-analyses, clinical guidelines, and larger observational studies directly addressing LUTS, urinary tract endometriosis, urodynamic findings, or postopera- tive urinary dysfunction. Mechanistic, anatomical, histo- logical, and pain-related studies were included selectively when they provided relevant biological context for pro- posed pathways linking endometriosis with LUTS. Com- mentaries, case reports, case series, and meeting abstracts were generally not included. Both authors participated in the selection of relevant publications and in the thematic interpretation of the evidence. Differences in the perceived relevance or interpretation of individual publications were resolved by discussion and consensus. International Urogynecology Journal Evidence directly examining LUTS in women with DE was distinguished from indirect evidence derived from studies of endometriosis-associated pain, OAB, IC/BPS, pelvic-floor dysfunction, or experimental mechanisms. Such indirect evidence was used to provide biological con- text and generate hypotheses, rather than as direct proof of causation or treatment efficacy for DE-associated LUTS. A flowchart of literature search and selection is presented in Fig.  1. Because this was a narrative rather than a system- atic review, formal PRISMA or SWiM methodology and risk-of-bias assessment were not applied. The use of Pub- Med/MEDLINE as the principal bibliographic database and the non-systematic nature of study selection may have resulted in incomplete literature retrieval and introduced selection bias; but these limitations are inherent to the narrative-review design. Narrative Synthesis The identified literature was organized into four thematic domains: (1) prevalence and pathophysiological mechanisms of LUTS in endometriosis (2) LUTS due to direct urinary tract involvement (3) LUTS without direct urinary tract involvement (4) de novo LUTS after surgery for deep endometriosis. Prevalence and Pathophysiological Mechanisms of LUTS in Endometriosis Both endometriosis and LUTS are prevalent in the general female population, and patients with DE often experience LUTS [15]. A systematic review from 2024 showed that 15% of patients with DE had detrusor overactivity, 21% had preoperative voiding dysfunction, and 39% had an abnormal bladder sensation. On urodynamic evaluation, 18% had low maximum cystometric capacity, 35% low preoperative blad- der compliance, and 37% painful preoperative bladder filling [16]. In women with parametrial endometriosis, LUTS are present in 27% and dysuria in 15%, with rare reporting of voiding dysfunction before surgery [17]. Overactive bladder (OAB) and non-urinary tract endometriosis may co-occur in 20.5% of patients [11]. The mechanisms underlying LUTS in endometriosis are complex and multifactorial (Table 1). Endometriotic lesions may infiltrate the bladder, ureters, or other components of the urinary tract, resulting in structural and functional abnor- malities. However, LUTS can also occur in the absence of direct urinary tract involvement, suggesting that altered innervation or inflammatory mechanisms may contribute to bladder dysfunction [11]. Additionally, LUTS may arise postoperatively as a consequence of nerve injury, fibrosis, or altered pelvic anatomy following excision of deep lesions [18]. Despite the high prevalence of LUTS in women with endometriosis, they are often unrecognized or untreated. Notably, endometriosis commonly coexists with chronic pain syndromes such as migraine, interstitial cystitis/bladder pain syndrome (IC/BPS), and irritable bowel syndrome [19]. Women with endometriosis and dysmenorrhea are more likely to report dysuria and urgency, and LUTS are present in approximately 40% of patients with endometriosis [ 6]. These symptoms are strongly associated with diminished quality of life, daily functioning, and productivity. Similar to endometriosis itself, LUTS independently contribute to impaired physical and emotional well-being. Neuropathic and nociplastic mechanisms: indirect evidence from endometriosis‑associated pain An imbalance between sympathetic and sensory innerva- tion has been identified in peritoneal endometriosis, with a predominance of sensory nerve fibers promoting a pro- nociceptive environment. This neuroanatomical alteration may contribute to persistent pelvic pain and provides a biologically plausible basis for altered sensory processing involving adjacent pelvic organs. However, direct evidence linking these changes specifically to LUTS in women with DE remains limited [20]. Pelvic pain may improve or per - sist after excision of peritoneal lesions because of ongo - ing abnormal nerve activity, neurogenic inflammation, and peripheral sensitization in surrounding pelvic tissues [21, 22]. In addition to classical nociceptive and inflammatory pathways, recent work has highlighted a substantial neu- ropathic component in women with DE and chronic pelvic pain (CPP). In an observational study from 2025, which included 149 women with DE and CPP, neuropathic-like pain (defined by a positive Douleur Neuropathique 4 score) was identified in 36% of patients and was associated with significantly higher pain intensity, greater catastrophizing, and worse quality of life [9 ]. Although this cohort did not specifically evaluate urinary tract involvement or LUTS, it supports the presence of a neuropathic-like pain phenotype in a subset of women with DE. Whether this phenotype con- tributes directly to urinary symptoms remains uncertain. Features consistent with nociplastic pain, including wide- spread hypersensitivity, fatigue, and coexisting pain condi- tions, have been described in women with endometriosis, even when lesion burden is limited [23]. In this context, persistent urgency, frequency, or suprapubic pain after technically successful excision could potentially be influ- enced by central sensitization, although direct evidence demonstrating this mechanism in DE-associated LUTS is lacking. Brain imaging studies in women with CPP and International Urogynecology Journal Fig. 1 Literature-search framework and thematic organization of the narrative review International Urogynecology Journal endometriosis demonstrate altered structure and connectiv - ity in pain-modulating regions such as the periaqueductal gray and anterior insula, supporting a central contribution to pain amplification; these findings provide indirect rather than LUTS-specific evidence [24]. The potential therapeutic implications of these pain phenotypes for DE-associated LUTS remain uncertain. Neuromodulatory agents such as gabapentinoids or seroto- nin–noradrenaline reuptake inhibitors, as well as multidisci- plinary approaches, including pain neuroscience education, cognitive-behavioral therapy, and pelvic-floor rehabilitation, are used in selected chronic pain populations [25, 26]. How- ever, their efficacy for LUTS specifically associated with DE has not been established. Assessment of neuropathic-like or nociplastic features may therefore be useful for charac- terizing the broader pain phenotype, but its role in guiding LUTS-specific treatment requires prospective validation. Emerging and Experimental Mechanisms: JAK–STAT Signaling, Mast Cells, and Neuroangiogenesis An emerging conceptual advance in endometriosis pain biol- ogy is the recognition of the JAK/STAT pathway as a central hub linking inflammation, angiogenesis, and neurogenesis. Evidence for this pathway derives primarily from mecha- nistic and endometriosis-pain research, and direct clinical evidence linking JAK/STAT signaling specifically to LUTS in women with DE is currently lacking. Neuroinflamma- tion in endometriosis lesions, including activation of dorsal root ganglia and lesion-associated nerve fibers, converges on JAK/STAT signaling, with mast cells acting as key effector cells in this network [14]. Mast cells, via mediators such as tryptase, histamine, and nerve growth factor (NGF), can promote growth and sensitization of afferent fibers; in deep lesions involving the bladder wall or ureter, this provides a plausible but unproven mechanistic link to LUTS via increased activity of vesical afferents (Fig.  2). Cytokines and growth factors associated with JAK/STAT- related pathways, including IL-6-family mediators, PDGF, and VEGF, have also been implicated in angiogenic and neu- roinflammatory processes in endometriosis [14, 27]. From a translational perspective, JAK inhibitors and mast-cell-stabilizing agents have been proposed as potential targets for future investigation in endometriosis-associated neuroinflammation [14]. However, no clinical trials have evaluated these agents for urinary tract endometriosis or DE- associated LUTS, and their relevance to urinary symptom management remains speculative. These pathways should therefore be regarded as hypothesis-generating targets for future mechanistic and clinical research rather than estab- lished therapeutic options. Urinary Tract Endometriosis: Bladder Symptoms and Ureteral Involvement Urinary tract endometriosis has been reported in approxi- mately 20–50% of women with DE, although estimates vary considerably according to referral setting, disease definition, and diagnostic method [12]. Among urinary tract sites, the bladder is most frequently involved, followed by the ure - ters; renal and urethral involvement are rare [28]. Bladder endometriosis may present with suprapubic pain, dysuria, hematuria, urgency, frequency, incomplete emptying, or recurrent urinary tract symptoms, often with a cyclical pat- tern. In contrast, ureteral endometriosis frequently causes no LUTS and may remain clinically silent until hydronephro- sis or impaired renal function develops [28, 29]. Because ureteral endometriosis may be clinically silent, assessment for ureteral involvement and upper urinary tract obstruction should be considered when disease location, imaging find- ings, or clinical suspicion suggest urinary tract involvement. Endometriotic lesions involving the bladder may be superficial, remaining confined to the peritoneal surface overlying the bladder, or deep, infiltrating the detrusor Table 1 Proposed pathophysiological mechanisms underlying LUTS in endometriosis Mechanism Description Clinical consequences Mechanical Caused by infiltration of endometriotic lesions into the bladder, ureters, and other components of the urinary tract, or adhesions and fibrosis, leading to structural and functional abnormalities Obstruction, reduced bladder compliance, LUTS, hematu- ria, suprapubic pain, dysuria Neural and nociplastic Altered afferent signaling from pelvic organs, possible central sensitization, and viscero-visceral cross-talk Potential contribution to persistent urgency, frequency, and bladder pain Chronic inflammation Potentially involving JAK/STAT signaling, mast cells, IL-1, IL-6, and NGF, which may promote growth and sensitization of afferent fibers Potential afferent sensitization and contribution to LUTS Iatrogenic Consequence of nerve injury, fibrosis, or altered pelvic anatomy following excision of DE de novo LUTS after surgery, detrusor underactivity, urinary retention International Urogynecology Journal muscle and, rarely, the urothelium. Transvaginal ultrasound is the first-line imaging modality, with MRI providing com- plementary evaluation when required. Cystoscopy may help determine whether the lesion involves the bladder mucosa and assess its relationship with the ureteric orifices. Hor - monal therapy may be considered for symptomatic bladder endometriosis, whereas surgery is appropriate when medical treatment is ineffective or unsuitable. Ureteral obstruction or hydronephrosis generally requires surgical treatment regard- less of symptoms because of the risk of irreversible loss of renal function [4, 30]. Histological studies have identified nerve fibers and neu- roinflammatory mediators in endometriotic lesions. How - ever, nerve bundle density and NGF and IL-1β expression vary substantially between lesions and anatomical subtypes within the same patient, without a uniform increase with lesion depth [31]. When lesions involve densely innervated regions such as the trigone, their proximity to intrinsic ganglia and sensory afferent pathways provides a plausible anatomical basis for urgency, frequency, and bladder pain, although direct clinical evidence linking lesion location to specific LUTS remains limited [32]. Transurethral resection of bladder endometriotic lesions is generally inadequate, as lesions typically invade from the outside inward and full excision via this approach is rarely achievable. When opting for surgical excision, the goal should be complete resection of the lesion, which may involve partial or full-thickness resection of the bladder wall depending on the depth of invasion [4 , 12]. Ureteral endometriosis may cause progressive ureteral obstruction, hydronephrosis, and potentially irreversible loss of renal function. Preoperative identification is there- fore important for surgical planning, and management should involve interdisciplinary collaboration between gynecologic and urologic surgeons. Depending on the type, location, and extent of ureteral involvement, surgical options include ureterolysis, segmental ureterectomy with end-to-end ureteroureterostomy, or ureteroneocystostomy. Patients should be counseled regarding the planned pro- cedure, its potential complications and outcomes, and the possible need for ureteral stenting or, in cases of severe obstruction, nephrostomy [30]. Diagnostic evaluation is tailored to the suspected site of disease and may include transvaginal ultrasonography, renal tract ultrasonography, pelvic MRI, and, when ure- teral obstruction requires further characterization, CT urography. While surgery remains the cornerstone of treat- ment in symptomatic cases, hormonal suppression therapy Fig. 2 Hypothesized role of JAK/STAT signaling in DE-associated LUTS. The diagram illustrates proposed links between local inflam- mation, JAK/STAT activation, mast-cell activity, angiogenesis, neu- rogenesis, and altered bladder afferent signaling. These pathways are supported mainly by indirect or experimental evidence; their specific contribution to LUTS in women with DE remains unproven. DE deep endometriosis; LUTS lower urinary tract symptoms; JAK/STAT Janus kinase/signal transducer and activator of transcription; NGF nerve growth factor International Urogynecology Journal with gonadotropin-releasing hormone (GnRH) analogs or progestins may help control symptoms and reduce recur - rence risk following lesion excision [4 , 12]. Recent outcome studies indicate that urinary symptom trajectories after surgery for bladder or ureteral endome- triosis are heterogeneous. Although dysuria and cyclical hematuria often improve after complete lesion excision, OAB-like symptoms or bladder pain may persist in some patients [4]. Persistent symptoms after technically successful surgery may reflect mechanisms beyond residual structural disease, including pelvic-floor dysfunction or altered sen- sory processing; however, the relative contribution of these mechanisms remains uncertain. LUTS Without Direct Involvement of the Urinary Tract In most cases of DE, the urinary tract is not directly affected by endometriotic lesions. Nevertheless, many patients expe- rience LUTS even in the absence of identifiable urinary tract infiltration. These symptoms appear to be independent of disease extent [4, 6]. IC/BPS is defined as chronic pelvic pain with discomfort perceived to originate in the bladder, accompanied by at least one symptom of urinary urgency or frequency in the absence of infection or other identifiable pathology. The co- occurrence of endometriosis and IC/BPS has been described as the “evil twin syndrome,” due to their overlapping clini- cal features and pathophysiological similarities. Studies of selected populations with chronic pelvic pain have reported substantial overlap between endometriosis and IC/BPS [33]. The reported prevalence of their coexistence ranges from 15.5% to 78.3% across chronic pelvic pain cohorts, with sub- stantial variation in patient selection, diagnostic criteria, and assessment instruments [34]. Differences include whether validated symptom questionnaires were used and whether assessment relied on clinical symptoms, cystoscopy with hydrodistension, or combinations of these approaches. These estimates should not be interpreted as the prevalence of IC/ BPS among all women with endometriosis. Although the precise relationship between endometrio- sis and IC/BPS remains unclear, shared inflammatory and sensory mechanisms have been proposed. In IC/BPS, dis - ruption of the urothelial barrier, including alterations of the glycosaminoglycan layer, may increase bladder permeabil- ity and facilitate exposure of underlying tissues to urinary irritants, thereby contributing to pain and urinary symp- toms [35]. Whether endometriosis-associated inflamma- tory mediators directly promote such urothelial dysfunction remains uncertain. Because of the substantial symptomatic overlap between the two conditions, IC/BPS may be under- recognized in women with endometriosis. When IC/BPS is suspected as a coexisting condition, management should follow established IC/BPS principles rather than being inter- preted as treatment of DE itself. Management may include lifestyle and dietary modification, pain-directed therapy, pelvic-floor management, and selected bladder-directed treatments according to applicable IC/BPS guidelines [36]. Persistent or recurrent bladder-related pain or urinary symp- toms after adequate endometriosis treatment should there- fore prompt consideration of coexisting IC/BPS. Pelvic floor dysfunction, including muscle hypertonic- ity and myofascial pain, has been frequently observed in women with endometriosis, potentially exacerbating LUTS through non-neurogenic mechanisms. Assessment of pelvic floor muscle abnormalities may therefore be appropriate in women with endometriosis and LUTS, particularly when pelvic-floor hypertonicity or myofascial pain is present [37]. Recent evidence indicates that oxidative stress plays a role in the pathogenesis of endometriosis, contributing to both the establishment and progression of the disease. Elevated levels of reactive oxygen species (ROS) in the peritoneal fluid of affected women may disrupt cellular homeostasis, promote inflammation and sensitize peripheral nerves. These mechanisms may contribute to peripheral sensitization and pain generation in endometriosis; however, a direct role of oxidative stress in the development of LUTS has not been established [38]. Urodynamic studies suggest that functional bladder abnormalities may occur even in the absence of direct blad- der wall involvement, although the relative contributions of autonomic dysfunction and inflammation remain uncertain [39]. Peripheral innervation of the bladder can be affected directly by endometriotic lesions or indirectly via pro- inflammatory mediators. Lesions involving the posterior pelvic compartment, particularly the uterosacral ligaments, frequently contribute to LUTS. In up to 50% of such cases, these ligaments undergo fibrotic retraction. The cardinal and uterosacral ligaments contain autonomic nerve fibers, including sympathetic fibers in the hypogastric nerve and parasympathetic fibers via the pelvic splanchnic nerves, which converge in the inferior hypogastric plexus [40]. His- tological studies have confirmed the presence of autonomic and sensory (C and Aδ) nerve fibers within resected endo- metriotic lesions from these ligaments [41]. These lesions promote a pro-inflammatory microenvironment rich in cytokines and neurotransmitters, leading to peripheral nerve sensitization, altered synaptic transmission, and potentially central sensitization. Central sensitization refers to the heightened respon- siveness of central neurons to nociceptive stimuli, result- ing in exaggerated and persistent pain responses to ther - mal, mechanical, or chemical stimuli [42]. Chronic nociceptive input from endometriotic lesions can lead to International Urogynecology Journal hyperexcitability of spinal cord neurons, which relay signals to the thalamus and cortex. Over time, stimuli of constant intensity may be perceived as increasingly painful. Build- ing on the concept of central sensitization, recent work has proposed distinct pain phenotypes in endometriosis: (i) a predominantly nociceptive/inflammatory phenotype, (ii) a neuropathic-like phenotype, and (iii) a nociplastic phenotype characterized by widespread pain and sensory amplification [23]. These pain phenotypes may also influence the clinical expression of LUTS. Pelvic-floor hypertonicity may contrib- ute to dysuria and obstructive voiding symptoms, whereas neuropathic-like pain may include burning or electric-shock- like sensations. Nociplastic mechanisms could contribute to persistent or fluctuating urgency and frequency that are disproportionate to identifiable pelvic pathology. However, direct evidence linking specific pain phenotypes to distinct LUTS patterns in endometriosis remains limited. Recogniz- ing these overlapping mechanisms may nevertheless help guide individualized therapeutic priorities [43]. Moreover, cross-sensitization between pelvic organs may occur—a phenomenon known as viscero-visceral hyperal- gesia—where pain originating from one organ (e.g., uterus) sensitizes sensory pathways shared with adjacent organs (e.g., bladder), thereby generating LUTS even in the absence of direct pathology [42]. Management of LUTS without direct urinary tract involvement is individualized based on symptom severity. First-line therapies include lifestyle modification, bladder retraining, pelvic floor relaxation techniques, and dietary adjustments to minimize bladder irritation. Pharmacologic treatments such as antimuscarinics and β3-adrenergic ago- nists are used for overactive bladder symptoms. In refrac - tory cases, intravesical botulinum toxin injections and neuro- modulatory techniques—including sacral nerve stimulation (SNS) and percutaneous tibial nerve stimulation (PTNS)— may be beneficial [44]. A proposed, phenotype-based frame- work could stratify women with DE-related LUTS into: (1) inflammatory/nociceptive-dominant phenotype, in whom treatment may primarily target endometriosis itself when clinically indicated; (2) neuropathic-like phenotype, in whom treatment of coexisting neuropathic pain may be considered accord- ing to established chronic-pain principles; and (3) central sensitization/nociplastic-dominant phenotype, in whom multidisciplinary pain management and pel- vic-floor assessment may be appropriate. These categories are conceptual and hypothesis-generat- ing and have not been prospectively validated as treatment pathways for DE-associated LUTS. Pelvic-floor physiother- apy may be considered in women with documented pelvic- floor dysfunction or hypertonicity. However, evidence for improvement of urinary symptoms specifically in women with DE remains limited; in the randomized trial by Del Forno et al., pelvic-floor physiotherapy did not significantly improve urinary-function outcomes [45]. The principal clini- cal presentations, associated mechanisms, and established versus proposed management considerations are summa- rized in Table  2. De Novo LUTS After Surgery for Deep Endometriosis Surgical treatment of deep endometriosis (DE) is indicated for patients with severe symptoms, visible lesions and failure of conservative management. However, owing to the pres- ence of adhesions and proximity of lesions to critical pel- vic structures, these procedures carry a substantial risk of complications. Among them, LUTS that arise de novo after surgery are frequently overlooked. Although some patients experience symptomatic improvement in LUTS after DE surgery, others experience deterioration of LUTS [ 46–48], particularly those with extensive parametrial and pelvic nerve involvement [47]. Postoperative lower urinary tract dysfunction may therefore represent true de novo dysfunc- tion related to surgical injury, persistence or worsening of pre-existing dysfunction, or unmasking of previously sub- clinical abnormalities. Endometriotic lesions may directly involve autonomic nerves responsible for urinary tract function. In cases where lesions infiltrate the hypogastric nerve, inferior hypogastric plexus, or pelvic splanchnic nerves, their resection may

in neural injury. These autonomic pathways provide sympathetic and parasympathetic innervation to the bladder and contribute to visceral afferent signaling involved in blad- der sensation and voiding. Postoperative lower urinary tract dysfunction has been reported after surgery for DE, particu- larly when extensive dissection involves the parametrium, uterosacral ligaments, or pelvic autonomic nerves. Reported rates vary according to the extent of disease, surgical tech- nique, and definition of postoperative dysfunction [51, 52]. Excision of endometriotic lesions from the rectovaginal septum, uterosacral ligaments, or parametria may damage autonomic innervation of the bladder. The inferior hypogas- tric plexus comprises parasympathetic fibers via pelvic splanchnic nerves and sympathetic fibers via the hypogastric nerve. Surgical disruption of this plexus can have segment- specific consequences. The functional consequences of injury depend on the location and extent of neural damage and may include impaired bladder sensation, reduced detru- sor contractility, and postoperative urinary retention [50]. Parasympathetic fibers are located a few centimeters below the cul-de-sac (Douglas pouch) and are at risk during resection of the rectovaginal septum or rectosigmoid colon. International Urogynecology Journal Table 2 Clinical presentations, relevant mechanisms, and established versus proposed management considerations for lower urinary tract symptoms in deep endometriosis Urinary symptom/clinical phenotype Relevant mechanism Established/standard approach Hypothetical/proposed approach Supporting references Dysuria, hematuria, urgency or fre- quency with bladder endometriosis Direct bladder-wall involvement; local inflammation and fibrosis Imaging according to suspected disease extent; hormonal or surgical treatment according to symptoms and lesion characteristics Persistent LUTS after treatment may also involve pelvic-floor or sensory mechanisms [4, 12, 28, 31, 32] Ureteral obstruction/hydronephrosis Direct ureteral infiltration and/or fibrosis causing obstruction Assessment of the upper urinary tract when ureteral involvement is sus- pected; surgical treatment when clini- cally significant obstruction is present / [28–30] OAB-like symptoms without direct urinary tract involvement Functional bladder abnormalities; possi- ble altered autonomic or inflammatory signaling Management according to established OAB principles An endometriosis-specific neuroinflam- matory contribution remains unproven [11, 39, 44] Bladder pain with coexisting IC/BPS Urothelial and sensory dysfunction related to IC/BPS Management according to established IC/BPS principles A direct contribution of endometriosis- associated inflammation to IC/BPS remains uncertain [19, 33–36] LUTS with pelvic-floor hypertonicity or myofascial pain Pelvic-floor dysfunction and altered pelvic-floor coordination Pelvic-floor assessment when dysfunc- tion is suspected Pelvic-floor physiotherapy may be considered when dysfunction is docu- mented, but improvement of urinary symptoms specifically in DE has not been established [37, 45] LUTS with neuropathic-like or nociplas- tic pain features Possible peripheral and central sensitiza- tion; evidence is largely indirect Treatment of coexisting chronic pain according to established chronic-pain/ endometriosis principles Whether pain phenotyping can guide LUTS-specific therapy remains unvalidated [9, 10, 20–26, 43] Postoperative voiding dysfunction/uri- nary retention Pelvic autonomic nerve injury, impaired bladder sensation and/or reduced detru- sor contractility Postvoid residual assessment, intermit- tent self-catheterization when indi- cated, and nerve-sparing surgery when technically feasible Sacral neuromodulation may be consid- ered in selected persistent cases [13, 18, 46–57] Experimental neuroinflammatory mechanisms JAK/STAT signaling, mast-cell activa- tion and neuroangiogenesis No established LUTS-specific treatment JAK/STAT- or mast-cell-directed thera- pies remain experimental and require clinical validation [14, 27, 31] International Urogynecology Journal International Urogynecology Journal Damage to afferent sensory fibers in the distal hypogastric nerve—typically during uterosacral ligament excision—may initially be asymptomatic but later result in progressive blad- der dysfunction [58]. Prospective and retrospective studies confirm that lower urinary tract dysfunction (LUTD) after DE surgery is not rare, particularly when resection involves the uterosacral ligaments, parametrium or rectovaginal septum. In a cohort of 198 women undergoing surgery for posterior compart- ment DE, 41% initially had postoperative voiding dysfunc- tion, defined as a postvoid residual volume > 100 mL at the second bladder scan. This proportion decreased to 11% at hospital discharge [52]. Seventeen women required self- catheterization after discharge, with a median duration of 41 days before recovery. In the same study, ENZIAN com- partment B involvement, particularly lesions > 3 cm, was associated with postoperative voiding dysfunction. Benoit et al. reported that combined resection of the torus uterinus, uterosacral ligaments, parametrium, and vagina was associ- ated with postoperative voiding dysfunction compared with uterosacral ligament resection alone (adjusted odds ratio 37.3, 95% confidence interval 6.8–203.1) [53]. The wide confidence interval indicates substantial imprecision, and residual confounding by disease severity and surgical com- plexity may partly explain the magnitude of the association. Additionally, colorectal surgery for endometriosis is asso- ciated with postoperative voiding dysfunction despite the use of nerve-sparing techniques. The incidence is highest in segmental colorectal resection and lower in discoid excision and rectal shaving [54, 55]. According to the meta-analysis by Vesale et al., self-catheterization was mainly required after segmental colorectal resection [54]. Bladder afferent signaling is mediated principally by myelinated Aδ fibers and unmyelinated C fibers traveling through pelvic and hypogastric pathways. Aδ fibers are pri- marily involved in physiological bladder-filling sensation, whereas C fibers are relatively quiescent under normal con- ditions and become increasingly active during inflammation, chemical irritation, or other noxious stimuli [59]. Surgical injury to pelvic autonomic pathways may impair bladder sensation and detrusor function, leading to prolonged void- ing intervals, increased bladder capacity, incomplete empty- ing, and, in severe cases, urinary retention [50]. More recent prospective work using pre- and post- operative multichannel urodynamics in women treated for DE reported both pre-existing and de novo detrusor underactivity or acontractile bladder in a substantial minority, highlighting that lower urinary tract dysfunction may already be present before surgery and that surgery may unmask or exacerbate pre-existing abnormalities [18]. These observations reinforce the importance of system- atic preoperative counseling regarding the risk of LUTD, especially in women requiring extensive dissection near the inferior hypogastric plexus, ureteric tunnels or bladder base. They also support the use of selective nerve-sparing techniques and careful intraoperative identification of neural structures wherever feasible. Early postoperative screening with bladder scanning and, in selected cases, formal urodynamics allows prompt initiation of appropri- ate management, including intermittent catheterization when clinically indicated. Where technically feasible, nerve-sparing approaches are associated with a lower risk of postoperative urinary retention compared with non- nerve-sparing techniques [18, 58]. Delayed bladder dysfunction has been described after extensive pelvic nerve injury, and patients with persistent voiding symptoms may require longitudinal assessment of postvoid residual volume. When clinically significant incomplete bladder emptying is present, clean intermit- tent self-catheterization may be required to prevent chronic bladder overdistension and secondary detrusor deterioration. Increased urethral outlet resistance following autonomic denervation has also been proposed as an additional con- tributor to postoperative urinary retention [50]. Postopera- tive voiding dysfunction may result from injury to pelvic autonomic pathways, leading to impaired bladder sensa- tion, reduced detrusor contractility, and incomplete bladder emptying. Functional outlet obstruction due to inadequate relaxation of the pelvic floor or urethral sphincter may also contribute in some patients. Management should be indi- vidualized according to the underlying dysfunction. Early postoperative assessment of spontaneous voiding and post- void residual volume is important, with clean intermittent self-catheterization when clinically indicated. Subsequent management may include bladder rehabilitation, pelvic-floor physiotherapy and, in selected persistent cases, sacral neu- romodulation [56]. In a retrospective cohort of 61 women discharged with intermittent self-catheterization after DE surgery, Boulus et al. reported that 43 (70.5%) discontin- ued catheterization during a median follow-up of 25 weeks (range 7–223 weeks). The estimated probability of recovery sufficient to discontinue self-catheterization reached 77% at 78 weeks [57]. Preoperative bladder dysfunction was the only statistically significant independent predictor of cath- eterization cessation in the multivariable model and was associated with a lower recovery hazard (hazard ratio 0.36, 95% confidence interval 0.15–0.83). These findings support assessment of baseline voiding function and counseling about the possibility of prolonged postoperative dysfunction. Fig. 3 Proposed pathophysiological mechanisms of lower urinary tract symptoms in deep endometriosis. Neuroinflammatory and noci- plastic pathways represent proposed mechanisms whose specific con- tribution to DE-associated LUTS remains incompletely established. DE deep endometriosis; LUTS lower urinary tract symptoms; IL interleukin; NGF nerve growth factor; JAK/STAT Janus kinase/signal transducer and activator of transcription ◂ International Urogynecology Journal

Endometriosis, particularly DE, may be associated with LUTS through both direct urinary tract involvement and extra-urinary mechanisms. Multiple pathophysiological mechanisms may contribute to LUTS in these patients, including direct infiltration of urinary organs, neuroin- flammatory processes, autonomic nerve involvement, and postoperative complications (Fig.  3). Symptoms may range from urinary urgency and frequency to pain, voiding dys- function, and retention. Effective management of LUTS in endometriosis requires a multidisciplinary approach, involving gynecolo- gists, urologists, physiotherapists, and clinical psycholo- gists. Treatment strategies must be individualized and may include conservative measures, pelvic floor rehabili- tation, pharmacotherapy, pain management, and surgical intervention when indicated. Where surgery is indicated, nerve-sparing techniques should be considered when tech- nically feasible to reduce the risk of postoperative urinary dysfunction. Reconstructive procedures, such as uretero - neocystostomy or bladder reconstruction, may be required in selected cases of extensive urinary tract involvement. Importantly, delayed urinary dysfunction may occur after extensive pelvic nerve injury, initially presenting with prolonged voiding intervals and later increased postvoid residual volumes. Early recognition and timely interven- tion are critical to preventing irreversible detrusor damage. Ultimately, the goal of treating deep pelvic endometriosis is to improve patients’ quality of life—an objective that includes the proactive identification and management of LUTS both before and after treatment. Future Directions Looking ahead, three areas appear particularly promising for improving outcomes in women with deep pelvic endo- metriosis and LUTS. First, pain phenotyping—distinguish- ing nociceptive, neuropathic-like, and nociplastic profiles using validated questionnaires and clinical assessment— may warrant further evaluation in prospective studies [9 ]. If validated, this approach could support personalized treatment plans combining lesion-directed surgery or hor - monal therapy with neuromodulators and multidisciplinary rehabilitation for patients with prominent neuropathic or centrally mediated features. Second, advanced imaging biomarkers may help clar - ify relationships between lesion characteristics and LUTS phenotypes. Prospective studies correlating standardized ultrasound and MRI findings with urinary symptom pro- files could improve understanding of clinically relevant disease patterns. Third, molecular biomarkers and neu- roinflammatory pathways, including JAK/STAT signal - ing and mast-cell activation, warrant further investigation [14]. These approaches remain experimental and require mechanistic and clinical validation before their relevance to DE-associated LUTS management can be established. Author Contributions RS conceived the review, performed the litera- ture search, synthesized the evidence, prepared the figures, and drafted the manuscript. TS contributed to the conceptualization of the review, critically revised the manuscript for important intellectual content, and approved the final version. Both authors read and approved the final manuscript. Funding This work was supported by the Slovenian Research and Inno- vation Agency (ARIS), with project number P3-0327. Data Availability No datasets were generated or analyzed during the current study. All information discussed in this narrative review is derived from previously published literature cited in the reference list. Declarations Ethical Approval Ethical approval was not required because this study is a narrative review based exclusively on previously published litera- ture and did not involve human participants, animals, or identifiable patient data. Conflicts of Interest None. Open Access This article is licensed under a Creative Commons Attri- bution 4.0 International License, which permits use, sharing, adapta- tion, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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