Biomechanical Formation Mechanism of the “Avascular Plane” in the Pelvis and Retroperitoneum: Redefining Surgical Cleavage Planes Created by Fetal Poisson Compression and Shear Stress

1. Introduction

In total mesorectal excision (TME) for rectal cancer and robot-assisted radical prostatectomy (RARP), surgeons proceed with dissection using the "avascular plane" as a guide. Conventionally, this cleavage plane has been explained broadly by two embryological concepts. One is the "embryological plane," a boundary formed where different embryological compartments (e.g., hindgut and urogenital) adjoin. The other is the "fusion fascia," represented by the adhesion of the mesocolon to the retroperitoneum. Among surgeons, the former compartment model—asserting that "a natural plane where vascular networks do not cross is maintained between organs of different embryological origins"—is frequently cited in clinical settings.

However, these classical models harbor significant logical contradictions that are inconsistent with modern anatomical knowledge and intraoperative observations. Even if the parenchyma of organs (such as epithelium) originates from different primordia, the mesenchymal tissues surrounding them and forming the boundaries are both derived from the same mesoderm. In vivo, there is no intrinsic mechanism that completely rejects capillary network formation (angiogenesis) between tissues of the same mesodermal origin simply because "they are in different compartments" or "they are in static contact." Furthermore, these models cannot explain clinical facts such as why blood vessels cannot invade yet nerves exclusively remain in that boundary space, the bilateral asymmetry of cleavage planes, and the lateral condensation of the NVB.

To organize these contradictions, the conventional models can be systematized as follows:

Table 1. Conventional Models Explaining the Cleavage Planes of the Retroperitoneum and Pelvis and Their Limitations.

Conventional Model	Central Concept	What It Can Explain	What It Cannot Explain (Resolved by This Study)
Embryological plane (Compartment) model	Boundary formed by adjoining different embryological compartments (primordia)	Location of the boundary for each organ compartment	Physical reason why vessels do not cross/invade despite identical mesodermal origin of mesenchyme / Selectivity of why only nerves exist
Fusion fascia model	Membrane formed by contact and fusion of tissues such as different peritonea	Existence of Denonvilliers' fascia (DF) and other fasciae	Reason why simple contact inhibits angiogenesis / Fiber alignment of DF (tension direction) / Bilateral asymmetry
Rectal support ligament model	Lateral ligament is a ligament supporting the rectum	Existence of lateral ligament and rectal fixation function	Histological true nature of the lateral ligament being the proximal root of the NVB / Formation mechanism as a shear refuge
DF = Fusion fascia model	DF is a product of fetal fusion	Location of DF	DF being a tension-induced lamina (Kim 2015) / Central high-density and lateral exclusion due to AP compression
Nerve "coincidental remnant" model	Nerves just happen to be on the outside of the membrane	Course of the nerves	Pre-wiring of nerves / Shear stress resistance conferred by the perineurium

Table 1. Conventional Models Explaining the Cleavage Planes of the Retroperitoneum and Pelvis and Their Limitations.

Conventional Model	Central Concept	What It Can Explain	What It Cannot Explain (Resolved by This Study)
Embryological plane (Compartment) model	Boundary formed by adjoining different embryological compartments (primordia)	Location of the boundary for each organ compartment	Physical reason why vessels do not cross/invade despite identical mesodermal origin of mesenchyme / Selectivity of why only nerves exist
Fusion fascia model	Membrane formed by contact and fusion of tissues such as different peritonea	Existence of Denonvilliers' fascia (DF) and other fasciae	Reason why simple contact inhibits angiogenesis / Fiber alignment of DF (tension direction) / Bilateral asymmetry
Rectal support ligament model	Lateral ligament is a ligament supporting the rectum	Existence of lateral ligament and rectal fixation function	Histological true nature of the lateral ligament being the proximal root of the NVB / Formation mechanism as a shear refuge
DF = Fusion fascia model	DF is a product of fetal fusion	Location of DF	DF being a tension-induced lamina (Kim 2015) / Central high-density and lateral exclusion due to AP compression
Nerve "coincidental remnant" model	Nerves just happen to be on the outside of the membrane	Course of the nerves	Pre-wiring of nerves / Shear stress resistance conferred by the perineurium

All of these conventional models are limited to explaining the "morphological results" and fail to provide a causal mechanism for why such cleavage planes are formed.

Historically, Tandler (1923) described the massive connective tissue stock penetrating the entire urogenital system as the "Tela urogenitalis," and Tobin (1944) and Sato (1988) demonstrated the "caudal extension" of the renal fascia continuing down to the pelvic floor. According to D’Arcy Thompson’s (1917) principle that "form is a diagram of forces," these vast fascial continuities serve as historical evidence that a systemic tension field existed during the mid-trimester of fetal development. Furthermore, through detailed histological analysis, Kim et al. (2015) demonstrated that DF is not merely a fusion fascia but a "tension-induced lamina" with fibers aligned along the direction of tension, aligning consistently with the mechanical model of this study.

This study redefines the avascular plane not as a static embryological boundary, but as a "biomechanical fault line" carved by the mechanical field (tension × Poisson compression × shear stress) generated during fetal life. Due to the phase transition of the ECM and the stiffening of the truncal skeleton during the mid-trimester, the fasciae of the retroperitoneum to the pelvis undergo simultaneous lamination, and shear stress associated with organ movement is hypothesized to continuously disrupt the anchoring of capillaries, contributing to an avascular state. Conversely, autonomic nerves establish their wiring prior to fascial lamination, and because they withstand shear stress due to the robust perineurium, they remain safely in the gliding plane.

To clarify the structural advantages of this new paradigm, this study introduces the following novel perspectives:

• Mechanical Vascular Exclusion: Proposing that capillary anchoring is physically disrupted by fetal shear stress rather than being inhibited by simple tissue compartmentalization.
• Temporal Offset of Nerve Wiring: Explaining nerve preservation in avascular planes through the temporal gap between early neurogenesis and subsequent tension-induced fascial lamination.
• NVB Condensation and Shear Refuge: Reinterpreting the lateral ligament and NVB as dynamic products of lateral mechanical exclusion and shear refuges.
• Asymmetric Mechanical Boundary Conditions: Introducing the concept that differential retroperitoneal fixation of the ascending and descending colonic mesenteries establishes asymmetric mechanical boundary conditions, thereby contributing to the bilateral asymmetry of pelvic fascial development.

The purpose of this study is to reconstruct the cleavage planes of the retroperitoneum and pelvis as "products of the fetal mechanical field" and to present a novel anatomical paradigm that integratively explains the inevitability of the three-layered structure of the Holy Plane, the mechanical origin of the lateral ligament, the lateral condensation and caudal extension of the NVB, and the bilateral asymmetry of the prehypogastric nerve fascia.

2. Materials and Methods

To verify the "biomechanical fault line formation model" presented in the previous chapter, this study was structured as a theoretical-clinical hybrid investigation integrating anatomy, embryology, materials science, mechanical modeling, and clinical insights. To reconstruct the phenomena that conventional models could not explain (vascular exclusion, nerve preservation, lamination, bilateral asymmetry, NVB condensation) as mechanical causal mechanisms, we established the following four methodological pillars.

2.1. Systematic Literature Review (Historical–Mechanical Synthesis)

Using PubMed, Scopus, and Web of Science, we searched the keywords: “pelvic fascia”, “avascular plane”, “retroperitoneum”, “shear stress”, “Poisson effect”, “fetal ECM”, “hypogastric nerve”, “Denonvilliers’ fascia”, and “NVB development”. Including historical anatomical literature since 1900 (Tandler, Tobin, Sato), a total of 126 articles were screened, and 53 were ultimately selected. In particular, the following literature groups were intensively evaluated:

• Lamination and the fibrous period of fetal fascia (Fritsch 1994, Kim 2015, Kinugasa 2008, Cho 2009, Matsubara 2009)
• Poroelastic transition of the ECM (Chaudhuri 2020, Mow 1980)
• Anomalous Poisson effect in collagen networks (Ban 2019, Storm 2005)
• Shear stress sensitivity of angiogenesis (Chien 2007)
• Gliding layer formation by fasciacytes (Stecco 2018)

By integrating these, we clarified the limitations of conventional models and constructed the theoretical foundation for the fetal mechanical field model.

2.2. Integration of Embryological Data (Developmental Timing Analysis)

By comparing key histological studies analyzing human fetal specimens from 8 to 30 weeks of gestation (Fritsch 1994, Kinugasa 2008, Cho 2009, Matsubara 2009), we extracted a "temporal offset" between:

• Lamination of pelvic connective tissue (fibrous period: 13–20 weeks of gestation, when connective tissue becomes fibrous)
• Establishment of autonomic nerve wiring: prior to the completion of the aforementioned lamination. This temporal offset constitutes the core of the mechanical model in this study, wherein nerves pre-establish wiring and withstand shear stress to remain intact even after fascial lamination.

2.3. Construction of the Biomechanical Field Model (Biomechanical Field Modeling)

The materials science properties of the ECM (poroelasticity, viscoelasticity) were reconstructed based on Chaudhuri (2020) and Mow (1980), and the "tension → Poisson compression → lamination" models of Ban (2019), Vader (2009), and Storm (2005) were applied to the anatomical structures of the retroperitoneum and pelvis. Furthermore, the sources of shear stress caused by organ movement were defined as "respiratory excursions," "bladder filling/voiding," and "cyclic volumetric changes of the rectum." These cyclic loads were modeled as a mechanical exclusion mechanism that continuously and physically disrupts the anchoring of capillaries.

2.4. Integration with Clinical Perspectives

We theoretically verified the consistency between the predictive structures derived from this mechanical model and numerous intraoperative observations (the density of cleavage planes, the degree of lamination, bilateral asymmetry, the location of preserved nerves, lateral condensation of the NVB, and central high-density of Denonvilliers' fascia) experienced by the author during robot-assisted radical prostatectomy (RARP) and total mesorectal excision (TME). This allowed us to evaluate how the footprints of the fetal mechanical field remain in the adult cleavage planes.

3. Results

3.1. Integration of the Fetal Mechanical Model: Phase Transition, Poisson Compression, and Shear Stress

During the fibrous period (13–20 gestational weeks), the pelvic connective tissue undergoes a phase transition from a hyaluronic acid-dominated undifferentiated mesenchyme to a poroelastic solid composed primarily of loosely cross-linked collagen networks, acquiring a fibrous laminated arrangement (Fritsch, 1994; Chaudhuri et al., 2020). Concurrently, the truncal skeleton rapidly stiffens, causing the energy of volumetric expansion to lose its escape routes and accumulate as multiaxial tension throughout the ECM.

According to previous reports, this tension field induces an anomalous Poisson effect (orthogonal compression) in the collagen networks, likely causing simultaneous lamination of the fasciae from the retroperitoneum to the pelvis (Ban et al., 2019; Storm et al., 2005). Furthermore, shear stress from the cyclic volumetric changes of the rectum, bladder, and intestines continues to concentrate at the boundary surfaces. As demonstrated by the mechanotransduction model of Chien (2007), shear stress destabilizes the anchoring of endothelial cells; therefore, it is mechanically consistent to explain that angiogenesis is permanently excluded by this mechanism. Added to this is the hyaluronic acid secretion by Fasciacytes, completing the "avascular gliding plane" (Stecco et al., 2018). Conversely, pelvic autonomic nerves establish their wiring earlier than the completion of fascial lamination (Kinugasa et al., 2008), and because they withstand shear stress due to the robust perineurium, the clinical fact that only nerves remain in the gliding plane is explained.

3.2. Cleavage Plane Spectrum: The Balance of Tension and Shear Stress

The structure of each cleavage plane is determined by the balance of tension and shear stress engraved during fetal life.

Table 2. Mechanical spectrum of tension, shear stress, and histological characteristics in each cleavage plane.

Cleavage Plane	Tension	Shear	Lamina	Foamy layer	Areolar tissue
Gerota's fascia	Strong	Moderate	Thick	Distinct	Sparse
Space of Retzius	Weak (Shielded)	Strong	Thin	Sparse	Abundant
Holy plane	Weak (Shielded)	Strong	Extremely thin	Sparse	Extremely abundant

Table 2. Mechanical spectrum of tension, shear stress, and histological characteristics in each cleavage plane.

Cleavage Plane	Tension	Shear	Lamina	Foamy layer	Areolar tissue
Gerota's fascia	Strong	Moderate	Thick	Distinct	Sparse
Space of Retzius	Weak (Shielded)	Strong	Thin	Sparse	Abundant
Holy plane	Weak (Shielded)	Strong	Extremely thin	Sparse	Extremely abundant

This spectrum represents the first model to mechanically explain the density, lamination, and gliding properties of the cleavage planes observed intraoperatively.

3.3. Mechanical Formation of the Three-Layered Structure of the Holy Plane

In the presacral space during TME, the following three-layered structure inevitably forms:

• Rectal proper fascia (Primary Lamina): The longitudinal tension of the rectum (σy) induces primary Poisson compression, casting an organ-dependent lamina closely attached to the rectal wall.
• Prehypogastric nerve fascia (Partial densification sheet): The anterior surface of the sacrum resides in a tension shadow where biaxial tension cannot be established, preventing it from becoming a complete lamina, and safely leaving the hypogastric nerves on its lateral aspect.
• Parietal pelvic fascia (Passive Lamina): Due to tension shielding from the early stiffening of the sacrum, this layer undergoes compaction as a passive lamina.

3.4. The Mechanical Origin of the Lateral Ligament: A Shear Refuge

While the lateral ligament holds a clinical function as a ligament fixing the rectum, it is reasonable to understand that it is essentially a shear refuge formed between the rectal proper fascia and the prehypogastric nerve fascia, functioning as the region where the pelvic plexus (the cranial component of the NVB) condenses (i.e., the proximal root of the NVB).

3.5. Mechanism of NVB Formation: Caudal Extension and Condensation from the Lateral Ligament

Due to the localized expansion of the prostate and rectum, strong anterior-posterior (AP) compression is applied to the central portion of DF. This mechanical pattern of "central compression and lateral exclusion" perfectly matches the fiber alignment (central high-density and lateral tension escape) observed by Kim et al. (2015) in fetal DF. Consequently, the neurovascular network is physically displaced and condensed laterally into the lateral pillars, where tension is relatively low. As a result, it is appropriate to understand the NVB as a continuous structure extending caudally from the neurovascular root of the lateral ligament.

3.6. Mechanical Boundary Conditions Underlying Bilateral Asymmetry of the Prehypogastric Nerve Fascia

A pronounced bilateral asymmetry is frequently observed in the fascial structures surrounding the hypogastric nerves and ureters during pelvic dissection. Embryologically, Kinugasa et al. (2008) demonstrated that the developmental pattern of the human hypogastric nerve sheath differs substantially between sides: on the left side, the prehypogastric nerve fascia extends laterally and envelops the ureter, whereas on the right side such fascial extension is much less distinct, and the ureter is often located ventral to the fascia.

The present model suggests that this asymmetry may reflect differences in the mechanical boundary conditions established by retroperitonealization of the ascending and descending colonic mesenteries during fetal development. In the Poisson Compression Theory (PCT), fascial lamination requires not only the generation of developmental tension but also the presence of sufficiently rigid fixation interfaces capable of accumulating and concentrating that tension. Without effective mechanical constraints, tensile forces are dissipated rather than stored within the extracellular matrix, reducing the likelihood of tissue condensation and lamina formation.

On the left side, the extensive retroperitoneal fixation associated with the descending colonic mesentery provides a broad mechanical boundary that is continuous with the posterior abdominal wall and pelvic connective tissue. This extensive attachment likely functions as a mechanical anchor, facilitating the accumulation and concentration of developmental tension throughout the connective tissue continuum extending into the pelvis. Under these conditions, enhanced Poisson compression may promote fascial condensation and formation of a distinct prehypogastric nerve fascia.

In contrast, the right-sided retroperitoneal fixation associated with the ascending colonic mesentery may provide a less extensive boundary condition for concentrating developmental tension within the pelvic connective tissue. Consequently, mechanical energy is more readily dissipated, resulting in reduced Poisson compression, incomplete fascial condensation, and persistence of areolar connective tissue rather than formation of a sharply defined lamina.

This interpretation provides a biomechanically plausible explanation for the asymmetrical fascial development reported by Kinugasa et al. (2008). More broadly, it suggests that the establishment of fetal fascial planes depends not only on the magnitude of developmental forces but also on the anatomical distribution and extent of retroperitoneal fixation boundaries that govern how those forces are accumulated and transformed into tissue architecture.

4. Discussion

This study redefined the "avascular plane" in the retroperitoneum and pelvis not as a conventional static fusion fascia or compartment model, but as a biomechanical fault line carved by the tension field, Poisson compression, and shear stress generated during fetal life. This mechanical model systematically resolves fundamental contradictions that could not previously be explained, such as "why blood vessels cannot invade boundaries derived from the same mesoderm," "why only nerves remain in the gliding plane," "the continuity between the lateral ligament and the neurovascular bundle (NVB)," "the bilateral asymmetry of the prehypogastric nerve fascia," and "the inevitability of the three-layered structure of the Holy Plane." As the scientific foundation supporting this, we integrated major publications spanning materials science, mechanobiology, and embryology, verifying the validity of our mechanical model from multiple angles.

4.1. Resolving the Logical Contradictions of Conventional Models

This study mechanically resolved three fundamental contradictions harbored by conventional static embryological models.

• Reason why blood vessels cannot invade: Anchoring failure (mechanical exclusion) due to Poisson compression and shear stress.
• Reason why only nerves remain: Nerves establish wiring before fascial lamination and withstand shear stress due to the perineurium.
• Continuity between the lateral ligament and NVB: Lateral ligament = proximal root of NVB; NVB = caudal extension of lateral ligament.

4.2. Scientific Foundation of the Mechanical Model Based on Materials Science, Mechanics, and Embryology

4.2.1. Chaudhuri et al. 2020: The Poroelastic Transition of Fetal ECM

The change in the material state of the ECM during fetal life is the starting point of the mechanical model in this study. Chaudhuri et al. (2020) demonstrated that the ECM undergoes a phase transition from a hyaluronic acid-dominated gel to a poroelastic solid primarily composed of loosely cross-linked collagen networks. Through this phase transition, the ECM shifts to a material state capable of "accumulating tension," "irreversibly memorizing deformation," and "permitting Poisson compression." The process of "tension → Poisson compression → lamination" presented in this study is established only upon the premise of this materials science phase transition. That is, the phase transition of the fetal ECM is the materials science prerequisite enabling widespread lamination of the retroperitoneum and pelvis.

4.2.2. Storm et al. 2005: Nonlinear Stress Response and Fiber Alignment of Collagen Networks

Storm et al. (2005) showed that collagen networks exhibit nonlinear stiffening and that fibers align in the direction of stress upon tension loading (tension-induced alignment). This finding proves that the fiber arrangement of DF and the rectal proper fascia is not "fusion" but a phenomenon of alignment toward the tension direction, perfectly consistent with the central high-density and lateral tension escape of DF demonstrated by Kim et al. (2015). Furthermore, it shares continuity with the Poisson compression models of Ban (2019) and Vader (2009). The assertion of this study that the fetal tension field determines the ultimate fiber architecture of the fascia is corroborated in terms of materials science by Storm's model. In a previous study (Tokuchi, 2026), it was also pointed out that widespread lamination of the retroperitoneal fascia might be driven by the anomalous Poisson effect, which aligns with this discussion.

4.2.3. Chien 2007: Anchoring Failure of Angiogenesis due to Shear Stress

The mechanotransduction model of Chien (2007) demonstrated that endothelial cells are extremely sensitive to shear stress, and that shear stress destabilizes integrin-mediated anchoring; this is consistent with the vascular exclusion model of this study. It can be interpreted that angiogenesis is not "materially inhibited" but "likely mechanically excluded." The inability of blood vessels to invade the cleavage plane can be explained by fetal shear stress loading, where the cyclic volumetric changes of organs (rectum, bladder, intestines) concentrate shear stress at the boundary interfaces. The causal mechanism of vascular exclusion, which could not be explained by the conventional fusion fascia model, is hereby clearly elucidated.

4.2.4. Ingber 1993–2014: The Tensegrity Model and Structural Determination by the Fetal Mechanical Field

Ingber's tensegrity theory proposed the concept that cells and the ECM maintain structure through a balance of tension and compression. The fetal mechanical field model of "tension × Poisson compression × shear stress" in this study directly connects to this theory. The fetal ECM exists in a material state capable of forming tensegrity structures through the accumulation of a tension field (Chaudhuri 2020) and collagen alignment (Storm 2005). This structure creates a structural selectivity where blood vessels are vulnerable to shear stress, while nerves possess resistance due to the perineurium. Ingber's theory provides the theoretical foundation for the mechanical selectivity of "nerve preservation and vascular exclusion" in this study.

4.2.5. Temporal Consistency Between Fetal Fascial Lamination (Fritsch 1994) and Nerve Pre-Wiring (Kinugasa 2008)

Fritsch (1994) showed that pelvic connective tissue in the fetus becomes denser and is organized into layered systems during the "fibrous period" between 13 and 20 gestational weeks (note that while the gestational week definition of the fibrous period varies slightly among studies, this study followed Fritsch 1994). This guarantees the temporal consistency of the "ECM phase transition → tension field → lamination" model in this study. Furthermore, in a study on the development of the hypogastric nerve sheath, Kinugasa et al. (2008) demonstrated that the basic wiring of the autonomic nervous system is established earlier than the completion of full fascial lamination. This knowledge of the temporal offset embryologically resolves the problem of "why only nerves remain in the avascular plane," which conventional models could not explain. In our model, a mechanical selectivity is established wherein nerves determine their position before lamination and withstand shear stress via the perineurium, while blood vessels that subsequently attempt to bridge the gap undergo anchoring failure due to shear stress. The conventional static explanation that "nerves just happen to be on the outside" is completely replaced by this model.

4.3. The Integrative Significance of the Fetal Mechanical Field

By integrating the above scientific pillars, the central thesis of this study is clarified as follows: "The avascular plane is a 'biomechanical fault line' carved continuously by the tension field, Poisson compression, and shear stress generated during fetal life, which likely disrupt the anchoring of angiogenesis." This mechanical field provides the first theoretical framework to causally explain the characteristics of the cleavage planes routinely observed by surgeons: it "laminates" the fascia, "excludes" angiogenesis, and "preserves" nerves.

4.4. The Inevitability of the Holy Plane and Mesorectal Fascia: Integration of Findings by Kim et al. (2015) and Dogaru et al. (2026)

The fact that the fascial structures surrounding the rectum and pelvis are not the result of "simple fusion or coalescence" is strongly supported by recent embryological findings. The lamination of the fetal Denonvilliers’ fascia (DF) demonstrated by Kim et al. (2015)—characterized by central densification and lateral tension evasion—is perfectly consistent with the "tension-induced lamina" model proposed in this study. Furthermore, recent findings by Dogaru et al. (2026) suggest that the mesorectal fascia development involves a distinct process of lateral divergence and "condensation" rather than simple peritoneal coalescence. Their observations are consistent with the mechanical interpretation proposed here, suggesting that the 'Holy plane' between the mesorectal fascia and the presacral fascia, navigated by surgeons during TME, is an anatomically pre-existing developmental entity rather than a surgically created artifact. Viewed through the lens of the Poisson Compression Theory (PCT), this anatomical "condensation" observed by Dogaru et al. may be interpreted as the direct macroscopic manifestation of tension-induced Poisson compression and poroelastic syneresis. In other words, the integration of these findings supports that the triple-layered fascial structure of the pelvis, including the Holy plane, is the logical product dynamically carved out as a "biomechanical fault line" by the fetal mechanical field (tension and orthogonal compression).

4.5. Biological Consequences of Vascular Exclusion: Angiogenesis-Adipogenesis Coupling and Fibrosis

While the current mechanical model successfully elucidates the physical exclusion of capillaries via shear stress and Poisson compression, it concomitantly explains another critical histological hallmark of the avascular plane: the profound absence of adipose tissue. In developmental and metabolic biology, the differentiation and expansion of adipose tissue are strictly dependent on the prior establishment of a local capillary network, a principle established as “angiogenesis-adipogenesis coupling” (Cao, 2007). Because mesenchymal progenitors and preadipocytes predominantly reside within the perivascular niche, the mechanical exclusion of blood vessels fundamentally deprives these cells of their developmental habitat. Furthermore, the resultant avascular microenvironment inevitably induces local hypoxia. Hypoxic signaling, primarily mediated by hypoxia-inducible factor 1-alpha (HIF-1α), strongly suppresses adipogenic differentiation while upregulating the expression of extracellular matrix proteins such as collagens (Sun et al., 2013). Therefore, in the mechanically excluded avascular planes, adipogenesis is inherently aborted, and compensatory fibrogenesis is promoted. This biological cascade—triggered by fetal mechanical forces—mechanistically elucidates why surgical cleavage planes, such as Denonvilliers’ fascia, are uniquely characterized as dense, fat-poor, fibrous laminas. Although the avascular plane is typically characterized as a dense, fat-poor lamina, a subset of individuals exhibits a noticeable amount of adipose tissue within the Holy plane. This variation is biologically and mechanically consistent with the proposed model. Because adipogenesis strictly depends on the presence of pre-existing microvasculature (angiogenesis–adipogenesis coupling), adipose tissue can only develop in regions where fetal shear stress loading was insufficient to completely eliminate capillary anchoring. In such cases, residual microvessels remain in the surrounding areolar tissue, allowing adipose tissue to secondarily infiltrate thin lamina margins during adulthood, particularly in individuals with higher adiposity. Importantly, the central lamina of the avascular plane remains devoid of vasculature, and fat infiltration is limited to peripheral zones where microvascular preservation occurred. Thus, the presence of adipose tissue in the Holy plane represents a natural expression of inter-individual mechanical variation rather than a contradiction to the avascular plane concept.

4.6. Anatomical Interpretation of the Continuity Between the Lateral Ligament and the NVB

It is reasonable to interpret that the lateral ligament should not be viewed merely as a "static fixation ligament of the rectum," but essentially as a shear refuge formed between the rectal proper fascia and the prehypogastric nerve fascia, serving as the region where the pelvic plexus (cranial component of the NVB) condenses (proximal Root). It is reasonable to understand the NVB as a continuous structure extending caudally from the neurovascular base of the lateral ligament, formed retrospectively as it is laterally excluded by the AP compression of the prostate and rectum.

4.7. Clinical Implications: Safety Strategies in Dissection

These findings mechanically redefine the safety strategies for dissection in TME and RARP, providing a clear checklist for surgical navigation:

• [ ] Identify the Proper Fascia: Do not breach the rectal proper fascia; maintaining this boundary prevents wandering into the mechanically excluded vascular network.
• [ ] Navigate Lateral to the Prehypogastric Nerve Fascia: Dissecting along this specific shear-resistant plane ensures optimal nerve preservation.
• [ ] Reassess the Lateral Ligament: Treat the lateral ligament not merely as a supportive structure to be transected, but as the proximal root and base of the NVB; careless transection is contraindicated.
• [ ] Utilize the Parietal Pelvic Fascia: Recognize this passive lamina as a safe, avascular gliding zone.
• [ ] Anticipate Bilateral Asymmetry: Exercise caution on the left side, where high tension creates a sharp but misleadingly thin membrane, and on the right side, where weak tension results in indistinct areolar tissue requiring careful layer identification.

4.8. Limitations and Future Prospects

Limitations of this study include the lack of direct measurement of the tension field using fetal MRI elastography, the need for intraoperative sensors to verify shear stress quantification, and the future necessity of mechanically verifying the three-layered fascia through cadaveric dissection. Future endeavors will focus on proving the phase transition through materials science measurements of fetal ECM, constructing shear stress mapping of cleavage planes, developing 3D mechanical reconstruction models of the NVB, and creating "mechanical navigation" systems for pelvic surgery.

5. Conclusions

The "avascular plane" in the pelvis and retroperitoneum is not a static concept representing embryological tissue boundaries. It may be better understood as a "biomechanical fault line" continuously carved by the systemic tension field, Poisson compression, and shear stress from organ movement generated during fetal life, which likely destabilize the anchoring of blood vessels. When surgeons select optimal cleavage planes and preserve nerves, they are doing nothing less than intraoperatively tracing the mechanical structures formed during fetal life in today's operating rooms. This study provides a novel anatomical paradigm that dramatically enhances the safety of pelvic surgery.