The connective tissue supports of the pelvic organs are collectively referred to as the “endopelvic fascia.” This fascia is a continuous, complex web of connective tissue that envelops and supports the bladder, vagina, and rectum (1). Pelvic fascia can be divided into two types. The parietal fascia, which covers the levator ani and other skeletal muscles, is composed of a dense layer of organized collagen. In contrast, the visceral fascia, which envelops the pelvic organs, is a loose, poorly organized connective tissue layer (2). On a histologic basis, this is a loose, areolar connective tissue layer composed of smooth muscle, collagen, and elastin fibers (2). Much of the collagen and smooth muscle in the visceral fascia is perivascular (3). The contrast between parietal and visceral fascia parallels the functions of these two layers: the parietal fascia provides support for the muscles of the pelvic floor and abdominal cavity, while the visceral fascia envelops the organs, providing autonomic innervation to these organs and allowing for dramatic changes in their volumes (e.g., bladder filling).

Within the endopelvic fascia, there are several surgically identifiable structures, such as the arcus tendineus fascia pelvis (ATFP) and the uterosacral and cardinal ligaments. However, these “ligaments” are not discrete structures but rather condensations of connective tissue (4). Anatomic landmarks are vague, variable, or disputed (4,5). Nevertheless, the uterosacral and cardinal ligaments are thought to provide important support to the uterus and upper vagina (6). They originate along the greater sciatic foramen and lateral sacrum and insert into the lateral aspect of the vaginal apex. In the standing position, these bands of connective tissue provide vertical support for the uterus and vaginal apex (6). In addition, the uterosacral and cardinal ligaments keep the vaginal apex over the levator plate (7). If these ligaments are deficient or lax, the vaginal apex might be positioned above the levator hiatus, thereby increasing the risk of prolapse.

Laterally, the anterior vagina is attached to the pelvic sidewall at the ATFP or “white line” (3,6,8). This line is a condensation of the fascia of the obturator internus muscle. Separations in the lateral attachment have been observed in women with vaginal wall prolapse (6,9). Posteriorly, there is a similar attachment of the vaginal wall to the arcus tendineus fascia rectovaginalis (ATFR), which is a condensation along the fascia of the levator ani muscle (10). The ATFR fuses with the ATFP at a point 4 cm above the posterior fourchette (10).

The composition and role of the rectovaginal (Denonvilliers) fascia and pubocervical fascia are debated (2,11). In the distal rectovaginal septum, there is a dense connective tissue layer (12). However, this is limited to the lower vagina, and there is no histologic evidence of a substantial fascial layer in the upper rectovaginal septum (12,13). Histologically, there is little evidence for pubocervical
“fascia.” Cadaveric studies of the anterior vaginal wall suggest that the visceral fascia in this location is composed of a thin areolar layer that separates the vaginal wall from the bladder (3,12,14). Surgical repair of cystocele and rectocele has long relied on repair of the “endopelvic fascia,” but the anatomic absence of a supportive, organized fascial layer in this location casts doubt on this concept of surgical repair. The “fascia” used in vaginal repairs is more accurately described as “vaginal submucosa” or “vaginal muscularis” (10,12,13), in recognition that this layer is part of the vaginal wall. However, others have suggested that defects in these layers result in cystocele and rectocele. This theory is the argument for the “defect-directed” approach to the correction of cystocele and rectocele (9,15,16). Objective defects cannot always be demonstrated, however (2). Debate continues regarding the role of endopelvic connective tissue in the genesis of pelvic organ support defects and the implications for surgical repair of these defects.

Levator ani muscles are important structures with respect to pelvic organ function, and there is increasing evidence of their role in pelvic organ support (1). The tone of the levator muscles keeps the levator hiatus closed (7,17) and likely prevents chronic tension on the parietal fascia. In addition to baseline tone, the normal response of the levator ani to Valsalva effort is increased tone, thereby closing the levator hiatus (17). Laxity of the levator ani leads to a widening of the genital hiatus, and this has been suggested to be a potential initiating event for pelvic organ prolapse. We know that women with prolapse have a wider genital hiatus on magnetic resonance imaging (18,19) and on physical examination (20). However, while this association has been consistently demonstrated, it might not be causal.

Preliminary research suggests an association between prolapse and the shape and size of the bony pelvis. Two studies suggested that women with prolapse have a wider pelvic diameter than women without prolapse (21,22). In one study, prolapse was also associated with a shorter obstetrical conjugate (21). An “at risk” bony pelvis could explain apparent racial differences in prolapse. Specifically, prolapse is less common in Black women (23), who are more likely to have an anthropoid pelvis, with a narrow transverse inlet and wide obstetrical conjugate (24).