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The Vagina

The vagina is a fibromuscular tubular organ running from the vulvar vestibule to the uterine cervix.

See also The Vulva for the introital and vestibular anatomy; Female Urethra for the anterior-wall urethral structures; and Perineum for the perineal body and posterior-compartment anchors.

Female reproductive system — frontal schematic

Blausen Medical — Female reproductive system, frontal schematic. (CC BY 3.0)

Dimensions and Shape​

Vaginal dimensions vary with the person, measurement method and degree of distension. In one MRI study of undistended volunteers, mean cervix-to-introitus length was 62.7 mm; a separate cast study reported a substantially wider range in a different cohort.[1][2] In the MRI cohort, mean width was 32.5 mm proximally, 27.8 mm at the pelvic diaphragm and 26.2 mm at the introitus.[1] Surface area is likewise method-dependent.[3]

The vagina is not a straight tube. In the supine pelvis the axis bends predictably:[3]

  • Approximately 90° relative to the horizontal in the lower vagina (nearly vertical)
  • Approximately 72° in the mid-vagina
  • Approximately 41° at the apex, directed toward the hollow of the sacrum

Contrast-distended MRI shows three vaginal zones that correspond broadly to DeLancey's support levels:[5]

ZoneLocationKey features
Superficial sphincteric (distal)Surrounded by pelvic-floor muscles and perineal membranePerineal body anchor; bulbospongiosus and superficial transverse perinei
Central transition (mid)Between levator plate and pelvic sidewallLateral attachments to ATFP; the paravaginal territory
Deep forniceal (proximal)Expanded around the cervix; anterior, posterior, lateral fornicesApical support from the cardinal–uterosacral ligament (CUL) complex

Anatomical relations​

AspectRelation
AnteriorUrethra (distal), bladder base and trigone (mid), cervix/vesicocervical space (proximal)
PosteriorPerineal body (distal), rectum (mid), rectouterine pouch of Douglas (proximal, peritoneum)
LateralLevator ani (pubovisceral), pelvic plexus, cardinal ligament, vaginal artery, ureter near the cervix as it passes beneath the uterine artery; distance varies
ApexCervix with anterior, posterior, and lateral fornices

The ureter at the vaginal apex. The ureter passes beneath the uterine artery near the cervix; the often-quoted 1.5–2-cm separation is an approximate teaching landmark, not a fixed safe distance. It is at risk during hysterectomy and some apical or paracervical dissections, with risk depending on the actual course and any distortion of anatomy. See The Ureters.

Wall Structure​

Three layers:[4][7]

LayerCompositionOperative relevance
MucosaNon-keratinised stratified squamous epithelium, hormone-responsive, glycogen-rich with rugae; ~26–28 cell layers in reproductive years[8]Relevant to colporrhaphy and fistula repair; estrogen can improve atrophy symptoms and the tissue appearance judged by surgeons[6][26]
Muscularis (fibromuscular layer)Inner circular and outer longitudinal smooth muscle in a collagen/elastin matrix; the lamina propria belongs to the mucosaIn anterior colporrhaphy, dissection splits vaginal muscularis and repair plicates muscularis and adventitia. Pubocervical and rectovaginal “fascia” are operative terms, not discrete vaginal histologic layers.[4]
AdventitiaLoose connective tissue carrying vessels, lymphatics, and nervesDissection between the vaginal wall and bladder or proximal rectum can follow local areolar planes in fistula, prolapse and hysterectomy surgery. Behind the distal vagina, connective tissue is fused to adjacent perineal and rectal tissues, so a continuous avascular plane cannot be assumed.[4][35]

Unlike the columnar endocervix, the superficial epithelium of both the vagina and ectocervix lacks classical tight junctions. The cited experiment demonstrated IgG penetration through apical ectocervical layers; vaginal junctions were assessed by staining.[10]

Hormone responsiveness. Estrogen thickens the epithelium and increases glycogen, which can support lactobacillus-dominant communities and an acidic vaginal pH in reproductive years.[9] Postmenopausal hypoestrogenism may thin the epithelium and raise pH, contributing to genitourinary symptoms.[6][26]

DeLancey's Three-Level Support — the Prolapse Framework​

The mechanical support of the vagina is best understood through DeLancey's three-level model.[19][21][22]

LevelStructuresClinical failure
Level I — apicalCardinal ligament + uterosacral ligament complex (CUL); suspends the vaginal apex and cervix from the sacrum and pelvic sidewallApical prolapse: uterine descent, vaginal vault prolapse, enterocele
Level II — mid-vaginal / lateralParavaginal attachments to the arcus tendineus fasciae pelvis (ATFP) ("white line") and superior fascia of levator aniAnterior (cystocele) and posterior (rectocele) compartment descent
Level III — distalPerineal membrane, perineal body, and levator–bulbospongiosus complexDistal anterior wall descent, perineal deficiency, gaping introitus

Two operative rules follow:

  • Apical support matters to compartment descent. Biomechanical modeling links levator impairment, hiatus size and apical support with anterior-wall prolapse severity.[21] An apical defect should be assessed when planning compartment repair.
  • Paravaginal (Level II) and distal (Level III) defects may coexist with apical descent and require individual assessment.

Vascular Supply and Drainage​

Arterial supply is polysegmental, with four paired contributions:[7][12]

ArteryOriginTerritory
Vaginal arteryInternal iliac (anterior division)Dominant middle / lower vagina
Descending vaginal branch of uterine arteryUterine artery (at the point where it crosses the ureter)Upper vagina and cervix
Internal pudendal artery (perineal branches)Internal iliacLower vagina and introitus
Middle rectal arteryVariable origin; often from the internal pudendal or inferior gluteal artery[38]Posterior vaginal wall

In anterior-wall biopsies from 32 women, microvessel density was greater in the distal third than in the proximal third in both the lamina propria and muscle layer.[13]

Venous drainage parallels the arteries to the vaginal venous plexus and into the internal iliac veins.

Lymphatic drainage split:

  • Upper vagina. Drains to the internal iliac and external iliac (obturator) nodes.
  • Middle vagina. Drains to the internal and external iliac nodes.
  • Lower vagina and introitus. Drains to the superficial inguinal nodes.

For surgically treated stage I primary vaginal squamous carcinoma, the 2023 ESTRO/ESGO/SIOPe guideline recommends pelvic lymph-node assessment for tumors involving the upper two-thirds of the vagina and surgical inguinal lymph-node assessment for lower-third involvement (both [IV, A]).[36]

Innervation​

Two distinct territories:[13][14][15][16]

RegionDominant supplyFunctional notes
Upper vagina (above pelvic diaphragm)Autonomic fibers from the inferior hypogastric (pelvic) plexus — sympathetic T10–L2 and parasympathetic S2–S4Sparse sensory supply; dilation and distension are the main perceived sensations; visceral afferents travel with the pelvic nerve
Lower vagina (below pelvic diaphragm)Pudendal nerve (S2–S4) — perineal branches to introitus and distal vaginal mucosaDense somatic sensation; the introital territory shares its sensory map with the vestibule

In anterior-wall biopsies from 32 women, small-nerve-fiber density was greater in the distal third than the proximal third.[13] The authors proposed that distal anterior repair could disrupt this neurovascular tissue and affect sexual function, but they did not measure sensation or postoperative outcomes.[13]

Autonomic input drives transudation-based lubrication during arousal, smooth-muscle tone, and vascular engorgement.

Secretion, pH, and the Microbiome (operative level)​

The vagina has no glands. Luminal fluid comes from:

  • Transudate across the permeable superficial epithelium
  • Cervical mucus descending from the endocervix
  • Bartholin and Skene-gland secretions
  • Desquamated epithelial cells

In many reproductive-age patients, vaginal pH is approximately 3.8–4.5. Estrogen supports epithelial glycogen accumulation; its breakdown products can be metabolized by lactobacilli to lactic acid. Lactobacillus-dominant communities include L. crispatus, L. iners, L. gasseri and L. jensenii.[9][17][40][41] Practical consequences:

  • Postmenopausal atrophy can raise vaginal pH, reduce lactobacilli, and present with atrophic vaginitis. Bacterial vaginosis and candidiasis can also occur after menopause.[34] Elevated pH alone does not establish either diagnosis; Candida vaginitis is usually associated with pH <4.5.[32][33]
  • Vaginal estrogen may be considered for bothersome menopause-associated genitourinary symptoms. For GSM-related vulvovaginal discomfort or irritation, dryness or dyspareunia, the 2025 AUA/SUFU/AUGS guideline gives a Strong Recommendation (Grade C) to offer local low-dose vaginal estrogen.[42] In the IMPROVE trial, surgeons rated estrogen-treated tissue more favorably at surgery.[6]

Biomechanics — What Fails in Prolapse​

The vagina is fibromuscular, and murine testing demonstrates biaxial mechanical responses and pressure-dependent creep.[11][18] In a 2025 human biaxial study, directional stiffness differences appeared in some premenopausal groups but not in postmenopausal or stage III prolapse groups.[39] A finite-element model simulated pelvic-support loading.[20]

Prolapse may involve several interacting supports:

  1. Levator ani (pubovisceral) impairment leads to opening of the genital hiatus
  2. Apical (Level I) support failure leads to proximal descent
  3. Paravaginal (Level II) and distal (Level III) failure leads to a compartment-specific bulge

Operative planning assesses apical, compartment and levator findings together. Apical suspension and compartment repair are selected for the patient's actual defects.

Developmental Origin​

Human fetal immunostaining and histologic reconstructions support replacement of Müllerian by urogenital-sinus epithelium during vaginal development; an earlier immunostaining series interpreted fornix epithelium as Müllerian in origin.[23][24][25] Müllerian epithelium is progressively replaced by UGS epithelium in a caudal-to-cranial direction, beginning around weeks 10–13 and reaching the uterovaginal junction around weeks 15–19 in the series reviewed by Hülsman et al.[23]

Clinical consequences:

  • Müllerian anomalies (vaginal agenesis, transverse septum, duplicated vagina) reflect disordered Müllerian-duct fusion and descent but not UGS development.
  • In-utero DES exposure is associated with a small risk of clear-cell adenocarcinoma of the vagina or cervix, estimated at approximately 1 in 1,000 exposed women through age 34.[37]
  • Vaginal elongation or neovaginal reconstruction in Müllerian agenesis (MRKH) usually begins with primary dilation when the patient is ready; surgery may use a skin graft (McIndoe), peritoneum (Davydov), buccal mucosa, or a bowel segment (sigmoid or ileum). A short distal vagina or vaginal dimple may be present.[30] Tissue-engineered scaffolds have been described in a four-patient pilot series.[31]

Clinical Correlations for the Reconstructive Surgeon​

  • Apical prolapse reconstruction. Sacrocolpopexy (mesh to sacral promontory), uterosacral ligament suspension (USLS) and sacrospinous ligament fixation (SSLF) are established apical options with different routes and trade-offs. Add anterior, posterior or paravaginal repair when the patient's compartment findings warrant it; none is universally required with every apical suspension.
  • Paravaginal defect repair. Loss of lateral anterior-wall support at the ATFP can contribute to cystocele, but physical examination does not consistently identify a paravaginal defect or distinguish it from levator-related descent.[46] Paravaginal repair reattaches the pubocervical fascia to the ATFP via retropubic or vaginal approach.
  • Anterior colporrhaphy. Addresses a central (distension) Level-II defect; apical support is assessed at the same operation. Mesh-augmented anterior repair has been curtailed by the FDA-mandated transvaginal-mesh limitations.
  • Posterior colporrhaphy and rectocele repair. Plicates the rectovaginal fascia; the perineal body is reconstructed at the distal (Level-III) terminus. A perineal-body deficiency can account for some "recurrent rectoceles" after posterior colporrhaphy.
  • Vaginal hysterectomy. Uses the vaginal fornices as the access route; the apex is anchored to the uterosacral-cardinal complex at closure to prevent subsequent vault prolapse.
  • Vesicovaginal fistula (VVF). Pelvic surgery is an important cause of non-obstetric VVF, but location and mechanism vary. Latzko partial colpocleisis and transvaginal layered closure, sometimes with tissue interposition, are useful options; an abdominal route may be appropriate for a high fixed vault fistula or other anatomy inaccessible vaginally. The approach and flap choice are tailored to size, tissue quality, prior radiation and ureteric involvement.[27] For radiation-associated fistula repair, the EAU weakly recommends a tissue interposition graft.[27]
  • Rectovaginal fistula (RVF). Obstetric (OASIS-related), inflammatory (Crohn's), or post-radiation. Repair depends on etiology, location, and sphincter status: transvaginal advancement flap, transperineal rectovaginal septum repair, gracilis interposition, or definitive diversion.
  • Urethrovaginal fistula (UVF). Most commonly iatrogenic (anti-incontinence surgery, diverticulectomy). Layered vaginal-flap repair with catheter drainage; an interposition flap (Martius, peritoneal, or gracilis) may be used when tissue quality or defect complexity warrants it.[27] Urethrovaginal fistula repair may be complicated by stress urinary incontinence, urethral stricture or shortening, which may require long-term follow-up.[27]
  • Vaginal stenosis and reconstruction. Post-radiation, post-LS, post-FGM, post-radical cystectomy, or congenital (MRKH). Options: dilator therapy, vaginal-wall flaps, buccal-graft neovagina, sigmoid / ileal neovagina, peritoneal (Davydov) neovagina.
  • Vaginoplasty.
    • Primary neovagina (MRKH, DSD, gender-affirming): McIndoe (split-thickness graft on stent), Davydov (peritoneum), Vecchietti (traction-dilation), sigmoid (ample length, self-lubricating but colitis risk, rare adenocarcinoma), ileum (adequate length, less mucus output).
    • Gender-affirming vaginoplasty. Penile skin inversion, scrotal graft, or pedicled bowel is used as the neovaginal lining; in penile-inversion vaginoplasty, the canal is dissected posterior to the prostate and urethra and anterior to the rectum, ending at the peritoneal reflection when the peritoneum is not used.[47] Peritoneal-flap techniques use peritoneum to construct the vaginal apex.[48]
  • Vaginal cuff dehiscence. A complication of hysterectomy (particularly total laparoscopic hysterectomy); presents as postcoital bleeding, evisceration or acute abdomen with bowel through the cuff. Emergent repair may be transvaginal or abdominal, with tissue-preserving closure. Smoking is an identified risk factor after minimally invasive hysterectomy.[43]
  • Clear-cell adenocarcinoma of the vagina. A DES-exposure sequela arising from residual Müllerian vaginal epithelium; historically seen in the upper anterior vagina of women exposed in utero.
  • Vaginal SCC. Rare, usually upper vagina, HPV-associated. Treatment depends on stage: radiation for most, surgery for small, superficial, or distal tumors (partial or radical vaginectomy with LND dictated by site).
  • Pessary fitting. Vaginal dimensions and support, genital-hiatus size, patient comfort and the chosen device all matter; more than one fitting may be needed.[28][29] Consider vaginal estrogen for concomitant menopause-associated genitourinary symptoms.[28] A 2025 placebo-controlled ring-pessary trial did not improve its 12-month continuation-plus-improvement primary outcome.[29] In secondary outcomes, erosion or ulcer (4/208 versus 14/203) and bleeding (3/208 versus 13/203) were less frequent with estrogen; these findings need cautious interpretation.[29]
  • Perioperative vaginal estrogen. In the Rahn 2023 IMPROVE trial, estrogen-treated tissue appeared more estrogenized and was rated more robust by surgeons, and some participants with bothersome atrophy symptoms improved. However, 12-month composite surgical failure was not lower with estrogen (model-estimated 19% versus 9% with placebo; adjusted HR 1.97, 95% CI 0.92–4.22)[6]; a 36-month follow-up likewise found no significant surgical-success benefit.[26] In a separate 2026 trial of postmenopausal women having primary native-tissue prolapse repair (311 randomized; 293 had surgery and started treatment; 57 dropped out), 92% in the perioperative estriol group versus 80% in the placebo group reported their prolapse symptoms were “much” or “very much” improved on the PGI-I at 12 months; anatomic and composite surgical success did not differ.[49]
  • Vaginal packing. Packs may be used selectively for hemostasis, flap support or graft splinting. Routine packing after vaginal hysterectomy showed no clear reduction in bleeding, hematoma or cuff infection across four trials (337 participants), and a systematic review advised against routine use.[44] If a pack is used, 24-hour dwell is not obligatory: a trial found no benefit to retaining both pack and catheter for 24 rather than 3 hours after vaginal surgery.[45]

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