|Vagina in the female human reproductive system.|
|Vulva with vaginal opening|
|Gray's||subject #269 1264|
|Artery||superior part to uterine artery, middle and inferior parts to vaginal artery|
|Vein||uterovaginal venous plexus, vaginal vein|
|Nerve||Sympathetic: lumbar splanchnic plexus
Parasympathetic: pelvic splanchnic plexus
|Lymph||upper part to internal iliac lymph nodes, lower part to superficial inguinal lymph nodes|
|Precursor||urogenital sinus and paramesonephric ducts|
The vagina is a fibromuscular elastic tubular tract (passage) which is a sex organ and mainly functions for the facilitation of sexual intercourse and childbirth. In mammals (especially primates), menstruation, which is the periodic discharge of blood and mucosal tissue (the endometrium) from the uterus and vagina, is another primary function of the vagina and usually signals fertility. The location and size of the vagina varies among species, and may vary in size within the same species. In humans, the vagina leads from the opening of the vulva to the uterus (womb), but the vaginal tract ends at the cervix.
Unlike mammalian males, who usually have only one genital orifice, mammalian females usually have two, the urethra and the vagina. The vaginal opening is much larger than the urethral opening, and both openings are protected by the labia.12 The vagina's inner mould has a foldy texture which can create friction for the penis during sexual intercourse. During sexual arousal, vaginal moisture increases (vaginal lubrication) to facilitate the entrance of the penis.
The female reproductive tract may also be termed the vagina with regard to amphibians, birds, reptiles and monotremes, but is generally known among zoologists as the cloaca in these species and may additionally serve as intestinal and urinary tracts.
- 1 Etymology and definition
- 2 Structure
- 3 Function
- 4 Clinical significance
- 5 Other animals
- 6 See also
- 7 References
- 8 External links
Etymology and definition
The term vagina is from Latin vāgīna, literally "sheath" or "scabbard." It is often referred to as the birth canal in the context of pregnancy and childbirth, though the term is, by definition, the area between the outside of the vagina and the fully dilated uterus.3
The Latinate plural "vaginae" is rarely used in English. Colloquially, the word vagina is often used to refer to the vulva or to the female genitals in general.4 However, by its dictionary and anatomical definitions, vagina refers exclusively to the specific internal structure.
The vagina is derived from the embryonic Mullerian duct.5 The human vagina is an elastic muscular canal that extends from the cervix to the vulva.6 It, along with the inside of the vulva, is reddish pink in color, and it connects the superficial vulva to the cervix of the deep uterus. The vagina, posterior to the urethra and bladder, reaches across the perineum superiorly and posteriorly toward the cervix; at approximately a 90 degree angle, the cervix protrudes into the vagina.7
The vagina's internal lining consists of stratified squamous epithelium.8 Beneath this lining is a layer of smooth muscle, which may contract during vaginal intercourse and when giving birth. Beneath the muscle is a layer of connective tissue called adventitia.9
Regions and layers
Where the vaginal lumen surrounds the cervix of the uterus, it is divided into four regions of fornices (the vaginal fornix); these are the anterior, posterior, and the right lateral and left lateral (the lateral fornix).6 Supporting the vagina are its upper third, middle third and lower third. The upper third concerns the levator ani muscles (transcervical, pubocervical) and the sacrocervical ligaments; these areas are also described as the cardinal ligaments laterally and uterosacral ligaments posterolaterally. The middle third of the vagina concerns the urogenital diaphragm (also described as the paracolpos and pelvic diaphragm). The lower third concerns the perineal body; it is sometimes described as containing the perineal body, pelvic diaphragm and urogenital diaphragm.610
Three layers, sometimes categorized as four layers, compose the vaginal walls.78911 When categorized as three layers, they may be described as follows: The first layer is made up of a stratified squamous non-keratinized epithelium and is an underlying lamina propria of connective tissue (a layer of connective tissue that is highly vascular under the base area lining the epithelium). The second layer is the muscular layer, which is composed of smooth muscle fibers and situated longitudinally and circularly. The third layer is the adventitia, which is a dense connective tissue that blends with the fascia surrounding the area.79
When categorized as four layers, the vaginal walls may be described in significantly more detail: The first layer is an inner layer of non-keratinized squamous epithelium, which forms the folds or rugae and facilitate the vagina's ability to expand large enough for child birth. The rugae are a series of ridges produced by folding of the wall of the outer third of the vagina; they are transverse epithelial ridges and their function is to provide the vagina with increased surface area for extension and stretching. The second layer of the vagina is connective tissue, which contains blood vessels. The third layer is the muscle layer; it is an outer layer of longitudinal muscle, as well as the inner layer of circular muscle. The fourth layer is an outer layer of connective tissue; it is continuous with the other pelvic organs and is made up of blood and lymphatic vessels and fibers.812
The vaginal opening is at the caudal end of the vulva, behind the opening of the urethra. The upper one-fourth of the vagina is separated from the rectum by the recto-uterine pouch. Above the vagina is a cushion of fat called the mons pubis which surrounds the pubic bone and provides protective support during vaginal intercourse.
The Bartholin's glands, located near the vaginal opening and cervix, were originally thought to be the primary source for vaginal lubrication, but they provide only a few drops of mucus for vaginal lubrication;13 the significant majority of vaginal lubrication is generally believed to be provided by plasma seepage from the vaginal walls, which is called vaginal transudation. Vaginal transudation, which initially forms as sweat-like droplets, is caused by vascular engorgement of the vagina (vasocongestion); this results in the pressure inside the capillaries increasing the transudation of plasma through the vaginal epithelium.131415
Before and during ovulation, the cervix's mucus glands secrete different variations of mucus, which provides an alkaline environment in the vaginal canal that is favorable to the survival of sperm. "Vaginal lubrication typically decreases as women age, but this is a natural physical change that does not normally mean there is any physical or psychological problem. After menopause, the body produces less estrogen, which, unless compensated for with estrogen replacement therapy, causes the vaginal walls to thin out significantly."16
Variations and size
In its normal state, there is anatomical variation in the length of the vagina of a woman of child-bearing age. The length is approximately 7.5 cm (2.5 to 3 in) across the anterior wall (front), and 9 cm (3.5 in) long across the posterior wall (rear), making the posterior fornix deeper than the anterior.8 During sexual arousal, the vagina expands in both length and width.
If a woman stands upright, the vaginal tube points in an upward-backward direction and forms an angle of slightly more than 45 degrees with the uterus and of about 60 degrees to horizon.10
The hymen is a membrane of tissue that surrounds or partially covers the external vaginal opening. The effects of vaginal intercourse and childbirth on the hymen are variable. If the hymen is sufficiently elastic, it may return to nearly its original condition. In other cases, there may be remnants (carunculae myrtiformes), or it may appear completely absent after repeated penetration.1718 Additionally, the hymen may be lacerated by disease, injury, medical examination, masturbation or physical exercise. For these reasons, it is not possible to definitively determine whether or not a girl or woman is a virgin by examining her hymen.17181920
The vagina has several biological functions.
The concentration of the nerve endings that lie close to the entrance of a woman's vagina (the lower third) can provide pleasurable sensations during sexual activity when stimulated in a way that a woman enjoys, and many women additionally derive pleasure from a feeling of closeness and fullness during vaginal penetration.2122 The vagina as a whole, however, lacks nerve endings, which generally hinders a woman's ability to receive sufficient sexual stimulation, including orgasm, solely from vaginal sexual activity.21232425 The outer one-third of the vagina, especially near the opening, contains the majority of the vaginal nerve endings, making it more sensitive to touch than the inner two-thirds of the vaginal barrel.212425 This factor is considered to make the process of child birth significantly less painful, because an increased number of nerve endings means that there is an increased possibility for pain as well as pleasure.242627
The clitoris contains an abundance of nerve endings and is a sex organ of multiplanar structure with a broad attachment to the pubic arch and via extensive supporting tissue to the mons pubis and labia, centrally attached to the urethra and vagina. Clitoral tissue forms a tissue cluster with the vagina. The tissue is more extensive in some women than in others, which may contribute to orgasms experienced vaginally.232528 During sexual arousal, and particularly the stimulation of the clitoris, the walls of the vagina lubricate. This reduces friction that can be caused by various sexual activities.16
With sexual arousal, the vagina lengthens rapidly,16 to an average of about 4 in.(10 cm), but can continue to lengthen in response to pressure. As the woman becomes fully aroused, the vagina tents (last ²⁄₃) expands in length and width, while the cervix retracts. The elastic walls of the vagina stretch or contract, with support from the pelvic muscles, to the size of the inserted penis or other object,16 stimulating the penis and helping to cause the male to experience orgasm and ejaculation; this in turn enables fertilization.
An area in the vagina that may be an erogenous zone is the G-spot (also known as the Gräfenberg Spot); it is typically defined as being located at the anterior wall of the vagina, about five centimeters in from the entrance. Some women experience intense pleasure, and sometimes an orgasm, if this area is stimulated during sexual activity. A G-spot orgasm may be responsible for female ejaculation, leading some doctors and researchers to believe that G-spot pleasure comes from the Skene's glands, a female homologue of the prostate, rather than any particular spot on the vaginal wall.293031 Other researchers consider the connection between the Skene's glands and the G-spot to be weak.323334 They contend that the Skene's glands do not appear to have receptors for touch stimulation, and that there is no direct evidence for their involvement.34 The G-spot's existence, and existence as a distinct structure, is still under dispute, as its location can vary from woman to woman, appears to be nonexistent in some women,262832 and it is hypothesized to be an extension of the clitoris and therefore the reason for orgasms experienced vaginally.232835
During childbirth, the vagina provides the channel to deliver the newborn from the uterus to its independent life outside the body of the mother. During birth, the elasticity of the vagina allows it to stretch to many times its normal diameter.
Vaginal ecosystem and acidity
The vagina is a nutrient rich environment that harbors a unique and complex microflora. It is a dynamic ecosystem that undergoes long term changes, from neonate to puberty and from the reproductive period (menarche) to menopause. Moreover, under the influence of hormones, such as estrogen (estradiol), progesterone and follicle stimulating hormone (FSH), the vaginal ecosystem undergoes cyclic or periodic changes, i.e. during menses and pregnancy.36373839
One important variable parameter is the vaginal pH, which varies significantly during a woman‘s lifespan, from 7.0 in premenarchal girls, to 3.8-4.4 in women of reproductive age to 6.5-7.0 during menopause without hormone therapy and 4.5-5.0 with hormone replacement therapy.36 Estrogen, glycogen and lactobacilli are important factors in this variation.36
Microflora and possible role in acidification
The vagina of a newborn is affected by the residual maternal estrogen still present. At birth, the vaginal mucosa is rich in glycogen and the vagina becomes colonized by lactic-acid producing bacteria, such as Lactobacillus spp., within the first day after birth.40 These estrogen effects will slowly disappear by the fourth week after birth and the glycogen content will diminish. The vaginal pH becomes neutral or alkaline, likely due to the almost absence of lactic-acid producing microorganisms.3741 In premenarchal girls, the vaginal microflora is composed of anaerobic and aerobic cocci and rods with low loads of lactobacilli, Gardnerella vaginalis and Mobiluncus spp.3641 During puberty, the estrogen levels rise until they reach the concentrations found in adult women. The estrogen causes the vaginal epithelium to thicken and the intracellular glycogen production to rise,42 which consequently causes a shift in the composition of the vaginal microflora.41 At this moment, lactobacilli, probably from the rectum,4344 become the most important inhabitants colonizing the vaginal econiche, utilizing the available glycogen, which is converted to lactic acid, resulting in the acidification (pH < 4.4) of the vagina.36434445 In addition, besides lactic acid, the principal vaginal acidifier, other organic acids, i.e. acetic and linoleic acid, are also normally found in vaginal fluid.46
Estrogen vs. lactobacilli
The source of the lactic acid has been subject to debate. Some studies suggest that the presence of estrogen and not Lactobacillus is primarily related to acidification of the vagina,47 and even that lactobacilli cannot produce lactic acid from glycogen. The overall vaginal pH can be attributed to the total of estrogen mediated lactic acid production by the epithelial cells (producing only the L-isomer of lactate) and the lactic acid contribution by the endogenous vaginal bacteria (producing both D- and L-isomers of lactate).4648 Boskey et al.,49 studying vaginal lactate production in 11 women, found that D-lactate (bacterial origin) in vaginal secretions ranged from 6% to 75%, with a mean of 55%. They concluded that these findings supported the role of Lactobacillus as the primary source for vaginal acidification, although the wide range found was not indicative for a dominant bacterial source of lactate in all women. Moreover, the midportion of the vagina has a higher pH than the vaginal fornix, although the lactobacilli concentration is uniform throughout the vaginal canal.46 This is indicative for the fact that the vaginal mucosal metabolism may be more dominant in determining the final pH.46
However, in a pyrosequencing study by Ravel et al.50 of the vaginal microflora of 396 asymptomatic North American women, representing four ethnic groups (white, black, Hispanic, and Asian), the higher median pH values in Hispanic (pH 5.0 ± 0.59) and black (pH 4.7 ± 1.04) women reflected a higher prevalence of communities not dominated by Lactobacillus spp. in these two ethnic groups, when compared with Asian (pH 4.4 ± 0.59) and white (pH 4.2 ± 0.3) women. Ravel et al.50 found that the lowest pH values were associated with vaginal ecosystems dominated by L. iners and L. crispatus, and the highest pH values were associated with vaginal ecosystems not dominated by species of Lactobacillus.5051 The results of Ravel may be controversial for L.iners, which was strongly associated with Bacterial vaginosis-like vaginal microflora, which is characterized by alkaline pH.5253 Hummelen et al.51 stated in their pyrosequencing study that L. crispatus is associated with a low pH, but when L. crispatus is not present, a large fraction of L. iners is required to predict a low pH.51 Nevertheless, these results indicate that bacteria play an important role in the acidification of the vagina and more research, e.g. regarding the resource of glycogen, used to produce lactic acid and regarding the bacterial species that can metabolize glycogen, is needed to understand the various factors that govern vaginal pH.
Next to the protective effects of pH and the endogenous vaginal microflora, pathogen colonization is also prevented by the local components of the innate and acquired immune systems.54 The innate immune system recognizes pathogen-associated molecular patterns (PAMPs) on microbial pathogens and includes soluble factors (e.g. mannose-binding lectin, complement components, defensins, secretory leukocyte protease inhibitor (SLPI) and nitric oxide), membrane-associated components (e.g. Toll-like receptors) and tissue-associated phagocytes (macrophages and neutrophils).46545556 The vaginal adaptive (acquired) immunity produces locally IgG and IgA, which will recognize and bind to specific antigens on microorganisms in the vagina.57 For instance, an IgA response against G. vaginalis vaginolysin has been reported and a correlation between this response and BV has been shown.5859
Finally, after the reproductive years, women enter the menopause, which is characterized by the cessation of menstruation because of the loss of follicular activity.38 The circulating estrogen levels are low and the glycogen content is low to absent, resulting in a rise of the vaginal pH, and consequently the vagina is colonized by bacteria associated with intermediate/disturbed vaginal microflora.37386061 It has been shown that estrogen therapy can augment the loads of lactobacilli, which in turn can diminish the increased risk for BV and urinary tract infections.6062 However, the absence of lactobacilli by itself is not related to an elevated prevalence of BV,63 and estrogen replacement may merely potentiate the effect of lactobacilli present on the vaginal pH.64
The vaginal ecosystem is under the influence of many factors, endogenous (hormonal, innate immunity, ethnicity), as well as exogenous (behavioral factors, such as sexual activity, cigarette smoking, douching and antibiotic treatment in general),656667 that are determinative for the vaginal health. The endogenous susceptibility for disturbance of the vaginal microflora and for infections is determined by the genetic characteristics of each individual woman,5054 the specific composition of her vaginal microflora at a certain point in time and the genotypic differences between the vaginal lactobacilli present (at species and strain level).6869
The vagina is self-cleansing and therefore usually needs no special treatment. Doctors generally discourage the practice of douching.70 Since a healthy vagina is colonized by a mutually symbiotic flora of microorganisms that protect its host from disease-causing microbes, any attempt to upset this balance may cause many undesirable outcomes, including but not limited to abnormal discharge and yeast infection.
The vagina is examined during gynecological exams, often using a speculum, which holds the vagina open for visual inspection of the cervix or taking of samples (see pap smear). Medical activities involving the vagina, including examinations, administration of medicine, and inspection of discharges, are also referred to as being per vaginam (or p.v.).71
The healthy vagina of a woman of child-bearing age is acidic, with a pH normally ranging between 3.8 and 4.5.72 This is due to the degradation of glycogen to the lactic acid by enzymes secreted by the Döderlein's bacillus. This is a normal commensal of the vagina. The acidity retards the growth of many strains of pathogenic microbes.73
An increased pH of the vagina (with a commonly used cut-off of pH 4.5 or higher), can be caused by bacterial overgrowth, as occurs in bacterial vaginosis and trichomoniasis, or rupture of membranes in pregnancy.72
Vaginismus, not to be confused with vaginitis (an inflammation of the vagina), refers to an involuntary tightening of the vagina due to a conditioned reflex of the muscles in the area. It can affect any form of vaginal penetration, including sexual intercourse, insertion of tampons and menstrual cups, and the penetration involved in gynecological examinations. Various psychological and physical treatments are possible to help alleviate it.
Signs of disease
The presence of unusual lumps in the wall or base of the vagina is always abnormal. The most common of these is Bartholin's cyst.74 The cyst, which can feel like a pea, is formed by a blockage in glands which normally supply the opening of the vagina. This condition is easily treated with minor surgery or silver nitrate. Other less common causes of small lumps or vesicles are herpes simplex. They are usually multiple and very painful with a clear fluid leaving a crust. They may be associated with generalized swelling and are very tender. Lumps associated with cancer of the vaginal wall are very rare and the average age of onset is seventy years.75 The most common form is squamous cell carcinoma, then cancer of the glands or adenocarcinoma and finally, and even more rarely, melanoma.
Most vaginal discharges occur due to normal bodily functions such as menstruation or sexual arousal. Abnormal discharges, however, can indicate disease.
Normal vaginal discharges include blood or menses (from the uterus), the most common, and clear fluid either as a result of sexual arousal or secretions from the cervix. Other non-infective causes include dermatitis. Non-sexually transmitted discharges occur from bacterial vaginosis and thrush or candidiasis. The final group of discharges include the sexually transmitted diseases gonorrhea, chlamydia, and trichomoniasis. The discharge from thrush is slightly pungent and white, that from trichomoniasis more foul and greenish, and that from foreign bodies resembling the discharge of gonorrhea, greyish or yellow and purulent (pus-like).76
All sores involve a breakdown in the walls of the fine membrane of the vaginal wall. The most common of these are abrasions and small ulcers caused by trauma. While these can be inflicted during rape most are actually caused by excessive rubbing from clothing or improper insertion of a sanitary tampon. The typical ulcer or sore caused by syphilis is painless with raised edges. These are often undetected because they occur mostly inside the vagina. The sores of herpes which occur with vesicles are extremely tender and may cause such swelling that passing urine is difficult. In the developing world a group of parasitic diseases also cause vaginal ulceration such as Leishmaniasis but these are rarely encountered in the west. HIV/AIDS can be contracted through the vagina during intercourse but is not associated with any local vaginal or vulval disease.77 All the above local vulvovaginal diseases are easily treated. Often only shame prevents patients from presenting for treatment.78
Route of administration
Intravaginal administration is a route of administration where the substance is applied to the inside of the vagina. Pharmacologically, it has the potential advantage to result in effects primarily in the vagina or nearby structures (such as the vaginal portion of cervix) with limited systemic adverse effects compared to other routes of administration.
|This section does not cite any references or sources. (March 2013)|
The vagina (along with the penis) is a general feature of animals in which the female is internally fertilised (other than by traumatic insemination). The shape of the vagina varies among different animals.
In placental mammals and marsupials, the vagina leads from the uterus to the exterior of the female body. In birds, monotremes, and some reptiles, a homologous part of the oviduct leads from the shell gland to the cloaca.citation needed In some jawless fish, there is neither oviduct nor vagina and instead the egg travels directly through the body cavity (and is fertilised externally as in most fish and amphibians). In insects and other invertebrates, the vagina is part of the oviduct (see insect reproductive system).
- Clinical pediatric urology: A. Barry Belman, Lowell R. King, Stephen Alan Kramer (2002)
- Kinetics, Human (15 May 2009). Health and Wellness for Life. Human Kinetics 10%. p. 221. ISBN 978-0-7360-6850-5. Retrieved 30 July 2013.
- "Princeton University's Wordnet search results for Birth Canal". Princeton. Retrieved 24 May 2010.
- Words meaning vulva ('vagina'), female genitalia Online Slang Dictionary
- Cai Y (2009). "Revisiting old vaginal topics: conversion of the Müllerian vagina and origin of the "sinus" vagina.". Int J Dev Biol 2009; 53:925-34 53 (7): 925–34. doi:10.1387/ijdb.082846yc. PMID 19598112.
- Snell, Richard S. (2004). Clinical Anatomy: An Illustrated Review with Questions and Explanations. Lippincott Williams & Wilkins. p. 98. ISBN 978-0-7817-4316-7. Retrieved 19 February 2014.
- Mulhall, John P. (2011). John P. Mulhall, Luca Incrocci, Irwin Goldstein, Ray Rosen, ed. Cancer and Sexual Health. Springer. pp. 13–22. ISBN 1-60761-915-6. Retrieved February 21, 2014.
- Wylie, Linda (2005). Essential Anatomy and Physiology in Maternity Care. Elsevier Health Sciences. pp. 157–158. ISBN 0-443-10041-1. Retrieved 19 February 2014.
- Young, B, ed. (2006). Wheater's Functional Histology: A Text and Colour Atlas (5th ed.). Elsevier. p. 377. ISBN 978-0443068508.
- Manual of Obstetrics. (3rd ed.). Elsevier. 2011. pp. 1–16. ISBN 9788131225561.
- Brown, Laurence (2012). Pathology of the Vulva and Vagina. Springer. pp. 6–7. ISBN 0857297570. Retrieved February 21, 2014.
- Sabaratnam Arulkumaran, Lesley Regan, Aris Papageorghiou, Ash Monga, David Farquharson (2011). Oxford Desk Reference: Obstetrics and Gynaecology. Oxford University Press. p. 471. ISBN 0191620874. Retrieved February 21, 2014.
- Sloane, Ethel (2002). Biology of Women. Cengage Learning. pp. 32, 41–42. ISBN 0-7668-1142-5. Retrieved 19 February 2014.
- Bourcier, A.; McGuire, Edward J.; Abrams, Paul (2004). Pelvic Floor Disorders. Elsevier Health Sciences. p. 20. ISBN 0-7216-9194-3. Retrieved 19 February 2014.
- Wiederman, Michael W.; Whitley, Jr., Bernard E. (1 August 2001). Handbook for Conducting Research on Human Sexuality. Psychology Press. p. 143. ISBN 978-1-135-66340-7. Retrieved 19 February 2014.
- "Vagina". health.discovery.com. Retrieved 11 February 2012.
- Knight, Bernard (1997). Simpson's Forensic Medicine (11th ed.). London: Arnold. p. 114. ISBN 0-7131-4452-1.
- Jacoby, David B.; Youngson, Robert M. (2005). Encyclopedia of Family Health (3rd ed.). Marshall Cavendish. p. 889. ISBN 0-7614-7486-2.
- Rogers DJ, Stark M (August 1998). "The hymen is not necessarily torn after sexual intercourse". BMJ 317 (7155): 414. doi:10.1136/bmj.317.7155.414. PMC 1113684. PMID 9694770.
- Perlman, Sally E.; Nakajyma, Steven T. and Hertweck, S. Paige (2004). Clinical protocols in pediatric and adolescent gynecology. Parthenon. p. 131. ISBN 1-84214-199-6.
- "I'm a woman who cannot feel pleasurable sensations during intercourse". Go Ask Alice!. 8 October 2004 (Last Updated/Reviewed on 17 October 2008). Archived from the original on January 7, 2011. Retrieved September 13, 2012.
- "No stimulation from intercourse". Go Ask Alice!. 13 May 2011. Archived from the original on January 7, 2011. Retrieved 10 November 2012.
- O'Connell HE, Sanjeevan KV, Hutson JM (October 2005). "Anatomy of the clitoris". The Journal of Urology 174 (4 Pt 1): 1189–95. doi:10.1097/01.ju.0000173639.38898.cd. PMID 16145367. Time for rethink on the clitoris: Lay summary – BBC News (11 June 2006).
- Weiten, Wayne; Dunn, Dana; Hammer, Elizabeth (1 January 2011). Psychology Applied to Modern Life: Adjustment in the 21st Century. Cengage Learning. p. 386. ISBN 1-111-18663-4. Retrieved 19 February 2014.
- Sex and Society, Volume 2. Marshall Cavendish Corporation. 2009. p. 590. ISBN 9780761479079. Retrieved 17 August 2012.
- Richard Balon, Robert Taylor Segraves (2009). Clinical Manual of Sexual Disorders. American Psychiatric Pub. p. 258. ISBN 1585629057. Retrieved February 21, 2014.
- Rosenthal, Martha (6 January 2012). Human Sexuality: From Cells to Society. Cengage Learning. p. 76. ISBN 0-618-75571-3. Retrieved 19 February 2014.
- Kilchevsky A, Vardi Y, Lowenstein L, Gruenwald I. (January 2012). "Is the Female G-Spot Truly a Distinct Anatomic Entity?". The Journal of Sexual Medicine 2011 (3): 719–26. doi:10.1111/j.1743-6109.2011.02623.x. PMID 22240236. G-Spot Does Not Exist, 'Without A Doubt,' Say Researchers - Lay summary – The Huffington Post (19 January 2012).
- Crooks, R; Baur, K (1999). Our Sexuality. California: Brooks/Cole.
- Jannini E, Simonelli C, Lenzi A (2002). "Sexological approach to ejaculatory dysfunction". Int J Androl 25 (6): 317–23. doi:10.1046/j.1365-2605.2002.00371.x. PMID 12406363.
- Jannini E, Simonelli C, Lenzi A (2002). "Disorders of ejaculation". J Endocrinol Invest 25 (11): 1006–19. PMID 12553564.
- Hines T (August 2001). "The G-Spot: A modern gynecologic myth". Am J Obstet Gynecol 185 (2): 359–62. doi:10.1067/mob.2001.115995. PMID 11518892.
- Santos, F Taboga, S. (2003). "Female prostate: a review about biological repercussions of this gland in humans and rodents" (PDF). Animal Reproduction. 3 (1): 3–18. Retrieved 2012-03-11.
- Alzate H Hoch Z (1986). "The "G spot" and "female ejaculation": a current appraisal". J Sex Marital Ther. 12 (3): 211–20. doi:10.1080/00926238608415407. PMID 3531529.
- Alexander, Brian (18 January 2012). "Does the G-spot really exist? Scientists can't find it". MSNBC.com. Retrieved 2 March 2012.
- Danielsson, D., P. K. Teigen, and H. Moi. 2011. The genital econiche: Focus on microbiota and bacterial vaginosis" Ann. N. Y. Acad. Sci 1230:48-58
- Farage, M., and H. Maibach. 2006. Lifetime changes in the vulva and vagina. Arch. Gynecol.
- Farage, M. A., S. Neill, and A. B. MacLean. 2009. Physiological changes associated with the
- Golub, S. 1992. Periods: From menarche to menopause. Sage Publications, Inc.
- Marshall WA, T. J. 1981. Puberty. Heinemann.
- Thoma, M. E., R. H. Gray, N. Kiwanuka, S. Aluma, M.-C. Wang, N. Sewankambo, and M. J. Wawer. 2011. Longitudinal changes in vaginal microbiota composition assessed by Gram stain among never sexually active pre- and postmenarcheal adolescents in Rakai, Uganda. J. Pediatr. Adolesc. Gynecol. 24:42-47.
- Paavonen, J. 1983. Physiology and ecology of the vagina. Scand. J. Infect. Dis. Suppl. 40:31-35.
- El Aila, N. A., I. Tency, G. Claeys, H. Verstraelen, B. Saerens, G. Lopes dos Santos Santiago, E. De Backer, P. Cools, M. Temmerman, R. Verhelst, and M. Vaneechoutte. 2009. Identification and genotyping of bacteria from paired vaginal and rectal samples from pregnant women indicates similarity between vaginal and rectal microflora. BMC Infect. Dis.9:167.
- El Aila, N. A., I. Tency, B. Saerens, E. De Backer, P. Cools, G. Lopes dos Santos Santiago, H. Verstraelen, R. Verhelst, M. Temmerman, and M. Vaneechoutte. 2011. Strong correspondence in bacterial loads between the vagina and rectum of pregnant women. Res. Microbiol. 162:506-513.
- Antonio, M. A., L. K. Rabe, and S. L. Hillier. 2005. Colonization of the rectum by Lactobacillus species and decreased risk of bacterial vaginosis" J. Infect. Dis 192:394-398.
- Linhares, I. M., P. R. Summers, B. Larsen, P. C. Giraldo, and S. S. Witkin. 2011. Contemporary perspectives on vaginal pH and lactobacilli" Am. J. Obstet. Gynecol 204:120.e1-120.e5.
- Weinstein L, H. J. 1939. The effect of estrogenic hormone on the H-ion concentration and the bacterial content of the human vagina with special reference to the Doderline bacillus" Am. J. Obstet. Gynecol 37:698-703.
- Gorodeski, G. I., U. Hopfer, C. C. Liu, and E. Margles. 2005. Estrogen acidifies vaginal pH by up-regulation of proton secretion via the apical membrane of vaginal-ectocervical epithelial cells. Endocrinol. 146:816-824.
- Boskey, E. R., R. A. Cone, K. J. Whaley, and T. R. Moench. 2001. Origins of vaginal acidity:High D/L lactate ratio is consistent with bacteria being the primary source" Hum. Reprod 16:1809-1813.
- Ravel, J., P. Gajer, Z. Abdo, G. M. Schneider, S. S. Koenig, S. L. McCulle, S. Karlebach, R. Gorle, J. Russell, C. O. Tacket, R. M. Brotman, C. C. Davis, K. Ault, L. Peralta, and L. J. Forney. 2011. Vaginal microbiome of reproductive-age women. Proc. Natl. Acad. Sci. U S A.108:4680-4687.
- Hummelen, R., A. D. Fernandes, J. M. Macklaim, R. J. Dickson, J. Changalucha, G. B. Gloor, and G. Reid. 2010. Deep sequencing of the vaginal microbiota of women with HIV. PloS One 5:e12078.
- De Backer, E., R. Verhelst, H. Verstraelen, M. A. Alqumber, J. P. Burton, J. R. Tagg, M. Temmerman, and M. Vaneechoutte. 2007. Quantitative determination by real-time PCR of four vaginal Lactobacillus species, Gardnerella vaginalis and Atopobium vaginae indicates an inverse relationship between L. gasseri and L. iners. BMC Microbiol. 7:115.
- Verhelst, R., H. Verstraelen, G. Claeys, G. Verschraegen, L. Van Simaey, C. De Ganck, E. De Backer, M. Temmerman, and M. Vaneechoutte. 2005. Comparison between Gram stain and culture for the characterization of vaginal microflora: Definition of a distinct grade that resembles grade I microflora and revised categorization of grade I microflora. BMC Microbiol. 5:61.
- Witkin, S. S., I. M. Linhares, and P. Giraldo. 2007. Bacterial flora of the female genital tract:function and immune regulation. Best Pract. Res. Clin. Obstet. Gynaecol. 21:347-354.
- Klein, N. J. 2005. Mannose-binding lectin: Do we need it?" Mol. Immunol 42:919-924.
- Wira, C. R., and J. V. Fahey. 2004. The innate immune system: Gatekeeper to the female reproductive tract. Immunol. 111:13-15.
- Mestecky, J., and M. W. Russell. 2000. Induction of mucosal immune responses in the human genital tract. FEMS Immunol. Med. Microbiol. 27:351-355.
- Cauci, S., S. Driussi, R. Monte, P. Lanzafame, E. Pitzus, and F. Quadrifoglio. 1998. Immunoglobulin A response against Gardnerella vaginalis hemolysin and sialidase activity in bacterial vaginosis" Am. J. Obstet. Gynecol 178:511-515.
- Cauci, S., F. Scrimin, S. Driussi, S. Ceccone, R. Monte, L. Fant, and F. Quadrifoglio. 1996. Specific immune response against Gardnerella vaginalis hemolysin in patients with bacterial vaginosis" Am. J. Obstet. Gynecol 175:1601-1605.
- Burton, J. P., and G. Reid. 2002. Evaluation of the bacterial vaginal flora of 20 postmenopausal women by direct (Nugent score) and molecular (polymerase chain reaction and denaturing gradient gel electrophoresis) techniques" J. Infect. Dis 186:1770-1780.
- Hillier, S. L., and R. J. Lau. 1997. Vaginal microflora in postmenopausal women who have not received estrogen replacement therapy" Clin. Infect. Dis 25:S123-S126.
- Stamm, W. E., and R. Raz. 1999. Factors contributing to susceptibility of postmenopausal women to recurrent urinary tract infections" Clin. Infect. Dis 28:723-725.
- Cauci, S., S. Driussi, D. De Santo, P. Penacchioni, T. Iannicelli, P. Lanzafame, F. De Seta, F. Quadrifoglio, D. de Aloysio, and S. Guaschino. 2002. Prevalence of bacterial vaginosis and vaginal flora changes in peri- and postmenopausal women" J. Clin. Microbiol 40:2147-2152.
- Ginkel, P. D., D. E. Soper, R. C. Bump, and H. P. Dalton. 1993. Vaginal flora in postmenopausal women: The effect of estrogen replacement. Infect. Dis. Obstet. Gynecol. 1:94-97.
- Cherpes, T. L., S. L. Hillier, L. A. Meyn, J. L. Busch, and M. A. Krohn. 2008. A delicate balance: Risk factors for acquisition of bacterial vaginosis include sexual activity, absence of hydrogen peroxide-producing lactobacilli, black race, and positive herpes simplex virus type 2 serology. Sex. Transm. Dis. 35:78-83.
- Verstraelen, H. 2008. Bacterial vaginosis: A sexually enhanced disease. Int. J. STD AIDS 19:575-576.
- Verstraelen, H., R. Verhelst, M. Vaneechoutte, and M. Temmerman. 2010. The epidemiology of bacterial vaginosis in relation to sexual behaviour. BMC Infect. Dis. 10:81.
- Martin, R., and J. E. Suarez. 2010. Biosynthesis and degradation of H2O2 by vaginal lactobacilli" Appl. Environ. Microbiol 76:400-405.
- McLean, N. W., and I. J. Rosenstein. 2000. Characterisation and selection of a Lactobacillus species to re-colonise the vagina of women with recurrent bacterial vaginosis. J. Med. Microbiol. 49:543-552.
- "Vaginal Problems — Home Treatment". Women's Health. WebMD, LLC. Retrieved 2009-08-28.
- See, e.g., Colin Hinrichsen, Peter Lisowski, Anatomy Workbook (2007), p. 101: "Digital examination per vaginam are made by placing one or two fingers in the vagina".
- Vaginal pH Test from Point of Care Testing, July 2009, at: University of California, San Francisco – Department of Laboratory Medicine. Prepared by: Patricia Nassos, PhD, MT and Clayton Hooper, RN.
- Todar, Kenneth (2008). "The Nature of Bacterial Host-Parasite Relationships in Humans". Online Textbook of Bacteriology. Retrieved 2009-08-28.
- "Bartholin cyst". Mayo Clinic.com. 19 January 2010. Retrieved 2011-08-18.
- Manetta A, Pinto JL, Larson JE, Stevens CW, Pinto JS, Podczaski ES (July 1988). "Primary invasive carcinoma of the vagina". Obstet Gynecol 72 (1): 77–81. PMID 3380510.
- Spence D, Melville C (December 2007). "Vaginal discharge". BMJ 335 (7630): 1147–51. doi:10.1136/bmj.39378.633287.80. PMC 2099568. PMID 18048541.
- "Hiv/Aids". MayoClinic.com. 11 August 2010. Retrieved 2011-08-18.
- Butcher J (January 1999). "Female sexual problems II: sexual pain and sexual fears". BMJ 318 (7176): 110–2. doi:10.1136/bmj.318.7176.110. PMC 1114576. PMID 9880287.