Little is known about the cause of vestibulodynia. A number of causes may be involved, including sub-clinical human papillomavirus infection, chronic recurrent candidiasis, or chronic recurrent bacterial vaginosis. Muscular causes have been implicated as well, since chronic vulvar pain may be the result of chronic hypertonic perivaginal muscles, leading to vaginal tightening and subsequent pain. Some investigators have postulated the existence of neurological causes, such as vestibular neural hyperplasia. Finally, psychological factors may contribute to or exacerbate the problem, since the anticipation of pain often results in a conditioned spasmodic reflex along with sexual desire and arousal problems.

Diagnosis is readily made by the cotton-swab test, in which pressure is applied in a circular fashion around the vulvar vestibule to assess complaints of pain. Laboratory tests are used to exclude bacterial or viral infection, and a careful examination of the vulvo/vaginal area is conducted to assess whether any atrophy is present.

A wide variety of possible causes and treatments for vulvodynia are currently being explored. Moreover, there are probably several causes of vulvodynia, and some may be individual to the patient.

Possible causes include Sjogren's syndrome, the symptoms of which include chronic vaginal dryness. Others include genetic predisposition to inflammation, allergy or other sensitivity (for example: oxalates in the urine), an autoimmune disorder similar to lupus erythematosus or to eczema or to lichen sclerosus, infection (e.g., yeast infections, bacterial vaginosis, HPV, HSV), injury, and neuropathy—including an increased number of nerve endings in the vaginal area. Some cases seem to be negative outcomes of genital surgery, such as a Labioplasty. Initiation of hormonal contraceptives that contain low- dose estrogen before the age of 16 could predispose women to vulvar vestibulitis syndrome. A significantly lower pain threshold, especially in the posterior vestibulum, has also been associated with the use of hormonal contraceptives in women without vulvar vestibulitis syndrome. Pelvic floor dysfunction may be the underlying cause of some women's pain.

The percentage of women affected is not entirely clear, but estimates range as high as 16%. Many other conditions that are not truly vulvodynia (diagnosis is made by ruling out other causes of vulvar pain) could be confused with it. Vulvar pain is a quite frequent complaint in women's health clinics. Vulvodynia is a new term in the medical literature.

Between 250,000 and 1 million American women are diagnosed with CIN annually. Women can develop CIN at any age, however women generally develop it between the ages of 25 to 35.

The disorder typically appears among young girls and adolescents but cases in children as young as 17 months have been reported.

Vulvitis, inflammation of the vulva, can have a variety of etiologies in children and adolescents, including allergic dermatitis, contact dermatitis, lichen sclerosus, and infections with bacteria, fungi, and parasites. Dermatitis in infants is commonly caused by a soiled diaper being left on for an extended period of time. Increasing the frequency of diaper changes and topical application of emollients are sufficient to resolve most cases. Dermatitis of the vulva in older children is usually caused by exposure to an irritant (e.g. scented products that come into contact with the vulva, laundry detergent, soaps, etc.) and is treated with preventing exposure and encouraging sitz baths with baking soda as the vulvar skin heals. Other treatment options for vulvar dermatitis include oral hydroxyzine hydrochloride or topical hydrocortisone.

Lichen sclerosus is another common cause of vulvitis in children, and it often affects an hourglass or figure eight-shaped area of skin around the anus and vulva. Symptoms of a mild case include skin fissures, loss of skin pigment (hypopigmentation), skin atrophy, a parchment-like texture to the skin, dysuria, itching, discomfort, and excoriation. In more severe cases, the vulva may become discolored, developing dark purple bruising (ecchymosis), bleeding, scarring, attenuation of the labia minora, and fissures and bleeding affecting the posterior fourchette. Its cause is unknown, but likely genetic or autoimmune, and it is unconnected to malignancy in children. If the skin changes are not obvious on visual inspection, a biopsy of the skin may be performed to acquire an exact diagnosis. Treatment for vulvar lichen sclerosus may consist of topical hydrocortisone in mild cases, or stronger topical steroids (e.g. clobetasol propionate). Preliminary studies show that 75% of cases do not resolve with puberty.

Organisms responsible for vulvitis in children include pinworms ("Enterobius vermicularis"), "Candida" yeast, and group A hemolytic "Streptococcus". Though pinworms mainly affect the perianal area, they can cause itching and irritation to the vulva as well. Pinworms are treated with albendazole. Vulvar "Candida" infections are uncommon in children, and generally occur in infants after antibiotic therapy, and in children with diabetes or immunodeficiency. "Candida" infections cause a red raised vulvar rash with satellite lesions and clear borders, and are diagnosed by microscopically examining a sample treated with potassium hydroxide for hyphae. They are treated with topical butoconazole, clotrimazole, or miconazole. "Streptococcus" infections are characterized by a dark red discoloration of the vulva and introitus, and cause pain, itching, bleeding, and dysuria. They are treated with antibiotics.

Some groups of women have been found to be at a higher risk of developing CIN:

- Women who become infected by a "high risk" type of HPV, such as 16, 18, 31, or 33

- Women who are immunodeficient

- Women who give birth before age 17

A number of risk factors have been shown to increase a woman's likelihood of developing CIN, including poor diet, multiple sexual partners, lack of condom use, and cigarette smoking.

The exact cause of VIN is unknown. Studies are being done to determine the cause of VIN. The following factors have been associated with VIN:

- HPV (Human Papilloma Virus)

- HSV-2 (Herpes simplex Virus - Type 2)

- Smoking

- Immunosuppression

- Chronic vulvar irritation

- Conditions such as Lichen Sclerosus

Vaccinating girls with HPV vaccine before their initial sexual contact has been claimed to reduce incidence of VIN.

Vaginal intraepithelial neoplasia (VAIN) is a condition that describes premalignant histological findings in the vagina characterized by dysplastic changes.

The disorder is rare and generally has no symptoms. VAIN can be detected by the presence of abnormal cells in a Papanicolaou test (Pap smear).

Like cervical intraepithelial neoplasia, VAIN comes in three stages, VAIN 1, 2, and 3. In VAIN 1, a third of the thickness of the cells in the vaginal skin are abnormal, while in VAIN 3, the full thickness is affected. VAIN 3 is also known as carcinoma in-situ, or stage 0 vaginal cancer.

Infection with certain types of the human papillomavirus ("high-risk types") may be associated with up to 80% of cases of VAIN. Vaccinating girls with HPV vaccine before initial sexual contact has been shown to reduce incidence of VAIN.

One study found that most cases of VAIN were located in the upper third of the vagina, and were multifocal. In the same study, 65 and 10% patients with VAIN also had cervical intraepithelial neoplasia and vulvar intraepithelial neoplasia, respectively.

In another study, most cases of VAIN went into remission after a single treatment, but about 5% of the cases studied progressed into a more serious condition despite treatment.

Lichen sclerosus may have a genetic component. Higher rates of lichen sclerosus have been reported among twins and among family members.

The disease can last for a considerably long time. Occasionally, "spontaneous cure" may ensue, particularly in young girls.

Lichen sclerosus is associated with a higher risk of cancer. Skin that has been scarred as a result of lichen sclerosus is more likely to develop skin cancer. Women with lichen sclerosus may develop vulvar carcinoma. Lichen sclerosus is associated with 3–7% of all cases of vulvar squamous cell carcinoma. In women, it has been reported that 33.6 times higher vulvar cancer risk is associated with LS. A study in men reported that "The reported incidence of penile carcinoma in patients with BXO is 2.6–5.8%".

Vulvitis is inflammation of the vulva, the external female mammalian genitalia that include the labia majora, labia minora, clitoris, and introitus (the entrance to the vagina). It may co-occur with vaginitis, inflammation of the vagina, and may have infectious or non-infectious causes.

The primary contributing factor to labial fusion is low estrogen levels. A vulva with low estrogen exposure, such as that of a preadolescent, has delicate epithelial lining and is therefore vulnerable to irritation. Conditions causing irritation, such as infection, inflammation and trauma, cause the edges of the labia minora to fuse together. The fusion typically begins at the posterior frenulum of the labia minora and continues anteriorly.

Most labial adhesions resolve spontaneously before puberty as estrogen levels increase and the vaginal epithelium becomes cornified.

Labial fusion can lead to urinary tract infection, vulvar vestibulitis and inflammation caused by chronic urine exposure. In severe cases, labial adhesions can cause complete obstruction of the urethra, leading to anuria and urinary retention.

Treatment is symptomatic, and usually of little value; in most cases, the ulcer heals spontaneously within four to six weeks, sometimes leaving scars. Topical analgesics and anesthetics, as well as topical application of disinfectants/astringents such as potassium permanganate (in sitz baths), is commonly used. In severe cases, a combination of systemic glucocorticoids and broad-spectrum antibiotics has been recommended.

Gardasil 6 is an HPV vaccine aimed at preventing cervical cancers and genital warts. Gardasil is designed to prevent infection with HPV types 16, 18, 6, and 11. HPV types 16 and 18 currently cause about 70% of cervical cancer cases, and also cause some vulvar, vaginal, penile and anal cancers. HPV types 6 and 11 are responsible for 90% of documented cases of genital warts.

Gardasil 9, approved in 2014 protects against HPV types 6, 11, 16, 18, 31, 33, 45, 52, and 58.

HPV vaccines do not currently protect against the virus strains responsible for plantar warts (verrucas).

A Cochrane review found little high quality evidence regarding the treatment of vaginismus in 2012. Specifically it is unclear if systematic desensitisation is better than other measures including nothing.

Some conditions such as lichen sclerosus, squamous dysplasia or chronic vulvar itching may precede cancer. In younger women affected with vulvar cancer, risk factors include low socioeconomic status, multiple sexual partners, cigarette use and cervical cancer. Patients that are infected with HIV tend to be more susceptible to vulvar cancer as well. Human papillomavirus (HPV) infection is associated with vulvar cancer.

True epidemiological studies of vaginismus have not been done, as diagnosis would require painful examinations that such women would most likely avoid. Data available is primarily reported statistics from clinical settings.

A study of vaginismus in people in Morocco and Sweden found a prevalence of 6%. 18-20% of people in British and Australian studies were found to have manifest dyspareunia, while the rate among elderly British people was as low as 2%.

A 1990 study of people presenting to sex therapy clinics found reported vaginismus rates of between 12% and 17%, while a random sampling and structured interview survey conducted in 1994 by National Health and Sexual Life Survey documented 10%-15% of people reported that in the past six months they had experienced pain during intercourse.

The most recent study-based estimates of vaginismus incidence range from 5% to 47% of people presenting for sex therapy or complaining of sexual problems, with significant differences across cultures. It seems likely that a society's expectations of person's sexuality may particularly impact on the people with the condition.

Studies show a link between HPV infection and penile and anal cancers. Sexually transmitted HPVs are found in a large percentage of anal cancers. Moreover, the risk for anal cancer is 17 to 31 times higher among gay and bisexual men than among heterosexual men

- though one survey did not find a difference between the HPV infection rate of men who had sex with men versus those who had sex only with women.

Anal Pap smear screening for anal cancer might benefit some subpopulations of men or women engaging in anal sex. No consensus exists, though, that such screening is beneficial, or who should get an anal Pap smear.

Vulvar cancer causes less than 1% of all cancer cases and deaths but around 6% of all gynecologic cancers diagnosed in the UK. Around 1,200 women were diagnosed with the disease in 2011, and 400 women died in 2012. Vulvar cancer causes about 0. 6% of all cancer cases but 5% of gynecologic cancers in the United States. About 4900 cases are diagnosed each year in the United States.

High-risk carcinogenic HPV types (including HPV 16 and HPV 18) are associated with an increasing number of head and neck cancers.

Sexually transmitted forms of HPV account for about 25% of cancers of the mouth and upper throat (the oropharynx). The latter commonly present in the tonsil area, and HPV is linked to the increase in oral cancers in nonsmokers. Engaging in anal or oral sex with an HPV-infected partner may increase the risk of developing these types of cancers. Oral infection with several types of HPV, in particular type 16, have been found to be associated with HPV-positive oropharyngeal cancer, a form of head and neck cancer. This association is independent of tobacco and alcohol use. In the United States, HPV is expected to replace tobacco as the main causal agent for oral cancer, and the number of newly diagnosed, HPV-associated head and neck cancers is expected to surpass that of cervical cancer cases by 2020.

In recent years, the United States has experienced an increase in the number of cases of throat cancer caused by HPV type 16. Throat cancers associated with HPV have been estimated to have increased from 0.8 cases per 100,000 people in 1988 to 2.6 per 100,000 in 2004. Researchers explain these recent data by an increase in oral sex. Moreover, findings indicate this type of cancer is much more prevalent in men than in women, something that needs to be further explored. Currently, two immunizations, Gardasil and Cervarix, are recommended to girls to prevent HPV-related cervical cancer, but not as a precaution against HPV-related throat cancer.

The mutational profile of HPV-positive and HPV-negative head and neck cancer has been reported, further demonstrating that they are fundamentally distinct diseases.

The virus is relatively hardy and immune to many common disinfectants. Exposure to 90% ethanol for at least 1 minute, 2% glutaraldehyde, 30% Savlon, and/or 1% sodium hypochlorite can disinfect the pathogen.

The virus is resistant to drying and heat, but killed by and ultraviolet radiation.