Fiona M. Lewis The main roles of the vulval epithelium are to provide a barrier function and to regulate an immune response. There are variations at different sites and at different times during life, with hormonal alterations being the predominant influence [1]. These normal changes can also be modified by oral contraceptives and hormone replacement therapy. The principal hormones involved in these changes are oestrogens, progestogens, and small amounts of androgens. Oestrogen has many effects on skin and mucosa [2]. It increases support by thickening the collagen, hydrates by increasing mucopolysaccharides and hyaluronic acid, and also stimulates melanogenesis. The effects of progesterone are not so well understood, but this hormone is known to increase vascularity and sebum secretion. Immunohistochemical studies have identified receptors for these hormones at different sites within human skin [3]. Further studies in the female genital skin have mapped out their distribution in the vulva and vagina, showing variation with different stages of the menstrual cycle [4], with oral contraceptive use [5], and at menopause [6]. Oestrogen receptors are mainly found in the labia minora and vagina. Androgen receptors are most commonly seen in the keratinocytes of the labia majora as well as the adnexal structures and fibroblasts. Progesterone receptors were found only on vaginal epithelium and inner labia minora. There is little difference in this distribution before and after menopause. The barrier function of skin is dependent on the degree of hydration, the presence of a stratum corneum, and occlusive factors. Vulval keratinised skin differs from that elsewhere in hydration, permeability, and friction, but there is no significant difference between pre‐and post‐menopausal age groups. There is little information on variations in these functions on the mucosal surface of the inner vulva, but it has been assumed that this will be similar to that of the oral mucosa, where there is a considerable increase in permeability. Transepidermal water loss (TEWL) is the rate at which water diffuses across the stratum corneum and is an indicator of hydration and therefore of barrier function. TEWL varies with the number of cell layers in the epidermis, which in turn varies at different body sites. This number is lowest in the genital area [7], and it has been shown that water diffuses faster across the stratum corneum of the labium majus than the forearm [8,9], therefore increasing hydration. The occlusive environment may also play a part in this. The coefficient of friction is higher on the vulva [9], making it more prone to mechanical damage. Friction can also be affected by occlusion, obesity, immobility, and use of sanitary wear. The vulva is less susceptible to irritants than forearm skin [10]. However, urinary ammonia levels will increase the pH and activate faecal enzymes, which will contribute to irritant features in patients with urinary incontinence [11]. The vulva is more permeable to hydrocortisone than the forearm [12], but this does not fall after the menopause as it does on the forearm. The difference in permeability and hydration will influence the effect and absorption of topically applied preparations [12,13], but it also has a practical application in cases of suspected contact irritancy and allergy. Routine patch testing may not be sufficient [14], and additional tests may be needed to allow for the effects of friction and epidermal morphology [15]. These physiological changes mainly studied in Caucasian women have also been confirmed in Asians [16]. The skin is an important site for antigen presentation, and intact immune surveillance is an important defence against infection. The immune response in the genital tract has a unique task as it has to balance protection from infection against tolerance to sperm, the embryo, and foetus. The innate and adaptive immune systems are influenced by hormonal changes, so in the secretory stage of the menstrual cycle, infection is a greater risk as the immune response reduces to prepare for a potential pregnancy [17]. Langerhans cells play a vital role in the skin immune system, and the vulva has the highest density and the vagina the lowest in the female genital tract [18]. This does not vary with the menstrual cycle [19], but cell‐mediated immunity reduces after menopause. Together with vaginal microbiota, the cervical mucus is an important component of the genital immune system. It contains antibodies, in particular secretory immunoglobulin A (IgA). This locally produced antibody is bactericidal in the presence of lysozyme and complement, and can agglutinate bacteria and present them for phagocytosis. It can also reduce the adhesion of the infective agent to the mucosa. Protection against viral infection also requires an effective cytolytic T‐lymphocyte response. Patients who are immunosuppressed secondary to primary immune deficiency or medication have a significant risk of viral infection such as human papillomavirus (HPV) and its associated oncogenic disease [20]. It has also been shown that oral contraception can reduce immune responses to infections such as HIV [21]. Large numbers of spermatozoa enter the female reproductive tract during coitus, and these are destroyed by a coital immune response which is limited by the immunosuppressive function of seminal fluid to the immediate postcoital period [22]. This ensures that the embryo, which expresses paternal alloantigens, is not subject to immune attack during implantation. Seminal fluid can also induce inflammatory cytokines after intercourse [23]. The changes in immunity throughout pregnancy are much more complex [24]. These are summarised in Table 3.1. At birth the vulva is still under the influence of maternal hormones that cross the placenta and persist for about 4 weeks. The vagina will be lined with a stratified squamous epithelium rich in glycogen as a direct effect of maternal oestrogen, and lactobacilli will be part of the normal flora. There will often be an obvious vaginal discharge, which can be bloodstained as the result of the endometrium breaking down as oestrogen levels begin to fall. The labia minora are relatively prominent in childhood and as the hymen is thickened the vaginal orifice is difficult to see. The vestibule and introitus is normally bright red, and this often gives rise to the mistaken suspicion of abnormality. Due to reduced oestrogen levels, adhesions of the labia minora can be seen. These can mimic disorders of sexual differentiation and are sometimes mistaken for pre‐pubertal lichen sclerosus. A line of demarcation between the clitoral hood and the labia minora under the clitoris is seen with adhesions (see Chapter 51). Milia are sometimes seen on the labia majora in childhood. Table 3.1 Normal changes in the vulva through life
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Vulval Physiology and Changes Through Life
Barrier function
Immune responsiveness
Changes through life
Neonate
Childhood
Labia majora
Labia minora
Vagina
Other
Neonate
Fat is increased
Milia (blocked eccrine ducts) may appear
Prominent
Lined by stratified epithelium, rich in glycogen
Lactobacilli present
May be white or slightly blood‐ stained discharge
Childhood
Fat reduces
May form adhesions
Lack of glycogenation makes vagina more alkaline
Puberty
Fat increases and also in the mons, which becomes more prominent
Pubic hair appears
Become more covered by labia majora
Increased pigmentation
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