Ridley's The Vulva. Группа авторов
and genetic factors and by obesity. There are significant ethnic differences in the onset of puberty, with 48% of African American girls having some signs of puberty at age 8 as opposed to only 14% of Caucasians [25]. Girls who present early do need follow‐up to exclude precocious puberty.
The adrenal glands mature first, usually about two years before menarche. The ovaries enlarge with an increase in the number of growing follicles, although they subsequently regress. The average age of menarche varies considerably, but it is estimated that about 95% of adolescent females have their menarche between the ages of 11 and 15 years. Menarche usually occurs within 2 years of breast budding.
It is thought that the pilosebaceous units are present at birth but do not develop until activated by hormonal stimulation at puberty. The apocrine glands of the axilla and vulva begin to function at about the time that axillary and pubic hair appears, and the sebaceous glands at all body sites become more active. The development of puberty is described according to Tanner [26], and growth of pubic hair is described in five stages:
1 No pubic hair
2 Sparse hair on the labia majora and on the mons pubis in the midline
3 Increase in hair density and texture, especially on mons pubis
4 Further increase so that only the upper lateral corners of the usual triangular distribution are deficient
5 Normal adult pubic hair pattern with its extension from the labia on to the medial aspects of the thighs, this is usually completed between 12 and 17 years
In the vulva, fat deposition increases the size of the labia majora and the prominence of the mons pubis. The labial skin becomes rugose, the clitoris increases in size, and the urethral orifice becomes more obvious. Coincidentally, Bartholin’s glands become active, and the hymenal ring enlarges.
The development of the ovarian follicles is associated with increasing levels of oestrogen production, which is responsible for the thickening of the vaginal epithelium and the glycogenation of the cells. The vaginal secretions increase in quantity and become more acidic, with a pH of between 4 and 5.
Reproductive years
The menstrual cycle is under endocrine and paracrine influence. Pituitary gonadotrophins, hypothalamic releasing factors, and numerous growth factors regulate intraovarian events, which occur in a cyclical pattern unless interrupted by pregnancy.
The first phase is the follicular phase, where oestradiol increases to reach a peak before the surge in luteinising hormone and ovulation. The endometrial layer grows at this time.
At ovulation, a mature oocyte is released, and the follicular remnants form a corpus luteum which produces progesterone that prepares the endometrium for possible implantation. The second phase of the cycle is the luteal phase where progesterone predominates. There is a small second peak in oestrogen secretion about 5 days after ovulation, and if pregnancy occurs, the corpus luteum persists and maintains the hormone levels. If it does not, then it will regress, and then both oestrogen and progesterone levels fall rapidly, and as the endometrial layer is not maintained, it will be lost as the next menses.
The cervical mucus secretion varies daily but becomes transparent, watery, and thin around ovulation to allow entry of sperm into the higher reproductive tract. In the luteal phase, it thickens and has more of a barrier function due to its consistency but also from the immunoglobulins it contains. There are several alterations in the protein and enzyme content of the mucus, but mucin glycosylation at ovulation is the main change [27]. It is these changes in the cervical mucus that lead to a subjective feeling of wetness on the vulva around the time of ovulation. A profuse discharge can lead to an irritant dermatitis.
The vaginal epithelium is very responsive to the influence of ovarian hormones. Oestrogen causes a thickening of the epithelium and its differentiation into the well‐recognised basal, intermediate, and superficial layers characteristic of the reproductive years. The percentage of superficial cells present in a vaginal smear is an indicator of the amount of oestrogenic activity. Progesterone produces a relative decrease in the number of superficial cells while increasing the number of intermediate cells.
The normal vaginal flora is mixed, but lactobacilli predominate and use glycogen to produce lactic acid and therefore lower the vaginal pH. During menses, there is a reduction in lactobacilli and an increase in G. vaginalis [28]. The acidity of the vaginal environment may be reduced by the alkaline secretions of the cervical glands, particularly in the presence of a large cervical erosion, menstrual flow, and ejaculate.
The thickness of the vulval epithelium is stable throughout the menstrual cycle but there may be an increase in parakeratosis, indicating increased skin turnover, at mid‐cycle [29]. One study of the vestibular mucosa showed no difference in the number of cell layers in users of oral contraceptives or with the normal cycle. There was an increased distance between the dermal papillae and the surface, possibly due to larger keratinocytes in those on oral contraceptives. An increase in vasculature was also seen, which may explain why the mucosa can sometimes look more erythematous in those taking oral contraceptives [30].
Sexual response
The sexual response is a sequence of events – desire, arousal, orgasm, and resolution – brought about by physiological changes triggered locally and centrally. The pathways are complex, but it is increasingly recognised that the clitoris is central to the process [31], and is regarded as the homologue of the penis in females [32]. Imaging techniques, particularly MRI and functional MRI, have led to a better understanding of clitoral anatomy and function [33]. There is conflicting evidence as to whether clitoral size plays a part in sexual function. One study found a smaller clitoral glans on MRI with an increased distance from the vagina in patients who were anorgasmic [34]. However, other studies have not shown any correlation between clitoral size and sexual function [35].
The clitorourethrovaginal complex is a term used to describe the interplay between the three structures and their role in the sexual response [36]. There is a long‐standing debate about the existence of an erogenous zone in the anterior vagina (G‐spot), but there is no evidence for any distinct structure.
The sexual response is a sequence of events involving initial stimulation of the sensory receptors and nerves of the clitoris, mainly via the sensory function of the epithelium, which stimulates the release of neurotransmitters [37]. Afferent fibres then transmit to the spinal cord roots at S2‐4, leading to activation of the parasympathetic system leading to vasodilatation in the erectile tissue. Genital arousal in females involves an increase in blood flow, clitoral engorgement and erection, and swelling of the labia minora, which is sufficient to induce some traction on the clitoris. The suspensory ligament in the female can restrict movement of the clitoris so that it can move up with arousal but it does not straighten [38]. If the threshold for orgasm is reached, there is then a central component which activates skeletal and autonomic smooth muscle contraction [39].
There is conflicting evidence about sexual desire and arousal in relation to the menstrual cycle, but it is generally accepted that sexual desire does peak mid‐cycle and in the pre‐menstrual phase. Hypoactive sexual desire disorder can be related to numerous physical, endocrine, and psychosocial factors [40], and it is helpful to screen patients and then refer appropriately.
Pregnancy
Several changes occur during pregnancy, mainly related to increased production of hormones via the placenta. There are changes in blood flow, pigmentation, and in the immune response (see above). A fivefold increase in blood flow through the pelvic circulation occurs during the first two months of pregnancy, and this doubles again during the third month. Progesterone causes increased venous distension, which predisposes to vulval varicosities (see Chapter 34). There is increased blood flow in the vulva which can give a bluish appearance. One case of a spontaneous vulval haematoma is described in pregnancy [41]. Isolated vulval oedema can occur in