The usual factor in VVA is decreasing oestrogen levels. This leads to a loss of vascularisation of vaginal tissues, reduced secretions and lubrication, and the vaginal epithelium becomes thinner. Tissue elasticity can be lost as connective tissue levels increase.^5,6

The natural microflora also changes. Under normal conditions, vaginal epithelial cells mature, die, and are then sloughed off. The cell breakdown process releases glycogen which is hydrolysed into glucose and commensal lactobacilli then convert this into lactic acid, making the vaginal content acidic at pH 4.5 or less.^5,8

However, oestrogen reduction means fewer epithelial cells are exfoliated. The resulting reduction in lactic acid production means vaginal pH increases (to pH 5.5 -6) and the commensal flora changes. Other bacteria (including streptococcus, staphylococci, corynebacteria, bifidobacterial, coliforms, and diphtheroids) start to grow and outcompete the lactobacilli, with the potential to cause symptomatic infection and inflammation. A trichomonas infection can see the vaginal pH increase to 6.5 or more.^5,8,9,10

The connection of oestrogen levels and the microbiota is shown by the effect of giving systemic oestradiol hormone replacement therapy. Lactobacilli levels will increase and become dominant again, with a reduction in vaginal pH, as well as other irritant symptoms easing.⁹