Vulvovaginitis occurs when the balance of the vaginal ecosystem is disturbed. Infection either in peripheral or directly in vagina can arouse strong immune/inflammatory reaction systematically or locally. The released cytokines and chemokines then act on the pituitary gland and reproductive organs, which may finally lead to menoxenia (abnormal menstruation), irregular ovulation, and infertility. These mediators have an important role in the control of reproductive neuroendocrine, ovarian physiology, fetal implantation and development, and placenta function.
Premature ovarian failure
Female mammals are born with a finite number of oocytes that gradually decreases during prepubertal development and adult life. Each oocyte is encircled by somatic granulosa cells (GCs) to form the basic functioning unit of the ovary - the follicle. The size of the oocytes at birth and the rate of endowment depletion dominate the ovarian functional lifespan. On the other hand, programmed cell death (apoptosis) has been considered one of the most prevalent mechanisms that contribute to the age-related exhaustion of oocytes. Therefore, a precise balance has to be achieved between prosurvival and proapoptotic molecules to maintain the final destiny of the follicle.
It is well recognized that immune/inflammatory response participates in many aspects of reproductive physiology, such as ovulation, menstruation, and implantation. Recent studies suggest that the inflammatory stress caused by infection may also affect ovarian reserve and cyclicity in women.