Edinburgh Napier University

  Ovarian cancer (OC) most frequently arises from the ovarian surface epithelium (OSE), which comprises a single layer of mesothelial, squamous-to-cuboidal cells covering the entire surface of the ovary (1). This dynamic cellular layer and underlying basement membrane is breached and repaired each time a follicle ovulates, which can happen up to around 400 times in an average woman’s lifetime. It is, therefore, perhaps not surprising that there is a positive association between ovulation and OC and that a majority of OCs arise from the OSE. OC has genetic and environmental aetiologies, and there is growing evidence for inflammatory involvement as well. Ovulation is a natural inflammatory process, the suppression of which by pregnancy, breast-feeding, or oral contraception reduces OC risk. On the other hand, environmental factors and medical conditions associated with ovarian inflammation such as use of talc, endometriosis, ovarian cysts, and hyperthyroidism increase OC risk (2). If inflammation promotes cancer (3,4), we argue that antiinflammation is quite likely to be protective. In this chapter, we rehearse evidence that inflammation is integral to ovulation and consider how associated antiinflammatory mechanisms might impact OC initiation and progression.