**6. Pain Receptors in Endometriosis-Associated Nerve Fibres**

The understanding of pain generation, as this is the main problem in EM patients, is of great importance: the ectopic lesions themselves release pain mediators and activate nociceptors (transduction and transmission). In most cases, this is strongly estrogen-dependent and leads to cyclical nociceptive pain (dysmenorrhoea and cyclical pelvic pain), which is treated by hormones or non-steroidal antiphlogistics (NSAP). However, with ongoing disease, the cyclical pain characterization shifts into an acyclical chronic pain (pain development under hormonal treatment, NSDAP resistant pain, increasing pain severity) [55,56]. We analyzed this phenomenon in nearly 100 patients with acyclical pain under hormonal treatment and found it in 100% of the peritoneal ectopic lesions with extended inflammatory reactions [16]. This phenomenon might especially be due to neurogenic inflammation and activation of peripheral sensory nerve fibres. The peripheral sensitization seems to be stressed and for this, the development of non-hormonal anti-inflammatory compounds is of great interest. So, besides the understanding of the inflammatory reaction, the peripheral sensitization of nerve fibres is also of great importance.
