Pelvic Mechanisms Involved in the Pathophysiology of Pain in Endometriosis
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Endometriosis involves richly innervated pelvic tissues with high nerve growth factor expression, contributing to varied pain perception and potentially neuropathic pain.
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Abstract
Endometriosis has been recognized as the principal cause of pelvic pain in most modern industrialized societies for the past 20 years, but mechanisms are remarkably poorly understood. There is great variability in the types and severity of pelvic pain experienced by women with endometriosis, and this is probably a reflection of a variable genetic background enhanced by highly variable environmental and reproductive experiences. Individual women exhibit great variability in perception and tolerance of pain experiences and in the possible development of hyperalgesia, allodynia and even neuropathic pain. The uterus (and especially the eutopic endometrium) and ectopic endometriotic lesions are richly innervated with a range of sensory and autonomic nerve fibers in a way which is never seen in women without endometriosis. These tissues show abundant expression of nerve growth factor, other neurotropins and their receptors, molecules that usually play a central role in sensitizing nociceptors to potential pain stimuli, as well as stimulating nerve fiber growth. Genetic control of secretion and function of neurotropins and the involvement of immune cells, such as macrophages, dendritic cells, B-cells, natural killer cells, mast cells and regulatory T-cells in controlling neurotropins are fields of current active research. Little is known about these mechanisms, other types of molecular stimuli and the processes influencing perception of chronic pelvic pain in endometriosis. A better understanding of these mechanisms will undoubtedly lead to more specific, and hopefully more effective, approaches to management of these very distressing symptoms.
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