Abstract

Pain is a complex subjective experience, associated with neurovegetative, affective and cognitive rapid changes. Biological, psychosocial and contextual factors may contribute. Chronic inflammation, of whatever cause, is the leading contributor to chronic pain. The mast cell directs both the inflammatory process and the shift to chronic pain, mediating through the production of Nerve Growth Factor (NGF) and other neurotrophic molecules. Women, in the fertile age, are biologically more vulnerable to chronic inflammation, as fluctuations of estrogens are agonist factors of mast cells degranulation, mostly in the premenstrual phase. Pain is defined as "nociceptive" when it indicates an ongoing damage; "neuropathic" when it becomes a disease per se. Chronic Pelvic Pain (CPP) indicates an invalidating, persistent or recurrent pelvic pain, persisting for more than 6 months. CPP is the main complaint of 10-15% of gynaecologic consultations, leading to 40% of diagnostic laparoscopies and 15% of hysterectomies. Comorbidity, i.e. the coexistence of pathologies and painful syndromes in different pelvic organs, is another common feature. Cystitis, vulvar vestibulitis, endometriosis, irritable bowel syndrome all play an important role and contribute to identifying the hyperactive mast cell and related chronic inflammation as the common pathophysiologic factor. The paper reviews nociception characteristics, the emerging role of mast cells, the pathophysiology of comorbidity, biological, psychosexual and contextual predictors, and stresses the need to move from a "hyperspecialistic" perspective to a multisystemic reading of CPP, with special attention to the urologic perspective.

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