Pathogenesis of endometriosis in adolescence: role of systemic inflammation, neoneuro- and neoangiogenesis
This study investigated the role of systemic inflammation, neoneurogenesis, and neoangiogenesis in the pathogenesis of endometriosis in adolescents.
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The paper reviews current concepts of endometriosis pathogenesis in adolescence, emphasizing systemic inflammation and the roles of neo-neurogenesis and neoangiogenesis, drawing together implantational, metaplastic (celomic), immunologic, disontogenetic, and hematogenous/lymphogenous hypotheses. It highlights findings such as estrogen-dependent chronic inflammation, dysregulated immune responses with impaired NK-cell cytotoxicity, macrophage-driven proinflammatory cytokine production (including TNF-α and IL-1β/IL-6/IL-8), altered adhesion/invasion mechanisms (e.g., ICAM-1, E-cadherin, CD-44), and reduced macrophage phagocytic function via prostaglandin E2–mediated effects, alongside mechanisms linking estrogen exposure to angiogenesis and pain-related nerve signaling. A stated limitation is that no single pathogenic theory has been conclusively confirmed, and adolescent epidemiology is difficult to determine due to a lack of population studies. This paper is centrally about endometriosis — it focuses on adolescent endometriosis pathogenesis and the roles of systemic inflammation, neurogenesis, and angiogenesis.
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