Essay On Estrogen Deprivation

Currently, the mechanism behind AIA is not clearly understood, though estrogen deprivation is thought to be a major cause of AIA. Joint pain could be related to various articular structures innervated with nociceptive fibers, such as joint capsule, synovium, periosteal bone, ligaments, and periarticular structures (Felson & Cummings, 2005). Estrogen is known to influence on changes of neurogenic pain response. High serum estrogen levels may cause the body to release endorphins and enkephalins that can help improve painful stimuli received by the brain (Felson & Cummings, 2005). Similarly, a decrease in estrogen level typically reduces the body’s ability to improve pain perception (Zubieta et al., 2005). This is particularly evident during pregnancy, when women have elevated thresholds for painful stimuli in the presence of increased levels of estrogen (Dawson-Basoa & Gintzler, 1996b).
Further, ERs are expressed in opioid-containing neurons in the spinal cord and brain (Eckersell, Popper, & Micevych, 1998; Flores, Shughrue, Petersen, & Mokha, 2003), indicating an even more direct effect of estrogen on opioid generation locally. In some species, aromatase has been found in dorsal horn cells; androgens, which are converted by aromatase to estrogens, could provide a source of estrogen in the spinal cord (Evrard et al., 2000). Given the possible effects of estrogen on nociceptive input, evidence has shown that estrogen may be a contributing factor to pain in animal models. In the Ma et