The Mechanisms of Action of Hormone Replacement Therapy and Selective Estrogen Receptor Modulators - Essay Example

The sex steroid hormone estrogen is important for various physiologic processes, such as bone remodeling; breast ductal tissue proliferation; growth, differentiation, and function of the reproductive system among others. Bone remodeling is a process that occurs throughout life. There are two types of cells in bone, osteoblasts, and osteoclasts. In health, there is a balance between bone-resorbing osteoclasts and bone deposition osteoblasts. Postmenopausal osteoporosis is characterized by low bone mass with architectural deterioration of bone tissue resulting in increased bone fragility. Logically, one can derive that postmenopausal osteoporosis that follows ovarian failure is a result of the acceleration of bone resorption due to enhanced osteoclast function. Osteoclasts (OC) are related to the macrophage family of cells, hence osteoclasts are regulated by the same family of cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1), and these mediate the bone resorptive function of OC.

Investigating the fact that oophorectomized prematurely menopausal women have enhanced bone loss, it has been established that estrogen deprivation enhances the production of proresorptive cytokines, IL-1 and TNF- α in excess in menopausal women, and those lead to a hormone-dependent increase in bone resorption and resultant accelerated loss of bone mass in the first 5 to 10 years of menopause. As regards bone density outcomes, many randomized controlled trials have shown consistently identical improved bone density with estrogen use; consequently, it was postulated that estrogen does this by reducing the production of catabolic cytokines by osteoclasts and mononuclear phagocytes.

Hence it could be concluded that neutralization of TNF-α and IL-1 protects against estrogen deficiency bone loss.