Abstract
Osteoporosis is the most prevalent metabolic bone disease that affects half the women in the sixth and seventh decade of life. Osteoporosis is characterized by uncoupled bone resorption that leads to low bone mass, compromised microarchitecture and structural deterioration that increases the likelihood of fracture with minimal trauma, known as fragility fractures. Several factors contribute to osteoporosis in men and women. In women, menopause – the cessation of ovarian function, is one of the leading causes of primary osteoporosis. Over the past three decades there has been growing appreciation that the adaptive immune system plays a fundamental role in the development of postmenopausal osteoporosis, both in humans and in mouse models. In this review, we highlight recent data on the interactions between T cells and the skeletal system in the context of postmenopausal osteoporosis. Finally, we review recent studies on the interventions to ameliorate osteoporosis.
Highlights
A great achievement of modern medicine is the increased lifespan of the human population
Suggest that Ocy are at the center of bone remodeling unit (BRU) balance and regulate bone resorption and formation according to biological needs
These results demonstrate that E2 loss promotes inflammation leading to the acute phase bone erosion
Summary
A great achievement of modern medicine is the increased lifespan of the human population. Studies suggested that E2 directly regulates OC [19,20,21,22] and OB [23, 24] and its loss results in long lived OC and impaired OB leading to uncoupled bone resorption [25]. We highlight recent advances in our understanding on how T cells and proinflammatory cytokines, namely TNFa and IL-17A, contribute to the pathogenesis of PMOP (Figure 1).
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