Osteoporosis: The Need for Prevention and Treatment

Abstract

Osteoporosis is a preventable, potentially crippling disease characterized by low bone density and increased bone fragility that affects millions of people. The seeds of this pernicious disease are sown during adolescence, when the skeleton is most active in absorbing dietary calcium and building up nearly all the bone mass that will carry the teenager throughout life. Dietary intake of calcium, vitamin D and vitamin K, particularly vitamin K2, is critical during this life stage for optimal bone growth; unfortunately, the majority of adolescents in the USA do not consume adequate amounts. In addition, many adolescents are now using oral contraceptives or intrauterine devices that prevent ovulation, thus inhibiting formation of progesterone required for the development of osteoblasts. Oral contraceptives also lower blood levels of vitamins B6 and B12, both of which are necessary to prevent elevated levels of homocysteine, whose impact on bone can be significant. In addition to "the pill," many commonly prescribed medications disrupt normal bone remodeling and promote osteoporosis. Other remediable factors that cause excessive bone loss include insufficiencies of key nutrients, such as vitamin D3, vitamin K2, and calcium, required for healthy bone remodeling. It is important to recognize key risk factors and manage those that can be modified to prevent disease and/or minimize risk of fracture. This article presents an overview of osteoporosis, pathophysiology of disease, diagnostic tests, risk factors, and clinical recommendations for healthy bones.

HDL-Associated Paraoxonase 1 as a Bridge between Postmenopausal Osteoporosis and Cardiovascular Disease

“…Direct reactions with the cells through receptor-mediated responses or via the formation of other inflammatory agents such as cytokines might cause the observed impacts of the oxidized lipids on bone cells. 33 , 34 , 35 , 36 Therefore, a reduction in PON1 in serum of patients with osteoporosis could be associated with the increase of those cytokines. 36 Owing to estrogen deficiency in the postmenopausal period, a higher prevalence of increased serum IL-17A levels has been observed.…”

“… 33 , 34 , 35 , 36 Therefore, a reduction in PON1 in serum of patients with osteoporosis could be associated with the increase of those cytokines. 36 Owing to estrogen deficiency in the postmenopausal period, a higher prevalence of increased serum IL-17A levels has been observed. Such enhancement in IL-17A might induce chronic inflammatory events, causing CVD and osteoporosis.…”

THE OSTEOPROTECTIVE EFFECT OF Azadirachta excelsa LEAVES EXTRACT ON BONE OF STREPTOZOTOCIN-INDUCED DIABETIC RATS

“…Recent evidences had verified that chronic hyperglyceamia induces bone fracture by delaying the bone healing process [7,8]. The DM also appears to be a major contributing factor in bone degeneration osteopenia and osteoporosis [9]. In spite of many observations, the exact mechanism of how DM induces osteoporosis remains elusive.…”