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EXPERIMENTAL RESEARCH OF 'JIANGUERXIANWAN'ON OSTEOPOROSIS

Osteoporosis is a systemic skeletal disease characterized by low bone mass and micro-architectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fractures. With the growth of age population,, the incidence rate of osteoporosis increase, Osteoporosis and its consequence have become a major source of mortality, morbidity ,medical expenditure and social problem worldwide. There are three categories of osteoporosis: primary osteoporosis, secondary osteoporosis and idiopathic osteoporosis. Primary osteoporosis can be divided into two types. Type I, or postmenopausal osteoporosis, characterized by the disproportionate loss of trabecular bone, is associated with fractures at sites rich in cancellous bone such as the vertebral body and distal radius. Type II, or age-associated osteoporosis which affects all skeletal sites with both cortical and cancellous bone such as the proximal femur, is a result of senile decline in bone mass. Osteoporosis is a multifactorial disease, where genetic, hormonal (such as estrogen, growth hormone, parathyroid hormone and calcitonin etc.), nutritional conditions, physical factors and immunologic functions interact in a complex way. They affect the peak bone mass achieving in the early adult years, the rate of bone loss during old age, and bone remodeling process. And these are the main factors that affect the probability of developing osteoporosis in later life. Osteoporosis belongs to the categories of i-syndrome? 態one hi-syndrome?and Flaccidity-syndrome involving the bone? and its pathogenesis is mainly because of deficiency of Kidney, or accompanied by deficiency of Spleen or Liver. The basic differential diagnoses are deficiency of Kidney, insufficiency of Kidney Yang, deficiency of Kidney Yin, deficiency of Yin and Yang, Deficiency of Kidney and Liver or insufficiency of Kidney and Spleen. Bone remodeling are regulated by hormone (such as growth hormone, estrogen and its receptors, parathyroid hormone, etc.) and cytokines (such as insulin-like growth factors, transforming Growth Factor 13, interferon, etc.) that modulating local metabolism of bone. Growth hormone (GH) and insulin-like growth factors (IGF- I & IGF- II) are the most important regulators among these factors. And there is an amazing resemblance between the physiological characteristics GH/IGFs-axis, the pathological changes when GH and IGFs is deficiency and the pathophysiolgical characteristics of idney Control the Bone Several lines of investigation support the importance of IGF- I in the skeleton and the bone remodeling. IGF- I enhances osteoblastic differentiation, helps to maintain the osteoblast phenotype, and inhibits collagenase activity. These IGF-dependent events result in an increase in matrix apposition and guarantee preservation of the skeleton. Studies have also confirmed that bone is a major depot for IGF- I and that aging produces a rather marked decline in skeletal production and storage of this peptide. IGF- I can also recruit premature osteoclasts and serve as a coupling agent in the bone remodeling cycle. Prevention is the most effective approach to osteoporosis. This may be done by optimizing peak bone mass at skeletal maturity, by preventing bone loss, or by restoring the bone mineral and archit

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