Abstract
million person the all over the world affected by osteoporosis as it is most common metabolic bone disorder. The general reason of bone loss are age and menopause, and the rates of bone loss variable between individuals. Physical activity and environmental factors as nutrition can contribute to bone health as they modify both peak bone mass and following bone loss. Medications embrace both antire- sorptive and anabolic types. Antiresorptive medications acts by reducing rates of bone remodeling like estrogens, selective estrogen receptor modulators (raloxifene), bisphosphonates (alendronate, risedronate, and ibandronate) and calcitonins. Para- thyroid hormone is the only anabolic medication. The nonmedical treatment must be used with pharmacologic treatment to maximize outcomes for osteoporotic patient. Some plant-derived natural products, mostly phytoestrogens (isoflavones, lignans, coumestanes, stilbenes) and many more novel estrogen-like compounds in plants have been greatly used to prevent depletion in bone mineral density. In this review an attempt has been made out to compile the mechanisms of glucocorticoids induced osteoporosis, the medicinal plants which are commonly utilized in osteoporosis with their prominent chemical ingredients and certain phar- macological actions.
Highlights
Bone consists of cells, extracellular organic components and non-organic components
Effect of glucocorticoids on osteoblasts The hypo function and apoptosis of osteoblasts is the first action of GC-induced bone loss as GCs induce a 30% increase in apoptosis of osteoblast and osteocyte[20]
Diagnosis of osteoporosis by biochemical markers The general laboratory evaluation are performed to do a differential diagnosis of bone fragility includes complete blood cell count and calcium, phosphorous, alkaline phosphatase, thyrotropin, renal and liver function, 25-hydroxyvitamin D and urinary calcium excretion[26]
Summary
Bone consists of cells (osteocytes, osteoblasts and osteoclasts), extracellular organic components (collagen and non-collagenous matrix protein) and non-organic components (calcium hydroxyapatite). The bone remodeling prevents fatigue damage and important in preserving calcium homeostasis and the loss of osteoblast – osteoclasts coupling lead to several metabolic bone diseases including osteoporosis, tumor related bone disease, rheumatoid arthritis[1,2]. Direct effects involve activation of monomeric glucocorticoid receptor signaling participates in excessive bone remodeling, it impairs osteoblast survival and differentiation, inhibit the production of bone matrix components, increase osteoblastic and osteocytic apoptosis, enhanced secretion of the osteoclast-promoting factor receptor activator of nuclear factor kappa B ligand (RANKL) by osteogenic cells, activation of osteoclastic cells and diminishing absorption of calcium.
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