The MicroRNAs in the Pathophysiology of Osteoporosis
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Globally, osteoporosis is the most common systemic skeletal disease. There are many factors that influence osteoporosis’ development and progression. During the pathogenesis of this disease, bone turnover is imbalanced between resorption and the formation of bone tissue. A growing interest has been devoted to the role that microRNA (miRNA) plays in osteoporosis regulation. A microRNA (miRNA) is a group of small single-stranded RNA molecules involved in regulating gene expression in eukaryotic organisms. As microRNAs (miRNAs) are key regulators of gene expression and can modulate processes related to bone metabolism, they have become increasingly important for studying osteoporosis pathogenesis. The available research suggests that miRNAs play an important role in regulating processes associated with bone metabolism, especially by influencing bone resorption and synthesis. Furthermore, microRNAs can also serve as potential therapeutic targets for osteoporosis, besides being a rapid and specific biomarker.Keywords:
Bone remodeling
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N-terminal telopeptide
Type I collagen
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Objective To investigate the effects of thyroid function on bonemetabolism.Methods Biochemical markers of bone metabolism such as carboxy terminal cross linked telopeptide of type Ⅰ collage (ICTP),osteocalin(OSC),parathyroid hormone (PTH) and other markers related to bone metabolism were respectively measured in 40 patients with hyperthyroidism and 40 normal subjects.Results The levels of bond resorption marker(ICTP) and bond formation markers(PICP and OSC) in experimental group were both significantly higher than those in normal subjects(P0.001).The levels of PTH showed no significant difference between two groups(P0.05).Significant positive correlations were found between ICTP and PICP, and between ICTP and FT 3 and FT 4 in patients with hyperthyroidism.Conclusion Patients with hyperthyroidism were characterized by increased function of bone resorption accompanied by increased activity of bone formation and by no secondary functional change of parathyroid.Thyroid hormone might speed up bone turnover directly,thus resulting in bone mass lose mainly by the process of bone resorption.
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Osteoporosis is a condition in which an imbalance appears between bone resorption and formation, with bone resorption exceeding formation. However since the rate of bone loss varies significantly from one individual to another resulting in different degrees of osteoporosis, new biochemical techniques to measure products of bone resorption and bone formation have been used in the last years allowing us to evaluate the degree of bone turnover. Bone tissue is constituted of an inorganic component and an organic matrix of collagen and noncollagenous proteins. Suitable bone marker should report the formation and degradation of all these constituents. Today markers of bone formation and markers of bone resorption are available. According to recent literature and personal data assessment of bone metabolism by the specific biochemical markers is helpful to select osteoporotic patients with high or low bone turnover and these parameters should be used to evaluate whether bone remains sensitive to different therapies.
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Bone remodeling
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Mechanical stress on bone is one of the determinants of bone morphology, bone mineral density and bone strength. Therefore, disuse accelerates bone resorption, especially of cancellous bone, and consequently bone becomes atrophic and fragile. Osteocytes embedded in the bone matrix respond to mechanical load and changes of bone metabolism. The gapjunction of the long processes of osteocytes plays an important role in transmitting mechanical load through intracellular signal transmitters (cAMP, cGMP) and extracellular signal transmitters (PGE(2), IGF- I , IGF- II , TGF-beta) , to induce bone formation by osteoblasts and bone resorption by osteoclasts, or a combination of the two. Bone metabolism markers reflect activities of osteoblasts and osteoclasts, so they provide information on bone turnover and bone metabolism. Bone resorption markers characteristically increase and remain high during bed rest and disuse, whereas ambulation and exercise, as in kinesiotherapy, decrease bone resorption markers. As for treatments of disuse bone atrophy, from the bone metabolic and pharmacological viewpoint, anti-resorption agents are recommended to inhibit bone loss. Bisphosphonates which are strong anti-resorption agents, are expected to inhibit bone resorption. Calcitonin and vitamin K(2) which are also anti-resorption agents effectively, reduce bone loss due to disuse and bed rest.
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Biochemical markers of bone turnover include markers of bone resorption which are produced by osteoclasts during bone resorption and markers of bone formation which are produced by osteoblasts during bone formation (Table1). Recently, ELISA based methods have been developed for measurement of other markers such as Osteoprotegerin and RANK ligand. They are proteins synthesised by osteoblasts and are seen to influence osteoclast formation, activation and bone resorption. Bone markers help to assess the overall rate of bone resorption or formation. But they cannot identify the type of bone or location of altered bone metabolism.
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The assay features of biochemical markers of bone turnover have markedly improved in the past few years. The most sensitive and specific markers of bone formation include serum bone alkaline phosphatase, total osteocalcin (including the intact molecule and the large N-Mid fragment) and the N extension peptide of type I collagen (PINP) measured with a recently developed radioimmunoassay. Among the various markers of bone resorption, measurements of the urinary excretion of the (deoxy) pyridinoline crosslinks and of N- and C- related telopeptides (NTX and CTX respectively) are the most sensitive and specific ones. In addition, a two-site immunoassay of serum CTX is now widely available. Bone markers can be used to predict the rate of bone loss in postmenopausal women. Three independent studies have shown that high bone turnover is associated with increased bone loss over 4 to 15 years in women aged 50 to 70 years. In addition, we have shown in elderly women that increased bone resorption, i.e. above the premenopausal range, is associated with a two-fold increase in the risk of hip fractures and that those with both a low BMD (T score < -2.5) and increased bone resorption have a 4- to 5- fold increase in hip fracture risk. We have recently confirmed that increased bone turnover predicts the risk of fragility fractures in a younger cohort of postmenopausal women followed for an average of 5 years. The mechanisms underlying the increased bone turnover in some (but not all) postmenopausal women are unknown. The increase appears to be independent from the residual secretion of 17 s estradiol (E2), assessed by a highly sensitive radioimmunoassay. Indeed, we found that a low serum E2 predicts the risk of fragility fractures in late postmenopausal women (but not in the elderly) independently of the rate of bone turnover. Bone markers can be used to monitor the efficacy of antiresorptive therapy such as hormone replacement therapy, raloxifene and bisphosphonates. We and others have shown that the short-term (3 to 6 months) decrease of bone turnover is significantly correlated with the long-term (2 years) increase in BMD of the spine. In addition, the decrease of serum osteocalcin is associated with the risk of vertebral fractures in osteoporotic women treated with raloxifene. Similar studies in patients using alendronate or risedronate show that the short-term decrease of bone turnover markers is correlated with the risk of subsequent fractures. Thus, with adequate cut-offs, individual patients can be monitored with bone markers earlier than with DXA. It remains to be assessed if such a monitoring can improve long-term compliance with therapy.
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Changes of bone remodeling markers reflect bone growth and bone turnover. Information on bone metabolism can be attained by blood and urine laboratory tests. Recently developed bone specific markers are categorized by bone remodeling process, i.e. bone formation and resorption. The formation markers include bone-specific alkaline phosphatase (BAP), osteocalcin (OC), undercarboxylated osteocalcin (ucOC), procollagene type I C- and N-terminal peptides (P1CP and P1NP). Bone resorption markers include deoxypyridinoline, collagen I C- and N-terminal telopeptides (CTX and NTX) , and tartrate resistent acid phosphatase (TRACP) isoform 5b. These laboratory tests offer lots of advantages for the diagnosis of bone metabolic disorders and for the evaluation of clinical states of primary osteoporosis and other metabolic skeletal diseases.
Bone remodeling
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Type I collagen
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Bone is a living tissue, metabolically very active, with the level of turnover of about 10% per year. Bone remodeling is a well-balanced process of bone resorption, induced by osteoclasts and bone formation maintained osteoblasts. Loss of bone remodeling balance, with increased bone resorption, leads to osteoporosis. Bone turnover markers are classified as markers of bone formation and of bone resorption. During the growth and development of skeleton, bone turnover markers show higher levels of activity than in the adult period. The increase in biochemical markers peaks again in the postmenopausal period, indicating accelerated bone remodeling. Bone mineral density is an important predictor of an osteoporotic fracture. Timely assessment of risk factors of osteoporosis and bone markers can detect subjects with accelerated bone remodeling and osteoporosis. This may introduce adequate therapy and prevent fracture.
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Bone metabolism is the course of dynamic balance between bone formation and bone resorption, and can produce some metabolites. These metabolites are named for markers of bone turnover, and classified into markers of bone formation and markers of bone resorption. Markers of bone formation represent the activity of osteoplast and metabolite of bone formation, and markers of bone resorption represent the activity of osteoclast and metabolite of bone resorption. In this review, the researches on neonatal markers of bone turnover were discussed.
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