scholarly journals PERAN ESTROGEN PADA REMODELING TULANG

2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Iknes Sihombing ◽  
Sunny Wangko ◽  
Sonny J.R. Kalangi
Keyword(s):  
Vitamin D ◽  
Hormone Replacement Therapy ◽  
Bone Resorption ◽  
Bone Remodeling ◽  
Bone Cells ◽  
Hormone Replacement ◽  
Vitamine D ◽  
Estrogen Action ◽  
Slowing Down ◽  
Fracture Risks

Abstract: Bone tissues experience continual regeneration of their extracellular components by overhauling the old components. This process is called bone remodeling, which involves several kinds of bone cells. The most important bone cells related to the bone remodeling are osteoblasts, osteocytes, and osteoclats. The bone remodeling is influenced by estrogen. This hormone inhibits bone resorption, resulting in slowing down the osteoporosis process. This antiresorptive effect can be provided also by the estrogen action on osteoblasts, which indirectly influences osteoclast activities. Estrogen has been proved to slow down the decrease of bone mass and fracture risks in women with osteoporosis. Hormone replacement therapy, aimed at replacing estrogen deficiency, consists of phytoestrogen and progesteron; besides that, calcium and vitamine D are needed, too. Keywords: estrogen, bone remodeling, osteoblast, osteocyte, osteoclast.     Abstrak: Tulang merupakan jaringan yang terus menerus melakukan regenerasi komponen-komponen ekstrasel dengan cara menghancurkan komponen tulang yang sudah tua dan menggantikannya dengan yang baru. Proses ini disebut remodeling tulang, yang melibatkan kerja sel-sel tulang tertentu. Sel-sel dalam tulang yang terutama berhubungan dengan pembentukan dan resorpsi tulang ialah osteoblas, osteosit, dan osteoklas. Remodeling tulang dipengaruhi oleh hormon estrogen. Hormon ini menekan resorpsi tulang sehingga dapat menghambat proses kerapuhan tulang. Efek antiresorptif tersebut dapat pula dihasilkan melalui kerjanya pada osteoblas, yang secara tidak langsung mempengaruhi aktivitas osteoklas. Estrogen terbukti dapat mengurangi laju penurunan massa tulang dan risiko fraktur pada wanita dengan osteoporosis. Terapi sulih hormon yang digunakan untuk mengganti defisisensi estrogen ialah fitoestrogen, progesteron, selain itu juga kalsium dan vitamin D. Kata kunci: estrogen, remodeling tulang, osteoblas, osteosit, osteoklas.

scholarly journals Minireview: Osteoprotective Action of Estrogens Is Mediated by Osteoclastic Estrogen Receptor-α

2010 ◽  
Vol 24 (5) ◽  
pp. 877-885 ◽  
Author(s):  
Yuuki Imai ◽  
Shino Kondoh ◽  
Alexander Kouzmenko ◽  
Shigeaki Kato
Keyword(s):  
Estrogen Receptor ◽  
Bone Resorption ◽  
Bone Remodeling ◽  
Bone Cells ◽  
Developed Countries ◽  
Estrogen Deficiency ◽  
Estrogen Signaling ◽  
Estrogen Action ◽  
Health Maintenance ◽  
Enhanced Production

Abstract The osteoprotective action of estrogen in women has drawn considerable attention because estrogen deficiency-induced osteoporosis became one of the most widely spread diseases in developed countries. In men, the significance of estrogen action for bone health maintenance is also apparent from the osteoporotic phenotype seen in male patients with genetically impaired estrogen signaling. Severe bone loss and high bone turnover, including typical osteofeatures seen in postmenopausal women, can also be recapitulated in rodents after ovariectomy. However, the expected osteoporotic phenotype is not observed in female mice deficient in estrogen receptor (ER)-α or -β or both, even though the degenerative defects are clearly seen in other estrogen target tissues together with up-regulated levels of circulating testosterone. It has also been reported that estrogens may attenuate bone remodeling by cell autonomous suppressive effects on osteoblastogenesis and osteoclastogenesis. Hence, the effects of estrogens in bone appear to be complex, and the molecular role of bone estrogen receptors in osteoprotective estrogen action remains unclear. Instead, it has been proposed that estrogens indirectly control bone remodeling. For example, the enhanced production of cytokines under estrogen deficiency induces bone resorption through stimulation of osteoclastogenesis. However, the osteoporotic phenotype without systemic defects has been recapitulated in female (but not in male) mice by osteoclast-specific ablation of the ERα, proving that bone cells represent direct targets for estrogen action. An aberrant accumulation of mature osteoclasts in these female mutants indicates that in females, the inhibitory action of estrogens on bone resorption is mediated by the osteoclastic ERα through the shortened lifespan of osteoclasts.

scholarly journals Pathogenic variants in GNPTAB and GNPTG encoding distinct subunits of GlcNAc-1-phosphotransferase differentially impact bone resorption in patients with mucolipidosis type II and III

2021 ◽  
Author(s):  
Giorgia Di Lorenzo ◽  
Lena M. Westermann ◽  
Timur A. Yorgan ◽  
Julian Stürznickel ◽  
Nataniel F. Ludwig ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Remodeling ◽  
Bone Cells ◽  
Collagen Crosslinks ◽  
Clinical Criteria ◽  
Pathogenic Variants ◽  
Bone Biopsies ◽  
Appropriate Therapy ◽  
Alpha Beta ◽  
Deficient Mice

Abstract Purpose Pathogenic variants in GNPTAB and GNPTG, encoding different subunits of GlcNAc-1-phosphotransferase, cause mucolipidosis (ML) II, MLIII alpha/beta, and MLIII gamma. This study aimed to investigate the cellular and molecular bases underlying skeletal abnormalities in patients with MLII and MLIII. Methods We analyzed bone biopsies from patients with MLIII alpha/beta or MLIII gamma by undecalcified histology and histomorphometry. The skeletal status of Gnptgkoand Gnptab-deficient mice was determined and complemented by biochemical analysis of primary Gnptgko bone cells. The clinical relevance of the mouse data was underscored by systematic urinary collagen crosslinks quantification in patients with MLII, MLIII alpha/beta, and MLIII gamma. Results The analysis of iliac crest biopsies revealed that bone remodeling is impaired in patients with GNPTAB-associated MLIII alpha/beta but not with GNPTG-associated MLIII gamma. Opposed to Gnptab-deficient mice, skeletal remodeling is not affected in Gnptgko mice. Most importantly, patients with variants in GNPTAB but not in GNPTG exhibited increased bone resorption. Conclusion The gene-specific impact on bone remodeling in human individuals and in mice proposes distinct molecular functions of the GlcNAc-1-phosphotransferase subunits in bone cells. We therefore appeal for the necessity to classify MLIII based on genetic in addition to clinical criteria to ensure appropriate therapy.

scholarly journals The Development of Molecular Biology of Osteoporosis

2021 ◽  
Vol 22 (15) ◽  
pp. 8182
Author(s):  
Yongguang Gao ◽  
Suryaji Patil ◽  
Jingxian Jia
Keyword(s):  
Bone Resorption ◽  
Molecular Biology ◽  
Bone Formation ◽  
Bone Mass ◽  
Bone Remodeling ◽  
Bone Cells ◽  
Cell Activity ◽  
Bone Cell ◽  
Bone Disorders ◽  
Molecular Aspects

Osteoporosis is one of the major bone disorders that affects both women and men, and causes bone deterioration and bone strength. Bone remodeling maintains bone mass and mineral homeostasis through the balanced action of osteoblasts and osteoclasts, which are responsible for bone formation and bone resorption, respectively. The imbalance in bone remodeling is known to be the main cause of osteoporosis. The imbalance can be the result of the action of various molecules produced by one bone cell that acts on other bone cells and influence cell activity. The understanding of the effect of these molecules on bone can help identify new targets and therapeutics to prevent and treat bone disorders. In this article, we have focused on molecules that are produced by osteoblasts, osteocytes, and osteoclasts and their mechanism of action on these cells. We have also summarized the different pharmacological osteoporosis treatments that target different molecular aspects of these bone cells to minimize osteoporosis.

scholarly journals Effect of hormone replacement therapy on the bone mass and urinary excretion of pyridinium cross-links

2000 ◽  
Vol 118 (1) ◽  
pp. 3-6 ◽  
Author(s):  
Dolores Perovano Pardini ◽  
Anibal Tagliaferri Sabino ◽  
Ana Maria Meneses ◽  
Teresa Kasamatsu ◽  
José Gilberto Henriques Vieira
Keyword(s):  
Hormone Replacement Therapy ◽  
Bone Resorption ◽  
Bone Mass ◽  
Urinary Excretion ◽  
Replacement Therapy ◽  
High Performance ◽  
Hormone Replacement ◽  
Mineral Density ◽  
Cross Links ◽  
Post Menopausal

CONTEXT: The menopause accelerates bone loss and is associated with an increased bone turnover. Bone formation may be evaluated by several biochemical markers. However, the establishment of an accurate marker for bone resorption has been more difficult to achieve. OBJECTIVE: To study the effect of hormone replacement therapy (HRT) on bone mass and on the markers of bone resorption: urinary excretion of pyridinoline and deoxypyridinoline. DESIGN: Cohort correlational study. SETTING: Academic referral center. SAMPLE: 53 post-menopausal women, aged 48-58 years. MAIN MEASUREMENTS: Urinary pyr and d-pyr were measured in fasting urine samples by spectrofluorometry after high performance liquid chromatography and corrected for creatinine excretion measured before treatment and after 1, 2, 4 and 12 months. Bone mineral density (BMD) was measured by dual energy X-ray absorptiometry (DEXA) before treatment and after 12 months of HRT. RESULTS: The BMD after HRT was about 4.7% (P < 0.0004); 2% (P < 0.002); and 3% (P < 0.01) higher than the basal values in lumbar spine, neck and trochanter respectively. There were no significant correlations between pyridinium cross-links and age, weight, menopause duration and BMD. The decrease in pyr and d-pyr was progressive after HRT, reaching 28.9% (P < 0.0002), and 42% (P < 0.0002) respectively after 1 year. CONCLUSIONS: Urinary pyridinoline and deoxypyridinoline excretion decreases early in hormone replacement therapy, reflecting a decrease in the bone resorption rate, and no correlation was observed with the bone mass evaluated by densitometry.

scholarly journals Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-17 ◽  
Author(s):  
Rinaldo Florencio-Silva ◽  
Gisela Rodrigues da Silva Sasso ◽  
Estela Sasso-Cerri ◽  
Manuel Jesus Simões ◽  
Paulo Sérgio Cerri
Keyword(s):  
Bone Resorption ◽  
Bone Formation ◽  
Bone Tissue ◽  
Bone Remodeling ◽  
Bone Cells ◽  
Current Data ◽  
Bone Diseases ◽  
Bone Homeostasis ◽  
Bone Biology ◽  
Structure And Functions

Bone tissue is continuously remodeled through the concerted actions of bone cells, which include bone resorption by osteoclasts and bone formation by osteoblasts, whereas osteocytes act as mechanosensors and orchestrators of the bone remodeling process. This process is under the control of local (e.g., growth factors and cytokines) and systemic (e.g., calcitonin and estrogens) factors that all together contribute for bone homeostasis. An imbalance between bone resorption and formation can result in bone diseases including osteoporosis. Recently, it has been recognized that, during bone remodeling, there are an intricate communication among bone cells. For instance, the coupling from bone resorption to bone formation is achieved by interaction between osteoclasts and osteoblasts. Moreover, osteocytes produce factors that influence osteoblast and osteoclast activities, whereas osteocyte apoptosis is followed by osteoclastic bone resorption. The increasing knowledge about the structure and functions of bone cells contributed to a better understanding of bone biology. It has been suggested that there is a complex communication between bone cells and other organs, indicating the dynamic nature of bone tissue. In this review, we discuss the current data about the structure and functions of bone cells and the factors that influence bone remodeling.

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