Application of chondroprotective agents to inhibit osteodestructive processes in the subchondral bone in patients with osteoarthritis

О. Gromova, А. M. Lila, I. Torshin, I. А. Reier
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引用次数: 1

Abstract

Background. Osteoarthritis (OA) is associated with an acute activation of local and systemic inflammation and involves subchondral tissue of the joint.Objective: to conduct a systemic analysis of the publications on the association between OA and metabolic disorders in bones.Material and methods. The authors analyzed 3,296 publications on the studies of OA and metabolic disorders in bones tissue by the method of a topologic theory of recognition selected by the request “osteoarthritis AND (bone resorption OR osteopenia OR osteoporosis)” in the database of biomedical publications PubMed/MEDLINE. The control sampling included 4,000 articles randomly selected out of 97,331 found by the request “osteoarthritis NOT bone NOT resorption NOT osteopenia NOT osteoporosis” (i.e. publications on OA that do not cover issues of bone metabolism).Results. The associations between cartilaginous pathology and bone tissue destruction are mediated by anti-inflammatory cytokines, osteoblast and osteoclast balance impairments, steroid hormone imbalance, and carbohydrate metabolism. Bone metabolism disorders are associated with an intensification of OA-associated pain syndrome. Chondroprotective agents (chondroitin sulfate (CS), glucosamine sulfate (GS), and undenaturated collagen) block the activity of antiinflammatory cytokines (NF-κB and toll-receptors), stimulate the activity of osteoblasts (bone tissue synthesizing cells), and decrease the excessive activity of osteoclasts (cells that degrade bone tissue).Conclusion. Pharmaceutically standardized forms of CS and GS can be used for the normalization of bone metabolism along with safe osteoptotective means (vitamin D, calcium, etc.) in patients with OA.
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应用软骨保护剂抑制骨关节炎患者软骨下骨的骨破坏过程
背景。骨关节炎(OA)与局部和全身炎症的急性激活有关,涉及关节软骨下组织。目的:对骨关节炎与骨骼代谢紊乱之间关系的文献进行系统分析。材料和方法。作者根据PubMed/MEDLINE生物医学出版物数据库中“骨关节炎与(骨吸收或骨质减少或骨质疏松)”的要求选择了一种拓扑识别理论,分析了3296篇关于骨性关节炎和骨组织代谢紊乱研究的出版物。对照样本包括根据“骨关节炎、骨吸收、骨减少、骨质疏松”(即不涉及骨代谢问题的OA出版物)的要求从97,331篇文章中随机抽取的4,000篇。软骨病理和骨组织破坏之间的关联是由抗炎细胞因子、成骨细胞和破骨细胞平衡受损、类固醇激素失衡和碳水化合物代谢介导的。骨代谢紊乱与oa相关疼痛综合征的加重有关。软骨保护剂(硫酸软骨素(CS)、硫酸氨基葡萄糖(GS)和不饱和胶原)可阻断抗炎细胞因子(NF-κB和toll受体)的活性,刺激成骨细胞(骨组织合成细胞)的活性,降低破骨细胞(骨组织降解细胞)的过度活性。在OA患者中,药物标准化的CS和GS可用于骨代谢的正常化以及安全的保骨手段(维生素D,钙等)。
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来源期刊
Farmakoekonomika
Farmakoekonomika Medicine-Health Policy
CiteScore
1.70
自引率
0.00%
发文量
43
审稿时长
8 weeks
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