Bone Homeostasis Editorial

K. Mano
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Abstract

Editorial The elements of bone(s) are (I) mechanical help of delicate tissues, (ii) switches for muscle activity, (iii) security of the focal sensory system, (iv) arrival of calcium and different particles for the upkeep of a consistent ionic climate in the extracellular liquid, and (v) lodging and backing of hemopoiesis. The design and measure of bone, both at the plainly visible and minute level, are dictated by the hereditary outline and by administrative components that assist convey with trip bone capacities. Hereditary data is liable for the profoundly preserved anatomical state of bones and doubtlessly for reestablishing that shape after break. To achieve its capacities, bone goes through persistent decimation, called resorption, completed by osteoclasts, and development by osteoblasts. In the grown-up skeleton, the two cycles are in equilibrium, keeping a steady, homeostatically controlled measure of bone. This reality, just as the histological perception that osteoclastic bone resorption is trailed by osteoblastic bone development, prompted the idea that the two cycles are unthinkingly "coupled" and to the quest for "coupling factors." No single factor has been demonstrated to connect the two cycles. Existing proof recommends that various factors presumably are engaged with the upkeep of bone homeostasis. Development factors found in bone, for example, IGFs or TGFβs, were proposed to be delivered during resorption and start neighborhood bone arrangement. Elements saved on the bone surface by osteoclasts toward the finish of the resorption stage were proposed to start the bone development that follows. Humoral components, for example, parathyroid chemical and prostaglandin E, that animate both bone resorption and bone development, could expand the two cycles couple. The activity of these components and different chemicals and cytokines on osteoclasts was proposed to be interceded by osteoblast-genealogy
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骨稳态编辑
骨(s)的元素是(I)精细组织的机械帮助,(ii)肌肉活动的开关,(iii)焦点感觉系统的安全性,(iv)钙和不同颗粒的到达,以维持细胞外液体中一致的离子气候,以及(v)造血的寄主和支持。骨的设计和尺寸,无论是在明显可见的还是微小的水平上,都是由遗传轮廓和辅助传达旅行骨容量的管理组件决定的。遗传数据对骨骼保存完好的解剖状态负有责任,毫无疑问对骨折后的形状重建负有责任。为了实现它的功能,骨经历了持续的破坏,称为再吸收,由破骨细胞完成,并由成骨细胞发育。在成熟的骨骼中,这两个循环处于平衡状态,保持着稳定的、自我平衡控制的骨骼测量。这一事实,正如组织学上认为破骨细胞骨吸收落后于成骨细胞骨发育一样,促使人们认为这两个周期是不假思索地“耦合”的,并促使人们寻求“耦合因素”。没有一个单一的因素被证明将这两个周期联系起来。现有证据表明,可能有多种因素参与了骨骼稳态的维持。在骨中发现的发育因子,如igf或TGFβs,被认为在吸收过程中被递送,并开始邻近骨排列。在骨吸收阶段结束时,破骨细胞保存在骨表面的元素被认为可以开始随后的骨发育。体液成分,例如甲状旁腺化学物质和前列腺素E,促进骨吸收和骨发育,可以扩大这两个循环。这些成分和不同的化学物质和细胞因子对破骨细胞的活性被认为是通过成骨细胞谱系来调解的
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