Boden S D, Kaplan F S
Department of Orthopaedic Surgery, George Washington University Medical Center, Washington, DC.
Orthop Clin North Am. 1990 Jan;21(1):31-42.
Precise maintenance of the physiologic levels of both extracellular and intracellular ionized calcium is essential to life. Calcium and phosphate homeostasis is complex, yet three important hormones are responsible for modulating most of the extracellular control of these minerals. Parathyroid hormone acts directly on bone and kidney and indirectly on the intestine to maintain or restore the serum calcium level. The signal for increased PTH synthesis and secretion is a decrease in the serum ionized calcium concentration and a decrease in serum levels of 1,25(OH)2-D. Calcitonin is produced in parafollicular cells of the thyroid and inhibits bone resorption in pharmacologic doses. These cells recognize the calcium signal in a different way. A diminution in serum calcium decreases calcitonin production and release. The role of calcitonin in normal human physiology, however, remains in dispute. Finally, the biologically potent metabolite of vitamin D, 1,25(OH)2-D, stimulates intestinal absorption of calcium and phosphate. It also probably plays a role in the orderly mineralization and resorption of bone and has some influence on renal resorption of filtered calcium and phosphorus. A major stimulus to its production by proximal renal tubule cells is elevated PTH and decreased serum levels of calcium and phosphate. The absence of PTH as well as high serum calcium and phosphate levels can reduce its synthesis and secretion. These three hormones along with other mediators and messengers work in concert to maintain the normal calcium homeostasis. A disturbance at any level in this intricate regulatory network will result in a host of compensatory changes that may lead to clinical disease. A complete understanding of these normal mechanisms is a prerequisite to investigating the etiology and treatment of the various pathologic responses seen with many of the metabolic bone disorders.
精确维持细胞外和细胞内游离钙的生理水平对生命至关重要。钙和磷的稳态很复杂，但三种重要激素负责调节这些矿物质在细胞外的大部分控制。甲状旁腺激素直接作用于骨骼和肾脏，间接作用于肠道，以维持或恢复血清钙水平。甲状旁腺激素合成和分泌增加的信号是血清游离钙浓度降低以及血清1,25(OH)2-D水平降低。降钙素由甲状腺滤泡旁细胞产生，在药理剂量下抑制骨吸收。这些细胞以不同方式识别钙信号。血清钙降低会减少降钙素的产生和释放。然而，降钙素在正常人体生理学中的作用仍存在争议。最后，维生素D的生物活性代谢产物1,25(OH)2-D刺激肠道对钙和磷的吸收。它可能还在骨骼的有序矿化和吸收中起作用，并对肾脏对滤过钙和磷的重吸收有一定影响。近端肾小管细胞产生它的主要刺激因素是甲状旁腺激素升高以及血清钙和磷水平降低。甲状旁腺激素缺乏以及血清钙和磷水平升高会减少其合成和分泌。这三种激素与其他介质和信使协同作用，以维持正常的钙稳态。这个复杂调节网络中任何一个层面的紊乱都会导致一系列代偿性变化，可能引发临床疾病。全面了解这些正常机制是研究许多代谢性骨病所见各种病理反应的病因和治疗方法的先决条件。
