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氟化物治疗骨质疏松症:剂量反应、治疗持续时间及作用骨骼部位的综述

Fluoride therapy for osteoporosis: a review of dose response, duration of treatment, and skeletal sites of action.

作者信息

Dure-Smith B A, Kraenzlin M E, Farley S M, Libanati C R, Schulz E E, Baylink D J

机构信息

Department of Medicine, Loma Linda University, CA.

出版信息

Calcif Tissue Int. 1991;49 Suppl:S64-72. doi: 10.1007/BF02555092.

Abstract

Osteoporosis is a disease characterized by a reduction in bone density which predisposes to fracture after even minimal trauma. Fluoride, because it has consistently been shown to stimulate bone formation and increase trabecular bone density, has been widely studied for the treatment of osteoporosis. The article focuses on the dose response, duration of treatment, and skeletal sites of action of fluoride; we also include comments on the effect of fluoride on vertebral and appendicular fracture rates. The skeletal response to fluoride doses, ranging from 15 to 43 mg elemental fluoride per day, included a linear increase in spinal bone density at an average rate of 1.25 +/- 0.91 mg/cm3 per month. The rate of increase in spinal bone density was related to the dose of fluoride (r = 0.34, P less than 0.03). Spinal bone density had increased above the fracture threshold in 44% of patients treated with fluoride for 32 +/- 10 months. The time required to achieve this goal was, however, influenced by the pretreatment spinal bone density and interpatient variation in response to fluoride treatment. Patients whose spinal bone density remained below the fracture threshold had lower pretreatment bone densities and/or slower rates of increase in spinal bone density (P less than 0.001). The osteogenic effect of fluoride was not limited to the spine. After 2 years of fluoride therapy, we found bone density in the femoral condyle (measured by QCT) to have increased by 13 +/- 2.6 mg/cm3 (n = 38, P less than 0.001); bone density in the hip (measured by DPA) was increased by 0.0261 +/- 0.015 g/cm2 (n = 55, P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

骨质疏松症是一种以骨密度降低为特征的疾病,即使受到极小的创伤也容易发生骨折。由于一直显示氟化物能刺激骨形成并增加骨小梁骨密度,因此对其治疗骨质疏松症进行了广泛研究。本文重点关注氟化物的剂量反应、治疗持续时间和作用的骨骼部位;我们还对氟化物对椎体和四肢骨折发生率的影响进行了评论。每天摄入15至43毫克元素氟的剂量时,骨骼的反应包括脊柱骨密度以平均每月1.25±0.91毫克/立方厘米的速度呈线性增加。脊柱骨密度的增加速率与氟化物剂量相关(r = 0.34,P<0.03)。在接受氟化物治疗32±10个月的患者中,44%的患者脊柱骨密度已增加到骨折阈值以上。然而,达到这一目标所需的时间受治疗前脊柱骨密度和患者对氟化物治疗反应的个体差异影响。脊柱骨密度仍低于骨折阈值的患者治疗前骨密度较低和/或脊柱骨密度增加速率较慢(P<0.001)。氟化物的成骨作用不仅限于脊柱。氟化物治疗2年后,我们发现股骨髁的骨密度(通过定量计算机断层扫描测量)增加了13±2.6毫克/立方厘米(n = 38,P<0.001);髋部的骨密度(通过双能X线吸收法测量)增加了0.0261±0.015克/平方厘米(n = 55,P<0.025)。(摘要截短为250字)

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