Intervention Review

Fluoride for treating postmenopausal osteoporosis

  1. Didier Haguenauer1,*,
  2. Beverley Shea2,
  3. Peter Tugwell3,
  4. George A Wells4,
  5. Vivian Welch5

Editorial Group: Cochrane Musculoskeletal Group

Published Online: 23 OCT 2000

Assessed as up-to-date: 29 AUG 2000

DOI: 10.1002/14651858.CD002825


How to Cite

Haguenauer D, Shea B, Tugwell P, Wells GA, Welch V. Fluoride for treating postmenopausal osteoporosis. Cochrane Database of Systematic Reviews 2000, Issue 4. Art. No.: CD002825. DOI: 10.1002/14651858.CD002825.

Author Information

  1. 1

    Hopital Ste Perine, Paris, France

  2. 2

    University of Ottawa, Institute of Population Health, Ottawa, Ontario, Canada

  3. 3

    Ottawa Hospital, Centre for Global Health, Institute of Population Health, Department of Medicine, Ottawa, Ontario, Canada

  4. 4

    University of Ottawa Heart Institute, Cardiovascular Research Reference Centre, Ottawa, Ontario, Canada

  5. 5

    University of Ottawa, Centre for Global Health, Institute of Population Health, Ottawa, Ontario, Canada

*Didier Haguenauer, Hopital Ste Perine, 11 rue Chardon Lagache, Paris, 75016, France. didier.haguenauer@spr.ap-hop-paris.fr.

Publication History

  1. Publication Status: Edited (no change to conclusions)
  2. Published Online: 23 OCT 2000

SEARCH

 

Abstract

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

Background

Osteoporosis is a condition that results in an increased risk of fractures due to the reduction of bone volume, which is caused by an imbalance between bone formation and bone resorption. Because of this property, fluoride has been used for over 30 years as a treatment for osteoporosis.

Objectives

To assess the efficacy of fluoride therapy on bone loss, vertebral and non-vertebral fractures and side effects in postmenopausal women.

Search methods

We searched MEDLINE, Current Contents and the Cochrane Controlled Trial Registry up to December 1998.

Selection criteria

Two independent reviewers selected RCTs which met predetermined inclusion criteria.

Data collection and analysis

Two reviewers independently extracted data using predetermined forms and assessed the methodological quality of the trials using a validated scale. For dichotomous outcomes, relative risks (RR) were calculated and for continuous outcomes, weighted mean differences (WMD) of percentage change from baseline were calculated. Where heterogeneity existed (determined by a chi-square test) a random effects model was used.

Main results

Eleven studies (1429 subjects) met the inclusion criteria. The increase in lumbar spine bone mineral density (BMD) was found to be higher in the treatment group than in the control group with a WMD 8.1% (95%CI: 7.15,9.09) after two years of treatment and 16.1%(95%CI: 14.65,17.5) after four years. The RR for new vertebral fractures was not significant at two years [0.87 (95%CI: 0.51,1.46)] or at four years [0.9(95%CI: 0.71,1.14)]. The RR for new non-vertebral fractures was not significant at two years 1.2(95%CI: 0.68,2.1) but was increased at four years in the treated group 1.85(95%CI: 1.36,2.5), especially if used at high doses and in a non slow release form. The RR for gastrointestinal side effects was not significant at two years 2.18(95%CI: 0.86,1.21) but was increased at four years in the treated group 2.18(95%CI: 1.69,4.57) especially if fluoride was used at high doses and in a non slow release form. There is no evidence of an important difference in the number of withdrawals and dropouts between treated and control groups at two and four years.

Authors' conclusions

Although fluoride has an ability to increase BMD at lumbar spine, it does not result in a reduction of vertebral fractures. In increasing the dose of fluoride, one increases the risk of non-vertebral fracture and gastrointestinal side effects without any effect on the vertebral fracture rate.

 

Plain language summary

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

Fluoride can increase bone mineral density at the lumbar spine, it does not reduce vertebral fractures.

When considering that other therapies have been shown to reduce vertebral fracture rates, fluoride may not be the first choice of therapy for the treatment and prevention of osteoporotic fractures. The evidence showed an increase risk of gastrointestinal side effects and non vertebral fractures with fluoride.

 

摘要

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

背景

氟化物用於治療停經後婦女的骨質疏鬆症

骨質疏鬆症因骨質密度減少,導因於骨質吸收及形成不平衡,而容易導致骨折,氟化物已經用於治療骨質疏鬆症超過30年。

目標

研究氟化物治療骨質疏鬆症於骨質流失、脊椎及非脊椎骨折及副作用的效果。

搜尋策略

搜尋包括MEDLINE, Current Contents and the Cochrane Controlled Trial Registry (直到1998年12月)。

選擇標準

兩位作者獨立進行收錄文章之資料摘錄。

資料收集與分析

兩位作者獨立進行資料摘錄於預定表單,並已經信度評估之工具摘錄資料的品質。針對二元性的結果(骨折),我們使用固定效果模式計算相對風險(relative risk, RR)。針對連續性的結果,則計算由基礎值改善的百分比之加權平均差異(weighted mean difference, WMD),若有異質性(卡方檢定)則使用隨機效應模型進行檢定。

主要結論

11篇臨床隨機對照試驗(1429位患者)符合納入標準。腰椎骨密度在治療組較安慰劑組高,加權平均差異(WMD)在2年為8.1% (95%CI 7.15 – 9.09),4年為16.1% (95%CI 14.65 – 17.5)。新脊椎骨折的發生相對風險(RR)在2年為0.87 (95%CI 0.51 – 1.46),4年為0.9 (95%CI 0.71 – 1.14)皆不顯著。新非脊椎骨折的發生相對風險(RR)在2年為1.2 (95%CI 0.68 – 2.1)不顯著,但4年時為增加1.85 (95%CI 1.36 – 2.5),尤其使用高劑量及非緩釋型。胃腸副作用相對風險在2年無顯著差異2.18 (95%CI 0.86 – 1.21),但4年時為增加2.18 (95%CI 1.69 – 4.57),尤其氟化物使用高劑量及非緩釋型。病人退出及流失率在2年及4年時兩組並無差異。

作者結論

氟化物使用雖然可以增加腰椎骨密度,但未降低新椎骨骨折的發生。增加氟化物劑量會增加新非脊椎骨折的發生風險及胃腸副作用,但未降低椎骨骨折發生率。

翻譯人

本摘要由林口長庚醫院余光輝翻譯。

此翻譯計畫由臺灣國家衛生研究院(National Health Research Institutes, Taiwan)統籌。

總結

氟化物可以增加腰椎骨密度,但未降低椎骨骨折的發生。在有其他預防骨質疏鬆治療藥物下,以氟化物預防骨質疏鬆不是優先考量。增加氟化物劑量會增加胃腸副作用及非脊椎骨折的發生風險。