The Effects of Smoking on Bone Health

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Clinical Science (2007) 113, 233–241 (Printed in Great Britain) doi:10.1042/CS20060173 233

R E V I E W

The effects of smoking on bone health

Peter K. K. WONG∗

, Jemma J. CHRISTIE† and John D. WARK†‡∗Department of Rheumatology, Royal Melbourne Hospital, Parkville, Victoria 3050, Australia, †Department of Medicine,University of Melbourne, Royal Melbourne Hospital, Parkville, Victoria 3050, Australia, and ‡Bone and Mineral Service,Royal Melbourne Hospital, Parkville, Victoria 3050, Australia

A B S T R A C T

Osteoporotic fractures are a major public health problem in most developed countries and

an increasing concern in much of the developing world. This healthcare burden will increase

significantly worldwide over the next 20 years due to aging of the population. Smoking is a key

lifestyle risk factor for bone loss and fractures that appears to be independent of other risk factors

for fracture such as age, weight, sex and menopausal status. This review discusses the effects of smoking on bone health in pre-menopausal and post-menopausal women and men. Data from twin

studies and the three main published meta-analyses are presented. Possible mechanisms by which

smoking affects bone mass are reviewed. Despite smoking being a major lifestyle risk factor for

osteoporosis, the mechanisms underlying smoking-associated bone loss and fracture risk remain

poorly understood. The effect appears dose-dependent, and may be, at least partially, reversible.

However, more work is required to confirm and characterize the reversibility of smoking-

associated bone defects. Finally, strategies for quitting smoking are discussed. Encouragement

of lifestyle alterations, including smoking cessation, should be a major component of any bone

therapeutic programme.

INTRODUCTION

Osteoporotic fractures are a major public health problem

in most developed countries and an increasing concern in

much of the developing world. Patients sustaining a hip

fracture have up to a 33% mortality rate in the following

12 months [1–3]. Approximately one-thirdof hip fracture

patients subsequently require admission to residential

care [4]. Clinical manifestations of osteoporosis affect

nearly 10% of the population of Australia, a developed

country of 20 million people [5]. This results in direct

and indirect annual costs to the Australian community

of AU$ 7.4 billion [6]. This healthcare burden will

significantly increase worldwide over the next 20 years

due to aging of the population. For example, in the most

populous Australianstate of NewSouthWales, the annual

incidence of hip fractures in people aged 65 years or older

is projected to increase from 5201 in 1994–1995 to over

9800 by the year 2021, an increase of over 90% [7].

Fracture prevention is therefore a major public

health priority. Strategies to achieve this may be

either population-based or targeted at high-risk groups.

Addressing modifiable risk factors for osteoporosis and

low-trauma fractures is an important component of both

approaches. Smoking was recognized over 30 years ago

as a key lifestyle risk factor for both bone loss and

fractures [8]. Since then, the association between smoking

and low BMD (bone mineral density) and osteoporotic

fractures has become increasingly recognized [9–11]. The

DOES (Dubbo Osteoporosis Epidemiologic Study), a

community-based longitudinal study of men and women

aged more than 60 years at study enrolment, found

that smoking was associated, independently of calcium

intake or body mass, with lower BMD (5–8%) at

Key words: bone, bone mineral density, fracture, osteoporosis, public health, smoking.

Abbreviations: BMD, bone mineral density; BMI, body mass index; CI, confidence interval; DHEA, dehydroepiandrosterone;

HRT, hormone replacement therapy; OR, odds ratio; RR, risk ratio; SHBG, sex hormone-binding globulin.

Correspondence: Professor John D. Wark (email [email protected]).

C The Authors Journal compilation C 2007 Biochemical Society

www.clinsci.org

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234 P. K. K. Wong, J. J. Christie and J. D. Wark

the femoral neck and spine in both men and women

[12]. The Nurses’ Health Study, a prospective cohort

study involving 121701 female nurses 30–55 years of age

when recruitment opened in 1976, found that current

smokers had a dose-dependent increase in hip fracture

rates compared with never-smokers [13]. A Norwegian

cohortstudyfollowed 34856 adultsaged 50 yearsor olderfor 3 years, and found an increased risk of hip frac-

ture for both female [RR (risk ratio) 1.5, 95% CI

(confidence interval) 1.0–2.4] and male smokers (RR

1.8, 95% CI 1.2–2.9) compared with non-smokers [14].

Interestingly, the effect of smoking on fracture risk

appeared largely independent of BMD in this study, as the

RR forhip fracture associated with a variety of risk factors

adjusted for age was similar, with and without correction

for BMD [15]. Hence smoking may alter fracture risk by

influencing other variables, including body mass [16] or

oestrogen levels [17].

This review will discuss the effects of smoking onbone health in pre-menopausal and post-menopausal

women and men. Data from twin studies and the three

main published meta-analyses will be presented. Possible

mechanisms by which smoking affects bone mass will be

reviewed. Finally, strategies for quitting smoking will

be discussed.

METHODS

To identify published studies we performed a computer-

ized literature search of the entirePubMed database usingthe key words ‘smoking’ and ‘bones’ in papers published

in the English language for the last 10 years. All key

articles were retrieved online with articles in all journals

considered. The reference lists of published papers

were also explored to identify any additional papers of

relevance to the review topic. The authors independently

reviewed and judged the selected publications on their

contribution to the body of knowledge on the topic, then

reached a consensus on which publications to include in

the present review.

FINDINGS

Pre-menopausal womenAn Australian cross-sectional study in pre-menopausal

parous women (118 current smokers, 158 non-smokers;

mean age 33 years) found a 4–5% deficit in BMD at the

femoral neck, lumbar spine and total body in smokers

[18]. This association was more pronounced in women

with a BMI (body mass index) <25 kg/m2 and who

had breastfed at least one child [18]. Sporting activity

appeared protective against bone loss. Another study of

healthy community-dwelling young women found that,

at 2 years of follow-up, smokers aged 20–39 years had a

lower spinal BMD than non-smokers [19].

Post-menopausal womenBone density at the radius was inversely related to pack-

years of smoking exposure in post-menopausal women,

even when controlled for BMI and the number of years post-menopause [20]. The annual rate of post-

menopausal bone loss at this site was also greater in

smokers [20]. A Danish study of 2015 women aged

45–58 years and within 2 years of their last menstrual

period reported significant negative associations between

smoking and bone mass in the lumbar spine, femoral

neck and total body, with a 3 % deficit at the femoral neck

in current smokers compared with non-smokers [21].

As reported in pre-menopausal women [18], the most

significant effect was seen in thinner women. BMD

levels in women who had stopped smoking more than

5 years previously were not significantly different fromvalues in women who had never smoked. Serum 25-

hydroxyvitamin D levels inversely correlated with the

number of cigarettes smoked per day. In a study of 153

early post-menopausal women, smoking was associated

with a 4% lower BMD at the spine compared with non-

smokers [22]. Although the increase in serum oestradiol

in these early post-menopausal smokers receiving HRT

(hormone replacement therapy) was half that seen in

non-smokers [22], a prospective study of 6159 post-

menopausal women found that the protective effect

of HRT on hip fracture was strongest in current and

ex-smokers [23]. A prospective study of 8600 post-

menopausal Southern Californian women found that

current smokers had an increased risk of hip fracture

compared with never-smokers [24]. A population-based

cohort study of subjects aged 60 years and older found

that smoking levels recorded 16–18 years earlier were

predictive of lower BMD at the hip in women (and

men) after adjustment for multiple covariates such as age,

exercise, alcohol use, BMI and oestrogen use [25].

Effects of smoking on bone health in menAlthough there are less data regarding the effects of

smoking on bone health in men, smoking appears to

be a significant risk factor for bone loss [9,26]. Afteradjusting for potentially confounding variables, current

male smokers had a 7.3% reduction in lumbar spine

BMD compared with non-smokers [27]. Each decade

of smoking was associated with a 0.015 g/cm2 reduction

in BMD. Cross-sectional data collected as part of the

Framingham Study, a population-based cohort study

with over 40 years of follow-up, found a 4–15.3% lower

BMD in male smokers at all skeletal sites [28]. Further

analysis of longitudinal data over 4 yearsfrom this cohort

found that men (but not women) who smoked lost more

BMD at the hip than men who had never smoked [29]. A

French study of 719 men aged 51–85 years reported that




The effects of smoking on bone health 235

former smokers had a higher BMD at the forearm than

current smokers [30]. However, following adjustment for

age, body mass, alcohol intakeand caffeine intake,the two

groups had a similar BMD at the lumbar spine, hip and

whole body. Despite this, current smokers had increased

urinary levels of bone resorption markers compared with

former smokers and subjects who had never smoked.Formersmokers had a lower BMD atthe hip,whole body

and distal forearm than subjects who had never smoked.

Current and past smokers in the Hawaii Osteoporosis

Study (1303 men, aged 51–82 years at recruitment) had a

lower BMD, especially at the calcaneus and radius [31].

A dose-dependent relationship with both the duration

and quantity of cigarettes smoked was noted [31]. These

results suggested a 10–30% increase in fracture risk per

decade of smoking. A prospective study of 5049 Southern

Californian men found that current smokers had an

increased risk of hip fracture compared with never-

smokers [24]. A Finnish prospective cohort study of menaged 9–18 years at study entry found that after 11 years of

follow-up,aninversecorrelationbetweenBMD(adjusted

for mass) and smoking existed for both the lumbar spine

and hip [32]. However, probably due to a lack of power,

this study found no consistent association between BMD

and smoking in women.

Results from twin studiesThe use of same-sex twins discordant for smoking is a

powerful research toolthat controls for threemajor deter-

minants of BMD, namely age, sex and genetic back-

ground. A cross-sectional twin study found that forevery

10 pack-years of smoking, the BMD of the smoking twin

was 2% lower at the lumbar spine and 0.9% lower at the

femoral neck compared with the non-smoking twin [33].

Theauthors of this study concluded that women smoking

one pack of cigarettes per day through adulthood would

have a 5–10% lower BMD by the time of menopause,

a biologically and clinically relevant effect [33]. Other

Australian twin studies have found bone deficits at

multiple skeletal sitesin twinpairsdiscordant for cigarette

use [11,34]. A more recent cross-sectional co-twin study

involving 146 female twin pairs, aged 30–65 years, found

that the within-pair difference in lifetime smoking was an

independent predictor of BMD at the hip, lumbar spineand total body [35]. The modelling included height, lean

mass, fat mass, current calcium intake, physical activity

and alcohol consumption as covariates. A discordance

of 10 pack-years smoking was related to a 2.7–3.3%

lower BMD at the hip and lumbar spine respectively,

but not at the forearm, with more marked effects in

post-menopausal women [35]. This may have arisen due

to a greater cumulative tobaccoexposurein older smokers

or a greater sensitivity to smoking-induced bone loss

after the menopause. In addition, some of the smoking-

associated BMD deficit was explained by a difference in

body fat mass.

Variability in findingsOther studies have suggested that, unlike age, mass,

muscle strength and oestrogen use, smoking is not a

major determinant of BMD and fracture risk [36,37]. A

longitudinal study (769 subjects aged 60 years or older at

baseline) showed current smoking had no apparent effect

on the rate of bone loss [38]. Earlier smallerstudies foundno difference in bone mass in smokers matched for sex,

age, weight, height, calcium intake, menopausal history

andoestrogen usewith non-smokers[39–41].Daniel et al.

[41] (n= 52 subjects) found no significant difference in

BMD between healthy female smokers and non-smokers

aged20–35 years (mean age for smokers, 29.5 years; mean

age for non-smokers, 28.7 years), which were closely

matched for anthropometric measures, physical activity

levels and age at menarche. They did find, however, that

smokers had higher levels of the SHBG (sex hormone-

binding globulin) and lower oestradiol levels, which have

previously been associated with increased bone loss inolder women. Other work has suggested that smoking

might exert an indirect effect on bone health by regulating

body mass [16] or oestrogen levels [17].

There are several possible explanations for the

discrepancies in published findings. Study subjects are

usually classified as current smokers and non-smokers.

However, there may be crossover between these two

groups at different times in people’s lives. For a variety of

reasons, current smokers may sometimes deny smoking.

Variability in the number and/or duration of cigarettes

smoked per day may not be captured during data

collection. This makes evidence of a dose-dependent

response relationship difficult to obtain. Data collection

may be subject to recall bias. Confounding factors such as

body mass, physical activity and alcohol intake may not

always be considered. This is a major problem as several

factors that influence bone mass may be distributed

unequally across study groups. Compared with non-

smokers, some of these factors appear more prevalent

in smokers, for example, lower physical activity, lower

calcium intake and higher alcohol consumption. There

are also often variations in age and menopausal status

of subjects and controls. Finally studies, especially some

earlier ones, were not sufficiently powered to detect

a significant difference in outcome measures betweengroups.

Results of meta-analysesThreemeta-analyses publishedover the past10 yearshave

attempted to clarify the effects of smoking on bone health

(Table 1) [15,42,43]. A meta-analysis of 29 published

cross-sectional studies examining 2156 smokers and 9705

non-smokers, and 19 cohort and case-control studies

representing 3889 hip fractures yielded the following

results [42]: (i) in women, one in eight hip fractures

may be attributable to smoking; (ii) the relative risk of

hip fracture in smokers compared with non-smokers





Table 1 Fracture risk associated with smoking from three meta-analyses (95 % CI)

Authors n Study design and population Fracture risk compared with non-smokers BMD compared with non-smokers

Law and Hackshaw, 15 750 29 cross-sectional studies , 41 % increase in hip fracture Decreased at femoral neck,

1997 [42] 19 cohort and case-control studies; risk at age 70 years radius and calcaneus

multi-ethnic sample, mean age 54.0 years,

mostly female

Ward and Kle sges , 40 753 86 cross- sectional and prospective Increase in li fet ime r isk Decreased at hip, lumbar spine ,

2001 [43] studies, multi-ethnic sample, of fracture: woman, hip − 31 %; forearm and calcaneus

74 % female, mean men, hip − 40 %; women, vertebral

age 53.3 years − 13 %; men, vertebral − 32 %

Kanis et al., 59 232 10 prospective cohort studies worldwide; 25 % increase overal l; 84 % increase Not reported

2005 [15] 74 % female, mean age 62.8 years in hip fracture

was strongly associated with age (e.g. the risk of hip

fracture was41 % greater in smokers compared with non-

smokers at the age of 70); (iii) the difference in BMDat the femoral neck, radius and calcaneus in smokers

compared with non-smokers increased with age (for

every 10 year increase in age, the BMD of smokers fell

2% more than that of non-smokers); (iv) the association

between smoking and lower BMD was not explained

by variations in body mass, menopausal history, exercise

levels or oestrogen replacement, suggesting a direct effect

of smoking on bone; (v) no effect of smoking on

BMD in pre-menopausal women was noted, suggesting

a protective role for oestrogen; and (vi) data in men were

limited, but suggested similar effects to those seen in

women.

A second meta-analysis of pooled data from 86

studies representing 40753 subjects [43], reported that:

(i) smokers had less bone mass at all measured sites

(hip, lumbar spine, forearm and calcaneus), although

especially at the hip; (ii) these effects were greatest in men

and the elderly, and were dose-dependent; (iii) smoking

cessation had a beneficial effect on bone mass, as former

smokers had an intermediate bone phenotype compared

with either life-long non-smokers or current smokers;

(iv) bone mass differences remained significant after

correction for age and body mass; (v) smoking appeared

to increase the lifetime risk of hip fracture by 31% in

women and 40% in men, and of vertebral fracture by13% in females and 32% in males; and (vi) up to 10%

of all hip fractures were attributable to smoking (this

corresponds to approx. 34000 additional hip fractures

per year in the U.S.A. alone).

The most recent and extensive meta-analysis examined

59232 subjects from ten prospective cohorts in five

continents [15] and reported that: (i) current smoking was

associated with a 25% increase in fracture risk compared

with the risk in subjects who had never smoked, the

highest risk was seen for hip fracture (RR 1.84; 95%

CI 1.52–2.22); (ii) BMD accounted for only 23% of the

increased risk of hip fracture; and (iii) BMI appeared to

have only a small effect on smoking-associated fracture

risk.

Effects of smoking on fallsIn addition to increasing bone fragility, it has been

suggested that smoking also contributes to an increase

in the risk of falls [44]. With increasing age comes an

increase in the risk of falls and injuries, largely due

to involutional changes in sensory and musculoskeletal

structure and function [45]. Compared with non-

smokers, smokers are weaker, have poorer balance and

impaired neuromuscular performance [44]. In the study

by Nelson et al. [44], smokers had a decrease in

physical and neuromuscular function, compared with

non-smokers,50–100%asgreatasthatassociatedwitha5year increase in age. Theauthors commentedthat vascular

effects of smoking could explain the poorer function

of smokers in this study. Another observational study

conducted in older community-dwelling women found

no significant association between smoking and reported

falls in the previous year [46]. However, a recent large

Canadian survey of older people found that smoking

was an independent predictor of unintentional injuries

in the home [47]. However, fall-related injuries were

not reported separately in this study [47]. Overall the

evidence is inconclusive, butsmoking may be a risk factor

for falls with consequent injuries including fractures.

Possible mechanisms by which smokingmay affect BMD and fracture riskSeveral mechanisms have been proposed to explain the

differences in BMD between smokers and non-smokers

(Figure 1) [30,42,43]. However, to date, no study has

been appropriately designed, sufficiently comprehensive

or adequately powered to provide a clear understanding

of how smoking effects bone.

It has been known for some time that smokers are

thinner and have lower body fat compared with non-

smokers [18,30,48]. The mechanism for this association





Figure 1 Potential mechanisms of decreased bone strength and increased fracture risk in smokers

25-OH vitamin D, 25-hydroxyvitamin D.

remains unclear, but appetite suppression may be

responsible [49]. These differences may partly explain

observed BMD differences [16]. In our studies of

smoking-discordant female twin pairs, the difference in

total fat mass explained a minority (22–31%) of the

difference in regional BMD at the hip and forearm

(J.D. Wark, unpublished work). Of interest, a significant

(P= 0.01) 3.8% difference in age- and height-adjusted

lumbar spine BMD fell to a non-significant 1.9% after

adjustingforfatmass,suggestingthatlowbodyfatmaybe

an important mediator of smoking effects at this skeletal

site.

There are several possible mechanisms by which fat

mass may influence BMD. Higher body mass/increased

mechanicalloadingmayprovideanosteogenicstimulusin

non-smokers [41]. Body fat may provide a site for extra-

ovarian aromatization of androgens to oestrogen [50,51].Serum levels of the fat-derived hormone leptin correlated

with bone mass at the spine, hip and total body in

healthy non-obese women aged 20–91 years [52]. Leptin

appeared to be an independent predictor of BMD and

vertebral fractures in post-menopausal women [53,54].

However, there appears to be an inconsistent relationship

between smoking and serum leptin levels, with some

studies reporting lower [55] or unchanged [56,57] levels

in smokers compared with non-smokers.

In female smokers, the age of menopause is up to

2 years earlier than in non-smokers, suggesting pre-

menopausal ovarian dysfunction [58,59]. Smoking may

have an oestrogen-lowering effect, possibly by increasing

oestradiol 2-hydroxylation, producing a metabolite with

minimal oestrogenic activity which is rapidly cleared

from the circulation [60]. In pre-menopausal female

smokers, concentrations of SHBG were higher and free

testosterone indices were lower [61]. Pre-menopausal

female smokers also had lower luteal phase oestrogen

levels [62]. Oestrogen production may be reduced due

to inhibition of aromatase activity by components

of cigarette smoke such as nicotine, cotinine and

anabasine [63]. In post-menopausal smokers, oestrogen

levels during HRT were less than in similarly treated

non-smoking women, suggesting increased oestrogen

clearance in smokers [22].

Smoking may also affect bone loss by altering

levels of adrenal cortical hormones. A study of 233

post-menopausal women, aged 60–79 years, found thatsmokers had higher levels of DHEA-S (dehydroepi-

androsterone sulfate) and androstenedione than non-

smokers [64]. Mean levels of oestrone, oestradiol,

testosterone and SHBG remained unchanged. Others

have found that smoking elevated basal levels of

androstenedione, DHEA and cortisol [65]. In male

smokers, total testosterone and oestradiol levels tend to

be higher than in non-smokers, but free hormone levels

may be normal because SHBG is higher in male [66,67]

and female [41] smokers.

Lower 25-hydroxyvitamin D levels in smokers

compared with non-smokers have been reported in





several studies, but the mechanism of this association

is unclear [18,68–70]. One possible explanation may be

enhanced hepatic metabolism of vitamin D metabolites

followinginduction of liver enzymes dueto smoking [18].

Another contributing factor to enhanced bone loss in

smokers may be impaired calcium absorption. Calcium

absorption was lower in smokers compared with non-smokers after adjustment for age, gender, use of calcium

supplements and dietary calcium/vitamin D intake,

especially in those smoking more than 20 cigarettes

per day [20,70]. However, the authors of these studies

considered it unlikely that this mechanismfully explained

the observed difference in rates of bone loss between

smokers and non-smokers. The effect of calcium and

vitamin D supplementation, as measured by increases

in urinary calcium/creatinine excretion, was lower in

smokers compared with non-smokers [70]. This may

be due to reduced enteric absorption from impaired

mesenteric blood flow in smokers [71]. A Finnish studysuggested that smoking seemed to nullify the bone-

protective effects of calcium supplementation in post-

menopausal women, especially at the lumbar spine [72].

Parathyroid hormone levels have been reported to

correlate negatively with smoking [68,69]. Bone turnover

markers have been measured in several studies. Lower

levelsof thebone formationmarker osteocalcin have been

reported in pre-menopausal and early post-menopausal

female smokers [21,69]. A rise in bone resorption

markers (C-terminal telopeptide, and free and total

deoxypyridinoline) has been reported in male smokers

[30].

Smoking is associated with increased concentrations

of free radicals, which may contribute to bone resorption

[73]. A prospective cohortstudyinvolving 66651 women,

aged 40–76 years of age, found that current smokers with

a low vitamin E and C intake had an increased risk of hip

fracture [OR (odds ratio) 3.0; 95% CI 1.6–5.4 and OR

3.0; 95% CI 1.6–5.6 respectively) [74]. Interestingly, the

OR fell to 1.1 (95% CI 0.5–2.4) and 1.4 (95 % CI 0.7–3.0)

respectively, with higher intakes of these vitamins. Levels

of β-carotene, selenium, calcium or vitamin B6 appeared

to have no effect on fracture risk.

It is unclear what component of cigarette smoke

adverselyaffects bone. In vitro studies have demonstrateddecreased proliferation and impaired collagen synthesis

in osteoblast-like cells exposed to high concentrations of

both nicotine [75,76] and the non-nicotine constituents

of cigarette smoke [77]. In a rabbit model of bone graft

revascularization, elevated systemic levels of nicotine

impaired vascularization of a cancellous bone graft

implantedinto thedistal femur [78]. Othershave reported

direct toxic effects of smoking on bone mass in rodents

in vivo [79].

The meta-analysis of Kanis et al. [15] found that only

23% of the increase in hip fracture risk associated with

smoking could be explained by the deficit in BMD.

This observation suggests that undetected defects in bone

quality and extra-skeletal effects of smoking need to be

considered.

Is smoking-related bone loss reversible?A small randomized smoking cessation trial in post-

menopausal women found that 6 weeks after stopping

smoking, subjects had a decrease in SHBG, DHEA and

urinary N-telopeptide (a markerof bone resorption) [80].

No significant changes in other biochemical or hormonal

indices were noted. Several cohort studies have re-

ported that ex-smokers have an intermediate BMD be-

tween that of current and never-smokers, suggesting that

the effects of smoking on bone may be partially reversible

[12,30]. This hypothesis has been supported by findings

from a meta-analysis, although there were insufficient

data to determine what length of time since quitting

was necessary for a meaningful biological effect [43].

One large well-controlled study found that both menand women had a significant dose-response relationship

between hip BMD and change in smoking status over 16–

18 years, suggesting that smoking cessation was helpful

in reducing bone loss [25]. However, the Nurses’ Health

Study found that fracture risk fell only after 10 or more

years of abstinence from smoking [13].

The available strategies to encourage quitting smoking

have been extensively reviewed [81–83]. In brief, various

self-help, counselling, support and pharmacological

interventions are beneficial. The provision of self-help

resources combined with telephone callback counselling

achieved a 24% smoking cessation rate at 12 weeks and22% at 12 months [84]. Pharmacological interventions

such as nicotine replacement therapy further improve

success rates [82]. Transdermal nicotine replacement in

combination with intensive group counselling produced

cessation rates of 59% compared with 40% for

intensive group counselling alone at the end of the 8-

week intervention [85]. These figures fell to 37% and

20% respectively, when the intensity of counselling

was reduced. Although published success rates for

smoking cessation are less than ideal, they highlight the

opportunity of modifying smoking habits and altering

the risk of osteoporosis and, therefore, fracture. What is

now needed are data to show a positive effect of smokingcessation on bone health.

CONCLUSIONS

Much attention has focused on pharmacological

measurements to both preserve and increase bone mass.

However, it is also important to address lifestyle factors

that affect bone health. Smoking appears to exert a

negative effect on bone mass at the major sites of

osteoporotic fracture, namely the hip, lumbar spine

and forearm. This influence appears independent of





other risk factors for fracture, such as age, weight, sex

and menopausal status. Despite smoking being a major

lifestyle risk factor for osteoporosis, the mechanisms

underlying smoking-associated bone loss remain poorly

understood. The effect appears dose-dependent and may

be, at least partially, reversible. However, more work

is required to confirm and characterize the reversibilityof smoking-associated bone defects. The magnitude of

the effect seems more pronounced in older individuals

and, possibly, in men. Some evidence suggests that the

deleterious effect of smoking on fracture risk is at

least partly due to mechanisms other than low BMD.

Although efforts should be directed towards appropriate

pharmacological therapy of osteoporosis, encouragement

of lifestyle alterations, including smoking cessation,

should be a major component of any bone therapeutic

programme.

ACKNOWLEDGMENTS

This work was supported in part by the Australian

National Health and Medical Research Council.

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Received 4 July 2006/28 February 2007; accepted 29 March 2007

Published on the Internet 1 August 2007, doi:10.1042/CS20060173


The Effects of Smoking on Bone Health

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