Abstract :
Objective: Cigarette smoking is the
most preventable cause of premature death in this country, and
is responsible for one in five deaths from all causes. Millions
of other people are living with serious illnesses caused by
smoking. Smoking has been linked with many health problems
including an array of orthopaedic conditions and complications.
In the past, there have been many individual reports that deal
with these relationships separately but very few published
comprehensive reviews. The objective of this study is to review
the available literature to find out the effects of smoking on
the musculoskeletal system and the subsequent orthopaedic
problems.
Data sources: We have used predominantly online
facilities mainly pubmed google search engine, yahoo and alta
vista search engine. In addition orthogate and orthopedic
weblinks were utilized for the study purpose. English language
papers have been quoted in the present review. Time period of
review started from selected topics of 1976-2005.
Study selection: All international indexed journals were
used based on smoking related musculoskeletal disorders.
Data extraction: Majority of articles were chosen from
the journals with good impact factor.
Data synthesis: An elaborate discussion over smoking
related orthopedic problems is presented in the present review.
Conclusion: There is a real and reproducible
relationship between smoking and musculoskeletal system. So
therefore quitting smoking help our body regain its normal
healthy functioning. If someone is smoker, he should talk to his
physician about stop-smoking techniques.
Key words: smoking, musculoskeletal disorders,
osteoporosis, arthritis, fracture
J.Orthopaedics 2006;3(2)e5
Introduction:
Tobacco smoking is the second major cause of
death in the world. It is currently responsible for the death of
one in ten adults worldwide (about 5 million deaths each year).
If current smoking patterns continue, it will cause some 10
million deaths each year by 2020. Half of the 650 million people
that smoke today will eventually be killed by tobacco.
“Cigarette smoking continues to impose substantial health and
financial costs on individuals and society. It’s in everyone’s
best interest to prevent and reduce tobacco use”.
Cigarette contains about 109 known chemicals
including nicotine, benzene, tar etc which harm an individual.
Nicotine has a significant negative role on musculoskeletal
system. Nicotine in tobacco products causes peripheral
vasoconstriction and tissue ischemia and decreases oxygen
tension. Moreover, nicotine depresses osteoblast activity, may
inhibit revascularization of bone graft (1), has a negative
impact on bone healing (2) and inhibits the expression of a wide
range of cytokines including those associated with
neovascularization and osteoblast differentiation (3). It
increases the risk of bone fractures, reduces estrogen
effectiveness, and can counter the antioxidant properties of
vitamins C and E.
The objective of this study is to review the
available literature to find out the effects of smoking on the
musculoskeletal system and the subsequent orthopaedic problems.
Smoking and
osteoporosis:
Lowering of bone mineral density in smokers
was shown 20 years ago, (4). Post-menopausal women who smoke
loose significantly more cortical bone, and have more spinal
osteoporosis than nonsmoking counterparts. Cigarette smoking may
increase bone resorption at the fracture ends (5,6). In addition
smoking may negate the protective skeletal effects of estrogen
replacement therapy (7). Smoking also lowers bone mineral
density, and is a result of decreased calcium absorption
associated with secondary hyperparathyroidism and increased bone
resorption (8). Subsequent studies have also demonstrated a
direct relationship between tobacco use and decreased bone
density. In addition, a relationship between cigarette smoking
and low bone density in adolescence and early adulthood has been
identified.
In order to elucidate the influence of
nicotine smoking on bone mass in elderly women, bone mass was
assessed by dual energy X-ray absorptiometry (DXA) in total
body, hip and lumbar spine, as well as with ultrasound of
calcaneus and phalanges of the hand. Gerdhem concluded that
nicotine smoking has a negative influence on bone mass
independent of differences in weight and physical activity (9).
It has been found that while estrogen
replacement protected women from fracture, this protective
effect was eliminated in women who smoked. The results support
an anti-estrogenic effect of cigarette smoking that is
consistent with the conclusions of other researchers. Other
reports have suggested that smokers have less effective
absorption of calcium, opposite to the effect of estrogen, which
is believed to enhance calcium absorption. The anti-estrogen
effect of tobacco use may help explain the increased risk for
osteoporosis among female smokers. Postmenopausal smokers have
lower estrogen levels than non-smokers and smokers tend to have
an earlier menopause than their non-smoking counterparts. This
reduction in estrogen is likely to result in an increase in bone
resorption, contributing to osteoporosis.
In men, smoking at any stage of life had
adverse effects on the skeleton that was independent of weight,
alcohol or caffeine use, implying other mechanisms of effect on
bone. Among men, a consistently lower bone mineral density (BMD)
at all skeletal sites was observed for smokers regardless of
when in their life they smoked. While, in women who had used
estrogen, BMD was lower in current or recent smokers than it was
in non-smokers. Studies have shown that smoking reduces the
blood supply to bones and that nicotine slows the production of
bone-forming cells (osteoblasts) and impairs the absorption of
calcium. With less bone mineral, smokers develop fragile bones
(osteoporosis).
Smoking and risk of
fracture:
While the first suggestion of an association
between tobacco smoking and osteoporosis was published in 1976
(4), several studies have examined the effect of tobacco smoking
on bone mineral density and risk of fracture. Smoking is widely
considered a risk factor for future fracture. Several biological
effects of tobacco may influence the risk of fracture in
smokers. Smoking may exert adverse effects on bone strength
through direct toxicity of nicotine and non-nicotine components
of cigarette smoke on bone cells, as demonstrated in vitro
(10,11). Further, smoking may indirectly affect bone strength
through decreased intestinal calcium absorption (12), increased
metabolism or decreased production of estrogen (13), and through
hypercortisolism (14). In addition, smoking may influence the
fracture risk through other mechanisms unrelated to
osteoporosis, such as poorer balance and physical performance
due to neurovascular and peripheral vascular deleterious effects
of smoking (15). Nicotine can counteract the antioxidant effects
of vitamins C and E and lead to a significantly higher risk of
bone fracture. Recent meta-analyses on the effects of smoking on
the bone revealed that current smokers sustained decreased bone
mass and increased fracture risk at age 50 years and older.
These relationships remained significant after adjustment for
the effects of age, years since menopause and body weight
regardless of sex. The raised risk of fractures was observed to
be consistent at all sites (16). Ex-smoker ran the intermediate
risk between non-smoker and current smoker, which implies
beneficial effect of quitting smoking (17, 18).
It has recently been indicated that
intrauterine exposure to tobacco smoke retards skeletal growth
resulting in increased risk for fracture later in life, which
should be confirmed by further studies(16). It is estimated that
smoking increases the lifetime risk of developing a vertebral
fracture by 13% in women and 32% in men. Kanis et al,
quantified the risk of smoking on an international basis and
explored the relationship of this risk with age, sex and bone
mineral density (BMD) (19). Risk ratios were significantly
higher in men than in women for all fractures. At the hip,
smoking is estimated to increase lifetime fracture risk by 31%
in women and 40% in men (18). Cigarette smoking is a risk factor
for hip fracture among postmenopausal women; risk decreases
after cessation (20). A meta-analysis based on these studies
recently concluded that postmenopausal bone loss is greater in
smokers than in non-smokers and that tobacco smoking increases
lifetime risk of hip fracture in women by about 50% (21). A
similar adverse effect of smoking is suspected to be present in
men, but recent bone mineral density studies have raised the
concern that men may be more sensitive to the deleterious effect
of smoking on bone than women (22, 23). Smoking cessation
reduces the risk of hip fracture in men after 5 years, while the
deleterious effect of smoking seems to be more long-lasting in
female ex-smokers Association between BMD, smoking and risk of
fractures was studied (20) and low BMD accounted for only 23% of
the smoking-related risk of hip fracture. Adjustment for body
mass index had a small downward effect on risk for all fracture
outcomes. For fracture associated with osteoporosis, the risk
ratio increased with age but not for fracture around hip.
Current smokers have lower risk compared to chronic smokers.
While the association between tobacco use and decreased bone
density is fairly strong, Most studies suggest at least a slight
association between cigarette smoking and fracture, especially
hip fracture and vertebral fracture.
It appears that smoking has an independent,
dose-dependent effect on bone loss, which increases fractures.
risk, and may be partially reversed by smoking cessation. Given
the public health implications of smoking on bone health, it is
important that this information be incorporated into smoking
prevention and cessation efforts (24).
Smoking and healing problems: Current data
show smoking is associated with a number of complications of the
fracture healing process. Current smokers are more than twice as
likely to develop an infection and develop osteomyelitis.
Previous smokers are more likely to develop osteomyelitis but
are at no greater risk for other types of infection. It is
concluded that Smoking places the patient at risk for increased
time to union and complications. Previous smoking history also
appears to increase the risk of osteomyelitis and increased time
to union (25)
Smoking decreases unions, slows healing (26,
27, 28) and increases complications such as increase rate of
flap failure (29, 30). For smokers in one arm of the study, time
to union was significantly longer, and there were more
complications smokers had a 4.1 fold risk of tibial shaft
fracture caused by low-energy injury, compared with non-smokers
(31). An accelerated failure time model showed that the more
comminuted or open the fracture, the higher the number of
cigarettes smoked and the older the patient, the longer was the
time to clinical union of the tibia shaft fracture. Female sex
appeared to be a further risk factor for delayed healing in this
group (26) Smoking is negatively associated with the healing of
open tibia fractures. In smoking patients, the time to
consolidation is on average statistically significantly longer
and they suffered more from osteitis. Smokers remained longer in
hospital and underwent more re-operation (32).
The pathophysiological effects are
multidimensional, including arteriolar vasoconstriction,
cellular hypoxia, demineralization of bone, and delayed
revascularisations. Nicotine seems to play a significant role in
causing the lack of oxygen to the tissues. Research has begun to
accumulate definitely linking smoking to difficulty in healing
fractures. It is felt that smokers have a significant deficiency
of oxygen (hypoxia) at the cellular level where the fracture is
trying to heal. Fractures heal normally in areas which have good
blood supply and a very adequate oxygen supply in the region of
the fracture. Micro vascular and trauma surgeons have documented
the adverse effect of smoking in the healing of skin flaps and
increased complication rates in the treatment of nonunion. In
addition, spine surgeons have shown the adverse effects of
smoking in fusion rates (33) An increased rate of pseudarthrosis
has been documented following posterolateral lumbar spine
grafting in patients who smoke (34). Smoking had a significant
negative impact on healing and clinical recovery after
multilevel anterior cervical decompression and fusion with
autogenous interbody graft for radiculopathy or myelopathy (34).
A review of the smoking habits in 426 patients who had been
followed prospectively for 2 years after a lumbar spinal fusion
procedure was conducted. It was to analyze the effect of pre-
and postoperative smoking on clinical and functional outcome
after lumbar spinal fusion. Smoking was shown to have a negative
effect on fusion and overall patient satisfaction. Smoking
cessation increased fusion rates to near those of nonsmokers
(35).
In a study on spinal fusions in the lower
back, the success rate was 80 to 85 percent for patients who
never smoked or who quit smoking after their surgery. The
success rate dropped to under 73 percent for smokers. More than
70 percent of nonsmokers and previous smokers were able to
return to work. But only about half of the smokers were able to
resume working. Another study on spinal fusions in the neck
showed successful fusion in 81 percent of nonsmokers, but in
only 62 percent of smokers. The effects of nicotine appear to
involve more than just local area (3) because nicotine inhibits
expression of a wide range of cytokines, including those
associated with neovascularization and osteoblast
differentiation.
The problem has also been observed in other
orthopaedic procedures in which a bone graft is done to fuse a
particular area of the body. Examples of this would be a fusion
of an arthritic ankle joint fusion of joints in the foot (36-38)
and sometimes in the hand. In fact, some orthopaedic surgeons in
their practice have insisted that patients stop smoking before
elective bone graft surgery is done. They feel that the
incidence of delayed healing of bone graft procedures is so high
that it would not be worth proceeding with the bone graft
surgery while the patient is still smoking. This delayed process
of healing has been observed in almost every type of fracture
that orthopaedic surgeons deal with when they are treating
patients who smoke. Nicotine has been shown in previous studies
to decrease production of fibroblasts (the main cells
responsible for tissue repair). In addition, the carbon monoxide
found in tobacco smoke reduces cellular oxygen tension levels,
which are vital for cellular metabolism and tissue healing (39).
To investigate the success of exchange reamed
femoral nailing in the treatment of femoral nonunion after
intramedullary (IM) nailing, and to analyze factors that may
contribute to failure of exchange reamed femoral nailing, Hak
David and coauthors did a retrospective study among smokers and
nonsmokers. They found a detrimental impact on the success of
exchange reamed nailing in smokers. All eight of the non-smokers
healed after exchange reamed nailing, whereas only ten of the
fifteen smokers (66.7 percent) healed after exchange reamed
nailing. Tobacco use appears to have an adverse effect on
nonunion healing after exchange reamed femoral nailing (40).
McKee, et al have done a retrospective review
of 84 adult patients (86 limbs) who underwent Ilizarov
reconstruction to determine the effect of smoking on outcome and
complication rates following Ilizarov reconstruction. There was
a higher incidence of nonunion in the smoking group .They
concluded that smokers had a higher percentage of poor results
due primarily to higher complication rates (41). Smoking is a
significant, potentially remediable risk factor for failure
following Ilizarov reconstruction, and cessation strategies are
of paramount importance prior to initiating treatment.
In one other study smokers had a
significantly higher rate of nonunion than did nonsmokers (18.6%
vs. 7.1%). However, quitting smoking seems to improve the
healing process in most cases, except for long-term, heavy
smokers who have permanent artery damage due to smoking. Delayed
or impaired healing of skeletal trauma in patients who smoke has
been attributed to vascular responses of nicotine absorption
and/or a direct effect of nicotine or other smoke components on
bone cells. In vivo studies indicate variability in
osteosynthetic response to nicotine versus smoke inhalation. It
has been hypothesized that components of cigarette smoke other
than nicotine may be responsible for the adverse skeletal
effects of smoking.
The negative effects of smoking gained
increased interest among plastic and micro vascular surgeons,
because smokers have been shown to suffer higher rates of flap
failure, tissue necrosis, and haematoma formation. Especially
smokers presenting with an open tibia fracture will suffer the
negative effects of their smoking behavior because these
fractures are inextricably bound up with soft-tissue injury.
Their fractures will need a significantly longer time to heal
than in non-smokers, and will have a higher incidence of
non-union. If micro vascular surgery is to be performed,
persistent smoking significantly increases the rate of
postoperative complications, with wound infection, partial flap
necrosis, and skin graft loss being more common(42).
Cessation of smoking has both short- and
long-term beneficial effects. Nowadays, there is strong evidence
to be very insistent that patients presenting with a (open)
tibia fracture should refrain from smoking immediately to
promote bone healing and to lower the complication rate. In case
of elective reconstructive procedures, patients should refrain
from smoking at least 4 weeks before surgery. In both
situations, cessation should continue during the full
rehabilitation period.
Smoking and increase
morbidity:
Smoking has been shown to increase morbidity
and mortality in surgical procedures Smoking is an important
risk factor for the development of postoperative pulmonary
complications after major surgical procedures Moller et al,
studied 811 consecutive patients who had undergone hip or knee
arthroplasty, recording current smoking and drinking habits, he
recorded any postoperative complications occurring before
discharge from hospital. They found that smoking was the single
most important risk factor for the development of postoperative
complications, particularly those relating to wound healing,
cardiopulmonary complications, and the requirement of
postoperative intensive care. A delay in discharge from hospital
was usual for those suffering a complication. In those patients
requiring prolonged hospitalisation (>15 days) the proportion of
smokers with wound complications was twice that of non-smokers.
(43)
A study was done to assess the effects of
smoking on the incidence of short term complications, resource
consumption, and length of hospital stay of patients undergoing
arthroplasty of the hip and knee. Patients who smoked were found
to have statistically longer surgical time and higher charges
adjusted for age, procedure, and surgeon than patients who did
not smoke. Patients who smoked also had longer anesthesia times.
Preoperative screening for nicotine use can predict operative
time and health resource consumption. The exact reasons why
patients who smoked had higher hospital charges remain elusive.
Probable reasons include higher degree of operative complexity (orthopaedic
severity of illness). In addition patients who smoked previously
also had better short term outcome than patients who currently
smoke. This indicates the importance of smoking abstinence
before joint replacement surgery and other surgical procedures.
Regardless of the exact causes, it is more expensive to treat
patients who smoke. Therefore contracting for orthopaedic care
should include a history of smoking (44).
In addition according to Lindstrom et al (45)
preoperative cessation of smoking seems to reduce the frequency
of complications. Tobacco smokers suffer from postoperative
complications after surgery more often than non-smokers. This
has been proven in general, orthopaedic and plastic surgery. In
recent years, preoperative smoking cessation has been evaluated
in several studies. It has been shown that smoking cessation
four to eight weeks prior to surgery significantly reduces wound
healing complications. There are still some unanswered questions
concerning the necessary length of preoperative smoking
cessation to affect the complication rate. There is also lacking
evidence on smoking cessation in emergency surgery, and the
cost-effectiveness of a smoking cessation intervention programme.
Therefore, further studies on preoperative smoking cessation are
needed. Smokers had slightly higher post treatment self-reported
pain and disability ratings mixed and limited. Overall, there is
evidence for the widely held belief that smoking negatively
affects tertiary rehabilitation (46).
Smoking and spinal
problems:
There is a definite link between smoking and
low back pain that increases with the duration and frequency of
the smoking (47). In several studies, smoking has been
associated with the occurrence of spinal pain, mostly low back
pain, and also neck pain and prolapsed cervical intervertebral
discs (48). Exposure to secondhand smoke during childhood may
increase the risk of developing back and neck problems in later
life.
Associations between back pain prevalence and
lifestyle factors (smoking and obesity) were analysed. Back pain
prevalence rose with increasing levels of smoking, with a
relative risk of 1.47 for persons reporting 50 or more
pack-years of smoking. This association was strongest in persons
under the age of 45 years, however, for whom the corresponding
relative risk was 2.33. (49)
Vogt MT, investigated the association between
the smoking status of spinal patients, duration and severity of
symptoms, and their self-reported health status: Smokers and
nonsmokers had had spinal symptoms for similar duration, but the
smokers reported more severe symptoms, which were present for a
greater proportion of time each day. Also, the smokers had lower
physical and mental health status scores than did nonsmokers
(50).
Numerous studies confirm that smoking is a
strong risk factor for back pain and associated with an
increased risk for prolapsed disc. Several explanations for the
association have been proposed. Smoking might provoke disc
herniation through coughing, or lead to pathological changes in
the intervertebral disc through alterations in its nutrition,
pH, or mineral content. Another possibility is that smoking has
a pharmacological effect on pain perception (51-55).
The most widely accepted explanations for the
association between smoking and disc degeneration is
malnutrition of spinal disc cells by carboxy-hemoglobin-induced
anoxia or vascular disease. Nicotine, a constituent of tobacco
smoke, present in most body fluids of smokers is known to have
detrimental effects on a variety of tissues. It may also be
directly responsible for intervertebral disc (IVD) degeneration
by causing cell damage in both the nucleus pulposus and annulus
fibrosus. Experimental investigation has been done to determine
the effect of nicotine on intervertebral spinal disc nucleus
pulposus (NP) cells cultured in vitro. It was to evaluate the
effects of nicotine on cell proliferation, extra cellular matrix
production, and viability of NP cells. There was significant
inhibition of cell proliferation and extra cellular matrix
synthesis. Hence nicotine in tobacco smoke may have a role in
pathogenesis of disc degeneration.
Spine surgeons have shown the adverse effects
of smoking in fusion rates (33) An increased rate of
pseudarthrosis has been documented following posterolateral
lumbar spine grafting in patients who smoke. (34) Smoking had a
significant negative impact on healing and clinical recovery
after multilevel anterior cervical decompression and fusion with
autogenous interbody graft for radiculopathy or myelopathy (34).
A review of the smoking habits in 426 patients who had been
followed prospectively for 2 years after a lumbar spinal fusion
procedure was conducted. It was to analyze the effect of pre-
and postoperative smoking on clinical and functional outcome
after lumbar spinal fusion. Smoking was shown to have a negative
effect on fusion and overall patient satisfaction. Smoking
cessation increased fusion rates to near those of nonsmokers
(35)
In a study on spinal fusions in the lower
back, the success rate was 80 to 85 percent for patients who
never smoked or who quit smoking after their surgery. The
success rate dropped to under 73 percent for smokers. More than
70 percent of nonsmokers and previous smokers were able to
return to work. But only about half of the smokers were able to
resume working. Another study on spinal fusions in the neck
showed successful fusion in 81 percent of nonsmokers, but in
only 62 percent of smokers. The effects of nicotine appear to
involve more than just local because nicotine inhibits
expression of a wide range of cytokines, including those
associated with neovascularization and osteoblast
differentiation (3).
Smoking and
Inflammatory polyarthropathies:
Anecdotal suggestions and retrospective
studies indicate an inverse relationship between the incidence
of osteoarthritis and individuals who smoke. As a possible
explanation, studies confirm that nicotine upregulates
glycosaminoglycan and collagen synthetic activity of articular
chondrocytes at physiological levels seen in individuals who
smoke (56). Rheumatoid arthritis (RA) is considered to be a
multifactorial disease, resulting from the interaction of both
genetic and environmental factors, which contribute to its
occurrence and expression.The main genetic risk factor for RA is
the shared epitope (SE) of HLA-DR, while smoking is an important
environmental risk factor particularly rheumatoid factor (RF)
positive RA .(57) The disease risk of RF-seropositive RA
associated with one of the classic genetic risk factors for
immune-mediated diseases (the SE of HLA-DR) is strongly
influenced by the presence of an environmental factor (smoking)
in the population at risk (58) and also there is strong
association between smoking and rheumatoid nodule in early
seropositive RA. (59). smoking also seems to influence the
disease outcome. Data suggest that disease outcome in female RA
patients with a history of smoking is significantly worse than
in those who have never smoked. According to a recent study,
maternal smoking in pregnancy is regarded as a determinant of
rheumatoid arthritis and other inflammatory polyarthropathies
during the first 7 years of life.There is a potential effect of
foetal exposure to tobacco smoke on the risks of RA & IP
(Inflammatory polyarthropathies) and juvenile rheumatoid
arthritis in girls (60). Gender interacts with smoking in by an
unknown mechanism to lead to differential risk of RA. (61)
Smoking and soft
tissue problems :
Cigarette smokers have an increased risk of
rotator cuff tears,a strong trend was found between smoking and
history of rotator cuff tear . Rotator cuff (shoulder) tears in
smokers are nearly twice as large as those in nonsmokers.
Smoking also has a negative impact on
surgeries that focus on muscles, such as rotator cuff repairs
(62). One study compared the results of 235 patients treated at
two different medical institutions. Results in nonsmokers were
significantly better than results in smokers. Nonsmokers
experienced less pain and a higher degree of function after
surgery than smokers.
Dupuytren's contracture is a deforming,
fibrotic condition of the palmar fascia The etiology of
Dupuytren's disease is still unknown in spite of significant
recent advances in identifying the type of cell responsible for
initiating the process (63).Smoking is linked statistically to
Dupuytren's disease and may be involved in its pathogenesis by
producing microvascular occlusion and subsequent fibrosis and
contracture (64).
Miscellaneous:
Perthes' disease is an idiopathic necrosis of
the capital femoral epiphysis. Passive smoking is a significant
factor. The risk of Legg-Calve-Perthes disease (LCPD) in passive
smoking children is more than five times higher than in children
who are not exposed to smoke. It seems that passive smoking is a
factor directly or indirectly associated with LCPD (65). Parents
who smoke at home put children at risk of developing LCPD.
Statistical analysis shows an extremely strong association
between smoking in the home and the presence of second-hand
smoke seem to be significant risk factors in the development of
LCPD (66). Secondhand smoke exposure while in utero and during
childhood appears to lower stimulated tissue plasminogen
activator activity and additionally may depress heritable low
stimulated tissue plasminogen activator activity, leading to
hypofibrinolysis. Hypofibrinolysis may facilitate thrombotic
venous occlusion in the head of the femur, leading to venous
hypertension, hypoxic bone death and LCPD (67).
There is a known association of alcohol
intake, cigarette smoking, occupation, and other factors with
the development of idiopathic osteonecrosis of the femoral head
(68-70).
Smoking has a detrimental effect on athletic
performance. Because smoking slows lung growth and impairs lung
function, there is less oxygen available for muscles used in
sports. Smokers suffer from shortness of breath almost three
times more often than nonsmokers. Smokers cannot run or walk as
fast or as far as nonsmokers.
Conclusion:
Experience has shown that there are many cost-effective tobacco
control measures that can be used in different settings and that
can have a significant impact on tobacco consumption. The most
cost-effective strategies are population-wide public policies,
like bans on direct and indirect tobacco advertising, tobacco
tax and price increases, smoke-free environments in all public
and workplaces, and large clear graphic health messages on
tobacco packaging Smoking has been linked with many health
problems, surgeons have known about the relationships that
putatively exist between smoking and an array of orthopaedic
conditions and complications. Although scientific and clinical
information on smoking and its consequences suggests differing
degrees of correlation between smoking and orthopaedic
conditions, most available data do suggest a real and
reproducible relationship. In the past, there have been many
individual reports that deal with these relationships separately
but very few published comprehensive reviews. This summary of
the current literature regarding the relationship between
smoking and musculoskeletal diseases provides information that
can be used clinically. Every tissue in the human body is
affected by smoking, but many effects are reversible. By
avoiding or quitting smoking, we can reduce our risk for
incurring many conditions.
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