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Smoking Related Musculoskeletal Disorders- A Review

* Vijay Kumar Jain, #Deepali Jain, *B.S. Murthy, *Deepak Mittal,

*Department of Orthopaedics, Dr RML Hospital, New Delhi, India
#Department of Pathology,  All India Institute of Medical Sciences, New Delhi, India

Address for Correspondence

Dr Vijay Kumar Jain,
Medical Officer, Dr RML Hospital, New Delhi, 110001, India.
Phone No. 098685-68031

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


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).


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.


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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This is a peer reviewed paper 

Please cite as : Vijay Kumar Jain: Smoking Related Musculoskeletal Disorders- A Review

J.Orthopaedics 2006;3(2)e5





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