Musculoskeletal conditions refer to many different conditions that affect the muscles, bones, joints and associated tissues. They include short-term issues such as injuries and fractures, as well as chronic disabling conditions such as arthritis (inflamed joints) and osteoporosis (bone weakening). Musculoskeletal conditions are the leading contributor to disability worldwide, with lower back pain being the leading global cause of disability.1
Musculoskeletal conditions such as arthritis are very common in Australia, affecting almost 1 in 3 people. Although rarely fatal, they cause considerable illness, pain and morbidity.2
3.13.1 Bone density, osteoporosis and the risk of fractures
3.13.1.1 Effect of smoking on bone mineral density
Osteoporosis is a skeletal disease characterised by low bone mineral density (BMD) and deterioration of bone, with a consequential increase in bone fragility and risk of fractures. The diagnosis of osteoporosis is based on low BMD. The most common osteoporotic fractures are of the hip, lumbar spine and wrist. Hip fractures are the most severe.3
Osteoporosis is common and is associated with older age and female gender. Women have an almost 50% lifetime risk of an osteoporotic fracture.3 In Australia, there were 7,382 hospitalisations in 2016–17 with a principal diagnosis of osteoporosis for people aged 50 and over.4
Smoking is a risk factor for osteoporosis, as smokers have a higher risk of low BMD.5 There has been debate about whether smoking, or other risk factors present in smokers, are the causes of low BMD. Smokers may be thinner than non-smokers, drink more alcohol, may be less physically active, and have poorer diets.6 Women who smoke also tend to have an earlier menopause than non-smokers (see Section 3.6.1). These risk factors will likely impact on BMD and the risk of osteoporosis.
Taking into account the epidemiological and mechanistic evidence, the 2004 US Surgeon General’s report concluded that smoking causes low BMD in postmenopausal women.5 BMD is lower in post-menopausal smoking women than non-smokers, and the difference increases linearly with age. For every 10 years additional age, BMD decreases by about an additional 2% compared with non-smokers, leading to a difference of about 6% by the age of 80. Data for men were more limited but suggested a similar effect.7
The 2004 report of the US Surgeon General concluded only that smoking may cause low BMD in older men.5 Seemingly counterintuitively, given that smoking is an established cause of low BMD in post-menopausal women, a meta-analysis of the effect of smoking on BMD that included data from more than 40,000 subjects found that smoking has a greater deleterious effect on bone mass for men than women.8 This meta-analysis also found that the effect of smoking on BMD is dose dependent. The more that people smoked—reflected in higher pack-years, cigarettes per day or number of years smoked—the lower their bone mass.
Both this meta-analysis and the US Surgeon General’s report found insufficient evidence that smoking lowers BMD in younger people.5, 8 The meta-analysis authors suggested that this is because the total exposure to smoking in young adults is insufficient to produce discernible decrements in BMD. They cited several studies that demonstrate a significant negative impact of smoking on BMD in young adults who are heavy smokers.8
Smoking may be causing low BMD in post-menopausal women through a number of plausible mechanisms. Cadmium in cigarette smoke may have a direct effect on bone cells,9 and smokers’ bone density could also be impaired through lower absorption of calcium and vitamin D and altered metabolism of some other hormones. Smoking also affects oestrogen levels and the effectiveness of hormonal replacement therapy. Smokers have altered levels of some proteins that regulate bone formation and a lower bone turnover than non-smokers.10, 11 There may also be indirect effects of smoking on BMD. Smokers tend to have a lower body weight (see Section 3.29.1) and be less physically active than non-smokers. Both of these factors adversely affect BMD. Smokers also reach menopause earlier, on average, thereby extending the postmenopausal period of accelerated bone mineral loss.5 Emphysema, which is often caused by smoking (see Section 3.2.4.1), is a strong, independent risk factor for low BMD.12
Smoking cessation may slow or even partially reverse the loss of bone mass.8 A small randomised controlled trial showed that smoking cessation for post-menopausal women led to increases in BMD measured at the femoral trochanter (protrusion at the top of the femur) and hip, but not at three other sites.13 In a 12-month longitudinal study of 81 adults smoking cessation was associated with increased bone density as well as increased muscle mass, muscle strength and weight gain.14 Smoking cessation led to a significant increase in the levels of bone formation markers by 124 days after cessation, indicating the benefits of cessation on bone health.15
3.13.1.2 Effect of smoking on osteoporotic hip fractures
As smoking is a risk factor for osteoporosis, it would be expected that bone fractures would also increase in smokers. The 2004 Surgeon General’s report concluded that smoking increases the risk of hip fractures.5 The evidence from numerous meta-analyses discussed in the Surgeon General’s report came from studies that included diverse populations,16-20 hence the conclusion of increased risk of hip fractures was not solely for post-menopausal women.5
A meta-analysis published in 1997 found that female smokers had a 41% increase in hip fractures at age 70 years.7 A 2001 meta-analysis predicted the smoking-attributable increases in risk of hip fracture to be 31% in women and 40% in men.8 Another meta-analysis from 2005 included data for almost 60,000 people and reported a 25% increase in risk of any fracture, and an 84% increase in the risk of hip fracture, associated with smoking.21 This study suggested that smoking may also increase the risk of fractures independently of its effect on BMD.21 There was still a 12% increase in the risk of any fracture associated with smoking, after adjustment for age, BMD and body mass index. The authors suggested that this effect could be due to the poorer balance and poorer physical function that has been reported in smokers (see Section 3.13.4).22 An increase in hip fractures caused by smoking in men was also supported by a meta-analysis of 14 prospective cohort studies from 201623 and a 2012 meta-analysis of 55 studies of men.24
The role of smoking in hip fractures is also supported by a four-decade analysis using data from the Framingham Heart Study in the US.25 The incidence of hip fracture decreased over the period from 1970 to 2010, alongside a decrease in smoking and heaving drinking, while hip fractures remained more common among smokers than non-smokers. The presence of other risk factors for hip fracture were stable over the same period in this cohort of people, indicating that smoking and alcohol consumption were the most likely contributors to this increased risk of fractures.25
Smoking cessation may reduce the risk of hip fractures. A large study of female nurses aged from 35 to 59 found a reduction in the risk of hip fractures for those who quit smoking. The risk of hip fracture was 0.70 times that of current smokers for women who had quit for at least 10 years.26 A 2015 meta-analysis of studies in women also found that former smokers, who had quit for 10 years, had a reduced risk of hip fracture compared to current smokers.27 One study has found a significantly reduced risk of hip fractures in male former smokers after 5 years cessation, but did not find a similar reduction in females over this time period.28
3.13.2 Delayed bone union
There is increasing evidence from both observational and experimental studies that smoking delays bone healing (union) after fracture or surgery.29-32 After elective foot surgery, for example, a 42% increase in the time to bone healing has been reported.33 Smoking has been found to increase the chance of non-union after spinal fusion surgery34 and to worsen outcomes.35 In a study of 249 people undergoing rotator cuff surgery, smokers showed a significantly higher healing failure rate than non-smokers.36
3.13.3 Back pain
Back pain is caused by various factors such as muscle strain or displacement of discs between the vertebrae in the spine.2, 37 Lower back pain is estimated to be the single leading cause of disability globally.1
There have been suggestions in the medical and health economic literature that smoking causes lower back pain and increases the incidence of sick leave due to back pain.38, 39 Assessing the association of smoking with lower back pain and the potential for a causative relationship is challenging because smoking is associated with, and causes, many different chronic conditions that could impact on physical functioning and sedentary lifestyle. Considerable effort is required to adjust for potential bias and confounding factors in order to assess whether smoking is a direct cause of lower back pain. Although many studies have demonstrated an association of smoking and lower back pain, further research that better accounts for bias and confounding factors is required to determine whether this relationship is causative.
A meta-analysis of all studies published until February 2009 has shown an increase in lower back pain in current and former smokers.40 The association was stronger in adolescents than adults and was more pronounced for chronic back pain and severe back pain. The authors of the meta-analysis speculated that the effect could be due to reduced perfusion of intervertebral discs. An analysis of the link between smoking and lower back pain in more than 70,000 Canadians was published in 2010.41 Smoking increased the likelihood that survey participants of all ages would have lower back pain, after adjustment for body mass index, level of activity and other factors that could have explained the association. The risk of having lower back pain was about 80% higher in daily smokers aged 20 to 29 years. The excess risk decreased with age but was still statistically significant at all ages. That smoking increases the risk of lower back pain was also the conclusion of a 2019 population-based longitudinal study of Finnish people.42 A study of 200 adults with back pain found that smokers had increased risk of lumbar disc degeneration than non-smokers. This risk remained higher even when other risk factors such as systemic disease, heavy working conditions, obesity, trauma and family history were accounted for.43 A large registry study of over 200,000 men found that smokers had small increases in risk, compared to non-smokers, of lower back pain, intervertebral disc disease, spinal stenosis (pressure on nerves in the spine due to narrowing of the space), spinal instability and spondylolisthesis (where a vertebrae has slipped forward onto the bone beneath it).44 This analysis took account of other risk factors such as age, physical activity, alcohol intake and socioeconomic status.
Some plausible mechanisms by which smoking may increase lower back pain have been described. Nicotine may alter the perception and threshold for pain, thereby increasing the self-reporting of pain. A smoking-induced increase in circulating pro-inflammatory cytokines and inflammation, may lead to amplification of pain. An increase in coughing by smokers may also increase lower back pain through muscle strains.45
3.13.4 Arthritis
For rheumatoid arthritis, see Section 3.17.1.
Osteoarthritis is a common chronic condition in Australia that involves the wearing down and loss of cartilage in the joints, most commonly the knees, hips and fingers.46 Smoking may be associated with joint cartilage loss.47
A 2011 meta-analysis of 48 studies, including more than 500,000 participants, investigated the association between smoking and osteoarthritis.48 The analysis found that the protective effect of smoking observed in some studies, but not others, is likely to be false and may be caused by selection bias. The effect was seen in hospital-based case-control studies (where the control subjects are more likely to have smoking-related conditions), but not in community-based case-control studies, cohort studies or cross-sectional studies. A study from 2016 concluded that long-term smoking provided no benefits to knee osteoarthritis patients while exposing them to other well-documented serious health risks.49 More studies are required to clarify the relationship between smoking and osteoarthritis.
Smoking may affect joint cartilage through the toxicity of cadmium found in smoke.50
3.13.5 Other musculoskeletal problems
A study of almost 10,000 women aged 65 years and over in the US found that smokers had poorer physical function than non-smokers, as measured by tests of muscle strength, agility, co-ordination, gait and balance, and self-reported physical status.22 The researchers likened the poorer physical function to a hastening of ageing by about five years, and suggested that the effect may be due to the poorer vascular function consequential to smoking.
Smoking has been reported to increase the risk of tears of the rotator cuff (the muscles and tendons that stabilise the shoulder).51 Tobacco, as well as alcohol use, is also associated with secondary musculoskeletal injury after lower limb amputation.52
Sarcopenia is a progressive loss of skeletal muscle mass and strength that occurs with ageing and/or physical immobility. A prospective study of people aged 65 and over showed that smokers were over-represented in those who developed sarcopenia.53 Smoking may therefore be a risk factor for sarcopenia, but more research is required to confirm this and determine whether smoking may have a causative role.
Relevant news and research
For recent news items and research on this topic, click here. ( Last updated October 2024)
References
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