3.13 Musculoskeletal diseases

Last updated:  August 2020

Suggested citation: Winnall, WR, Hurley, S & Winstanley, MH. 3.13 Musculoskeletal conditions. In Greenhalgh, EM, Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2020. Available from http://www.tobaccoinaustralia.org.au/chapter-3-health-effects/3-13-musculoskeletal-conditions  

 

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 counterintuitive, a meta-analysis of the effect of smoking on BMD that included data from more than 40,000 subjects found that smoking has a more 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 women and younger men.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, 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.9 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

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.10 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.11

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, but found that there was inadequate evidence at that time to reach the same conclusion about smoking and fractures of other bones.5 The evidence from numerous meta-analyses discussed in the Surgeon General’s report has come from studies that included diverse populations,12-16 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.17 This study suggested that smoking may also increase the risk of fractures independently of its effect on BMD.17 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 Chapter 3, Section 3.13.4).18 An increase in hip fractures caused by smoking in men was also supported by a meta-analysis of 14 prospective cohort studies from 201619 and a 2012 meta-analysis of 55 studies of men.20

Smoking cessation may reduce the risk of hip and other fractures. A 10-year prospective observational study followed 1,033 women from the age of 75 to study fracture risk. Multivariate analysis was used to adjust for different levels of other risk factors such as alcohol intake and BMD. In this study, smoking cessation decreased the risk of vertebral fractures, but not other fractures. However, by adjusting for differences in BMD, this study may not have detected fracture risk caused by smoking-induced loss of BMD.21 

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.22-25 After elective foot surgery, for example, a 42% increase in the time to bone healing has been reported.26 Smoking has been found to increase the chance of non-union after spinal fusion surgery27 and to worsen outcomes.28 In a study of 249 people undergoing rotator cuff surgery, smokers showed a significantly higher healing failure rate than non-smokers.29 

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, 30 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.31, 32 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.33 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 2010.34 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.35  

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.36

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.37 Smoking may be associated with joint cartilage loss.38

A 2011 meta-analysis of 48 studies, including more than 500,000 participants, investigated the association between smoking and osteoarthritis.39 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.40 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.41

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.18 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).42


Relevant news and research

For recent news items and research on this topic, click  here. (Last updated October 2020)

 

References 

1. World Health Organization. Musculoskeletal conditions. Geneva, Switzerland: WHO, 2020. Available from: https://www.who.int/news-room/fact-sheets/detail/musculoskeletal-conditions.

2. Australian Institute for Health and Welfare. Chronic musculoskeletal conditions. Canberra, Australia: AIHW, 2019. Available from: https://www.aihw.gov.au/reports-data/health-conditions-disability-deaths/chronic-musculoskeletal-conditions/about.

3. Johnell O and Kanis J. Epidemiology of osteoporotic fractures. Osteoporosis International, 2005; 16 Suppl 2:S3-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15365697

4. Australian Institute for Health and Welfare. Osteoporosis web report. Canberra, Australia: AIHW, 2019. Available from: https://www.aihw.gov.au/getmedia/507c3057-c3cd-4894-83e3-0fb68e357a37/Osteoporosis.pdf.aspx?inline=true.

5. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: https://www.cdc.gov/tobacco/data_statistics/sgr/2004/index.htm.

6. NIH Osteoporosis and Related Bone Diseases National Resource Center. Smoking and bone health. Bethesda, US: NIH, 2018. Available from: https://www.bones.nih.gov/health-info/bone/osteoporosis/conditions-behaviors/bone-smoking.

7. Law MR and Hackshaw AK. A meta-analysis of cigarette smoking, bone mineral density and risk of hip fracture: recognition of a major effect. BMJ, 1997; 315(7112):841-6. Available from: https://www.ncbi.nlm.nih.gov/pubmed/9353503

8. Ward KD and Klesges RC. A meta-analysis of the effects of cigarette smoking on bone mineral density. Calcified Tissue International, 2001; 68(5):259-70. Available from: https://www.ncbi.nlm.nih.gov/pubmed/11683532

9. Jorde R, Stunes AK, Kubiak J, Grimnes G, Thorsby PM, et al. Smoking and other determinants of bone turnover. PLoS ONE, 2019; 14(11):e0225539. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31765401

10. Oncken C, Prestwood K, Kleppinger A, Wang Y, Cooney J, et al. Impact of smoking cessation on bone mineral density in postmenopausal women. Journal of Women's Health, 2006; 15(10):1141-50. Available from: https://www.ncbi.nlm.nih.gov/pubmed/17199455

11. Rom O, Reznick AZ, Keidar Z, Karkabi K, and Aizenbud D. Smoking cessation-related weight gain--beneficial effects on muscle mass, strength and bone health. Addiction, 2015; 110(2):326-35. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25312589

12. Baron JA, Farahmand BY, Weiderpass E, Michaelsson K, Alberts A, et al. Cigarette smoking, alcohol consumption, and risk of hip fracture in women. Archives of Internal Medicine, 2001; 161(7):983-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/11295961

13. Burger H, de Laet CE, Weel AE, Hofman A, and Pols HA. Added value of bone mineral density in hip fracture risk scores. Bone, 1999; 25(3):369-74. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10495142

14. Forsen L, Bjartveit K, Bjorndal A, Edna TH, Meyer HE, et al. Ex-smokers and risk of hip fracture. American Journal of Public Health, 1998; 88(10):1481-3. Available from: https://www.ncbi.nlm.nih.gov/pubmed/9772848

15. Kanis J, Johnell O, Gullberg B, Allander E, Elffors L, et al. Risk factors for hip fracture in men from southern Europe: the MEDOS study. Mediterranean Osteoporosis Study. Osteoporosis International, 1999; 9(1):45-54. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10367029

16. Melhus H, Michaelsson K, Holmberg L, Wolk A, and Ljunghall S. Smoking, antioxidant vitamins, and the risk of hip fracture. Journal of Bone and Mineral Research, 1999; 14(1):129-35. Available from: https://www.ncbi.nlm.nih.gov/pubmed/9893075

17. Kanis JA, Johnell O, Oden A, Johansson H, De Laet C, et al. Smoking and fracture risk: a meta-analysis. Osteoporosis International, 2005; 16(2):155-62. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15175845

18. Nelson HD, Nevitt MC, Scott JC, Stone KL, and Cummings SR. Smoking, alcohol, and neuromuscular and physical function of older women. Study of Osteoporotic Fractures Research Group. JAMA, 1994; 272(23):1825-31. Available from: https://www.ncbi.nlm.nih.gov/pubmed/7990216

19. Wu ZJ, Zhao P, Liu B, and Yuan ZC. Effect of Cigarette Smoking on Risk of Hip Fracture in Men: A Meta-Analysis of 14 Prospective Cohort Studies. PLoS ONE, 2016; 11(12):e0168990. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28036356

20. Drake MT, Murad MH, Mauck KF, Lane MA, Undavalli C, et al. Clinical review. Risk factors for low bone mass-related fractures in men: a systematic review and meta-analysis. Journal of Clinical Endocrinology and Metabolism, 2012; 97(6):1861-70. Available from: https://www.ncbi.nlm.nih.gov/pubmed/22466344

21. Thorin MH, Wihlborg A, Akesson K, and Gerdhem P. Smoking, smoking cessation, and fracture risk in elderly women followed for 10 years. Osteoporosis International, 2016; 27(1):249-55. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26302684

22. Adams CI, Keating JF, and Court-Brown CM. Cigarette smoking and open tibial fractures. Injury, 2001; 32(1):61-5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/11164405

23. Al-Mukhtar SA. The effect of cigarette smoking on bone healing in elderly individuals with Colle’s fracture. Tobacco Use Insights, 2010; 3:17–22. Available from: https://journals.sagepub.com/doi/10.4137/TUI.S3009?icid=int.sj-abstract.similar-articles.1&

24. Schmitz MA, Finnegan M, Natarajan R, and Champine J. Effect of smoking on tibial shaft fracture healing. Clinical Orthopaedics and Related Research, 1999; 365(365):184-200. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10627703

25. Sloan A, Hussain I, Maqsood M, Eremin O, and El-Sheemy M. The effects of smoking on fracture healing. Surgeon, 2010; 8(2):111-6. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20303894

26. Krannitz KW, Fong HW, Fallat LM, and Kish J. The effect of cigarette smoking on radiographic bone healing after elective foot surgery. Journal of Foot and Ankle Surgery, 2009; 48(5):525-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19700113

27. Andersen T, Christensen FB, Laursen M, Hoy K, Hansen ES, et al. Smoking as a predictor of negative outcome in lumbar spinal fusion. Spine, 2001; 26(23):2623–8. Available from: https://pubmed.ncbi.nlm.nih.gov/11725245/

28. Luca A, Mannion AF, and Grob D. Should smoking habit dictate the fusion technique? European Spine Journal, 2011; 20(4):629-34. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20960013

29. Park JH, Oh KS, Kim TM, Kim J, Yoon JP, et al. Effect of Smoking on Healing Failure After Rotator Cuff Repair. American Journal of Sports Medicine, 2018:363546518789691. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30129777

30. Australian Institute for Health and Welfare. Back problems. Canberra, Australia: AIHW, 2019. Available from: https://www.aihw.gov.au/reports/chronic-musculoskeletal-conditions/back-problems/contents/what-are-back-problems.

31. Alkherayf F and Agbi C. Cigarette smoking and chronic low back pain in the adult population. Clinical and Investigative Medicine, 2009; 32(5):E360-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19796577

32. Skillgate E, Vingard E, Josephson M, Holm LW, and Alfredsson L. Is smoking and alcohol consumption associated with long-term sick leave due to unspecific back or neck pain among employees in the public sector? Results of a three-year follow-up cohort study. Journal of Rehabilitation Medicine, 2009; 41(7):550-6. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19543666

33. Shiri R, Karppinen J, Leino-Arjas P, Solovieva S, and Viikari-Juntura E. The association between smoking and low back pain: a meta-analysis. American Journal of Medicine, 2010; 123(1):87 e7-35. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20102998

34. Alkherayf F, Wai EK, Tsai EC, and Agbi C. Daily smoking and lower back pain in adult Canadians: the Canadian Community Health Survey. Journal of Pain Research, 2010; 3:155-60. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21197319

35. Shiri R, Falah-Hassani K, Heliovaara M, Solovieva S, Amiri S, et al. Risk Factors for Low Back Pain: A Population-Based Longitudinal Study. Arthritis Care Research, 2019; 71(2):290-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30044543

36. Green BN, Johnson CD, Snodgrass J, Smith M, and Dunn AS. Association Between Smoking and Back Pain in a Cross-Section of Adult Americans. Cureus, 2016; 8(9):e806. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27790393

37. Australian Institute for Health and Welfare. Osteoarthritis. Canberra, Australia: AIHW, 2019. Available from: https://www.aihw.gov.au/reports/chronic-musculoskeletal-conditions/osteoarthritis/contents/what-is-osteoarthritis.

38. Davies-Tuck ML, Wluka AE, Forbes A, Wang Y, English DR, et al. Smoking is associated with increased cartilage loss and persistence of bone marrow lesions over 2 years in community-based individuals. Rheumatology, 2009; 48(10):1227-31. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19696062

39. Hui M, Doherty M, and Zhang W. Does smoking protect against osteoarthritis? Meta-analysis of observational studies. Annals of the Rheumatic Diseases, 2011; 70(7):1231-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21474488

40. Dube CE, Liu SH, Driban JB, McAlindon TE, Eaton CB, et al. The relationship between smoking and knee osteoarthritis in the Osteoarthritis Initiative. Osteoarthritis and Cartilage, 2016; 24(3):465-72. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26432984

41. Yessica Eduviges ZC, Martinez-Nava G, Reyes-Hinojosa D, Mendoza-Soto L, Fernandez-Torres J, et al. Impact of cadmium toxicity on cartilage loss in a 3D in vitro model. Environmental Toxicology and Pharmacology, 2020; 74:103307. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31830724

42. Baumgarten KM, Gerlach D, Galatz LM, Teefey SA, Middleton WD, et al. Cigarette smoking increases the risk for rotator cuff tears. Clinical Orthopaedics and Related Research, 2010; 468(6):1534-41. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19283436