We all know that smoking can have negative effects on the body but have you ever considered the effects smoking can have on your bone health, tissue health and your recovery from injury? This blog is here to address just that – and the effects it can have may just stop you from reaching for that next cigarette.
Smoking can contribute to a loss of bone density and the risk of developing osteoporosis. In a study of 14,000 people, exposure to tobacco smoke was found to reduce bone mineral density in the femoral head (top of your thigh bone), tibia (shin bone) and the calcaneus (heel bone) (Gerdhem & Obrant, 2002). Reductions in bone mineral density have also been found in the hip and lumbar spine due to smoking (Rudang et al, 2012). For women who have gone through the menopause, smoking can further reduce bone density. One study examined 41 pairs of female twins and showed that for women who smoke one pack of cigarettes each day as an adult, come the menopause, bone density had reduced by 5-10%, significantly increasing their risk of fractures (Bączyk et al, 2012).
It’s notable that within the UK, smoking is no longer allowed within bars and restaurants, reducing the risk of passive smoking. However, if you are a passive smoker, second hand smoke has also been linked to osteoporosis in the lumbar spine and femoral head (Kim et al, 2012). It is therefore evident based on epidemiologic studies that smoking can detrimentally affect bone health in terms of bone density. This can thus increase the risk of consequent bone fractures. The level of bone density reduction shows a strong relationship to the number of cigarettes smoked and length of exposure. Interestingly, it hasn’t been linked to age, sex, BMI or other lifestyle choices which smokers may have, such as reduced calcium intake or lack of physical activity and sun exposure (Kim et al, 2012).
If you’re interested in how smoking affects bone health then here comes the scientific part. Research indicates that the pathogenesis of bone density loss is a complex process. Smoking is thought to reduce osteogenesis, angiogenesis and collagen synthesis which impairs or reduces the balance between osteoblast and osteoclast activity. Osteoblasts are responsible for depositing new bone tissue whilst osteoclasts resorb and remove bone tissue. Therefore, maintaining the balance between these two types of cell is of particular importance for bone health. Meanwhile, smoking contributes to increased oxidative stress within the body, induces chronic inflammation and reduces calcium absorption within the intestines. Calcium absorption is largely affected as smoking alters vitamin D metabolism which is critical for calcium absorption to occur. Oestrogen and testosterone normally have a protective element towards skeletal bones. However, smoking can cause a reduction in both oestrogen and testosterone levels, reducing their ability to support bone health. Whilst these hormones reduce, cortisol levels increase. If cortisol levels remain high, this can adversely affect bone formation due to the stress hormone’s inhibitory effect on osteoblast activity. Smoking can also disadvantageously affect the levels of parathormone, a hormone which is secreted by the parathyroid glands to aid bone remodelling. As a result, bone mineral content is reduced by a combination of direct toxic activity on the bone cells together with indirect involvement from sexual, calciotropic and adrenocortical hormones together with changes in the vascular system and oxygen supply (Walker et al, 2001; Rothem et al, 2009; Gullihorn et al, 2005; Yoon et al, 2012; Falahati-Nini et al, 2000; Meier et al, 2008; Need et al, 2002). All in all, not a great combination if you’re keen to look after your bone health.
If smoking reduces bone mineral content then it’s obvious that as your bones grow weaker, the risk of osteoporosis and fractures will increase. Smoking can increase the risk of developing a vertebral fracture by 32% in men and 13% in women and can increase the risk of a hip fracture by 40% and 31% respectively. If you stop smoking this can certainly help matters. However, notably, stopping smoking only reduces the risk of hip fractures in men after a period of five years whilst for women this can take far longer (Kanis et al, 2005). Therefore, the detrimental effects of smoking can remain in your system long after you’ve given up smoking for good.
Evidently, whilst fractures are most strongly linked to a reduced bone mineral content, other deleterious effects of smoking such as changes to the vascular system, oxygen supply and muscle strength can affect both balance and overall performance, increasing the risk of falls for smokers and thus increasing the likelihood of a fracture.
For a fracture to heal it must go through a series of different phases. These include the haematoma and inflammatory response, callus formation, ossification, and remodelling. These phases encompass a cascade of synthesis and activation of matrix proteins, growth factors, cytokines, and angiogenic stimulators which aim to restore mechanical stability at the fracture site.
Without doubt, fracture healing is delayed by smoking. One study examined 146 consecutive closed and grade I open tibia shaft fractures, treated with cast immobilization, external fixation, or intramedullary rod fixation. The study found that clinical healing for a smoker took on average 269 days versus 136 days for non-smokers – a huge difference of 133 days (Schmitz et al, 1999). Cigarette smoke can also negatively affect graft healing after surgery (Ziran et al, 2007).
One study which examined mice, found that at seven days post-injury, mice which were exposed to cigarette smoke had a smaller callus formation at the fracture site with a smaller cartilage matrix and more immature cell proliferation. At 14 days, despite increased chondrogenesis a lower percentage of bone was found in contrast to controls (El Zawaway et al, 2006). In other words, this research clearly indicates that bone healing is significantly slowed and delayed if you regularly reach for a cigarette.
Nicotine has been shown to inhibit bone healing (Yamano et al, 2010). Nicotine has a directly toxic affect by reducing the proliferation of various cells which are essential for bone healing. Nicotine is also a powerful vasoconstrictor which reduces blood flow, essential for tissue healing. It also promotes platelet adhesiveness which increases the chances of microvascular occlusion. As a result, a reduction in blood supply, increased levels of carbon monoxide within the blood and the toxic impact of hydrogen cyanide on the mitochondrial respiratory chain can lead to tissue hypoxia. This lack of oxygen to the tissues is a crucial contributory factor to the impaired formation of a cartilaginous callus at the fracture site. This is because, oxygen is critical in the synthesis of type II collagen which is essential for bone healing (Williams et al, 2008). It’s simple. Smoking reduces blood flow and oxygen which in turn impedes type II collagen laydown which is critical for a bone to knit back together.
In order for wounds to heal, wound healing is dependent on fibroblast and mesenchymal stem cell activity. These cells produce various cytokines which are essential in the formation of granulation tissue. Substances within cigarette smoke can disadvantageously affect growth factor production which in turn can lead to poor tissue healing. At times, this can lead to a chronic wound which fails to heal at all.
In the short-term, if a wound doesn’t heal, it’s not just the wound that’s an issue, it’s the risk of potential complications which can arise from this. This can include the risk of osteomyelitis or bone infection, pulmonary infections, cardiac failure or cardiac rhythm disorders. This can often result in a stay in hospital or admission to intensive care following surgery. Indeed, it is notable that if a smoker undergoes orthopaedic surgery then their stay in hospital is often far longer compared to a non-smoker (Gabbiani, 2003).
Back pain is one of the most prevalent musculoskeletal conditions and it’s thought that 80% of us will be affected by it at some point in our lives. Independent of age, sex, physical activity and life style choices, smoking can be strongly linked to back pain (Kassel et al, 2003). But why?
Research indicates that an organic pathogenesis underlies the link between smoking and back pain. One animal study exposed animals to passive smoking at the equivalent of 20 cigarettes per day for a period of eight weeks. Pretty horrible for the animals, right? However, the study identified that these animals showed cell necrosis and fibrosis in the nucleus pulposus, chondrocyte degeneration, reduced collagen synthesis, misalignment of collagen layers and increased degradation of extracellular matrix proteins (Nemoto et al, 2006).
Meanwhile, another study exposed mice to directly inhaled tobacco smoke. These mice demonstrated a reduction in proteoglycan synthesis and increased degradation of a key disc extracellular matrix protein, aggrecan, within its interglobular domain. Without getting overly specific, aggrecan is critical for attracting water within the spinal discs. With reduced aggrecan levels and therefore water, this predisposes spinal discs to increased compressive forces and therefore can make them more likely to sustain damage, leading to back pain (Vo et al, 2011).
Whilst there are a variety of causes underlying back pain, it is strongly evident that smoking doesn’t help back pain sufferers. The research shows that smoking is linked to disc degeneration due to the toxic effects of nicotine. Smoking also causes degradation of collagen, reduces blood and oxygen supplies and can cause vascular damage and vasoconstriction adjacent to the intervertebral discs. If you want good back health then smoking isn’t for you.
Various studies have examined the link between smoking and the relatively common condition of osteoarthritis. A couple of studies have interestingly found that, after adjusting for age, sex and weight, smoking was found to have a possible protective effect against osteoarthritis, possibly due to an anabolic action of nicotine on chondrocytes. Indeed this research found that over thirty-six years, smokers had a lower rate of osteoarthritis than non-smokers at 28% and 37.5% respectively (Felson et al, 1989; Ying et al, 2012). Hurrah! Finally, there’s some research that puts a slightly more positive spin on smoking!! However, look at this research a little more closely and it’s evident that study limitations such as inaccurate methods of evaluation and selection bias exist. Additionally, these studies were not designed to examine the effect of smoking and the suggested protective effect of smoking was not deemed to be largely significant in terms of data analysis. So, whilst this research is out there it doesn’t mean that smoking will help your joints in the long-term.
More recent research has examined MRI scans which indicate a significant reduction in knee cartilage at the medial tibiofemoral joint and the patellofemoral joint in smokers. This study examined 271 middle-aged smokers over a two year period. Those who smoked or had smoked in the past showed an increased loss of medial tibial and patella cartilage on an annual basis. The study identified that individuals with bone marrow lesions had an increased risk of medial cartilage loss perhaps indicating that cartilage loss may be linked to an initial bone marrow lesion. In other words, smoking may encourage and mediate the development of a healthy joint to a diseased one (Davies-Tuck et al, 2009).
Rheumatoid arthritis (RA) has been linked to a variety of different environmental factors. And you’ve guessed it, it’s also linked to smoking which is one of the best known causes of this condition. Meta-analysis attributes smoking to 25% of the RA population. Scarily, only a moderate intensity of smoking over a long period of time can be a causative factor. In other words, you don’t have to be a heavy smoker for years to increase the risk of developing RA. Meanwhile, if you’re male you may have a slightly increased risk compared to the female population (Lahiri et al, 2012).
Epidemiologically, genotype can play a role in whether or not smoking will increase your chances of developing RA (Klareskog et al, 2006). Overall, smoking can act as an inflammatory mediator and can certainly increase the chances of developing more aggressive joint damage. It is also more strongly linked to developing extra-articular problems such as sub-cutaneous nodules together with interstitial lung disease (Nyhall-Wahlin et al, 2009).
In many cases, RA patients will often take disease modifying anti-rheumatic medication. However, smoking has been found to negatively affect the effects of these medications with smokers showing less improvement in disease activity (Saevarsdottir et al, 2011).
If you’re getting older and are hoping to maintain your muscle mass and strength then stopping smoking is a good place to start. This is because smoking can reduce muscle mass and strength as found by Kok et al, 2012. This study measured quadriceps strength at the ages of 21, 27, 32 and 36 years in both men and women. The research discovered that smoking 100g of tobacco per week reduces muscle mass and strength by 2.9% in men and 5.0% in women. This was entirely independent of any variations in lifestyle. Smoking was to blame.
Clinical research has identified that cigarette smoke encourages skeletal muscle damage by impairing muscle metabolism, increasing inflammation and increasing oxidative stress. It also causes increased activity of atrophy related genes (Rom et al, 2012). In other words, the impact of cigarette smoke can significantly weaken your muscles.
Alongside reduced muscle mass and strength, smoking is linked to increased levels of muscle pain. In a study which compared 13,000 subjects, musculoskeletal pain, for example in the neck, upper and lower limbs, was found to be considerably higher over the life-time of a smoker compared to a non-smoker. It’s possible that smoking may cause increased pain due to a pharmacological effect although it has been proposed that perhaps people with a lower pain threshold are perhaps more inclined to start smoking if they are in pain (Palmer et al, 2003).
Chronic tendons can be notoriously difficult to treat. Studies show that smoking is linked to ongoing shoulder pain and tendinopathy and is a significant risk factor for the development of a rotator cuff tear (Bodin et al, 2012). One study incorporated 408 patients who underwent an arthroscopic repair of a rotator cuff tear. The study found that smoking can affect the severity of a rotator cuff tear. In those who had smoked a higher number of cigarettes over a longer period of time, their rotator cuff tears were significantly worse (Carbone et al, 2012).
Aside from shoulder complaints, smoking can increase the risk of distal biceps tendon ruptures. Smokers have been shown to have a rupture risk 7.5 times higher than non-smokers (Safran et al, 2002) which is significant. Those who sustain bilateral distal biceps tendon ruptures are commonly middle-aged men with a higher level of nicotine intake (Schneider et al, 2009).
Not only does smoking increase the risk of tendon injury in the first place, it can also negatively affect tendon healing once injury has occurred. Animal studies, examining Achilles and rotator cuff tendon tears, have found that nicotine slows tissue repair, is linked to degeneration of fibroblasts which are critical for healing to occur and results in disorganisation of fibrils which are required for tendon strength (Duygulu et al, 2006). Again, we’re yet to find any benefits of smoking when it comes to tendon health and repair.
So What Does This Mean When We Put it All Together?
We’re used to hearing that smoking’s bad for us and detrimental to our health but this sweeping statement often doesn’t go much further than just that. The effects of smoking on musculoskeletal problems are widespread. It ranges from reducing bone density and increasing the risk of osteoporosis and bone fractures. It has also been linked to osteoarthritis, rheumatoid arthritis, intervertebral disc degeneration, reduced muscle mass and strength, muscle pain, tendon degeneration and tendon rupture. It also significantly impacts upon wound healing and tissue repair.
This isn’t an article written to condemn smokers. However, the range of adverse side effects from a musculoskeletal perspective is far reaching. If you’re struggling from pain or are wondering why that injury is taking such a long time to heal then it may be worth thinking twice before you light up that next cigarette. I for one would much rather have strong bones and a nicely healed wound than a broken leg and a systemic infection.