The Effect of Tobacco Smoking on Musculoskeletal Health: A Systematic Review
Major advances have been made by applying modern genetic technologies to examine the relationship between exposure to tobacco smoke and the. smoke (18,19). In contrast to the information on cigarette smoking, few studies have examined the relationship between cigarette smoking and novel risk factors . AIMS: To examine comorbidity between tobacco use, substance-use disorders METHOD: Data from the Australian National Survey of Mental Health and.
There were few studies on the musculoskeletal health outcomes of secondhand smoke, smoking cessation, or other modes of smoking, such as waterpipes or electronic cigarettes. This review found evidence that suggests tobacco smoking has negative effects on the health outcomes of the musculoskeletal system.
There is a need for further research to understand mechanisms of action for the effects of smoking on the musculoskeletal system and to increase awareness of healthcare providers and community members of the adverse effects of smoking on the musculoskeletal system.
Introduction Tobacco smoke has more than 7, harmful chemical compounds that enter a human body either directly through smoking, indirectly through secondhand exposure to smoke exhaled by a smoker, or through downstream smoke released from a cigarette or pipe [ 1 ].
Both smokers and nonsmokers are at risk of exposure to the compounds of smoked tobacco that accumulate on the surfaces in a poorly ventilated environment; this method of exposure is known as thirdhand smoke exposure [ 2 ]. In the United States, there are approximatelyannual deaths causally related to smoking and secondhand exposure to smoke [ 3 ].
Tobacco smoking has known adverse consequences on most human body systems. Researchers have focused more attention on the deleterious effects of smoking for high mortality diseases, such as cancer and diseases of the cardiovascular and respiratory systems, with less research attention on other body systems, such as the musculoskeletal system [ 3 ].
The musculoskeletal system is one of the largest human body systems, comprised of bones, joints, muscles, cartilage, tendons, ligaments, and other connective tissues [ 4 ]. An intact and functioning musculoskeletal locomotor system is necessary to perform activities of daily living and maintain quality of life [ 56 ]. Several studies have investigated the association between smoking and musculoskeletal disorders. According to the recent Surgeon General report, the causal relationship between tobacco smoking and rheumatoid arthritis, periodontitis, and hip fractures has been confirmed [ 3 ]; however, there is inconclusive evidence to support causality between smoking and many other musculoskeletal disorders.
Searching online databases revealed significant growth in the body of literature investigating relationships between tobacco smoking and the musculoskeletal system.
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During our comprehensive online search, we did not encounter any systematic reviews examining those relationships; however, we did find 10 systematic reviews of the effects of tobacco smoking on components of the musculoskeletal system. Five systematic reviews focused on smoking and the effects on dental implants and found smoking increases the risk of peri-implant bone loss and implant failure [ 7 — 11 ].
Another systematic review revealed an association between smoking and lumbar disc herniation [ 12 ]. Three other reviews found smoking was related to negative postoperative outcomes on knee ligaments [ 13 ], higher complication rates after anterior cruciate ligament ACL reconstruction [ 14 ], and slowed healing of rotator cuff repair [ 15 ]. Also, one review found smoking was associated with rotator cuff tears and other shoulder symptoms [ 16 ].
Our review will be the first to collect and assess all the recent literature on the effects of smoking on the musculoskeletal system. This systematic review will orient scientists interested in the health effects of smoking about the state of the science over the last decade as they conduct more advanced research. Also, the amalgamation of these data in one document will be helpful to the research community as there is a high degree of similarity and shared characteristics between musculoskeletal system components.
This systematic review evaluated literature published in the last decade to summarize the evidence regarding the effect of smoking on the musculoskeletal system. This systematic review will answer two main questions: Is there an association between tobacco smoking and musculoskeletal health? What are the effects of tobacco smoking on the musculoskeletal health?
Before the onset of the systematic review, a specific protocol was developed to minimize bias. This protocol included a priori research questions, a comprehensive literature search, inclusion criteria for studies, screening methods and reasons for exclusion, data abstraction, scientific study quality, data analysis, and synthesis.
This search covered 10 years from January 1,to March 18,and included only articles written in English.
The search strategies included a combination of the following key words: This step was helpful to expand the search; for example, the entry terms for MeSH of smoking were as follows: All retrieved records were pulled from databases using EndNote X7. After that, abstracts of the retained records were screened for inclusion criteria: English language, human subjects, published January 1, —March 18,and investigating effects of smoking on the musculoskeletal system.
Retained records then underwent full-text screening and records that did not meet the inclusion criteria or were editorials, commentaries, dissertations, case studies, or reviews e. A total of final full-text articles were included in the review and used for data abstraction. Two independent authors first and second extracted data using a standard form.
The data abstraction process was piloted for the first 10 articles; it was successful and was used for the remaining articles. Any disagreements between authors were resolved through discussion. The findings in this review were synthesized qualitatively as there was heterogeneity in study designs and populations.
Our narrative analyses considered study design and quality. Results The comprehensive search of the literature identified 8, potentially relevant records; however, only records met the inclusion criteria and underwent data abstraction and synthesis Figure 1.
The articles were reviewed and the effects of tobacco smoking on musculoskeletal system were classified into 7 categories: Process of literature search.
This review included studies using various designs: Table 1 presents the classification of study designs and related information based on the categories and subcategories.
Table 2 summarizes the effect of smoking on major outcomes of musculoskeletal health. Table 3 provides comprehensive information on each study in the review. Summary of study characteristics. Summary for the effect of smoking on major outcomes of musculoskeletal health.
Tobacco smoking and musculoskeletal system. Table 3 provides comprehensive details on the findings from those studies for effects of smoking on selected bone-related outcomes. According to a majority of studies, smoking had adverse effects on BMD across age categories and sex.
In males, regardless of age, method, and site of measurement for bone density, the cross-sectional studies found smokers had significantly lower BMD than nonsmokers [ 2742 — 4446525455 ]. The cohort studies found male smokers exhibited a significant decline in BMD [ 32335054 ]. There was only one cross-sectional study that reported no significant difference in calcaneus BMD between 3 groups: In adolescent females, 2 cross-sectional studies found a high frequency of smoking was associated with lower rate of total body BMC [ 29 ] and hip BMD [ 2829 ]; these findings were supported by cohort studies that found initiation of smoking at age 13 affected bone accrual and was associated with low mean BMD at age 17 [ 3347 ].
Another cross-sectional study of adolescent females reported significant linear relationships between urinary cotinine and BMD of the femoral neck, total femur, and lumbar spine [ 48 ]. However, only one cross-sectional study in adolescent females found no significant difference in BMC and BMD between smokers and nonsmokers [ 30 ]. In premenopausal women, one cross-sectional study reported the BMD of smokers was not significantly different than the BMD of nonsmokers [ 20 ].
In postmenopausal women, cross-sectional study findings demonstrated postmenopausal women who smoked had significantly lower BMD than postmenopausal women who did not smoke [ 2356 ] and an increased risk of falls regardless of the BMD T-score [ 21 ]. Two randomized control studies were conducted in postmenopausal women. Another study found quitting smoking significantly associated with increased body weight, fat, muscles, and functional mass that affected BMD [ 41 ].
Finally, two cross-sectional studies enrolled both males and females, and one reported BMD and BMC were significantly lower in smokers than those of nonsmokers [ 26 ]; the second study used a small sample and found no association between pack-years and BMD [ 31 ]. Biological mechanisms were examined in several studies, most of which were cross-sectional.
The correlational analysis did not find a significant effect for serum osteocalcin OC or tartrate resistant acid phosphatase isoenzyme 5b TRACP 5b [ 55 ]. The interaction between smoking and genetic factors was also investigated.
A potential interaction was reported between smoking and receptor-related Protein 5 LRP5 CT rs on osteoporosis in postmenopausal women [ 35 ] and between smoking and polymorphism of glutathione S-transferases GSTT1 on bone quality index in young adult men [ 45 ]. Table 3 provides comprehensive details on studies which examined the prevalence of fracture in smokers, the association between smoking and fracture risk, fracture healing, the biological mechanism of fracture in smokers, and the interaction of smoking and other fracture risks.
Smoking was also found to increase the likelihood of fracture. Two prospective cohort studies of both sexes investigating the postsurgery level of serum transforming growth factor-beta 1 TGF-beta 1 found TGF-beta 1 was lower in smokers than in nonsmokers at 4 weeks [ 65 ] and 8 weeks [ 63 ].
The trend of lower level of TGF-beta 1 in smokers than that of nonsmokers was observed in both groups of patients with normally healed fractures and delayed healed fractures [ 65 ]. Finally, two studies examined interactional effect of smoking and other factors. In the first study, changes in BMI had an effect on fracture risk in nonsmokers, but not in smokers [ 72 ]. The second study did not find smoking significantly correlated with alveolar crest height loss [ 75 ].Smoking Causes Cancer, Heart Disease, Emphysema
Table 3 provides comprehensive details on the 4 studies that examined the effect of smoking on the alveolar bone. The characteristics of these studies were as follows: Twenty-four studies were cross-sectional, 5 studies were RCTs, 4 studies were cohort, and 1 study was a case-control.
Two studies out of 34 obtained data or samples from large-scale longitudinal studies. All the studies used self-report to assess smoking, with the exception of three studies that assessed levels of cotinine [ 8899]. Table 3 provides comprehensive details on the studies that examined the relationship between smoking and periodontitis. Eleven studies investigated the prevalence and association of smoking on periodontitis and periodontal parameters.
Ten studies were cross-sectional. The comparative analysis found smokers compared to nonsmokers had significantly deeper periodontal pockets [ 77899092], higher mean clinical attachment loss CAL [ 789192], higher mean plaque scores [ 789192 ], greater fraction of teeth with apical periodontitis [ 79 ], higher marginal bone loss, and a greater number of missing teeth [ 92 ]. Heavy smoking was also associated with higher prevalence [ 7994 ] and severity of periodontitis [ 7794 ].
Two studies compared cigarettes smokers to waterpipe and narghile users and found a similarity between groups on most periodontal parameters [ 9295 ]. Fourteen studies examined the potential biological mechanism for smoking in periodontitis and what potential biomarkers may be affected. Thirteen studies were cross-sectional designs and enrolled both sexes.
Seven studies enrolled both smokers and nonsmokers in groups with or without periodontitis.
Smoking is one of the greatest risks for periodontitis and may increase host susceptibility to tissue destruction especially in presence of other factors such as the functional defect of leukocyte and monocyte [ 98 ]. The combined effect was 3. Eight interventional studies examined therapies to manage periodontitis. Another prospective observational study found periodontal maintenance therapy every months inhibited the progression of CAL, probing depth, and tooth loss in smokers [ 86 ].
Three RCTs found adjunct treatments of low-dose doxycycline for 6 months [ ], systemic azithromycin [ 81 ], or a daily dose of mg of aspirin [ ] did not significantly improve periodontal parameters in smokers with chronic periodontitis.
In contrast, 2 RCTs in smokers with chronic periodontitis successfully improved some periodontal parameters.
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Compared with treatment using only scaling and root planing SRPthe treatment using Simvastatin 1. Smoking is one of the greatest risks for periodontitis and is associated with poor periodontal parameters; such finding provides evidence that the treatment used Simvastatin besides SRP in smokers suffering from chronic periodontitis was more effective in reducing the negative effect of smoking on the periodontal parameter than the treatment using only SRP.
Also, this finding provides evidence that the use of mYJ Chinese medicinal herbs in a nonsurgical treatment was effective in reducing the negative effect of smoking on the periodontal parameter as evidenced by the increases in radiographic alveolar bone density.
Eleven studies had small samples. All studies used self-report to assess smoking. Table 3 provides comprehensive detail on these studies exploring the effects of smoking on bone implants.
Thirteen studies examined the effect of smoking on dental implant survival with special consideration of implant type and time of follow-up. Eleven studies were cohort studies.
Two studies investigated smoking and early implant failure and the first study found early implant failure was threefold higher in smokers than nonsmokers [ ] while the second study found frequency of tobacco smoking was not associated with early implant failure [ ]. Two studies reported smoking did not influence implant survival rates , although 8 studies provided contradictory findings.
A correlation analysis found smoking status , and pack-years [ ] were inversely associated with dental implant survival. A comparative analysis between smokers and nonsmokers found smokers had lower implant survival rates [,]. A subgroup analysis based on implant type found smokers had higher failure rates for turned [ ] and smooth-surface implants [ ].
One study of only tobacco smokers found implant survival with turned or screw surfaces was similar in tobacco smokers regardless of periodontal status [ ]. Five of 13 studies measured marginal bone loss; 4 reported smokers demonstrated significantly greater marginal bone loss than nonsmokers [,], and two studies did not report a significant difference . Six studies examined the clinical effects of implants on surrounding tissue in smokers.
One retrospective cohort study found smoking was associated with overall complications e. Smoking is associated with increased risk of bone implant failure due to its negative effect on tissues surrounding the implant; such finding indicates that the negative effect of smoking on histometric measurements after dental mini-implants was significantly minimized through using of implants with sandblasted acid-etched but it was not improved with the use of implants with machined surfaces.
Eight studies examined the biological mechanism of smoking on tissue surrounding dental implants and explored potential biomarkers that could be affected by this mechanism. One case-control study found heavy smokers with an IL-1 polymorphism did not increase their risk for peri-implantitis [ ].
One short-term prospective study found a 7-day follow-up for the whole genome array of implant adherent cells was not different between smokers and nonsmokers [ ]. The long-term prospective cohort study found smokers with previous periodontal disease had significant clinical signs of inflammation and significantly higher counts of pathogenic bacteria [ ].
Four studies were randomized control trials; 2 measured peri-implant parameters for implants with different configurations. One trial found smoking did not influence peri-implant soft tissue response recession and the papilla index [ ]; a second study found smoking doubled marginal bone loss regardless of treatment [ ]. One methodological RCT using stereolithographic surgical guides found smoking was associated with inaccurate implant placement [ ]. A therapeutic RCT found mechanical debridement with adjunct antimicrobial did not significantly improve parameters of bleeding on probing, probing depth, or crestal bone loss in smokers [ ].
There were positive outcomes high implant survival, bone level, and low rate of biological complications reported by one retrospective cohort study where the authors monitored dental implant rehabilitation in patients with systemic disorders and smoking habits [ ].
The first trial found smokers who received an acellular dermal matrix graft ADMG with enamel matrix derivative EMD had a higher mean gain in recession height and root coverage than smokers who received ADMG alone [ ].
A second trial found regenerative treatment of platelet-rich plasma combined with a bovine-derived xenograft did not improve periodontal parameters in smokers [ ]. Three long-term prospective cohorts compared smokers to nonsmokers and found smokers had significantly higher marginal bone loss up to 4 years after onlay bone grafting in the atrophic maxilla [ ].
These patients also had higher tissue inflammation around augmentation sites once they received bone graft titanium- reinforced ePTFE membranes [ ] and had similar survival rates for dental implants after A Le Fort I osteotomy and interpositional bone graft in combination with implants in the atrophic maxilla [ ]. Table 3 provides comprehensive details on the 5 studies that examined the effects of smoking on bone graft. Twelve studies obtained data or samples from large-scale longitudinal studies and all used self-report to assess smoking habits with an exception of one study that assessed level of cotinine [ ].
Table 3 provides comprehensive detail about studies that examined the effect of smoking on several outcomes in patients with RA. Five studies of varying design 2 cross-sectional studies, 2 prospective cohort studies, and 1 case-control study enrolled patients from both sexes of similar age.
These studies examined the effect of smoking on RA clinical outcomes, such as disease activity, functional capacity, radiographic damage, serology, and existence of extraarticular manifestations.
Overall, the collective results were that smokers had significantly higher scores on the Disease Activity Score of 28 joints DAS 28 , the functional disability score Health Assessment Questionnaire [ ], the simple erosion narrowing score [ ], CRP [ ], and a rheumatoid factor titer [ ].
These patients demonstrated severe extraarticular RA [ ] and took significantly more disease-modifying antirheumatic drugs DMARD [ ]. One study reported no difference in DAS28 and radiographic scores between smokers and nonsmokers [ ]. Those with less formal education were more likely to smoke, as were those who were unemployed, and had greater social disadvantage.
Finally, those with higher levels of neuroticism i. Anxiety and affective disorders were more than twice as common among smokers, with around one in 10 smokers having an anxiety disorder 9. In comparison, only around one in 20 non-smokers had an anxiety 4. Smokers also reported significantly higher levels of psychological distress and disability due to emotional problems than non-smokers.
These significant differences all remained even after the effects of demographic factors, neuroticism and other drug use were taken into account. Substance use disorders were even more strongly related to smoking. Again, these relationships remained significant even after accounting for demographics, neuroticism and other drug use.
These findings indicated that tobacco use is strongly related to mental health problems as assessed with symptom measures or as mental disorders and other substance use problems. These relationships persisted after accounting for a range of confounding variables. Research has found that mental health problems reduce the likelihood of quitting smoking. Hence, it appears that there is a need to further examine interventions for smokers with mental health and substance use problems.
Furthermore, general practitioners and health professionals need to consider the possibility that smokers may have a number of other problems that will decrease their chances of successfully giving up smoking.