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Clinical Orthopaedics and Related Research®

, Volume 475, Issue 3, pp 903–905 | Cite as

CORR Insights®: Exposure to Secondhand Smoke Impairs Fracture Healing in Rats

CORR Insights

Keywords

Nicotine Polycyclic Aromatic Hydrocarbon Smoking Cessation Tobacco Smoke Fracture Healing 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Where Are We Now?

We do not need double-blind crossover randomized clinical trials to understand that smoking causes cancer. Though we are not “lung doctors or cancer doctors” (as I tell my patients), we understand that when the preponderance of clinical results—along with experimental and mechanistic data—strongly indicate a detrimental affect, we scientifically accept those conclusions and use them to guide and treat our patients.

Following that paradigm, but focusing on musculoskeletal tissues, multiple systematic reviews have shown that smoking has negative consequences in the healing of ligament, cartilage [8], tendon, labrum [13], and specifically relevant to the paper by Santiago and colleagues, bone [11, 14]. Mechanistically, we have come to understand the osteobiologic underpinnings of some of the effects of cigarette smoke, including its modulation of the osteoprogenitor population [1], preosteogenic chondrogenesis [3], and osteoblastic gene expression [12]. The conclusion is clear: Smoking is bad for the bone.

While surgeons strive to decrease smoking in their patients with fractures in an attempt to avoid complications and improve healing, we must also consider the issue of secondhand smoke, which is even less under our control. Among the many undesired compounds in secondhand smoke are polycyclic aromatic hydrocarbons, which have been implicated in specific-receptor mediated loss of bone mass [7], and likely impair callus generation in fractures [9].

Santiago and colleagues conclude that if you smoke cigarettes, or are close enough to it to inhale it, you are at risk. The consistency in the results only enhances their conclusion—callus maturity, density, and mechanical resistance were all negatively affected by secondhand smoke. A more clinically relevant finding in their study showed that exposure to secondhand smoke before the fracture was less detrimental to the patient than exposure before and after the fracture. This is a compelling scientific rationale to strongly encourage cessation at the time of injury, which is typically the orthopaedic surgeon’s first encounter with a patient.

In other words, being a nonsmoker is best, but stopping after the fracture still is helpful.

Where Do We Need To Go?

Several topics pertaining to tobacco smoke and fractures call for further elucidation. First, while the results from Santiago and colleagues provide a rational association between secondhand smoke and negative effects on fracture healing, they do so in a controlled experimental setting. We do not yet know whether secondhand smoke, as inhaled by people in real life, is in fact linked to poor fracture healing.

Second, we do not clearly know the relative negative contributions of the components of tobacco smoke (first or secondhand) such as polycyclic aromatic hydrocarbons or the active stimulant ingredient of nicotine. This may become increasingly important as marketing efforts for, and the popularity of, nicotine-containing smokeless products increase; it also presents a dilemma for cessation efforts as we do not clearly know how nicotine from a gum or a patch, without the rest of tobacco smoke, may affect fracture healing.

Third, our data (including those from the current study) do not provide a robust dose-response relationship. Does some reduction help or is there a threshold that must be crossed? Is that threshold essentially zero, including secondhand smoke? Answers to these questions will improve our ability to properly counsel and treat our patients.

That said, this information would be much less necessary, if we could get all of our patients to quit smoking (except perhaps the understanding of inhaled nicotine, should this become a popular independent “habit” rather than a proxy for cigarette smoking). That brings me to another important place for us to go: Leading our patients with fractures to smoking cessation.

How Do We Get There?

We have amassed enough good scientific evidence to conclude that eliminating tobacco smoke from our patients with fractures will help them heal, and will save medical-economic resources. But it is beyond the scope of this commentary to delineate the scientific experiments and clinical studies to resolve the three issues mentioned in the section above. Rather, I will consider the larger problem at hand: Getting our patients with fractures to stop smoking. Here, we not only have a challenge, but an opportunity.

Consider that for some of our patients, hospital admission is part of the care of the fracture; this generally provides temporary disruption of smoking, which has been associated with cessation [6]. Further, the acute event of fracture and surgeon intervention may provide a “teachable moment,” which has been used successfully to improve healthy-heart practices after myocardial infarction [4, 5], and to promote smoking cessation within other hospital settings [2]. Consistent with the Health Belief Model for healthcare change, McBride and colleagues [10] have formalized a model to study such interventions. For example, an acute fracture can become a teachable moment for smoking cessation because it: (1) Increases expectation of personal risk, (2) prompts a strong emotional response, and (3) redefines self-concept.

Our real challenge is to use the lessons learned from others regarding healthcare behavior change, combine them with insights gleaned as orthopaedic surgeons to further understand the critical issues, and help our fracture patients quit smoking.

References

  1. 1.
    Beyth S, Mosheiff R, Safran O, Daskal A, Liebergall M. Cigarette smoking is associated with a lower concentration of CD105(+) bone marrow progenitor cells. Bone Marrow Res. 2015;2015:914935.CrossRefPubMedPubMedCentralGoogle Scholar
  2. 2.
    Dohnke B, Ziemann C, Will KE, Weiss-Gerlach E, Spies CD. Do hospital treatments represent a ‘teachable moment’ for quitting smoking? A study from a stage-theoretical perspective. Psychol Health. 2012;27:1291–1307.CrossRefPubMedGoogle Scholar
  3. 3.
    El-Zawawy HB, Gill CS, Wright RW, Sandell LJ. Smoking delays chondrogenesis in a mouse model of closed tibial fracture healing. J Orthop Res. 2006;24:2150–2158.CrossRefPubMedGoogle Scholar
  4. 4.
    Flocke SA, Clark E, Antognoli E, Mason MJ, Lawson PJ, Smith S, Cohen DJ. Teachable moments for health behavior change and intermediate patient outcomes. Patient Educ Couns. 2014;96:43–49.CrossRefPubMedPubMedCentralGoogle Scholar
  5. 5.
    Fonarow GC. In-hospital initiation of statins: taking advantage of the ‘teachable moment’. Cleve Clin J Med. 2003;70:502, 504–506.Google Scholar
  6. 6.
    Glasgow RE, Stevens VJ, Vogt TM, Mullooly JP, Lichtenstein E. Changes in smoking associated with hospitalization: Quit rates, predictive variables, and intervention implications. Am J Health Promot. 1991;6:24–29.CrossRefPubMedGoogle Scholar
  7. 7.
    Iqbal J, Sun L, Cao J, Yuen T, Lu P, Bab I, Leu NA, Srinivasan S, Wagage S, Hunter CA, Nebert DW, Zaidi M, Avadhani NG. Smoke carcinogens cause bone loss through the aryl hydrocarbon receptor and induction of Cyp1 enzymes. Proc Natl Acad Sci U S A. 2013;110:11115–11120.CrossRefPubMedPubMedCentralGoogle Scholar
  8. 8.
    Kanneganti P, Harris JD, Brophy RH, Carey JL, Lattermann C, Flanigan DC. The effect of smoking on ligament and cartilage surgery in the knee: A systematic review. Am J Sports Med. 2012;40:2872–2878.CrossRefPubMedPubMedCentralGoogle Scholar
  9. 9.
    Kung MH, Yukata K, O’Keefe RJ, Zuscik MJ. Aryl hydrocarbon receptor-mediated impairment of chondrogenesis and fracture healing by cigarette smoke and benzo(a)pyrene. J Cell Physiol. 2012;227:1062–1070.CrossRefPubMedPubMedCentralGoogle Scholar
  10. 10.
    McBride CM, Emmons KM, Lipkus IM. Understanding the potential of teachable moments: the case of smoking cessation. Health Educ Res. 2003;18:156–170.CrossRefPubMedGoogle Scholar
  11. 11.
    Patel RA, Wilson RF, Patel PA, Palmer RM. The effect of smoking on bone healing: A systematic review. Bone J Res. 2013;2:102–111.CrossRefGoogle Scholar
  12. 12.
    Rothem DE, Rothem L, Dahan A, Eliakim R, Soudry M. Nicotinic modulation of gene expression in osteoblast cells, MG-63. Bone. 2011;48:903–909.CrossRefPubMedGoogle Scholar
  13. 13.
    Santiago-Torres J, Flanigan DC, Butler RB, Bishop JY. The effect of smoking on rotator cuff and glenoid labrum surgery: A systematic review. Am J Sports Med. 2015;43:745–751.CrossRefPubMedGoogle Scholar
  14. 14.
    Scolaro JA, Schenker ML, Yannascoli S, Baldwin K, Mehta S, Ahn J. Cigarette smoking increases complications following fracture: A systematic review. J Bone Joint Surg Am. 2014;96:674–681.CrossRefPubMedGoogle Scholar

Copyright information

© The Association of Bone and Joint Surgeons® 2016

Authors and Affiliations

  1. 1.University of PennsylvaniaPhiladelphiaUSA

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