Fracture Healing: How Strong Is the Effect of Smoking on Bone Healing?

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Chapter 50 Fracture Healing: How Strong Is the Effect of Smoking on Bone Healing?

The negative sequelae of cigarette smoking on the musculoskeletal system and wound healing have become a popular topic of study.¹^–⁴ A variety of specialties and institutions (especially those responsible for healthcare costs) have focused on smoking as a potentially remediable risk factor for negative outcome after a variety of medical interventions. For example, epidemiologic and experimental studies in the plastic surgery literature identify nicotine as a deleterious constituent of cigarette smoke, leading to increased rates of wound complications and pedicle flap necrosis secondary to vasoconstriction and microthrombus formation.⁵^–⁷

For years, orthopedic experts have anecdotally described the negative impact of cigarette smoking on the musculoskeletal system. More recently, this effect has been the subject of a number of reports: cigarette smoking leads to an increased incidence of pseudarthrosis after spinal fusion,^8,⁹ increased time to union in tibial fractures¹⁰^–¹³ lower bone mineral density,³ and poor outcome after treatment of chronic osteomyelitis.^11,¹⁴ In addition, clinical and experimental evidence suggests that cigarette smoking leads to decreased mineralization and mechanical strength of regenerate bone during tibial lengthening.¹⁴^–¹⁷

The purpose of this chapter is to critically analyze the evidence available in the literature on the effect of smoking on fracture healing, outline areas of uncertainty, and provide some recommendations for future care. Because it is not a topic that lends itself well to randomization, or even prospective studies, most of the evidence available is contained in basic science studies and relatively low-quality Level III and IV retrospective clinical reviews.

EVIDENCE

Basic Science Research

Regenerate bone is vulnerable to the vasoconstrictive and hypoxic effects of cigarette smoke and nicotine.14–17 In a model of tibial lengthening in rabbits, Ueng and colleagues¹⁵ demonstrate decreased production, maturation, and torsional strength of regenerate bone formation in subjects exposed to cigarette smoke. The same group demonstrated improved mechanical strength of regenerate bone in animals treated with hyperbaric oxygen, suggesting that local tissue oxygen tissue tension is of paramount importance.¹⁶ El-zawawy and coworkers¹⁷ show that the chondrogenic phase of tibial fracture healing in a mouse model was delayed by exposure to nicotine. Similarly, Skott and coauthors¹⁸ studied the effect of tobacco extract on the healing of a closed femoral fracture model in the rat. They found that the rats given tobacco extract had a 20% to 26% decrease in the mechanical strength of the femur 21 days after fracture. In a rabbit model, Raikin and colleagues¹⁹ conducted a study examining the effect of administration of nicotine on the mechanical strength of midshaft tibial osteotomies. They found a nearly identical 26% decrease in mechanical strength in the nicotine group with a corresponding decrease in callous size. In summary, abundant basic science evidence illustrates the negative effects of smoking in general and nicotine in particular on fracture healing (Table 50-1).

TABLE 50-1 Basic Science Studies on the Effect of Smoking on Bone Healing

Clinical Research

Numerous clinical studies describe the effects of smoking on various aspects of fracture healing, regenerate bone formation, spinal fusion, arthrodeses, or osteotomy healing.^3,^5,^10–^14,^{20, 21} Because of the nature of the condition, it is not possible to randomize patients into smoking and nonsmoking groups; therefore, most reports are Level III retrospective reviews, although there are some studies with prospectively gathered information in a comparative study (Level II).^11,^{12, 14} However, even though it is of relatively low quality, the clinical information that is available is overwhelming in its description of the negative effects of smoking on bone healing (Table 50-2).

TABLE 50-2 Clinical Studies on the Effect of Smoking on Bone Healing

In the upper extremity, Chen and colleagues ²¹ describe a 30% nonunion rate with a mean time to healing of 7.1 months in smokers versus a 0% nonunion rate and a mean healing time of 4.1 months in nonsmokers after ulnar shortening osteotomy. Similarly, in a series of 64 patients, Little and colleagues²² found that smokers were 3.7 times more likely (P = 0.005) than nonsmokers to have failure of their scaphoid nonunion repair.

In the lower extremity, Hak and coauthors ²³ found that all 8 smokers had a healed femoral nonunion after exchange reamed femoral nailing versus only 10 of 15 smokers. Folk, Starr, and Early ⁵ found that smoking was a significant negative risk factor for wound complications in a series of 190 calcaneal fractures treated with surgery (relative risk, 1.2; P = 0.03). McKee and colleagues,¹⁴ in a series of 84 adult patients treated with Ilizarov reconstruction, found that smokers had a 38% chance of a poor outcome versus 10% in nonsmokers (P = 0.003). Significantly, all five amputations in their series were in smokers.

Perhaps the most closely studied aspect of orthopedic trauma with respect to smoking is that of the fracture that continues to plague orthopedic surgeons with poor outcomes, nonunion, infection, and limb loss: the open tibia fracture. In retrospective reviews, Harvey and investigators,¹² Schmitz and researchers,¹³ and Adams, Keating, and Court-Brown¹⁰

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