Indian Journal of Dental Research

Historians believe that the Native Americans began using tobacco for medicinal and ceremonial purposes before the first century B.C. According to a Huron Indian myth,[¹] “In ancient times, when the land was barren and the people were starving, the Great Spirit sent forth a woman to save humanity. As she travelled over the world, everywhere her right hand touched the soil, there grew potatoes. And everywhere her left hand touched the soil, there grew corn. And in the place where she sat, there grew tobacco.”

Tobacco was introduced into India by the Portuguese traders during 16^th century. Tobacco use and production have greatly increased to such an extent that today India is the second largest producer of tobacco in the world.[¹]

Usage of tobacco harms almost every organ of the body and has been associated with coronary heart diseases, stroke, atherosclerosis, respiratory diseases such as COPD, and pneumonia, and various carcinomas.[¹]

Also, usage of tobacco affects oral tissues causing various pre-cancerous lesions and carcinomas of the mouth and pharynx. Smoking tobacco has been attributed to have a negative effect on the healing process of oral tissues after surgical and nonsurgical extractions, periodontal procedures, orthognathic surgeries, and implant therapies. This article aims at reviewing the effects of tobacco upon the healing capacity of oral tissues following routine surgical procedures performed in the oral cavity.

CIGARETTE SMOKING AND WOUND HEALING

Tobacco is a peripheral vasoconstrictor influencing the rate at which the oral wound heals.[²] Carbon monoxide and other chemicals produced during the combustion of tobacco can reduce the capillary blood flow. A clinical study has shown that a single cigarette can reduce the peripheral blood velocity by 40% in one hour.[²]

The mechanism by which smoking may affect wound healing is unknown. One possible explanation is that the substances in tobacco and its smoke, particularly nicotine, cotinine, carbon monoxide, and hydrogen cyanide are cytotoxic to those cells that are involved in wound healing. Nicotine increases platelet adhesiveness, raising the risk of microvascular occlusion, and tissue ischemia. Smoking is associated with catecholamines release, resulting in vasoconstriction and decreased tissue perfusion.[³] In the author's experience, a patient reported with delayed healing of an ulcer in the lip was found to be a smoker [Figure 1].

DRY SOCKET

Cryer et al.,[⁴] postulated that smoking is associated with endogenous catecholamines release resulting in vasoconstriction and decreased tissue perfusion. Sweet et al.,[⁵] had evaluated the relationship between smoking and localized osteitis in 200 patients, who had 400 mandibular third molars removed. Information on the number of cigarettes smoked each day and the postoperative smoking habit of each patient were recorded. The authors suggest that the heat from the burning tobacco, and tobacco along with its byproducts could act as a contaminant in the surgical site together with the suction applied to the cigarette that might dislodge the clot from the alveolus interrupting healing of the socket.

According to Meechan et al.,[⁶] fibrinolytic activity caused by smoking reduces alveolar blood supply after dental extractions and dry socket was found common among smokers. Incidence of painful socket was analyzed in 3541 extractions performed in 2417 patients. It was observed that sockets with poor filling of blood postoperatively, were found more likely to develop painful sockets (P> 0.02). Postoperative socket filling with blood was significantly reduced in smokers compared with nonsmokers (P> 0.01). The incidence of painful socket in heavy smokers (20 or more cigarettes per day) was higher compared with nonsmokers (P> 0.05).

Larsen[⁷] in a prospective study assessed the risk factors associated with the development of dry socket after extraction of 138 third molars. Usage of tobacco was found to significantly increase the incidence of alveolar osteitis compared to other factors like age, sex, usage of oral contraceptives, and increased surgical time.

Al-Belasy et al.,[³] in a study determined the risk of developing dry socket in water-pipe (shisha) smokers and found that cigarette and shisha smokers were 3-times more prone to develop dry socket than nonsmokers. The authors had observed that smoking on the day of surgery and increased frequency of smoking increased the incidence of dry socket.

Lopez Carriches et al.,[⁸] in their study observed that after third molar extraction, smokers were more prone to develop trismus than nonsmokers. However, they did not observe statistically significant difference in terms of pain.

In the author's experience, smoking on the day of tooth extraction seemed to increase the susceptibility to dry socket formation [Figure 2].

According to Sweet et al., the suction associated with cigarette smoking might dislodge the clot from the alveolus and interrupt healing. However, Alexander denies the fact that suction during smoking causes physical dislodgement of the clot.[⁹] Al-Belasy et al.,[³] believe that dry socket is caused by destruction of the clot rather than physical dislodgement. Though the exact mechanism by which smoking predisposes the socket to become dry remains unclear, smoking definitely seems to be positively associated with the occurrence of dry socket.

IMPLANT FAILURE

Though plaque-induced inflammation and occlusal loading are considered as the most important factors influencing the prognosis of oral implant treatment, smoking is also an important factor related to the loss of, and soft tissue changes around implants.[^10,11,12,13]

Some clinicians believe that smoking is a relative contraindication for dental implant therapy.[¹⁴] De Bruyn found that the early failures before loading in the maxilla were higher in smokers (9%) than nonsmokers (2%).[¹¹] Over an average of a thirty-eight months follow-up, Bain and Moy[¹⁰] reported that implant failure rates were more than twice as high in smokers (11.28%) as nonsmokers (4.76%). Effects were more pronounced in the maxillary arch, where the failure rate for smokers was (16.82%) in the anterior region as compared to 3.6% in nonsmokers.

Weyant[¹⁵] in a large multicentre population-based study, reported that the usage of tobacco negatively affects peri-implant soft tissue health. Another multicentre study was conducted by Gorman et al.,[¹²] to analyze the implant survival at stage-2 surgery in more than 2000 implants placed in 433 patients in 310 cases. Correlating the results of the interim analysis, the authors have concluded that smoking is detrimental to implant success.

Lindquist et al.,[¹⁶] studied the association of smoking with the peri-implant bone loss around mandibular implants in 45 edentulous patients (21 smokers and 24 nonsmokers) for a period of 10 years after treatment. Information about smoking habits of patients was collected based on an interview. Peri-implant bone level was measured on intraoral radiographs. Though the long-term results of the implant were good, the mean marginal bone loss was significantly greater in smokers (P< 0.001) than nonsmokers, correlating to the numbers of cigarettes consumed. Based on a multivariate analysis, smoking was observed as the most significant factor affecting the rate of peri-implant bone loss compared to oral hygiene, and those associated with occlusal loading. The authors have stressed that smoking habits should be included in the analysis of implant survival and peri-implant bone loss.

EFFECT OF NICOTINE ON DISTRACTION OSTEOGENESIS

An experimental study was performed by Cheung et al.,[¹⁷] to evaluate the dose-dependent effect of nicotine on bone regeneration, using a rabbit model of mandibular distraction osteogenesis with sham, placebo control, low-dose nicotine (0.75 g), and high-dose nicotine (1.5 g) groups. Nicotine was administered with 60 daytime-release nicotine pellets implanted subcutaneously in the nicotine groups. When the sacrificed animals were subjected to examination by radiography, computed tomography, and histological analysis, significantly lower volume of bone and chondrocytes were found in the high-dose nicotine group compared to the low-dose nicotine, sham, and placebo-control groups. The authors imply that bone formation following distraction osteogenesis may be compromised by high-dose nicotine exposure.

EFFECT OF SMOKING UPON BONE HEALING FOLLOWING ROUTINE ORAL SURGICAL PROCEDURES

Smoking is reported to be an important factor responsible for postoperative infections leading to plate removal in orthognathic surgeries and fracture management.

Hollinger et al.,[¹⁸] based on an experimental study, hypothesized that nicotine has a negative effect on bone healing by diminishing osteoblast function. It also seems to cause autogenous bone graft morbidity and interferes with the biomechanical properties of the graft.

Cheynet et al.,[¹⁹] in their retrospective study of infectious complications of 60 mandibular osteotomies, smoking was observed as the important patient-related risk factor responsible for postoperative infection.

Levin et al.,[²⁰] observed high degree of complications following surgeries or implant failures in smokers. The authors had suggested that the heat released from main-stream cigarette smoke and the toxic by-products of tobacco such as nicotine, carbon monoxide, and hydrogen cyanide, could be the risk factors affecting the success of dental implants and grafting procedures like maxillary sinus augmentation, etc.

Saldanha et al.,[²¹] investigated the effect of smoking on the dimension of alveolar process and radiographic bone density in 21 patients (11 nonsmokers and 10 smokers) after nonmolar extractions. Reduction in alveolar height and radiographic bone density was more pronounced in smokers than nonsmokers. The authors believe that cigarette smoking increases bone resorption at the fractured ends, interfering with the osteoblastic function.

In the author's experience, a male patient treated for fracture of the mandibular angle, reported with flap laceration and plate exposure was found to have a history of cigarette smoking during the postoperative period [Figure 3].

The plate was removed since the bone healing was not compromised. Thus, cigarette smoking may be an important factor predisposing to wound dehiscence or flap laceration following surgeries.

INFLUENCE OF SMOKING ON PERIODONTAL THERAPY

Cigarette smoking is a significant risk factor for periodontal diseases and impaired healing after periodontal surgeries.[²²] Unlike usage of smoking tobacco that causes widespread periodontal destruction, the usage of smokeless tobacco causes gingival recession at the site of placement.[²³]

Many periodontal interventional studies had consistently demonstrated that smokers do not heal as well as nonsmokers.[²⁴] Two population-based epidemiological studies done by Tomar et al.,[²⁵] and Beck et al.,[²⁶] found that periodontitis is more common in smokers than in nonsmokers. Former smokers had lower rates of periodontitis than smokers.[²⁵] Smokers were also reported to have more alveolar bone loss.

A number of clinical studies have compared the response of smokers and nonsmokers to various types of surgical and nonsurgical periodontal therapy.[^{26,27,28,29,30}] It was found that smoking has a strong negative impact on regenerative therapy,[³¹] including osseous grafting, guided tissue regeneration,[^31,32,33,34] or a combination of these treatments,[³⁵] and 80% failure rate in the treatment of furcation defects.[³⁶] The majority of studies found that gingival grafting for root coverage is less successful in smokers than nonsmokers.[^37,38,39]

CONCLUSION

Tobacco, apart from being positively associated with pre-cancerous and cancerous lesions is also reported to negatively affect the outcome of almost all routine therapeutic procedures performed in the oral cavity, starting from simple nonsurgical periodontal therapy to orthognathic surgeries. Dental surgeons should aid smoking patients to become tobacco-free, educating the patients by imparting these adverse effects.

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