Year : 2008 | Volume
: 19 | Issue : 4 | Page : 344--348
Tobacco smoking and surgical healing of oral tissues: A review
Consultant Oral and Maxillofacial Surgeon and Director, Balaji Dental and Craniofacial Hospital, 30/1, Kavingar Bharadidasan Road, Teynampet, Chennai - 600 018, India
S M Balaji
Consultant Oral and Maxillofacial Surgeon and Director, Balaji Dental and Craniofacial Hospital, 30/1, Kavingar Bharadidasan Road, Teynampet, Chennai - 600 018
It is believed that the crew of Columbus had introduced tobacco from the «SQ»American India«SQ» to the rest of the world, and tobacco was attributed as a medicinal plant. It was often used to avert hunger during long hours of work. But in reality, tobacco causes various ill effects including pre-malignant lesions and cancers. This article aims at reviewing the literature pertaining to the effect of tobacco smoking upon the outcome of various surgical procedures performed in the oral cavity.
Tobacco affects postoperative wound healing following surgical and nonsurgical tooth extractions, routine maxillofacial surgeries, implants, and periodontal therapies. In an experimental study, bone regeneration after distraction osteogenesis was found to be negatively affected by smoking. Thus, tobacco, a peripheral vasoconstrictor, along with its products like nicotine increases platelet adhesiveness, raises the risk of microvascular occlusion, and causes tissue ischemia. Smoking tobacco is also associated with catecholamines release resulting in vasoconstriction and decreased tissue perfusion. Smoking is believed to suppress the innate and host immune responses, affecting the function of neutrophils - the prime line of defense against infection. Thus, the association between smoking and delayed healing of oral tissues following surgeries is evident. Dental surgeons should stress on the ill effects of tobacco upon the routine postoperative healing to smoker patients and should aid them to become tobacco-free.
|How to cite this article:|
Balaji S M. Tobacco smoking and surgical healing of oral tissues: A review.Indian J Dent Res 2008;19:344-348
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Balaji S M. Tobacco smoking and surgical healing of oral tissues: A review. Indian J Dent Res [serial online] 2008 [cited 2019 Sep 20 ];19:344-348
Available from: http://www.ijdr.in/text.asp?2008/19/4/344/44540
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,  "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. 
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. 
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.  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. 
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.  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].
Cryer et al.,  postulated that smoking is associated with endogenous catecholamines release resulting in vasoconstriction and decreased tissue perfusion. Sweet et al.,  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.,  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  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.,  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.,  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.  Al-Belasy et al.,  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.
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. ,,,
Some clinicians believe that smoking is a relative contraindication for dental implant therapy.  De Bruyn found that the early failures before loading in the maxilla were higher in smokers (9%) than nonsmokers (2%).  Over an average of a thirty-eight months follow-up, Bain and Moy  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  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.,  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.,  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 et al.,  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.,  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.,  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.,  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.,  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.  Unlike usage of smoking tobacco that causes widespread periodontal destruction, the usage of smokeless tobacco causes gingival recession at the site of placement. 
Many periodontal interventional studies had consistently demonstrated that smokers do not heal as well as nonsmokers.  Two population-based epidemiological studies done by Tomar et al.,  and Beck et al.,  found that periodontitis is more common in smokers than in nonsmokers. Former smokers had lower rates of periodontitis than smokers.  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. ,,,, It was found that smoking has a strong negative impact on regenerative therapy,  including osseous grafting, guided tissue regeneration, ,,, or a combination of these treatments,  and 80% failure rate in the treatment of furcation defects.  The majority of studies found that gingival grafting for root coverage is less successful in smokers than nonsmokers. ,,
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.
|1||Reddy KS, Gupta PC, editors. Report on Tobacco Control in India. Ministry of Health and Family Welfare, New Delhi: Government of India; 2004.|
|2||Mayfield L, Soderholm G, Hallstrom H, Kullendorff B, Edwardsson S, Bratthall G, et al. Guided tissue regeneration for the treatment of intraosseous defects using a bioabsorbable membrane: A controlled clinical study. J Clin Periodontol 1998;25:585-95.|
|3||Al-Belasy FA. The relationship of "shisha" (water pipe) smoking to postextraction dry socket. J Oral Maxillofac Surg 2004;62:10-4.|
|4||Cryer PE, Haymond MW, Santiago JV, Shah SD. Norepinephrine and epinephrine release and adrenergic mediation of smoking-associated hemodynamic and metabolic events. N Engl J Med 1976;295:573-7.|
|5||Sweet JB, Butler DP. The relationship of smoking to localized osteitis. J Oral Surg 1979;37:732-5.|
|6||Meechan JG, Macgregor ID, Rogers SN, Hobson RS, Bate JP, Dennison M. The effect of smoking on immediate post-extraction socket filling with blood and on the incidence of painful socket. Br J Oral Maxillofac Surg 1988;26:402-9.|
|7||Larsen PE. Alveolar osteitis after surgical removal of impacted mandibular third molars: Identification of the patient at risk. Oral Surg Oral Med Oral Pathol 1992;73:393-7.|
|8||López-Carriches C, Gómez-Font R, Martνnez-Gonzαlez JM, Donado-Rodrνguez M. Influence of smoking upon the postoperative course of lower third molar surgery. Med Oral Patol Oral Cir Bucal 2006;11:E56-60.|
|9||Alexander RE. Dental extraction wound management: A case against medicating postextraction sockets. J Oral Maxillofac Surg 2000;58:538-51. |
|10||Bain CA, Moy PK. The association between the failure of dental implants and cigarette smoking. Int J Oral Maxillofac Implants 1993;8:609-15.|
|11||De Bruyn H, Collaert B. The effect of smoking on early implant failure. Clin Oral Implants Res 1994;5:260-4.|
|12||Gorman LM, Lambert PM, Morris HF, Ochi S, Winkler S. The effect of smoking on implant survival at second-stage surgery: DICRG Interim Report No 5: Dental Implant Clinical Research Group. Implant Dent 1994;3:165-8.|
|13||Lindquist LW, Rockler B, Carlsson GE. Bone resorption around fixtures in edentulous patients treated with mandibular fixed tissue-integrated prostheses. J Prosthet Dent 1988;59:59-63.|
|14||Hwang D, Wang HL. Medical contraindications to implant therapy: Part II: Relative contraindications. Implant Dent 2007;16:13-23.|
|15||Weyant RJ. Characteristics associated with the loss and peri-implant tissue health of endosseous dental implants. Int J Oral Maxillofac Implants 1994;9:95-102.|
|16||Lindquist LW, Carlsson GE, Jemt T. Association between marginal bone loss around osseointegrated mandibular implants and smoking habits: A 10-year follow-up study. J Dent Res 1997;76:1667-74.|
|17||Cheung LK Ma L, Zheng LW. Inhibitory effect of nicotine on bone regeneration in mandibular distraction osteogenesis. Front Biosci 2007;12:3256-62.|
|18||Hollinger JO, Schmitt JM, Hwang K, Soleymani P, Buck D. Impact of nicotine on bone healing. J Biomed Mater Res 1999;45:294-301.|
|19||Cheynet F, Chossegros C, Richard O, Ferrara JJ, Blanc JL. Infectious complications of mandibular osteotomy. Rev Stomatol Chir Maxillofac 2001;102:26-33.|
|20||Levin L, Schwartz-Arad D. The effect of cigarette smoking on dental implants and related surgery. Implant Dent 2005;14:357-61.|
|21||Saldanha JB, Casati MZ, Neto FH, Sallum EA, Nociti FH Jr. Smoking may affect the alveolar process dimensions and radiographic bone density in maxillary extraction sites: A prospective study in humans. J Oral Maxillofac Surg 2006;64:1359-65.|
|22||Winn DM. Tobacco use and oral disease. J Dent Educ 2001;65:306-12.|
|23||Johnson GK, Slach NA. Impact of tobacco use on periodontal status. J Dent Educ 2001;65:313-21. Review.|
|24||Mecklenburg RE, Grossi SG. Tobacco use and intervention. In: Rose LF, Genco RJ, Cohen DW, Mealey BL, editors. Periodontal medicine. Hamilton, Ontario: Decker; 2000. p. 99-119.|
|25||Tomar SL, Asma S. Smoking-attributable periodontitis in the United States: Findings from NHANES III: National Health and Nutrition Examination Survey. J Periodontol 2000;71:743-51.|
|26||Beck JD, Cusmano L, Green-Helms W, Koch GG, Offenbacher S. A 5-year study of attachment loss in community-dwelling older adults: Incidence density. J Periodontal Res 1997;32:506-15.|
|27||Ah MK, Johnson GK, Kaldahl WB, Patil KD, Kalkwarf KL. The effect of smoking on the response to periodontal therapy. J Clin Periodontol 1994;21:91-7.|
|28||Preber H, Bergstrom J. Effect of non-surgical treatment on gingival bleeding in smokers and non-smokers. Acta Odontol Scand 1986;44:85-9.|
|29||Grossi SG, Zambon J, Machtei EE, Schifferle R, Andreana S, Genco RJ, et al . Diabetics and smokers. J Periodontol 1996;67:1094-102.|
|30||Grossi SG, Zambon J, Machtei EE, Schifferle R, Andreana S, Genco RJ, et al . Effects of smoking and smoking cessation on healing after mechanical periodontal therapy. J Am Dent Assoc 1997;128:599-607.|
|31||Rosen PS, Marks MH, Reynolds MA. Influence of smoking on long-term clinical results of intrabony defects treated with regenerative therapy. J Periodontol 1996;67:1159-63.|
|32||Rosenberg ES, Cutler SA. The effect of cigarette smoking on the long-term success of guided tissue regeneration: A preliminary study. Ann R Australas Coll Dent Surg 1994;12:89-93.|
|33||Kaldahl WB, Johnson GK, Patil KD, Kalkwarf KL. Levels of cigarette consumption and response to periodontal therapy. J Periodontol 1996;67:675-81|
|34||Trombelli L, Kim CK, Zimmerman GJ, Wikesjo UM. Retrospective analysis of factors related to clinical outcome of guided tissue regeneration procedures in intrabony defects. J Clin Periodontol 1997;24:366-71.|
|35||Luepke PG, Mellonig JT, Brunsvold MA. A clinical evaluation of a bioresorbable barrier with and without decalcified freeze-dried bone allograft in the treatment of molar furcations. J Clin Periodontol 1997;24:440-6.|
|36||The effect of smoking on implant survival at second-stage surgery: DICRG Interim Report No 5: Dental Implant Clinical Research Group. Implant Dent 1994;3:165-8.|
|37||Miller PD Jr. Root coverage with the free gingival graft: Factors associated with incomplete coverage. J Periodontol 1987;58:674-81.|
|38||Muller HP, Eger T, Schorb A. Gingival dimensions after root coverage with free connective tissue grafts. J Clin Periodontol 1998;25:424-30.|
|39||Zucchelli G, Clauser C, De Sanctis M, Calandriello M. Mucogingival versus guided tissue regeneration procedures in the treatment of deep recession type defects. J Periodontol 1998;69:138-45.|