References
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Vellappally S, Fiala Z, Smejkalová J, Jacob V, Somanathan R. Smoking related systemic and oral diseases. Acta Medica (Hradec Kralove). 2007; 50:161-166
Balaji SM. Tobacco smoking and surgical healing of oral tissues: a review. Indian J Dent Res. 2008; 19:344-348
Petti S. Lifestyle risk factors for oral cancer. Oral Oncolog. 2009; 45:340-350
Geneva: World Health Organization; 2008
Scully C. Cancer and potentially malignant disorders, 3rd edn. Oxford: Churchill Livingstone; 2013
Just-Sarobé M. Smoking and the skin. Actas Dermosifiliogr. 2008; 99:173-184
Rom O, Avezov K, Aizenbud D, Reznick AZ. Cigarette smoking and inflammation revisited. Respir Physiol Neurobiol. 2013; 187:5-10
Katsiki N, Papadopoulou SK, Fachantidou AI, Mikhailidis DP. Smoking and vascular risk: are all forms of smoking harmful to all types of vascular disease?. Public Health. 2013; 5:435-441
Cancer Research UK. http://www.cancerresearchuk.org/cancer-info/cancerstats/keyfacts/lung-cancer/
Khullar D, Maa J. The impact of smoking on surgical outcomes. J Am Coll Surg. 2012; 3:418-426
Blondon M, Wiggins KL, McKnight B, Psaty BM, Rice KM, Heckbert SR, Smith NL. The association of smoking with venous thrombosis in women. A population-based, case-control study. Thromb Haemost. 2013; 5:891-896
Benowitz NL. Cigarette smoking and cardiovascular disease: pathophysiology and implications for treatment. Prog Cardiovasc Dis. 2003; 46:91-111
Reibel J. Tobacco and oral diseases. Update on the evidence, with recommendations. Med Princ Pract. 2003; 12:22-32
Sham AS, Cheung LK, Jin LJ, Corbet EF. The effects of tobacco use on oral health. Hong Kong Med J. 2003; 9:271-277
Johnson NW, Bain CA. Tobacco and oral disease. EU-Working Group on Tobacco and Oral Health. Br Dent J. 2000; 189:200-206
Johnson GK, Hill M. Cigarette smoking and the periodontal patient. J Periodontol. 2004; 75:196-209
Darwazeh AM, Al-Dwairi ZN, Al-Zwairi AA. The relationship between tobacco smoking and oral colonization with Candida species. J Contemp Dent Pract. 2010; 11:17-24
Shulman JD, Rivera-Hidalgo F, Beach MM. Risk factors associated with denture stomatitis in the United States. J Oral Pathol Med. 2005; 34:340-346
Calsina G, Ramon JM, Echeverria JJ. Effects of smoking on periodontal tissues. J Clin Periodontol. 2002; 29:771-776
Amagasa T, Yamashiro M, Uzawa N. Oral premalignant lesions: from a clinical perspective. Int J Clin Oncol. 2011; 16:5-14
Hashibe M, Brennan P, Benhamou S, Castellsague X, Chen C, Curado MP Alcohol drinking in never users of tobacco, cigarette smoking in never drinkers, and the risk of head and neck cancer: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. J Natl Cancer Inst. 2007; 99:777-789
Jerjes W, Upile T, Radhi H, Petrie A, Abiola J, Adams A The effect of tobacco and alcohol and their reduction/cessation on mortality in oral cancer patients: short communication. Head Neck Oncol. 2012; 4
Krueger JK, Rohrich RJ. Clearing the smoke: the scientific rationale for tobacco abstention with plastic surgery. Plast Reconstr Surg. 2001; 108:1063-1073
Wolfram D, Tzankov A, Pulzl P, Piza-Katzer H. Hypertrophic scars and keloids a review of their pathophysiology, risk factors, and therapeutic management. Dermatol Surg. 2009; 35:171-181
Kolokythas A, Olech E, Miloro M. Alveolar osteitis: a comprehensive review of concepts and controversies (review article). Int J Dent. 2010; 1-10
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; 73:393-397
Bortoluzzi MC, Capella DL, Barbieri T, Marchetti S, Dresch CP, Tirello C. Does smoking increase the incidence of postoperative complications in simple exodontia?. Int Dent J. 2012; 62:106-108
Sloan A, Hussain I, Maqsood M, Eremin O, El-Sheemy M. The effects of smoking on fracture healing. Surgeon. 2010; 8:111-116
Levin L, Schwartz-Arad D. The effect of cigarette smoking on dental implants and related surgery. Implant Dent. 2005; 14:357-361
Kalantzis A, Scully C., 3rd edn. Oxford: Oxford University Press; 2009
Koorbusch GF, Fotos P, Goll KT. Retrospective assessment of osteomyelitis. Etiology, demographics, risk factors, and management in 35 cases. Oral Surg Oral Med Oral Pathol. 1992; 74:149-154
Baldi D, Izzotti A, Bonica P, Pera P, Pulliero A. Degenerative periodontal-diseases and oral osteonecrosis: the role of gene-environment interactions. Mutat Res. 2009; 667:118-131
Ajmal M, Cheng EY. Biologic factors influencing osteonecrosis: steroids, statins, ethanol, human immunodeficiency virus and antiretroviral therapy, and smoking. Semin Arthroplasty. 2007; 18:180-183
Kluth EV, Jain PR, Stuchell RN, Frich JC. A study of factors contributing to the development of osteoradionecrosis of the jaws. J Prosthet Dent. 1988; 59:194-201
Snider TN, Cottrell D, Batal H. Summary of current consensus on the effect of smoking on implant therapy. J Mass Dent Soc. 2011; 59:20-22
Liddelow G, Klineberg I. Patient-related risk factors for implant therapy. A critique of pertinent literature. Aust Dent J. 2011; 56:417-426
Tobacco habit-associated oral disease and the negative effects on surgical outcomes
From Volume 44, Issue 11, December 2017 | Pages 1065-1070
Article
Tobacco is obtained from the leaves of the plant Nicotiana, with nicotine being the main psychoactive alkaloid. Named after the Lisbon based diplomat, Jean Nicot, in the 16th Century, the leaf was chewed, taken nasally in powder form or applied locally in the treatment of cough, asthma, headaches, stomach cramps, gout, diseases of women, intestinal parasites, open wounds and cancers.1 By the latter part of the 16th Century, tobacco was being used mainly for pleasure, with smoking being the dominant mode of administration. Over the following 200 years, evidence of the harmful effects of tobacco on almost every system in the body became documented.2 Tobacco use is now accepted as being a leading cause of preventable illness and premature death and has a significant public health impact. It affects multiple organ systems, resulting in numerous tobacco-related diseases, primarily in the cardiovascular and respiratory systems. Tobacco use is also involved in the causation of numerous types of cancer.3,4
The World Health Organization now accords tobacco usage as the main contributing factor in the early death of 50% of its users,5 and it is estimated that almost 6 million people die each year due to tobacco-related diseases, these being users, ex-users as well as second-hand smokers. These figures do not include data from e-cigarette smoking or ‘vaping’ and neither does this paper attempt to address the effects of this rapidly expanding form of ‘tobacco’ use. Despite such tobacco-related mortality, tobacco consumption is still increasing globally, although some reduction is seen in pockets of high income and upper-middle income households/communities.4
Tobacco smoke contains over 250 harmful compounds, including carbon monoxide (CO), hydrogen cyanide (HC) and polycyclic aromatic hydrocarbons such as benzpyrene, nitrosamines, aldehydes and aromatic amines.6,7 Many of these substances exist in both a gaseous as well as a solid phase. A number of these substances are listed in Table 1. Tobacco-related oral diseases and pathological processes include acute necrotizing gingivitis, periodontitis, xerostomia, candidosis, halitosis, extrinsic tooth staining, hairy tongue, infected extraction socket, delayed bone healing, implant failure, oral cancer and premalignant lesions.
| Solid Phase (Particles) | Gas Phase |
|---|---|
| Phenol | Carbon monoxide |
| Catechol | Hydrogen cyanide |
| Quinoline | Nitrogen oxides |
| Aniline | Acetone |
| Toluidine | Formaldehyde |
| Nickel | Acrolein |
| N-Nitrosodimethylamine | Ammonium |
| Benzopyrenes | Pyridine |
| Benzanthracene | 3-Vinylpyridine |
| 2-Naphthylamine | N-Nitrosodimethylamine, N-Nitrosopyrrolidine |
Systemic diseases
It is not the authors' intention to give a detailed discussion of those tobacco-related systemic diseases that may have an indirect impact on the delivery of oral surgery. It is evident, however, that, for example, in the management of tobacco-associated malignancies, that the chemotherapeutic agents used may complicate management and surgical outcomes. For example, lung cancer is the commonest cause of cancer death in the UK, accounting for more than 1 in 5 cancer deaths, and smoking is the main avoidable risk factor for lung cancer, linked to an estimated 86% of lung cancer cases in the UK.8
Cardiovascular disease
The association of tobacco habit with coronary artery disease, peripheral arterial disease, abdominal aortic aneurysm and stroke was recently reviewed by Katsiki et al.9 Cigarette smoking dramatically increases inflammatory markers such as C-reactive protein and haemostatic factors, affecting plasma viscosity and raising tissue plasminogen activator antigen.10 Atherosclerosis is also promoted, which is a major contributory factor in ischaemic heart disease.9 The enhanced risks of complications due to cardiac disease impacts upon fitness for GA, sedation and ambulatory treatment generally, eg angina. Long-term CO exposure in smokers causes an increase in the red cell population to compensate for oxygen requirements, which results in an increased blood viscosity, which may also contribute to venous thrombosis and other hypercoagulopathies.11,12 The requirement for anticoagulant therapy will further complicate the practice of surgery.
Chronic obstructive pulmonary disease (COPD)
COPD is a chronic, slowly progressing disorder, usually a combination of chronic bronchitis and emphysema. Increased levels of inflammatory markers and cytokines, such as tumour necrosis factor-α (TNF-α), interleukin-1, interleukin-6 and interleukin-8 cause extensive tissue damage, resulting in reduced lung function. Smoking also affects host antibacterial immune responses predisposing them to infection.13
Oral diseases
The effects of tobacco range from harmless staining of teeth and dental restorations, to a reduction in ability to taste and smell, to more serious effects including periodontal disease, benign mucosal lesions, precancerous lesions and carcinoma of the mouth and pharynx.14 Also of note in the mouth as with skin, the healing process following various forms of surgery can be frustrated.3
Aesthetics
Smoking causes discoloration of teeth, dental restorations and dentures. Evidence suggests that tobacco staining is more significant than that of tea and coffee consumption.15
Smell and taste
There are numerous reports in the literature suggesting that tobacco smoking negatively impacts the acuity of smell and taste. Also, smoking is the major contributing factor to halitosis.16
Dental caries
Saliva flow rate is increased in the short term by tobacco usage and its pH rises during smoking, however, long-term smokers tend to have a lower salivary pH than non-smokers. There is not a direct aetiological relationship between caries and smoking, however, the lower salivary pH, as observed in long-term smokers, results in a shift of bacterial population towards lactobacillus and cariogenic streptococci in smokers, which may argue for increased risk of dental caries.17
Oral candidiasis
Controversy exists in the literature with regards to establishing a link between cigarette smoking and oral candidiasis. A leukoplakia in a smoker, affecting the commissure of the lip, is a lesion from which a fungal overgrowth is often isolated (Figure 1). It has been observed that infection by Candida species may disappear following cessation of smoking.2 A quantitative study showed a slight increase in the prevalence of candidal growth in smokers when compared to non-smokers.18 Further studies have suggested an increased prevalence in heavy smokers (>15/day) compared to non-smokers.19
Periodontal disease
There is a well demonstrated connection between smoking and periodontal disease prevalence and severity, indicating that smoking is a significant risk factor.2 Other commonly observed features include increased marginal bone loss, periodontal pockets, greater number of teeth with furcation involvement and more severe attachment loss.16 Smoking has a direct impact on periodontal health irrespective of age, gender or socioeconomic status.2 Smokers are approximately three times more likely to have severe periodontitis than non-smokers and exhibit only half as much improvement following periodontal therapy compared to non-smokers.20 In summary, smoking-related periodontal disease will commonly lead to the demand for ‘premature’ tooth removal.
Premalignant conditions
The common oral lesions accepted as having a premalignant potential include erythroplakias, leukoplakias (of various subtypes), actinic cheilitis, lichenoid lesions and submucous fibrosis. Those that have an accepted association with a tobacco habit are erythroplakias (erythroplasias), leukoplakias and sublingual keratosis. An example of an erythroplasia of the palate is shown in Figure 2. A six-fold increase in the risk of developing leukoplakia is documented for smokers compared to non-smokers, with floor of mouth leukoplakia occurring significantly more frequently in smokers. Regression or complete resolution of leukoplakia may occur following cessation of smoking in association with reversal of dysplastic change.2,16 The rate of malignant transformation of oral leukoplakia varies in the literature from 0.13%–17.5%, with observation periods ranging from 1–30 years. Dysplasia within leukoplakia is a key factor in determining transformation to squamous cell carcinoma.21
Stomatitis nicotina
It is an asymptomatic lesion associated with tobacco use that occurs in the hard palate. It appears as a white plaque with multiple red dots occasionally located centrally in a small elevated nodule (Figure 3). It disappears following cessation of smoking,16 whereas palatal keratosis, associated with reverse smoking, is considered a premalignant lesion.2
Oral malignancy
Head and neck cancers are a group of related neoplasms arising in the oral cavity, pharynx and larynx. Cigarette smoking has been implicated in 25% of head and neck cancers in patients who have never drunk alcohol, and a clear dose relationship for the frequency, duration and number of pack-years of cigarettes has been demonstrated.22 A pack-year is calculated by the number of years the patient has been smoking multiplied by the number of packs they smoke on average in a day. The relative risk of head and neck cancer increases markedly in a patient with 20 pack-years.22
The mechanisms involved in oral carcinogenesis have been extensively researched but are still not fully understood. It is believed to involve mutations at the DNA level that activates oncogenes to cause abnormal proliferation of cells.23 Oral SCC (Figure 4) represents 3–4% of all cancer in the UK, with 7700 new cases per year.8 Squamous cancer accounts for approximately 90% of all oral cancer and its association with smoking and alcohol drinking is well established.7 It is well-documented that the risk is decreased with cessation of smoking.2,14
Other mucosal conditions
Smoker's melanosis
Heavy smokers have a higher prevalence of oral pigmentation; greyish-brown macular lesions caused by tar deposits mostly seen on the attached gingiva. The condition is not considered premalignant and regression of pigmentation may occur following cessation of smoking.2,7,16
Hairy tongue
‘Hairy tongue’ or ‘black hairy tongue’ is a condition characterized by hypertrophy of the filiform papillae on the dorsum of the tongue and accompanied by black pigment deposition. The furry appearance of the dorsum of the tongue has been associated with heavy smoking, however, it can also be seen in non-smokers. Other causes that contribute to this condition include antibiotic use, chromogenic bacterial growth and high levels of tea or coffee consumption.2,7,14
Tobacco smoking and wound healing
The toxic components of cigarette smoke, and particularly nicotine, carbon monoxide, and hydrogen cyanide, impede the cellular processes involved in wound healing. Nicotine and catecholamines stimulate chalones, which are hormones that inhibit epithelialization. Carbon monoxide binds to haemoglobin to become carboxyhaemoglobin, so reducing oxygen-carrying capacity and leading to impaired wound healing. Nicotine inhibits prostacyclin, which increases platelet adhesiveness and forms thrombi, leading to microvascular occlusion and eventual tissue ischaemia. This results in delayed healing, wound dehiscence, an increase in post-operative infections and increased scarring.24 These hypertrophic scars represent excessive collagen synthesis and, as they are linked to cigarette smoking, should influence the consenting process when a smoker is being considered for cosmetic surgery, such as synthetic fillers and grafts.25 A minimum time period of pre-operative abstinence from smoking in an attempt to reduce these deleterious effects is not well established, but it has been suggested that cessation for 4 weeks before surgery and continuing for between 5 and 28 days post-surgery is associated with improved healing and reduced scarring.7
Dry socket/Alveolar osteitis (AO)
The recorded incidence of AO varies in the literature from 0.55%–5% for simple exodontia to 1%–37.5% for mandibular third molar removal.26 A dose-dependent relationship has been demonstrated between smoking and AO occurrence, with a 4–5 fold increase in the incidence of AO reported for patients who smoke half a pack of cigarettes a day compared to non-smokers.2 Smoking on the day of surgery appears to be particularly detrimental.27,28 A period of pre- and post-operative cessation of tobacco use, as previously described, would be expected to decrease the incidence of AO.7
Bone healing
One of the factors responsible for delayed or poor healing is smoking. Components of tobacco smoke are toxic to proliferating osteoblasts, reduce the blood supply to the injured site and have been implicated in the development of osteoporosis.29 Studies have demonstrated that smoking is responsible for post-operative infection following osteotomy and trauma surgery.3 Bone augmentation procedures have also been shown to be adversely affected by a tobacco habit.30
Osteomyelitis
Osteomyelitis by definition is the ‘inflammation of bone marrow and associated structures’, although the term has become synonymous with an infection of bone with a pyogenic organism. This process manifests in either an acute or chronic form.31 A tobacco habit has been cited as a risk factor in osteomyelitis of the jaw.32
Osteonecrosis
This disease is defined as ‘avascular necrosis of bone’. Several risk factors have been identified as predisposing to this condition as it affects the jaws. Most recently, a number of the bisphosphonate drugs have been associated with this oral condition, but usually where co-morbidities exist, including extreme of age and local factors. Smoking has been demonstrated to act both as a general and local risk factor in this condition, with the vasoconstrictive and microthrombolic effects of tobacco leading to ischaemia, which may predispose to both osteonecrosis and osteomyelitis.33 In most cases, it is considered a weak risk factor but can have a cumulative and dose-related effect. It has been suggested that a smoking habit equal to 20-pack years or more represents a significant risk factor for developing osteonecrosis.34
Osteoradionecrosis
Smoking has also been cited as a risk factor in the development of this post-irradiation condition.35 It is, however, difficult to demonstrate an evidential link between this, radiation-associated condition and a frequent user tobacco habit among sufferers.
Implant failure
Successful and stable osseointegration is essential for long-term success and function of implants. A number of factors have been cited in implant failure and a tobacco habit is one of these.30 An increased incidence of complications during implantation procedures has been observed in smokers and includes the following, marginal bone loss, peri-implant inflammation, pocket formation and radiographic mesial and distal bone loss.36 A dose relationship has also been reported between smoking and peri-implant marginal bone loss, with an associated higher incidence of peri-implantitis.37
Conclusion
Tobacco use is harmful to general and oral health. It is a common cause of addiction, preventable illness, disability and death. It is well recognized that a tobacco habit increases the risk for periodontal disease, premalignancy and oral cancer. A tobacco habit can also impair wound healing and increases the risk and severity of surgical complications. With the increased responsibility of clinicians to tailor consent to the individual patient before them, the presence of a smoking habit should be addressed directly in relation to any invasive/surgical procedure under consideration. It is hoped that this article will support clinicians in this process and provide relevant references for further reading.