ABSTRACT and its frequency . Thus it is


The role of smoking in the development of lung cancer and cardiovascular disease is well known. Smokers have a 2.5 to 3.5 times greater risk of severe gum disease, which is recognised by the amount of bone lost around a particular tooth due to gum disease. Smokers also tend to lose more teeth than non-smokers.It also has a part to play in several diseases and lesions in the mouth; the most common being gum disease. It affects the mucosa of the oral cavity and may result in pigmentation of the intra oral surface .It’s carbon monoxide and nicotine content are carcinogenic in nature and start revealing their nature by slow and gradual pigmentation of the oral mucosa. It  may further lead to other complications like , atrophy of the mucosa , restricted mouth opening , halitosis and so on. But these changes in the mucosa can be reversed once the habit is controlled and gradually stopped.  Some of these changes are very characteristic and have varying clinical appearance and features. Pre-cancerous conditions are easily detected with regard to the mucosal changes . The pigmentation and lesions vary from one individual to another. The key factor depends upon the type of the tobacco product and its frequency . Thus it is of utmost importance to understand these mucosal changes for diagnosis and treatment . When detected at an early stage cessation of the habit is of prime concern and may aid in reversal of the lesion or pigmentation. 

Key words – Mucosal atrophy , pigmentation of oral cavity , smokers , malignancy associated with smoking, tobacco chewing , palatal change

             Disease of the oral mucosa is quite common when a person uses tobacco both smokeless and smoking type. More often it appears that smoking interferes with the normal function of gum tissue cells. This interference makes smokers more prone to various infection , particularly bacteria infection, periodontal disease affecting gums are also seen, and this will further lead to reduced wound healing capacity . 1 It becomes harder to quit smokeless types of tobacco products due to their high nicotine content, whereas the usual cigars contains reasonably lesser concentration. This nicotine content in the tobacco products  irritate your gum tissue, causing it to recede or pull away from your teeth. Once the gum tissue recedes, your teeth roots become exposed, creating an increased risk of tooth decay. Such cases where the roots are exposed, leads to immense sensitivity .2Tobacco use is responsible for approximately 30% of all cancer-related deaths in the United States 1. Usuage of tobacco causes multiple human malignancies including cancers of the lung, oral cavity, pharynx, esophagus, stomach, liver, pancreas, kidney, bladder, and cervix 2. More than 60 carcinogens are found in cigarette smoke 3. In addition to being a major cause of cancer, smoking alters the activity of chemo preventive agents4,5 stimulates the clearance of selected targeted anticancer therapies 6, reduces the efficacy of cancer treatment and increases the risk of second primary tumors 7-10 Three common bacteria are involved in gum disease. Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Prevotella intermedia, are all present in higher amounts in smokers than non-smokers3There is less inflammation and bleeding in smokers than in non-smokers. The reason for this is due to a constriction in blood vessels in the facial area. This constriction does not simply go away once people stop smoking but lasts for a while after smoking has stopped. The reduction in inflammation around the gums may also lead to a false sense of security that the gums are healthy, as one of the indicators dentists use to measure gum health is the amount of inflammation around the gums.1,2.Combining smoking and excessive alcohol intake increases the risk of getting oral cancer, and it has been estimated that 75-90% of all cases of oral cancer are explained by the combined effect of smoking and alcohol use.2.

              Smoking alters the way the body responds to the bacteria that is in plaque. It reduces the ability of the body to respond well to the bacteria and thus causes gum disease.There are many compounds in smoke that can cause a reduction in the immune system (e.g. nicotine)11,12 .The main way our body responds to bacteria is through inflammation, and neutrophils are the most critical cell in protection against gum disease. Smokers have more neutrophils in the body in total; however fewer neutrophils reach the gums mainly due to the effects of nicotine.13-16 As neutrophils cannot control the bacteria as well as usual (due to the fewer amount reaching the gums), there is a much higher chance gum disease will occur.The destruction of the gums also occurs much faster in smokers due to the presence of a higher number of matrixmetalloproteinases (MMPs), elastase, interleukin-1 and prostanglandin-2.12 These are components of the body’s immune response that are involved in inflammation, loss of collagen, and loss of bone.It is clear that nicotine and various compounds in tobacco may impose detrimental effects on the blood system, inflammatory process and immune system. This results in a progression of gum disease, and a poor response to treatment.15

Gaseous and particulate CS constituents first interface with the immune system at the mucosal surfaces lining the oral cavity, sinuses, and airways. Thousands of ROS are produced in the burning cigarette and are not removed by cigarette butt filters 16. ROS contained in the gaseous phase are often short-lived and affect primarily the upper airways. Those in the particulate phase, particularly the semiquinone radicals, have the ability to secondarily generate more free radicals. ROS damage epithelial cells lining the airways by inducing peroxidation of lipids and other cell membrane constituents, activate oxidative-sensitive cellular pathways, and induce DNA damage 17. CS constituents (particularly ROS) activate epithelial cell intracellular signaling cascades that lead to inflammatory gene activation e.g., interleukin-8 or IL-8 and tumor necrosis factor-alpha (TNF?)18,19.CS alters many cell-signaling pathways involved in cellular activation. CS constituents activate several cell-signaling pathways, including mitogen-activated protein kinases (MAPK), nuclear factor kappa-B (NF-?B), signal transducer and activator of transcription (STAT), and activatory protein-1 (AP-1), all of which are also involved in the regulation of inflammatory, cell cycle, and other genes20-23.CS induces qualitative and quantitative defects in circulating natural killer cells which are important in host anti-tumor and viral responses 24,25. In smokers, natural killer cells produce significantly less IFN? and TNF? upon activation, when compared with non-smokers. CS-extract also reduces cytotoxic functions of natural killer cells 26.There are several mechanisms by which CS-induced modulation of innate immune responses in the oral cavity facilitates colonization and chronic infection.Human gingival epithelial cells incubated with CS-extract produce substantially fewer anti-microbial peptides when activated with TLR ligands 27CS causes diverse changes in immunity that lead to heightened constitutive inflammation, skewing of adaptive T-cell-mediated immunity, impaired responses to pathogens, and suppressed anti-tumor immune cell functions. When the exposure to CS is sustained, a chronic inflammatory process ensues that has the potential to promote enhanced microbial colonization and infection, persistence of apoptotic material and abnormal processing of cellular debris, induction of autoimmunity to self-antigen, and architectural remodeling. The consequences of unchecked CS-induced inflammation and immune dysregulation continue to be an area of active research. While a potential solution to the tobacco disease epidemic may be attainable with widespread and effective smoking cessation methodologies, the unfortunate reality is that tobacco use is actually on the rise on a global level 28.


Tobacco in its many forms is a risk factor for oral cancer, oral mucosal lesions, periodontal disease, gingival recession, and coronal and root caries. Available evidence suggests that the risks of oral diseases increase with greater use of tobacco and that ceasing to use tobacco can result in decreased risks. The magnitude of the effect of tobacco on the occurrence of oral diseases is generally very high, with users having many times the risks of non-users.  Tobacco use leads to additional consequences for persons with periodontal disease and oral cancer.  Tobacco adversely affects healing after periodontal treatment, while among persons with oral cancer, continued use of tobacco increases the risk of a second primary cancers.  There is a clear benefit to quitting tobacco use because the risks of oral cancer and periodontal disease decline with increasing time after smoking cessation and some oral mucosal lesions may resolve with cessation of smokeless tobacco use. The risk of oral cancer appears to decline to the level of nonsmokers in most studies, but it may take two decades or more for this to occur. Several biological mechanisms appear to be responsible for the increased risks of oral and dental diseases among tobacco users . Although tobacco contributes to the pathogenesis of oral diseases through many pathways, some may have a greater impact on the disease burden than others. Among the many carcinogens in tobacco smoke, the polycyclic aromatic hydrocarbons, aromatic amines, and nitrosamines are very significant. 29 As smokeless tobacco products are not burned, the tobacco-specific nitrosamines may be the main etiologic factor in smokeless tobacco-related oral cancers.  The effect of tobacco on the immune system plays a major role in the development of periodontal disease and in impaired healing after treatment for the disease. The risk for caries may be elevated in users as a consequence of the high amounts of sugar in chewing tobacco.  There is an increasing recognition that genetic factors play a role in the development of tobacco-related oral diseases. Genetic factors affecting susceptibility to oral cancers include genotypes affecting metabolism of tobacco carcinogens and DNA repair.26Specific genotypes for interleukin-1 are associated with adult periodontal disease.51,52 It has been estimated that smoking accounts for half of all periodontal disease30  and 91 percent of 310 oral cancers among males and 59 percent of oral cancers among females.31 Because tobacco accounts for such a high proportion of periodontal disease and oral cancer, controlling tobacco use will be important if we are to make progress in reducing the burden of tobacco-related oral diseases. Effective treatments to prevent tobacco use and increase successful quitting32  are available and need to be more widely adopted. Dental practices may provide a uniquely effective setting for prevention and cessation of smoking and smokeless tobacco use.33,34


Periodontitis is defined  as “inflammatory  disease of supportive tissue of  teeth  caused by  specific  microorganisms  which  lead to  progressive  destruction  of  periodontal  membrane  and alveolar  bone,  with  formation of periodontal pockets  and gingival recession  35. Opinions  have  been  divided about  the effect  of smoking  on  chronic inflammatory  periodontal  disease. Earlier reviews  of  the epidemiology  of  periodontal  disease concluded that smoking  was  a possible causative factor. Few  studies have  conclusively  demonstrated  any relevant  microbiological  changes  in  the periodontal  tissues  attributable to  smoking.  Some  authors 36,37using self-reported smoking  data, investigated the relationship between  periodontal  pathogens  and cigarette consumption.  They  reported an  increased risk  for smokers to  have  subgingival  infection  with  Porphyromonas gingivalis  although  this  was  not  found to  be  statistically significant.  In  this  same  study the  investigators  found smokers  were 3 times  more likely  to harbor  A. actinomycetemcomitans. Many  authors 38,39 investigated  the relationship between  cigarette  smoking  and the prevalence of  periodontal  pathogens using polymerase chain  reaction techniques.  In  this  study,  which included  equal  numbers  of smoking  and non-smoking  subjects  with  generalised aggressive  periodontitis, the investigators  could find  no significant differences  in the  occurrence of  any  of  the pathogenic species  which  included  Porphyromonas  gingivalis, Prevotella  intermedia, Tanarella  forsythensis, Actinobacillus  actinomycetemcomitans  and  Tanarella denticola. 
                      Response to periodontal therapy is poorer in smokers than in nonsmokers. In one study, seventyfour patients were followed for up to seven years. The smokers had less periodontal depth reduction and less clinical attachment level gain after treatment than either prior smokers or nonsmokers.40Findings from other studies are also consistent with an adverse effect of smoking on healing after various forms of periodontal therapy.41-45  One of these studies found that former smokers were similar to nonsmokers in their response to therapy,42 suggesting that quitting smoking may promote healing.
                 Smoking as we know causes major destruction of the periodontal structures . Smokers have   deeper pockets and greater attachment loss, increased radiographic evidence of furcation involvement, increased alveolar bone loss. Many studies show that , smoking may hinder surgical procedures including: modified Widman flap surgery guided tissue regeneration implants and supportive periodontal treatment.Smoking  affects the neutrophils and macrophages, which are essential  gingival immunocompetent cells. Especially, smoking impairs neutrophils chemotaxis and/or phagocytosis. It has an immunosuppressive effect on the host thereby  affecting host-bacterial interactions, and this change may be due to changes in the composition of subgingival plaque. It creates a suitable environment for the bacteria to thrive making it a risk factor in periodontal disease development. 45

Smoker’s melanosis may be due to the effects of tobacco smoke on melanocytes located in the lining epithelium of the oral mucosa. It has been shown that melanin may bind many substances, including a variety of drugs, and has a high affinity for nicotine. Studies have also found that nicotine and tobacco-specific compounds (N-nitrosamines and benzopyrene) may accumulate in melanin-containing human tissues and affect melanogenesis. 46


A clinical definition of leukoplakia was formulated by the World Health Organization in 1978. Oral leukoplakia is currently defined as a predominantly white lesion of the oral mucosa that cannot be characterised as any other definable lesion; some of these lesions will develop into cancer 47  The recent classification and staging system also incorporates provisional and definitive  diagnoses on the basis of histopathological features of persistent lesions lasting longer than 2 to 4 weeks, such as the size of the leukoplakia and the presence of epithelial dysplasia.  A diagnosis of oral leukoplakia results from the recognition of several levels of certainty, an approach that is analogous to the use of the C-factor in the tumour-nodemetastatis classification system.47Smokers with oral premalignant lesions such as leukoplakia and erythroplakia (red patches or plaques that cannot be characterised clinically or pathologically as any other conditions) have an annual cancer transformation rate of about 5% 48 A case-control study,  conducted by Shiu et al49   in Taiwan, showed that the adjusted ratio for betel nut chewing and smoking on the occurrence of leukoplakia were 17.43 and 3.22, respectively.  These findings suggested that stopping smoking may reduce the number of leukoplakia cases by 36%, while elimination of betel nut influence may prevent 62% cases of leukoplakia and 26% of cases of malignant transformation to oral carcinoma.

    Habit of chewing or holding of pan masala and gutkha in oral cavity – allows absorption of nicotine and other carcinogens through oral mucosa. Orally absorbed nicotine also stays longer in the blood stream.  As an early sign of damage to the oral mucosa, chewers of BQ  with or  without tobacco often develop clinically visible whitish (leukoplakia) or reddish (erythroplakia) lesions and/or stiffening of the oral mucosa and oral submucous fibrosis (OSF).  Quid-related lesions should be categorized conceptually into two categories: first, those that are diffusely outlined and second, those localized at the site where a quid is regularly placed. Additional or expanded criteria and guidelines were proposed to define, describe or identify lesions such as chewer’s mucosa, areca nut chewer’s lesion, oral submucous fibrosis and other quid-related lesions. A new clinical entity, betel-quid lichenoid lesion, was also proposed to describe an oral lichen planus-like lesion associated with the betel quid habit. The Betel quid or pan is mixture of areca nut (Areca catechu), catechu (Acacia catechu), slaked lime (calcium oxide and calcium hydroxide) and several condiments according to taste, wrapped in a betel leaf (Piper betle). Pan placed between the teeth and the buccal mucosa, and is gently chewed or sucked over a period of several hours.49-52  The slaked lime acts to release an alkaloid from the areca nut, which produces a feeling of euphoria and well-being.53.Other substances of local preference may be added, such as grated coconut or a variety of spices, for example, aniseed, peppermint, cardamom and cloves.54Variants of pan include use of sliced areca nut alone and addition of sweeteners to make the product particularly attractive to younger children, to whom it is sold under the names sweet supari, gua, mawa or mistee pan. Other variants such as kiwam, zarda and mitha pan (also known as gutkha) may contain a variety of substances, including tobacco.55.


OSF is predominantly caused by the use of areca nut.54Besides being regarded as a precancerous condition; it is a seriously debilitating and progressive disease. Marked by stiffening of the oral mucosa and development of fibrous bands, loss of elasticity of the mucosa results in a progressive restriction of mouth opening. Affected users experience a burning sensation of the oral mucosa, occasional mucosal ulceration, a peculiar marble-like blanching of the mucosa and palpable fibrous bands of the buccal mucosa, soft palate. Moreover, the frequency of chewing rather than the total duration of the habit was directly correlated with OSF.53  Oesophageal subepithelial fibrosis, an extension of oral submucosal fibrosis, was seen more frequently in patients who had consumed pan masala, gutka, areca nut, tobacco or a combination of some or all of these, with or without betel leaf.The pathogenesis of OSMF is believed to be multifactorial. Factors that trigger the disease include consumption of chewing areca nut, chilies, nutritional deficiencies, and immunologic processes.  Areca nut chewing is known to cause local trauma and injury to the oral mucosa due to its abrasive nature. This could be more severe in users of pan masala and gutkha due to their fine particulate nature, with the high probability of particle adhesion to the traumatized mucosa, leading to morphological changes and membrane damage. This continuous local irritation by pan masala, gutkha or areca nut can lead to injury related chronic inflammation, oxidative stress and cytokine production. Oxidative stress and subsequent Reactive oxygen species (ROS) generation can induce cell proliferation, cell senescence or apoptosis, depending upon the level of ROS production. During chronic exposure, these events can lead to preneoplastic lesions in the oral cavity and subsequently to malignancy.55

Apart from these pathologies, tobacco smoking is associated with discolouration of teeth, halitosis, with a coated tongue also called black hairy tongue and it delays the wound healing following minor surgical procedures 56. Further there is association of smokers with candidiasis and there is higher rate of implant failures as compared to non-smokers 57. There also exists an association between tobacco smoking and aphthous ulcerations although the cause is unknown 58. Tobacco smoking stimulates the oral melanocytes resulting in increased melanin production resulting in pigmentations on the oral mucosa. These diffuse irregular brownish pigmentations are called Smokers Melanosis is reversible on cessation of the habit 38. Smokers palate is also a common lesion presenting in smokers as a white, plaque-like change on the palatal mucosa due to hyperkeratosis combined with multiple red dots located centrally in small elevated nodules representing the dilated and inflamed duct openings of minor salivary glands. It is attributed to thermal and chemical agents, released from the cigars.  and several studies have shown that the DMFT values are higher in tobacco users and compared to non users59. Smokers are generally associated with increased incidence of root surface lesions and a significant difference in the median values of salivary lactobacillus counts are observed in smokers and non-smokers 60. Tobacco usage impairs the salivary function, which has a vital role in caries prevention. The buffering capacity also varies and these also affect the susceptibility to caries 59. Smokeless tobacco are rich in sugar content and this results in increased susceptibility to dental caries, predominantly cervical and root surface caries 56. 

 Various studies show that proper education on the affects of smoking gives the population general knowledge and helps them understand the hazards of using such products . This markedly reduces the use of  tobocco products .61

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