INTRODUCTION for a while even after the cessation if

INTRODUCTION 
             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. As the gingiva recedes , the root of the tooth starts to expose , which in turn makes it a highly prone region to caries. Apart from caries , these areas will also be highly sensitive to hot and cold food. .2Approximately 32% of cancer related deaths in the United States are due to tobacco use   1. Usage of tobacco causes multiple human malignancies including cancers of the lung, oral cavity, pharynx, oesophagus, 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-smokers3However the level of inflammation is markedly reduced in the smokers when compared to non smokers. This occurs due to the constriction of blood vessels at the facial site.This is not a reversible state and may be present for  a while even after the cessation if the smoking habit . 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 the body reacts to the plaque and calculus over the teeth surface and gums. It decrease the body’s immune system to the bacteria and thus results in the gum disease.Nicotine is the major component  in tobacco which causes the decreases the the hosts immune response to the varying microbial agents. 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

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IMMUNITY OF THE ORAL ENVIRONMENT 
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.

ORAL DISEASE

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

PERIODONTAL DISEASE

Periodontitis is an inflammatory condition where this is gingival recession periodontal pocket formation and complete alveolar bone loss. In certain cases , mobility if teeth may also be present.  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.  Porphyromonas gingivalis  was commonly seen  as an important constituent of the sun gingival region,  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, seventy four 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

SMOKERS MELANOSIS
Tobacco smoke on melanocytes located in the lining epithelium of the oral mucosa acts as the primary causative agent for  smokers Melanesia. It has been shown that melanin may bind many substances, including a variety of drugs, and has a high affinity for nicotine. Nicotine and tobacco-specific compounds (N-nitrosamines and benzopyrene) may accumulate in melanin-containing human tissues and alter the melanogensis , breed on study results . 46

LEUKOPLAKIA AND ERYTHROPLAKIA 

A clinical definition of leukoplakia was formulated by the World Health Organization in 1978. Leukoplakia is a white lesion which cannot be compared or mistaken for another white lesion if the oral cavity, due to its characteristic  mud wall appearance 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.  The results of the study conducted shows that 36% of the cases showed reduced changes with the decreased usage of tobacco , and 62% of cases showed completed disappearance of leukoplakia and 29% shows that there is malignant transformation to oral carcinoma.

SMOKELESS TOBACCO INDUCED CHANGES 
    Absorption of nicotine and the various carcinogens for long periods due to placement of the pan or Gutkha in the oral cavity, gets into the mucosa . The blood stream may show increased content of nicotine in cases where the tobacco products are consumed orally.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) as an early sign prior to severity of condition .  Quid-related lesions are significantly classified into two types based on their margins. They are diffusely lined and the other is localised based on the site of the betel quid placement. There are various theories and researchers that are conducted to help identify and differentiate each type of mucosal lesion from another. The various identified lesions are such as chewer’s mucosa, areca nut chewer’s lesion, and other quid-related lesions. The betel-quid lichenoid lesion,was a new clinical entity which  was also proposed to describe an oral lichen planus-like lesion associated with the betel quid habit. A mixture of areca nut (Areca catechu), catechu (Acacia catechu), slaked lime (calcium oxide and calcium hydroxide) and several components  according to taste, wrapped in a betel leaf (Piper betle) are the major constituents of the beetle quid or most commonly used Pan in India . Pan is commonly placed between the teeth and the gingiva . From this site they are sucked or chewed upon  resulting in their prolonged absorption into the mucosa..49-52  The slaked lime acts to release an alkaloid from the areca nut, which produces a feeling of euphoria and well-being.53. Spices such as aniseed, peppermint, cardamom and cloves are added along with grated coconut and introduced into the leaf for chewing.54Variants of pan include use of sliced areca nut alone and addition of sweeteners to make the product particularly attractive to younger children, and most commonly  sold as sweet supari, gua, mawa or mistee pan. This thereby starts the addiction at a much younger age due to false advertisement  Other variants such as kiwam, zarda and mitha pan (also known as gutkha) may contain a variety of substances, including tobacco.55.

ORAL SUBMUCOUS FIBROSIS 

Areca Nut is the primary cause if OSMF .54 It is highly deteriorating and progressive in nature ,though it is a precancerous condition . Stiffening of the oral mucosa and development of fibrous bands seen along the entire vertical lines of the buccal mucosa , loss of elasticity of the mucosa results in a progressive restriction of mouth opening. The most common symptoms include 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 in individuals suffering from oral submoucous fibrous . 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.  Local trauma and injury to oral mucosal structures in very common while using Areca nut due to its primary abrasive nature which erodes the Mucosal lining. 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. Injury related chronic inflammation, oxidative stress and cytokine production is seen to occur as an indirect response to the prolonged use of Areca nut, pan masala etc . Depending on the level of ROS,  Oxidative stress and subsequent Reactive oxygen species (ROS) generation can induce cell proliferation, cell senescence or apoptosis.This further leads to oral cancer which is a malignant transformation from the dormant state , as a result of chronic exposure to these causative agents.55

OTHER AFFECTS ON THE MUCOSA
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 There is diffuse  pigmentation of the oral mucosa due to the increased number of melanocytes being produced as a result of increased usage of tobacco. These diffuse irregular brownish pigmentations are called Smokers Melanosis is reversible on cessation of the habit 38 in certain individuals  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 are commonly seen in individuals smoking tobacco products for longer periods of time . It is attributed to thermal and chemical agents, released from the cigars. The Tobacco smokers show increased DMFT score when compared to non smokers .59. Significant difference in mean values of salivary lactobacillus was seen between the smokers and non smokers. It’s also observed that smokers have increased risk of root surface lesions, which make them highly sensitive60. 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. 

CONCLUSION 
 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