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. 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
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. 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. 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.
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