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Tobacco contains various toxic contents which produce oxygen-free radicals that damage oral tissues. Since saliva encounters tobacco, it has antioxidant defense system and also can serve as a biomarker for oral diseases. Thus, the present study aims to evaluate salivary oxidative stress levels among smokers and chewers. Unstimulated saliva from 240 males who visited tobacco cessation clinic for the first time was collected. Standard protocol was followed to collect saliva and assess salivary antioxidant levels from 80 participants with the habit of smoking, smokeless, and both (smoking and smokeless) tobacco users. The collected data were statistically analyzed. The mean salivary superoxide dismutase and malonyldialdehyde levels were significantly high for participants with both habits (P < 0.000). There was a significant high reduction of glutathione peroxidase and catalase in participants with both habits (P < 0.000). Both smoking and smokeless tobacco modify salivary antioxidant activity. The estimation of salivary oxidative stress can serve as a diagnostic and prognostic biomarker for oral tissue damage and dysplasia. Furthermore, they can function as early biomarkers in preventing dysplastic changes in the oral cavity.

Background: Smoking and chewing tobacco carry significant risks for the development of oral cancer and premalignant lesions. The present study was conducted to find the prevalence of tobacco-related habits in Hazaribagh population and its association with oral mucosal lesion. Methodology: The present study was carried out on patients who visited the Department of Oral Medicine And Radiology, Hazaribagh College of Dental Sciences And Hospital. A total of 5,000 subjects were screened for tobacco-related habits and associated mucosal changes. Detailed clinical history about tobacco-related habits was obtained. Oral mucosal lesions were screened using the WHO format for diagnosis of oral lesions. The findings were tabulated and analyzed statistically. Results: Of the 5,000 subjects enrolled for the study, 1,085 (21.7%) used tobacco in some forms. Habit of smoking tobacco was present among 273 (25.2%) and using smokeless tobacco among 811 (74.7%) individuals. Tobacco pouch keratosis (46.1%) was found to be most common lesion, followed by oral submucous fibrosis (OSMF) (16.1%), lichenoid reaction (14.1%), smokers palate/melanosis (12.2%), leukoplakia (7.2%), erythroplakia (2.3%), and oral cancer in (2%). Conclusion: The results provide insight into prevalent tobacco habits and associated oral mucosal lesions in Hazaribagh population. These may act as baseline data for the formulation of preventive programs and help future studies explore the prevalence of tobacco-associated lesions in vulnerable populations. Current knowledge, including findings from the present study, about the prevalence of tobacco use and various oral lesions associated with it may help primary health care physicians to promote among patients visiting them the awareness about the adverse effects of tobacco consumption and treatment options available for tobacco-related lesions at the early stage.

Tobacco contains various toxic contents which produce oxygen-free radicals that damage oral tissues. Since saliva encounters tobacco, it has antioxidant defense system and also can serve as a biomarker for oral diseases. Thus, the present study aims to evaluate salivary oxidative stress levels among smokers and chewers. Unstimulated saliva from 240 males who visited tobacco cessation clinic for the first time was collected. Standard protocol was followed to collect saliva and assess salivary antioxidant levels from 80 participants with the habit of smoking, smokeless, and both (smoking and smokeless) tobacco users. The collected data were statistically analyzed. The mean salivary superoxide dismutase and malonyldialdehyde levels were significantly high for participants with both habits (P < 0.000). There was a significant high reduction of glutathione peroxidase and catalase in participants with both habits (P < 0.000). Both smoking and smokeless tobacco modify salivary antioxidant activity. The estimation of salivary oxidative stress can serve as a diagnostic and prognostic biomarker for oral tissue damage and dysplasia. Furthermore, they can function as early biomarkers in preventing dysplastic changes in the oral cavity. [ABSTRACT FROM AUTHOR]

Background: There is paucity of data on tissue levels of Survivin and Caspase 3 in south Indian tobacco chewers with oral Squamous cell carcinoma (OSCC). Oral cancer is a rapidly growing, highly prevalent head and neck malignancy; it involves a mucosal epithelium of a buccal cavity exposed to tobacco and other carcinogens. The basis of the survival of a tumor cell or transformed normal cell into a neoplastic cell is by the suppression of apoptosis regulation. Recently, researchers have focused on Survivin, an inhibitor of apoptosis family of proteins (IAP), involved in apoptosis regulation in cancer cells targeting the executioner Caspase 3. The current study aims to quantify the cellular levels of Survivin and Caspase 3 in tobacco chewers with OSCC and in habitual tobacco chewers without OSCC, in comparison to controls. Methods: A single centric case control study included 186 study subjects, categorized into: Group I (n = 63), habitual tobacco chewers with OSCC; Group 2 (n = 63), habitual tobacco chewers without OSCC; and Group 3 (n = 63), the controls. Resected tumor tissue from Group 1 and buccal cell samples from Groups 2 and 3 were collected into phosphate buffer saline (PBS) and assayed for Survivin and Caspase 3 levels by the ELISA sandwich method. Results: The mean ± SD of the Survivin protein in Group 1 was (1670.9 ± 796.21 pg/mL); in Group 2, it was (1096.02 ± 346.17 pg/mL); and in Group 3, it was (397.5 ± 96.1 pg/mL) with a significance of p < 0.001. Similarly, the level of Caspase 3 in Group 1 was (7.48 ± 2.67 ng/mL); in Group 2, it was (8.85 ± 2.41 ng/mL); and in Group 3, it was (2.27 ± 2.24 ng/mL) with a significance of p < 0.001. Conclusion: The progressive transformation of buccal cells to neoplastic cells is evident; in the case of OSCC, this indicates that the over-expression of Survivin compared to Caspase 3 confirms the suppression and dysregulation of apoptosis. [ABSTRACT FROM AUTHOR]

Background: Smoking and chewing tobacco carry significant risks for the development of oral cancer and premalignant lesions. The present study was conducted to find the prevalence of tobacco-related habits in Hazaribagh population and its association with oral mucosal lesion. Methodology: The present study was carried out on patients who visited the Department of Oral Medicine And Radiology, Hazaribagh College of Dental Sciences And Hospital. A total of 5,000 subjects were screened for tobacco-related habits and associated mucosal changes. Detailed clinical history about tobacco-related habits was obtained. Oral mucosal lesions were screened using the WHO format for diagnosis of oral lesions. The findings were tabulated and analyzed statistically. Results: Of the 5,000 subjects enrolled for the study, 1,085 (21.7%) used tobacco in some forms. Habit of smoking tobacco was present among 273 (25.2%) and using smokeless tobacco among 811 (74.7%) individuals. Tobacco pouch keratosis (46.1%) was found to be most common lesion, followed by oral submucous fibrosis (OSMF) (16.1%), lichenoid reaction (14.1%), smokers palate/melanosis (12.2%), leukoplakia (7.2%), erythroplakia (2.3%), and oral cancer in (2%). Conclusion: The results provide insight into prevalent tobacco habits and associated oral mucosal lesions in Hazaribagh population. These may act as baseline data for the formulation of preventive programs and help future studies explore the prevalence of tobacco-associated lesions in vulnerable populations. Current knowledge, including findings from the present study, about the prevalence of tobacco use and various oral lesions associated with it may help primary health care physicians to promote among patients visiting them the awareness about the adverse effects of tobacco consumption and treatment options available for tobacco-related lesions at the early stage. [ABSTRACT FROM AUTHOR]

Introduction: Periodontal disease is a multifactorial disease and one of the most common chronic diseases of the oral cavity. Smoking has a long-term chronic effect on many important aspects of the inflammatory and immune responses. Tobacco smoke has been found to affect both cell-mediated immunity and humoral immunity. Oral smokeless tobacco consumption has been considered a major risk factor for oral cancer. Its role as a risk factor for periodontal disease is less well-documented when compared to that of the relationship between smoking and periodontal disease. Materials and Methods: One hundred and eighty participants willing to sign informed consent were selected randomly with no gender bias, and the purpose of the study was explained. The periodontal examination was conducted, and the oral hygiene index-simplified (OHI-S), community periodontal index (CPI) score and loss of attachment (LOA) score were recorded. The collected data were analysed using SPSS 20 software. Results: Sixty participants in each group were examined. OHI-S mean score in Group 1 was 1.77 ± 0.43, in Group 2, it was 1.70 ± 0.65 and in Group 3, it was 1.73 ± 0.55. The mean value of CPI was 3.32 ± 0.47 in Group 1, 2.17 ± 0.46 in Group 2 and 2.67 ± 0.54 in Group 3. In comparison, the mean value of CPI-LOA was 1.35 ± 0.48 in Group 1, 1.65 ± 0.5 in Group 2 and 1.18 ± 0.65 in Group 3. Conclusion: The present survey concluded that tobacco consumption in both the forms caused poor periodontal status, with smokers having more pocket depth than tobacco chewers and non-tobacco users and tobacco chewers having more LOA than smokers and non-tobacco users.

Aim: We aimed to evaluate the prevalence of tobacco-associated oral mucosal lesions in Mahabubnagar district of Telangana state in South India. Methodology: A cross-sectional study was conducted in Mahabubnagar district for 6 months on 3200 subjects of both rural and urban people and the study was carried out by conducting camps at the Government Hospitals to assess the prevalence of oral mucosal lesions. People aged from 16 to 75 years, both men and women in same proportions, were included in the study. Results: 750 subjects had the habit of tobacco usage among a total of 3200 subjects. Among the 750 subjects, 225 (30.0%) subjects were being diagnosed with oral mucosal lesions. Of 225 subjects, 6 (2.67%) subjects had erythroplakia, 22 (9.78%) subjects had leukoplakia, 58 (25.78%) subjects had lichenoid reaction, 62 (27.56%) subjects had oral submucous fibrosis (OSMF), 45 (20.0%) subjects had palatal hyperkeratosis, and 32 (14.22%) subjects had tobacco pouch keratosis. Conclusion: From this study, we can conclude that prevalence of oral mucosal lesions was seen in tobacco-related oral habits where palatal hyperkeratosis was found among smokers; similarly OSMF was more among tobacco chewers and potentially malignant disorders were more prevalent in tobacco chewers than smokers.

Objective: Our study aims to determine the influence of smoking or tobacco chewing and the association of Interleukin 6 (IL-6) polymorphism, where G is substituted by A at the position − 596 (IL-6 − 596 G/A) and substitution of G by cytosine (C) at position − 572 (IL-6 − 572 G/C) on the susceptibility of precancerous oral lesions and oral cancer. Materials and methods: The participants consisted of 250 subjects among which 75 were suffering from oral cancer, 75 subjects with precancerous oral lesions and 100 were healthy controls. Single-nucleotide polymorphism study (SNP) was done by polymerase chain reaction and restriction fragment length polymorphism (PCR–RFLP). Results: IL-6 − 596 G/A SNP revealed genotypes, GG, and GA in subjects with precancerous oral lesions and oral cancer, and AA genotype was not found in any subject. IL-6 − 596 G/A was strongly associated with oral precancerous lesions but not with oral cancer. The present study reports that smokers carrying GA for IL-6 − 596 G/A were at several folds higher risk of developing oral precancerous lesions. Smokers with GC and CC for IL-6 − 572 G/C were at higher risk of developing oral precancerous lesions. No significant interaction was observed between these habits and IL-6 − 596 G/A and IL-6 − 572 G/C SNP with oral cancer. Conclusion: The interaction of variant A allele of IL-6 − 596 G/A and C allele of IL-6 − 572 G/C polymorphism with smoking and increases the risk of oral precancerous lesions. Tobacco chewing was not related with IL-6 − 596 G/A or IL-6 − 572 G/C in oral precancerous lesions or oral cancer. Clinical relevance: The study will help to determine the susceptibility of individuals with smoking or chewing habits to the development of oral precancerous lesion and oral cancer by monitoring the IL-6 SNPs which can be used as a biomarker for risk determination. [ABSTRACT FROM AUTHOR]

Brief Background The main reason for oral cancer is tobacco consumption in various forms, such as chewing and smoking. Micronuclei in oral exfoliated cells are markers of chromosomal damage caused by toxic genetic agents from tobacco-related substances, alcohol, etc. The number of micronuclei indicates the cell's genotoxic effect and can be used as a biomarker to assess the changes in the cellular changes. Recently research is focused on determining early genotoxicity changes using exfoliative cytology in human buccal epithelial cells. Aim Quantitative analysis of micronuclei in oral exfoliated oral, buccal mucosal cells using Papainicolous stain with Giemsa stain in tobacco users in the form of chewing and smoking in comparison with healthy individuals. Materials and Methods A total of seventy-five cases were selected for this study. The seventy-five participants were divided into three groups based on the habits; tobacco smokers (n=25), tobacco chewers (n=25), and healthy individuals (n=25). Results The mean number of micronuclei in Giemsa stain was 255.2 ± 78 compared with PAP stain 155.12 ± 78.5. The increased mean number of micronuclei in chewers 273.24 ± 80.7, and different stain comparison Giemsa stain showed highest in chewers. A mean number of micronuclei showed statistically highly significant (p=0.05). Pair-wise comparison of micronuclei inter and intra groups in all three groups, smokers and chewers showed highly statistically substantial (p= 0.0001) compared with healthy individuals. Summary and Conclusion Micronuclei provide evidence that consumption of smokeless tobacco may be developing oral cancer, and micronuclei assay can be used as biomarkers of genotoxicity and carcinogenesis progression. [ABSTRACT FROM AUTHOR]

Background: There is paucity of data on tissue levels of Survivin and Caspase 3 in south Indian tobacco chewers with oral Squamous cell carcinoma (OSCC). Oral cancer is a rapidly growing, highly prevalent head and neck malignancy; it involves a mucosal epithelium of a buccal cavity exposed to tobacco and other carcinogens. The basis of the survival of a tumor cell or transformed normal cell into a neoplastic cell is by the suppression of apoptosis regulation. Recently, researchers have focused on Survivin, an inhibitor of apoptosis family of proteins (IAP), involved in apoptosis regulation in cancer cells targeting the executioner Caspase 3. The current study aims to quantify the cellular levels of Survivin and Caspase 3 in tobacco chewers with OSCC and in habitual tobacco chewers without OSCC, in comparison to controls. Methods: A single centric case control study included 186 study subjects, categorized into: Group I (n = 63), habitual tobacco chewers with OSCC; Group 2 (n = 63), habitual tobacco chewers without OSCC; and Group 3 (n = 63), the controls. Resected tumor tissue from Group 1 and buccal cell samples from Groups 2 and 3 were collected into phosphate buffer saline (PBS) and assayed for Survivin and Caspase 3 levels by the ELISA sandwich method. Results: The mean ± SD of the Survivin protein in Group 1 was (1670.9 ± 796.21 pg/mL); in Group 2, it was (1096.02 ± 346.17 pg/mL); and in Group 3, it was (397.5 ± 96.1 pg/mL) with a significance of p < 0.001. Similarly, the level of Caspase 3 in Group 1 was (7.48 ± 2.67 ng/mL); in Group 2, it was (8.85 ± 2.41 ng/mL); and in Group 3, it was (2.27 ± 2.24 ng/mL) with a significance of p < 0.001. Conclusion: The progressive transformation of buccal cells to neoplastic cells is evident; in the case of OSCC, this indicates that the over-expression of Survivin compared to Caspase 3 confirms the suppression and dysregulation of apoptosis.

INTRODUCTION Cancer is defined as the uncontrollable growth of cells that invade and cause damage to surrounding tissue. Oral diseases and conditions share modifiable risk factors with the leading NCDs (Cardiovascular diseases, cancer, chronic respiratory diseases and diabetes). This study was carried out to assess the knowledge regarding prevention of oral cancer and to find out the effectiveness of video assisted teaching program among tobacco chewers. MATERIAL AND METHODS A pre-experimental one group pre-test post-test design study was conducted to find the effectiveness of video assisted teaching for prevention of oral cancer among tobacco chewers in Dhakdahi village of Rohini rural municipality of Rupandehi District, Nepal. The total duration ofthe study was three months 5/5/2019 to 26/8/2019. The study samples tobacco chewers were selected by non-probability convenient sampling. Self-administered structured questionnaire was used for socio-demographic variables and video in local language for prevention of oral cancer was used as a intervention for the study group and collected data was analysed by using descriptive and inferential statistics with SPSS software version 20.0 RESULTS The findings ofthe study show that the mean score pre-test knowledge was 7.23 and standard deviation 1.801. After the intervention, the mean score of post-test knowledge was 9.96 and standard deviation 1.56. No significant association was found between socio-demographic variables and post-test knowledge level. CONCLUSION Based on the study findings, the knowledge level on prevention of cancer is inadequate before intervention of video assisted teaching and after the video assisted teaching the knowledge on prevention was found to be improved. There was overall gain in the knowledge score teaching program following the video assisted teaching program. [ABSTRACT FROM AUTHOR]

Aim: This study aims to assess the usefulness of salivary sialic acid (SA) as a tumor marker in the detection of oral squamous cell carcinoma (OSCC) among tobacco chewers.Materials and Methods: After the approval of study protocol by the Institutional Ethics Committee and informed voluntary consent, salivary samples were collected from 96 participants in each group of tobacco chewers with OSCC, tobacco chewers without precancerous or cancerous lesion, and healthy controls. Salivary protein-bound SA (PBSA) and salivary-free SA (FSA) were measured by Yao et al.'s method of acid ninhydrin reaction, and the data were subjected to appropriate statistical analysis.Results: The salivary PBSA and FSA levels in the Groups 1, 2, and 3 participants were 31.17 ± 7.6 mg/dL and 63.45 ± 9.8 mg/dL, 25.45 ± 16.61 mg/dL and 33.18 ± 11.38 mg/dL, and 22.73 ± 3.01 mg/dL and 21.62 ± 8.86 mg/dL, respectively. Salivary FSA levels were significantly increased among the tobacco chewers with OSCC patients (Group 1) and tobacco chewers with no premalignant lesions of the oral cavity (Group 2) compared to the healthy controls (Group 3) with P < 0.05 being statistically significant. Salivary FSA levels were significantly increased in Group 1 as compared with Group 2. The salivary PBSA was high among Group 1 as compared to the control Group 3; there was however no significant difference in the levels of salivary PBSA between Group 1 and Group 2. There was no significant difference in the PBSA levels between OSCC patients of Group 1 and the tobacco chewers without precancerous or cancerous lesion in the oral cavity of Group 2.Conclusion: Salivary PBSA and FSA are significantly raised in both tobacco chewers with OSCC and in tobacco chewers with no precancerous or cancerous lesions in the oral cavity. SA should therefore be used cautiously while considering it as a marker for the early detection of oral cancer. Tobacco can be a crucial confounding factor when SA is used as a biomarker in OSCC since their levels are elevated to some extent even in tobacco chewers without any clinically obvious precancerous or cancerous lesions in the oral cavity. [ABSTRACT FROM AUTHOR]

Background & Objective: Relationship between cotinine and oral cancer is still an unexplored area. Limited availability of studies embarks to investigate its importance in cancer. This study aims to quantify serum cotinine level as a biomarker for tobacco exposure related oral cavity malignancy. Methodology: Patients (n=150) of either sex, aged between 31-80 years, were distributed into group A (Oral cancer), group B (Chronic tobacco chewers) and group C (Control) with 50 in each group. Details of gender, age and tobacco habit were recorded. For Group A, clinical data for anatomical site of tumour, type of lesion and pathology oral hygiene were collected. Serum cotinine levels were estimated by ELISA. Chi-square test, unpaired t-test, two-sample proportion test were performed using SPSS software. Results: Significant difference was observed in the duration, frequency of tobacco consumption and serum cotinine levels among group A and B (P<0.01). Group B showed higher levels of serum cotinine (32.458 ±0.31ng/ml). The mean serum cotinine levels in group A, B and C were 6.218±0.34ng/ml, 5.753±0.62ng/ ml and 0.245 ±0.81ng/ml. Conclusion: Chronic tobacco chewers had high serum cotinine levels and could be at high-risk group for oral cavity cancer indicating the effectiveness of serum cotinine as a tobacco exposure related biomarker in oral cancer. [ABSTRACT FROM AUTHOR]

Tobacco chewing is one of the known risk factors for oral cancer and it is widely consumed by residents of India. The present study was aimed at assessing the free and total sialic acid in the saliva and compared among smokers and tobacco chewers. In order to quantify the total and free sialic acid concentration in saliva, A total of 20 patients (n=20) were selected from the department of oral medicine and radiology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Chennai, and divided two different groups. Group-I served as smokers while Group-II served as tobacco chewers. The sialic acid concentrations were measured by standard biochemical methods and data obtained were statistically analyzed using spectrophotometer. Results of the present study showed that the total sialic acid concentration was found to be higher in the tobacco chewers (14.78±1.20 mg/dl) compared to smokers (9.23±0.56 mg/dl). Similarly, free sialic acid concentration was also significantly higher in the tobacco chewers (25.25±1.82mg/dl) than smokers (16.65±1.37). In both the groups studied, the free sialic acid concentration was higher in tobacco chewers (Group-II) than the total free sialic acid (Group-I). Our present finding indicates that the free sialic and total sialic acid levels are higher in group B (Tobacco Chewers) than group A (Smokers). Our present findings clearly show that salivary total and free sialic acid levels were significantly higher in the tobacco chewers when compared to the people who are having smoking habits which could be due to the carcinogenic effect of smokeless tobacco (Tobacco chewers). It is concluded from the present findings that measurement of total and free sialic acid in saliva may be useful in early detection of oral cancer progression. [ABSTRACT FROM AUTHOR]

Introduction: Tobacco usage is mainly in the form of smoking and smokeless tobacco. Some studies commented that smokeless tobacco has high nicotine and toxic effect, but the studies with depictive data have been limited. Cotinine is one of the nicotine metabolite, which is used as a marker to quantify tobacco exposure. Aim: To estimate serum cotinine (CTN) levels in tobacco smokers and smokeless tobacco users and to compare them with tobacco non-users. Materials and Methods: This cross-sectional study was performed in 240 study subjects divided into four groups- only tobacco smokers (G1), only smokeless tobacco users (G2), dual tobacco smokers and smokeless tobacco users (G3), and tobacco non-users (G4). G2 was divided into G2a, G2b, and G2c. Serum CTN levels were estimated using enzyme linked immunosorbant assay (ELISA) kit. Chi-square test, unpaired t-test, ANOVA and regression analysis were used for statistical analysis. Results: The mean serum CTN levels in groups G1, G2a, G2b, G2c, G3 and G4 were found to be 117.45 ng/mL, 138.09 ng/mL, 72.35 ng/mL, 100.34 ng/mL, 145.21 ng/mL and 5.28 ng/mL respectively. When the mean values were compared between the groups the values were found to be statistically highly significant. The finding suggests significantly higher CTN levels in tobacco users compared with tobacco non-users, also in tobacco chewers compared with tobacco smokers, as well as for dual tobacco smokers and smokeless tobacco users compared with smokers. Conclusion: Dual tobacco smokers and smokeless tobacco users tend to have relatively high level of serum CTN, which suggests tobacco dependence.

Introduction: Tobacco usage is mainly in the form of smoking and smokeless tobacco. Some studies commented that smokeless tobacco has high nicotine and toxic effect, but the studies with depictive data have been limited. Cotinine is one of the nicotine metabolite, which is used as a marker to quantify tobacco exposure. Aim: To estimate serum cotinine (CTN) levels in tobacco smokers and smokeless tobacco users and to compare them with tobacco non-users. Materials and Methods: This cross-sectional study was performed in 240 study subjects divided into four groups-only tobacco smokers (G1), only smokeless tobacco users (G2), dual tobacco smokers and smokeless tobacco users (G3), and tobacco non-users (G4). G2 was divided into G2a, G2b, and G2c. Serum CTN levels were estimated using enzyme linked immunosorbant assay (ELISA) kit. Chi-square test, unpaired t-test, ANOVA and regression analysis were used for statistical analysis. Results: The mean serum CTN levels in groups G1, G2a, G2b, G2c, G3 and G4 were found to be 117.45 ng/mL, 138.09 ng/mL, 72.35 ng/mL, 100.34 ng/mL, 145.21 ng/mL and 5.28 ng/mL respectively. When the mean values were compared between the groups the values were found to be statistically highly significant. The finding suggests significantly higher CTN levels in tobacco users compared with tobacco non-users, also in tobacco chewers compared with tobacco smokers, as well as for dual tobacco smokers and smokeless tobacco users compared with smokers. Conclusion: Dual tobacco smokers and smokeless tobacco users tend to have relatively high level of serum CTN, which suggests tobacco dependence. [ABSTRACT FROM AUTHOR]

Background: Histopathological diagnosis of lesions arising from the intake of tobacco is based on subjective evaluation of morphological alterations within the lesional tissue. Oral exfoliative cytology is a non-invasive diagnostic technique for early detection of oral premalignant and malignant lesions. Morphometric techniques have been advocated as objective and reproducible methods of detecting changes before they are visible by routine microscopy and can facilitate differentiation of normal and abnormal epithelium. This study was conducted to assess the morphometric parameters (cell diameter, nuclear diameter and nuclear cytoplasmic ratio [N:C ratio]) in tobacco smokers and chewers and to evaluate the variations, if any. Materials and Methods: The study was conducted on cytological smears obtained from oral lesions of patients with habit of tobacco smoking (Group B) and tobacco chewing (Group C). Group A comprised of subjects free from oral lesions and not using tobacco in any form. Patients with both the habits were excluded. The smears were stained using Papanicoloaou staining method. For morphometric analysis, Microimage 3.0 image analysis software was employed. The statistical test employed was an analysis of variance and P < 0.05 was considered as significant. Results: The results of this study showed that the cellular diameter was progressively reduced and nuclear diameter progressively increased from Group A to Group B to Group C. The N:C ratio also showed a progressive increase from Group A to Group C. Conclusion: The results confirmed that tobacco chewing and smoking influenced the cytomorphology of normal appearing buccal mucosa and the degree of these changes were found to be greater in chewers as compared to smokers.

Introduction: Tobacco consumption is a serious health hazard and most important avoidable cause of death worldwide. Tobacco is recognized as lethal toxin, ripping off 7-11 minutes of human life with each cigarette through harmful compounds and inducing free radical synthesis and a high rate of lipid peroxidation. These free radicals are scavenged by the endogenous antioxidants viz. S. Glutathione (S.GSH) and S.αLipoic acid (S. α-LA), thus preventing the endothelial damage. Aim: The present study was designed with an aim to find out the lipid peroxidative stress through S. Malondialdehyde (S.MDA) and its correlation with antioxidant levels like S. Glutathione (S. GSH) and S. α- Lipoic acid (S. α- LA) among tobacco users (in both smokers and chewers). Materials and Methods: A case control cross-sectional study was carried out in the Department of Physiology among 200 subjects; aged 18-50 years of both sexes which were chosen randomly from institutional campus and healthy volunteers. The subjects were broadly divided into two groups (A & B); group A comprised of tobacco users (n=150) with history of smoking cigarette/biddies and chewing tobacco daily, for at least one year and group B had controls (non tobacco users) (n=50). S. MDA, S.GSH and S. α-LA levels were estimated by standardized methods. The data was analysed by unpaired student t-test and Pearson’s correlation coefficient (r) for finding the correlation between antioxidants and S.MDA in group-A and group-B. Results: The present study reports the significantly higher (p

Introduction: Tobacco consumption is a serious health hazard and most important avoidable cause of death worldwide. Tobacco is recognized as lethal toxin, ripping off 7-11 minutes of human life with each cigarette through harmful compounds and inducing free radical synthesis and a high rate of lipid peroxidation. These free radicals are scavenged by the endogenous antioxidants viz. S. Glutathione (S.GSH) and S.a- Lipoic acid (S. a-LA), thus preventing the endothelial damage. Aim: The present study was designed with an aim to find out the lipid peroxidative stress through S. Malondialdehyde (S.MDA) and its correlation with antioxidant levels like S. Glutathione (S. GSH) and S. a- Lipoic acid (S. a- LA) among tobacco users (in both smokers and chewers). Materials and Methods: A case control cross-sectional study was carried out in the Department of Physiology among 200 subjects; aged 18-50 years of both sexes which were chosen randomly from institutional campus and healthy volunteers. The subjects were broadly divided into two groups (A & B); group A comprised of tobacco users (n=150) with history of smoking cigarette/biddies and chewing tobacco daily, for at least one year and group B had controls (non tobacco users) (n=50). S. MDA, S.GSH and S. a-LA levels were estimated by standardized methods. The data was analysed by unpaired student t-test and Pearson's correlation coefficient (r) for finding the correlation between antioxidants and S.MDA in group-A and group-B. Results: The present study reports the significantly higher (p<0.0001) levels of S.MDA and lower (p<0.0001) levels of S.GSH and S. a-LA in tobacco users as compared to nontobacco users. The observed value of S.MDA was (2.72±0.87, 1.39±0.47) nmol/ ml, S. a-LA was (9.94±5.96, 14.24 ± 4.34) µg/ml and S.GSH was (23.24±7.04, 32.82±2.95) mg/dl respectively in group-A and group-B. A significant (p<0.01) strong negative correlation was observed between S. MDA and antioxidants (S.GSH and S. a-LA) with a Pearson co-efficient of r=-0.619, r= -0.625 respectively, in group A. Conclusion: The decreased level of S. a-LA and S. GSH, in our study clearly indicates potential risk of cellular damage in tobacco users due to lipid peroxidation. Hence, the present study recommends supplementation of S. a-LA and Vitamin C in tobacco users to prevent this damage whereas quitting this evil habit will be the best available option. [ABSTRACT FROM AUTHOR]

Objective: To assess the expression of Endoglin (CD-105) and Microvessel Density in clinically normal oral mucosa of non-tobacco and tobacco habituated patients & also histopathologically confirmed cases of oral squamous cell carcinoma (OSCC) patients. Materials and Methods: Twenty cases of clinically normal oral mucosa with tobacco habituation in the form of chewing or smoking, 20 histopathologically confirmed cases of OSCC and twelve normal healthy oral mucosal cases without tobacco habituation in any form, served as control group, were immunohistochemically analysed for expression of Endoglin (CD-105). Chi-square test is used to determine statistical analysis and significance. Result & Conclusion: The finding of 65% of Endoglin CD - 105 positivity and microvessel density (MVD) in the mucosal specimens of tobacco users may be attributed as neoangiogenesis or angiogenic squamous dysplasia like phenomenon occurring as important pathological biomarker preceding oral cancer development, and may therefore be useful as a predictive marker of malignancy.

Objective: The objective of the present study was to evaluate the expression of cyclin D1 in normal oral mucosa of both non tobacco habituated and tobacco habituated individuals histologically and also compare and correlate cyclin D1 expression with histopathologically confirmed cases of oral squamous cell carcinomas. Study Design: The present study involved 20 cases of tobacco habituated individuals with normal oral mucosal tissue and 20 histopathologically confirmed cases of squamous cells carcinomas. Twelve cases of non tobacco habituated individuals served as control group. Chi-square analysis was used to determine statistical significance. Results: Fifty percent of control cases, 70% of squamous cell carcinoma cases and 80% of tobacco habituated individuals of clinically normal mucosa showed cyclin D1 positivity. Thirteen cases with tobacco chewing habit, with clinically normal mucosa, showed dysplasia, out of which seven were mildly dysplastic and six were moderately dysplastic. A larger percentage of cyclin D1 expression was observed in lower grade dysplasias (53.8%) than higher grade dysplasias (46.1%). However statistical analysis showed no significant association between groups. Chi-square value was < 7.82 for p=0.05. Conclusion: The finding of cyclin D1 expression in 80% of tobacco users with clinically normal mucosa indicates that the mutation of cyclin D1 occurs early, even before clinical changes are apparent. This finding appears to be previously unreported. The presence of dysplasia in the same group and cyclin D1 expression in 84.6% of dysplastic cases show that the patients are susceptible for further changes, including progression to higher grades of dysplasia and development of carcinoma. Relatively lower expression of cyclin D1 positivity (70%), in oral cancer patients, when compared with tobacco users with clinically normal mucosa (80%) is indicative of increased traverse of the cell through the cell cycle, which may occur early in tumor progression. Cyclin D1 immunoreactivity was detected in all the three study groups.

Background: Histopathological diagnosis of lesions arising from the intake of tobacco is based on subjective evaluation of morphological alterations within the lesional tissue. Oral exfoliative cytology is a non-invasive diagnostic technique for early detection of oral premalignant and malignant lesions. Morphometric techniques have been advocated as objective and reproducible methods of detecting changes before they are visible by routine microscopy and can facilitate differentiation of normal and abnormal epithelium. This study was conducted to assess the morphometric parameters (cell diameter, nuclear diameter and nuclear cytoplasmic ratio [N:C ratio]) in tobacco smokers and chewers and to evaluate the variations, if any. Materials and Methods: The study was conducted on cytological smears obtained from oral lesions of patients with habit of tobacco smoking (Group B) and tobacco chewing (Group C). Group A comprised of subjects free from oral lesions and not using tobacco in any form. Patients with both the habits were excluded. The smears were stained using Papanicoloaou staining method. For morphometric analysis, Microimage 3.0 image analysis software was employed. The statistical test employed was an analysis of variance and P < 0.05 was considered as significant. Results: The results of this study showed that the cellular diameter was progressively reduced and nuclear diameter progressively increased from Group A to Group B to Group C. The N:C ratio also showed a progressive increase from Group A to Group C. Conclusion: The results confirmed that tobacco chewing and smoking influenced the cytomorphology of normal appearing buccal mucosa and the degree of these changes were found to be greater in chewers as compared to smokers. [ABSTRACT FROM AUTHOR]

Objective: To assess the expression of Endoglin (CD-105) and Microvessel Density in clinically normal oral mucosa of non-tobacco and tobacco habituated patients & also histopathologically confirmed cases of oral squamous cell carcinoma (OSCC) patients. Materials and Methods: Twenty cases of clinically normal oral mucosa with tobacco habituation in the form of chewing or smoking, 20 histopathologically confirmed cases of OSCC and twelve normal healthy oral mucosal cases without tobacco habituation in any form, served as control group, were immunohistochemically analysed for expression of Endoglin (CD-105). Chi-square test is used to determine statistical analysis and significance. Result & Conclusion: The finding of 65% of Endoglin CD - 105 positivity and microvessel density (MVD) in the mucosal specimens of tobacco users may be attributed as neoangiogenesis or angiogenic squamous dysplasia like phenomenon occurring as important pathological biomarker preceding oral cancer development, and may therefore be useful as a predictive marker of malignancy. [ABSTRACT FROM AUTHOR]

Objective: The objective of the present study was to evaluate the expression of cyclin D1 in normal oral mucosa of both non tobacco habituated and tobacco habituated individuals histologically and also compare and correlate cyclin D1 expression with histopathologically confirmed cases of oral squamous cell carcinomas. Study Design: The present study involved 20 cases of tobacco habituated individuals with normal oral mucosal tissue and 20 histopathologically confirmed cases of squamous cells carcinomas. Twelve cases of non tobacco habituated individuals served as control group. Chi-square analysis was used to determine statistical significance. Results: Fifty percent of control cases, 70% of squamous cell carcinoma cases and 80% of tobacco habituated individuals of clinically normal mucosa showed cyclin D1 positivity. Thirteen cases with tobacco chewing habit, with clinically normal mucosa, showed dysplasia, out of which seven were mildly dysplastic and six were moderately dysplastic. A larger percentage of cyclin D1 expression was observed in lower grade dysplasias (53.8%) than higher grade dysplasias (46.1%). However statistical analysis showed no significant association between groups. Chi-square value was < 7.82 for p=0.05. Conclusion: The finding of cyclin D1 expression in 80% of tobacco users with clinically normal mucosa indicates that the mutation of cyclin D1 occurs early, even before clinical changes are apparent. This finding appears to be previously unreported. The presence of dysplasia in the same group and cyclin D1 expression in 84.6% of dysplastic cases show that the patients are susceptible for further changes, including progression to higher grades of dysplasia and development of carcinoma. Relatively lower expression of cyclin D1 positivity (70%), in oral cancer patients, when compared with tobacco users with clinically normal mucosa (80%) is indicative of increased traverse of the cell through the cell cycle, which may occur early in tumor progression. Cyclin D1 immunoreactivity was detected in all the three study groups. [ABSTRACT FROM AUTHOR]

Background: Tobacco smoking in any form (cigarette, bidi etc.) has long been established as a risk factor for CAD (coronary artery disease) but a very little research has been done on tobacco chewing, which is restricted to South Asia (India, Pakistan, Nepal, Bangladesh, Sri Lanka) whether it increases risk for cardiovascular morbidity or not. Aims & Objective: To assess the cardiovascular risks in tobacco chewers as compared to normal population of Aligarh a city of Western Uttar Pradesh. Materials and Methods: The study was conducted in Department of Physiology, Department of TB Chest and Department of Medicine JNMCH, AMU Aligarh. The study consisted of 30 tobacco chewers (in any form) and 30 subjects without any history of tobacco consumption in any form. The age group varied from 20-60years. Anthropometric measurement age, weight, height, BMI, Pulse, SBP (systolic BP), DBP (Diastolic BP) and Lipid Profile estimation from blood sample. Results: Anthropometric measurements did not show any significant change when compared in two groups (p > 0.05). Cardiovascular Parameters like, Systolic pressure (117.46 ± 11.07); diastolic pressure (83.37 ± 8.74); mean arterial pressures (93.40 ± 6.33) and pulse rate (84.29 ± 5.70), were significantly increased in chewers as compared to normal population (p < 0.05). Lipid Profile Parameters like, Total cholesterol (237.04 ± 82.6); HDL (45.54 ± 5.46); LDL (161.16 ± 76.7) were increased in chewers as compared to control (p < 0.05). Atherogenic index T Choles./HDL (5.22 ± 1.90); LDL/HDL (3.57±1.35); Non-HDL/HDL (4.3 ± 1.0), were also showed a significant increase (p < 0.05). Conclusion: All these findings are suggestive that tobacco chewers are at increased risk of cardiovascular diseases as compared to non-tobacco consuming population. [ABSTRACT FROM AUTHOR]

Oral cancer is a major health problem in tobacco users all over the world. It is one of the ten most common cancers in the world. Oral cancer is almost always preceded by some type of precancerous lesion. The precancerous lesions can be detected up to 15years, prior to their change to an invasive carcinoma. It usually affects between the ages of 15 and 40 years. It may be triggered by factors like frequency and duration of tobacco consumption, alcohol, poor oral hygiene etc. This study was conducted primarily to screen chronic tobacco chewers for the presence of oral pre-malignant conditions and secondly to educate them about the hazards of tobacco and motivate them to quit the habit. This was a cross sectional study conducted at Badi gawaltoli area of Indore. Tobacco chewers using tobacco for more than 5yrs were included in the study. Chronic tobacco chewers were screened for oral pre-malignant lesions followed by an educational intervention about the harmful effects of tobacco. Two follow ups were made to motivate them to quit the habit and to get treatment for their lesions. An open ended semi-structured questionnaire was administered to chronic tobacco chewers to assess their habit of tobacco chewing, smoking, their knowledge regarding lesions in their mouth, hazards of tobacco and any cessation efforts. Among the 80 identified chronic tobacco chewers, 60 were males and 20 were females. Lesions such as leukoplakia, erythroplakia and oral sub-mucosal fibrosis were found in 10 females (50%) and 24 males (40%).

Data on the microbial composition among tobacco chewers and oral cancer patients in Rajasthan, India is of interest. NGS analysis from tobacco chewers and oral cancer comprised the most abundant and core microbial taxa in the oral cavity. It shows that highly pathogenic phylum consisting of 6% Fusobacteria and 9% Firmicutes are observed in oral cancer samples; whereas, 0.6% Treponema, 34% Firmicutes, 0.02% Mollicutes, and 4% Fusobacteria are seen in tobacco chewers. Thus, data shows that the most abundant and core microbial taxa are found in the oral cavity of tobacco chewers and oral cancer patients in Rajasthan, India., Competing Interests: There is no conflict of interests among the authors regarding the present publication., (© 2022 Biomedical Informatics.)

Objective: The purpose of this study was to compare effects of smoking and smokeless forms of tobacco consumption (tobacco chewing) on periodontal disease parameters and response of these subjects to non-surgical periodontal therapy., Methods: One hundred sixty-eight patients with chronic periodontitis were screened for the study. Eighteen patients were excluded as they decided to quit the tobacco habit. One hundred fifty patients fulfilling the inclusion and exclusion criteria were grouped as: Group 1, 50 smokers; Group 2, 50 tobacco chewers; and Group 3, 50 non-smokers, non-tobacco chewers (controls). Scaling and root planing was performed at the initial visit as a part of initial therapy. The clinical parameters recorded at baseline, 1 month, 2 months and 3 months were plaque index (PI), gingival index (GI), probing depth (PD), gingival recession (GR), and gingival crevicular fluid (GCF) measurement., Results: With respect to the comparison between smokers and tobacco chewers, smokers had significantly more probing depth at baseline examination, while tobacco chewers had more gingival recession. Gingival inflammation, response to non-surgical treatment and oral hygiene maintenance were more suppressed in smokers as compared to tobacco chewers., Conclusion: Tobacco consumption in both forms affects the severity of periodontal disease. It affects the response of periodontal tissues to non-surgical treatment. In addition it leads to poorer oral hygiene and hampers maintenance of oral hygiene., (Copyright© by the International Academy of Periodontology.)

Prostate cancer is responsible for major deaths globally after lung cancer. However, etiology of prostate cancer is still unknown. Individual risk and incidence of prostate cancer may result from the interaction of genetic susceptibility with exposure to environmental factors such as infectious agents, tobacco, occupational exposure, dietary carcinogens, and/or hormonal imbalances leading to injury of the prostate and to the development of chronic inflammation. About 30% of all human cancers are caused by tobacco smoking and inhaled pollutants. Inflammation is now regarded as an important hallmark of cancer. The present study has been aimed to explore the pro-inflammatory levels in prostate carcinoma patients by examining the serum levels of novel cytokine interleukin-18 (IL-18) expression in tobacco exposed population. A total of 578 (n = 284 biopsy proven prostate cancer patients, n = 294 controls with and without tobacco exposed population) were recruited. Serum IL-18 (Interleukin-18) level was done by ELISA. The IL-18 levels between cancer patients and controls within same mode tobacco exposure as tobacco smoking (overall) showed significant difference (P < 0.0001) and further we compared within stratified group, it significantly differ (P < 0.0001) in bidi and cigarette smoking than control non users. Furthermore, IL-18 levels in tobacco chewers (overall) with gutkha and khaini chewers showed significant difference (P < 0.01) than controls non users. Moreover, the IL-18 levels between cancer patients and controls with in of combined mode chewers smokers and alcohol (CSA), smokers with alcohol showed significant difference (P < 0.01) than controls. The IL-18 levels also differed significantly (P < 0.05) with smokers and chewers in higher stages of III and IV, and showed non significant with in lower stages. Tobacco exposure enhance the inflammation in prostate carcinoma patients in stratified group as it have been represented as a risk factors in various cancers, but this study provide further its role that seems to influence inflammation especially in prostate carcinoma.