SciDoc Publishers | Open Access | Science Journals | Media Partners


International Journal of Dentistry and Oral Science (IJDOS)  /  IJDOS-2377-8075-08-6064

Analysis Of Periodontal Status Among Smokers And Non-Smokers - A Retrospective Study


Pooja Umaiyal. M1, Deepika Rajendran2*, Jaiganesh Ramamurthy3

1 Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Science, Saveetha University, Chennai, India.
2 Senior Lecturer, Department of Oral Medicine and Radiology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India.
3 Professor and Head, Department of Periodontics, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India.


*Corresponding Author

Deepika Rajendran,
Senior lecturer, Department of Oral Medicine and Radiology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, 162, PH Road, Chennai 600077, TamilNadu, India.
E-mail: deepikar.sdc@saveetha.com

Received: May 28, 2021; Accepted: June 16, 2021; Published: June 25, 2021

Citation: Pooja Umaiyal. M, Deepika Rajendran, Jaiganesh Ramamurthy. Analysis Of Periodontal Status Among Smokers And Non-Smokers - A Retrospective Study. Int J Dentistry Oral Sci. 2021;8(6):2894-2899.doi: dx.doi.org/10.19070/2377-8075-21000587

Copyright: Deepika Rajendran©2021. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.



Abstract

Periodontitis is defined as an inflammatory disease of the supporting tissue of the teeth caused by specific microorganisms or a specific group of microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both. Smoking is a known risk factor and it adversely affects the periodontal health. The aim of the study was to analyse the periodontal status among smokers and non-smokers. We reviewed and analysed the data of 86000 patients between June 2019 and March 2020, among which a total of 2320 patients’ details containing both smokers and non-smokers along with their periodontal status were collected. The documented information included patients age, gender, habits and periodontal score. Periodontitis among the smokers and non-smokers was predominant among 46-60 years (53.1%) of age group. The prevalence of Gingivitis was highly predominant among smokers (89.14%) and non-smokers (71.98%) when compared to periodontitis. On comparing the periodontal status, the highest prevalence of periodontitis with periodontal score was 2-5 among the non-smokers (46.3%) and smokers (47.62%). Within the limits of this study, periodontal score of 2-5 was highly prevalent among the smokers and non-smokers with periodontal disease being more prevalent among the non-smokers than the smokers, predominantly affecting the age group of 46-60 years. Hence, regular dental visits and enrollment of smokers in smoking cessation programs will prevent periodontitis among non-smokers and smokers respectively.



1.Keywords
2.Introduction
6.Conclusion
8.References


Keywords

Periodontitis; Smokers; Non-Smokers; Gingivitis, Periodontal Score.


Introduction

Perodontitis is defined as an inflammatory disease of the supporting tissue of the teeth caused by specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both [1]. Dental plaque causes periodontal disease but risk factors can modify the host response to microbial aggression [2]. Diabetes, smoking, microbial tooth deposits and pathogenic bacteria are some of the known factors for the cause of periodontal disease.

For many diseases smoking is a known risk factor and increasing evidence suggests that smoking adversely affects the periodontal health [3]. The concept that smoking tobacco could also be detrimental to periodontal health isn’t new. The newest plaque of the twentieth century is tobacco and its utilisation is still expanding around the world. 182 million smokers abide in India among the humongous population of 930 million worldwide tobacco users. By 2020 World Health Organization appraisal evaluated that tobacco related demise may surpass 1.5 million every year or 13% of all passing in India [4].

A major modifiable risk factor for health is the use of tobacco. Both the mental and physical dependence are included in Nicotine dependence. There are numerous unfriendly consequences for oral and dental being on smoking cigarettes [5]. Oral malignant growth, periodontal illness, delayed healing of extraction socket, a main source of tooth loss, discoloured teeth and tongue, awful breath, decreased feeling of taste and smell are among the impacts [4].

Nearly 60 years ago, Pindburg observed an association between acute Necrotizing ulcerative gingivitis and smoking [6]. Since then there are various studies and investigations on the role of tobacco smoking in the etiology of periodontal diseases. These studies suggest that smoking might be a single, modifiable environmental risk factor liable for excess prevalence of periodontitis within the population and features a direct influence on periodontal variables. A number of studies were reviewed by the 1996 World Workshop in periodontitis and confirmed that “smoking entailed an overall increased risk for severe periodontal disease and estimated overall odds ratio 2.85” [7]. Earlier investigators had attributed the increased severity and prevalence of periodontitis was seen in smokers to the greater presence of plaque and calculus than compared to non-smokers. Besides, in chronic smokers the gingiva bleeds less and appears hardened as compared to that of nonsmokers. The gingival inflammation is reduced in smokers due to the vasoconstrictive properties of cigarette smoke. However, on better understanding of the host response, evidence suggests that the effect of smoking on periodontal status is independent from the plaque index and oral hygiene of the individual. So this clearly suggests that smoking features a direct influence on periodontal tissues.

Individuals smoking have been associated with deeper pockets, pronounced radiographic evidence of furcation involvement, greater attachment loss and increased alveolar bone loss. The negative effect of smoking on periodontal issues, has an established biologic rationale. It has an immunosuppressive effect on the host, adversely affecting host- bacterial interactions and this alteration may be due to the change on the composition of subgingival plaque. The Conductive environment for some periodontal pathologies in the plaque may be provided by smoking and might be a risk factor in periodontal disease development. Smoking exerts a strong, chronic and dose dependent suppressive effect on gingival bleeding on probing. Bleeding on probing was less evident in smokers when compared to the non-smokers which indicates its effect on gingival blood vessels [8]. The exact mechanisms by which smoking suppresses gingival bleeding is not understood yet [9]. Based on the observation that smokers may present with a lower level of gingival inflammation, it has been speculated that the gingival blood flow in smokers may be lesser than in non-smokers [10, 11]. This would also induce a decreased local host response, so smoking is assumed to affect the periodontal tissues mainly by the vascular and immunological response of the body [12].

The mechanisms that may predispose smokers to periodontitis remain to be fully elucidated, while there is overwhelming clinical evidence to associate smoking with destructive periodontal disease.Previously our team has a rich experience in working on various research projects across multiple disciplines [13-27]. The aim of this study was to analyse the periodontal status among the smokers and non-smokers.


Materials And Methods

A retrospective study was conducted in a University setting. Ethical approval was obtained from the institutional ethical committee. We reviewed and analysed the data of 86000 patients between june 2019 and march 2020, among which a total of 2320 patients’ details containing both 1160 smokers and 1160 non-smokers along with their periodontal status were collected. To evaluate and nullify the effect of all the other possible contributing factors, patients belonging to the same age group (15-60 yrs and above) with no other known systemic problems were selected for the study. The documented information included patients age, gender, habits and periodontal score. The collected data was reviewed and subjected to statistical analysis using IBM SPSS software version 20.0. Chi Square test was performed and the p value was determined to evaluate the significance of the variables.


Results And Discussion

In this study a total of 2320 patients were involved with an equal number of smokers and non smokers and with a mean age of 40 yrs. The prevalence of Gingivitis was highly predominant among smokers (89.14%) and non-smokers (71.98%) when compared to periodontitis among smokers (10.86%) and non-smokers (28.02%) (Figure 1 & Figure 2). Among the non-smokers, the highest prevalence of periodontal score was 2-5 (46.3%), followed by the score of 1-2 (27.16%), 0-1 (14.81%) and the least being 5-8 (11.73%) (Figure 3). Among the smokers, the highest prevalence of periodontal score was 2-5 (47.62%), followed by the score of 1-2 (22.22%), 5-8 (16.67%) and the least being 0-1 (14.81%) (Figure 4). However, on comparing the association between the periodontal score and the smoking status of the study population,it was found to be statistically not significant with a p value >0.05 (Figure 5). According to the age group of the non-smokers, highest prevalence of periodontal score was 2-5 among the age group of 15-30 years (66.67%), 31-45 years (46.43%) and among the age group of 46-60 years (45.86%), followed by the score of 1-2 among the age group of 15-30 yrs (33.33%), 31-45 yrs (26.43%), 46-60 yrs (27.62%). The least predominant periodontal score was 0-1 among the age group of 46-60 yrs (11.05%) and the score of 5-8 among the age group of 31-45 yrs (7.14%). However, it was statistically not significant with a p value >0.05 (Figure 6). And according to the age group of smokers, highest prevalence of periodontal score was 2-5 among the age group of 15-30 years (46.67%), 31-45 years (58.33%) and among the age group of 46- 60 years (50%), followed by the score of 1-2 among the age group of 15-30 yrs (33.33%), 31-45 yrs (19.44%), 46-60 yrs (18.97%). The most predominant periodontal score among the age group of 60 yrs and above was 5-8 (47.06%) whereas it was the least score among the age group of 31-45 yrs (8.33%). However, the association between the periodontal score and the age group of the smokers was found to be statistically significant with a p value <0.05 (Figure 7).

Tobacco smoking is considered as the absolute most preventable reason for driving worldwide mortality and the main source of tooth loss in adults being the periodontal disease. Females were purposely excluded from the study for the main purpose that it would be difficult to recruit females who admit that they smoke. Since patients with any known systemic problems were not included, it was considered reasonable that comparisons reflected on the influence of smoking on periodontium. Whereas in contrast to the present study, Chilcan institutional study represented 70.7% of female samples [28].

Gingival bleeding is considered as an important sign associated with gingivitis and periodontitis. There is some evidence that tobacco may be associated with expression of lesser symptoms in periodontal inflammation. In this study, there were significantly less periodontal issues among the smokers than the non-smokers, which is in agreement with earlier studies [29-32].

In the NHANES III [33], the smoking attributable fraction of periodontitis for current smokers was almost 82% in the age group of 20-49 and near 84% among those aged 50 years or more likely reflects the decreased prevalence of smoking and the greater prevalence of severe periodontal disease seen in older individuals. In our current study periodontitis among the smokers and non-smokers was predominant among 46-60 years (53.1%) of age group. In the present study the mean age of the periodontitis patients was 40 yrs which was in accordance with the study by Sreedevi et al.[34], and Luzzi et al.[35], showing a mean age of 35.12 yrs and 40.6 yrs respectively on the highest prevalence of periodontitis.

In the current study, periodontal score was interpreted using Russell's periodontal score, in which the score of 0-1 showed healthy gingiva or simple gingivitis, 1-2 showed beginning of destructive periodontal disease, 2-5 showed established destructive periodontal disease and the score of 5-8 showed terminal disease. According to the current study, established destructive periodontal disease with a score of 2-5 was the most predominant among smokers and non-smokers. In accordance, shah et al., [36] showed an evident negative influence of tobacco, particularly for probing depth and clinical attachment loss. There was a tendency of greater probing depth and clinical attachment loss means in all regions analyzed in smokers than in non-smokers. Similarly sreedevi et al., [34]. showed a comparison of probing depth among smokers and non-smokers in which it was higher among smokers than nonsmokers but it was not statistically significant.

This study was done to know the effect of smoking on the periodontium by studying the clinical parameters. To evaluate and nullify the effect of all the other possible contributing factors, patients belonging to the same age group (15-60 yrs and above) with no other known systemic problems were selected for the study. Although some of the previous studies [37, 3, 38] included subjects who had quit smoking for a period of 2-5 years or more under the non-smokers category, it was decided in this study to exclude former smokers so as to eliminate any long term effect of smoking on periodontal tissues. The discoveries from the present examination of patients calls for attention to the necessities for building up a suitable instructive, preventive and treatment measures combined with successful reconnaissance for tobacco end. Our institution is passionate about high quality evidence based research and has excelled in various fields [39-49].

The limitation of the study conducted includes provision of not getting fully reliable data from the self reported amount of tobacco of the individuals, reduction or the availability of location specific datas. Hence, the results of this study must be interpreted within the limitations of this study and further cohort studies must be done including larger sample size. Such study should also include other associated parameters like, systemic medical condition, plaque index, current smokers or not, duration, etc.



Figure 1: Bar graph depicting the percentage distribution of age groups of diabetic patients with chronic periodontitis. X axis represents age groups and Y axis represents percentage of diabetic patients with chronic periodontitis. The age group of 36-45 years (blue) 17.65%, 46-55 years (green) 44.12% , 56-65 years (beige) 32.35%, and above 65 years (violet) 5.882%. From the figure we can infer that periodontitis with diabetes was more prevalent at the age of 46-55 years (44.12%).



Figure 2: Bar graph depicting the percentage distribution of gender of diabetic patients with chronic periodontitis. X axis represents gender and Y axis represents percentage of diabetic patients with chronic periodontitis. 67.65% were male (blue) and the remaining 32.35% were female (green). From the figure we can infer that patients with periodontitis and diabetes were mostly male gender (67.65%).



Figure 3: Bar graph depicting the percentage distribution of probing depth of upper right molar among the diabetic patients with chronic periodontitis . X axis represents probing depth from 2mm-8mm and Y axis represents percentage of diabetic patients with chronic periodontitis.Most of the periodontitis patients with diabetes had a probing depth of 3mm by 35.29% (green) and least number of patients with periodontitis and diabetes had a probing depth of 8mm by 2.941% (grey). From the figure we can infer that periodontitis patients with diabetes had a maximum probing depth of 3mm by 35.29%.



Figure 4: Bar graph depicting the percentage distribution of age groups of diabetic patients with chronic periodontitis. X axis represents age groups and Y axis represents percentage of diabetic patients with chronic periodontitis. The age group of 36-45 years (blue) 17.65%, 46-55 years (green) 44.12% , 56-65 years (beige) 32.35%, and above 65 years (violet) 5.882%. From the figure we can infer that periodontitis with diabetes was more prevalent at the age of 46-55 years (44.12%).



Figure 5: Bar graph depicting the percentage distribution of gender of diabetic patients with chronic periodontitis. X axis represents gender and Y axis represents percentage of diabetic patients with chronic periodontitis. 67.65% were male (blue) and the remaining 32.35% were female (green). From the figure we can infer that patients with periodontitis and diabetes were mostly male gender (67.65%).



Figure 6: Bar graph depicting the percentage distribution of probing depth of upper right molar among the diabetic patients with chronic periodontitis . X axis represents probing depth from 2mm-8mm and Y axis represents percentage of diabetic patients with chronic periodontitis.Most of the periodontitis patients with diabetes had a probing depth of 3mm by 35.29% (green) and least number of patients with periodontitis and diabetes had a probing depth of 8mm by 2.941% (grey). From the figure we can infer that periodontitis patients with diabetes had a maximum probing depth of 3mm by 35.29%.



Figure 7. Bar chart depicts correlation of periodontal score based on the age group of the smokers. X axis denotes the age group of the smokers based on their periodontal score and Y axis denotes the number of patients. The prevalence of periodontal score of 2-5 was more predominant among the smokers under the age group of 31-45 years. However, the association between the periodontal score and the age group of the smokers was found to be statistically significant with a p value <0.05. Pearson’s Chi Square= 20.419 df= 9, p value= 0.015 (<0.05).


Conclusion

Within the limits of this study, periodontal score of 2-5 was highly prevalent among the smokers and non-smokers. Irrespective of their habits, periodontal disease was more prevalent among both the population in the age group between 46-60 years. Hence regular dental visits and enrollment of smokers in smoking cessation programs will prevent periodontitis among non-smokers and smokers respectively.


Acknowledgment

I am sincerely thankful to Saveetha Dental College and Hospital, Chennai for providing me with the opportunity to write a research paper in the form of a dissertation on the topic “ Analysis of periodontal status among smokers and non-smokers- A retrospective study.”

I am also thankful to Dr. Deepika Rajendran for guiding me in every stage of this research paper. Without her support it would have been very difficult for me to prepare the paper so meaningfully.

I also would like to thank the department of Information Technology of Saveetha Dental College and Hospital, who had helped me during the course of this research paper for the collection of required datas of the patients.


References

  1. Novak MJ, Novak KF. Chronic periodontitis. R Carranzas Clinical Periodontology 9th ed …. 2006;
  2. Gloria Calsina, Ramón JM, Echeverría JJ. Effects of smoking on periodontal tissues. J Clin Periodontol. 2002 Aug;29(8):771-6.
  3. Haber J, Wattles J, Crowley M, Mandell R, Joshipura K, Kent RL. Evidence for cigarette smoking as a major risk factor for periodontitis. J Periodontol. 1993 Jan;64(1):16-23.
  4. Vellappally S, Jacob V, Smejkalová J, Shriharsha P, Kumar V, Fiala Z. Tobacco habits and oral health status in selected Indian population. Cent Eur J Public Health. 2008 Jun 1;16(2) :77–84.
  5. D'Souza MS, Markou A. Neuronal mechanisms underlying development of nicotine dependence: implications for novel smoking-cessation treatments. Addict Sci Clin Pract. 2011 Jul;6(1):4-16.Pubmed PMID: 22003417.
  6. Pindborg JJ. Tobacco and gingivitis. J Dent Res. 1947 Jun;26(3):261-4.
  7. Papapanou PN. Periodontal diseases: epidemiology. Ann Periodontol. 1996 Nov;1(1):1-36.
  8. Ramamurthy J, Nd J, Varghese S. Comparison of Salivary Beta Glucuronidase Activity in Chronic Periodontitis Patients with and without Diabetes Mellitus. J Clin Diagn Res. 2014 Jun;8(6):ZC19-21.Pubmed PMID: 25121058.
  9. Dietrich T, Bernimoulin JP, Glynn RJ. The effect of cigareté smoking on gingival bleeding. J Periodontol. 2004 Jan;75(1):16-22.
  10. Ramamurthy JA, Mg V. Comparison of effect of Hiora mouthwash versus Chlorhexidine mouthwash in gingivitis patients: A clinical trial. Asian J Pharm Clin Res. 2018 Jul 7;11(7):84-8.
  11. Ramamurthy J, Lakshmi T. Pharmacological aspects of tea tree oil (TTO) and its role in dentistry-a comprehensive review. Int J Pharma Bio Sci. 2011;2(4).
  12. Panda S, Jayakumar ND, Sankari M, Varghese SS, Kumar DS. Platelet rich fibrin and xenograft in treatment of intrabony defect. Contemp. Clin. Dent. 2014 Oct;5(4):550-4.
  13. Hafeez N. Accessory foramen in the middle cranial fossa. Res J Pharm Technol. 2016;9(11):1880-2.
  14. Krishnan RP, Ramani P, Sherlin HJ, Sukumaran G, Ramasubramanian A, Jayaraj G, et al. Surgical Specimen Handover from Operation Theater to Laboratory: A Survey. Ann Maxillofac Surg. 2018 Jul-Dec;8(2):234-238. Pubmed PMID: 30693238.
  15. Somasundaram S, Ravi K, Rajapandian K, Gurunathan D. Fluoride Content of Bottled Drinking Water in Chennai, Tamilnadu. J Clin Diagn Res. 2015 Oct;9(10):ZC32-4.Pubmed PMID: 26557612.
  16. Felicita AS. Orthodontic extrusion of Ellis Class VIII fracture of maxillary lateral incisor - The sling shot method. Saudi Dent J. 2018 Jul;30(3):265- 269.Pubmed PMID: 29942113.
  17. Kumar S, Rahman R. Knowledge, awareness, and practices regarding biomedical waste management among undergraduate dental students. Asian J Pharm Clin Res. 2017;10(8):341.
  18. Gurunathan D, Shanmugaavel AK. Dental neglect among children in Chennai. J Indian Soc Pedod Prev Dent. 2016 Oct 1;34(4):364.
  19. Sneha S. Knowledge and awareness regarding antibiotic prophylaxis for infective endocarditis among undergraduate dental students. Asian J Pharm Clin Res. 2016 Oct 1:154-9.
  20. Dhinesh B, Lalvani JI, Parthasarathy M, Annamalai K. An assessment on performance, emission and combustion characteristics of single cylinder diesel engine powered by Cymbopogon flexuosus biofuel. Energy Convers Manage. 2016 Jun 1;117:466-74.
  21. Choudhari S, Thenmozhi MS. Occurrence and Importance of Posterior Condylar Foramen. Res J Pharm Technol .2016;9(8):11–43.
  22. Paramasivam A, Vijayashree Priyadharsini J, Raghunandhakumar S. N6- adenosine methylation (m6A): a promising new molecular target in hypertension and cardiovascular diseases. Hypertens Res. 2020 Feb;43(2):153- 154.Pubmed PMID: 31578458.
  23. Wu F, Zhu J, Li G, Wang J, Veeraraghavan VP, Krishna Mohan S, et al. Biologically synthesized green gold nanoparticles from Siberian ginseng induce growth-inhibitory effect on melanoma cells (B16). Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):3297-3305.Pubmed PMID: 31379212.
  24. Palati S, Ramani P, Shrelin HJ, Sukumaran G, Ramasubramanian A, Don KR, et al. Knowledge, Attitude and practice survey on the perspective of oral lesions and dental health in geriatric patients residing in old age homes. Indian J Dent Res. 2020 Jan-Feb;31(1):22-25.Pubmed PMID: 32246676.
  25. . Saravanan M, Arokiyaraj S, Lakshmi T, Pugazhendhi A. Synthesis of silver nanoparticles from Phenerochaete chrysosporium (MTCC-787) and their antibacterial activity against human pathogenic bacteria. Microb Pathog. 2018 Apr;117:68-72.Pubmed PMID: 29427709.
  26. Govindaraju L, Gurunathan D. Effectiveness of Chewable Tooth Brush in Children-A Prospective Clinical Study. J Clin Diagn Res. 2017 Mar;11(3):ZC31-ZC34.Pubmed PMID: 28511505.
  27. Vijayakumar Jain S, Muthusekhar MR, Baig MF, Senthilnathan P, Loganathan S, Abdul Wahab PU, et al. Evaluation of Three-Dimensional Changes in Pharyngeal Airway Following Isolated Lefort One Osteotomy for the Correction of Vertical Maxillary Excess: A Prospective Study. J Maxillofac Oral Surg. 2019 Mar;18(1):139-146.Pubmed PMID: 30728705.
  28. Rivera C, Jones-Herrera C, Vargas P, Venegas B, Droguett D. Oral diseases: a 14-year experience of a Chilean institution with a systematic review from eight countries. Med Oral Patol Oral Cir Bucal. 2017 May 1;22(3):e297- e306.Pubmed PMID: 28390130.
  29. Bastiaan RJ, Waite IM. Effects of tobacco smoking on plaque development and gingivitis. J. Periodontol. 1978 Sep 1;49(9):480-2.
  30. Feldman RS, Bravacos JS, Rose CL. Association between smoking different tobacco products and periodontal disease indexes. J. Periodontol. 1983 Aug;54(8):481-7.
  31. Lie MA, van der Weijden GA, Timmerman MF, Loos BG, van Steenbergen TJ, van der Velden U. Oral microbiota in smokers and non-smokers in natural and experimentally-induced gingivitis. J Clin Periodontol. 1998 Aug;25(8):677-86.Pubmed PMID: 9722273.
  32. Danielsen B, Manji F, Nagelkerke N, Fejerskov O, Baelum V. Effect of cigarette smoking on the transition dynamics in experimental gingivitis. J Clin Periodontol. 1990 Mar;17(3):159-64.Pubmed PMID: 2319002.
  33. Hyman JJ, Reid BC. Epidemiologic risk factors for periodontal attachment loss among adults in the United States. J Clin Periodontol. 2003 Mar;30(3):230-7.
  34. . Sreedevi M, Ramesh A, Dwarakanath C. Periodontal status in smokers and nonsmokers: a clinical, microbiological, and histopathological study. Int J Dent. 2012;2012:571590.Pubmed PMID: 22505904.
  35. Luzzi LI, Greghi SL, Passanezi E, Sant'Ana AC, Lauris JR, Cestari TM. Evaluation of clinical periodontal conditions in smokers and non-smokers. J Appl Oral Sci. 2007 Dec;15(6):512-7.
  36. Shah PM, Geetha RV, Thangavelu L. Prevalence of periodontitis among smokers and non-smokers. Int. J. Pharm. Sci. Res. 2019;10(2):1161–6.
  37. Haber J, Kent RL. Cigarette smoking in a periodontal practice. J Periodontol. 1992 Feb;63(2):100-6.
  38. Varadan M, Ramamurthy J. Association of periodontal disease and pre-term low birth weight infants. J Obstet Gynaecol India. 2015 May;65(3):167-71.
  39. Vijayashree Priyadharsini J. In silico validation of the non-antibiotic drugs acetaminophen and ibuprofen as antibacterial agents against red complex pathogens. J Periodontol. 2019 Dec;90(12):1441-1448.Pubmed PMID: 31257588.
  40. Pc J, Marimuthu T, Devadoss P, Kumar SM. Prevalence and measurement of anterior loop of the mandibular canal using CBCT: A cross sectional study. Clin Implant Dent Relat Res. 2018 Apr 6;20(4):531-4.
  41. Ramesh A, Varghese S, Jayakumar ND, Malaiappan S. Comparative estimation of sulfiredoxin levels between chronic periodontitis and healthy patients - A case-control study. J Periodontol. 2018 Oct;89(10):1241-1248.Pubmed PMID: 30044495.
  42. Ramadurai N, Gurunathan D, Samuel AV, Subramanian E, Rodrigues SJ. Effectiveness of 2% Articaine as an anesthetic agent in children: randomized controlled trial. Clin Oral Investig. 2019 Sep;23(9):3543-50.
  43. Sridharan G, Ramani P, Patankar S, Vijayaraghavan R. Evaluation of salivary metabolomics in oral leukoplakia and oral squamous cell carcinoma. J Oral Pathol Med. 2019 Apr;48(4):299-306.
  44. Ezhilarasan D, Apoorva VS, Ashok Vardhan N. Syzygium cumini extract induced reactive oxygen species-mediated apoptosis in human oral squamous carcinoma cells. J Oral Pathol Med. 2019 Feb;48(2):115-121.Pubmed PMID: 30451321.
  45. Mathew MG, Samuel SR, Soni AJ, Roopa KB. Evaluation of adhesion of Streptococcus mutans, plaque accumulation on zirconia and stainless steel crowns, and surrounding gingival inflammation in primary molars: randomized controlled trial. Clin Oral Investig. 2020 Sep;24(9):3275-3280.Pubmed PMID: 31955271.
  46. Samuel SR. Can 5-year-olds sensibly self-report the impact of developmental enamel defects on their quality of life? Int J Paediatr Dent. 2021 Mar;31(2):285-286.Pubmed PMID: 32416620.
  47. R H, Ramani P, Ramanathan A, R JM, S G, Ramasubramanian A, et al. CYP2 C9 polymorphism among patients with oral squamous cell carcinoma and its role in altering the metabolism of benzo[a]pyrene. Oral Surg Oral Med Oral Pathol Oral Radiol. 2020 Sep;130(3):306-312.Pubmed PMID: 32773350.
  48. Chandrasekar R, Chandrasekhar S, Sundari KKS, Ravi P. Development and validation of a formula for objective assessment of cervical vertebral bone age. Prog Orthod. 2020 Oct 12;21(1):38.Pubmed PMID: 33043408.
  49. Vijayashree Priyadharsini J, Smiline Girija AS, Paramasivam A. In silico analysis of virulence genes in an emerging dental pathogen A. baumannii and related species. Arch Oral Biol. 2018 Oct;94:93-98.Pubmed PMID: 30015217.

         Indexed in

pubhub  CGS  indexcoop  
j-gate  DOAJ  Google_Scholar_logo

       Total Visitors

SciDoc Counter

Get in Touch

SciDoc Publishers
16192 Coastal Highway
Lewes, Delaware 19958
Tel :+1-(302)-703-1005
Fax :+1-(302)-351-7355
Email: contact.scidoc@scidoc.org


porn