Assessment of Periodontal Status in Patients with Oral Leukoplakia
S. Sivaharini1, M. Jeevitha2*, Vivek Narayan3
1 Saveetha Dental College and Hospital, Saveetha Institute of Medical and Technical Sciences, Saveetha University (SIMATS), Chennai, India.
2 Senior lecturer, Department of Periodontics, Saveetha Dental College and Hospital, Saveetha Institute of Medical and Technical Sciences (SIMATS), Saveetha University, Chennai, India.
3 Senior lecturer, Department of Oral Medicine and Radiology, Saveetha Dental College and Hospital, Saveetha Institute of Medical and Technical Sciences (SIMATS), Saveetha University, Chennai, India.
*Corresponding Author
Dr. M. Jeevitha,
Senior lecturer, Senior lecturer, Department of Periodontics, Saveetha Dental College and Hospital, Saveetha Institute of Medical and Technical Sciences (SIMATS), Saveetha
University, Chennai - 600077, India.
Tel: +91 7904613787
E-mail: jeevitham.sdc@saveetha.com
Received: July 30, 2021; Accepted: August 10, 2021; Published: August 17, 2021
Citation:S. Sivaharini, M. Jeevitha, Vivek Narayan. Assessment of Periodontal Status in Patients with Oral Leukoplakia. Int J Dentistry Oral Sci. 2021;8(8):3866-3870. doi: dx.doi.org/10.19070/2377-8075-21000791
Copyright: Dr. M. Jeevitha©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
The occurrence of periodontal diseases in humans has been a global problem. Certain risk factors affect the initiation, progression and severity of periodontitis. The present study has been designed to assess the periodontal status in patients with oral leukoplakia. The study was carried out among 27 subjects with oral leukoplakia. The required data were collected and imported to SPSS analysis software for analysis. A total of 44.4% were reported to have generalized chronic gingivitis and 55.6% were having generalized chronic periodontitis. It was observed that elderly patients between 50 to 80 years (55.6%) are more prone to generalised chronic periodontitis. The p value obtained is 0.503 which is not significant (p>0.05). We also observed that males (96.3%) were more commonly reported with oral leukoplakia and diagnosed with periodontal diseases than females (3.7%).The results of this study provide the prevalence of periodontal diseases in oral leukoplakia. The association of periodontitis with premalignant lesions may influence the risk of disease progression and thus preventive therapeutic measures for periodontal diseases can be planned for oral leukoplakia patients.
2.Introduction
3.Conclusion
4.References
Keywords
Periodontal Disease; Periodontitis; Premalignant Lesions; Oral Cancer; Oral Leukoplakia; Gingivitis.
Introduction
Oral leukoplakia is a potentially malignant disorder affecting mucosa
of the oral cavity. Other than smoking and liquor, the risk
factors for the development of this oral lesion are still less recognised
[4]. Leukoplakia is an asymptomatic, potentially malignant
lesion in the oral mucosa. However, leukoplakia increases
your risk of oral cancer. Oral cancers often form near leukoplakia
patches. Stress and socio-economic factors may be additive risk
factors for leukoplakia and acute infections in the oral cavity may
contribute to the risk [45].
It is known that one of the most frequent potentially malignant
disorders of oral mucosa is Oral leukoplakia. It was first defined
by the world health organisation in 1978 as ‘a white patch
or plaque which cannot otherwise be characterized clinically or
pathologically as any other disease’ [44]. As oral leukoplakia can
mimic a large variety of lesions, a possible causal factor is suspected
such as dental restoration, mechanical irritation [4]. The
studies done on oral leukoplakia are very rare, so it is difficult
to value its real malignant transformation rate due to different
regional habits [28].
Periodontitis is a very common disease caused by oral bacterial
inflammation and leading to irreversible attachment loss, bone
destruction and eventually tooth loss. It is a multi-factorial disease
modified by numerous risk factors such as smoking, social background,
diabetes, genetic susceptibility, attitude towards health
and supragingival plaque control [7].
Periodontitis is related to different pathological states in the oral
cavity including pre malignant and malignant lesions. This is also
true for smoking, the most important risk factor for oral leukoplakia
and for periodontitis [17]. The occurrence of periodontal
disease in humans is a global problem [29]. Periodontal disease
is found to affect the Male gender more than the females [49].
Furthermore lack of oral hygiene encourages plaque formation,
which leads to increase in pathogenic bacteria that are associated with severe forms of periodontal disease [10]. Periodontal diseases
are prevalent both in developed and developing countries
and affect about 20-50% of global population. High prevalence
of periodontal disease in adolescents, adults and older individuals
make it a public health concern [47]. The risk of periodontal disease
increases with the advancing age that is why the high prevalence
of periodontal disease is seen among elderly population.
Previous studies identified that age is associated with periodontal
disease [19].
Previously our team has a rich experience in working on various
research projects across multiple disciplines. (Ramamurthy and
Mg, 2018)[33], (Gupta, Ariga and Deogade, 2018)[12], (Vikram
et al., 2017)[54], (Paramasivam, Vijayashree Priyadharsini and
Raghunandhakumar, 2020)[25], (Palati et al., 2020)[23], (Samuel,
Acharya and Rao, 2020)[43], (Muthukrishnan and Wanakulasuriya,
2018)[22], (Govindaraju, Neelakantan and Gutmann, 2017)
[11], (Chen et al., 2019)[6], (Priyanka et al., 2017)[31], (Sitharthan
et al., 2019)[46], (Priyadharsini et al., 2018)[30], (Azeem and
Sureshbabu, 2018)[3], (Wu et al., 2019)[56], (Abitha and Santhanam,
2019)[1].Now the growing trend in this area motivated us to
pursue this project.
Taking into consideration the lack of data about periodontal disease
in Indian population of oral leukoplakia cases, the present
study has been designed to assess the periodontal status of patients
with oral leukoplakia in an institutional setup.
Materials And Methods
In this retrospective study, records of 86000 patients visited
Saveetha Dental College and Hospitals from June 2019 to march
2020 were reviewed and the data were analysed. In this study, we
reviewed data of 27 patients diagnosed with oral leaukoplakia.
Data collected regarding age, gender and different types of periodontal
diseases such as generalised chronic gingivitis, localised
chronic periodontitis, generalised chronic periodontitis and localised
chronic gingivitis diagnosed in oral leukoplakia patients. The
data collected were tabulated into excel sheets. It was then transferred
to SPSS and analysed by Chi- square test.
Results & Discussion
The study population consisted of 27 individuals of which 26
(96.3%) were males and 1 patient (3.7%) was female. [Figure 1]
Regarding age 50-80 (55.6%) years of age group were most commonly
affected followed by 30-50 years (40.7%) and 10-30 years
(3.7%). The most commonly observed diagnosis in our study is
generalised chronic periodontitis (55.6%) and it is followed by
generalised chronic gingivitis (44.4%). [Figure 2] The data was
analysed using SPSS software Chi-square tests was done and the p
value obtained is 0.503, which is not significant, (p>0.05). There
were no reported cases of localised chronic periodontitis and localised
chronic gingivitis in oral leukoplakia patients.
In our present study, periodontal diseases were more commonly
observed in 50-80 years of age. Most studies suggest that periodontal
disease is more severe in older adults because of cumulative
tissue destruction over a lifetime rather than an age-related,
intrinsic deficiency or abnormality which affects periodontal susceptibility.
However, it is still unclear in the case of whether aging
is a risk factor for severe periodontal disease, or if its impact is
due to the prolonged exposure of older subjects to true etiologic
factors.
The main objective in oral leukoplakia’s management of care is
to detect and to prevent malignant transformation.(Meyer et al.,
2008) At the first, the ceasing of the risk activities such as smoking
is recommended. Further the histopathological evaluation is
needed. Oral leukoplakia presenting low malignant risk may be either
completely removed or not and the decision should consider
other factors such as location size and in the case of smokers, the
patient’s engagement in smoking cessation [50].
Therefore, cessation of smoking can prevent periodontal cases,
since smoking is a major risk factor for periodontal disease. [16].
Smoking cessation not only inhibits further progression of periodontal
disease but can also decrease the periodontal tissue destruction
[15].
Chronic periodontitis is the most common and widely recognised
infection worldwide with high clinical significance for dentists.
Chronic periodontitis triggers the development of (OSCC) oral
squamous cell carcinoma [13]. Recently, there is improving enthusiasm
in the development of various types of cancer and their
contribution to inflammation as also the underlying pathophysiological
factors that lead to malignant transformation [34, 14].
Periodontitis is treated by dental professionals with scaling and
root planing of bacteria and calculus to address the inflammation
deep into the root. Topical antibiotics (metronidazole, minocycline,
and doxycycline) and systemic antibiotics (doxycycline 100
mg daily, metronidazole 500 mg twice daily) are also used [38,
37] Chlorhexidine rinses may also be prescribed. Oral hygiene
is an essential aspect of management and can be supported by
medical professionals. Oral hygiene should include brushing twice
daily with fluoridated toothpaste, ideally using an electric oscillating
toothbrush, flossing daily, avoiding sugary snacks and drinks,
avoiding tobacco products, and regular dental visits and cleanings.
[31, 9].
Oral Leukoplakia around the world is around 1-2% for all ages together.
There are geographical differences with regard to gender
distribution. Leukoplakias are usually more typical among smokers
than non-smokers [55].
WHO recommends employing integrated public health preventive
strategies which should be based on the common risk factor
approach. Risk factors such as smoking,stress and low socioeconomic
status are associated with periodontal disease as well as
other systemic chronic diseases; therefore inclusion of oral disease
prevention strategies in chronic systemic disease is needed.
Preventive initiatives can curtail the burden of disease of the level
of population [27].
Proper mouth cleaning, regular tooth brushing and dental flossing
are most effective in preventing oral disease and periodontitis
[51]. Despite utmost significance of tooth brushing, about half
of the population brush twice a day. There are various types of
toothbrushes in reducing dental plaque [34].
Although the role of diet in the prevention of dental caries is
more significant compared with preventing periodontal disease;
nonetheless poor diet can negatively affect periodontal tissues
causing rapid progression of disease [52].
A diet high in fruits, vegetables and low in fat and sugars is required
for healthy periodontal tissues [2]. Stannous fluoride has
antiplaque and antigingivitis effects and it reduces the proportion
of bacteria and spirochetes in subgingival areas, thus can help to
promote gingival health [24]. Chlorhexidine, triclosan, essential
oils and zinc in toothpastes, mouthwashes and gels are used to
control specific periodontal bacteria as well as plaque [21]. Moreover
research data from several clinical trials support that antibacterial
mouth rinses have equal or greater efficiency in controlling
gingival disease than the use of interproximal dental floss [39].
The limitations of the present study are small sample size. There
was insufficient data of female patients with oral leukoplakia to
statistically analyse the association of oral leukoplakia and periodontal
diseases based on gender. Our institution is passionate
about high quality evidence based research and has excelled in
various fields ( (Pc, Marimuthu and Devadoss, 2018 [26]; Priyadharsini
et al., 2018 [30]; Ramesh et al., 2018 [36]; Ezhilarasan,
Apoorva and Ashok Vardhan, 2019 [8]; Ramadurai et al., 2019
[32]; Sridharan et al., 2019 [48]; Vijayashree Priyadharsini, 2019
[53]; Chandrasekar et al., 2020 [5]; Mathew et al., 2020 [18]; R et
al., 2020 [41]; Samuel, 2021 [42]). We hope this study adds to this
rich legacy.
Figure 1: The graph shows association of distribution of gender reported with oral leukoplakia. X-axis represents the gender type and Yaxis represents the patient count. Males (96.3%) were higher than females (3.7%)
Figure 2: The graph shows the association of prevalence of periodontal diseases in relation to age. The X axis represents the age group and Y axis represents the patient count. Blue denotes Generalised chronic gingivitis and red denotes generalised chronic periodontitis. Generalised chronic gingivitis (22.22%) and generalised chronic periodontitis (33.33%) were more commonly observed in participants in the age group of 50 to 80 years than in participants of other age groups; however it is not statistically significant. Chi square test, p value: 0.503 (p<0.05 which is not statistically significant).
Conclusion
Further research is needed to explore the underlying mechanics
and risk factors of periodontal diseases and oral leukoplakia, to
develop initiative preventive strategies. Preventive programs for
periodontal disease should utilize common risk approaches to
reduce the magnitude of other chronic diseases. Decreased periodontal
disease burden can minimize treatment needs and can
reduce financial impact on healthcare systems.
The role of the dentist and general practitioner is important in the
early diagnosis when leukoplakia is usually asymptomatic. Ideal
dental diagnosis and procedures should be evaluated.
References
-
[1]. Abitha T, Santhanam A. Correlation between bizygomatic and maxillary
central incisor width for gender identification. Brazilian Dental Science.
2019 Oct 31;22(4):458-66.
[2]. Oliveira Alves MG, Almeida JD, Balducci I, Guimarães Cabral LA. Oral lichen planus: A retrospective study of 110 Brazilian patients. BMC Res Notes. 2010 Jun 3;3:157. Pubmed PMID: 20525297.
[3]. Azeem RA, Sureshbabu NM. Clinical performance of direct versus indirect composite restorations in posterior teeth: A systematic review. J Conserv Dent. 2018 Jan-Feb;21(1):2-9. Pubmed PMID: 29628639.
[4]. Campisi G, Giovannelli L, Aricò P, Lama A, Di Liberto C, Ammatuna P, D'Angelo M. HPV DNA in clinically different variants of oral leukoplakia and lichen planus. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 Dec;98(6):705-11. Pubmed PMID: 15583544.
[5]. Chainani-Wu N, Silverman S Jr, Lozada-Nur F, Mayer P, Watson JJ. Oral lichen planus: patient profile, disease progression and treatment responses. J Am Dent Assoc. 2001 Jul;132(7):901-9. doi: 10.14219/jada.archive. 2001.0302. PMID: 11480643.
[6]. 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.
[7]. Chen F, Tang Y, Sun Y, Veeraraghavan VP, Mohan SK, Cui C. 6-shogaol, a active constiuents of ginger prevents UVB radiation mediated inflammation and oxidative stress through modulating NrF2 signaling in human epidermal keratinocytes (HaCaT cells). J Photochem Photobiol B. 2019 Aug;197:111518. Pubmed PMID: 31202076.
[8]. Chen QM, Deng JX, Zeng X. [Development and chinization of diagnostic criteria for oral lichen planus]. Zhonghua Kou Qiang Yi Xue Za Zhi. 2020 Mar 9;55(3):191-195. Chinese. Pubmed PMID: 32193918. [9]. Costa NL, Gonçalves JAM, de Lima SLG, de Arruda JAA, Miranda ACC, Mesquita RA, da Silveira ÉJD, Batista AC. Evaluation of PD-L1, PD-L2, PD-1 and cytotoxic immune response in oral lichen planus. Oral Dis. 2020 Apr 7. Pubmed PMID: 32259363.
[10]. Crincoli V, Di Bisceglie MB, Scivetti M, Lucchese A, Tecco S, Festa F. Oral lichen planus: update on etiopathogenesis, diagnosis and treatment. Immunopharmacol Immunotoxicol. 2011 Mar;33(1):11-20. Pubmed PMID: 20604639.
[11]. Day T, Wilkinson E, Rowan D, Scurry J; ISSVD Difficult Pathologic Diagnoses Committee*. Clinicopathologic Diagnostic Criteria for Vulvar Lichen Planus. J Low Genit Tract Dis. 2020 Jul;24(3):317-329. PMID: 32205763.
[12]. Eisen D. The clinical features, malignant potential, and systemic associations of oral lichen planus: a study of 723 patients. J Am Acad Dermatol. 2002 Feb;46(2):207-14. Pubmed PMID: 11807431.
[13]. 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.
[14]. Farhi D, Dupin N. Pathophysiology, etiologic factors, and clinical management of oral lichen planus, part I: facts and controversies. Clin Dermatol. 2010 Jan-Feb;28(1):100-8. Pubmed PMID: 20082959. [15]. Gheena S, Ezhilarasan D. Syringic acid triggers reactive oxygen species-mediated cytotoxicity in HepG2 cells. Hum Exp Toxicol. 2019 Jun;38(6):694- 702. Pubmed PMID: 30924378.
[16]. Govindaraju L, Neelakantan P, Gutmann JL. Effect of root canal irrigating solutions on the compressive strength of tricalcium silicate cements. Clin Oral Investig. 2017 Mar;21(2):567-571. Pubmed PMID: 27469101.
[17]. Gupta V, Ramani P. Histologic and immunohistochemical evaluation of mirror image biopsies in oral squamous cell carcinoma. J Oral Biol Craniofac Res. 2016 Sep-Dec;6(3):194-197. Pubmed PMID: 27761383.
[18]. Hannah R, Ramani P, Sherlin HJ, Ranjith G, Ramasubramanian A, Jayaraj G, Don KR, Archana S. Awareness about the use, ethics and scope of dental photography among undergraduate dental students dentist behind the lens. Res J Pharm Technol. 2018;11(3):1012-6.
[19]. Hasan S. Lichen planus of lip - Report of a rare case with review of literature. J Family Med Prim Care. 2019 Mar;8(3):1269-1275. Pubmed PMID: 31041290. [20]. Jablonska E, Garley M, Surazynski A, Grubczak K, Iwaniuk A, Borys J, Moniuszko M, Ratajczak-Wrona W. Neutrophil extracellular traps (NETs) formation induced by TGF-ß in oral lichen planus - Possible implications for the development of oral cancer. Immunobiology. 2020 Mar;225(2):151901. Pubmed PMID: 31882256.
[21]. Jangid K, Alexander AJ, Jayakumar ND, Varghese S, Ramani P. Ankyloglossia with cleft lip: A rare case report. J Indian Soc Periodontol. 2015 Nov- Dec;19(6):690-3. Pubmed PMID: 26941523.
[22]. Jayaraj G, Sherlin HJ, Ramani P, Premkumar P, Anuja N. Cytomegalovirus and Mucoepidermoid carcinoma: A possible causal relationship? A pilot study. J Oral Maxillofac Pathol. 2015 Sep-Dec;19(3):319-24. Pubmed PMID: 26980959.
[23]. Jayaraj G, Ramani P, Sherlin HJ, Premkumar P, Anuja N. Inter-observer agreement in grading oral epithelial dysplasia–A systematic review. Journal of Oral and Maxillofacial Surgery, Medicine, and Pathology. 2015 Jan 1;27(1):112-6.
[24]. Jayaraj G, Sherlin HJ, Ramani P, Premkumar P, Natesan A. Stromal myofibroblasts in oral squamous cell carcinoma and potentially malignant disorders. Indian J Cancer. 2015 Jan-Mar;52(1):87-92. Pubmed PMID: 26837985.
[25]. Kämmerer, P. (no date) ‘QUANTIFIABLE ANGIOGENESIS PARAMETERS IN ASSOCIATION WITH THE GRADUAL MALIGNANT TRANSFORMATION AND THE PROGNOSIS OF LEUKOPLAKIADERIVED ORAL SQUAMOUS CELL CARCINOMA’.
[26]. Krasowska D, Pietrzak A, Surdacka A, Tuszynska-Bogucka V, Janowski K, Rolinski J. Psychological stress, endocrine and immune response in patients with lichen planus. Int J Dermatol. 2008 Nov;47(11):1126-34. Pubmed PMID: 18986442.
[27]. Liu W, Ma L, Song C, Li C, Shen Z, Shi L. Research trends and characteristics of oral lichen planus: A bibliometric study of the top-100 cited articles. Medicine (Baltimore). 2020 Jan;99(2):e18578. Pubmed PMID: 31914037. [28]. Lozada-Nur F, Miranda C. Oral lichen planus: epidemiology, clinical characteristics, and associated diseases. Semin Cutan Med Surg. 1997 Dec;16(4):273-7. Pubmed PMID: 9421218. [29]. Manohar J. A Study on the Knowledge of Causes and Prevalance of Pigmentation of Gingiva among Dental Students. Indian J Pub Health Res Dev. 2019 Aug 1;10(8).
[30]. 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.
[31]. Munde AD, Karle RR, Wankhede PK, Shaikh SS, Kulkurni M. Demographic and clinical profile of oral lichen planus: A retrospective study. Contemp Clin Dent. 2013 Apr;4(2):181-5. Pubmed PMID: 24015006.
[32]. Murti PR, Daftary DK, Bhonsle RB, Gupta PC, Mehta FS, Pindborg JJ. Malignant potential of oral lichen planus: observations in 722 patients from India. J Oral Pathol. 1986 Feb;15(2):71-7. Pubmed PMID: 3083065. [33]. Muthukrishnan A, Warnakulasuriya S. Oral health consequences of smoke less tobacco use. Indian J Med Res. 2018 Jul;148(1):35-40. Pubmed PMID: 30264752.
[34]. Prasad TS, Nair AK, Sreela LS. Oral Lichen Planus-Clinical and Psychological Stress Profile-A Preliminary Study.
[35]. Nosratzehi T. Oral Lichen Planus: an Overview of Potential Risk Factors, Biomarkers and Treatments. Asian Pac J Cancer Prev. 2018 May 26;19(5):1161-1167. Pubmed PMID: 29801395.
[36]. Ozbagcivan O, Akarsu S, Semiz F, Fetil E. Comparison of serum lipid parameters between patients with classic cutaneous lichen planus and oral lichen planus. Clin Oral Investig. 2020 Feb;24(2):719-725. Pubmed PMID: 31129877.
[37]. Palati S, Ramani P, Shrelin HJ, Sukumaran G, Ramasubramanian A, Don KR, Jayaraj G, Santhanam A. 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.
[38]. 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.
[39]. J PC, Marimuthu T, C K, 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 Aug;20(4):531-534. Pubmed PMID: 29624863.
[40]. 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.
[41]. Priyanka S, Kaarthikeyan G, Nadathur JD, Mohanraj A, Kavarthapu A. Detection of cytomegalovirus, Epstein-Barr virus, and Torque Teno virus in subgingival and atheromatous plaques of cardiac patients with chronic periodontitis. J Indian Soc Periodontol. 2017 Nov-Dec;21(6):456-460. Pubmed PMID: 29551863.
[42]. Rakhshan A, Toossi P, Amani M, Dadkhahfar S, Hamidi AB. Different distribution patterns of plasmacytoid dendritic cells in discoid lupus erythematosus and lichen planopilaris demonstrated by CD123 immunostaining. An Bras Dermatol. 2020 May-Jun;95(3):307-313. Pubmed PMID: 32299739.
[43]. Ramadurai N, Gurunathan D, Samuel AV, Subramanian E, Rodrigues SJL. Effectiveness of 2% Articaine as an anesthetic agent in children: randomized controlled trial. Clin Oral Investig. 2019 Sep;23(9):3543-3550. Pubmed PMID: 30552590.
[44]. 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.
[45]. R H, Ramani P, Ramanathan A, R JM, S G, Ramasubramanian A, K M. 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.
[46]. SA Anandan S, Prasanthi G. Oral Lichen Planus. Lichen Planus. 2013:97– 97.
[47]. Sachdev R, et al. Demographic Prevalence of Oral Lichen Planus in Males: A Retrospective Study. Acta Scientific Dental Sciences. 2019;3(8):111–114. [48]. 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.
[49]. Samuel SR, Acharya S, Rao JC. School Interventions-based Prevention of Early-Childhood Caries among 3-5-year-old children from very low socioeconomic status: Two-year randomized trial. J Public Health Dent. 2020 Jan;80(1):51-60. Pubmed PMID: 31710096.
[50]. Scully C, Carrozzo M. Oral mucosal disease: Lichen planus. Br J Oral Maxillofac Surg. 2008 Jan;46(1):15-21. Pubmed PMID: 17822813.
[51]. Kumar A, Sherlin HJ, Ramani P, Natesan A, Premkumar P. Expression of CD 68, CD 45 and human leukocyte antigen-DR in central and peripheral giant cell granuloma, giant cell tumor of long bones, and tuberculous granuloma: An immunohistochemical study. Indian J Dent Res. 2015 May- Jun;26(3):295-303. Pubmed PMID: 26275199.
[52]. Hema Shree K, Ramani P, Sherlin H, Sukumaran G, Jeyaraj G, Don KR, Santhanam A, Ramasubramanian A, Sundar R. Saliva as a Diagnostic Tool in Oral Squamous Cell Carcinoma - a Systematic Review with Meta Analysis. Pathol Oncol Res. 2019 Apr;25(2):447-453. Pubmed PMID: 30712193.
[53]. Sitharthan R, Sundarabalan CK, Devabalaji KR, Yuvaraj T, Mohamed Imran A. Automated power management strategy for wind power generation system using pitch angle controller. Measurement and Control. 2019 Mar;52(3-4):169-82.
[54]. Sivaramakrishnan SM, Ramani P. Study on the Prevalence of Eruption Status of Third Molars in South Indian Population [Internet]. Vol. 07, Biology and Medicine. 2015.
[55]. 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. Pubmed PMID: 30714209.
[56]. 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. Pubmed PMID: 30714209.
[57]. Sridharan G, Ramani P, Patankar S. Serum metabolomics in oral leukoplakia and oral squamous cell carcinoma. J Cancer Res Ther. 2017 Jul- Sep;13(3):556-561. Pubmed PMID: 28862226.
[58]. Swathy S, Gheena S, Varsha SL. Prevalence of pulp stones in patients with history of cardiac diseases. Res J Pharm Technol. 2015;8(12):1625-8.
[59]. Thangaraj SV, Shyamsundar V, Krishnamurthy A, Ramani P, Ganesan K, Muthuswami M, Ramshankar V. Molecular Portrait of Oral Tongue Squamous Cell Carcinoma Shown by Integrative Meta-Analysis of Expression Profiles with Validations. 2016 Jun 9;11(6):e0156582. Pubmed PMID: 27280700.
[60]. Thorn JJ, Holmstrup P, Rindum J, Pindborg JJ. Course of various clinical forms of oral lichen planus. A prospective follow-up study of 611 patients. J Oral Pathol. 1988 May;17(5):213-8. Pubmed PMID: 3144584.
[61]. Varghese SS, George GB, Sarojini SB, Vinod S, Mathew P, Mathew DG, Sebastian J, George A. Epidemiology of Oral Lichen Planus in a Cohort of South Indian Population: A Retrospective Study. J Cancer Prev. 2016 Mar;21(1):55-9. Pubmed PMID: 27051650.
[62]. Venu H, Raju VD, Subramani L. Combined effect of influence of nano additives, combustion chamber geometry and injection timing in a DI diesel engine fuelled with ternary (diesel-biodiesel-ethanol) blends. Energy. 2019 May 1;174:386-406.
[63]. 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.
[64]. Viveka TS, Shyamsundar V, Krishnamurthy A, Ramani P, Ramshankar V. p53 Expression Helps Identify High Risk Oral Tongue Pre- malignant Lesions and Correlates with Patterns of Invasive Tumour Front and Tumour Depth in Oral Tongue Squamous Cell Carcinoma Cases. Asian Pac J Cancer Prev. 2016;17(1):189-95. Pubmed PMID: 26838208.
[65]. Wang F, Tan YQ, Zhang J, Zhou G. Insulin-like growth factor 1 exhibits the pro-autophagic and anti-apoptotic activity on T cells of oral lichen planus. Int J Biol Macromol. 2019 Jul 15;133:640-646. Pubmed PMID: 31026523.
[66]. Wang Y, Zhang Y, Guo Y, Lu J, Veeraraghavan VP, Mohan SK, Wang C, Yu X. Synthesis of Zinc oxide nanoparticles from Marsdenia tenacissima inhibits the cell proliferation and induces apoptosis in laryngeal cancer cells (Hep-2). J Photochem Photobiol B. 2019 Dec;201:111624. Pubmed PMID: 31722283.
[67]. Jayaraj G, Sherlin HJ, Ramani P, Premkumar P, Natesan A. Stromal myofibroblasts in oral squamous cell carcinoma and potentially malignant disorders. Indian J Cancer. 2015 Jan-Mar;52(1):87-92. Pubmed PMID: 26837985.
[68]. Wu F, Zhu J, Li G, Wang J, Veeraraghavan VP, Krishna Mohan S, Zhang Q. 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.
