Muthusamy Mudiyayirakkani, Ramani Pratibha, Arumugam Paramasivam, Rudrapathy Parthiban, Kangusamy Boopathi, Veeraraghavan Vishnu Priya, Jayaraman Selvaraj, Kannan Balachander, Pandi Anitha
Department of Oral and Maxillofacial Pathology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, 162, Poonamallee High Road, Velappanchavadi, Chennai, Tamil Nadu, 600077, India.
Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, 162, Poonamallee High Road, Velappanchavadi, Chennai, Tamil Nadu, 600077, India.
BMC Oral Health. 2025 Jan 13;25(1):62. doi: 10.1186/s12903-024-05406-z.
Oral squamous cell carcinoma (OSCC) is one of the most prevalent oral cancers in the world. The major etiological factors are considered to be tobacco and alcohol. However, the etiological factors for non-habit associated oral squamous cell carcinoma (NHOSCC) remains an enigma. So we focused in assessing various etiological factors like genetic factor, microbial factor, dental factor and the biochemical factor of non-habit associated oral squamous cell carcinoma. The aim was to assess Harvey Rat Sarcoma Virus gene (HRAS) mutation, total bacterial count, Herpes Simplex Virus-1 (HSV-1), regressive changes of teeth, total antioxidant capacity and its association with NHOSCC.
A total of 564 (n = 564) patients with OSCC were included in the study. Out of 564 patients, 282 patients had NHOSCC and 282 patients had habit associated oral squamous cell carcinoma (HOSCC). The isolated DNA from the tissue was subjected to Sanger's sequencing analysis for mutation analysis of the HRAS gene. The isolated serum was subjected to HSV-1 ELISA analysis and TAC ELISA analysis. The dental cast used to analyze the presence of sharp teeth/ any other form of regressive changes of teeth.
Firstly, we found 3 novel pathogenic mutations c.16C > A/p.L6M (missense mutation), c.359 T > C/p.L120P (point mutation), c.382C > T/p.R128W (missense mutation) of HRAS gene in NHOSCC samples by genetic analysis. No significant difference was noted in the total bacterial count between the non-habit associated and habit associated oral squamous cell carcinoma (HOSCC). The binary logistic regression showed patients with HSV1 infection have 2.667 odds (2.667 OR, CI, 1.589- 4.484) of getting NHOSCC and it was found to be statistically significant (p < 0.001).The dental analysis revealed that patients with regressive changes have 4.432 odds (4.432 OR, CI, 2.807- 6.998) of getting NHOSCC and it was found to be statistically significant (p < 0.001). The biochemical analysis revealed patients with lower total antioxidant capacity have 0.671 odds (0.671 OR, CI, 0.621-0.725) of getting NHOSCC and was found to be statistically significant (p < 0.001). Our results suggest that the frequency of HRAS mutation in NHOSCC is high. HSV1, oxidative stress and regressive changes of teeth are associated with NHOSCC.
Our results suggest that the frequency of HRAS mutation in NHOSCC is high. HSV1, oxidative stress and regressive changes of teeth are associated with NHOSCC.
口腔鳞状细胞癌(OSCC)是世界上最常见的口腔癌之一。主要病因被认为是烟草和酒精。然而,非习惯相关口腔鳞状细胞癌(NHOSCC)的病因仍然是个谜。因此,我们专注于评估各种病因,如遗传因素、微生物因素、牙齿因素和非习惯相关口腔鳞状细胞癌的生化因素。目的是评估哈维鼠肉瘤病毒基因(HRAS)突变、总细菌计数、单纯疱疹病毒1型(HSV-1)、牙齿的退行性变化、总抗氧化能力及其与NHOSCC的关联。
本研究共纳入564例OSCC患者。在564例患者中,282例患有NHOSCC,282例患有习惯相关口腔鳞状细胞癌(HOSCC)。从组织中分离的DNA进行桑格测序分析,以检测HRAS基因的突变。分离的血清进行HSV-1 ELISA分析和总抗氧化能力(TAC)ELISA分析。用牙模分析尖锐牙齿的存在/牙齿的任何其他形式的退行性变化。
首先,通过基因分析,我们在NHOSCC样本中发现了HRAS基因的3种新的致病突变:c.16C>A/p.L6M(错义突变)、c.359T>C/p.L120P(点突变)、c.382C>T/p.R128W(错义突变)。非习惯相关和习惯相关口腔鳞状细胞癌(HOSCC)之间的总细菌计数没有显著差异。二元逻辑回归显示,HSV1感染患者患NHOSCC的几率为2.667(比值比2.667,置信区间1.589 - 4.484),差异有统计学意义(p<0.001)。牙齿分析显示,有退行性变化的患者患NHOSCC的几率为4.432(比值比4.432,置信区间2.807 - 6.998),差异有统计学意义(p<0.001)。生化分析显示,总抗氧化能力较低的患者患NHOSCC的几率为0.671(比值比0.671,置信区间0.621 - 0.725),差异有统计学意义(p<0.001)。我们的结果表明,NHOSCC中HRAS突变的频率很高。HSV1、氧化应激和牙齿的退行性变化与NHOSCC有关。
我们的结果表明,NHOSCC中HRAS突变的频率很高。HSV1、氧化应激和牙齿的退行性变化与NHOSCC有关。