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Bringing Light to Dental Trauma and Oral Cavity Cancer—Reply

Bringing Light to Dental Trauma and Oral Cavity Cancer—Reply In Reply The focus of much current research has been the role of human papilloma virus (HPV) in oropharyngeal cancer, especially as a separate risk factor, or even disease process, compared with smoking-related cancer of the oropharynx. Our data1 support previous research showing that oral cavity cancer is slightly more prevalent than oropharyngeal cancer, and that this disparity is largely due to increased numbers of nonsmokers, especially women, who develop oral cavity cancers. In our series, oral cavity cancers occurred in lifelong nonsmokers in 87 patients compared with only 48 patients with oropharyngeal cancer. Mentioning HPV in the title of our article1 was partly to bring attention to the fact that despite the significant research focus on HPV oropharyngeal cancers, nonsmokers are much more likely to develop oral cavity cancers, and a risk factor more important than HPV may be as yet be unrecognized or underinvestigated. In our data, 66% of oral cavity cancers occurred on the lateral tongue in nonsmokers lacking other major risk factors. In smokers and ex-smokers, these tumors also occurred on the lateral tongue in over one-third of cases. As Frustino et al rightly have pointed out, our article only makes an association, rather than proves causation, between dental trauma and oral cavity cancer. However, this is a large cohort of patients with a significant difference in location of oral cavity cancer development by smoking status. Also, the data were initially collected by a number of physicians who were not explicitly examining or making notes regarding the status of teeth in close proximity to the site of the tumor. As the clinic became more aware of this potential risk factor, it became apparent that a significant proportion of patients who were presenting with oral cavity cancer, especially nonsmokers, had lesions occurring adjacent to sharp or medialized teeth, large and rough dental work, or at sites of denture rubbing. A number of patients subsequently have had oral cavity premalignant changes resolve with repair of irritating teeth. These factors have led to our assertion that dental trauma is a potential carcinogen in the oral cavity that should be corrected for treating both premalignant and malignant conditions. Other conditions of the oral cavity, such as lichen planus and proliferative verrucous leukoplakia, were not commented on in the article1 but were also not mentioned commonly in the patient notes examined, and we think these are likely to be a factor in only a small subset of patients. Human papilloma virus is known to implant at sites of chronic trauma and thus may be a causative or potentiating factor for dental trauma carcinogenesis. However, only 3 of our nonsmoking, nondrinking patients with oral cavity cancer were p16-positive. We are currently collecting data prospectively to examine for HPV genetic changes in new patients to our clinics. Even if HPV is found to be involved in these cancers, it may be a synergistic effect with dental trauma. Back to top Article Information Corresponding Author: Christopher F. L. Perry, MBBS, DTM&H, FRACS, Watkins Medical Centre, 225 Wickham Terrace, Brisbane, Queensland, Australia 4000 (admin@brisbaneent.com.au). Conflict of Interest Disclosures: None reported. References 1. Perry BJ, Zammit AP, Lewandowski AW, et al. Sites of origin of oral cavity cancer in nonsmokers vs smokers: possible evidence of dental trauma carcinogenesis and its importance compared with human papillomavirus. JAMA Otolaryngol Head Neck Surg. 2015;141(1):5-11. doi:10.1001/jamaoto.2014.2620.PubMedGoogle ScholarCrossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Otolaryngology - Head & Neck Surgery American Medical Association

Bringing Light to Dental Trauma and Oral Cavity Cancer—Reply

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References (6)

Publisher
American Medical Association
Copyright
Copyright © 2015 American Medical Association. All Rights Reserved.
ISSN
2168-6181
eISSN
2168-619X
DOI
10.1001/jamaoto.2015.2410
Publisher site
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Abstract

In Reply The focus of much current research has been the role of human papilloma virus (HPV) in oropharyngeal cancer, especially as a separate risk factor, or even disease process, compared with smoking-related cancer of the oropharynx. Our data1 support previous research showing that oral cavity cancer is slightly more prevalent than oropharyngeal cancer, and that this disparity is largely due to increased numbers of nonsmokers, especially women, who develop oral cavity cancers. In our series, oral cavity cancers occurred in lifelong nonsmokers in 87 patients compared with only 48 patients with oropharyngeal cancer. Mentioning HPV in the title of our article1 was partly to bring attention to the fact that despite the significant research focus on HPV oropharyngeal cancers, nonsmokers are much more likely to develop oral cavity cancers, and a risk factor more important than HPV may be as yet be unrecognized or underinvestigated. In our data, 66% of oral cavity cancers occurred on the lateral tongue in nonsmokers lacking other major risk factors. In smokers and ex-smokers, these tumors also occurred on the lateral tongue in over one-third of cases. As Frustino et al rightly have pointed out, our article only makes an association, rather than proves causation, between dental trauma and oral cavity cancer. However, this is a large cohort of patients with a significant difference in location of oral cavity cancer development by smoking status. Also, the data were initially collected by a number of physicians who were not explicitly examining or making notes regarding the status of teeth in close proximity to the site of the tumor. As the clinic became more aware of this potential risk factor, it became apparent that a significant proportion of patients who were presenting with oral cavity cancer, especially nonsmokers, had lesions occurring adjacent to sharp or medialized teeth, large and rough dental work, or at sites of denture rubbing. A number of patients subsequently have had oral cavity premalignant changes resolve with repair of irritating teeth. These factors have led to our assertion that dental trauma is a potential carcinogen in the oral cavity that should be corrected for treating both premalignant and malignant conditions. Other conditions of the oral cavity, such as lichen planus and proliferative verrucous leukoplakia, were not commented on in the article1 but were also not mentioned commonly in the patient notes examined, and we think these are likely to be a factor in only a small subset of patients. Human papilloma virus is known to implant at sites of chronic trauma and thus may be a causative or potentiating factor for dental trauma carcinogenesis. However, only 3 of our nonsmoking, nondrinking patients with oral cavity cancer were p16-positive. We are currently collecting data prospectively to examine for HPV genetic changes in new patients to our clinics. Even if HPV is found to be involved in these cancers, it may be a synergistic effect with dental trauma. Back to top Article Information Corresponding Author: Christopher F. L. Perry, MBBS, DTM&H, FRACS, Watkins Medical Centre, 225 Wickham Terrace, Brisbane, Queensland, Australia 4000 (admin@brisbaneent.com.au). Conflict of Interest Disclosures: None reported. References 1. Perry BJ, Zammit AP, Lewandowski AW, et al. Sites of origin of oral cavity cancer in nonsmokers vs smokers: possible evidence of dental trauma carcinogenesis and its importance compared with human papillomavirus. JAMA Otolaryngol Head Neck Surg. 2015;141(1):5-11. doi:10.1001/jamaoto.2014.2620.PubMedGoogle ScholarCrossref

Journal

JAMA Otolaryngology - Head & Neck Surgery – American Medical Association

Published: Nov 1, 2015

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