Does human papillomavirus modify the risk of oropharyngeal cancer related to smoking and alcohol drinking? A systematic review and meta‐analysis

Abstract

Objective To synthesize evidence for interactions of traditional oropharyngeal squamous cell carcinoma (OPSCC) risk factors—tobacco smoking and alcohol drinking—with human papillomavirus (HPV). Data Sources MEDLINE, Embase, Cochrane Database of Systematic Reviews, ProQuest, and Global Health were searched with no restrictions on language or publication date. Methods All case–control studies assessing interactions between these factors in OPSCC were considered. Quality was assessed using the Newcastle‐Ottawa Scale for case–control studies. The main outcome was the OR for developing OPSCC for the following interactions: (1) HPV and smoking, (2) HPV and alcohol drinking, and (3) HPV, alcohol drinking, and smoking. Interactions were assessed from stratified analysis (by HPV status) and/or joint effect analysis (synergy index and multiplicative index). Results The search provided 3084 relevant studies, of which 9 were included. In the stratified analysis, the OR of developing OPSCC among smokers with HPV was less than that among smokers without HPV. A similar pattern was observed for alcohol drinking. This effect persisted among smokers and heavy alcohol drinkers with HPV compared with those without HPV. Joint effect analysis on the additive scale showed sub‐additive antagonistic interactions between HPV and smoking, and between HPV and alcohol. On the multiplicative scale, sub‐multiplicative interactions were found between HPV and smoking, and HPV and alcohol. Conclusions This meta‐analysis suggests a negative directed interaction of HPV and smoking; and HPV and heavy alcohol drinking in the development of primary OPSCC on stratified analysis and joint effect analysis. Level of Evidence 3A.

A SEER-based analysis of trends in HPV-associated oropharyngeal squamous cell carcinoma

“…First, we conducted a retrospective analysis of data from the SEER database, noting the absence of smoking and alcohol history, as well as molecular characterization. A systematic review and meta-analysis indicated a negative interaction between smoking and alcohol in the development of HPV (+) OPSCC [ 21 ]. In a previous study involving 157 OPSCC patients, gene alterations associated with oxidative stress were observed more frequently in HPV-positive cases, whereas those related to the p53 signaling and cell cycle control pathways were more prevalent in HPV-negative cases [ 22 ].…”

The Impact of Alcohol Consumption and Oral Microbiota on Upper Aerodigestive Tract Carcinomas: A Pilot Study

“…In particular, the present retrospective study strongly focused at the level of (i) the EtG hair values and (ii) the oral occurrence of Streptococcus mitis , Candida albicans , Candida glabrata , and Neisseria subflava . In order to unveil the risk of alcohol consumption at the onset of UADT carcinoma, previous studies were mainly based on interviews that aimed to discover alcohol drinking habits without measuring the real, long-lasting alcohol consumption [ 69 , 70 , 71 ].…”

The Influence of the Oral Microbiome on Oral Cancer: A Literature Review and a New Approach

“…All the above-mentioned factors are controllable: it is a matter of lifestyle choice in the case of the first two and being vaccinated in the case of the latter. It should be noted that the meta-analysis by Arif et al implied a negative synergy between HPV infection and smoking tobacco as well as HPV infection and high alcohol consumption, increasing the risk of primary OC development in a tiered and cumulative effect analysis [47]. Other risk indicators include Epstein-Barr virus (EBV, for nasopharyngeal carcinoma) [48,49], Candida albicans [50,51], a diet low in vitamin A and carotenoids, inadequate dental hygiene, including the regularity of tooth brushing, and chronic mouth trauma [52].…”