Prevalence of Alpha, Beta, and Gamma Human Papillomaviruses in Patients With Head and Neck Cancer and Noncancer Controls and Relation to Behavioral Factors.

BACKGROUND: Human papillomaviruses (HPVs) cause head and neck cancer (HNC), which is increasing in incidence in developed countries. We investigated the prevalence of alpha (α), beta (ß), and gamma (γ) HPVs among HNC cases and controls, and their relationship with sociodemographic, behavioral, and oral health factors. METHODS: We obtained oral rinse and brush samples from incident HNC cases (n = 369) and hospital-based controls (n = 439) and tumor samples for a subsample of cases (n = 121). We genotyped samples using polymerase chain reaction with PGMY09-PGMY11 primers and linear array for α-HPV and type-specific multiplex genotyping assay for ß-HPV and γ-HPV. Sociodemographic and behavioral data were obtained from interviews. RESULTS: The prevalence of α-, ß-, and γ-HPV among controls was 14%, 56%, and 24%, respectively, whereas prevalence among cases was 42%, 50%, and 33%, respectively. Prevalence of α- and γ-HPV, but not ß-HPV, increased with increase in sexual activity, smoking, and drinking habits. No HPV genus was associated with oral health. Tumor samples included HPV genotypes exclusively from the α-genus, mostly HPV-16, in 80% of cases. CONCLUSIONS: The distribution of α- and γ-HPV, but not ß-HPV, seems to vary based on sociodemographic and behavioral characteristics. We did not observe the presence of cutaneous HPV in tumor tissues.

Immunosuppression and cancer risk in kidney transplant recipients: A retrospective cohort study.

We assessed whether contemporary immunosuppression agents were associated with cancer among kidney transplant recipients (KTR), and if this association varied by age and sex. We studied a retrospective province-wide cohort of primary KTR (1997-2016). Employing multivariable Cox models, we estimated associations of cumulative doses of prednisone, mycophenolate and tacrolimus administered over the past 10 years, lagged by 2 years, with the incidence of primary malignant neoplasms (PMN). We assessed interactions with age and sex. To assess the impact of exposure recency, we used weighted cumulative exposure (WCE) modeling. Among 1064 KTR, 108 (10.2%) developed PMN over median follow-up of 73 months (interquartile range: 32-120). Adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) of 0.96 (0.64-1.43), 1.34 (0.96-1.86), and 1.06 (0.88-1.29) were estimated for cumulative daily doses of prednisone (5 mg), mycophenolate (1000 mg), and tacrolimus (2 mg) administered continuously over the past 10 years, respectively. PMN risk associated with cumulative tacrolimus exposure was modified by age (interaction p = .035) and was more pronounced in 15-year and 30-year-old KTR (aHRs of 1.57 [1.08-2.28] and 1.31 [1.03-1.66], respectively) in comparison to older KTR. PMN risk increase associated with higher cumulative mycophenolate dose was more pronounced in females (aHR = 1.86 [1.15-3.00]) than in males (aHR = 1.16 [0.74-1.81]; interaction p = .131). WCE analyses suggested increased PMN risk the higher the mycophenolate doses taken 5-10 years ago. A trend toward increased PMN risk with long-term mycophenolate exposure, particularly in females, and more pronounced risk with long-term tacrolimus exposure in younger KTR, identify opportunities for tailored immunosuppression to mitigate cancer risk.

Neighbourhood social deprivation and risk of prostate cancer.

BACKGROUND: Striking geographic variations in prostate cancer incidence suggest an aetiological role for spatially-distributed factors. We assessed whether neighbourhood social deprivation, which can reflect limited social contacts, unfavourable lifestyle and environmental exposures, is associated with prostate cancer risk. METHODS: In 2005-2012, we recruited 1931 incident prostate cancer cases and 1994 controls in a case-control study in Montreal, Canada. Lifetime residential addresses were linked to an area-based social deprivation index around recruitment (2006) and about 10 years earlier (1996). Logistic regression estimated adjusted odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Men residing in areas characterised by greater social deprivation had elevated prostate cancer risks (ORs of 1.54 and 1.60 for recent and past exposures, respectively; highest vs lowest quintiles), independently from area- and individual-level confounders and screening patterns. The increase in risk with recent high social deprivation was particularly elevated for high-grade prostate cancer at diagnosis (OR 1.87, 95% CI 1.32-2.64). Associations were more pronounced for neighbourhoods with higher proportions of separated/divorced or widowed individuals in the past, and with higher percentages of residents living alone recently. CONCLUSIONS: These novel findings, suggesting that neighbourhood-level social deprivation increases the risk of prostate cancer, point out to potential targeted public health interventions.

Association between the second- and fourth-digit ratio and oral squamous cell carcinoma.

OBJECTIVES: Using an established proxy measure of intra-utero testosterone and estrogen levels-the ratio of second- and fourth-digit lengths-we estimated its association with the oral cancer risk among a population from Southern India. MATERIAL AND METHODS: In a hospital-based case-control study, incident oral cancer cases (N = 350) and non-cancer controls (N = 371), frequency-matched by age and sex, were recruited from two major referral hospitals in Kerala, India. Structured interviews collected information on several domains of exposure via detailed life course questionnaires. Digit lengths were measured using a ruler in a standardized manner. Unconditional logistic regression was performed to estimate the odds ratios and 95% confidence intervals. RESULTS: Second- and fourth-digit ratio lower than 1, which indicates relatively higher intra-utero level of testosterone and lower intra-utero level of estrogen, was associated with higher oral cancer risk (OR = 1.60, 95% CI: 1.02-2.52), after accounting for several confounders. CONCLUSION: Our findings suggest that intra-utero hormonal levels measured by second- and fourth-digit ratio are associated with oral cancer risk. Further studies in different population should confirm these results.

In Vitro Toxicity Evaluation of Carrageenan on Cells and Tissues of the Oral Cavity.

Carrageenan is a highly potent anti-human papillomavirus (HPV) agent with the potential for formulation as a mouthwash against oral HPV infection. However, its toxic effect on tissues of the oral cavity is currently unknown. This study aims to evaluate the safety of carrageenan on human cells and tissues of the oral cavity. Human salivary gland cells and reconstructed human oral epithelium (RHOE) were used for this in vitro study. The cells were subjected to 0.005-100 µg/mL of carrageenan for 4, 12, and 24 h in quadruplicate. RHOE were exposed to 100 µg/mL of carrageenan for 24 h in triplicate and stained with hematoxylin/eosin for histological analyses. All experiments had saline and 1% sodium dodecyl sulphate (SDS) as negative and positive controls, respectively. Carrageenan tissue toxicity was evaluated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to quantify cell viability. Tissue toxicity was further evaluated histologically by an oral pathologist to assess morphological changes. Our data showed that carrageenan did not significantly decrease cell and tissue viability when compared to the positive control. The histological evaluation of the RHOE also showed no loss of viability of the carrageenan-treated sample compared to untreated tissue. In contrast, 1% SDS-treated RHOE showed extensive tissue destruction. Our experiments suggest that carrageenan is safe for use in the oral cavity.

Association between periodontitis and severity of COVID-19 infection: A case-control study.

AIM: COVID-19 is associated with an exacerbated inflammatory response that can result in fatal outcomes. Systemic inflammation is also a main characteristic of periodontitis. Therefore, we investigated the association of periodontitis with COVID-19 complications. MATERIALS AND METHODS: A case-control study was performed using the national electronic health records of the State of Qatar between February and July 2020. Cases were defined as patients who suffered COVID-19 complications (death, ICU admissions or assisted ventilation), and controls were COVID-19 patients discharged without major complications. Periodontal conditions were assessed using dental radiographs from the same database. Associations between periodontitis and COVID 19 complications were analysed using logistic regression models adjusted for demographic, medical and behaviour factors. RESULTS: In total, 568 patients were included. After adjusting for potential confounders, periodontitis was associated with COVID-19 complication including death (OR = 8.81, 95% CI 1.00-77.7), ICU admission (OR = 3.54, 95% CI 1.39-9.05) and need for assisted ventilation (OR = 4.57, 95% CI 1.19-17.4). Similarly, blood levels of white blood cells, D-dimer and C Reactive Protein were significantly higher in COVID-19 patients with periodontitis. CONCLUSION: Periodontitis was associated with higher risk of ICU admission, need for assisted ventilation and death of COVID-19 patients, and with increased blood levels of biomarkers linked to worse disease outcomes.

HIV Modifies the Effect of Tobacco Smoking on Oral Human Papillomavirus Infection.

BACKGROUND: People living with HIV (PLWH) are more likely to smoke and harbor oral human papillomavirus (HPV) infections, putting them at higher risk for head and neck cancer. We investigated effects of HIV and smoking on oral HPV risk. METHODS: Consecutive PLWH (n = 169) and at-risk HIV-negative individuals (n = 126) were recruited from 2 US health centers. Smoking history was collected using questionnaires. Participants provided oral rinse samples for HPV genotyping. We used multivariable logistic regression models with interaction terms for HIV to test for smoking effect on oral HPV. RESULTS: PLWH were more likely to harbor oral HPV than HIV-negative individuals, including α (39% vs 28%), ß (73% vs 63%), and γ-types (33% vs 20%). HIV infection positively modified the association between smoking and high-risk oral HPV: odds ratios for smoking 3.46 (95% confidence interval [CI], 1.01-11.94) and 1.59 (95% CI, .32-8.73) among PLWH and HIV-negative individuals, respectively, and relative excess risk due to interaction (RERI) 3.34 (95% CI, -1.51 to 8.18). RERI for HPV 16 was 1.79 (95% CI, -2.57 to 6.16) and 2.78 for ß1-HPV (95% CI, -.08 to 5.65). CONCLUSION: Results show tobacco smoking as a risk factor for oral HPV among PLWH.

Oscillating-rotating electric toothbrushes may have a better effect on gingivitis and plaque control than sonic and manual toothbrushes in adults.

ARTICLE TITLE AND BIBLIOGRAPHIC INFORMATION: Grender J, Adam R, Zou Y. The effects of oscillating-rotating electric toothbrushes on plaque and gingival health: A meta-analysis. Am J Dent. 2020 Feb;33(1):3-11. PMID: 32,056,408. SOURCE OF FUNDING: Industry (Procter & Gamble Company). TYPE OF STUDY/DESIGN: Systematic review with meta-analysis of data.

Latency of tobacco smoking for head and neck cancer among HPV-positive and HPV-negative individuals.

Human papillomavirus (HPV) infection and tobacco smoking are well-known risk factors for head and neck cancers (HNC). Although an effect modification between oral HPV infection and tobacco smoking may exist, evidence is lacking on how they interact temporally. We investigated the latency and life course effects of tobacco smoking on risk of HNC among HPV-positive (HPV+ve ) and negative (HPV-ve ) individuals. We used data from 631 ever-smoker participants of a hospital-based case-control study conducted in four major hospitals in Montréal, Canada. Cases (n = 320), incident, histologically confirmed, primary squamous cell carcinomas, were frequency-matched to controls (n = 311) by age and sex. Sociodemographic and behavioral factors (e.g., tobacco and alcohol use and sexual history) were collected using a structured interview applying a life grid technique. Oral exfoliated cells were used for HPV DNA detection and genotyping. Latency effects were estimated flexibly using a Bayesian relevant exposure model and further extended with a life course approach. Retrospective smoking trajectories for HPV+ve cases and controls had similar shapes. Exposure to tobacco smoking even 40 years before diagnosis was associated with an increased HNC risk among both HPV+ve and HPV-ve participants. The effect of smoking before the start of sexual activity compared to afterwards was higher among HPV+ve individuals. This pattern of association was less profound among HPV-ve participants. Temporal interactions may exists between oral HPV infection and life course smoking trajectories in relation to HNC risk.

Stressed-Out Oral Immunity: A Gateway From Socioeconomic Adversity to Periodontal Disease.

OBJECTIVE: It has been suggested that adverse socioeconomic conditions "get under the skin" by eliciting a stress response that can trigger periodontal inflammation. We aimed to a) estimate the extent to which socioeconomic position (SEP) is associated with periodontal disease (PD) and proinflammatory oral immunity, and b) determine the contribution of psychosocial stress and stress hormones to these relationships. METHODS: In this cross-sectional study (n = 102), participants (20-59 years old) completed financial and perceived stress questionnaires and underwent full-mouth periodontal examinations. SEP was characterized by annual household income and educational attainment. Cortisol, a biological correlate of chronic stress, was assessed in hair samples. Oral immunity was characterized by assessing oral inflammatory load and proinflammatory oral neutrophil function. Blockwise Poisson and logistic regression models were applied. RESULTS: Compared with lower SEP, individuals in the middle- and higher-income categories had a significantly lower probability of PD (incidence rate ratio [IRR] = 0.5 [confidence interval {CI} = 0.3-0.7] and IRR = 0.4 [95% CI = 0.2-0.7]) and oral inflammatory load (IRR = 0.6 [95% CI = 0.3-0.8] and IRR = 0.5 [95% CI = 0.3-0.7]) and were less likely to have a proinflammatory oral immune function (odds ratio [OR] = 0.1 [95% CI = 0.0-0.7] and OR = 0.1 [95% CI = 0.0-0.9]). PD and oral immune parameters were significantly associated with financial stress and cortisol. Adjusting for financial stress and cortisol partially attenuated the socioeconomic differences in PD to IRR = 0.7 (95% CI = 0.5-0.8) and IRR = 0.6 (95% CI = 0.5-0.7) for the middle- and higher-income categories, respectively. Similar results were observed for proinflammatory immunity (OR = 0.2 [95% CI = 0.0-1.8] and OR = 0.3 [95% CI = 0.0-2.3]). CONCLUSION: These findings suggest that psychosocial stress may contribute to a proinflammatory immunity that is implicated in PD pathobiology and provide insight into social-to-biological processes in oral health.

Maternal Mental Disorders before Delivery and the Risk of Dental Caries in Children.

Prevention of childhood caries is an ongoing public health challenge, but the possibility of an association with maternal mental disorders has received limited attention. We estimated the extent to which maternal mental disorders are associated with an increased risk of hospitalization due to dental caries. We conducted a longitudinal cohort study of 790,758 infants born in Quebec, Canada between 2006 and 2016, with follow-up extending to 2018. We identified women with mental disorders before or during pregnancy and computed the incidence of dental caries in their children. We estimated HR and 95% CI for the association of maternal mental disorders with the risk of dental caries, adjusted for personal characteristics. Infants of women with mental disorders before or during pregnancy had a higher incidence of dental caries compared to children of women with no mental disorder (56.1 vs. 27.2 per 10,000 person-years). Maternal stress and anxiety disorders (HR = 1.73; 95% CI 1.60-1.86), depression (HR = 1.81; 95% CI 1.60-2.03), schizophrenia and delusional disorders (HR = 1.69; 95% CI 1.29-2.22), and personality disorders (HR = 1.89; 95% CI 1.70-2.11) were associated with the risk of dental caries. The associations were present throughout childhood, including after 7 years (HR = 1.65; 95% CI 1.38-1.96). Maternal mental disorders were associated with caries of the enamel, dentin, and cementum and caries that reached the dental pulp. Maternal mental disorders before or during pregnancy, especially stress and anxiety, depression, schizophrenia, and personality disorders, are associated with the risk of childhood caries. Women with a history of mental disorders may benefit from enhanced strategies for prevention of dental caries in their children.

Oral Health Implications of Cannabis Smoking: A Rapid Evidence Review.

OBJECTIVES: To summarize evidence relating cannabis smoking and oral disease and highlight any potential influence of cannabis smoking on clinical care and dental public health. METHODS: Using rapid evidence review, a librarian facilitated a systematic search of 5 electronic databases in August and September 2018 and updated it in March 2019, yielding 581 publications. Two researchers screened the documents using pre-established inclusion criteria: article was based on primary or secondary data; cannabis smoking was an exposure; at least 1 cannabis-related oral health outcome was reported; participants were humans; and the article was available in English or French. Data from retained articles were analyzed for themes without meta-analysis. RESULTS: We synthesized and summarized 23 articles in 2 broad categories: cannabis and oral disease; and cannabis, clinical care and dental public health. Current evidence shows that smoking cannabis is harmful to the health of the periodontium. The association between smoking cannabis and other oral disease (dental caries, soft tissue lesions and oral cancers) is sparse and inconsistent, although studies suggest that cannabis smoking is an underlying risk factor. Cannabis smoking can lead to an altered mental state that can delay dental treatment of the patient. Further, interactions between smoked cannabis and adrenaline-containing local anesthetics can result in life-threatening consequences. CONCLUSIONS: Cannabis smoking is harmful to the periodontium. Further research is needed to fully understand how cannabis smoking affects oral disease and how dental professionals should integrate this knowledge into clinical care and dental public health.

Genetic variants in CYP and GST genes, smoking and risk for head and neck cancers: a gene-environment interaction hospital-based case-control study among Canadian Caucasians.

The evidence for genetic polymorphisms in genes encoding cytochrome P450 (CYP) and glutathione S-transferase (GST) enzymes as risk factors for squamous cell carcinomas of the head and neck (SCCHN) in Caucasians is conflicting. Furthermore, the interactive effects with smoking have not been documented. We estimated the effects of five single nucleotide polymorphisms and two copy number variants associated with CYP and GST genes, as well as their interactive effects with smoking, on SCCHN risk among Caucasians from a case-control study conducted in Montreal, Canada. The study involved 389 incident SCCHN cases and 429 controls, frequency-matched by age and sex, recruited from four main hospitals between 2005 and 2013. Life-course-based interviews collected information on tobacco smoking history and other risk behaviors. DNA was isolated from oral exfoliated cells and genotyped for genetic variants. Unconditional logistic regression models estimated odds ratios (OR) and 95% confidence intervals (CI) for main, joint effect, stratum-specific and interaction estimates among non-, moderate and heavy smokers. Carriers of GSTP1 105Val (versus non-carriers) had a lower risk of SCCHN (OR = 0.71, 95% CI: 0.53, 0.95), which was observed for heavy smokers (OR = 0.59, 95% CI: 0.36, 0.95) and non-smokers alike (OR = 0.49, 95% CI: 0.24, 0.98). The decreased risk associations were also conserved among human papillomavirus negative individuals. There was no evidence for statistical interaction with smoking on additive or multiplicative scales for any of the variants analyzed. Of CYP and GST polymorphisms detected in Canadian Caucasians, only GSTP1 105Val was associated with a decreased risk for SCCHN.

Shared social mechanisms underlying the risk of nine cancers: A life course study.

Identifying life periods during which social conditions have the highest impact on risk of common cancers in a population may help to reveal their underlying shared social mechanisms. We used the life course framework to estimate the extent to which life course SEP is associated with risk of nine cancers. In addition, we tested whether these associations conform to a critical period or cumulative life course model. Data were from a population-based case-control study of occupational exposures and cancer conducted in Montreal, Canada. Participants were males aged 35-70 years (n = 2,547) residing in the Montreal metropolitan area with primary, histologically confirmed cancers diagnosed between 1979 and 1985. Population controls (n = 512) were sampled from electoral lists. SEP was measured at three different periods of life based on respondent's report: during childhood, young adulthood and mid-life. We used a structured modeling approach using a series of unconditional logistic regressions to test which models best fit the data. Life course SEP increased the risk of all cancers. SEP in childhood was identified as a critical period for prostate and all gastrointestinal tract cancers except for esophagus cancer. In addition, the accumulation model best explained the data for melanoma and lung squamous cell carcinoma. Our findings suggest that childhood social circumstances are a common risk factor for several cancers among men; our results provide insights into the mechanisms involved in the etiology of nine cancers.

Socioeconomic inequalities in oral health-related quality of life in adolescents: a cohort study.

PURPOSE: Socioeconomic inequalities are recognized as a major problem with people in low socioeconomic groups having worse subjective oral health outcomes, including oral health-related quality of life (OHRQoL). However, only a few longitudinal studies assessed the impact of contextual and individual socioeconomic determinants in adolescents' OHRQoL. We estimate the impact of socioeconomic inequalities on adolescents' OHRQoL over a 2-year period. METHODS: This study followed up a random sample of 1134 12-year-old schoolchildren for 2 years in Brazil. OHRQoL was assessed by the Brazilian version of the Child Perceptions Questionnaire for 11- to 14-year-old Children (CPQ11-14) at baseline and follow-up. Participants were clinically examined for dental caries, gingival bleeding, and malocclusion. The schoolchildren's parents answered a questionnaire regarding socioeconomic status, social capital, and adolescents' use of dental service. Socioeconomic contextual variables were collected from official city publications. Multilevel linear regression models fitted the associations between socioeconomic factors and overall CPQ11-14 scores over time. RESULTS: A total of 747, 14-year-old adolescents were reassessed for OHRQoL (follow-up rate of 66%). Adolescents with lower mean income school's neighborhood (P < 0.05), household income (P < 0.05), and maternal schooling (P < 0.05) had higher overall CPQ11-14 scores. Female sex, attending a dentist by toothache, dental caries, and malocclusion were also associated with higher overall CPQ11-14 scores. CONCLUSIONS: Adolescents from low socioeconomic background reported worse OHRQoL at 2-year follow-up compared to those from high socioeconomic background. Actions toward health inequalities need to address socioeconomic factors in adolescence.

A Comprehensive Clinical Care Pathway for Microvascular Maxillofacial Reconstructive Surgery.

PURPOSE: Clinical care pathways (CCPs) for major surgical procedures are less developed. We describe the development of a comprehensive microvascular maxillofacial reconstruction CCP and evaluate the impact. MATERIALS AND METHODS: Our team developed a comprehensive CCP for patients undergoing microvascular free flap reconstruction for benign or malignant tumors. Patient data before (n = 48) and after (n = 47) implementation of the CCP were used to evaluate the impact. Bayesian negative binomial and logistic regression analyses were used to estimate the associations between the CCP and clinical outcomes (length of stay [LOS], readmission to the operating room, and readmission within 3 months of discharge). RESULTS: The average total hospital LOS was high in the pre-CCP group (16.9 days) compared with the post-CCP group (9.8 days). Being in the post-CCP group reduced the LOS in the intensive care unit and surgical ward and reduced the risk of readmission to the operating room. CONCLUSION: Our results underscore the importance of standardized evidence-based patient care through CCPs for complex patient populations.

Inconclusive Evidence Exists Regarding the Association Between Dental Caries and BMI in Children Under Age 18 Years.

ARTICLE TITLE AND BIBLIOGRAPHIC INFORMATION: Association between dental caries and BMI in children: a systematic review and meta-analysis. Chen D, Zhi Q, Zhou Y, Tao Y, Wu L, Lin H.Caries Res 2018;52:230-45. SOURCE OF FUNDING: None declared. TYPE OF STUDY/DESIGN: Systematic review with meta-analysis.

Aetiological heterogeneity of head and neck squamous cell carcinomas: the role of human papillomavirus infections, smoking and alcohol.

Tobacco and alcohol consumption are the main risk factors for head and neck squamous cell carcinoma (HNSCC). In addition, human papillomavirus (HPV) infection plays a causal role in oropharyngeal cancer (OPC), a subset of HNSCC. We assessed the independent effects of tobacco, alcohol and HPV infection on OPC risk in the head and neck cancer (HeNCe) Life study, a hospital-based case-control study of HNSCC with frequency-matched controls by age and sex from four Montreal hospitals. Interviewers collected information on socio-demographic and behavioural factors. We tested exfoliated oral cells for HPV DNA by polymerase chain reaction (PCR). We included only OPC cases (n = 188) and controls (n = 427) without missing values for HPV, smoking or alcohol. We examined associations by estimating odds ratios (ORs) and corresponding 95% confidence intervals (CI) using unconditional logistic regression. Smoking (OR = 1.90, 95% CI: 1.04-3.45) and alcohol (OR = 2.74, 95% CI: 1.45-5.15) were associated with an increased risk of OPC independent of HPV status. Positivity for HPV 16 among heavy smokers and heavy alcohol users was associated with a 30.4-fold (95% CI: 8.94-103.26) and 18.6-fold (95% CI: 5.75-60.13) elevation in risk of OPC relative to participants who were HPV negative, respectively. Moreover, the combined effect of heavy smoking and alcohol comsumption with HPV 16 infection substantially increased OPC risk (OR = 48.76, 95% CI: 15.83-150.17) and (OR = 50.60, 95% CI: 15.96-160.40), respectively. Our results support the independent roles of smoking, alcohol and HPV infection in OPC risk and a possible combined effect. Efforts should be made to tackle these major risk factors simultaneously.

Periodontal diseases and risk of oral cancer in Southern India: Results from the HeNCe Life study.

Some studies suggest that periodontal diseases increase the risk of oral cancer, but contradictory results also exist. Inadequate control of confounders, including life course exposures, may have influenced prior findings. We estimate the extent to which high levels of periodontal diseases, measured by gingival inflammation and recession, are associated with oral cancer risk using a comprehensive subset of potential confounders and applying a stringent adjustment approach. In a hospital-based case-control study, incident oral cancer cases (N = 350) were recruited from two major referral hospitals in Kerala, South India, from 2008 to 2012. Controls (N = 371), frequency-matched by age and sex, were recruited from clinics at the same hospitals. Structured interviews collected information on several domains of exposure via a detailed life course questionnaire. Periodontal diseases, as measured by gingival inflammation and gingival recession, were evaluated visually by qualified dentists following a detailed protocol. The relationship between periodontal diseases and oral cancer risk was assessed by unconditional logistic regression using a stringent empirical selection of potential confounders corresponding to a 1% change-in-estimates. Generalized gingival recession was significantly associated with oral cancer risk (Odds Ratio = 1.83, 95% Confidence Interval: 1.10-3.04). No significant association was observed between gingival inflammation and oral cancer. Our findings support the hypothesis that high levels of periodontal diseases increase the risk of oral cancer.