Dataset Information

Number of teeth is associated with all-cause and disease-specific mortality

ABSTRACT:

Background

Tooth loss has been shown to correlate with multiple systemic comorbidities. However, the associations between the number of remaining natural teeth (NoT) and all-cause mortality have not been explored extensively. We aimed to investigate whether having fewer NoT imposes a higher risk in mortality. We tested such hypotheses using three groups of NoT (20–28,10–19, and 0–9), edentulism and without functional dentition (NoT < 19).

Methods

The National Health and Nutrition Examination Survey in the United States (NHANES) (1999–2014) conducted dental examinations and provided linkage of mortality data. NHANES participants aged 20 years and older, without missing information of dental examination, age, gender, race, education, income, body-mass-index, smoking, physical activities, and existing systemic conditions [hypertension, total cardiovascular disease, diabetes, and stroke (N = 33,071; death = 3978), or with femoral neck bone mineral density measurement (N = 13,131; death = 1091)] were analyzed. Cox proportional hazard survival analyses were used to investigate risks of all-cause, heart disease, diabetes and cancer mortality associated with NoT in 3 groups, edentulism, or without functional dentition.

Results

Participants having fewer number of teeth had higher all-cause and disease-specific mortality. In fully-adjusted models, participants with NoT0-9 had the highest hazard ratio (HR) for all-cause mortality [HR(95%CI) = 1.46(1.25–1.71); p < .001], mortality from heart diseases [HR(95%CI) = 1.92(1.33–2.77); p < .001], from diabetes [HR(95%CI) = 1.67(1.05–2.66); p = 0.03], or cancer-related mortality [HR(95%CI) = 1.80(1.34–2.43); p < .001]. Risks for all-cause mortality were also higher among the edentulous [HR(95%CI) = 1.35(1.17–1.57); p < .001] or those without functional dentition [HR(95%CI) = 1.34(1.17–1.55); p < .001].

Conclusions

Having fewer NoT were associated with higher risks for all-cause mortality. More research is needed to explore possible biological implications and validate our findings.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12903-021-01934-0.

SUBMITTER: Yu Y

PROVIDER: S-EPMC8574051 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:BackgroundDysfunctional mitochondria have an influence on inflammation and increased oxidative stress due to an excessive production of reactive oxygen species. The mitochondrial DNA copy number (mtDNA-CN) is a potential biomarker for mitochondrial dysfunction and has been associated with various diseases. However, results were partially contrasting which might have been caused by methodological difficulties to quantify mtDNA-CN.ObjectiveWe aimed to investigate whether mtDNA-CN is associated with peripheral arterial disease (PAD) as well as all-cause mortality and cardiovascular events during seven years of follow-up.MethodsA total of 236 male patients with PAD from the Cardiovascular Disease in Intermittent Claudication (CAVASIC) study were compared with 249 age- and diabetes-matched controls. MtDNA-CN was measured with a well-standardized plasmid-normalized quantitative PCR-based assay determining the ratio between mtDNA-CN and nuclear DNA.ResultsIndividuals in the lowest quartile of mtDNA-CN had a twofold increased risk for PAD which, however, was no longer significant after adjusting for leukocytes and platelets. About 67 of the 236 patients had already experienced a cardiovascular event at baseline and those in the lowest mtDNA-CN quartile had a 2.34-fold increased risk for these events (95% CI 1.08-5.13). During follow-up, 37 PAD patients died and 66 patients experienced a cardiovascular event. Patients in the lowest mtDNA-CN quartile had hazard ratios of 2.66 (95% CI 1.27-5.58) for all-cause-mortality and 1.82 (95% CI 1.02-3.27) for cardiovascular events compared with the combined quartile 2-4 (adjusted for age, smoking, CRP, diabetes, prevalent cardiovascular disease, leukocytes and platelets).ConclusionThis investigation supports the hypothesis of mitochondrial dysfunction in peripheral arterial disease and shows an association of low mtDNA-CNs with all-cause-mortality and prevalent and incident cardiovascular disease in PAD patients with intermittent claudication.

Project description:ImportanceHispanics are the largest minority group in the United States and face a disproportionate burden of risk factors for cardiovascular disease (CVD) and low socioeconomic position. However, Hispanics paradoxically experience lower all-cause mortality rates compared with their non-Hispanic white (NHW) counterparts. This phenomenon has been largely observed in Mexicans, and whether this holds true for other Hispanic subgroups or whether these favorable trends persist over time remains unknown.ObjectiveTo disaggregate a decade of national CVD mortality data for the 3 largest US Hispanic subgroups.Design, setting, and participantsDeaths from CVD for the 3 largest US Hispanic subgroups-Mexicans, Puerto Ricans, and Cubans-compared with NHWs were extracted from the US National Center for Health Statistics mortality records using the underlying cause of death based on coding from the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (I00-II69). Mortality data were evaluated from January 1, 2003, to December 31, 2012. Population estimates were calculated using linear interpolation from the 2000 and 2010 US Census reports. Data were analyzed from November 2015 to July 2016.Main outcomes and measuresMortality due to CVD.ResultsParticipants included 688 074 Mexican, 163 335 Puerto Rican, 130 397 Cuban, and 19 357 160 NHW individuals (49.0% men and 51.0% women; mean [SD] age, 75 [15] years). At the time of CVD death, Mexicans (age, 67 [18] years) and Puerto Ricans (age, 68 [17] years) were younger compared with NHWs (age, 76 [15] years). Mortality rates due to CVD decreased from a mean of 414.2 per 100 000 in 2003 to 303.3 per 100 000 in 2012. Estimated decreases in mortality rate for CVD from 2003 to 2012 ranged from 85 per 100 000 for all Hispanic women to 144 per 100 000 for Cuban men, but rate differences between groups vary substantially, with Puerto Ricans exhibiting similar mortality patterns to NHWs, and Mexicans experiencing lower mortality. Puerto Ricans experienced higher mortality rates for ischemic and hypertensive heart disease compared with other subgroups, whereas Mexicans experienced higher rates of cerebrovascular disease deaths.Conclusions and relevanceSignificant differences in CVD mortality rates and changes over time were found among the 3 largest Hispanic subgroups in the United States. Findings suggest that the current aggregate classification of Hispanics masks heterogeneity in CVD mortality reporting, leading to an incomplete understanding of health risks and outcomes in this population.

Project description:ObjectiveTo estimate all cause mortality and cause specific mortality among patients taking proton pump inhibitors (PPIs).DesignLongitudinal observational cohort study.SettingUS Department of Veterans Affairs.ParticipantsNew users of PPIs (n=157 625) or H2 blockers (n=56 842).Main outcome measuresAll cause mortality and cause specific mortality associated with taking PPIs (values reported as number of attributable deaths per 1000 patients taking PPIs).ResultsThere were 45.20 excess deaths (95% confidence interval 28.20 to 61.40) per 1000 patients taking PPIs. Circulatory system diseases (number of attributable deaths per 1000 patients taking PPIs 17.47, 95% confidence interval 5.47 to 28.80), neoplasms (12.94, 1.24 to 24.28), infectious and parasitic diseases (4.20, 1.57 to 7.02), and genitourinary system diseases (6.25, 3.22 to 9.24) were associated with taking PPIs. There was a graded relation between cumulative duration of PPI exposure and the risk of all cause mortality and death due to circulatory system diseases, neoplasms, and genitourinary system diseases. Analyses of subcauses of death suggested that taking PPIs was associated with an excess mortality due to cardiovascular disease (15.48, 5.02 to 25.19) and chronic kidney disease (4.19, 1.56 to 6.58). Among patients without documented indication for acid suppression drugs (n=116 377), taking PPIs was associated with an excess mortality due to cardiovascular disease (22.91, 11.89 to 33.57), chronic kidney disease (4.74, 1.53 to 8.05), and upper gastrointestinal cancer (3.12, 0.91 to 5.44). Formal interaction analyses suggested that the risk of death due to these subcauses was not modified by a history of cardiovascular disease, chronic kidney disease, or upper gastrointestinal cancer. Taking PPIs was not associated with an excess burden of transportation related mortality and death due to peptic ulcer disease (as negative outcome controls).ConclusionsTaking PPIs is associated with a small excess of cause specific mortality including death due to cardiovascular disease, chronic kidney disease, and upper gastrointestinal cancer. The burden was also observed in patients without an indication for PPI use. Heightened vigilance in the use of PPI may be warranted.