Chronic periodontitis is a local inflammatory condition that affects the tooth-supporting tissues. There is an association between periodontitis and higher levels of locally produced proinflammatory markers, contributing to low-grade systemic inflammation. It is possible that periodontitis contributes to decline in kidney function because: (1) periodontitis contributes to overall systemic inflammatory burden, possibly triggering kidney function decline; and (2) periodontal bacteria and related products can be found in the bloodstream, possibly damaging the kidney epithelium.
There are limited data on the relationship between chronic periodontitis and kidney function. Christin Wangerin, DDS, and colleagues recently conducted a population-based cohort study designed to examine the association between current and cumulative periodontal disease status with kidney function. Results of the study were reported in the American Journal of Kidney Diseases [2019;73(4):513-524].
The researchers utilized 11-year follow-up data from the population-based prospective Study of Health in Pomerania (SHIP). Glomerular filtration rate estimated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) creatinine-cystatin C equation (eGFRcr-cys) and urinary albumin-creatinine ratio (UACR) were used to assess kidney function. Periodontal disease was assessed via analysis of five exposure variables to evaluate the consistency of the potential exposure-outcome effects using continuous rather than categorial variables.
Baseline SHIP data were available on 2297 participants, and 11-year follow-up data were available on 1512 participants. Eligible participants for the current analysis were 20 to 59 years of age. The outcomes of interest were eGFRcr-cys and moderately increased albuminuria, defined as UACR >30 mg/g.
Periodontal disease is characterized by current (pocket probing depth [PPD]) and cumulative (clinical attachment level [CAL]) characteristics. For the current analysis, the researchers evaluated variables quantifying disease severity (mean value) and extent (percentage of diseased sites) on the participant level, using both PPD and CAL measures. The analysis also evaluated total PPD to quantify current exposure to periodontal inflammation and account for the reduction in inflammatory exposure due to tooth loss.
At baseline, mean age of participants included in the eGFRcr-cys analyses was 40 years, 47% of participants were men, 20% were highly educated, and 39% were current smokers. There were significant differences across categories of total PPD in covariate levels; low education, current smoking status, and high consumption of alcohol were seen more often in periodontally diseased individuals (highest category).
Those with periodontal disease also were more likely to have known diabetes mellitus, dyslipidemia, and hypertension than those with lower PPD levels. The remaining variables were significantly greater across greater categories of total PPD. In addition, across categories of total PPD, average eGFRcr-cys at baseline and follow-up decreased from 121.8 to 115.2 and from 105.0 to 101.8 mL/min/1.73 m2, respectively. Median UACR at baseline and at follow-up increased from 6.6 to 7.8 mg/g and from 7.6 to 9.1 mg/g, respectively, across categories of total PPD.
In linear and logistic mixed models, comprehensive modeling of various exposure and outcome variables did not reveal consistent statistically significant associations. In eGFRcr-cys models, effect estimates for periodontal variables were consistently nonsignificant. In UACR (long-transformed) models, there were significant associations between mean PPD, mean interproximal CLA, and percentage of sites with interproximal CAL ≥3 mm and UACR. Those with higher levels of periodontitis measures had greater worsening of UACR over time. There were no significant associations with any of the periodontitis variables when moderately increased albuminuria (UACR ≥30 mg/g) was used as the outcome.
In mixed models, evaluation of eGFRcr-cys as the outcome yielded significant hits for total PPD (b=0.222 for highest versus reference category) and percentage of sites with interproximal CAL ≥3 mm. However, because effect estimates had implausible directions such that higher levels of periodontitis variables were associated with less pronounced decreases in eGFRcr-cys, the initial hypothesis that periodontitis might be associated with decreased eGFR was not supported by these results.
There were several study limitations cited by the authors, including the partial recording protocol of periodontal status that may have led to underestimation of severity of periodontal disease; basing changes in eGFR and albuminuria on only two measurements; assessing UACR using a spot urine sample; excluding individuals mainly due to missing confounder (only baseline) or outcome data (baseline and follow-up); and incomplete data on gum treatment during follow-up.
“In summary, mixed models failed to indicate consistent associations of periodontitis with decreased kidney function in a general population examined over 11 years. Thus, or results do not support the hypothesis that periodontitis might be a risk factor for decreased kidney failure,” the researchers said.
- Researchers conducted a population-based cohort study to determine whether chronic periodontitis is associated with subsequent decreases in kidney function.
- Baseline and 11-year follow-up data from the Study of Health in Pomerania were used in the study; outcomes were glomerular filtration rate estimated from serum creatinine and serum cystatin C and increases in albuminuria.
- The results did not support the hypothesis that periodontitis is an important risk factor for chronic kidney disease.