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Abstract
Aim
To examine the associations between bone turnover markers and periodontitis in two cross‐sectional population‐based studies.
Materials and Methods
We used data from two independent adult samples (N = 4993), collected within the Study of Health in Pomerania project, to analyse cross‐sectional associations of N‐procollagen type 1 amino‐terminal propeptide (P1NP), C‐terminal cross‐linking telopeptide, osteocalcin, bone‐specific alkaline phosphatase (BAP), fibroblast growth factor 23, wingless‐type mouse mammary tumour virus integration site family member 5a (WNT5A), and sclerostin values with periodontitis. Confounder‐adjusted gamma and fractional response regression models were applied.
Results
Positive associations were found for P1NP with mean pocket probing depth (PPD; eβ=1.008; 95% confidence interval [CI]: 1.001–1.015), mean clinical attachment loss (mean CAL; eβ=1.027; 95% CI: 1.011–1.044), and proportion of sites with bleeding on probing (%BOP; eβ=1.055; 95% CI: 1.005–1.109). Similar associations were seen for BAP with %BOP (eβ=1.121; 95% CI: 1.042–1.205), proportion of sites with PPD ≥4 mm (%PPD4) (eβ=1.080; 95% CI: 1.005–1.161), and sclerostin with %BOP (eβ=1.308; 95% CI: 1.005–1.704). WNT5A was inversely associated with mean PPD (eβ=0.956; 95% CI: 0.920–0.993) and %PPD4 (eβ=0.794; 95% CI: 0.642–0.982).
Conclusions
This study revealed scattered associations of P1NP, BAP, WNT5A, and sclerostin with periodontitis, but the results are contradictory in the overall context. Associations reported in previous studies could not be confirmed.
Abstract
Study Objective
Long‐term intake of proton pump inhibitors (PPIs) might increase the risk of cardiovascular events. One suggested mechanism is that PPIs inhibit the enzyme dimethylarginine dimethylaminohydrolase (DDAH) and thereby block the degradation of endothelial asymmetrical dimethylarginine (ADMA). Excess ADMA in turn leads to impaired endothelial nitric oxide (NO) generation. So far, this mechanism has only been established in human cell cultures. Previous studies that examined this pathway in human populations measured circulating ADMA and found no association with PPI use and excess plasma ADMA. But in a recent study, plasma ADMA was not correlated with intracellular ADMA. We therefore focused on changes in plasma citrulline as an indicator for potential DDAH inhibition.
Design
We analyzed the association between regular daily PPI intake and flow‐mediated dilation (FMD) of the brachial artery as well as plasma concentrations of citrulline, arginine, ADMA, and symmetric dimethylarginine using inverse probability weighting to adjust for confounding and censoring.
Data Source
Data of 1298 participants from two independent cohorts of the population‐based Study of Health in Pomerania were used.
Participants
Participants of the population‐based Study of Health in Pomerania are a stratified random sample of the study region.
Exposure
Regular daily intake of PPIs.
Measurements
FMD of the brachial artery and plasma concentrations of citrulline, arginine, ADMA, and symmetric dimethylarginine.
Main Results
Eighty‐seven participants (57.5% female) were regular daily users of PPIs. In the fully adjusted models, associations were identified for FMD and plasma citrulline concentrations. PPI users revealed a 0.99% (95% CI: −1.96 to −0.02) lower FMD and 3.03 µmol/L (95% CI: −4.96 to −1.10) lower plasma citrulline levels as compared to non‐users.
Conclusion
Our data provide evidence that long‐term intake of PPIs might inhibit human DDAH activity, resulting in impaired endothelial NO production and reduced vascular function. In the long run, this might explain an increased risk for cardiovascular diseases associated with long‐term PPI use.