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Abstract
Aim
Observational research suggests that periodontitis affects psoriasis. However, observational studies are prone to reverse causation and confounding, which hampers drawing causal conclusions and the effect direction. We applied the Mendelian randomization (MR) method to comprehensively assess the potential bi‐directional association between periodontitis and psoriasis.
Materials and Methods
We used genetic instruments from the largest available genome‐wide association study of European descent for periodontitis (17,353 cases, 28,210 controls) to investigate the relationship with psoriasis (13,229 cases, 21,543 controls), and vice versa. Causal Analysis Using Summary Effect (CAUSE) estimates and inverse variance‐weighted (IVW) MR analyses were used for the primary analysis. Robust MR approaches were used for sensitivity analyses.
Results
Both univariable methods, CAUSE and IVW MR analyses, did not reveal any impact of periodontitis on psoriasis (CAUSE odds ratio [OR] = 1.00, p = 1.00; IVW OR = 1.02, p = .6247), or vice versa (CAUSE OR = 1.01, p = .5135; IVW OR = 1.00, p = .7070). The null association was corroborated by pleiotropy‐robust methods with ORs close to 1 and p‐values >.59. Overall, MR analyses did not suggest any effect of periodontitis on psoriasis. Similarly, there was no evidence to support an effect of psoriasis on periodontitis.
Conclusions
Within the limitations of this MR study, the outcomes supported neither periodontitis affecting psoriasis nor psoriasis affecting periodontitis.
Abstract
Background
Twenty five‐hydroxy vitamin D (25OHD) levels have been proposed to protect against periodontitis based on in vitro and observational studies but evidence from long‐term randomized controlled trials (RCTs) is lacking. This study tested whether genetically proxied 25OHD is associated with periodontitis using Mendelian randomization (MR).
Methods
Genetic variants strongly associated with 25OHD in a genome‐wide association study (GWAS) of 417,580 participants of European ancestry were used as instrumental variables, and linked to GWAS summary data of 17,353 periodontitis cases and 28,210 controls. In addition to the main analysis using an inverse variance weighted (IVW) model, we applied additional robust methods to control for pleiotropy. We also undertook sensitivity analyses excluding single nucleotide polymorphisms (SNPs) used as instruments with potential pleiotropic effects and used a second 25OHD GWAS for replication. We identified 288 SNPs to be genome‐wide significant for 25OHD, explaining 7.0% of the variance of 25OHD levels and providing ≥90% power to detect an odds ratio (OR) of ≤ 0.97.
Results
MR analysis suggested that a 1 standard deviation increase in natural log‐transformed 25OHD was not associated with periodontitis risk (IVW OR = 1.04; 95% confidence interval (CI): 0.97–1.12; P‐value = 0.297). The robust models, replication, and sensitivity analyses were coherent with the primary analysis.
Conclusions
Collectively, our findings suggest that 25OHD levels are unlikely to have a substantial effect on the risk of periodontitis, but large long‐term RCTs are needed to derive definitive evidence on the causal role of 25OHD in periodontitis.
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.