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Objective: We investigated the bidirectional relationship between rheumatoid arthritis (RA) and periodontitis and their cross‐sectional association using national administrative health care data. Methods: The sample included 3,308,903 individuals aged 20 to 79 years who resided in Denmark in 2000 and had remained free of RA and periodontitis in the previous 10 years. RA and periodontitis were defined using diagnosis and treatment codes. Marginal structural survival models were employed to estimate the effects of RA on periodontitis incidence and vice versa from 2000 to 2017. Using a cross‐sectional sample of 2,574,536 individuals from 2017, the association of periodontitis with RA was investigated using regression analyses and probabilistic quantitative bias analyses, simulating RA and periodontitis misclassification and unmeasured confounding of smoking. Results: Between 2000 and 2017, 20,348 individuals developed RA and 740,799 developed periodontitis. The estimated hazard ratio (HR) for the effect of periodontitis on incident RA was 1.05 (95% confidence interval [CI] 0.88–1.25), resulting in a restricted mean survival time difference of one day. The HR for the effect of RA on incident periodontitis was 0.84 (95% CI 0.80–0.88), corresponding to a restricted mean survival time difference of 151 days. Cross‐sectionally, the unadjusted prevalence ratio for the association was 1.15 (95% CI 1.11–1.19), whereas the estimate adjusted for measured and simulated confounding was practically null (0.99, 95% simulation interval 0.93–1.04). Conclusion: These findings challenge previously reported bidirectional relationships between periodontitis and RA, pointing to potential residual confounding as an important link and prompting reconsideration of the biologic plausibility and clinical significance of these associations. [ABSTRACT FROM AUTHOR]

Over the years, several reviews of periodontal risk assessment tools have been published. However, major misunderstandings still prevail in repeated attempts to use these tools for prognostic risk prediction. Here we review the principles of risk prediction and discuss the value and the challenges of using prediction models in periodontology. Most periodontal risk prediction models have not been properly developed according to guidance given for the risk prediction model development. This shortcoming has led to several problems, including the creation of arbitrary risk scores. These scores are often labelled as 'high risk' without explicit boundaries or thresholds for the underlying continuous risk estimates of patient‐important outcomes. Moreover, it is apparent that prediction models are often misinterpreted as causal models by clinicians and researchers although they cannot be used as such. Additional challenges like the critical assessment of transportability and applicability of these prediction models, as well as their impact on clinical practice and patient outcomes, are not considered in the literature. Nevertheless, these instruments are promoted with claims regarding their ability to deliver more individualized and precise periodontitis treatment and prevention, purportedly resulting in improved patient outcomes. However, people with or without periodontitis deserve proper information about their risk of developing patient‐important outcomes such as tooth loss or pain. The primary objective of disseminating such information should not be to emphasize assumed treatment efficacy, hype individualization of care, or promote business interests. Instead, the focus should be on providing individuals with locally validated and regularly updated predictions of specific risks based on readily accessible and valid key predictors (e.g. age and smoking). [ABSTRACT FROM AUTHOR]

Once a while, disease classifications have needed revision because new knowledge has accumulated, and new technologies and better treatments have emerged. Changes made to disease classifications should be trustworthy and openly justified. The periodontitis definition and classification system was changed in 2017 by the 'World Workshop on the Classification of Periodontal and Peri‐Implant Diseases and Conditions'. The workshop, comprising clinicians and researchers, resulted in the production of a 23‐article special issue that introduced the new definitions and classifications of periodontitis. In this narrative review, we critically review how the changes made to the periodontitis definition and classification were justified in the light of the Checklist for Modifying Disease Definitions. Under each of the eight items of the checklist, we have discussed how the item was or could have been considered in the light of the checklist and its guidance. In our view, the new definition and classification of periodontitis was presented in an understandable way, even though the changes from the previous definition were not made visible. However, the issues of (1) estimated changes in prevalence or incidence, (2) triggers for the change, (3) prognostic ability, (4) repeatability or reproducibility, (5) incremental benefits, (6) incremental harms or (7) net benefits and harms related to the introduction of new classification were not considered in the way suggested in the checklist. Thereby, a balanced assessment of potential benefits and harms associated with the new periodontitis classification system was not presented, and to a large extent it remains unknown if the use of the new classification system will provide more net benefits to patients and to the community than previous systems. It is our view that patients and societies deserve transparent and balanced assessments of the potential benefits and harms associated with the periodontitis classification. Importantly, these should reflect the values and preferences also of the patients and the wider community and consider the impact on resource usage. [ABSTRACT FROM AUTHOR]

The article contends that acceptance of a multi-causation approach to the prevention and treatment of periodontitis is hindered by the focus on mono-causal microbiological etiology. A historical overview of the specific microbial and ecological plaque hypotheses, dysbiosis and keystone pathogen hypothesis is presented. It highlights the application of the sufficient-component cause model to periodontitis and calls for the recognition of periodontitis as a chronic multi-factorial disease.