Association of periodontitis with blood pressure

Inoue et al. [1] evaluated the association of periodontitis with blood pressure (BP) in a sample of Japanese workers examined at enrolment and 1 year later. They conducted cross‐sectional analyses at both time points and reported significantly higher systolic and diastolic BP in patients with periodontitis. They argued that an increase in BP may be an underlying pathway linking periodontitis and cardiovascular disease. Although their hypothesis is biologically plausible, their analysis has several limitations and provides little support for an increased risk of hypertension in people with periodontitis. First, subjects undergoing antihypertensive treatment should have been excluded from the analysis because their BP should be “artificially” low regardless of the presence of periodontitis. Inclusion of treated hypertensives should dilute any BP difference between patients with and without periodontitis. Second, it is impossible to know whether BP elevation preceded or followed the development of periodontitis, since only cross‐sectional analyses were conducted, although longitudinal data were available. Third, a closer look at Inoue's data suggests that periodontitis was unrelated to BP elevation. From their Table III, one can appreciate that the average systolic BP did not change much during the study period. In fact, the mean adjusted systolic BP at the time of enrolment was practically identical to that 1 year later in both people with and without periodontitis (121.1 and 123.4 mmHg in those without and 127.1 and 127.1 mmHg in those with periodontitis). Similarly, changes in diastolic BP from enrolment to 1‐year of follow up, estimated from their Table III, were 4.1 mmHg (95% confidence interval, CI 4.0–4.2) in people without periodontitis and 4.4 mmHg (95% CI 3.9–4.9) in those with periodontitis. Therefore, diastolic BP increased significantly, but the increase was virtually identical in subjects with and without periodontitis. Since changes in BP in a period of 1 year should be relatively small, longer periods of follow‐up may be needed to ascertain if an increase in BP could indeed be a consequence of periodontitis. This could be important since the nature of the relationship between BP and chronic inflammation is yet to be established.