Periodontal Disease Independently Associated With White Matter Hyperintensity Volume: A Measure of Cerebral Small...

White matter hyperintensities (WMHs), cerebral microbleeds (CMBs), and lacunar infarcts are radiographic markers of cerebral small vessel disease (CSVD), which is associated with an increased risk of stroke and cognitive decline. Periodontal disease (PD), a chronic inflammatory condition, has been linked to vascular pathology and may contribute to CSVD. The aim of this study was to assess the independent association between PD and MRI-verified CSVD features using data from the Atherosclerosis Risk in Communities (ARIC) cohort.

Periodontal status was classified as PD (n = 800) or periodontal health ([PH]; n = 343). CSVD features included WMH volume (WMHV), CMBs, and lacunar infarcts. WMHV was derived from fluid-attenuated inversion recovery images and categorized into quartiles. Multinomial logistic regression was used to evaluate associations between PD and WMHV quartiles, and binomial logistic regression assessed associations between PD and the presence of CMBs and lacunar infarcts. Models were adjusted for demographic and vascular risk factors including age, sex, race-center, hypertension, diabetes, smoking status, and time between visits.

We analyzed 1,143 ARIC participants (mean age 77 years; 45% male; 76% White, 24% African American) who underwent periodontal assessment at Visit 4 and brain MRI at Visit 5. Participants with PD had significantly greater WMHV compared with those with PH (median WMH%: 2.83 vs 2.52; p = 0.012). PD was associated with the highest WMHV quartile (Q4 >21.36 cm³), with a crude odds ratio (OR) of 1.77 (95% CI 1.23-2.56) and an adjusted OR of 1.56 (95% CI 1.01-2.40). A weak but significant correlation was found between WMHV and World Workshop Periodontal Profile Class (ρ = 0.076, p = 0.011). No statistically significant adjusted associations were found between PD and CMBs (adj. OR 1.16, 95% CI 0.83-1.63) or lacunar infarcts (adj. OR 1.14, 95% CI 0.77-1.69).

PD was independently associated with greater WMH burden, a key imaging marker of CSVD, but not with CMBs or lacunar infarcts after adjustment for confounders. This suggests that PD may contribute to CSVD pathology, particularly WMHs, through mechanisms involving systemic inflammation. Limitations include the temporal gap between dental and imaging assessments and potential residual confounding. Interventions targeting PD could be explored as a modifiable risk factor for CSVD prevention.