{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T06:34:10Z","timestamp":1777358050402,"version":"3.51.4"},"reference-count":202,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T00:00:00Z","timestamp":1777334400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oral Health"],"abstract":"<jats:p>Epidemiological studies have reported a distinct link between periodontitis and cardiovascular diseases (CVD). However, the underlying mechanisms\u2014except for systemic inflammation\u2014are still poorly understood. This review examines the evidence that mitochondrial dysfunction represents a key pathological denominator in both periodontitis and CVD. We explain the mechanisms through which dysbiotic periodontal microenvironment and related inflammation can disrupt key mitochondrial functions, including redox balance and quality control. This disruption can exacerbate local tissue damage in the oral cavity and contribute to CVD. Important mechanisms include abnormal mitochondrial dynamics, impaired mitophagy, and impaired mitochondrial biogenesis, which are involved in both periodontitis and CVD. Examining the relationship through the perspective of mitochondrial dysfunction may elucidate the underlying mechanism and allow for new treatment possibilities. Targeting these shared mitochondrial pathways may unveil new strategies to reduce the impact of both periodontitis and CVD.<\/jats:p>","DOI":"10.3389\/froh.2026.1791758","type":"journal-article","created":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T05:36:30Z","timestamp":1777354590000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Periodontitis and cardiovascular diseases: bridging the gap through mitochondrial dysfunction"],"prefix":"10.3389","volume":"7","author":[{"given":"Weiquan","family":"Li","sequence":"first","affiliation":[{"name":"Center of Oral Implantology, Stomatological Hospital, School of Stomatology, Southern Medical University","place":["Guangzhou, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mingshu","family":"Huang","sequence":"additional","affiliation":[{"name":"Center of Oral Implantology, Stomatological Hospital, School of Stomatology, Southern Medical 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