{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T12:27:47Z","timestamp":1790166467929,"version":"4.1.0"},"reference-count":27,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Periodontitis is a chronic oral inflammatory disease that is caused by dental plaque pathogens. Periodontal disease development and evolution are based on the host immune system, humoral and cellular immunity, the integrity of the tissues, and certain endocrine and nutritional factors. Mitochondria are significantly involved in periodontal infections and inflammation, which play a role in the inflammatory response in a variety of ways. In general, oxidative stress causes a stressful environment that subsequently leads to tissue damage and chronic inflammation. Several mutations and alterations in mitochondrial DNA lead the disease to an aggressive condition, by causing dysregulated mitochondrial function. Such mutations are significantly associated with various diseases. Numerous studies indicate chronic periodontitis patients have a decreased level of mitochondrial membrane potential, as well as adenosine triphosphate, and an increased level of reactive oxygen species production, which causes cell death in the periodontium and affects tissue growth. Further studies into the association between mitochondria and periodontitis might be helpful for the treatment and prevention of the diseases.<\/jats:p>","DOI":"10.4103\/jisp.jisp_678_21","type":"journal-article","created":{"date-parts":[[2024,4,17]],"date-time":"2024-04-17T11:05:10Z","timestamp":1713351910000},"page":"126-130","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":17,"title":["The implication of mitochondrial DNA mutation and dysfunction in periodontal diseases"],"prefix":"10.4103","volume":"27","author":[{"given":"Balachander","family":"Kannan","sequence":"first","affiliation":[{"name":"Centre for Cellular and Molecular Research, Department of Molecular Biology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, Tamil Nadu, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paramasivam","family":"Arumugam","sequence":"additional","affiliation":[{"name":"Centre for Cellular and Molecular Research, Department of Molecular Biology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, Tamil Nadu, India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2023,3,4]]},"reference":[{"key":"R2-20240828","doi-asserted-by":"crossref","first-page":"37","DOI":"10.1034\/j.1600-0757.2001.22250104.x","article-title":"Periodontal risk assessment, diagnosis, and treatment planning","volume":"25","author":"Pihlstrom","year":"2001","journal-title":"J Periodontol"},{"key":"R3-20240828","doi-asserted-by":"crossref","first-page":"26","DOI":"10.1111\/prd.12297","article-title":"The role of inflammation and genetics in periodontal 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