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However, the physiology of mitochondria within gingival tissues and human gingival fibroblasts (HGFs) in patients with chronic periodontitis (CP) remains unclear. The objective of this study was to investigate the structure profile and function of mitochondria in gingival tissues and in HGFs derived from patients with or without CP. These features of mitochondria in HGFs were further analyzed when HGFs were induced by lipopolysaccharide (LPS) from <jats:italic>Porphyromonas gingivalis<\/jats:italic> (<jats:italic>P.g<\/jats:italic>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Gingival tissues and HGFs were collected from CP and healthy patients. Mitochondrial structure was assessed by transmission electron microscopy. Tissues or cells lysis was performed for mitochondrial DNA (mtDNA) quantification, and real\u2010time polymerase chain reaction (RT\u2010PCR) tests were used to determine mtDNA copy numbers. Western blot analysis was used to evaluate autophagy\u2010related protein (ATG)\u20105, microtubule\u2010associated protein light chain 3 (LC3), and mitochondrial matrix protein pyruvate dehydrogenase kinase isozyme 2 (PDK2) levels in tissues and HGFs from CP and healthy individuals.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Tissues and HGFs from CP showed a significant greater mitochondrial structure destruction, lower mtDNA level, increased ATG5, LC3\u2010II, and lower PDK2 protein levels than those of healthy individuals. In addition, LPS from <jats:italic>P.g<\/jats:italic> also triggered the same results in HGFs from healthy donors. Moreover, the challenge of HGFs from CP with LPS worsened these parameters.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Mitochondrial structure and function within gingival tissues and HGFs from CP individuals were abnormal compared to those from healthy donors, and LPS could promote mitochondrial destruction.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jre.12941","type":"journal-article","created":{"date-parts":[[2021,11,26]],"date-time":"2021-11-26T18:24:39Z","timestamp":1637951079000},"page":"94-103","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":51,"title":["Abnormal mitochondrial structure and function are retained in gingival tissues and human gingival fibroblasts from patients with chronic periodontitis"],"prefix":"10.1111","volume":"57","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5336-8712","authenticated-orcid":false,"given":"Jia","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Periodontology Peking University School and Hospital of Stomatology  Beijing China"},{"name":"National Clinical Research Center for Oral Diseases  Beijing China"},{"name":"National Engineering Laboratory for Digital and Material Technology of Stomatology  Beijing China"},{"name":"Beijing Key Laboratory of Digital Stomatology  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoxuan","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Periodontology Peking University School and Hospital of Stomatology  Beijing China"},{"name":"National Clinical Research Center for Oral Diseases  Beijing China"},{"name":"National Engineering Laboratory for Digital and Material Technology of Stomatology  Beijing 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