{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T13:01:39Z","timestamp":1791378099353,"version":"4.3.2"},"reference-count":279,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:00Z","timestamp":1791331200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:00Z","timestamp":1791331200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Periodontal Research"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Periodontitis research has traditionally focused on pathogenesis; however, understanding why some individuals remain resistant to the disease may be even more important. The concept of salutogenesis (\u201csalutology\u201d) has evolved around the capacity to remain resilient to life's stressors. An individual's sense of coherence (SOC) is based on generalized resistance resources (GRRs), including physiological, biological, material, psychological, interpersonal, and sociocultural factors. This review focuses mainly on physiological and biological resistance resources and briefly considers psychosocial coping, which together can generate actions that mitigate periodontal stressors, that is, periodontal risk factors. We focus on dental biofilm compositions compatible with resistance to periodontal destruction and host responses that promote homeostasis and resolve inflammation. Putative physiological and biological salutogenic factors described here are summarized in a five\u2010cluster model. First, people may be resistant to periodontitis because their dental biofilm communities do not promote inflammation and exhibit resilience that maintains eubiosis. Furthermore, inherited DNA variants may modulate non\u2010destructive, tolerant immunological and inflammatory responses. Protective epigenetic factors may also induce trained immunity with enhanced protective and inflammation\u2010resolving capacity. Lifestyle\u2010related salutogenic factors for periodontal health are better understood because they are also associated with general health. From an oral health standpoint, maintaining a consistent and effective daily oral hygiene routine is a straightforward way to protect against gingivitis. In addition, we emphasize dietary components that may support the resolution of inflammation, including specific omega\u20106 and omega\u20103 polyunsaturated fatty acids that serve as precursors of specialized pro\u2010resolving mediators (e.g., lipoxins and resolvins); sufficient vitamins and other micronutrients may also be salutogenic. More broadly, systemic health may protect against systemic inflammation and its adverse effects on distant tissues and organs, including the periodontium. Finally, the absence of plaque\u2010retentive factors in the dentition may be salutogenic by helping to prevent the transition from eubiosis to dysbiosis. We propose that resistance to periodontitis does not depend on any single cluster or specific factor but on individually variable, combined, and synergistic effects of multiple factors that maintain eubiosis, immune tolerance, and resolution of gingival inflammation. The key pillars of salutogenesis support a more holistic interpretation of resistance to periodontitis. This state\u2010of\u2010the\u2010art review provides new insights into potential mechanisms that maintain periodontal health and enhance resistance to the onset of periodontitis.<\/jats:p>","DOI":"10.1111\/jre.70173","type":"journal-article","created":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T12:18:11Z","timestamp":1791375491000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Periodontal Salutogenesis: Why Are Some People Resistant to Oral Microbial Dysbiosis and Destructive Inflammation?"],"prefix":"10.1111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8794-552X","authenticated-orcid":false,"given":"Bruno G.","family":"Loos","sequence":"first","affiliation":[{"name":"Department of Periodontology, Academic Centre for Dentistry Amsterdam (ACTA) University of Amsterdam and Vrije Universiteit Amsterdam  Amsterdam the Netherlands"},{"name":"Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine Harvard University  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2293-3392","authenticated-orcid":false,"given":"Magda","family":"Feres","sequence":"additional","affiliation":[{"name":"Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine Harvard University  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7102-9746","authenticated-orcid":false,"given":"William V.","family":"Giannobile","sequence":"additional","affiliation":[{"name":"Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine Harvard University  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4395-3958","authenticated-orcid":false,"given":"Hatice","family":"Hasturk","sequence":"additional","affiliation":[{"name":"Department of Immunology and Inflammation ADA Forsyth Institute  Somerville Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1432-6194","authenticated-orcid":false,"given":"Egija","family":"Zaura","sequence":"additional","affiliation":[{"name":"Department of Preventive Dentistry, Academic Centre for Dentistry Amsterdam (ACTA) University of Amsterdam and Vrije Universiteit Amsterdam  Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,10,7]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/jre.13424"},{"key":"e_1_2_12_3_1","doi-asserted-by":"publisher","DOI":"10.1177\/0022034514552491"},{"key":"e_1_2_12_4_1","doi-asserted-by":"publisher","DOI":"10.1111\/jcpe.13769"},{"key":"e_1_2_12_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.adaj.2018.04.023"},{"key":"e_1_2_12_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/jcpe.12978"},{"key":"e_1_2_12_7_1","doi-asserted-by":"publisher","DOI":"10.1111\/jre.13337"},{"key":"e_1_2_12_8_1","doi-asserted-by":"publisher","DOI":"10.1111\/jcpe.13506"},{"key":"e_1_2_12_9_1","doi-asserted-by":"publisher","DOI":"10.1002\/JPER.21\u20100111"},{"key":"e_1_2_12_10_1","doi-asserted-by":"publisher","DOI":"10.1111\/jcpe.14058"},{"key":"e_1_2_12_11_1","doi-asserted-by":"publisher","DOI":"10.1111\/prd.12305"},{"key":"e_1_2_12_12_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41577\u2010020\u201000488\u20106"},{"key":"e_1_2_12_13_1","doi-asserted-by":"publisher","DOI":"10.1111\/prd.12616"},{"key":"e_1_2_12_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.canep.2024.102595"},{"key":"e_1_2_12_15_1","doi-asserted-by":"publisher","DOI":"10.1111\/prd.12540"},{"issue":"1","key":"e_1_2_12_16_1","doi-asserted-by":"crossref","first-page":"10","DOI":"10.1016\/S0035-8819(25)00469-6","article-title":"Senescence, Cancer and \u2018Endogenous Parasites\u2019: A Salutogenic Hypothesis","volume":"30","author":"Charlton B. 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