{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:42:01Z","timestamp":1791276121354,"version":"4.1.0"},"reference-count":363,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,4,11]],"date-time":"2013-04-11T00:00:00Z","timestamp":1365638400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Periodontology 2000"],"published-print":{"date-parts":[[2013,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>During the last two to three decades our understanding of the immunobiology of periodontal disease has increased exponentially, both with respect to the microbial agents triggering the disease process and the molecular mechanisms of the host engagement maintaining homeostasis or leading to collateral tissue damage. These foundational scientific findings have laid the groundwork for translating cell phenotype, receptor engagement, intracellular signaling pathways and effector functions into a \u2018picture\u2019 of the periodontium as the host responds to the \u2018danger signals\u2019 of the microbial ecology to maintain homeostasis or succumb to a disease process. These findings implicate the chronicity of the local response in attempting to manage the microbial challenge, creating a \u2018Double Indemnity\u2019 in some patients that does not \u2018insure\u2019 health for the periodontium. As importantly, in reflecting the title of this volume of <jats:italic>Periodontology 2000<\/jats:italic>, this review attempts to inform the community of how the science of periodontal immunology gestated, how continual probing of the biology of the disease has led to an evolution in our knowledge base and how more recent studies in the postgenomic era are revolutionizing our understanding of disease initiation, progression and resolution. Thus, there has been substantial progress in our understanding of the molecular mechanisms of host\u2013bacteria interactions that result in the clinical presentation and outcomes of destructive periodontitis. The science has embarked from observations of variations in responses related to disease expression with a focus for utilization of the responses in diagnosis and therapeutic outcomes, to current investigations using cutting\u2010edge fundamental biological processes to attempt to model the initiation and progression of soft\u2010 and hard\u2010tissue destruction of the periodontium. As importantly, the next era in the immunobiology of periodontal disease will need to engage more sophisticated experimental designs for clinical studies to enable robust translation of basic biologic processes that are in action early in the transition from health to disease, those which stimulate microenvironmental changes that select for a more pathogenic microbial ecology and those that represent a rebalancing of the complex host responses and a resolution of inflammatory tissue destruction.<\/jats:p>","DOI":"10.1111\/prd.12005","type":"journal-article","created":{"date-parts":[[2013,4,11]],"date-time":"2013-04-11T09:13:59Z","timestamp":1365671639000},"page":"163-202","source":"Crossref","is-referenced-by-count":129,"title":["Periodontal disease immunology: \u2018double indemnity\u2019 in protecting the host"],"prefix":"10.1111","volume":"62","author":[{"given":"Jeffrey 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