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Unlike periodontitis, peri\u2010implant tissues lack a periodontal ligament and epithelial junction integrity and interface with metal oxides on titanium surfaces. The inflammatory changes in peri\u2010implant disease not only affect the host but also extend to the implant surfaces, which undergo corrosion and particle release. These specific ecological features must be accurately captured in preclinical experimental models to provide mechanistic insight and enable translational success.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>This review evaluates preclinical and microengineered models of peri\u2010implantitis, focusing on how well they recapitulate the peri\u2010implant mucosal barrier, the biomaterial interface, and systemic modifiers. We propose minimum criteria for \u201ctrue\u201d peri\u2010implantitis models and outline ecosystem\u2010specific platforms for translational research.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>A literature search for this narrative review was conducted in PubMed, prioritizing in\u00a0vivo peri\u2010implantitis models and their use in assessing systemic comorbidities (e.g., diabetes) and local risk factors on peri\u2010implant disease. Furthermore, emerging implant\u2010specific organ\u2010on\u2010a\u2010chip systems for 3D peri\u2010implant mucosa are reviewed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Ligature\u2010 and infection\u2010based rodent and large\u2010animal models have elucidated key bacterial\u2010driven inflammatory pathways around dental implants, but careful consideration is needed to ensure long\u2010term chronicity and to account for titanium degradation as a costimulatory pathogenic factor. Comorbidity\u2010integrated models demonstrate that diabetes, vascular disease, and antiresorptive therapy amplify peri\u2010implant bone loss and can precipitate MRONJ\u2010like lesions. Organ\u2010on\u2010a\u2010chip peri\u2010implant mucosa platforms now enable controlled bacterial and titanium exposure, biomechanical strain, and human\u2010relevant barrier readouts, aligned with reduction principles and prioritizing Human\u2010Centered models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Clinical Relevance<\/jats:title>\n                    <jats:p>Ecosystem\u2010specific models that incorporate microrough titanium, inflammatory biomaterial corrosion, barrier biology, and systemic risk factors are essential to advance the study of peri\u2010implantitis. Such models provide a strong foundation for implant\u2010specific investigations that move peri\u2010implantitis management beyond biofilm\u2010centric debridement into the management of host\u2013microbial\u2013biomaterial equilibrium.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/prd.70076","type":"journal-article","created":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T06:13:38Z","timestamp":1787724818000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Decoding host\u2013microbial dynamics in peri\u2010implantitis: Ecosystem\u2010specific experimental models"],"prefix":"10.1111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8635-9422","authenticated-orcid":false,"given":"Georgios A.","family":"Kotsakis","sequence":"first","affiliation":[{"name":"Department of Oral Biology and Clinical Research Center Rutgers School of Dental Medicine  Newark New Jersey 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