{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T21:56:30Z","timestamp":1791582990449,"version":"4.3.4"},"reference-count":160,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"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":["Periodontology 2000"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background\/Aim<\/jats:title>\n                    <jats:p>Antiresorptive therapy represents a cornerstone in the management of osteoporosis and cancer\u2010related bone disease through suppression of osteoclast\u2010mediated bone resorption. As implant therapy becomes more common in aging populations, clinicians increasingly encounter patients receiving these medications, thus making their impact on peri\u2010implant tissues clinically relevant.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>This narrative review critically examines clinical evidence on implant survival, peri\u2010implant bone stability, peri\u2010implantitis progression, and treatment considerations in patients receiving antiresorptive therapy, while integrating mechanistic insights.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Evidence suggests that implant survival and marginal bone loss in osteoporotic patients are generally comparable to untreated individuals, indicating that suppression of bone resorption does not inherently compromise osseointegration. However, these outcomes may not fully reflect peri\u2010implant tissue dynamics. Antiresorptives alter osteoclast functions and bone remodeling, potentially affecting the osteoimmune balance required to adapt to mechanical and oral microbial challenges. While these effects may remain subclinical under healthy conditions, they may become relevant during chronic peri\u2010implant inflammation or repeated surgical interventions, where remodeling demands are increased. Altered remodeling may result in lesion persistence, impaired structural recovery, and late complications. Although medication\u2010related osteonecrosis of the jaw remains rare, antiresorptives may modify osteoimmune interactions within inflamed tissues. Therefore, peri\u2010implantitis may act as a contextual modifier influencing healing outcomes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Antiresorptive therapy should not be regarded as an absolute contraindication to implant therapy in appropriately selected patients, particularly those receiving osteoporosis\u2010dose regimens. However, chronic peri\u2010implant inflammation, repeated surgical intervention, and high\u2010dose oncologic antiresorptive exposure may impair osteoimmune adaptation and increase susceptibility to delayed healing and MRONJ\u2010related complications.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Clinical Relevance<\/jats:title>\n                    <jats:p>Early control of peri\u2010implant inflammation, individualized risk stratification, and strict supportive maintenance should be considered central components of clinical management in antiresorptive\u2010exposed patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/prd.70085","type":"journal-article","created":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T17:42:59Z","timestamp":1789580579000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Antiresorptive therapy influence on peri\u2010implant diseases: Clinical implications and osteoimmunological perspectives"],"prefix":"10.1111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9243-1382","authenticated-orcid":false,"given":"Emilio A.","family":"Cafferata","sequence":"first","affiliation":[{"name":"Department of Oral Surgery, Implantology and Oral Medicine Goethe Universit\u00e4t  Frankfurt am Main Germany"},{"name":"Oral Peri\u2010Implant Research Group, Department of Oral Implantology, Postgraduate School of Dentistry Universidad Cient\u00edfica del Sur  Lima Peru"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5873-9903","authenticated-orcid":false,"given":"Frank","family":"Schwarz","sequence":"additional","affiliation":[{"name":"Department of Oral Surgery, Implantology and Oral Medicine Goethe Universit\u00e4t  Frankfurt am Main Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5400-9009","authenticated-orcid":false,"given":"Reinhard","family":"Gruber","sequence":"additional","affiliation":[{"name":"Department of Oral Biology University Clinic of Dentistry, Medical University of Vienna  Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,16]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"crossref","first-page":"898","DOI":"10.1016\/S2213-8587(17)30188-2","article-title":"Osteoporosis treatment: recent developments and ongoing challenges","volume":"5","author":"Khosla S","year":"2017","journal-title":"Lancet Diabetes Endocrinol"},{"key":"e_1_2_12_3_1","doi-asserted-by":"crossref","first-page":"25","DOI":"10.1038\/s41413-022-00204-1","article-title":"mTORC1 induces plasma membrane depolarization and promotes preosteoblast senescence by regulating the sodium channel 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