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However, accumulating evidence indicates that periodontal bone loss is more accurately understood as a state of pathological uncoupling of bone remodeling, in which exaggerated bone resorption coexists with inadequate bone formation response. In this review, we reposition periodontitis within the broader context of inflammatory skeletal diseases and synthesize current mechanistic insights from osteoimmunology, bone biology, and mechanobiology. We discuss how excessive osteoclastogenesis in periodontitis is sustained by receptor activator of nuclear factor kappa\u2010B ligand (RANKL) dominance derived from osteocytes, osteoblast\u2010lineage cells, stromal cells, monocytes\/macrophages, B and T lymphocytes, and neutrophils within a cytokine\u2010rich microenvironment characterized by tumor necrosis factor (TNF)\u2010\u03b1, interleukin (IL)\u20101\u03b2, IL\u20106, and IL\u201017A signaling. Persistent activation of nuclear factor kappa\u2010B (NF\u2010\u03baB) and mitogen\u2010activated protein kinase (MAPK) pathways further enhance osteoclast differentiation, survival, and resorptive activity. At the same time, inflammatory mediators actively suppress osteoblast\u2010lineage commitment by inhibiting Runx2 and Osterix, antagonizing canonical Wnt\/\u03b2\u2010catenin signaling through the upregulation of sclerostin and Dickkopf\u20101 (DKK1), and impairing bone matrix production and mineralization. We further examine how disruption of key osteoclast\u2013osteoblast coupling mechanisms, including ephrinB2\/EphB4 and semaphorin signaling, prevents the effective transition from resorption to formation, while osteocyte dysfunction amplifies the uncoupled phenotype by integrating inflammatory and mechanical signals. Comparisons with rheumatoid arthritis, inflammatory bowel disease\u2010associated bone loss, and peri\u2010implantitis reveal shared immune\u2010driven mechanisms of remodeling imbalance, whereas the unique features of alveolar bone, including high turnover, continuous mechanical loading, and chronic microbial exposure, make it particularly susceptible to inflammatory uncoupling. Together, these concepts support a therapeutic shift toward restoring physiological coupling instead of solely inhibiting resorption and position periodontitis as a clinically accessible model for understanding and targeting inflammatory bone loss across skeletal diseases.<\/jats:p>","DOI":"10.1111\/jre.70148","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T09:05:27Z","timestamp":1783328727000},"page":"662-694","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Periodontitis as a Model for Inflammatory Uncoupling of Bone Remodeling"],"prefix":"10.1111","volume":"61","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1110-6233","authenticated-orcid":false,"given":"Rafael Scaf","family":"de Molon","sequence":"first","affiliation":[{"name":"Department of Diagnostic and Surgery, School of Dentistry S\u00e3o Paulo State University (UNESP)  Ara\u00e7atuba Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0157-1855","authenticated-orcid":false,"given":"Sotirios","family":"Tetradis","sequence":"additional","affiliation":[{"name":"Division of Diagnostic and Surgical Sciences UCLA School of Dentistry  Los Angeles California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1391-320X","authenticated-orcid":false,"given":"Rolando","family":"Vernal","sequence":"additional","affiliation":[{"name":"Periodontal Biology Laboratory, Department of Conservative Dentistry, Faculty of Dentistry Universidad de Chile  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8053-4517","authenticated-orcid":false,"given":"Fabio Renato Manzolli","family":"Leite","sequence":"additional","affiliation":[{"name":"Section of Population Health University of Utah School of Dentistry  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0568-124X","authenticated-orcid":false,"given":"Thomas E.","family":"Van Dyke","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Research ADA Forsyth Institute  Somerville Massachusetts USA"},{"name":"Department of Oral Medicine Infection and Immunity, Faculty of Medicine Harvard University  Cambridge Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,7,6]]},"reference":[{"key":"e_1_2_19_2_1","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2024.1385436"},{"key":"e_1_2_19_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/jre.13337"},{"key":"e_1_2_19_4_1","doi-asserted-by":"publisher","DOI":"10.1186\/s12903-025-06108-w"},{"key":"e_1_2_19_5_1","doi-asserted-by":"publisher","DOI":"10.1007\/s15010-025-02568-y"},{"key":"e_1_2_19_6_1","doi-asserted-by":"publisher","DOI":"10.1113\/JP272427"},{"key":"e_1_2_19_7_1","doi-asserted-by":"publisher","DOI":"10.3390\/jcm14103415"},{"key":"e_1_2_19_8_1","doi-asserted-by":"publisher","DOI":"10.4317\/medoral.27304"},{"key":"e_1_2_19_9_1","doi-asserted-by":"publisher","DOI":"10.1111\/prd.70037"},{"key":"e_1_2_19_10_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1301970"},{"key":"e_1_2_19_11_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms20184541"},{"key":"e_1_2_19_12_1","doi-asserted-by":"publisher","DOI":"10.3390\/jcm13195978"},{"key":"e_1_2_19_13_1","doi-asserted-by":"publisher","DOI":"10.3390\/jcm12155140"},{"key":"e_1_2_19_14_1","doi-asserted-by":"publisher","DOI":"10.1111\/prd.12427"},{"issue":"1","key":"e_1_2_19_15_1","first-page":"S1","article-title":"A New Classification Scheme for Periodontal and Peri\u2010Implant Diseases and Conditions \u2010 Introduction and Key Changes From the 1999 Classification","volume":"89","author":"Caton J. 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