{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T08:12:50Z","timestamp":1778227970762,"version":"3.51.4"},"reference-count":40,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2026,5,5]],"date-time":"2026-05-05T00:00:00Z","timestamp":1777939200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Delta Dental of Michigan Foundation"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["JDR Clinical &amp; Translational Research"],"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>This investigation evaluated the predictive capacity of the oral microbiome and host salivary biomarkers on treatment outcomes for periodontitis in patients with type 2 diabetes mellitus (T2DM).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Two patient cohorts were enrolled: T2DM without periodontitis (DWoP; n = 32) and T2DM with periodontitis (DWP; n = 29). Whole saliva was collected at baseline and 4 to 7 wk posttreatment (i.e., DWoP, supragingival prophylaxis; DWP, scaling and root planing). The oral microbiome (operational taxonomic units; OTUs) and targeted salivary biomarkers were assessed in pre- and posttreatment saliva.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Most OTUs (57%\u201368%) and salivary biomarkers (43%\u201355%) decreased after treatment in both groups. Supragingival prophylaxis in the DWoP patients altered a limited number of taxa (V. dispar, P. denticola, Rothia, Neisseria), showing substantial increases in the microbiome, whereas predominantly gram-negative OTUs decreased. In the DWP, decreases were observed following therapy for Bacillota, Bacteroidetes, and Proteobacteria, again representing primarily gram-negative taxa. Microbe-host response biomarker correlations increased posttherapy in DWoP and decreased in DWP samples. Importantly, poor response (PR) to therapy was independent of HbA1c levels but associated with higher pretreatment levels of multiple bacterial genera (i.e., Alloprevotella, Campylobacter, Corynebacterium, Fusobacterium, and Leptotrichia) and elevated levels of interleukin (IL)\u20131b, IL-6, matrix metalloprotease\u20138 (MMP-8), adiponectin, and resistin. After therapy, PR was characterized by increases in Lachnospiraceae, Prevotella, and a lack of effects on Leptotrichia, Alloprevotella, Porphyromonas, and Stomatobaculum.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Poor clinical response to therapy was characterized by (1) less microbiome diversity and elevated levels of specific bacteria and salivary analytes pretherapy and (2) posttherapy elevations in multiple taxa and sustained levels of IL-1b and MMP-8 in both groups of PR patients. These findings support that a panel of salivary features could enhance our prediction and earlier decisions on response to therapy at the biological level, thus opening the door for more precise patient-level management.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Knowledge Transfer Statement:<\/jats:title>\n                    <jats:p>These findings contribute to a pathway for understanding oral health using biological measures as a standard for better decisions in oral health care. Specifically, microbiome and host response parameters provided important insights with predictive value and differential biological presentation related to response to therapy. While these measures do not dictate disease causation, they appear to reflect the periodontal environment, hallmarks of disease, and response to therapy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/23800844261437825","type":"journal-article","created":{"date-parts":[[2026,5,6]],"date-time":"2026-05-06T06:48:11Z","timestamp":1778050091000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Salivary Biological Responses to Nonsurgical Periodontal Treatment in Type 2 Diabetics"],"prefix":"10.1177","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9743-6585","authenticated-orcid":false,"given":"J.L.","family":"Ebersole","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences, School of Dental Medicine, University of Nevada Las Vegas, Las Vegas, NV, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.S.","family":"Kirakodu","sequence":"additional","affiliation":[{"name":"Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2486-7931","authenticated-orcid":false,"given":"X.","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Kentucky, Lexington, KY, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"suffix":"III","given":"D.","family":"Dawson","sequence":"additional","affiliation":[{"name":"Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY, USA"},{"name":"Department of Oral Health Practice, Center for Oral Health Research, of Dentistry, University of Kentucky, Lexington, KY, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.S.","family":"Miller","sequence":"additional","affiliation":[{"name":"Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY, USA"},{"name":"Department of Oral Health Practice, Center for Oral Health Research, of Dentistry, University of Kentucky, Lexington, KY, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2026,5,5]]},"reference":[{"key":"e_1_3_3_2_1","doi-asserted-by":"crossref","unstructured":"Armitage GC; Research Science and Therapy Committee of the American Academy of Periodontology. 2003. 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Diabetes and periodontal diseases: consensus report of the joint EFP\/AAP workshop on periodontitis and systemic diseases. J Periodontol. 84(4 suppl):S106\u2013S112. https:\/\/doi.org\/10.1902\/jop.2013.1340011","DOI":"10.1902\/jop.2013.1340011"},{"key":"e_1_3_3_6_1","doi-asserted-by":"crossref","unstructured":"Chapple ILC et al. 2018. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: consensus report of Workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 89(suppl 1):S74\u2013S84. https:\/\/doi.org\/10.1002\/jper.17-0719","DOI":"10.1002\/JPER.17-0719"},{"key":"e_1_3_3_7_1","doi-asserted-by":"crossref","unstructured":"D\u2019Aiuto F et al. 2018. Systemic effects of periodontitis treatment in patients with type 2 diabetes: a 12 month single-centre investigator-masked randomised trial. 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