Student Theses, Dissertations and Capstones
Document Type
Thesis - NSU Access Only
Degree Name
Master of Science (M.S.) in Dentistry
Copyright Statement
All rights reserved. This publication is intended for use solely by faculty, students, and staff of Nova Southeastern University. No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, now known or later developed, including but not limited to photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author or the publisher.
Department
College of Dental Medicine
First Advisor
Xiaozhe Han
Date of original Performance / Presentation
January 2026
Publication Date / Copyright Date
1-1-2026
NSUWorks Citation
Jacques Christopher Jaar. 2026. Diabetes Exacerbates Experimental Peri-implantitis in Mice through Enhanced IL-17-mediated Pathogenesis and a Sustained Alteration of the Oral Microbiome. Master's thesis. Nova Southeastern University. Retrieved from NSUWorks, College of Dental Medicine. (172)
https://nsuworks.nova.edu/hpd_cdm_stuetd/172.
Abstract
Diabetes is a major risk factor for peri-implantitis. This study investigated the role of interleukin-17 (IL-17) in peri-implant inflammation and oral microbiome alterations under hyperglycemic and normoglycemic conditions. Wild-type (WT) and diabetic (db/db) mice with maxillary implants underwent ligature placement with or without IL-17A neutralization. Db/db mice exhibited greater peri-implant bone loss, increased osteoclastogenesis, and elevated RANKL/OPG ratio compared to WT. These changes were accompanied by higher Il17a expression, reduced anti-inflammatory cytokines (Il1rn, Il10, Vegfa), increased Th17 infiltration, and deficient Treg responses. Anti-IL-17A treatment attenuated inflammation and bone resorption in both groups. Notably, ligature-induced Il17f upregulation occurred only in db/db mice. Microbial alterations induced by ligature were partially alleviated by IL-17A inhibition in WT mice, whereas diabetes-associated alterations persisted regardless of ligation or treatment. Cellular pro-inflammatory responses to peri-implant microbiota could be more effectively alleviated by IL-17A inhibition in WT than in DB. These findings suggest that exacerbated peri-implantitis in diabetes is driven by heightened IL-17-mediated inflammation and persistent microbial alterations, underscoring the need for more comprehensive therapeutic approaches to address this disease under diabetic conditions.
Disciplines
Dentistry
Files
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