Diabetes mellitus exacerbates inflammation in a murine model of ligature-induced peri-implantitis: A histological and microtomographic study.

Silva, Davi N A; Monajemzadeh, Sepehr; Casarin, Maísa; Chalmers, Jaclyn; Lubben, Jacob; Magyar, Clara E; Tetradis, Sotirios; Pirih, Flavia Q

Silva, Davi N A; Monajemzadeh, Sepehr; Casarin, Maísa; Chalmers, Jaclyn; Lubben, Jacob; Magyar, Clara E; Tetradis, Sotirios; Pirih, Flavia Q.

Afiliação

Silva DNA; Section of Periodontics, School of Dentistry, University of California, Los Angeles, California, USA.
Monajemzadeh S; Section of Periodontics, School of Dentistry, University of California, Los Angeles, California, USA.
Casarin M; School of Dentistry, Federal University of Pelotas, Pelotas, Brazil.
Chalmers J; Section of Periodontics, School of Dentistry, University of California, Los Angeles, California, USA.
Lubben J; Section of Periodontics, School of Dentistry, University of California, Los Angeles, California, USA.
Magyar CE; Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
Tetradis S; Section of Oral and Maxillofacial Radiology, University of California, Los Angeles, California, USA.
Pirih FQ; Section of Periodontics, School of Dentistry, University of California, Los Angeles, California, USA.

J Clin Periodontol ; 2024 Aug 12.

Article em En | MEDLINE | ID: mdl-39135333

ABSTRACT

ABSTRACT

AIM:

To investigate the influence of diabetes mellitus (DM) in a murine model of peri-implantitis (PI). MATERIALS AND

METHODS:

Twenty-seven 4-week-old C57BL/6J male mice had their first and second maxillary left molars extracted. Eight weeks later, one machined implant was placed in each mouse. Four weeks after osseointegration, the mice were divided into three groups (a) control (C), (b) PI and (c) DM + PI. DM was induced by streptozotocin (STZ) administration. After DM induction, PI was induced using ligatures for 2 weeks. The hemimaxillae were collected for micro-CT and histological analyses. The primary outcomes consisted of linear (mm) and volumetric (mm3) bone loss. Secondary outcomes were based on histological analysis and included inflammatory infiltrate, osteoclastic activity, matrix organization, composition and remodelling. Data are presented as means ± SEM. Statistical analyses were performed using one-way ANOVA, followed by Tukey's test.

RESULTS:

Gingival tissue oedema was detected in the PI and DM + PI groups. Micro-CT showed significantly increased linear and volumetric bone loss in the DM + PI group compared to the C and PI groups. H&E staining showed greater inflammatory response and bone resorption in the PI and DM + PI groups than in the C group. The DM + PI group had significantly higher osteoclast numbers than the C and PI groups. Picrosirius red stained less for types I and III collagen in the PI and DM + PI groups than in the C group. There was a significant increase in monocyte/macrophage (CD-11b) counts and matrix metalloproteinases (MMP-2 and MMP-8) marker levels and a significant decrease in the matrix metalloproteinases inhibition marker (TIMP-2) levels in the DM + PI group compared to the C and PI groups.