School of Podiatric Medicine - Student Research

Document Type

Poster

Publication Date

Fall 7-26-2024

Abstract

Introduction and Hypothesis: Diabetes can impair implant osseointegration and impact implant functionality. While significant research has focused on osteogenesis during the osseointegration, little attention has been given to pre-osteoclast differentiation. We hypothesize that diabetes increases pre-osteoclast activity potentially leading to implant failure. This study aims to identify and localize osteoclast markers, specifically DC-STAMP (Dendritic Cell-Specific Transmembrane Protein) and NFATc2 (Nuclear Factor of Activated T-cells, cytoplasmic 2), in diabetic (D) and non-diabetic (ND) mice.

Methodology: Twenty-four 16-week-old male 129 Sv mice (12 diabetic and 12 non-diabetic) underwent implantation with a 0.5x1.5 mm commercially pure titanium screw in the right maxillary bone. Diabetes was induced in mice using a high-fat diet followed by two consecutive streptozotocin injections (100mg/kg) one week prior to surgery. At 7 and 21 days post-implantation, six mice from each group were euthanized, and samples were collected for immunofluorescence analysis targeting DC-STAMP (TRITC) and NFATc2 (FITC), with DAPI blue staining for nuclei.

Results: The D group exhibited signs of inflammation and incomplete epithelization, contrasting with the ND group, which showed signs of successful clinical healing. NFATc2 and DC-STAMP primarily co-localized in multinucleated cells, indicative of osteoclasts, in both groups. However, the intensity of both markers in ND group decreased significantly at 21 days, primarily found in remodeling trabeculae. Conversely, D-group from the same timeframe showed a widespread presence of co-localized DC-STAMP and NFATc2 cells, particularly in areas of implant failure.

Discussion and Conclusion: This study demonstrates that diabetes negatively impacts the osseointegration of titanium implants through the modulation of osteoclast differentiation and activity.

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