Type 2 Diabetes Impairs Alveolar Socket Healing: Immunohistochemical Analysis of Del-1, IL-17, RANKL, and OPG Expression in a Rat Model.

BACKGROUND

Type 2 diabetes (T2D) is known to impair bone healing, yet the molecular mechanisms underlying this process in alveolar sockets remain insufficiently understood. This study aimed to evaluate the expression of some key regulatory proteins related to angiogenesis and bone remodeling during alveolar socket healing in a diabetic rat model.

METHODS

Thirty-three male Sprague-Dawley rats were divided into control and T2D groups. T2D was induced by a high-fat diet combined with low-dose streptozotocin. Following mandibular molar extraction, animals were sacrificed at days 7, 14, and 28 postextraction. Alveolar bone tissues were examined using microcomputed tomography (micro-CT) for structural analysis. Immunohistochemical staining was performed to assess the expression patterns of developmental endothelial locus-1 (Del-1), interleukin 17 (IL-17), osteoprotegerin (OPG), and receptor activator of nuclear factor kappa-B ligand (RANKL) with semiquantitative evaluation. Parametric tests were used for group comparisons and correlation analyses.

RESULTS

Micro-CT analysis revealed reduced bone volume and trabecular integrity in the T2D group compared to controls. Del-1 was localized to vessel walls within the bone marrow, IL-17 was found in both bone tissue and marrow, while RANKL and OPG were detected in osteoblasts and osteocytes. Protein staining was mild or absent in diabetic groups (p  < 0.05) and declined over time.

CONCLUSION

T2D negatively affects bone healing, potentially by disrupting the expression balance of key proteins involved in angiogenesis and bone remodeling. These findings highlight the need for further research on molecular targets in diabetic bone repair.