Hyperglycemia in obese type 2 diabetes mellitus rats affects pulp wound healing

Hyperglycemia in individuals with type 2 diabetes mellitus is associated with delayed wound healing, although the underlying mechanism remains unclear. Macrophages play a crucial role in the initiation, maintenance, and resolution of inflammation by polarizing into proinflammatory and anti-inflammatory subtypes. Hyperglycemia may interfere with odontoblast-like cell differentiation and cause persistent proinflammatory polarization in individuals with type 2 diabetes mellitus.

Eight-week-old spontaneously diabetic Torii fatty rats (model rats for type 2 diabetes mellitus) and Sprague-Dawley rats (control group, four rats per group) were used. The upper left first molars underwent pulpotomy and were capped with mineral trioxide aggregates for observation after seven days. Osteopontin expression was analyzed to assess the initiation of wound healing. Immunofluorescence analysis of nestin and alpha-smooth muscle actin was used to evaluate odontoblast-like cell differentiation. Double-positive cells among proinflammatory and anti-inflammatory macrophages were counted. Furthermore, the proliferating cell nuclear antigen (PCNA), Thy1, and CD146 were evaluated to assess cell proliferation and mesenchymal stem cells.

Inflammation persisted in the model rats, and no reparative dentin was formed. Macrophages in the model rats showed an increased proinflammatory response and a reduced anti-inflammatory response.

Hyperglycemia interferes with macrophage polarization and odontoblast-like cell differentiation, thus impairing wound healing in this model.