(c) Morphology of peri-implant trabecular separation. In the diabetic-GL group, the reduction in trabecular number caused by diabetes was relieved, but not eliminated. While in the control group, the trabeculae got denser and well organized. After another healing period of 4 weeks, however, the trabeculae became sparser and thinner among rats in the diabetic group. Four weeks after implantation, the trabecular thickness and number were quite similar in three groups. (b) Morphology of peri-implant trabeculae. (a) Quantification of BV/TV, Tb.N, Tb.Th, and Tb.Sp within the VOI. Inhibiting HMGB1 rescued impaired osseointegration in diabetic rats. Taken together, inhibiting HMGB1 can be an effective approach to relieve BMSC dysfunction and enhance osseointegration under diabetic environment. In diabetic rats, GL administration suppressed the upregulation of HMGB1, attenuated the lipoperoxide, and ameliorated the impaired trabecular structure and osseointegration. By these approaches, we demonstrated that inhibiting HMGB1 by GL significantly attenuated HG-induced upregulation of HMGB1, HMGB1 ligand receptor for advanced glycation end products (RAGE) and their interaction, relieved oxidative stress, and reversed the downregulation of osteogenic markers, resulting in improved osteogenic differentiation. After 4 and 8 weeks, plasma lipoperoxide detection, μCT analysis, and histomorphometric evaluation were conducted. Rats received GL (50 mg/kg, i.p.) or vehicle treatment daily after titanium implants were planted into the tibiae. In vivo, 8-week-old Sprague-Dawley rats were categorized to control, streptozotocin-induced diabetic, and diabetic-GL groups. Cell proliferation, osteogenic behaviors, and oxidative stress were determined. In vitro, BMSCs were treated with normal glucose (NG), high glucose (HG), and HG+glycyrrhizin (HMGB1 inhibitor, HG+GL). This article is aimed at investigating the effects of HMGB1 on dysfunction of bone marrow stromal cells (BMSCs) and impaired osseointegration under diabetic environment. High mobility group box 1 (HMGB1) participates actively in oxidative stress damage and the latter relates closely to diabetic complications, including poor implant osseointegration.
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