Potential role of high mobility group box protein 1 and intermittent PTH (1–34) in periodontal tissue repair following orthodontic tooth movement in rats
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Recent studies indicate that high mobility group box protein 1 (HMGB1) can be released by necrotic and damaged cells and functions as an alarmin that is recognized by the innate immune system. Little is known about the role of HMGB1 within the periodontal ligament (PDL). Therefore, we examined HMGB1 expression by PDL cells in vitro and compared the findings to an in vivo model of orthodontically induced tooth root resorption. In addition, we addressed the question of whether a potentially anabolic intermittent administration of parathyroid hormone (iPTH) would modulate the expression of HMGB1.
Materials and methods
In confluent PDL cell cultures, HMGB1 messenger RNA (mRNA) expression was quantified by real-time polymerase chain reaction. In a rat model comprising 25 animals, mechanical loading for 5 days was followed by administration of either iPTH (1–34) systemically or sham injections for up to 56 days. HMGB1 expression was determined by means of immunohistochemistry and histomorphometry.
The in vitro experiments revealed an inhibitory effect of iPTH on basal HMGB1 mRNA expression in confluent PDL cells. In vivo, the mechanical force-induced enhanced HMGB1 protein expression declined time dependently. Intermittent PTH further inhibited HMGB1 expression. The significantly higher basal HMGB1 protein expression in the former compression side was followed by a more pronounced time- and iPTH-dependent decline in the same area.
These data indicate a major role for HMGB1 in the regulation of PDL wound healing following mechanical load-induced tissue injury.
The findings point to the potential benefit of iPTH in the attempt to support these immune-associated reparative processes.
KeywordsPeriodontal ligament HMGB1 iPTH Tooth movement In vivo
The authors thank Mrs. Schaffrath for expert technical assistance and the German Research Foundation (DFG) as well as the Medical Faculty of the University of Bonn for providing a research grant (KFO 208, TP8, LO-1181/2-2). The authors declare that they have no conflict of interest.
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