Lithium chloride promotes osteogenesis and suppresses apoptosis during orthodontic tooth movement in osteoporotic model via regulating autophagy

Abstract

Osteoporosis is a widely distributed disease that may cause complications such as accelerated tooth movement, bone resorption, and tooth loss during orthodontic treatment. Promoting bone formation and reducing bone resorption are strategies for controlling these complications. For several decades, the autophagy inducer lithium chloride (LiCl) has been explored for bipolar . In this study, we investigated the autophagy-promoting effect of LiCl on bone remodeling under osteoporotic conditions during tooth movement. Ovariectomy was used to induce osteoporosis status in vivo. The results showed that LiCl rejuvenated autophagy, decreased apoptosis, and promoted bone formation, thus protecting tooth movement in osteoporotic mice. Furthermore, in vitro experiments showed that LiCl reversed the effects of ovariectomy on bone marrow-derived mesenchymal stem cells (BMSCs) extracted from ovariectomized mice, promoting osteogenesis and suppressing apoptosis by positively regulating autophagy. These findings suggest that LiCl can significantly decrease adverse effects of osteoporosis on bone remodeling, and that it has great potential significance in the field of bone formation during tooth movement in osteoporosis patients.

Tideglusib enhances odontogenic differentiation in human dental pulp stem cellsin vitro

“…Other small‐molecule GSK‐3β antagonists had a similar effect on apoptosis inhibition. The inhibitory effect of LiCl on apoptosis has been reported in mouse dental pulp cells (Vijaykumar & Mina, 2021) and bone marrow mesenchymal stem cells (Huang et al, 2021; Kazemi Mehrjerdi et al, 2018). 6‐bromoindirubin‐3′‐oxime also targets GSK‐3β.…”

Bone regeneration strategies based on organelle homeostasis of mesenchymal stem cells

“…Yin et al (148) reported that autophagy was suppressed in PDLSCs cultured under inflammatory conditions, and this inhibition of autophagic function was mediated by disorders of autophagosome-lysosome fusion and impaired activation of transcription factor EB (TFEB). Researchers have found that Lithium chloride inhibit apoptosis of MSCs in osteoporosis and reduces bone loss through upregulation of autophagic flux (149,150). Conversely, in wear particle-induced osteolysis models in vitro and in vivo, implant wear particles (CoCrMo metal particles) over activate autophagy and inhibit bone formation, becoming the most common cause of implant aseptic loosening and total hip arthroplasty failure (71).…”

Regulating Macrophage Polarization in High Glucose Microenvironment Using Lithium‐Modified Bioglass‐Hydrogel for Diabetic Bone Regeneration

“…Previous studies have shown that lithium chloride (LiCl) promoted osteogenesis and accelerates the time of bone fracture. Huang et al [ 14 ] applied LiCl in osteoporotic model, demonstrating that LiCl was beneficial to the proliferation of bone marrow‐derived mesenchymal stem cells (BMSCs) and promoted osteogenesis by regulating autophagy. Peng et al [ 15 ] found that the appropriate addition of lithium could enhance cell attachment and stimulate osteogenesis.…”