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.

Corticotomy is an effective approach in accelerating orthodontic tooth movement (OTM) in clinical treatment. Corticotomy causes regional acceleratory phenomenon (RAP) in the alveolar bone of surgical sites. However, the molecular mechanism of RAP after corticotomy remains unclear. Herein, we established a mouse model to study the biomechanical interfaces of corticotomy-assisted OTM and to investigate the histological responses and underlying cellular mechanism. A total of 144 male C57BL/6 mice were randomly assigned into four groups: corticotomy alone (Corti), sham operation (Sham), corticotomy with tooth movement (Corti + TM), and sham operation with tooth movement (Sham + TM). Nickel–titanium orthodontic springs were applied to trigger tooth movement. Mice were sacrificed on Post-Surgery Day (PSD) 3, 7, 14, 21, and 28 for radiographic, histological, immunohistochemical, and molecular biological analyses. The results reveal that corticotomy significantly promoted alveolar bone turnover and periodontal tissue remodeling. During orthodontic tooth movement, corticotomy significantly promoted osteogenic and proliferative activity, accelerated tooth movement, and eliminated root resorption by upregulating Wnt signal pathway.

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Aim The osseointegration of dental implants is impaired in patients with osteoporosis, leading to significantly higher failure rates. This study set out to investigate the potential effects of alpha‐ketoglutarate (α‐KG) on implant osseointegration in an osteoporotic mouse model. Materials and Methods Female C57BL/6 mice received ovariectomy and bilateral first maxillary molar extraction at the age of 7 weeks. Dental implants were inserted 8 weeks after tooth extraction. In one of the groups, α‐KG was administered via drinking water throughout the experimental period. Specimens were collected on post‐implant days (PIDs) 3, 7, 14, and 21 for micro‐CT, histological, and immunohistochemical analyses. At the same time, bone‐marrow‐derived mesenchymal stem cells (BMMSCs) treated with α‐KG were interrogated for osteogenic differentiation, autophagic activity, and apoptosis. Results α‐KG supplementation in drinking water resulted in enhanced dental implant osseointegration in ovariectomized mice, with up‐regulated osteogenic and autophagic activity and down‐regulated osteoclast differentiation and cell apoptosis. α‐KG‐treated BMMSCs showed enhanced activity in proliferation, survival, colony formation, and osteogenic differentiation, as well as autophagic activity. Conclusions Systemic α‐KG supplementation effectively prevents the failure of dental implant osseointegration in mice under an osteoporotic state.