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The Establishment of a Murine Mandibular Molar Extraction Socket Healing Model
Published on: January 13, 2023
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Denervation delays initial bone healing of rat tooth extraction socket
Zhenxian Sheng1,2, Fuju Zheng2, Jianbin Li1,2
1School of Stomatology, Binzhou Medical College, Yantai, 264000, Shandong, China.
Odontology
|December 13, 2022
Summary
Nerve damage (denervation) delays initial bone healing in rat tooth extraction sockets. This delay is linked to increased osteoclast activity and reduced Nrf2 expression, impacting bone regeneration.
Area of Science:
- Oral and Maxillofacial Surgery
- Bone Biology
- Regenerative Medicine
Background:
- Nerve function significantly influences bone healing processes.
- Understanding the role of the inferior alveolar nerve in mandibular bone repair is crucial.
Purpose of the Study:
- To investigate the impact of inferior alveolar nerve transection on initial bone healing following tooth extraction in rats.
- To elucidate the molecular mechanisms, including Nrf2 signaling and osteoclast activity, involved in denervation-induced changes in bone healing.
Main Methods:
- Wistar rats underwent tooth extraction with or without inferior alveolar nerve transection.
- Histological analysis, TRAP staining, immunofluorescence, immunohistochemistry, and micro-CT were employed at 1, 2, and 4 weeks post-extraction.
- In vitro studies assessed Nrf2 expression and osteoclast differentiation in bone marrow-derived macrophages.
Main Results:
- Denervation delayed initial bone healing, evidenced by reduced bone volume/total volume (BV/TV) and bone mineral density (BMD) at 4 weeks.
- Down-regulation of osteocalcin (OCN) and osteopontin (OPN) was observed in the denervated group.
- Increased TRAP-positive osteoclasts and decreased Nrf2 expression were noted at 2 weeks post-extraction.
- Reduced Nrf2 expression in vitro promoted osteoclast differentiation.
Conclusions:
- Denervation significantly delays initial bone healing in rat tooth extraction sockets.
- Decreased Nrf2 expression and subsequent osteoclast activation appear to be key mechanisms contributing to impaired bone regeneration after nerve injury.

