Trehalose-Coated Implant for Prevention of Inflammation in Bone
Min-Suk Kook DDS, PhD, Oral and Maxillofacial Surgery, Chonnam National University, Gwangju, South Korea
Hong-Ju Park DDS, PhD, Oral and Maxillofacial Surgery, Chonnam National University, Gwangju, South Korea
Hee-Kyun Oh DDS, PhD, Oral and Maxillofacial Surgery, Chonnam National University, Gwangju, South Korea
Sun-Youl Ryu DDS, PhD, Oral and Maxillofacial Surgery, Chonnam National University, Gwangju, South Korea
Sam-Young Park PhD, Oral Physiology, Chonnam National University, Gwangju, South Korea
Ji-Yeon Jung PhD, Oral Physiology, Chonnam National University, Gwangju, South Korea
Won-Jae Kim PhD, Oral Physiology, Chonnam National University, Gwangju, South Korea
Bone inflammation is one of major causes in dental implant failure. This study is aimed to investigate whether autophagy may ameliorate or prevent bone inflammation associated with dental implant failure. In the present study, autophagy was directly involved in odontogenic differentiation from human dental pulp stem cell but not in osteogenic differentiation from MC3T3 mesenchymal stem cell under differentiation inductive medium (DM) including 50 μM/L ascorbic acid and 5 mM/L β-glycerophosphate. Lipopolysaccharide(LPS), a bacterial endotoxin, inhibited osteogenic differentiation from MC3T3 stem cell co-cultured with RAW 264.7 cell, a macrophagy cell line but did not influence osteogenic differentiation from MC3T3 mesenchymal stem cell without RAW 264.7 cell under DM. LPS up-regulated and released inflammatory cytokines such as IL-1,6 and TNF in RAW 264.7 cell.
Trehalose, an autophagy enhancing agent, rescued LPS -induced impaired osteogenic differentiation from MC3T3 stem cell co-cultured with RAW 264.7 cell and ameliorated LPS -induced up-regulated and -released inflammatory cytokines such as IL-1 and 6 in RAW 264.7 cell. In the rabbit calvarium, implants coated with trehalose showed an increment of new bone formation and a decrement of inflammatory responses under P gingivalis and LPS treatment compared to the control.
From these results, autophagy reduces bone inflammation through inhibiting inflammatory cytokine production in macrophagy and implant coated with trehalose, an autophagy enhancer, is available for inflammed and infected bone.
References
1. Ravikumar et al,. Regulation of mammalian autophagy in physiology and pathology. Physiol. Review 2011
2. Waters et al,. Autophagy receptor Nbr1 and P62 co-regulate skeletal remodeling. Autophagy 2010
