Abstract
Dentin formation was dependent on osteo-/odontogenic differentiation of dental pulp stem cells (DPSCs). It was observed in previous studies that antibiotic treatment in a clinical and animal model resulted in impaired mineralization of dental tissues. We previously reported that microbiota maintained the function of bone marrow mesenchymal stem cells, while whether microbiota dysbiosis caused by antibiotic treatment contributed to DPSCs dysfunction and impaired dentin formation is still not known. In this study, we aimed to clarify the role of microbiota or its metabolic products on dental mineralization and the function of DPSCs. Mice were treated with antibiotics to disrupt microbiota; then, the growth rate and histological characteristics of incisors as well as the biological characteristics of DPSCs in vitro were compared with specific pathogen-free (SPF) mice. In antibiotic-treated mice (AbT), we found a diminished quantity of microbiota and reduced growth rate of mechanical injured incisor, as well as decreased colony-forming rate and impaired ability of osteo-/odontogenic differentiation of DPSCs, in comparison to SPF mice. Colonization of AbT mice with SPF mice replanted the microbiota by cohousing (conventionalized (ConvD)) and normalized the growth rate of injured incisors and colony-forming and osteo-/odontogenic differentiation ability of DPSCs. Giving short-chain fatty acids (SCFAs) by oral gavage after antibiotic treatment also rescued the growth rate of incisors and the differentiation ability of DPSCs and enhanced proliferation ability of DPSCs. Collectively, gut microbiota could make contribution to maintain continuous growth of injured rodent incisor and differentiation capacity of DPSCs; SCFAs might play a crucial role in this process.
Highlights
Antibiotics are by far the most common medications prescribed for children
We compared the growth rate of incisors. 2 mm of the right incisor was clipped in specific pathogen-free (SPF), antibiotic-treated mice (AbT), and conventionalized group (ConvD) mice (Figure 1(a)); the height difference of bilateral lower incisors was measured every 24 h (Figure 1(b))
We showed that the osteo-/odontogenic differentiation potential of dental pulp stem cells (DPSCs), dentin mineralization, and continuous growing of mouse incisors were impaired in antibiotic-treated mice, which were characterized by reduced quantity of gut microbes
Summary
Studies have suggested the association between early antibiotic use and disease phenotypes in adulthood. Many clinical studies have found that antibiotic use during pregnancy or early childhood growth is associated with an increased risk of molar-incisor hypomineralization (MIH) [1,2,3,4], suggesting that antibiotics may lead to abnormal mineralization of dental hard tissues. Studies have confirmed that the use of antibiotics can disrupt gut microbiota and contribute to the occurrence and development of various diseases [5]. The dysbiosis of microbiota in diseases such as diabetes or antibiotic treatment caused organ or tissue dysfunction [12, 13], via the alteration of pathogenassociated molecular patterns (PAMPs) including agents like peptidoglycans and lipopolysaccharide (LPS) or metabolites of microbiota such as short-chain fatty acids (SCFAs)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
