Premium
Delay of tooth eruption in null mice devoid of the type I IL‐1R gene
Author(s) -
Huang Heguang,
Wise Gary E.
Publication year - 2000
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1034/j.1600-0722.2000.108004297.x
Subject(s) - dental follicle , tooth eruption , gene expression , hair follicle , biology , gene , endocrinology , medicine , microbiology and biotechnology , molar , dentistry , genetics , stem cell
Interleukin‐one alpha (IL‐1α) is located in the stellate reticulum and its receptor, type I IL‐1R (IL‐1R), is present in the adjacent dental follicle. IL‐1α may play a role in initiating tooth eruption because of its ability to enhance the gene expression in the dental follicle of putative tooth eruption molecules – colony‐stimulating factor‐one (CSF‐1), monocyte chemotactic protein‐1 (MCP‐1), and nuclear factor kappa B (NFκB). To directly examine the effect of IL‐1α and IL‐1R on tooth eruption, we observed the times of tooth eruption in null mice devoid of the type I IL‐1R gene. The results showed that the time of eruption in the null mice was delayed by 2 d for the first mandibular molar and 1 d for incisors as compared to wild type controls. Reverse transcription‐polymerase chain reaction (RT‐PCR) techniques confirmed the absence of the IL‐1R gene in the null mice, but the genes for CSF‐1 and NFκB were still expressed. Thus, a molecule(s) other than IL‐1α also may enhance the expression of CSF‐1 and NFκB in the dental follicle. Because there is a slight delay of tooth eruption in IL‐1R null mice, IL‐1α may normally play a role in eruption. However, eruption eventually can occur without the signaling from IL‐1α.