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Enamel alterations in serotonin 2B receptor knockout mice
Author(s) -
Harichane Yassine,
DimitrovaNakov Sasha,
Marchadier Arnaud,
Collet Corinne,
Baudry Anne,
Vidal Catherine,
KamounGoldrat Agnès,
Kellermann Odile,
Goldberg Michel
Publication year - 2011
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 - 10.1111/j.1600-0722.2011.00908.x
Subject(s) - ameloblast , enamel paint , knockout mouse , chemistry , amelogenesis , serotonin , receptor , mineralization (soil science) , molar , endocrinology , medicine , biochemistry , dentistry , biology , organic chemistry , nitrogen
Harichane Y, Dimitrova‐Nakov S, Marchadier A, Collet C, Baudry A, Vidal C, Kamoun‐Goldrat A, Kellermann O, Goldberg M. Enamel alterations in serotonin 2B receptor knockout mice.
Eur J Oral Sci 2011; 119 (Suppl. 1): 177–184. © 2011 Eur J Oral Sci The role of the serotonin 2B receptor (5‐HT 2B R) in enamel formation and mineralization was explored in adult 5HT 2B R knockout (KO) mice compared with wild‐type (WT) mice. In the molar, quantitative data obtained by micro‐computed tomography imaging showed that the overall volume of the enamel layer was firmly reduced in KO mice. Defective mineralization was ascertained by energy‐dispersive X‐ray microanalysis. We also observed, using scanning electron microscopy, that parazones in the KO mice included two or three helicoidally twisted rods within Hunter–Schreger bands, instead of a single rod, as found in the WT mice. Minor disturbances were also detected in the incisors of KO mice. Structural modifications, thinner enamel crystallites, and porosities observed in KO mice indicate that the 5‐HT 2B R‐mediated signaling pathways as part of the enamel formation process. These data provide a basis for evaluating the role of 5‐HT 2B R in ameloblast functions. Defects observed in the mineralization and structure of enamel in KO mice highlight that the 5‐HT 2B R interferes with the mechanisms directing amelogenesis.