Msx2 −/− transgenic mice develop compound amelogenesis imperfecta, dentinogenesis imperfecta and periodental osteopetrosis

Aïoub, M.; Lézot, F.; Molla, M.; Castaneda, B.; Robert, B.; Goubin, G.; Néfussi, J.R.; Berdal, A.

doi:10.1016/j.bone.2007.07.023

Cited by 91dental development and anomaliesBone Metabolism and DiseasesBone and Dental Protein Studies

Msx2 −/− transgenic mice develop compound amelogenesis imperfecta, dentinogenesis imperfecta and periodental osteopetrosis

Aïoub, M., Lézot, F., Molla, M., Castaneda, B., Robert, B., Goubin, G., Néfussi, J.R., Berdal, A.·2007·Bone

DOI 10.1016/j.bone.2007.07.023

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Abstract

The physiological function of the transcription factor Msx2 in tooth and alveolar bone was analysed using a knock-in transgenic mouse line. In this mouse line, the beta-galactosidase gene was used to disrupt Msx2: thus, beta-galactosidase expression was driven by the Msx2 promoter, but Msx2 was not produced. This allowed to monitor Msx2 expression using a beta-galactosidase assay. Msx2 transgenic mice ubiquitously and continuously expressed the mutated Msx2-nlacZ gene in cells of the complex formed by tooth and alveolar bone. Msx2 -/- homozygous mice displayed a wide spectrum of alterations in tooth eruption and morphology as well as dental and periodontal defects from the first post-natal weeks up to 6 months. These defects culminated with the formation of an odontogenic tumour at the mandibular third molar site. This study suggests that bone resorption is a functional target of Msx2 in the alveolar compartment, since Msx2 was expressed in osteoclasts, with the highest expression levels found in the active sites of bone modelling associated with tooth eruption and root elongation. The RANK osteoclast differentiation pathway was affected in microdissected Msx2 -/- mouse alveolar bone (as inferred by RANK ligand mRNA levels) compared to basal bone and wild-type controls. Decreased alveolar osteoclast activity was observed in Msx2 -/- mice, similar to that seen in osteopetrosis, another condition in which osteoclast activity is impaired and odontogenic tumours form. These data suggest a pleiotropic role for Msx2 in oral bone growth from birth until adult homeostasis. RANK pathway appeared to be modulated by Msx2, in addition to the previously reported modulations of BMP4 and laminin5alpha3 in early tooth development. Non-overlapping Msx1 and Msx2 expression patterns suggested that these two homeogenes play non-redundant roles in skeletal growth, with Msx1 targeting basal bone and Msx2 targeting alveolar bone. This study provides a detailed analysis of the phenotype resulting from the Msx2 null mutation and identifies the impact of Msx1 and Msx2 on post-natal oral bone growth.

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Global Msx2 knockout impairs osteoclast formation, whereas loss of Irx3 has no effect on osteoclasts.
“According to previous studies, global Msx2 knockout impairs osteoclast formation, whereas loss of Irx3 has no effect on osteoclasts26,27.”
From Targeting Msx2 as a brake in the fusion fate of osteoclasts and an anabolic therapy in pre-clinical models of osteoporosis (2025) · cites this paper as [26]
Msx2 null mutation leads to periodontal osteopetrosis, with impaired osteoclast generation in alveolar bones.
“In a Msx2−/− transgenic mouse model, Msx2 null mutation leads to periodontal osteopetrosis, with impaired osteoclast generation in alveolar bones26.”
From Targeting Msx2 as a brake in the fusion fate of osteoclasts and an anabolic therapy in pre-clinical models of osteoporosis (2025) · cites this paper as [26]

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Distorted Patterns of Dentinogenesis and Eruption in Msx2 Null Mutants
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Experimental periodontitis in Msx2 mutant mice induces alveolar bone necrosis
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Authors: Aïoub, M., Lézot, F., Molla, M., Castaneda, B., Robert, B., Goubin, G., Néfussi, J. R., & Berdal, A.
Affiliations: Inserm (FR)
Centre National de la Recherche Scientifique (FR)
Corresponding author: Berdal, A.
ORCID: Lézot, F.
Berdal, A.
Venue: Bone
Publisher: Elsevier BV
Published: 2007-11
Volume: 41
Issue: 5
Pages: 851-859
ISSN: 1873-2763 (ISSN-L)
8756-3282
DOI: 10.1016/j.bone.2007.07.023
OpenAlex: W2119800259
Cited by: 91
References: 43
Citations by year: 2026: 3 · 2025: 4 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 3 · 2020: 4 · 2019: 8 · 2018: 3 · 2017: 8 · 2016: 4 · 2015: 6 · 2014: 8 · 2013: 4 · 2012: 3
FWCI: 2.64
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Bone (publishedVersion)
PubMed (publishedVersion)
Funders: Institut National de la Santé et de la Recherche Médicale
Université Paris Diderot
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › dental development and anomalies
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
Health Sciences › Medicine › Rheumatology › Bone and Dental Protein Studies
Keywords: Msx2, transcription factors, amelogenesis imperfecta, dentinogenesis imperfecta, alveolar bone, tooth eruption, odontogenic tumors, osteoclasts, RANK ligand, bone resorption, MSX1, tooth development, root elongation
MeSH terms: Animals, Base Sequence, Cell Communication, Cell Differentiation, DNA-Binding Proteins, Mice, Transgenic, Osteoclasts, Osteopetrosis, Phenotype, RNA, Messenger, Tooth Diseases, DNA Primers, Homeodomain Proteins, Reverse Transcriptase Polymerase Chain Reaction, Mice, RANK Ligand

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Msx2 −/− transgenic mice develop compound amelogenesis imperfecta, dentinogenesis imperfecta and periodental osteopetrosis

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