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Overexpression of Dlx2 leads to postnatal condyle degradation.

Dai J, Si J, Zhu X, Zhang L, Wu D, Lu J, Ouyang N, Wang X, Shen G - Mol Med Rep (2016)

Bottom Line: The model was constructed and the phenotype observed using gross observation, micro‑CT scan and histological examination.The model determined that overexpression of Dlx2 may lead to postnatal condyle malformation, subchondral bone degradation and irregular histological structure of the condylar cartilage.In addition, the expression of osteocalcin in the condyle region was markedly downregulated, whereas expression of msh homeobox 2 was upregulated.

View Article: PubMed Central - PubMed

Affiliation: Department of Oral and Cranio‑Maxillofacial Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, P.R. China.

ABSTRACT
Distal-less homeobox 2 (Dlx2), a member of the Dlx family of transcription factors, is important for the development of craniofacial tissues. Previous studies based on knock‑out mutant mice revealed that Dlx2 primarily disturbed the development of tissues from maxillary arch. The present study used a transgenic mouse model to specifically overexpress Dlx2 in neural crest cells in order to investigate the role of Dlx2 overexpression in post‑natal condyle in mice. The model was constructed and the phenotype observed using gross observation, micro‑CT scan and histological examination. The model determined that overexpression of Dlx2 may lead to postnatal condyle malformation, subchondral bone degradation and irregular histological structure of the condylar cartilage. In addition, the expression of osteocalcin in the condyle region was markedly downregulated, whereas expression of msh homeobox 2 was upregulated. The results of the present study suggest that Dlx2 overexpression in cranial neural crest cells would disrupt the development of post‑natal condyle, which demonstrates that the expression level and the spatiotemporal expression patterns of Dlx2 may be important in regulating the development of post-natal condyle in mice, and also offered a possible temporal‑mandibular joint osteoarthritis model animal for future studies.

No MeSH data available.


Related in: MedlinePlus

Overexpression of Dlx2 leads to postnatal condyle dysmorphia. (A) Small and abnormal condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. (B and D) and Alizarin red/Alcian blue staining (C and E) under an integrated microscope showed a thin cartilage cap (denoted with arrow heads) in the condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. Dlx2, distal-less homeobox 2.
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f2-mmr-14-02-1624: Overexpression of Dlx2 leads to postnatal condyle dysmorphia. (A) Small and abnormal condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. (B and D) and Alizarin red/Alcian blue staining (C and E) under an integrated microscope showed a thin cartilage cap (denoted with arrow heads) in the condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. Dlx2, distal-less homeobox 2.

Mentions: Observation under an integrated microscope demonstrated that P90 Wnt1Cre::iZEG-Dlx2 mice exhibited smaller mandible and condyle, and the condylar cartilage cap was malformed and thinner compared with the control group (Fig. 2). At P90, the reconstructed 3D images from micro-CT highlighted a cross-bite malocclusion, and bone defect in the mandible of Wnt1Cre::iZEG-Dlx2 mice (Fig. 3A and B). The 3D images and sagittal sections also showed osteoporosis in the condylar bone when compared with the control group (Fig. 3C and D). BMD analysis based on micro-CT examination suggested a significant decrease in BMD in the condylar bone in P90 Wnt1Cre::iZEG-Dlx2 mice compared with control mice (P<0.01; Fig. 3E). This demonstrated that osteoporosis occurred in the condyle, and implied that overexpression of Dlx2 may lead to condyle degradation or abnormal development.


Overexpression of Dlx2 leads to postnatal condyle degradation.

Dai J, Si J, Zhu X, Zhang L, Wu D, Lu J, Ouyang N, Wang X, Shen G - Mol Med Rep (2016)

Overexpression of Dlx2 leads to postnatal condyle dysmorphia. (A) Small and abnormal condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. (B and D) and Alizarin red/Alcian blue staining (C and E) under an integrated microscope showed a thin cartilage cap (denoted with arrow heads) in the condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. Dlx2, distal-less homeobox 2.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940110&req=5

f2-mmr-14-02-1624: Overexpression of Dlx2 leads to postnatal condyle dysmorphia. (A) Small and abnormal condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. (B and D) and Alizarin red/Alcian blue staining (C and E) under an integrated microscope showed a thin cartilage cap (denoted with arrow heads) in the condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. Dlx2, distal-less homeobox 2.
Mentions: Observation under an integrated microscope demonstrated that P90 Wnt1Cre::iZEG-Dlx2 mice exhibited smaller mandible and condyle, and the condylar cartilage cap was malformed and thinner compared with the control group (Fig. 2). At P90, the reconstructed 3D images from micro-CT highlighted a cross-bite malocclusion, and bone defect in the mandible of Wnt1Cre::iZEG-Dlx2 mice (Fig. 3A and B). The 3D images and sagittal sections also showed osteoporosis in the condylar bone when compared with the control group (Fig. 3C and D). BMD analysis based on micro-CT examination suggested a significant decrease in BMD in the condylar bone in P90 Wnt1Cre::iZEG-Dlx2 mice compared with control mice (P<0.01; Fig. 3E). This demonstrated that osteoporosis occurred in the condyle, and implied that overexpression of Dlx2 may lead to condyle degradation or abnormal development.

Bottom Line: The model was constructed and the phenotype observed using gross observation, micro‑CT scan and histological examination.The model determined that overexpression of Dlx2 may lead to postnatal condyle malformation, subchondral bone degradation and irregular histological structure of the condylar cartilage.In addition, the expression of osteocalcin in the condyle region was markedly downregulated, whereas expression of msh homeobox 2 was upregulated.

View Article: PubMed Central - PubMed

Affiliation: Department of Oral and Cranio‑Maxillofacial Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, P.R. China.

ABSTRACT
Distal-less homeobox 2 (Dlx2), a member of the Dlx family of transcription factors, is important for the development of craniofacial tissues. Previous studies based on knock‑out mutant mice revealed that Dlx2 primarily disturbed the development of tissues from maxillary arch. The present study used a transgenic mouse model to specifically overexpress Dlx2 in neural crest cells in order to investigate the role of Dlx2 overexpression in post‑natal condyle in mice. The model was constructed and the phenotype observed using gross observation, micro‑CT scan and histological examination. The model determined that overexpression of Dlx2 may lead to postnatal condyle malformation, subchondral bone degradation and irregular histological structure of the condylar cartilage. In addition, the expression of osteocalcin in the condyle region was markedly downregulated, whereas expression of msh homeobox 2 was upregulated. The results of the present study suggest that Dlx2 overexpression in cranial neural crest cells would disrupt the development of post‑natal condyle, which demonstrates that the expression level and the spatiotemporal expression patterns of Dlx2 may be important in regulating the development of post-natal condyle in mice, and also offered a possible temporal‑mandibular joint osteoarthritis model animal for future studies.

No MeSH data available.


Related in: MedlinePlus