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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

Histological analysis of condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. (A and B) Sagittal sections and H&E staining of iZEG-Dlx2 mice and P90 Wnt1Cre::iZEG-Dlx2 mice sections (Scale bar, 100 µm). Subchondral bone degradation and irregular cartilage histological structure was observed in the latter. (C–F) Sagittal sections and Alizarin red/Alcian blue staining showed irregular cartilage histological structure and less hypertrophic chondrocytes (blue) in the P90 Wnt1Cre::iZEG-Dlx2 mice. (E and F) Magnification corresponding to regions in C and D, respectively (Scale bar, 50 µm). H&E, hematoxylin and eosin; Dlx2, distal-less homeobox 2.
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f4-mmr-14-02-1624: Histological analysis of condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. (A and B) Sagittal sections and H&E staining of iZEG-Dlx2 mice and P90 Wnt1Cre::iZEG-Dlx2 mice sections (Scale bar, 100 µm). Subchondral bone degradation and irregular cartilage histological structure was observed in the latter. (C–F) Sagittal sections and Alizarin red/Alcian blue staining showed irregular cartilage histological structure and less hypertrophic chondrocytes (blue) in the P90 Wnt1Cre::iZEG-Dlx2 mice. (E and F) Magnification corresponding to regions in C and D, respectively (Scale bar, 50 µm). H&E, hematoxylin and eosin; Dlx2, distal-less homeobox 2.

Mentions: The condyle of P90 Wnt1Cre::iZEG-Dlx2 mice was analyzed in detail. H&E and Alizarin red/Alcian blue staining of coronal sections indicated that the Wnt1Cre::iZEG-Dlx2 mice exhibited an irregular condylar cartilage structure and a uneven condylar cartilage surface. Condylar cartilage were disorganized and narrower, irregular in size and lacked a regular arrangement of four layers, including resting layer, proliferative layer, hypertrophic layer and mineralized zone. Additionally, less hypertrophic chondrocytes were observed in the condylar cartilage in P90 Wnt1Cre::iZEG-Dlx2 mice (Fig. 4). Bone loss was also evident in the condylar bone region when compared with the control group (Fig. 4). The phenotype demonstrated was observed in six condyle from three mice. Although the three mice exhibited similar phenotype, the severity was not consistent in each mouse; therefore, the expression pattern of Dlx2 may not be the same across the different mice.


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)

Histological analysis of condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. (A and B) Sagittal sections and H&E staining of iZEG-Dlx2 mice and P90 Wnt1Cre::iZEG-Dlx2 mice sections (Scale bar, 100 µm). Subchondral bone degradation and irregular cartilage histological structure was observed in the latter. (C–F) Sagittal sections and Alizarin red/Alcian blue staining showed irregular cartilage histological structure and less hypertrophic chondrocytes (blue) in the P90 Wnt1Cre::iZEG-Dlx2 mice. (E and F) Magnification corresponding to regions in C and D, respectively (Scale bar, 50 µm). H&E, hematoxylin and eosin; Dlx2, distal-less homeobox 2.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4-mmr-14-02-1624: Histological analysis of condyle in P90 Wnt1Cre::iZEG-Dlx2 mice. (A and B) Sagittal sections and H&E staining of iZEG-Dlx2 mice and P90 Wnt1Cre::iZEG-Dlx2 mice sections (Scale bar, 100 µm). Subchondral bone degradation and irregular cartilage histological structure was observed in the latter. (C–F) Sagittal sections and Alizarin red/Alcian blue staining showed irregular cartilage histological structure and less hypertrophic chondrocytes (blue) in the P90 Wnt1Cre::iZEG-Dlx2 mice. (E and F) Magnification corresponding to regions in C and D, respectively (Scale bar, 50 µm). H&E, hematoxylin and eosin; Dlx2, distal-less homeobox 2.
Mentions: The condyle of P90 Wnt1Cre::iZEG-Dlx2 mice was analyzed in detail. H&E and Alizarin red/Alcian blue staining of coronal sections indicated that the Wnt1Cre::iZEG-Dlx2 mice exhibited an irregular condylar cartilage structure and a uneven condylar cartilage surface. Condylar cartilage were disorganized and narrower, irregular in size and lacked a regular arrangement of four layers, including resting layer, proliferative layer, hypertrophic layer and mineralized zone. Additionally, less hypertrophic chondrocytes were observed in the condylar cartilage in P90 Wnt1Cre::iZEG-Dlx2 mice (Fig. 4). Bone loss was also evident in the condylar bone region when compared with the control group (Fig. 4). The phenotype demonstrated was observed in six condyle from three mice. Although the three mice exhibited similar phenotype, the severity was not consistent in each mouse; therefore, the expression pattern of Dlx2 may not be the same across the different mice.

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