Meckel’s Cartilage: Discovery, Embryology and Evolution

Amano, Osamu; Doi, Takashi; Yamada, Tohru; Sasaki, Au; Sakiyama, Kazuo; Kanegae, Haruhide; Kindaichi, Koji

doi:10.2330/joralbiosci.52.125

Cited by 8 publications

(11 citation statements)

References 38 publications

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“…Thus, apoptosis was not involved in chondrocyte cell death and might play a role in chondroblast differentiation in the perichondrium of Meckel's cartilage. This result is in accord with other studies (Amano et al, 2010).…”

Section: Discussionsupporting

confidence: 82%

“…During the degeneration of Meckel's cartilage, MMP-2, MMP-9, MMP-13, and MMP-14 were detected, and crosstalk between them regulated the degradation of extracellular matrices (Sakakura et al, 2007). In endochondral ossification, MMPs were detected in hypertrophic chondrocytes, osteoblasts, young osteocytes, and bone matrices of the periosteal envelope (Sakakura et al, 2007;Amano et al, 2010). Hence, the activation cascade of MMPs is different between the two processes.…”

Section: Discussionmentioning

confidence: 99%

“…In endochondral ossification, RANKL is expressed in hypertrophic chondrocytes, and OPG is nearly negative in chondrocytes. However, in Meckel's cartilage, aside from hypertrophic chondrocytes, RANKL and OPG expressions were also detected in immature and mature chondrocytes (Sakakura et al, 2005;Amano et al, 2010). During the degeneration of Meckel's cartilage, MMP-2, MMP-9, MMP-13, and MMP-14 were detected, and crosstalk between them regulated the degradation of extracellular matrices (Sakakura et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

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Autophagy Prior to Chondrocyte Cell Death During the Degeneration of Meckel's Cartilage

Yang

Zhang

Liu

et al. 2012

The Anatomical Record

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The central portion of Meckel's cartilage degenerates almost immediately after birth. Whether autophagy is involved in this process remains unclear. Thus, to explore the role of autophagy during this process, we have detected the expression of autophagy and apoptosis-related markers in embryonic mice. In E15, Beclin1 and LC3 expressions were weak and negative in Meckel's cartilage, respectively. In E16, chondrocytes of the central portion became hypertrophic. Moderate immunoreactivities of Beclin1 and LC3 were observed in prehypertrophic and hypertrophic chondrocytes of the central portion. In E17, the degradation occurred in the central portion and expanded anteriorly and posteriorly. Beclin1 expression was observed in Meckel's cartilage with an increase in the hypertrophic chondrocytes of the central portion. The expression of LC3 was detected specifically in terminally differentiated hypertrophic chondrocytes. The mRNA expressions of LC3 and Beclin1 from E15 to E17 significantly increased. This result is in accord with the histologic findings. Terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick-end labeling assay and Caspase 3 expression demonstrated that apoptosis was detected in the lateral part of terminal hypertrophic chondrocytes along the degeneration area of Meckel's cartilage. In addition, Bcl2 expression increased significantly from E15 to E17. These results indicate that autophagy is involved in hypertrophic chondrocytes during the degradation of Meckel's cartilage and occurs prior to chondrocyte cell death during this process. Anat Rec,

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Autophagy Prior to Chondrocyte Cell Death During the Degeneration of Meckel's Cartilage

Yang

Zhang

Liu

et al. 2012

The Anatomical Record

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“…Although a number of reports have investigated the developmental process of the TMJ in various animals 7,9,11,14) , including human 2,4,15,16) , no view of the mouse TMJ has been established. In particular, in mouse, although the developmental period of the lower joint cavity showed variation, development occurred after birth in many studies [5][6][7] .…”

Section: Introductionmentioning

confidence: 99%

“…The ossification point of the mouse mandible is present in mesenchymal tissue near the lateral side of Meckel's cartilage, and mandibular development occurs upon intramembranous ossification of the point 8,10,18) . The posterior end region of Meckel's cartilage, which bends into a hooked shape, becomes the auditory ossicles, while the rest of the cartilage disappears during the fetal period 2,10) . The region lost during the fetal period is believed to be occupied by the mandible.…”

Section: Introductionmentioning

confidence: 99%

Morphological Observation of Process of Mouse Temporomandibular Joint Formation

Ohshima

Yonezu

Nishibori

et al. 2011

Bull. Tokyo Dent. Coll.

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The aim of this study was to clarify the developmental mechanism of the temporomandibular joint (TMJ) cavity, using the relationship between Meckel's cartilage and the mandible to morphologically observe the process of TMJ formation in mouse fetuses. We investigated the involvement of apoptosis in the development of the mouse TMJ cavity. We attempted to 3-dimensionally clarify the developmental process of the mandible and Meckel's cartilage by observing the developmental process optically and reconstructing 3-dimensional images to observe 3-dimensional locations of the mandible and Meckel's cartilage. Formation of the upper joint cavity began on embryonal day 16, and a complete joint cavity was formed on embryonal day 18. Formation of the lower joint cavity began on embryonal day 18, and formation was almost completed on embryonal day 19. Meckel's cartilage adjacent to the mandible decreased with development of the mandible but was vestigial on embryonal day 19. The posterior region of Meckel's cartilage developed toward the posterior direction, and it was 3-dimensionally confirmed that the mandible and Meckel's cartilage were separated. Histological observation by the TUNEL method revealed the presence of solitary and diffuse apoptotic cells not only in the joint cavity, but also around the condyle.

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