Role of Meckel's Cartilage in the Development and Growth of the Rat Mandible

Bhaskar, Surindar N.; Weinmann, Joseph P.; Schour, Isaac

doi:10.1177/00220345530320031401

Cited by 89 publications

(90 citation statements)

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“…68 Although chondrocytes located at the posterior end of Meckel's cartilage do ossify to form the malleus and incus bones of the inner ear, 69 chondrocytes within the body of Meckel's cartilage do not express type X collagen, mineralize, or form bone. 70,71 In Nell-1 transgenic mice, the number of apoptotic cells within the Meckel's cartilage was equivalent to that in wild-type mice (data not shown), thus the anatomy of this bone was not altered. Although the underlying reason is unknown, we speculate that the normal occurrence of apoptosis in this tissue could not be further affected by the increased presence of Nell-1, due to the non-osteogenic fate of cells within Meckel's cartilage and the fact that Nell-1's effects are restricted to osteochondral bone formation.…”

Section: Discussionmentioning

confidence: 84%

Nell-1 induces acrania-like cranioskeletal deformities during mouse embryonic development

Zhang

Cowan

Jiang

et al. 2006

Laboratory Investigation

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We previously reported NELL-1 as a novel molecule overexpressed during premature cranial suture closure in patients with craniosynostosis (CS). Nell-1 overexpression also results in premature suture closure/ craniosynostosis in newborn transgenic mice. On a cellular level, increased levels of Nell-1 induce osteoblast differentiation and apoptosis. In this report, mice over-expressing Nell-1 were examined during embryonic development as well as shortly after birth for further analysis of craniofacial defects including neural tube defects (NTDs). The results demonstrated that overexpression of Nell-1 could induce acrania at relatively late gestation stage (E15.5) in mouse embryos, through massive apoptosis in calvarial osteoblasts and neural cells. The induced apoptosis was associated with an increase in Fas and Fas-L production. In addition, transgenic E15.5 and newborn transgenic mice with the CS phenotype displayed distortion of the chondrocranium associated with premature hypertrophy and increased apoptosis of chondrocytes. These findings were also verified in vitro with primary chondrocytes transduced with AdNell-1. In conclusion, Nell-1 overexpression can induce craniofacial anomalies associated with neural tube defects during embryonic development and may involve mechanisms of massive apoptosis associated with the Fas/Fas-L signaling pathway. NELL-1: used when describing the human gene; NELL-1: used when describing the human protein; Nell-1: used when describing the rodent gene; Nell-1: used when describing the rodent protein Laboratory Investigation (2006) 86, 633-644.

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Section: Discussionmentioning

confidence: 84%

Nell-1 induces acrania-like cranioskeletal deformities during mouse embryonic development

Zhang

Cowan

Jiang

et al. 2006

Laboratory Investigation

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“…During the embryonic stage in mammals, ectomesenchymal cells derived from the neural crest migrate into mandibular processes, differentiate into chondrocytes, and develop into a characteristic rod-shaped hyaline cartilage called Meckel's cartilage (Bhaskar et al, 1953;Lee et al, 2001). Meckel's cartilage is present transiently in the developing mandible and usually disappears at early postnatal stages (Bhaskar et al, 1953).…”

Section: Introductionmentioning

confidence: 99%

“…Meckel's cartilage is present transiently in the developing mandible and usually disappears at early postnatal stages (Bhaskar et al, 1953). Meckel's cartilage provides mechanical strength and contributes to the normal development of the mandible (Tomo et al, 1997).…”

Section: Introductionmentioning

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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“…A study on mandibular growth in an early human fetal development (weeks 8 -14) revealed the mandibular ramus grew faster than the body, both in length and height; the greatest growth rate was found in the height of ramus; and the mandibular growth patterns differed significantly from those of successive developmental periods (Bareggi et al, 1995). Many authors had emphasized the importance of growth of the Meckel cartilage (Bhaskar et al, 1953), condylar head in mandibular growth (Kjaer 1978a;Morimoto et al, 1987;Shibata et al, 1996;Xu et al, 1983). A precise description of the prenatal human mandibular growth and developmental pattern, however, has not been reported.…”

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confidence: 99%

Prenatal development of the human mandible

et al. 2001

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In an effort to better understand the interrelationship of the growth and development pattern of the mandible and condyle, a sequential growth pattern of human mandibles in 38 embryos and 111 fetuses were examined by serial histological sections and soft X-ray views. The basic growth pattern of the mandibular body and condyle appeared in week 7 of fertilization. Histologically, the embryonal mandible originated from primary intramembranous ossification in the fibrous mesenchymal tissue around the Meckel cartilage. From this initial ossification, the ramifying trabecular bones developed forward, backward and upward, to form the symphysis, mandibular body, and coronoid process, respectively. We named this initial ossification site of embryonal mandible as the mandibular primary growth center (MdPGC). During week 8 of fertilization, the trabecular bone of the mandibular body grew rapidly to form muscular attachments to the masseter, temporalis, and pterygoid muscles. The mandible was then rapidly separated from the Meckel cartilage and formed a condyle blastema at the posterior end of linear mandibular trabeculae. The condyle blastema, attached to the upper part of pterygoid muscle, grew backward and upward and concurrent endochondral ossification resulted in the formation of the condyle. From week 14 of fertilization, the growth of conical structure of condyle became apparent on histological and radiological examinations. The mandibular body showed a conspicuous radiating trabecular growth pattern centered at the MdPGC, located around the apical area of deciduous first molar. The condyle growth showed characteristic conical structure and abundant hematopoietic tissue in the marrow. The growth of the proximal end of condyle was also approximated to the MdPGC on radiograms. Taken together, we hypothesized that the MdPGC has an important morphogenetic affect for the development of the human mandible, providing a growth center for the trabecular bone of mandibular body and also indicating the initial growth of endochondral ossification of the condyle.

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Role of Meckel's Cartilage in the Development and Growth of the Rat Mandible

Cited by 89 publications

References 5 publications

Nell-1 induces acrania-like cranioskeletal deformities during mouse embryonic development

Nell-1 induces acrania-like cranioskeletal deformities during mouse embryonic development

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

Prenatal development of the human mandible

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