Interface between intramembranous and endochondral ossification in human foetuses

Hayashi, Shogo; Kim, J. H.; Hwang, Si Eun; Shibata, Shunichi; Fujimiya, Mineko; Murakami, Gen; Cho, B. H.

doi:10.5603/fm.2014.0029

Cited by 15 publications

(18 citation statements)

References 20 publications

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“…Given these distinct developmental processes, unique gene-regulatory programs and biological mechanisms likely drive ossification of these two bone groupings in the head. Supporting this, differences in vascular invasion have been observed between endochondral and intramembranous bones of the human fetal head, and animal models exist with defects in a distinct subset of these craniofacial bones 16,17 . However, given the final product of both mechanisms is ossified bone, there are also likely overlapping genetic programs involved, although the degree of dependency on these programs may be different between these two bone populations 12 .…”

Section: Introductionmentioning

confidence: 79%

MEMO1 drives cranial endochondral ossification and palatogenesis

Otterloo

Feng

Jones

et al. 2016

Developmental Biology

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The cranial base is a component of the neurocranium and has a central role in the structural integration of the face, brain and vertebral column. Consequently, alteration in the shape of the human cranial base has been intimately linked with primate evolution and defective development is associated with numerous human facial abnormalities. Here we describe a novel recessive mutant mouse strain that presented with a domed head and fully penetrant cleft secondary palate coupled with defects in the formation of the underlying cranial base. Mapping and non-complementation studies revealed a specific mutation in Memo1 - a gene originally associated with cell migration. Expression analysis of Memo1 identified robust expression in the perichondrium and periosteum of the developing cranial base, but only modest expression in the palatal shelves. Fittingly, although the palatal shelves failed to elevate in Memo1 mutants, expression changes were modest within the shelves themselves. In contrast, the cranial base, which forms via endochondral ossification had major reductions in the expression of genes responsible for bone formation, notably matrix metalloproteinases and markers of the osteoblast lineage, mirrored by an increase in markers of cartilage and extracellular matrix development. Concomitant with these changes, mutant cranial bases showed an increased zone of hypertrophic chondrocytes accompanied by a reduction in both vascular invasion and mineralization. Finally, neural crest cell-specific deletion of Memo1 caused a failure of anterior cranial base ossification indicating a cell autonomous role for MEMO1 in the development of these neural crest cell derived structures. However, palate formation was largely normal in these conditional mutants, suggesting a non-autonomous role for MEMO1 in palatal closure. Overall, these findings assign a new function to MEMO1 in driving endochondral ossification in the cranium, and also link abnormal development of the cranial base with more widespread effects on craniofacial shape relevant to human craniofacial dysmorphology.

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Section: Introductionmentioning

confidence: 79%

MEMO1 drives cranial endochondral ossification and palatogenesis

Otterloo

Feng

Jones

et al. 2016

Developmental Biology

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“…Bones containing osteoblasts which terminally differentiate into osteocytes develop from a mesenchymal stem cell precursor which can undergo osteogenesis through two distinct mechanisms [10]. Endochondral ossification (with cartilage as an intermediate stage) is typical for the long bones, e.g., femur or tibia, whereas intramembranous ossification (related to a direct differentiation of mesenchymal stem cells into osteoblasts) is the main mechanism leading to a development of flat (e.g., craniofacial) bones [11].…”

Section: Vasculature Of the Bone: The Role In Skeleton Development Rmentioning

confidence: 99%

The role of vasculature in bone development, regeneration and proper systemic functioning

et al. 2017

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Bone is a richly vascularized connective tissue. As the main source of oxygen, nutrients, hormones, neurotransmitters and growth factors delivered to the bone cells, vasculature is indispensable for appropriate bone development, regeneration and remodeling. Bone vasculature also orchestrates the process of hematopoiesis. Blood supply to the skeletal system is provided by the networks of arteries and arterioles, having distinct molecular characteristics and localizations within the bone structures. Blood vessels of the bone develop through the process of angiogenesis, taking place through different, bone-specific mechanisms. Impaired functioning of the bone blood vessels may be associated with the occurrence of some skeletal and systemic diseases, i.e., osteonecrosis, osteoporosis, atherosclerosis or diabetes mellitus. When a disease or trauma-related large bone defects appear, bone grafting or bone tissue engineering-based strategies are required. However, a successful bone regeneration in both approaches largely depends on a proper blood supply. In this paper, we review the most recent data on the functions, molecular characteristics and significance of the bone blood vessels, with a particular emphasis on the role of angiogenesis and blood vessel functioning in bone development and regeneration, as well as the consequences of its impairment in the course of different skeletal and systemic diseases.

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“…Endochondral ossification occurs in a versican-rich matrix, while perichondral ossification occurs in tenascin-positive fibrous tissues [7]. Antibodies to these two proteins may therefore be associated with the development of fabella.…”

Section: Methodsmentioning

confidence: 99%