Meckel's Cartilage: Discovery, Embryology and Evolution

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

doi:10.1016/s1349-0079(10)80041-6

Cited by 16 publications

(19 citation statements)

References 35 publications

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“…Note that, in contrast to the termini of Meckel’s cartilage, which contribute to the mandible and auditory apparatus, the central portion under study in those papers is simply removed (55). Thus, from their earliest description, chondroclasts were seen as essentially identical to osteoclasts with the exception of their location on mineralized cartilage, as opposed to bone.…”

Section: Chondroclastsmentioning

confidence: 99%

The cast of clasts: catabolism and vascular invasion during bone growth, repair, and disease by osteoclasts, chondroclasts, and septoclasts

Odgren

Witwicka

Reyes-Gutierrez

2016

Connective Tissue Research

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Three named cell types degrade and remove skeletal tissues during growth, repair, or disease: osteoclasts, chondroclasts, and septoclasts. A fourth type, unnamed and less understood, removes non-mineralized cartilage during development of secondary ossification centers. “Osteoclasts,” best known and studied, are polykaryons formed by fusion of monocyte precursors under the influence of CSF-1 (M-CSF) and RANKL. They resorb bone during growth, remodeling, repair, and disease. “Chondroclasts”, originally described as highly similar in cytological detail to osteoclasts, reside on and degrade mineralized cartilage. They may be identical to osteoclasts, since to date there are no distinguishing markers for them. Because osteoclasts also consume cartilage cores along with bone during growth, the term “chondroclast” might best be reserved for cells attached only to cartilage. “Septoclasts” are less studied and appreciated. They are mononuclear perivascular cells rich in cathepsin B. They extend a cytoplasmic projection with a ruffled membrane and degrade the last transverse septum of hypertrophic cartilage in the growth plate, permitting capillaries to bud into it. To do this, antiangiogenic signals in cartilage must give way to vascular trophic factors, mainly VEGF. The final cell type excavates cartilage canals for vascular invasion of articular cartilage during development of secondary ossification centers. The “clasts” are considered in the context of fracture repair and diseases such as arthritis and tumor metastasis. Many observations support an essential role for hypertrophic chondrocytes in recruiting septoclasts and osteoclasts/chondroclasts by supplying VEGF and RANKL. The intimate relationship between blood vessels and skeletal turnover and repair is also examined.

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Section: Chondroclastsmentioning

confidence: 99%

The cast of clasts: catabolism and vascular invasion during bone growth, repair, and disease by osteoclasts, chondroclasts, and septoclasts

Odgren

Witwicka

Reyes-Gutierrez

2016

Connective Tissue Research

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“…Here Meckel described the relationship between a cartilage rod that ran along the jaw and the forming malleus, and compared this rod to similar structures previously described in fish, amphibians and birds ( Meckel, 1820 ). The cartilage was later named Meckel’s cartilage by his followers ( Amano et al, 2010 ). During development, MC begins life as two rods of cartilage, which meet in the midline to form a V-structure outlining the forming lower jaw ( Figures 1A,B ).…”

Section: Introductionmentioning

confidence: 99%

“…Meckel’s cartilage forms the lower jaw strut in all jawed vertebrates during embryonic development, and as such plays a key conserved role in vertebrate jaw development and evolution ( Anthwal et al, 2013 ). In mammals, the main body of Meckel’s cartilage is largely transient but acts as a template for later formation of the bones of the lower jaw, with defects leading to anomalies in the pattern and size of the jaw in mouse mutants and in human embryos ( Bhaskar et al, 1953 ; Amano et al, 2010 ). In addition to its role as a jaw support, MC also forms two of the three mammalian middle ear bones (malleus and incus), which sit in the middle ear cavity and, along with the stapes, form a chain of ossicles to transfer sound from the outer to the inner ear.…”

Section: Introductionmentioning

confidence: 99%

“…In this review the development of the mammalian MC is followed from initiation to final function, highlighting the molecular mechanisms involved in its creation, remodelling and loss, as documented in the research literature. In particular we aim to put into context the recent discoveries in MC development since the last review on this subject ( Amano et al, 2010 ), and highlight the gaps that call for further study of this important cartilage. Over the last ten years, the use of conditional transgenic mice has revealed many of the molecular aspects of MC, providing an understanding of the spatial and temporal dynamics of lower jaw development, and highlighting roles for processes such as autophagy.…”

Section: Introductionmentioning

confidence: 99%

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Diverse Fate of an Enigmatic Structure: 200 Years of Meckel’s Cartilage

Švandová

Anthwal

Tucker

et al. 2020

Front. Cell Dev. Biol.

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Meckel’s cartilage was first described by the German anatomist Johann Friedrich Meckel the Younger in 1820 from his analysis of human embryos. Two hundred years after its discovery this paper follows the development and largely transient nature of the mammalian Meckel’s cartilage, and its role in jaw development. Meckel’s cartilage acts as a jaw support during early development, and a template for the later forming jaw bones. In mammals, its anterior domain links the two arms of the dentary together at the symphysis while the posterior domain ossifies to form two of the three ear ossicles of the middle ear. In between, Meckel’s cartilage transforms to a ligament or disappears, subsumed by the growing dentary bone. Several human syndromes have been linked, directly or indirectly, to abnormal Meckel’s cartilage formation. Herein, the evolution, development and fate of the cartilage and its impact on jaw development is mapped. The review focuses on developmental and cellular processes that shed light on the mechanisms behind the different fates of this cartilage, examining the control of Meckel’s cartilage patterning, initiation and maturation. Importantly, human disorders and mouse models with disrupted Meckel’s cartilage development are highlighted, in order to understand how changes in this cartilage impact on later development of the dentary and the craniofacial complex as a whole. Finally, the relative roles of tissue interactions, apoptosis, autophagy, macrophages and clast cells in the removal process are discussed. Meckel’s cartilage is a unique and enigmatic structure, the development and function of which is starting to be understood but many interesting questions still remain.

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“…LGRs are specifically present in Meckel's cartilage of the mandible, which is normally resorbed in adults, yet has the ability to undergo ossification under BMP signaling pathway cues. (55)(56)(57) Interestingly, recent evidence points to an LGR-independent mechanism for R-spondins in limb development, where a triple transgenic LGR4/5/6 KO mouse model did not recapitulate the striking limb phenotype of RSPO2 −/− embryos. (49) Despite the possibility that RSPO-mediated limb formation may operate through an alternative mechanism, (58) it is clear that LGRs themselves play a role in skeletal development.…”

Section: Introductionmentioning

confidence: 99%

LGRs in Skeletal Tissues: An Emerging Role for Wnt‐Associated Adult Stem Cell Markers in Bone

Doherty

Sanjay

2020

JBMR Plus

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Leucine-rich repeat-containing G protein-coupled receptors (LGRs) are adult stem cell markers that have been described across various stem cell niches, and expression of LGRs and their corresponding ligands (R-spondins) has now been reported in multiple bonespecific cell types. The skeleton harbors elusive somatic stem cell populations that are exceedingly compartment-specific and under tight regulation from various signaling pathways. Skeletal progenitors give rise to multiple tissues during development and during regenerative processes of bone, requiring postnatal endochondral and intramembranous ossification. The relevance of LGRs and the LGR/R-spondin ligand interaction in bone and tooth biology is becoming increasingly appreciated. LGRs may define specific stem cell and progenitor populations and their behavior during both development and regeneration, and their role as Wnt-associated receptors with specific ligands poses these proteins as unique therapeutic targets via potential R-spondin agonism. This review seeks to outline the current literature on LGRs in the context of bone and its associated tissues, and points to key future directions for studying the functional role of LGRs and ligands in skeletal biology.

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Meckel's Cartilage: Discovery, Embryology and Evolution

Cited by 16 publications

References 35 publications

The cast of clasts: catabolism and vascular invasion during bone growth, repair, and disease by osteoclasts, chondroclasts, and septoclasts

The cast of clasts: catabolism and vascular invasion during bone growth, repair, and disease by osteoclasts, chondroclasts, and septoclasts

Diverse Fate of an Enigmatic Structure: 200 Years of Meckel’s Cartilage

LGRs in Skeletal Tissues: An Emerging Role for Wnt‐Associated Adult Stem Cell Markers in Bone

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