The nature of endochondral ossification in the mandibular condyle of the mouse

Silbermann, Michael; Frommer, Jack

doi:10.1002/ar.1091720406

Cited by 60 publications

(34 citation statements)

References 13 publications

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“…Therefore, the middle area of normal Meckel's cartilage bar does not form calcified cartilage. Essentially, since endochondral ossification including mandibular condyle (SILBERMANN andFROMMER, 1972, 1974) or the growth plate (EGGLI et al,1985;JEE,1988) usually occurs in the hypertrophic chondrocyte-associated areas of the chondro-osseous junction, the calcification throughout hypertrophic zone or, occasionally, maturating zone cells-such as observed in the present study-was a unique phenomenon. When Meckel's cartilage of the same stage was cultivated in vivo in the subcutaneous, muscle, or peritoneal cavity, hypertrophic chondrocytes degenerated rapidly and no calcified cartilage matrix was formed (ISHIZEKI, unpublished data).…”

Section: Discussionsupporting

confidence: 49%

Endochondral calcification by hypertrophic chondrocytes in the Meckel's cartilage grafted into the isogenic mouse spleen.

Ishizeki

Fujiwara

Sugawara

et al. 1990

Archives of Histology and Cytology

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Summary. We found that when the midsection of Meckel's cartilage bars obtained from mice on the eighteenth day of gestation were grafted into isogenic mouse spleen, chondrocytes induced an endochondral calcification. Concurrent with the onset of calcification throughout Meckel's cartilage matrix, periodic banded thick collagen fibrils and matrix vesicles were observed around the chondrocytes.Although most of the chondrocytes prior to grafting were hypertrophic cells, they survived for seven days in the splenic tissue and had well-developed secretory organelles. The cells which were surrounded by calcified matrix were relatively small, spherical, and showed a morphology closely resembling that of osteocytes.These findings suggest that the life span of hypertrophic chondrocytes is influenced by the microenvironment of the spleen.Meckel's cartilage, known as a fetal organ, is initially formed as the main support of the mandible. It is divided into three distinct subdivisions by the regional transformation of the cartilage (BHASKER et al., 1953; FROMMER and MARGOLIES, 1971). Among these regions, the rostral process (distal portion) and auricular end (proximal portion) of the Meckel's cartilage have been thought to undergo endochondraltype ossification, but not the midsection (BHASKER et al., 1953; GORET-NICAISE and PILET, 1983; RICHMAN and DIEWRT, 1988).The hypertrophic chondrocytes in the midsection of the normal Meckel's cartilage degenerate and are replaced by invading cells accompanied by membrane bone formation around the cartilage. Recently, it has been proposed that some of the hypertrophic cells following morphological changes transform into osteogenic cells (HOLTROP, 1972;SHIMOMURA and RAY, 1973;RICHMAN and DIEWERT, 1988;YOSHIOKA and YAGI, 1988). Thus, there is still some confusion regarding the ultimate fate of the terminal chondrocytes.The present study examined morphologically the fate of the hypertrophic chondrocytes in the middle area of Meckel's cartilage grafted into the spleen. MATERIALS AND METHODSMeckel's cartilage bars obtained from mouse (ddy strain) embryos on the eighteenth day of gestation (day of vaginal plug =day 0) were used because cartilage in this stage contains a large number of hypertrophic chondrocytes in the absence of degenerated chondrocytes.The mandibular arches containing Meckel's cartilage were dissected aseptically and placed in Hanks' balanced salt solution supplemented with Kanamycin (1 mg/ml). After they were immersed in 10 mM EDTA in magnesium-calcium free-phosphate buffer for 10 min to remove excessive cellular elements of the connective tissue from Meckel's cartilage bars, the Meckel's cartilage was removed mechanically. These spicules were immediately transferred to fresh Hanks' solution and one-third were cut away using scissors. The midsection was used for grafting because it was known that this region does not have endochondral calcification.These explants were grafted into the spleen of isogenic adult mice as previously reported (ISHIZEKI et al., 1987). Briefly, us...

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Section: Discussionsupporting

confidence: 49%

Endochondral calcification by hypertrophic chondrocytes in the Meckel's cartilage grafted into the isogenic mouse spleen.

Ishizeki

Fujiwara

Sugawara

et al. 1990

Archives of Histology and Cytology

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“…[ Carlson et al, 1980]. As lias been demonstrated in the present study this cartilage in fetal mandibular condyles exhibits all the cellular components involved in endochon dral ossification [Silbermann and Frommer, 1972;Lester and Ash, 1981;Ludcr. 1983;Bouvier and Hvlander.…”

Section: Youngsupporting

confidence: 81%

Structural Characterization of the Mandibular Condyle in Human Fetuses: Light and Electron Microscopy Studies

Ben-Ami¹,

Lewinson²,

Silbermann³

1992

Cells Tissues Organs

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Mandibular condyles from 18- to 20-week-old human fetuses were examined in the light and electron microscope with particular attention to intratissue organization and extracellular matrix. In the human fetus the condyle has been divided into five layers: (1) the most superficial, articular layer, (2) chondroprogenitor cell layer, (3) condroblast cell layer, (4) nonmineralized hypertrophic cell layer, and (5) mineralized hypertrophic cell layer. The articular layer is rich in collagen fibers (mostly of the type I collagen), but the cells seldom divide. By contrast, in the chondroprogenitor cell layer and upper part of the chondroblastic cell layer mitosis gives rise to new cells. The matrix in the latter layer is composed of thick banded ‘lucent’ fibrils in a loose feltwork of granules representing cartilage proteoglycans. The daughter cells in the progenitor cell layer undergo differentiation which is apparently completed along the lower border of the mineralized hypertrophic cell layer – the ossification front. The matrix in the hypertrophic cell layer reveals distinct matrix vesicles that undergo mineralization and subsequently coalesce to form larger sheets of mineralized extracellular matrix. Mineralized cartilage serves as a backbone for new bone formation as marrow-derived osteoblasts and osteoclasts attach to remnants of mineralized cartilage, which enables the turning on of the remodeling cycles involved in new bone formation. It can be concluded that the process of endochondral ossification as has been reported in lower animals is recapitulated in the human fetus, thus the dynamics associated with condylar morphogenesis is maintained through phytogeny.

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“…1, upper right) (18,19). One key gene previously noted to be expressed during and function within the growth plate of the condylar cartilage is Indian hedgehog (Ihh) (20)(21)(22).…”

mentioning

confidence: 99%

Temporomandibular joint formation requires two distinct hedgehog-dependent steps

Purcell

Joo

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

126

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We conducted a genetic analysis of the developing temporo-mandibular or temporomandi-bular joint (TMJ), a highly specialized synovial joint that permits movement and function of the mammalian jaw. First, we used laser capture microdissection to perform a genome-wide expression analysis of each of its developing components. The expression patterns of genes identified in this screen were examined in the TMJ and compared with those of other synovial joints, including the shoulder and the hip joints. Striking differences were noted, indicating that the TMJ forms via a distinct molecular program. Several components of the hedgehog ( Hh ) signaling pathway are among the genes identified in the screen, including Gli2 , which is expressed specifically in the condyle and in the disk of the developing TMJ. We found that mice deficient in Gli2 display aberrant TMJ development such that the condyle loses its growth-plate-like cellular organization and no disk is formed. In addition, we used a conditional strategy to remove Smo , a positive effector of the Hh signaling pathway, from chondrocyte progenitors. This cell autonomous loss of Hh signaling allows for disk formation, but the resulting structure fails to separate from the condyle. Thus, these experiments establish that Hh signaling acts at two distinct steps in disk morphogenesis, condyle initiation, and disk–condyle separation and provide a molecular framework for future studies of the TMJ.

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The nature of endochondral ossification in the mandibular condyle of the mouse

Cited by 60 publications

References 13 publications

Endochondral calcification by hypertrophic chondrocytes in the Meckel's cartilage grafted into the isogenic mouse spleen.

Endochondral calcification by hypertrophic chondrocytes in the Meckel's cartilage grafted into the isogenic mouse spleen.

Structural Characterization of the Mandibular Condyle in Human Fetuses: Light and Electron Microscopy Studies

Temporomandibular joint formation requires two distinct hedgehog-dependent steps

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