Transmission and scanning electron microscope studies of calcified cartilage resorption

Savostin-Asling, I; Asling, C. Willet

doi:10.1002/ar.1091830303

Cited by 37 publications

(24 citation statements)

References 27 publications

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“…As a general PubMed search term, “chondroclast” yielded 19 citations. The first occurrences of “chondroclast” in the literature that can be searched electronically are in papers by Savostin-Asling and Asling (53, 54). They showed light, transmission and scanning electron microscopic studies of calcified cartilage resorption.…”

Section: Chondroclastsmentioning

confidence: 99%

“…Specifically, they looked at the central region of Meckel’s cartilage in embryonic day 19 rat fetuses and describe their findings as follows:

“Chondroclasts (multinucleated cells identical with osteoclasts) dominate the erosion front.” (53)

“The many features which they showed in common with osteoclasts included abundant mitochondria, vacuolation, lysosomes, sparsity of rough-surfaced endoplasmic reticulum, and deep infoldings at loci of contact with calcified matrix. Crumbling of matrix (with mineral crystals penetrating between these foldings) and fragmentation of collagen fibrils were also seen.” (54)

…”

Section: Chondroclastsmentioning

confidence: 99%

“…Crumbling of matrix (with mineral crystals penetrating between these foldings) and fragmentation of collagen fibrils were also seen.” (54)…”

Section: Chondroclastsmentioning

confidence: 99%

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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%

“…Specifically, they looked at the central region of Meckel’s cartilage in embryonic day 19 rat fetuses and describe their findings as follows:

“Chondroclasts (multinucleated cells identical with osteoclasts) dominate the erosion front.” (53)

…”

Section: Chondroclastsmentioning

confidence: 99%

See 1 more Smart Citation

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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“…Another theory proposes that the canals grow by a phenomenon of 'invasion'; in this theory the chondrolytic action of perichondral cells [3. 6, 7], perivascular cells [14,15] and mesenchymal cells [4,8,9] is necessary for canal growth.…”

Section: Discussionmentioning

confidence: 99%

Morphogenesis of Cartilage Canals: Experimental Approach in the Rat Tibia

Delgado-Baeza¹,

Gimenez-Ribotta²,

Miralles-Flores³

et al. 1991

Cells Tissues Organs

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This paper studies the participation of vessels in the canal morphogenesis. The proximal chondroepiphysis of the left tibia of 44 five-day-old rats was exposed and the vessels of the intercondylar fossae, near the attachment of cruciate ligaments, were cauterized. In addition to the vascular lesion this assay induced a perichondral lesion. However, the canal appeared and joined to the secondary ossification center. 36 tibiae of 4-day-old rats were removed under sterile conditions and cultured in a serum-free chemically defined medium. The cultures were carried out for as long as 15 days. A canal lumen structure was found on the first days of culture, and grew in depth to the central region of the chondroepiphysis during the culture. The secondary ossification center was not found. The vessels and mesenchymal cells observed in the control canal were not found in the culture. We suggest that the presence of vessels, perivascular cells or perichondrium does not appear to be necessary in canal morphogenesis.

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“…Calcified cartilage matrix is degraded by chondroclasts (Bromley and Woolley 1984;Lee et al 1995;Lewinson and Silbermann 1992;Nordahl et al 1998;Savostin-Asling and Asling 1975;Schenk et al 1967), but chondroclasts have not been well characterized and are thought to be identical to osteoclasts which are tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cells and are responsible for bone resorption (Suda et al 1992(Suda et al , 1997. The ability to generate TRAP-positive This work was supported by the Special Coordination Funds for Science and Technology from the Science and Technology Agency, Japan clones would therefore facilitate the investigations into the biological properties of cells involved in cartilage and bone degradation.…”

Section: Introductionmentioning

confidence: 99%

Establishment and characterization of tartrate-resistant acid phosphatase and alkaline phosphatase double positive cell lines

Masuda¹,

Sakiyama²,

Nonaka

et al. 2001

Cell and Tissue Research

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Morphologically macrophage-like cells were cloned from hamster bone marrow cells by coculturing bone marrow cells with hamster chondrocytes. One of the clones (CCP-2) was characterized in the present study. CCP-2 cells were positive in an osteoclast marker enzyme, tartrate-resistant acid phosphatase (TRAP), alkaline phosphatase (ALP) and non-specific esterase (NSE). We showed CCP-2 cells degraded cartilage matrix and hydroxyapatite coated on Osteologic disks. A gelatinase secreted from CCP-2 cells was observed and purified from serum-free conditioned medium of the cells. N-terminal amino acid sequencing of the purified enzyme revealed it was matrix metalloproteinase-9. However, CCP-2 cells failed to express calcitonin receptors, a mature osteoclast marker, even after coculture with osteoblast ST2 cells in the presence of 1alpha, 25-dihydroxyvitamin D3 [1alpha, 25-(OH)2D3]. The cells showed high affinity to types X and I but not to type II collagen. In addition, histochemical studies have shown the presence of tartrate-resistant acid phosphatase and alkaline phosphatase double positive cells at the secondary ossification site of the hamster humerus. From these observations, we concluded that CCP-2 cells are similar to osteoclast but not the same. CCP-2 cells are therefore important tools for investigating chondroclastogenesis/osteoclastogenesis and endochondral ossification.

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Transmission and scanning electron microscope studies of calcified cartilage resorption

Cited by 37 publications

References 27 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

Morphogenesis of Cartilage Canals: Experimental Approach in the Rat Tibia

Establishment and characterization of tartrate-resistant acid phosphatase and alkaline phosphatase double positive cell lines

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