Osteoklasten, Chondroklasten, Mineraloklasten, Kollagenoklasten

Knese, Karl-Heinrich

doi:10.1159/000143863

Cited by 19 publications

(6 citation statements)

References 1 publication

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“…In 1962, Takuma S., for the first time, described a cell type that destroy and resorb cartilage, named them as chondroclasts. This type of cells also be later named as mineraloclasts and collagenoclasts [15,16]. Based on morphological and histo-chemical findings, these cells are usually taken to be the same as osteoclasts, which resorb bone and calcified cartilage.…”

Section: Discussionmentioning

confidence: 99%

The expression of osteoprotegerin is required for maintaining the intervertebral disc endplate of aged mice

Qian

Zhou

et al. 2011

Bone

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Objective Human chondrocytes and annulus fibrosus cells of intervertebral disc (IVD) express osteoprotegerin (OPG), but the effect of OPG on the pathogenesis of IVD degeneration remains unknown. Here we assessed the phenotype change of IVD in OPG−/− mice. Methods The IVDs from 12-, 20-, and 28-week-old OPG−/− mice and WT controls were subjected to histologic analyses including TRAP staining for osteoclasts, immunostaining for OPG and type I collagen protein expression, and TUNEL staining for apoptosis. The IVD tissues were also subjected to real time RT-PCR for mRNA expression of genes for osteoblast-osterix, ALP, and osteocalcin; for osteoclasts-trap, rank, mmp9 and cathepsin K, and for chondrocytes-aggrecan, mmp13 and Col10. Results OPG protein expresses at the cells of endplate cartilage and annulus fiborsis in IVDs of WT mice. Compared to WT mice, OPG−/− mice developed aging related cartilage loss and bony tissue appearance at the endplate. Stating from 20 weeks of age, IVDs from OPG−/− mice expressed significantly increased mmp13 and Col10 levels, which is associated with increased osteoblast number and elevated expression of osteoblast marker genes. Furthermore, TRAP+ osteoclasts were presented in the endplate cartilage of OPG−/− mice. These osteoclasts localized adjacently to and erosion into the cartilage. Increased expression of RANK, mmp9 and cathepsin k was detected in OPG−/− IVDs. Conclusions OPG at IVD plays an important role for maintaining the integrity of endplate cartilage during aging by preventing endplate cartilage from osteoclast-mediated resorption.

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Section: Discussionmentioning

confidence: 99%

The expression of osteoprotegerin is required for maintaining the intervertebral disc endplate of aged mice

Qian

Zhou

et al. 2011

Bone

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“…These ideas are based upon the extensive enzymatic repertoire of osteoclasts, evidence for endocytosis and exocytosis at the structurally-distinct, ruffled border (Gothlin & Ericsson 1972, Lucht 1972, Lucht & Norgaard 1976, and changes in the sizes of the ruffled border and extent of cytoplasmic vacuolization with changes in bone resorptive activity in vivo and in vitro (Holtrop et al 1974, King et al 1978, Miller 1981). An alternative mechanism has been proposed (Knese 1972, Heersche 1978 which involves an initial demineralization by osteoclasts and collagenolysis by trailing mononuelear cells such as monocytes or fibroblasts, two cells known to synthesize collagenase. This theory is based upon the absence of morphological evidence for collagen degradation in osteoclast vacuoles and the lack of biochemical evidence for collagenase in osteoclasts.…”

Section: The Evidence For Current Views Of the Origin Of Osteoclmentioning

confidence: 99%

The origin of osteoclasts:

1983

J Oral Pathology Medicine

152

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Recent evidence for an extraskeletal origin of osteoelasts and the historical record of the genesis of osteoelasts are examined critically. Reviews of the structure, function and development of osteoelasts from mononuclear precursors, the local regulation of bone resorption and the coupling of bone formation to preceding resorption are presented as a background for discussing the clinical implications for management of osteolytic bone diseases. The roles of osteoelasts and macrophages as phagocytes are compared and contrasted, and recent evidence for macrophage heterogeneity resulting from site-specific monoblastic precursors is reviewed. The implications of these recent developments in macrophage biology are extrapolated to osteoelasts and the existence of site-specific, extraskeletal tsteoclast precursors is proposed. Finally, the investigative challenges inherent in these perspectives are discussed.

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“…In 1962, Dr. Takuma, for the first time, described a type of cell that resorbed cartilage, and named them as chondroclasts. This type of cell was also later called mineraloclasts and collagenoclasts (5–6). Using electronic microscopy, Nordahl et al demonstrated that chondroclasts do not form ruffled borders and a clear zone, which are seen typically in activated osteoclasts, but they are stained positively for tartrate-resistant acid phosphatase (TRAP) (7).…”

Section: Introductionmentioning

confidence: 99%

Mice Deficient in NF-κB p50 and p52 or RANK Have Defective Growth Plate Formation and Post-natal Dwarfism

Xing

Chen

2013

Bone Res.

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NF-κBp50/p52 double knockout (dKO) and RANK KO mice have no osteoclasts and develop severe osteopetrosis associated with dwarfism. In contrast, Op/Op mice, which form few osteoclasts, and Src KO mice, which have osteoclasts with defective resorptive function, are osteopetrotic, but they are not dwarfed. Here, we compared the morphologic features of long bones from p50/p52 dKO, RANK KO, Op/Op and Src KO mice to attempt to explain the differences in their long bone lengths. We found that growth plates in p50/p52 dKO and RANK KO mice are significantly thicker than those in WT mice due to a 2–3-fold increase in the hypertrophic chondrocyte zone associated with normal a proliferative chondrocyte zone. This growth plate abnormality disappears when animals become older, but their dwarfism persists. Op/Op or Src KO mice have relatively normal growth plate morphology. In-situ hybridization study of long bones from p50/p52 dKO mice showed marked thickening of the growth plate region containing type 10 collagen-expressing chondrocytes. Treatment of micro-mass chondrocyte cultures with RANKL did not affect expression levels of type 2 collagen and Sox9, markers for proliferative chondrocytes, but RANKL reduced the number of type 10 collagen-expressing hypertrophic chondrocytes. Thus, RANK/NF-κB signaling plays a regulatory role in post-natal endochondral ossification that maintains hypertrophic conversion and prevents dwarfism in normal mice.

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Osteoklasten, Chondroklasten, Mineraloklasten, Kollagenoklasten

Cited by 19 publications

References 1 publication

The expression of osteoprotegerin is required for maintaining the intervertebral disc endplate of aged mice

The expression of osteoprotegerin is required for maintaining the intervertebral disc endplate of aged mice

The origin of osteoclasts:

Mice Deficient in NF-κB p50 and p52 or RANK Have Defective Growth Plate Formation and Post-natal Dwarfism

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