Aberrant death in dark chondrocytes of the avian growth plate

Erenpreisa, Jekaterina; Roach, Helmtrud I.

doi:10.1038/sj.cdd.4400320

Cited by 34 publications

(40 citation statements)

References 26 publications

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“…Many of the chondrocytes had the appearance previously described as 'dark' [6]. These dark cells exhibited condensed chromatin, abundant endoplasmic reticulum (ER) and dark cytoplasm.…”

Section: Discussionmentioning

confidence: 93%

“…Experimental fracture studies have concluded that endochondral ossification plays a role in bone remodelling and that this process involves removal of chondrocytes via apoptosis [6,15]. The study presented here uses a rabbit fracture model to investigate cell death in the soft callus and to localise deadldying chondrocytes in relation to their surrounding matrix at different time points during the fracture healing process.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The fate of soft callus chondrocytes during long bone fracture repair

Ford

Robinson

Scammell

2003

Journal Orthopaedic Research

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Following fracture, the cartilaginous tissue of the soft callus is eventually replaced by bone. Removal of the cartilage is a critical part of the bone healing process but information concerning the changes in chondrocytes during this process is sparse. The aim of the study was to investigate the fate of chondrocytes in the soft callus during the bone repair process using a rabbit tibia1 fracture model. Fracture tissue was processed for collagen 1-11 I and keratan sulphate immunohistochemistry to study changes in matrix composition and the TUNEL technique (terminal deoxynucleotidyl transferase medicated dUTP nick-end labelling) to identify death of soft callus chondrocytes. Transmission electron microscopy (TEM) was also carried out to investigate the ultrastructure of chondrocytes within the soft callus. Results showed that the size of the cartilage area decreased over time and that cartilage matrix was replaced with new matrix rich in collagen 1 and 111. Chondrocytes became engulfed in the new matrix and appeared to stop producing cartilage matrix. Chondrocyte cell death was seen at the border of the soft callus, just within the newly produced matrix. TEM revealed that these dying/dead cells were not typically apoptotic in appearance. In conclusion, results indicate that chondrocytes of the soft callus die as a result of the progressive production of bone matrix which eventually engulfs them and leads to the remodelling of the area and eventual bone repair.

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“…Many of the chondrocytes had the appearance previously described as 'dark' [6]. These dark cells exhibited condensed chromatin, abundant endoplasmic reticulum (ER) and dark cytoplasm.…”

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

The fate of soft callus chondrocytes during long bone fracture repair

Ford

Robinson

Scammell

2003

Journal Orthopaedic Research

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“…It is worth mentioning that their nuclear membrane often contains defects. The segments ravel into small inverted buds and dissolve together with adjacent chromatic clumps to release pore complexes [4,18,33,38].…”

Section: Dark Chondrocytesmentioning

confidence: 99%

“…These cells were unable to live or die analogous to a paralytic state, a form of cell death similar to dark chondrocytes (see below). These cells underwent autophagy [38,39] that is a process that involves the cell using its own components to degrade itself by lysosomes. These cells contain double-membrane autophagic vacuoles, termed autophagosomes that are used for self degradation.…”

Section: Authophagal Bodiesmentioning

confidence: 99%

Morphology and physiology of the epiphyseal growth plate.

Burdan

Szumiło²,

Korobowicz³

et al. 2009

Folia Histochem Cytobiol.

129

108

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Mammalian growth plate, also known as epiphyseal plate or physis, is highly specialized mesodermderived cartilaginous structure. It develops in the bone bud, secondary to presence of the primary ossification centers and is responsible for bone elongation. The plates are formed by numerous cells that rapidly divide and mature. Post puberty, the epiphyseal cartilage cell division decreases, bone completely replaces cartilage, and the epiphyseal plates fuse together with primary and secondary ossification centers [1,2]. Cartilage differentiation processPresently, four major stages of chondrocyte differentiation are known, i.a., mesenchymal precursor cells (MPCs), prechondrocytes, early chondroblasts and terminally differentiated chondrocytes [1][2][3][4]. Abstract: The epiphyseal growth plate develops from the cartilaginous-orientated mesenchymal cells that express SOX family genes. This multilayer structure is formed by the proliferation and hypertrophy of cells that synthesize the extracellular matrix composed of collagen (mainly type II, IX, X, XI) and proteoglycans (aggrecan, decorin, annexin II, V and VI). The resting zone is responsible for protein synthesis and maintaining a germinal structure. In the proliferative zone, cells rapidly duplicate. The subsequent morphological changes take place in the transformation zone, divided into the upper and lower hypertrophic layers. In the degenerative zone, the mineralization process becomes intensive due to increased release of alkaline phosphate, calcium and matrix vesicles by terminally differentiated chondrocytes and some other factors e.g., metaphyseal ingrowth vessels. At this level, as well as in the primary and secondary spongiosa zones, chondrocytes undergo apoptosis and are physiologically eliminated. Unlike adult cartilage, in fetal and early formed growth plates, unusual forms such as autophagal bodies, paralysis and dark chondrocytes are also observed. Their ultrastructure differs greatly from apoptotic and normal cartilage cells. Chondrocyte proliferation and differentiation are regulated by various endocrine, paracrine, and autocrine agents such as growth, thyroid and sex hormones, beta-catenin, bone morphogenetic proteins, insulin-like growth factor, iodothyronine deiodinase, leptin, nitric oxide, transforming growth factor beta and vitamin D metabolites. However, the most significant factor is parathyroid hormone-related protein (PTHrP) which is synthesized in the perichondrium by terminally differentiated chondrocytes. Secondary to activation of PTH/PTHrP receptors, PTHrP stimulates cell proliferation by G protein activation and delays their transformation into prehypertrophic and hypertrophic chondrocytes. When proliferation is completed, chondrocytes release Indian hedgehog (Ihh), which stimulates PTHrP synthesis via a feedback loop. Any disturbances of the epiphyseal development and its physiology result in various skeletal abnormalities known as dysplasia.

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“…Indeed, the complexity of the chondro-osseous (cartilage and bone) junction has been the cause of considerable debate, especially the morphological appearance of the terminal chondrocyte. For example, Roach and co-workers 5,6 have described cells that exhibited unusual ultramicroscopic features. It was suggested that these cells were in "limbo", unable to live or die.…”

Section: Introductionmentioning

confidence: 99%