Condensation of hypertrophic chondrocytes at the chondro‐osseous junction of growth plate cartilage in Yucatan swine: Relationship to long bone growth

Abstract

Chondrocytes of the cartilaginous growth plate are found in a spatial gradient of cellular differentiation beginning with cellular proliferation and ending with cellular hypertrophy. Although it is recognized that both proliferation and hypertrophy contribute significantly to overall bone growth, mechanisms acting on the chondrocyte to control the timing, the rate, and the extent of hypertrophy are poorly understood. Similarly, mechanisms acting on the terminal chondrocyte to cause its death at the chondro-osseous junction have not been investigated. In this study we examine the condensation of terminal hypertrophic chondrocytes in proximal and distal radial growth plates of Yucatan swine at 4 weeks of age. The animals were raised in a controlled environment where activity and feeding patterns were synchronized to a given time in the light/dark cycle. We analyzed cellular condensation both as a function of circadian rhythms in a 24-hr time period, and as a function of overall rate of growth. The data suggest that the magnitude of circadian influences on long bone growth is significantly damped at the level of the hypertrophic chondrocyte compared to that seen by previous investigators studying circadian influences on chondrocytic proliferation. Secondly, the condensation of hypertrophic chondrocytes at the chondro-osseous junction varies inversely with rate of growth in length of the bone. At any time period, a higher percentage of terminal chondrocytes in the condensed form was found in the slower-growing of the two growth plates. We relate these findings to current hypotheses concerning controls of chondrocytic hypertrophy and possible controls over the timing of hypertrophic cell death.

Chondrocyte apoptosis in endochondral ossification of chick sterna

“…The primary ossification center is resorbed from all surfaces rather than a single (metaphyseal) interface in the growth plate and thus has a greater relative resorption surface than the growth plate. As suggested by Farnum and Wilsman (Farnum and Wilsman, 1989b), the number of chondrocytes in condensed form is probably not directly related to the rate of bone elongation and by inference the rate of cartilage resorption (Farnum and Wilsman, 1989b) but reflects the rate at which condensed chondrocytes are removed from the tissue rather than the rate of cell death.…”

Indian hedgehog synchronizes skeletal angiogenesis and perichondrial maturation with cartilage development

“…One day later, at E18.5, the PECAMand TRAP-positive cells had disappeared, and the cartilage matrix was degraded. In addition, we noted a large number of condensing, terminally differentiated chondrocytes (Farnum and Wilsman, 1989;Roach and Clarke, 2000) in that region and only weak MMP9 expression remained in the disintegrated extracellular matrix (Fig. 2I,J,K, arrows).…”

Fate of growth plate hypertrophic chondrocytes: Death or lineage extension?

“…In contrast to necrosis, which is considered a form of passive cell death that involves cell swelling and rupture in response to stress and injury, apoptosis is characterized by cell shrinkage, nuclear condensation, preservation of membrane integrity and rapid elimination by phagocytosis (see review by Fuchs & Steller 2011). Since then, with refined fixation techniques to reduce artefactual changes during preservation of the growth plate and cellular structure for (2014a,b) and Zhou et al (2014) ª 2015 Japanese Society of Developmental Biologists electron microscopy (Hunziker et al 1983), apoptotic HCs have been found in avian dyschondroplastic tibia (Hargest et al 1985) and in normal mammalian growth plates (Farnum & Wilsman 1987, 1989bLewinson & Silbermann 1992). From thin serial histological sections of swine growth plate, it was estimated that about 12% of the terminal HCs in a single section are undergoing apoptosis (characterized as condensing cells) which takes as soon as 45 min, whereas the resultant empty lacuna remain observable for about 15 min (Farnum & Wilsman 1989a).…”