Chondroclasts and endothelial cells collaborate in the process of cartilage resorption

Abstract

The condylar cartilage of the young rat is a major growth center of the craniofacial complex. Differences between the mechanism that results in bone formation from growth centers in the epiphyseal plates of long bones are dictated primarily by the different character of the mineralization of the cartilage. In this ultrastructural study we demonstrate that the terminal hypertrophic chondrocytes undergo apoptosis and disintegration while simultaneously chondroclasts dissolve gaps in the calcified cartilage that engulfs them. The latter are also phagocytizing debris of the chondrocytes. The chondroclasts are intimately followed by tube-forming endothelial cells that most probably coalesce to create extensions of the invading capillaries into the evacuated lacunae. The chondroclasts have ultrastructural features similar to osteoclasts. They are multinucleate, are rich in mitochondria and vacuoles, form clear zones that adhere to the spicules of the calcified cartilage, and also form a sort of ruffled border. The latter is not as elaborate and orderly arranged as is known from osteoclasts. The capillaries that follow orient the stroma cells to the evacuated lacunae and, together with the calcified cartilaginous scaffold, supply the adequate environmental conditions for the stroma cells to differentiate into osteoblasts and to build up trabecular bone.

Insulin impairs the maturation of chondrocytes in vitro

“…In vivo and in vitro studies have demonstrated that terminally differentiated chondrocytes undergo programmed cell death (12,27). In vivo studies have shown that in the proximal tibial growth plate of young chicks, terminally differentiated chondrocytes undergo programmed cell death (28,29).…”

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).…”

Lead alters parathyroid hormone‐related peptide and transforming growth factor‐β1 effects and AP‐1 and NF‐κKB signaling in chondrocytes

“…Eventually the matrix surrounding hypertrophic chondrocytes calcifies and the cells undergo apoptosis [14,24]. As blood vessels invade the calcified cartilage, bone is deposited on the cartilaginous template completing the process of endochondral bone formation.…”