Abstract
ABSTRACTDuring early bone formation, mesenchymal cells condense and then differentiate into collagen type II‐expressing chondrocytes that make up the cartilaginous bone anlagen. This anlage then becomes enclosed by the perichondrium. The mechanisms by which the perichondrium forms are not known. The purpose of this study was to determine whether epiphyseal chondrocytes can differentiate into perichondrial cells. Novel perichondrium markers were identified by expression microarray of microdissected rat perichondrium and growth plate cartilage. A dissection method that allowed for removal of contaminating perichondrium was developed and the absence was confirmed by histological examination and by expression of perichondrium markers. Perichondrium formation surrounding chondrocyte pellets was studied using histology, real‐time PCR, and in situ hybridization for chondrocyte and perichondrium markers. Cultured chondrocyte pellets developed an exterior perichondrium‐like layer. This surrounding tissue did not express chondrocyte markers, collagen‐type II and type X, as assessed by in situ hybridization. Instead, perichondrium markers, periostin, Dickkopf 3 (Dkk3), roundabout 2, cadherin 2, L‐galectin 1 (Lgals1), and thrombospondin 2 (Thbs2) were upregulated following formation of the perichondrium‐like layer as assessed by real‐time PCR. Interestingly, markers specific for the cambium layer, Dkk3, Thbs2, and Lgals1, but not for the fibrous layer, collagen‐type XIV and decorin, were upregulated. The findings suggest that epiphyseal chondrocytes of postnatal animals retain the potential to differentiate into perichondrial cells, supporting the hypothesis that the perichondrium originates from collagen type II‐expressing chondrocytes at the periphery of the cartilaginous bone template. © 2018 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.
Highlights
During embryonic development, the formation of long bones starts with the condensation of mesenchymal cells that differentiate into collagen-type II-expressing chondrocytes.[1,2] Chondrocytes in the center of the bone template undergo hypertrophic differentiation, initiating the process of remodeling of the newly formed cartilage into bone
To identify perichondrium markers that can be used to study differentiation of perichondrium cells, we developed an algorithm that ranks the genes based on their differential expression in perichondrium compared with growth plate cartilage and prioritizes highly expressed genes as described above
The top-ranking marker for perichondrium, tenascin N (Tnn), showed mRNA levels in the perichondrium that were more than 150-fold higher than in the growth plate, followed by asporin (Aspn; 161-fold), tenascin C (Tnc; 68-fold), and Postn (46-fold; Table S1)
Summary
The formation of long bones starts with the condensation of mesenchymal cells that differentiate into collagen-type II-expressing chondrocytes.[1,2] Chondrocytes in the center of the bone template undergo hypertrophic differentiation, initiating the process of remodeling of the newly formed cartilage into bone. The chondrogenic capacity of the perichondrium has been appreciated for some time,(9,10) whereas the capacity of postnatal chondrocytes to differentiate into perichondrium cells has only been suggested by a small number of in vitro studies.[11,12,13,14,15] these previous studies did not confirm complete removal of contaminating perichondrium. It is, difficult to draw firm conclusions about the cellular origin of the perichondrium layer formed in these experiments. Previous studies have not determined whether this perichondrium-like layer is formed by contaminating perichondrium cells or by chondrocytes that differentiate into perichondrium cells
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