title: Chondrocytes isolated from tibial dyschondroplasia lesions and articular cartilage revert to a growth plate-like phenotype when cultured in vitro.
abstract: We report here a comparative study of the development and behavior of chondrocytes isolated from normal growth plate tissue, tibial dyschondroplasic lesions, and from articular cartilage. The objective of these studies was to determine whether the properties exhibited by chondrocytes in dysplasic lesions or in articular cartilage were due to their cellular phenotype, their environment, or both. We had previously analyzed the electrolytes and amino acid levels in the extracellular fluid of avian growth plate chondrocytes. Using these data, we constructed a culture medium (DATP5) in which growth plate cells essentially recapitulate their normal behavior in vivo. Here, we used DATP5 to examine the behavior of chondrocytes isolated from lesions of tibial dyschondroplasia (TD). We found that once isolated from lesion and grown in this supportive medium, dysplasic chondrocytes behaved essentially like normal growth plate cells. These findings suggest that the cause of TD is local factors operating in vivo to prevent these cells from developing normally. With respect to articular chondrocytes, our data indicate that they more closely retain normal protein and proteoglycan synthesis when grown in serum-free media. These cells readily induced mineral formation in vitro, both in the presence and absence of serum. However, in serum-containing media, mineralization was significantly enhanced when the cells were exposed to retinoic acid (RA) or osteogenic protein-1 (OP-1). Our studies support previous work indicating the presence of autocrine factors produced by articular chondrocytes in vivo that prevent mineralization and preserve matrix integrity. The lack of inhibitory factors and the presence of supporting factors are likely reasons for the induction of mineralization by articular chondrocytes in vitro.
authors.affiliation: Department of Chemistry and Biochemistry, University of South Carolina, Graduate Science Research Center, Columbia, South Carolina 29208, USA.
authors.forename: Licia N Y
authors.initials: LN
authors.lastname: Wu
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Ishikawa
authors.forename: Brian R
authors.initials: BR
authors.lastname: Genge
authors.forename: Roy E
authors.initials: RE
authors.lastname: Wuthier
mesh_terms: D000818:Animals; D019898:Autocrine Communication / Q000502:physiology; D055419:Bone Morphogenetic Protein 7; D019485:Bone Morphogenetic Proteins / Q000378:metabolism / Q000494:pharmacology; D002113:Calcification, Physiologic / Q000187:drug effects / Q000235:genetics*; D002114:Calcinosis / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D002358:Cartilage, Articular / Q000166:cytology / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D002645:Chickens; D019902:Chondrocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D020219:Chondrogenesis / Q000187:drug effects / Q000502:physiology*; D003470:Culture Media / Q000737:chemistry / Q000494:pharmacology; D016895:Culture Media, Serum-Free / Q000494:pharmacology; D006132:Growth Plate / Q000166:cytology / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D010009:Osteochondrodysplasias / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D011509:Proteoglycans / Q000096:biosynthesis; D013977:Tibia / Q000254:growth & development / Q000473:pathology / Q000503:physiopathology; D016212:Transforming Growth Factor beta / Q000378:metabolism / Q000494:pharmacology; D014212:Tretinoin / Q000494:pharmacology
chemical_list: D055419:Bone Morphogenetic Protein 7; D019485:Bone Morphogenetic Proteins; D003470:Culture Media; D016895:Culture Media, Serum-Free; D011509:Proteoglycans; D016212:Transforming Growth Factor beta; D014212:Tretinoin