title: Degree of degeneration and chondroitinase ABC treatment of human articular cartilage affect adhesion of chondrocytes.
abstract: The aim of the present study was to investigate whether degree of degeneration and chondroitinase ABC treatment of articular cartilage affect adhesion of chondrocytes to its surface. Human articular cartilage explants were harvested from patients undergoing total knee joint replacement arthroplasty, cut into discs of 0.5-0.8 mm thick and 3.75 mm in diameter, and then divided into three groups according to the degree of degeneration: G0, normal; G1, superficial fissures, and G2, deep fissures. These discs were stored at 70 degrees C until use. Chondrocytes (3 x 10(5) cell/mL in 100 microL of medium) isolated from articular cartilage by enzymatic digestion were transferred to a well plate containing cartilage discs and cultured for a maximum of 21 days. The cultures were divided into one of six groups according to the degree of degeneration and treatment of chondroitinase ABC of the disc. The morphologies of the disc surface and of cultured chondrocytes were assessed histologically. Chondrocyte adhesion, proliferation, and synthesis of proteoglycan and protein were analyzed. Chondrocyte adhesion significantly increased on the discs with higher degrees of degeneration, that is, maximum adhesion in G2, G1, and G0, subsequently. However, adhesion was not significantly different among the three groups at day 3. Chondrocyte adhesion on the chondroitinase ABC-treated disc significantly increased in comparison with that on the nontreated discs with the same degree of degeneration. However, proliferation of chondrocytes and synthesis of glycosaminoglycan and protein were not significant, regardless of degree of degeneration or chondroitinase ABC treatment. The present study demonstrated that chondrocyte adhesion on articular cartilage disc increased along with its degree of degeneration and with treatment of chondroitinase ABC, but that proliferation and synthesis of matrix of the cultured chondrocytes were not significantly influenced by both of them.
authors.affiliation: Department of Orthopedic Surgery, Seoul National University Boramae Hospital, Dongjak-gu, Seoul, Korea.
authors.forename: Chris H
authors.initials: CH
authors.lastname: Jo
authors.forename: Eun Mi
authors.initials: EM
authors.lastname: Kim
authors.forename: Hyung Jung
authors.initials: HJ
authors.lastname: Ahn
authors.forename: Hee Joong
authors.initials: HJ
authors.lastname: Kim
authors.forename: Sang Cheol
authors.initials: SC
authors.lastname: Seong
authors.forename: Myung Chul
authors.initials: MC
authors.lastname: Lee
mesh_terms: D000368:Aged; D002358:Cartilage, Articular / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology* / Q000648:ultrastructure; D002448:Cell Adhesion / Q000187:drug effects; D002452:Cell Count; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D019902:Chondrocytes / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology* / Q000648:ultrastructure; D019765:Chondroitin ABC Lyase / Q000494:pharmacology*; D006801:Humans; D018613:Microscopy, Confocal; D011509:Proteoglycans / Q000378:metabolism
chemical_list: D011509:Proteoglycans; D019765:Chondroitin ABC Lyase