title: An Articular Cartilage Repair Model in Common C57Bl/6 Mice.
abstract: To analyze the genetic and biomolecular mechanisms underlying cartilage repair, an optimized mouse model of osteochondral repair is required. Although several models of articular cartilage injury in mice have recently been established, the articular surface in adult C57Bl/6 mice heals poorly. Since C57Bl/6 mice are the most popular strain of genetically manipulated mice, an articular cartilage repair model using C57Bl/6 mice would be helpful for analysis of the mechanisms of cartilage repair. The purpose of this study was to establish a cartilage repair model in C57Bl/6 mice using immature animals. To achieve this goal, full-thickness injuries were generated in 3-week-old (young), 4-week-old (juvenile), and 8-week-old (adult) C57Bl/6 mice. To investigate the reproducibility and consistency of full-thickness injuries, mice were sacrificed immediately after operation, and cartilage thickness at the patellar groove, depth of the cartilage injury, cross-sectional width, and cross-sectional area were compared among the three age groups. The depth of cartilage injury/cartilage thickness ratio (%depth) and the coefficient of variation (CV) for each parameter were also calculated. At 8 weeks postoperatively, articular cartilage repair was assessed using a histological scoring system. With respect to the reproducibility and consistency of full-thickness injuries, cartilage thickness, depth of cartilage injury, and cross-sectional area were significantly larger in young and juvenile mice than in adult mice, whereas cross-sectional width and %depth were almost equal among the three age groups. CVs of %depths were less than 10% in all groups. With respect to articular cartilage repair, young and juvenile mice showed superior results. In conclusion, we established a novel cartilage repair model in C57Bl/6 mice. This model will be valuable in achieving mechanistic insights into the healing process of the joint surface, as it will facilitate the use of genetically modified mice, which are most commonly developed on a C57Bl/6 background.
authors.affiliation: Department of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine , Sapporo, Japan .
authors.forename: Masatake
authors.initials: M
authors.lastname: Matsuoka
authors.affiliation: Department of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine , Sapporo, Japan .
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Onodera
authors.affiliation: Department of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine , Sapporo, Japan .
authors.forename: Fumio
authors.initials: F
authors.lastname: Sasazawa
authors.affiliation: Department of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine , Sapporo, Japan .
authors.forename: Daisuke
authors.initials: D
authors.lastname: Momma
authors.affiliation: Department of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine , Sapporo, Japan .
authors.forename: Rikiya
authors.initials: R
authors.lastname: Baba
authors.affiliation: Department of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine , Sapporo, Japan .
authors.forename: Kazutoshi
authors.initials: K
authors.lastname: Hontani
authors.affiliation: Department of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine , Sapporo, Japan .
authors.forename: Norimasa
authors.initials: N
authors.lastname: Iwasaki
mesh_terms: D000375:Aging / Q000378:metabolism*; D000818:Animals; D002358:Cartilage, Articular / Q000293:injuries* / Q000502:physiology*; D004195:Disease Models, Animal; D051379:Mice; D012038:Regeneration