Repair of large osteochondral defects in rabbits using porous hydroxyapatite/collagen (HAp/Col) and fibroblast growth factor‐2 (FGF‐2)

Abstract

Articular cartilage has a limited capacity for self-renewal. This article reports the development of a porous hydroxyapatite/ collagen (HAp/Col) scaffold as a bone void filler and a vehicle for drug administration. The scaffold consists of HAp nanocrystals and type I atelocollagen. The purpose of this study was to investigate the efficacy of porous HAp/Col impregnated with FGF-2 to repair large osteochondral defects in a rabbit model. Ninety-six cylindrical osteochondral defects 5 mm in diameter and 5 mm in depth were created in the femoral trochlear groove of the right knee. Animals were assigned to one of four treatment groups: porous HAp/Col impregnated with 50 ml of FGF-2 at a concentration of 10 or 100 mg/ml (FGF10 or FGF100 group); porous HAp/Col with 50 ml of PBS (HAp/Col group); and no implantation (defect group). The defect areas were examined grossly and histologically. Subchondral bone regeneration was quantified 3, 6, 12, and 24 weeks after surgery. Abundant bone formation was observed in the HAp/Col implanted groups as compared to the defect group. The FGF10 group displayed not only the most abundant bone regeneration but also the most satisfactory cartilage regeneration, with cartilage presenting a hyaline-like appearance. These findings suggest that porous HAp/Col with FGF-2 augments the cartilage repair process. ß

In vitro and in vivo studies of a novel bacterial cellulose-based acellular bilayer nanocomposite scaffold for the repair of osteochondral defects

“…The subchondral bone formation may have resulted from osteoconductive property of nanocomposite BC-HA activated with BMP-2. This is in conjunction with previous reports 5,47,48 where subchondral bone formation is reported to enhance regeneration of the articular cartilage. In the current in vivo study, the size of the modified BC scaffold was significantly reduced at 3 months, indicating biodegradative resorption and integration in the surrounding tissue.…”

Evaluation of Cartilage Repair by Mesenchymal Stem Cells Seeded on a PEOT/PBT Scaffold in an Osteochondral Defect

“…In contrast, hypocellularity was observed in the cell-free scaffolds and there was no obvious cell orientation. Regarding fibrocartilage development, positive collagen type I staining was not observed to the same extent in the cell-seeded scaffold, suggesting fibrocartilage formation in 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 the cell-free scaffold and hyaline-like cartilage formation in the cell-seeded scaffold, echoing the observations of Maehara 14 Nonetheless, analysis with a modified O'Driscoll scoring system, revealed that there was no statistical difference observed between the cell-free scaffold and the cell-seeded scaffold (Table 2) other cartilage repair studies using a cell-free PEOT scaffold, these results compare well with Jansen, 6 where cartilage repair was not observed frequently, while bone repair and integration with native tissue was observed. In contrast, the cell-seeded PEOT/PBT scaffold in this study appeared to augment cartilage repair in addition to bone repair, with higher O'Driscoll scores for percentage hyaline cartilage, surface continuity, tidemark and thickness of repair tissue compared to the cell-free scaffolds (Fig.…”

Tissue engineered bone using select growth factors: A comprehensive review of animal studies and clinical translation studies in man

“…Tissue engineered bone and clinical translation revealed the most abundant member utilised within bone tissue engineering strategies in vivo was FGF-2, also known as basic FGF (Hirata et al, 2013;Hong et al, 2010;Maehara et al, 2009;Shirakata et al, 2010).…”

“…Considering related fold increases in bone formation within large (1.3 to 3 fold Shirakata et al, 2010)) and small animals (1.1 to 16.4 fold (Goodman et al, 2003;Hong et al, 2010)), it is interesting to note that higher dosages correlated with greater fold increases (defects with highest fold increase included tibial fracture and calvarial defect respective to large and small animals). Evidently, data suggest positive correlation between FGF-2 treatment and bone formation, potentially due to induced vessel ingrowth and ossification at the defect site (Guo et al, 2006;Maehara et al, 2009 (Bland et al, 1995;Dunstan et al, 1999;Kelpke et al, 2004), and one study utilised FGF-18 (Carli et al, 2012) which has been shown to promote chondrogenesis amongst many other functions. FGF-1 was administered between 3 and 7 µg in small animals including mouse (Dunstan et al, 1999), rabbit (Bland et al, 1995) and rat (Kelpke et al, 2004).…”