Abstract
Articular cartilage maturation is the postnatal development process that adapts joint surfaces to their site-specific biomechanical demands. Maturation involves gross morphological changes that occur through a process of synchronised growth and resorption of cartilage and generally ends at sexual maturity. The inability to induce maturation in biomaterial constructs designed for cartilage repair has been cited as a major cause for their failure in producing persistent cell-based repair of joint lesions. The combination of growth factors FGF2 and TGFβ1 induces accelerated articular cartilage maturation in vitro such that many molecular and morphological characteristics of tissue maturation are observable. We hypothesised that experimental growth factor-induced maturation of immature cartilage would result in a biophysical and biochemical composition consistent with a mature phenotype. Using native immature and mature cartilage as reference, we observed that growth factor-treated immature cartilages displayed increased nano-compressive stiffness, decreased surface adhesion, decreased water content, increased collagen content and smoother surfaces, correlating with a convergence to the mature cartilage phenotype. Furthermore, increased gene expression of surface structural protein collagen type I in growth factor-treated explants compared to reference cartilages demonstrates that they are still in the dynamic phase of the postnatal developmental transition. These data provide a basis for understanding the regulation of postnatal maturation of articular cartilage and the application of growth factor-induced maturation in vitro and in vivo in order to repair and regenerate cartilage defects.
Highlights
IntroductionRepair of adult cartilage is complicated in that this tissue is avascular, has a low cell to volume ratio and is rich in glycosaminoglycan containing proteoglycans producing a high negative fixed charge density [1]
Repair and regeneration of articular cartilage defects presents biologists and bioengineers with formidable challenges.From the biological perspective, repair of adult cartilage is complicated in that this tissue is avascular, has a low cell to volume ratio and is rich in glycosaminoglycan containing proteoglycans producing a high negative fixed charge density [1]
In vitro culture of articular cartilage explants excised from immature metacarpophalangeal joints in the presence of FGF2 (100 ng mlÀ1) and TGFb1 (10 ng mlÀ1) for 21 days results in profound morphological change [37]
Summary
Repair of adult cartilage is complicated in that this tissue is avascular, has a low cell to volume ratio and is rich in glycosaminoglycan containing proteoglycans producing a high negative fixed charge density [1]. These attributes limit active or passive cellular migration to the lesion site and characterise the poor intrinsic healing capacity of adult tissue [2]. Further complications arise as transplanted cells initially adopt an immature cartilage phenotype that appears to be subject to phenotypic instability [9], resulting in the inappropriate production of fibrocartilage or calcified tissue, both of which are to varying degrees deleterious to joint function [10,11]
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