Biomaterials and scaffolds for tissue engineering

Every day thousands of surgical procedures are performed to replace or repair tissue that has been damaged through disease or trauma. The developing field of tissue engineering (TE) aims to regenerate damaged tissues by combining cells from the body with highly porous scaffold biomaterials, which act as templates for tissue regeneration, to guide the growth of new tissue. This article describes the functional requirements, and types, of materials used in developing state of the art of scaffolds for tissue engineering applications. Furthermore, it describes the challenges and where future research and direction is required in this rapidly advancing field

Influence of shear stress in perfusion bioreactor cultures for the development of three-dimensional bone tissue constructs: a review.

Bone tissue engineering aims to generate clinically applicable bone graft substitutes in an effort to ease the demands and reduce the potential risks associated with traditional autograft and allograft bone replacement procedures. Biomechanical stimuli play an important role under physiologically relevant conditions in the normal formation, development, and homeostasis of bone tissue--predominantly, strain (predicted levels in vivo for humans \u3c2000\u3eμε) caused by physical deformation, and fluid shear stress (0.8-3 Pa), generated by interstitial fluid movement through lacunae caused by compression and tension under loading. Therefore, in vitro bone tissue cultivation strategies seek to incorporate biochemical stimuli in an effort to create more physiologically relevant constructs for grafting. This review is focused on collating information pertaining to the relationship between fluid shear stress, cellular deformation, and osteogenic differentiation, providing further insight into the optimal culture conditions for the creation of bone tissue substitutes

IV.3. Bioreactors in tissue engineering.

IV.3. Bioreactors in tissue engineering

Influence of a novel calcium-phosphate coating on the mechanical properties of highly porous collagen scaffolds for bone repair.

Lyophilised collagen scaffolds have shown enormous potential in tissue engineering in a number of areas due to their excellent biological performance. However, they are limited for use in bone tissue engineering due to poor mechanical properties. This paper discusses the development of a calcium-phosphate coating for collagen scaffolds in order to improve their mechanical properties for bone tissue engineering. Pure collagen scaffolds produced in a lyophilization process were coated by immersing them in sodium ammonium hydrogen phosphate (NaNH(4)HPO(4)) followed by calcium chloride (CaCl(2)). The optimal immersing sequence, duration, as well as the optimal solution concentration which facilitated improved mechanical properties of the scaffolds was investigated. The influence of the coating on composition, structural and material properties was analysed. This investigation successfully developed a novel collagen/calcium-phosphate composite scaffold. An increase in the mechanical properties of the scaffolds from 0.3 kPa to up to 90 kPa was found relative to a pure collagen scaffold, while the porosity was maintained as high as 92%, indicating the potential of the scaffold for bone tissue engineering or as a bone graft substitute

Estrogen plus estrogen receptor antagonists alter mineral production by osteoblasts in vitro.

In early postmenopausal women, estrogen withdrawal is associated with increased bone turnover leading to bone loss and increased risk of fracture. Recent studies have suggested that the remaining bone tissue is significantly stronger, stiffer and has an increased tissue-level mineral content. Such changes may occur to compensate for bone loss or as a direct result of estrogen deficiency. To date many details of the physiology of osteoblastic cells during estrogen deficiency are vague. In this study we test the hypothesis that osteoblastic matrix mineralisation is altered at the onset of estrogen deficiency. In vitro cell culture experiments were carried out up to 28 days to compare the mineral production of MC3T3-E1 osteoblastic cells subject to estrogen deficiency (fulvestrant), enhanced estrogen supplementation (17-β-estradiol) or a combination of both. Mineralisation was detected using von Kossa staining and was quantified with alizarin red absorbance readings. The expression of osteocalcin and osteopontin proteins, markers of osteoblast differentiation and mineralisation, was monitored using immunohistochemistry. Our results demonstrate that estrogen enhancement improves matrix mineralisation by MC3T3 cells in vitro. Furthermore this study found a significant reduction in the level of mineralisation when cells were treated with a combination of estrogen and fulvestrant. In an estrogen deficient environment mineralisation by osteoblastic cells was not altered. These findings suggest that altered tissue mineralisation following estrogen deficiency is not a direct result of estrogen deficiency on osteoblasts. Rather, we propose that altered tissue mineralisation may be a compensatory mechanism by bone to counter bone loss and reduced strength

Microcrack accumulation at different intervals during fatigue testing of compact bone.

Fatigue damage in bone occurs in the form of microcracks. This microdamage contributes to the formation of stress fractures and acts as a stimulus for bone remodelling. A technique has been developed, which allows microcrack growth to be monitored during the course of a fatigue test by the application of a series of fluorescent chelating agents. Specimens were taken from bovine tibiae and fatigue tested in cyclic compression at a stress range of 80MPa. The specimens were stained before testing with alizarin and up to three other chelating agents were applied during testing to label microcracks formed at different times. Microcracks initiated in interstitial bone in the early part of a specimen\u27s life. Further accumulation of microcracks is then suppressed until the period late in the specimen\u27s life. Microcracks were found to be longer in the longitudinal than in the transverse direction. Only a small proportion of cracks are actively propagating; these are longer than non-propagating cracks. These results support the concept of a microstructural barrier effect existing in bone, whereby cracks initiate easily but slow down or stop at barriers such as cement lines