Objecives of Tissue Engineering

Tissue exchange is an ancient art, but tissue engineering is a new concept. The new thinking about tissue engineering is supported by technologies that were developed during the twentieth century, including advanced cell culture, gene transfer, and materials synthesis. Tissue engineering arose from a diverse group of historical precedents that included pharmacology, surgery, and materials science; each historical line of inquiry engaged different motivations and diverse tools. Therefore, as a substitute for a single definition, this chapter observes tissue engineering from several different angles and attempts to illustrate the field by practical example. The field of tissue engineering can be subdivided in various ways; usually it is organized by organ system, as in hepatic tissue engineering or bone tissue engineering, which are concerned with engineering replacements for liver and bone function, respectively. A coarse subdivision can also be made according to the general objective; most tissue engineering strategies involve replacement of a tissue’s metabolic function, structural function, or both. Here, several overlapping views of tissue engineering are presented: tissue engineering as a logical extension of contemporary medical and surgical therapies; tissue engineering as a method for controlling the normal healing response of tissues; tissue engineering as an effort to repopulate the cellular component of tissues without replacement of the whole organ; tissue engineering as a variety of controlled drug delivery; and tissue engineering as a new method for developing models of human physiology. Metabolism is a coordinated ensemble of chemical transformations that are individually regulated by the action of enzymes. Many metabolic disorders are caused by the defective production of a single enzyme. It is sometimes possible to identify, produce, and use enzymes to reconstitute missing elements of metabolism. For example, the enzyme adenosine deaminase (ADA) is involved in the degradation of purine nucleosides; individuals who lack the gene for ADA cannot produce the enzyme in their bodies. As a result, high concentrations of certain purine nucleoside metabolites accumulate within cells; toxicity due to these metabolites is particularly harmful to B and T lymphocytes.