In Situ Material Transformations in Tissue Engineering
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tes through small holes in the body via minimally invasive surgery. Using such approaches, it has become possible to perform many complex surgical procedures in the joints, abdominopelvic cavity, thoracic cavity, and nasal sinuses, for example, using surgical instruments that are manipulated through surgical access holes less than 1 cm in diameter. Even procedures as complex as coronary-artery bypass surgery have been performed in this way. It still remains generally impossible however to implant devices in the body through such holes unless these implants are very small. If such devices were for example able to be delivered as liquids and then shaped into devices at the implant site, such minimally invasive surgical-device placement could be envisioned. Material Transformations to Modulate Interactions at Tissue Surfaces A host of interactions in tissue engineering occur at tissue surfaces. One set of examples involves healing at surgically manipulated tissue surfaces. Two cases will be considered here: arterial restenosis and postoperative adhesions. One approach for reopening a coronary artery that has been partially obstructed by disease is to inflate a stiff balloon within the artery to break the diseased plaque and force it into the arterial wall. This treatment, balloon angioplasty, damages the artery surface, permitting blood platelets to attach and thrombosis and blood clotting to ensue. Perhaps because of the arterial healing factors that are released by components of the clot on the arterial surface, a scar within the artery lumen may form. This process is called restenosis. It may be possible to partially prevent restenosis by blocking the recognition of the injured arterial surface by the blood platelets after arterial angioplasty. In the second example, when tissue surfaces are injured by sur-
gical manipulation—for example the removal of a cyst on the ovary—the healing response at the tissue surfaces can result in the formation of a scar-tissue bridge between that tissue surface and neighboring organ surfaces, with the scar being called a postoperative adhesion. It may be possible to prevent this untoward healing response by blocking inflammatory-cell activity and fibrin clot formation at the surgically damaged surface. Thus in both of these examples, it may be possible to engineer the tissue-healing response by engineering the tissue surface and the cellular interactions at the tissue surface. Our laboratory has developed approaches to convert liquid precursors into biomedical hydrogels on arterial surfaces to block platelet deposition after 1,2 arterial injury. This material transformation must be very rapid (tens of seconds at the most) to be clinically relevant; must utilize solvents, temperatures, and chemical environments that will retain the viability of the arterial tissue; and must produce a tissue treatment that conforms to the complex shape of the diseased artery. The resulting surface treatment must be nonadhesive to blood platelets and ideally would degrade over time or under the influenc
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