| Biocompatibility evaluation of nickel-titanium shape memory metal alloy: | ||
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On the basis of their interface reactions, materials may be classified as toxic, biologically inactive (nearly inert), bioactive, or resorptive (Hench 1996). Toxic materials are not used in implants. Metallic biomaterials are classified as nearly inert materials. Because of their mechanical strength and biocompatibility, metals are superior in load-bearing implants.
The biocompatibility of the implant material is closely related to the reactions between the surface of the biomaterial and the inflammatory host response (Thomsen et al. 1991). There are several factors that contribute to this. These may depend on individual patient characteristics, such as general health, age, tissue perfusion, immunological factors, or implant characteristics, such as surface roughness and porosity, chemical reactions at the surface, corrosion properties of the material, and the toxicity of the individual metals present in the alloy (Klinger et al. 1997). The surgery itself, the technique applied, and biomechanical considerations (stability) modify the inflammatory response.
The releasing agents from the cell may alter the characteristics of the material surface. The surface is also changed due to the influence of proteins absorbed from plasma (Anderson et al. 1990).
After implantation, a coagulating and vascularizing process takes place. The implant is covered by a blood clot containing leukocytes and erythrocytes, thrombocytes and coagulating proteins. The implant and the surgical trauma trigger an inflammatory reaction which eliminates the damaged tissue, clot and bacteria. Inflammatory cells, first polymorphonuclear granulocytes and later monocytes, arrive to expurgate the debris and foreign materials. If there is too much foreign substance for granulocytes, monocytes developed into macrophages. If there is a delay in removing the substance, the enzymes of activated macrophages affect the fibroblasts to make a fibrous capsule around the implant. As long as phagocytic activation is maintained, the capsule becomes thicker. In soft tissues, the inert material forms a thin, fibrous encapsule around the implant (Anderson 1996).
The implantation response in bone differs in some ways from that taking place in soft tissue. There is an inflammatory and a reparative response which occur one on the other. The reparative response starts 2-3 days after the implantation. The stem cells of bone develop into osteoblasts, which form a layer near the implant together with fibroblasts. Fibroblasts, osteoblasts and capillaries penetrate into the blood clot, replacing it, and fill the space between the implant and bone (Tarr et al. 1986). After the formation of a collagen-rich extracellular matrix (ECM), mineralization follows. Normally, there are vesicles in ECM and some of them include calcification focuses. The presence of vesicles with biomaterial in the early period is a sign of good primary acceptance. When the membranes of these vesicles rupture, the erupted apatite crystals unite and form calcifying structures (Davies 1991). Early trabecles grow and continue to mineralize, and some of them reach the implant surface. In an optimal situation, the material is covered by bone tissue and not by fibrous capsule. The healing of bone tissue continues like fracture healing. Remodelation of bone tissue begins after two weeks and continues for the lifetime. Woven bone is replaced by functionally oriented lamellar bone.
The changes in the local environment, such as acidity, oxygen content, electric charge, ion concentration, enzymes, growth factors, etc., have effects on the differentiation and migration of stem cells. The attachment of osteogenic stem cells to substrate and the formation of mineralized ECM are essential for the differentiation of osteoblasts (Davies 1991). When the material is biocompatible, there is an abundance of ECM and osteoblasts. This is confirmed by the close attachment and fast proliferation of these cells (Vrouwenvelder et al. 1993). Brånemark et al. (1969) first suggested that titanium may form direct bone contact. He defined this ”osseointegration” as direct metal-to-bone contact at the light-microscopic (0.5 µm) level. This definition appears to be somewhat inaccurate, and some clinically based definitions of osseointegration have been suggested (Albrektsson et al. 1993). In optimal situations, however, bone accepts the implant as part of its ECM, and clinically asymptomatic rigid fixation is achieved in bone during functional loading. Such fixation is possible with titanium implants. Other implant metals usually form some fibrous tissue between the bone and the implant and are often called “nearly inert”. Because of their mechanical strength and biocompatibility, metals are superior in load-bearing implants. Even chemical bone bonding (the establishment, by physico-chemial processes, of continuity between implant and bone) is seen with bioactive glasses, but their mechanical properties are inferior to metal biomaterials (Hench 1996).
Highly toxic material causes tissue necrosis. The signs of sub-acute toxicity or low tissue tolerance may be manifested in several ways. A large amount of foreign-body giant cells is usually a sign of a prolonged stimulus. Also, the presence of phagocytes at a later time may signify a rejection of the implant. The propagation of lymphocytes or plasma cells may indicate the activation of the immune system against the material. Profuse accumulation of neutrophils is a sign of infection. Vacualization and resorption of muscle are signs of an inferior tissue response (Williams 1986).
The response of individual cells to material can be considered to be dependent on how well the material mimics the natural (extracellular) environment of the cell. The physical structure of the surface may have an inferior influence on the biological response of the material, which is normally non-toxic and does not release any biologically active substance. Osteolysis, bone resorption and the formation of a thick fibrous layer between the implant and bone reflect poor biocompatibility. Also, microparticles of certain size of normally non-toxic materials may trigger an inflammatory response. These particles cause an irritation of phagocytic cells and activate them to produce and release cytokines, proteinases, growth factors and other proinflammatory factors, finally leading to chronic inflammation, fibrosis, osteolysis and porosis in bone (Shanbhag et al. 1994, Tang et al. 1996). In the case of aseptic loosening of the prosthesis, wear particles are expected to lead to the formation of a poorly vascularized, synovial-like interface membrane between the prosthesis and bone (Santavirta et al. 1998). The formation of necrotic focuses, granulomas and osteolysis may finally result in loosening of the prosthesis (Santavirta et al. 1996). The increase of metallic wear increases the surface of the metal material and the quantity of metal ions. The porous surface increases the surface area, but also particular wear.