Alloplastic and natural materials used as implants

Introduction

Alloplastic and natural materials have gained widespread use as replacements for tissues in a wide variety of applications. Allografts and xenografts have grown appreciably in their applications in a wide variety of clinical situations that range from the skeletal framework to the overlying soft tissue envelope (see Silver et al. for a review).

Synthetic materials, such as polyethylene terephthalate, polyethylene, and polytetrafluoroethylene, work well in many applications; metals, such as stainless steel, titanium, and cobalt chromium, are useful in stents; and natural materials, such as auto- and allografts, are used in many applications where cellular ingrowth and repair responses are required to promote long-term healing of tissues ( Table 12.1 ). Tissue responses to implants vary, depending on implantation site, material biocompatibility, implant porosity, and mechanical forces applied at the implant–tissue interface. Recent study results have suggested that mechanical mismatches at the tissue–implant interface can lead to implant failure due to upregulation of mechanotransduction processes.

The purpose of this chapter is to discuss the use of synthetic and natural materials in aesthetic surgery of the facial skeleton. This chapter will also discuss biologic materials within the context of a broader body of scientific data. The success of any implant depends not only on minimizing the inflammatory reaction of the material but also on the prosthetic porosity and stress at the tissue–implant interface.

Effects of implant material characteristics, porosity, and interfacial stress

All foreign materials have limited biocompatibility. Any material without vasculature, whether it is a metal, polymer, ceramic, allograft, or autograft, is treated as a foreign body, triggering biologic cascades, including natural blood clotting, fibrinolysis, and activation of the complement and kinin systems. This leads to natural and acquired immune responses, including influx of inflammatory cells, release of cytokines and lymphokines, destruction of host tissue, and vasodilation. Thus the goal of the surgeon is to minimize these responses to prevent implant failure.

Beyond this, the porosity of an implant will dictate whether the implant is encapsulated or tissue ingrowth leads to movement of fibroblasts, capillaries, and stem cells into the implant, leading to quiescence and toleration. Reaching quiescence will depend on implant material characteristics and the host response—these factors will vary from patient to patient. If a thick capsule forms around the implant, the capsule will attempt to contract and may lead to shifting of the implant or to implant ejection from the host. In the case of porous implants, with pore sizes averaging greater than 100 to 150 μm, implants are stabilized by tissue ingrowth. However, the pores must be connected internally for appropriate tissue ingrowth.

In addition, there is strong evidence that the biomechanics of load transfer between native tissue and the implant plays a significant role in the functional success or failure of the implant. ^, Implants fail at the junction because of anatomic and biomechanical discontinuities. Effective tissue repair with the use of allografts or synthetic implants should involve limiting the stress and strain at the implant–issue interface whether the implant is loaded in tension or compression. In addition, the stress–strain behavior of tissues is nonlinear ( Fig. 12.1 ), with the modulus increasing according to the degree of deformation so that excessive strain at the implant–tissue interface magnifies the stress concentration at the boundary.

The testing of materials has moved from ex vivo to in vivo with increasing sophistication of the technology. The clinician today can measure the modulus of the implant, host tissue, and the interface to minimize implant-related problems and to develop better biologic materials by using optical coherence tomography (OCT) and vibrational analysis.

Adverse reactions to implants

All implants, with the possible exception of vascularized autograft flaps, have the potential to lead to adverse reactions. Adverse reactions can lead to intense pain, excessive inflammation, and even implant failure and extrusion. Implants initiate a macrophage-mediated acute inflammatory response, followed by resolution, proliferation of somatic cells, tissue remodeling, and tissue homeostasis. Macrophage polarization by cytokines leads to activation and then macrophage secretion of cytokines in the presence of an implant.

All nonvascularized implants induce a foreign body response as a result of macrophage activation. The sequence of events leading to this response includes (1) protein adsorption to the implant, (2) macrophage recruitment to the wound area, (3) macrophage adhesion to the implant surface, (4) release of macrophage chemokines, (5) recruitment of additional macrophages and immune cells, and (6) induction of acute inflammation.

Unresolved inflammation can lead to chronic inflammation that is accompanied by macrophage fusion into foreign body giant cells, followed by fibrous encapsulation of the implant. This can lead to movement of the implant and eventually implant failure. Proteins that are adsorbed to the implant and are involved in implant recognition include fibronectin, fibrinogen, vitronectin, and complement component C3b. Protein adsorption to foreign surfaces leads to initiation of a foreign body response.

Adverse reactions to metallic implants that contain nickel, cobalt, and chromium elements lead to cutaneous and systemic hypersensitivity. Adverse reactions to titanium, zirconium, cobalt–chromium, titanium–nickel, and steel have been reported.

Types of implant materials

A variety of implant materials, including polymers, metals, ceramics, and biologic tissues, have been used in surgery in the form of solid implants, porous materials, and injectables (see Table 12.1 ).