The Biology of Aseptic Loosening
Total joint replacement is an effective surgical intervention for those patients with end stage of joint diseases. The major factor limiting the survival of joint implants is wear debris which is primarily generated from the bearing articular surface of t
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Theofilos Karachalios and Antonios Koutalos
Introduction Total joint replacement is an effective surgical intervention for those patients with end stage of joint diseases. The major factor limiting the survival of joint implants is wear debris which is primarily generated from the bearing articular surface of the artificial joint. Aseptic loosening is a disabling condition affecting patients 10–20 years after joint replacement surgery, leading to the failure of the artificial joint. It appears as a subtle progression of bone tissue destruction (osteolysis, periprosthetic bone loss). It is a major challenge for orthopedic surgeons due to the fact that signs and symptoms may not be clinically apparent until the late stages of destruction and failure [1]. There are several theories related to the appearance of the biological phenomenon of aseptic loosing (wear particle disease, high fluid pressure, micromotion, stress shielding, endotoxin, genetic susceptibility). Particle disease (cement, polyethylene, metal, ceramic) is currently
T. Karachalios, MD, DSc (*) Orthopaedic Department, Faculty of Medicine, School of Health Sciences, University of Thessalia, CERETETH, University General Hospital of Larissa, Larissa, Mezourlo Region, 41110 Larissa, Hellenic Republic, Greece e-mail: [email protected] A. Koutalos, MD Orthopaedic Department, University General Hospital of Larissa, Larissa, Greece
the dominant theory. In order to understand osteolysis and aseptic loosening, we have first to consider that following the implantation of an either cemented or cementless prosthesis, the boneimplant interface passes from an initial face of trauma and inflammation to an early (3–4 months) static stage of healing and mechanical stability (early stability). The interface remains in a biological and mechanical steady state condition for a varying period of time. Later it becomes unstable due to inadequate initial fixation (rarely seen today because of improved surgical techniques and implants), mechanical loss of fixation over time, and biological loss of fixation due to particle-induced osteolysis. This phenomenon is really a complex network of mechanical, cellular, and inflammatory responses [1]. It first appeared in the literature as “the cement disease” (Fig. 11.1), and as a result a boost in the development of cementless implants took place. Later, it became obvious that osteolysis and aseptic loosening are also seen with the use of cementless implants (Fig. 11.2), and thus the multifactorial nature of this biological process was uncovered.
Comments on Causative Theories Micromotion Micromotion, as measured by radiostereometric analysis (RSA) on the clinical setting, if it exceeds a certain threshold, does not lead to
T. Karachalios (ed.), Bone-Implant Interface in Orthopedic Surgery, DOI 10.1007/978-1-4471-5409-9_11, © Springer-Verlag London 2014
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T. Karachalios and A. Koutalos
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Fig. 11.1 Radiographs of a failed cemented early THA design. This radiological appearance was initially named “cement disease”
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