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Taken together, approximately 50% of the patients develop a PJI with a higher risk for failure in total knee arthroplasty with a mean follow-up of approximately 4.2 years [15]. The first revision surgery is typically performed in the first year after the primary implantation procedure [14]. In addition, other risk factors are well known, namely previous surgery, obesity, revision surgery, prior infections, and immunosuppression [29]. The diagnosis of PJI after total joint arthroplasty is challenging. At present, the preoperative diagnosis is mainly based on conventional clinical criteria such as elevated erythrocyte sedimentation rate, white blood cell count, and elevated C-reactive protein. The postoperative diagnosis is mainly based on the clinical signs and symptoms, especially fever. The most sensitive clinical test for PJI is the presence of a suppurative acute inflammation in the joint space, the so-called purulence, together with elevated white blood cell count and elevated C-reactive protein [31]. Radiographic analysis may reveal soft-tissue swelling, cortical bone destruction, irregularity, or osteolysis. The management of a PJI is largely based on antibiotic treatment, with a goal of eradication of the causative microorganisms, and consists of debridement, retention of the prosthesis, antibiotic therapy for a minimum of 6 to 8 weeks, and further steps as necessary according to the progress of the infection. A two-stage revision arthroplasty has been recommended by most authors for the treatment of PJI, when a substantial amount of bone destruction is present. The role of revision arthroplasty in the treatment of PJI is controversial.
The bone cement interface is the most important factor in the failure of the prosthesis [9]. The most common failure point for total hip and knee arthroplasty is aseptic loosening of the metal-polymethylmethacrylate (PMMA) bearing and the subsequent migration of the femoral head. The optimal bone-cement interface is a bone-cement interface with a firm, nonporous, stable, and continuous structure and the absence of any lysis. There is excellent evidence that the cement mantle needs to be thick enough to compensate for cement-bone debonding and that the cement-bone interface needs to be firm and continuous in order to allow physiological changes in bone density, muscle activity, and mechanical loading [23].
2.- Osawa D. Prostodoncia total. 13 ed. Editorial Mxico Publicaciones, UNAM; Sharry JS. Prostodoncia dental completa. 1 ed. Editorial Trillas; Osawa D. Prostodoncia total. 13 ed. Editorial Mxico Publicaciones, UNAM;
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