Implant failure, mechanisms

The most well characterized of the p38 kinases, the final MAPK phosphorelay pathway, is p38a, which is expressed by most cells and regulates the expression of many cytokines. Interleukin 1, IL-1, a product of inflammatory cells, has been implicated in modulating the response to mechanical loading in a number of tissues. IL-1 is a product of inflammatory cells thought to be involved in cartilage destruction in osteoarthritis and in bone resorption associated with total joint implant failure. 

Although the use of implants has been documented since the 1950s, little attention has been directed to how mechanical forces at the implant interface affect tissue metabolism and the fate of the implant. Some interest has been expressed concerning the use of balloons for tissue expansion, pressure-induced necrosis (cell death) of skin and fat cells, and bone resorption as a result of stress shielding by hip and knee implants. These effects may need closer examination in light of the recent findings that most tissues are normally stretched in tension and that any interruption of this tension adversely affects homeostasis via perturbations in normal mechanochemi-cal transduction and could lead to implant failure. 

This paper presents results from a study of assemblies composed of glass fibre reinforced epoxy composites. First, tests performed to produce mixed mode fracture envelopes are presented. Then results from tests on lap shear and L-stiffener specimens are given. These enabled failure mechanisms to be examined in more detail using an image analysis technique to quantify local strain fields. Finally the application of a fracture-mechanics-based analysis to predict the failure loads of top-hat stiffeners with and without implanted bond-line defects is described. Correlation between test results and predictions is reasonable, but special attention is needed to account for size effects and micro-structural variations induced by the assembly process. 

Implant loosening invariably leads to clinical failure for a variety of reasons, which includes peri-prosthetic fracture of the implant or the bone adjacent to the implant. Numerous failure mechanisms limit the long-term success of endo-prosthetic implants including aseptic osteolysis, aseptic loosening, infection and implant instability (Holt et al., 2007). The key molecules of the host response at the protein level are chemokines, cytokines, nitric oxide metabolites and metallo-proteinases (Gallo et al., 2014). Aseptic osteolysis and subsequent implant failure occur because of a chronic inflammatory response to implant-derived wear particles. Despite many advances related to materials selection, and operation tool and techniques, aseptic osteolysis continues to limit implant longevity. 

Collagen molecules undergo self-assembly by lateral associations into fibrils and fibers and are able, therefore, along with other biological functions, to ensure the mechanical support of the connective tissue. Collagen also plays an important role in many bioadhesion processes. Collagen molecules bound to implant materials enhance adhesion of epidermal cells to the surfaces of biomaterials and prevent implant failure. 

Each of the fixation mechanisms has an idiosyncratic behavior, and their load transfer characteristics as well as the failure mechanisms are different. Further complexity arises from prostheses which combine two or more of the fixation mechanisms in different regions of the implant. Multiple mechanisms of fixation are used in an effort to customize load transfer to requirements of different regions of bone in an effort to preserve bone mass. Loosening, unlocking, or de-bonding between implant and bone constitute some of the most important mechanisms of prosthetic failure. 

Endovascular prosfheses, assembled from tubular textile fabric and wire stent components, are deployed and expanded non-invasively from catheters for the rq>air of aneurysms in medium and large caliber arteries. Now that the implantation procedure is no longer experimental and these devices are becoming widely accepted and used for a growing cohort of patients, so the incidence of reported cases of late complications continues to grow. Observations from our own implant retrieval programme have led us to report that certain styles and models of endovascular prostheses are associated with particular failure mechanisms, such as endoleaks, migration, thrombosis, stent disruption, as well as fabric distortion and perforation. 

The failure of silicone rubber in breast implants has received plenty of coverage in the popular press and several technical articles have been reviewed by Lewis (71). It appears that there have been a number of failure mechanisms but they all generally relate to lack of thorough testing to cover the expected lifetime and all service conditions. For cases of failed tissue expanders he suggests the causes were a combination of poor design and poor manufacturing. 

Still a third failure mechanism was not seen in animal studies, but was discovered clinically. Explanted and returned leads with crushed, flattened, and fractured conductor coils began to show up in the mid 1980s (Fig. 7) [17]. When polyurethane leads were introduced for human use, a new implant technique was developed. Instead of inserting the leads through a cephalic or jugular vein cut down, they were... 

Cardiac transplantation is one option for patients with severe heart failure. Candidates for cardiac transplantation generally present with New York Heart Association (NYHA) class III or IV symptoms and have an ejection fraction of less than 25%.1,3 The general indications for cardiac transplantation include rapidly declining cardiac function and a projected 1-year mortality rate of greater than 75%. Mechanical support with an implantable left ventricular assist device may be appropriate while patients await the availability of a viable organ.1,3 Some additional reasons for heart transplant include ... 

Leakage. By far the majority of implanted electronic devices fail due to mechanisms of the second type (i.e. leakage). In a poorly encapsulated implant, this failure mode can cause rapid deterioration in a matter of days, hours, or even minutes. As the size of the implant designs are reduced, the risk of this type of failure is greatly Increased because due to the small dimensions involved, the time for fluid entry into the package becomes very short. 

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