2.6. Non-invasive diagnosis of prosthesis infections

Many complications of joint prosthesis surgery can be diagnosed easily. However, differentiating infection from aseptic loosening is difficult, because these conditions are very similar clinically and histopathologically. Clinical signs, symptoms, laboratory tests and radiography are insensitive, non-specific or both. In the postoperative period, signs and symptoms that are associated with infection may be masked by normal postoperative changes. Anatomic imaging modalities provide high-quality details and are widely available. However, x-ray cannot exclusively differentiate infection from loosening, and cross-sectional imaging modalities, e.g. computer tomography and magnetic resonance imaging, are complicated by artefacts produced by metallic prostheses. Radionuclide imaging is not significantly affected by metallic objects and is therefore useful in the diagnosis of complicated prostheses. Another advantage is that, since scintigraphic images are based on functional tissue changes, infectious and inflammatory foci can be visualised in their early phases, when anatomical changes are not yet apparent. Over the past 30 years, many approaches have been developed to visualise infection and inflammation using radionuclides. Understanding the action of radionuclide tracers requires, however, understanding of the pathophysiology of inflammation and infection. (Itasaka et al. 2001, Palestro 1995, Rennen et al. 2001, Rosas et al. 1998)

Inflammation can be described as a reaction of the body to any kind of injury. Injuries range from trauma to ischaemia, neoplasm or invasion by microorganisms. There can be infection without overt inflammation, as in the case of a severely neutropaenic patient. In such cases, it is clear that, for the purposes of imaging, one would need an agent that directly interacts with the microorganims. Conversely, there is often inflammation without infection when tissue injury is not due to microorganisms but is caused by other stimuli, such as trauma, ischaemia, neoplasm or foreign particles. (Rennen et al. 2001)

The response to infection or inflammation is characterised by locally increased blood supply, increased vascular permeability, enhanced transudation of plasma proteins and enhanced influx of leukocytes. Defence mechanisms consisting of cells and plasma proteins are activated in response to tissue damage. Many mediators, both vasoactive and chemotactic, are involved in the process. These mediators are generated at the focus of inflammation or infection and amplify the local response by recruiting cells and plasma components from blood. Vasodilatation and increased endothelial permeability facilitate extravasation of proteins and cells. Expression of adhesion molecules on endothelial cells and leukocytes is also stimulated, which causes leukocytes to actively migrate from the circulation into the inflamed tissue. First, leukocytes adhere to the vascular endothelium due to locally enhanced expression of adhesion molecules (rolling, arrest and adhesion). Then they pass through the endothelium and the basal membrane (diapedesis) and migrate into the inflammatory focus (chemotaxis). In acute inflammation or infection, the infiltrating cells are predominantly polymorphonuclear cells. In chronic inflammation or infection, the cellular response is different from that in acute situation, and the infiltrating cells are predominantly mononuclear cells: lymphocytes, monocytes and macrophages. (Etzioni et al. 1999, Gahmberg et al. 1992, Gahmberg 1997, Gahmberg et al. 1997, Gahmberg et al. 1998, Rennen et al. 2001)