Zeitschrift für Rheumatologie
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To summarize the strategy of patient recruitment, applied methods and published results within the Ulm Osteoarthritis Study, a multicenter cross-sectional survey of patients with advanced hip and knee osteoarthritis. ⋯ Our innovative study design allows the non-invasive investigation of patient subgroups with established disease and a testing of relevant hypotheses in an appropriate setting. The data add to the evidence regarding the independent role of different systemic risk factors for OA. In an ongoing study the natural course of the disease of the contralateral, unoperated joint is currently being investigated in all recruited patients.
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The physiology of nociception involves a complex interaction of peripheral and central nervous system (CNS) structures, extending from the skin, the viscera and the musculoskeletal tissues to the cerebral cortex. The pathophysiology of chronic pain shows alterations of normal physiological pathways, giving rise to hyperalgesia or allodynia. After integration in the spinal cord, nociceptive information is transferred to thalamic structures before it reaches the somatosensory cortex. ⋯ Among the three subtypes of opioid receptors, mu- and delta-receptors either inhibit or potentiate NMDA receptor-mediated events, while kappa opioids antagonize NMDA receptor-mediated activity. Recently, CRH has been found to act at all levels of the neuraxis to produce analgesia. Modulation of nociception occurs at all levels of the neuraxis, thus, eliciting the multidimensional experience of pain involving sensory-discriminative, affective-motivational, cognitive and locomotor components.
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Traditionally, opioids were considered the prototype of centrally acting analgesics. In the past decade a substantial literature has emerged demonstrating that opioids can produce potent and clinically measurable analgesia by activation of opioid receptors on peripheral terminals of primary sensory neurons. ⋯ Major recent findings in peripheral opioid analgesia include the relative lack of tolerance under inflammatory conditions, tetrapeptides as novel peripherally restricted compounds, the potent antiinflammatory activity of mu- and kappa-agonists and the identification of selectins as important molecules governing the homing of opioid cells to injured tissue. In addition to the extensively documented efficacy of locally applied morphine in post-surgical pain, clinical studies have now moved into the field of chronic arthritic pain.
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Autoreactivity plays a major role in the pathogenesis of RA. The rheumatoid factor has been and still is for now more than 50 years the only autoreactivity that is clinically applied in the diagnosis of RA. This well reflects the current way of thinking that a single antigen or a single cause drives an individual into disease. ⋯ The massive influx of T cells into the arthritic joint is accompanied by the anergization of over 90% of T cells in this compartment--which further substantiates the concept of the RA attractor within the self-regulating immune system. Thereby, the RA-attracted immune system is not able to completely downregulate the inflammation and the local tissue damage/repair. Thus, the immune system is permanently stimulated and suddenly by chance shifts to a stable state different from the healthy system--reaching the wide fields of rheumatoid arthritis which in itself is self-sustaining as the healthy state before disease onset.