Pain measurements with cuff algometry have developed into a reliable method to evaluate pressure pain, which appears to be a good measure for pain sensitivity. With the new model of Dolocuff, intra- and inter-rater variation is being tested, and values for pain threshold and temporal summation response are being determined in a healthy pain-free population.
The Biochemistry and Physiology Laboratory
Acoustic myography is a non-invasive method to assess muscle activity during movement. It has the advantage over other present methods that measurements can take place in a wireless system, where it is possible to carry the small measuring devices around during sports activity and when carrying out daily activities. The setup has been evaluated in healthy subjects, and the plans are now to assess muscle activities in rheumatic patients and in chronic pain patients during daily activities.
One of the characteristics of OA is loss of articular cartilage. The process of cartilage catabolism may happen at different rate, and the question is if different interventions may slow down or stop the process. In a group of overweight OA patients exposed to a substantial weight loss, we are following collagen-II (the major collagen in cartilage) markers, as well as extra-cellular matrix markers from cartilage, to see if the intervention will be reflected in a decrease in cartilage breakdown.
The overall aim is to assess changes in biochemical markers with changes in disease progression, and with treatment, in rheumatoid arthritis, osteoarthritis and psoriatic arthritis.The project consists of several sub-projects: I Pro-inflammatory markers in paired samples from blood and synovial fluid from affected joint – How do these correlate to clinical assessments. II Pro-inflammatory activity of ex-vivo explants of synovial membrane from site-specific biopsies from inflamed joint – How do these correlate to clinical assessments. III Study comparing changes in ultrasound (US) Doppler with changes in plasma Vascular Endothelial Growth Factor (VEGF) and IL-6 in patients with rheumatoid arthritis treated with anti-TNF-α.