Influence of Oxidative Dysbalance on Secondary Osteoarthritis
Recruitment status was Recruiting
The important role of mechanical joint stress for the insert and progress of osteoarthritis (OA) is supported by recent studies. The degeneration of joint cartilage is caused either by unphysiological load of a healthy joint or physiological load of a damaged joint. The exact mechanisms leading from increased weight bearing and overuse to cartilage degeneration are mostly unknown.
The hypothesis of the study is that parameters of oxidative stress in the joint synovial space reflect damages possibly leading to OA. These parameters correlate with parameters of oxidative stress in the peripheral blood. Aim of the study is the identification of such non- invasive obtainable biomarkers which represent the degenerative and regenerative changes in joint.
|Study Design:||Time Perspective: Prospective|
|Official Title:||Biomechanical Factors of Secondary Osteoarthritis: Oxidative and Nitrosative Stress as Predictive Factors of Joint Destruction|
Arthroscopical obtained wash- out preparations of synovial space Synovial biopsies Blood serum samples
|Study Start Date:||October 2010|
|Estimated Study Completion Date:||November 2013|
|Estimated Primary Completion Date:||November 2012 (Final data collection date for primary outcome measure)|
Acute knee pain
Patients with a history of knee pain < 6 months. The radiologic and arthroscopic OA stadium is less or equal II°. n=20.
Chronic knee pain
Clinical manifestation of knee joint OA, radiological and arthroscopic III° or more. n=20
Patients coming for post- primary repair of the cruciate ligament, having no inflammation and no sign of OA. n=10
Patients with clinically manifest OA typically consult the physician at time of irreversible cartilage destruction. This is due to the long time clinically silent progress of the disease. A biomarker screening profile for joint damage is a valuable tool for the detection of over use and joint damaging conditions especially in competitive sports. This would provide a method for OA risk assessment for the patient before clinical symptoms occur. For this the first step is the identification of biological substances reflecting pathologic changes in the joint.
Since preterm chondrocyte senescence, apoptosis and ageing related changes are key factors in OA pathophysiology and each of these factors is closely related to oxidative dysbalance the measurement of these factors and correlation with the amount of joint damage is promising.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01228487
|Contact: Christoph Ziskoven, MDfirstname.lastname@example.org|
|Orthopedic Department, Heinrich-Heine University Medical School||Recruiting|
|Düsseldorf, NRW, Germany, D40225|
|Contact: Christoph Ziskoven, MD 004917622900348 email@example.com|