Serum and Synovium Protease Inhibitor Levels in Primary and Secondary Osteoarthritic Joints
Public ClinicalTrials.gov record NCT01613833. Field values are reproduced from the official study page; the official ClinicalTrials.gov record remains the source of truth for eligibility, enrollment, and contact information.
Data is sourced from official ClinicalTrials.gov public API records. Always review the official ClinicalTrials.gov record for the latest information.
Official title
Evaluation of Serum and Synovium Protease Inhibitor Levels in Primary and Secondary Osteoarthritic Joints, and Comparison for Patients Undergoing Joint Replacement
Brief summary
Reproduced verbatim from the official ClinicalTrials.gov record. Not medical advice.
Osteoarthritis (OA) is the irreversible degeneration of articular cartilage and underlying bone. It poses a major healthcare problem as it is the leading cause of joint disease and disability in the United States. It was traditionally thought that OA was a consequence of aging and joint trauma. However, it is now thought that OA is a result of the interplay of multiple genetic, biomechanical, and biochemical factors that disrupt the normal homeostasis of cartilage, bone, and synovium. OA is classified into two groups, primary and secondary. Primary OA is classically polyarticular and peripheral while secondary OA can commonly be attributed to a specific cause, limited to a singular joint, and a result of trauma. It is known as post-traumatic OA (PTOA). Other causes of secondary OA include congenital disorders, calcium pyrophosphate dehydrate deposition disease, and other diseases. Regardless of classification, genetic variation in the normal metabolism of cartilage and bone is thought to play a role in the progression of OA. Furthermore, the polyarticular presentation of primary idiopathic osteoarthritis suggests that it may have a stronger genetic component as compared to secondary OA, indicating a deviation from normal cartilage and bone homeostasis. Matrix metalloproteinases (MMP) and their inhibitors take part in the metabolism of cartilage and bone. MMPs are enzymes that catalyze the degradation of elements within joint spaces while their inhibitors cease this activity. Alpha-2-Macroglobulin (A2M) is a naturally-occurring plasma glycoprotein that functions throughout multiple tissues and extracellular spaces as a protease inhibitor but does not normally reach high levels within the intra-articular joint space. A2M is believed to modulate the systemic inflammatory response by its ability to bait, trap, and clear various MMPs and cytokines. Concentrated A2M directly addresses the roles of cytokines and catabolic enzymes known to participate in the development of osteoarthritis. Cytonics has shown that A2M can inhibit cartilage degradation in vitro. As the role of MMPs and protease inhibitors have emerged as key components of OA, the investigation of regulators of MMP has become of interest to elucidate the pathogenesis and possible novel treatments of OA. This study aims to measure and correlate the levels of alpha-2-Macroglobulin (A2M) in plasma and knee joint OA between primary post-traumatic (PTOA) and secondary osteoarthritis groups.
Study identification
- NCT ID
- NCT01613833
- Recruitment status
- Suspended
- Study type
- Observational
- Phase
- Not listed
- Enrollment
- 40 participants
Conditions and interventions
Conditions
Eligibility (public fields only)
- Age range
- 19 Years to 65 Years
- Sex
- All
- Healthy volunteers
- Healthy volunteers not accepted
This page does not interpret eligibility. Detailed inclusion and exclusion criteria are on the official ClinicalTrials.gov record.
Study timeline
- Start date
- Feb 29, 2012
- Primary completion
- Jul 31, 2018
- Completion
- Jul 31, 2018
- Last update posted
- Oct 8, 2017
2012 – 2018
United States locations
- U.S. sites
- 1
- U.S. states
- 1
- U.S. cities
- 1
| Facility | City | State | ZIP | Site status |
|---|---|---|---|---|
| Stanford University Hospital | Palo Alto | California | 94304 | — |
Site contact phone numbers, emails, and investigator names are intentionally not displayed here. Open the official ClinicalTrials.gov record for site contact information.
About this trial record page
- What this page shows
- Public field values for ClinicalTrials.gov record NCT01613833, including study identification, conditions, interventions, eligibility (age, sex, healthy volunteer), timeline, and U.S. site list.
- What this page does not do
- No medical advice, eligibility judgments, treatment recommendations, study quality scoring, or AI-generated medical summaries. No site contact phone numbers, emails, or investigator names.
- Where the data comes from
- Sourced from the official ClinicalTrials.gov public API. The official record is the source of truth.
- Last refresh
- Last update posted Oct 8, 2017 · Synced Sep 6, 2026
Related: full search, browse by condition, browse by drug or therapy, browse by sponsor, browse by U.S. city.
Open the official record
The complete protocol, eligibility criteria, and contact information for NCT01613833 live on ClinicalTrials.gov.