|Principal Investigator: Justin Haller|
|Keywords: Post traumatic osteoarthritis , joint injuries , knee osetoarthritis , ankle osetoarthritis||Department: Orthopedic Surgery Operations|
|IRB Number: 00051134|
|Specialty: Orthopaedic Surgery|
|Sub Specialties: Orthopaedic Trauma|
|Recruitment Status: Enrolling by invitation|
Main Study Purpose:
- This study wants to determine the relationship between the inflammatory response after a joint fracture (knee, ankle) and osteoarthritis (degeneration of joint cartilage and the underlying bone) that occurs after a traumatic injury, known as post-traumatic osteoarthritis (PTOA).
Main Study Objectives:
- Determine a correlation between intraarticular inflammatory response and PTOA by:
- Evaluating patient:
- inflammatory cytokine profile and
- cartilage injury
- Knee joint synovial fluid from patients with an intraarticular tibial plateau fracture.
- Ankle joint synovial fluid from patients with an intraarticular tibial plafond fracture
- Ankle joint synovial fluid from patients with an ankle fracture
- Evaluating patient:
And in combination with patient:
- Radiographs and
- Outcome measure scores
DoD Sub-Study Purpose/Objectives:
- Evaluate CPC gene expression and migratory capacity in normal human cartilage exposed to inflammatory cytokines.
- Examine the relationship between post-injury inflammation and human synoviocytes and chondrogenic progenitor cells.
- Compare CPC gene expression in acute pilon fracture versus CPC expression in healthy cartilage
(None of the procedures for the sub-study will require any additional specimen collection or procedure to the patient. All patient samples needed for sub-study objectives will come from already collected main study specimens.)
Post-traumatic osteoarthritis (PTOA) is a common cause of disability following a traumatic event involving a joint. It is estimated that PTOA may affect up to 12% of the population with symptomatic osteoarthritis, and it is associated with significant cost to the healthcare system (1). Given that the majority of trauma patients are younger, the impact of the condition can be particularly devastating for those in the prime of their working careers (2).PTOA can develop following a variety of joint injuries, but it most predictably occurs with articular fracture. The initial traumatic injury involves a complex process of articular impaction or displacement and soft tissue disruption that leads to articular exposure to blood and marrow, a local inflammatory response, abnormal joint loading, and subsequent chondrocyte necrosis and apoptosis (3). However, the mechanism(s) that lead to progression from the initial injury to end-stage PTOA are largely unknown. Inflammation can have deleterious effects on a joint. Though inflammatory cytokines have been shown to stimulate bone repair through osteoclastogenesis and recruitment of osteoblastic cells, multiple studies have demonstrated that these cytokines play a role in cartilage degradation (4-9). Increased IL-1 and TNF-a expression has been found in the cartilage of patients with osteoarthritis, and these cytokines are transiently increased after traumatic injury (10,11). Other matrix molecules including matrix metalloproteinase (MMP)-3 and cartilage oligomeric matrix protein (COMP) can be persistently elevated in synovial fluid after ACL injury (12,13)The effect of the initial inflammatory response after intraarticular fracture on the development of PTOA remains unknown. Several authors have found elevated levels of cytokines in joints affected by trauma (14-16). However, these studies evaluated patients following an anterior cruciate ligament (ACL) injury. An intraarticular fracture likely subjects the joint to more of an inflammatory response and may place the joint at greater risk for developing osteoarthritis. There are currently no studies that link elevated levels of the inflammatory cytokines and chemokines in the setting of intraarticular trauma with PTOA. Investigating the cytokine profile in a joint immediately following intraarticular injury could lead to early targeted drug therapy with cytokine inhibitors to modify the progression of PTOA.
1.) Patients between 18 and 60 years of age
2.) Patients presenting with a tibial plateau, tibial plafond, or ankle fracture shown by radiographs.
3.) Patients who are English speaking
1.) Patients previously diagnosed with knee or ankle osteoarthritis
2.) Patients with a history of autoimmune disease
3.) Patients considered a vulnerable adult population i.e. prisoner, ward of the state, decision impaired, or pregnant