Inflammatory Response Following Intraarticular Fracture
Inflammatory Response Following Intraarticular Fracture
The purpose of the study is to investigate a relationship between the inflammatory response
 following intraarticular fracture and post-traumatic osteoarthritis. The investigators plan
 to evaluate the inflammatory cytokine profile in knee joint synovial fluid and blood serum in
 patients who sustain an intraarticular tibial plateau fracture and ankle joint synovial fluid
 and blood serum in patients who sustain an intraarticular tibial plafond fracture. This
 information will be combined with radiographs and patient outcome measures to determine a
 correlation between intraarticular inflammatory response and post-traumatic osteoarthritis.
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. 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.

 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. 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. 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.
 Other matrix molecules including matrix metalloproteinase (MMP)-3 and cartilage oligomeric
 matrix protein (COMP) can be persistently elevated in synovial fluid after ACL injury.

 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. 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.
Inclusion Criteria:

 -  18 years of age or older

 -  Radiographic evidence of tibial plateau fracture

 Exclusion Criteria:

 -  Less than 18 years of age

 -  Greater than 60 years of age

 -  Any history of pre-existing knee osteoarthritis based on previous diagnosis or
 suggestive history

 -  Any history of autoimmune disease

 -  Any history of contralateral intra-articular knee injury