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Osteoarthritis (OA) is a leading cause of disability in the US and poses considerable economic burden to society. Further, the pain, psychosocial implications, and decreased quality of life for individual patients are great.
Clinically, OA is divided into two types: primary (cases with no known cause; a.k.a. “wear and tear degenerative joint disease”) and secondary. A large proportion of secondary OA is due to a prior traumatic joint injury that may have occurred up to 10 years previously. These cases are known as post-traumatic OA. Current treatments options for OA are limited. There is no medication that can be given to alter the course of the disease, and the medications available are limited to symptomatic relief (i.e. pain relief).
When the situation has become unacceptable to the patient, total knee arthroplasty (total joint replacement) may be an option. While this relieves pain, joint replacements have a limited life span and there are risks associated with the surgery. Thus, it is very desirable to have some intervention that can alter the disease course or decrease its prevalence.
The impact group, as we call ourselves, is primarily interested in studying the basic science of cartilage’s response to mechanical trauma. Early work has focused on comprehensively characterizing the effects of different levels of impact loading on articular cartilage. Our hypotheses were that a high level of impact would cause immediate changes to the tissue that we could observe through cell death, changes in levels of gene expression, alterations to the biochemistry of the tissue’s extra-cellular matrix (ECM), and detrimental changes to its mechanical properties. We expected these changes to worsen with time. In contrast, a low level of impact would not show immediate changes, but over time would experience a degenerative cascade that would eventually cause the cartilage to be functionally equivalent to the high impact group. Several studies we have performed show these hypotheses to be, in the most part, true.
We have identified several changes occurring at the tissue and cellular levels that we believe are responsible for cartilage degeneration. We are currently investigating several bioactive agents that have the potential to prevent or reverse the degradative changes we observe post-impact. The hope is that one day these agents will be used in animal models and clinical trials, either as intra-articular injections or oral medications, to treat post-traumatic OA.
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