Do you integrate some of the following principles/drugs in your clinical regimen as NSAID, chondroprotection (e.g. antioxidants, inhibition of apoptosis, protection of cell membrane integrity), inhibition of pro-inflammatory mediators (e.g. anti-TNFα, anti-IL-1/IL-1RA, NO-inhibitors), anabolic cytokines (e.g. BMP-7, bFGF, IGF-1, PRP), matrix protection/remodeling (e.g. MMP-inhibitors)?
As there is an inflammatory component in trauma, it is useful to use NSAIDs as anti-inflammatory analgesics acutely post-trauma for symptomatic relief. Following the acute injury, it remains debatable whether chondroprotective agents are of any use; clinically, only glucosamine/chondroitin/diacerein are available and can be tried, but the evidence is conflicting. The other suggestions are not really clinically used, more research options. For chronic post-traumatic OA, there should not be an inflammatory component, thus even NSAIDs should be used sparingly.
Thanks, very good summary. Have you thought about application of intraarticular HA (hyaluronic acid) in the course of early fracture treatment?
I use IA HA only in (selected) chronic OA cases. Have you any data on its efficacy in early trauma? I would be interested in any information you have. Thanks.
Among the NSAIDs, I still prefer traditional diclofenac, ibuprofen and indomethacin when the patients report with acute exacerbation.
If there is effusion in the knee, I perform aspiration and inject cortisone.
I use diacerin in all patients.
I have used in plenty intrarticular hyaluronic acid in the past ( of different molecular weights). It is too expensive and I am not convinced with its benefit.
For everyone's info, this is the latest 2014 guidelines from the OA Research Society International (OARSI) on non-surgical management of knee OA.
Dear Swan, using IA-HA for OA prevention was just an idea, but I have no data. Actually, there is a non-inferiority study showing equivalent effect of IA-HA and NSAID:
http://www.ncbi.nlm.nih.gov/pubmed/24443804
But in the OARSI guidelines IA-HA does not seem to play a role.
There are some papers that suggest that long-acting HA e.g. Synvisc may have cartilage protective effects:
http://www.ncbi.nlm.nih.gov/pubmed/22809835
http://www.ncbi.nlm.nih.gov/pubmed/21861935
Since they are expensive, I have stopped using even synvisc due to my own personal observations as well as lack of high level evidence in the literature.
Dr. Swan, I am sorry but I have to disagree with you as far as inflammatory changes in chronic posttraumatic OA are concerned. There are many such cases in which chronic non-specific inflammatory synovitis is observed. So I do not see any reason for rejecting the use of NSAID in similar cases. Actually, in late stages the etiology of OA is no longer so important (except for RA, Bechterew) and the pathoanatomic changes are similar - cartilage degeneration, joint deformity, ligament laxity accompanied by chronic non-specific inflammatory synovitis (not always !).
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