By Jordana Bieze Foster, Editor
Recent efforts to reduce utilization of opioid pain medications for lower extremity joint injuries and surgical rehabilitation have mostly focused on reducing the risk of addiction. But there’s another important reason to be concerned about the use of opioids in these patients—and other popular pain medications as well.
A Stanford University study published in September found in vitro evidence that intraarticular use of the opioid meperidine (Demerol) is associated with chondrocyte death, which contributes to the development of osteoarthritis. And although nonsteroidal anti-inflammatory drugs (NSAIDs) are often proposed as opioid alternatives for pain relief, the same study found that the NSAID ketorolac was also associated with in vitro chondrotoxicity (see “Intraarticular NSAIDs and opioid meds may contribute to cartilage cell death,” page 13).
Other studies have reported similar findings with other popular pain medications. The Stanford group found in 2012 that lidocaine injection was associated with cartilage cell death, and a 2013 study from the University of Connecticut in Farmington reported chondrotoxic effects of methylprednisone.
Granted, these are in vitro studies, and cartilage cells likely behave at least somewhat differently in vivo than in a petri dish. The oral medications typically given to patients after an injury or surgery also likely behave somewhat differently than intraarticular injections of the same medication. But the implications are still pretty scary.
Preliminary evidence suggests cartilage deterioration begins almost immediately after a joint injury (see “Early warnings: Data support aggressive intervention,” August, page 11). So it’s not a stretch to think that plying patients with potentially chondrotoxic medications after a joint injury will only exacerbate that degenerative process. That leaves us with the sobering possibility that efforts to improve patients’ quality of life by decreasing their pain in the short term are inadvertently setting those patients up for chronic pain in the same joint later in life.
On the positive side, some pain medications studied by the Stanford group and others have not been associated with chondrotoxicity; these include bupivacaine, ropivacaine, morphine, and fentanyl. It’s also possible that platelet-rich plasma (PRP) injections can help offset some chondrotoxic effects: The UConn study found that cartilage cell viability associated with ketorolac was significantly greater than placebo when the NSAID was supplemented with PRP. However, a 2013 review of basic science research on PRP and cartilage noted that, although such preliminary findings are encouraging, not all in vivo studies have found a positive effect of PRP on cartilage repair after surgery.
Less-invasive therapies also show promise as nondrug analgesic alternatives; for example, a systematic review and meta-analysis in the August issue of JAMA found moderate-certainty evidence to support acupuncture and electrotherapy after total knee arthroplasty. Bracing, foot orthoses, and physical therapy have all been associated with pain relief in various populations and would seem to be worthy of future study in this context, as well.
The fight against opioid addiction needs all the help it can get. If lower extremity researchers and clinicians can assist in this effort while reducing the risk of long-term cartilage damage at the same time, that definitely seems like a win-win proposition.
