Current Concepts In Treating Acute Charcot's Arthropathy
- Volume 19 - Issue 9 - September 2006
- 10226 reads
- 0 comments
Although offloading may prevent further trauma, which reduces inflammation over time, a more urgent antiinflammatory is needed. New and exciting research in Charcot treatments are focusing on interrupting the inflammatory cycle. After trauma initiates the Charcot process, there is an ensuing inflammatory cascade that involves tumor necrosis factor alpha (TNF-a) and interleukin-1 (IL-1).15 These pro-inflammatory cytokines induce RANK-L to mature more osteoclasts, resulting in bone loss.9
Several inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, Crohn’s disease and ulcerative colitis, respond to tumor necrosis factor-alpha (TNF-a) inhibitors. Researchers have shown that people with diabetes have persistent synthesis of TNF-a during cutaneous inflammation (blister formation) and they theorize that TNF-a inhibitors may play a role in treating diabetic foot conditions.16
However, it is yet unknown whether TNF-a plays a role in the pathogenesis of Charcot’s arthropathy or if its inhibition will prevent joint breakdown. Early stages of a randomized controlled trial utilizing one of these agents is in the planning stages at the Center for Lower Extremity Ambulatory Research (CLEAR) at Rosalind Franklin University of Medicine and Science in Chicago.
Some authors have shown that cryotherapy reduces inflammation after acute injury and others have proposed that cooling the diabetic foot may prevent foot wounds.17,18 However, further study is needed before cryotherapy can become an accepted tool in helping to remit a Charcot foot.
How To Address Osteopenia In Those With Acute Charcot
Medical and physical methods to increase bone mineral density are currently accepted methods of treatment for acute Charcot’s arthropathy. The bisphosphonates pamidronate (IV) and alendronate (PO) have both undergone randomized trials to determine their effectiveness.19,20 Their mechanism of action is induced apoptosis of osteoclasts.21 Studies have shown that both bisphosphonates reduce foot temperature and decrease the levels of bone turnover markers. The IV therapy has a much more rapid onset of action (within two weeks) whereas the oral therapy can require up to six months before one sees the benefit.
A recent study investigating the use of intranasal calcitonin in acute Charcot foot found a reduction in bone turnover markers in the first three months of follow-up.22 These authors concluded that the use of calcitonin may be superior to that of bisphosphonates since calcitonin acts directly on the RANK-L signaling pathway to reduce bone turnover whereas bisphosphonates indiscriminately induce death of osteoclasts and may have some effect on osteoblasts.22
One can achieve physical stimulation of bone growth through the use of bone stimulators. Various authors have utilized ultrasonic, combined and pulsed electromagnetic field, and implanted DC in patients with Charcot foot.23-25 Physicians would use the implantable stimulators at the time of surgical reconstruction whereas one can apply the external stimulators as an adjunct in treating acute Charcot foot.
Future directions for treating Charcot’s arthropathy are clear. There is still a need for more treatments that are designed to interrupt the natural history of the disease process. We must gain a more complete understanding of the pathophysiology of Charcot’s arthropathy at the biochemical level. As the governments of the world are recognizing diabetic foot disorders as a large financial burden, the funding of research will likely increase. Subsequently, more high quality trials will be initiated and physicians will be able to offer more effective treatments to those who suffer from Charcot foot.