A Closer Look At Bone Stimulators For Charcot

Pages: 52 - 58
By Michael S. Downey, DPM, FACFAS

     Charcot osteoarthropathy remains a chronic, progressive and destructive process that often affects the bony architecture and joints of the foot and ankle, primarily in patients with diabetic peripheral neuropathy. Despite advances in the diagnosis and management of this condition, the deformity continues to be associated with a high incidence of recurrence, treatment failure and resultant morbidity. If left untreated, Charcot foot predictably leads to deformity, ulceration, infection and amputation.      The mainstays of treatment for the Charcot foot have traditionally been immobilization and offloading or non-weightbearing. More recently, clinicians have attempted to utilize other modalities, including pharmacologic management with bisphosphonate therapy (i.e. IV pamidronate), early operative stabilization and bone growth stimulation. However, reports on electrical and mechanical bone growth stimulation are limited. Accordingly, let us take a closer look at the current evidence of their efficacy as adjunctive modalities in managing the Charcot foot.      Bone remodeling and repair involves a cascade of cellular and tissue activities that can potentially be modulated by external mechanical and electrical forces. Yasuda, et. al., first described electrically induced osteogenesis in 1953.1 Since the early 1970s, clinicians have used bone growth stimulators to attempt to positively influence osteoblasts (i.e. bone-making cells) in a variety of ways. While surgeons have traditionally used bone growth stimulators to manage nonunions and problematic delayed unions, one should consider bone growth stimulators as adjuncts to other well-documented bone healing methods such as immobilization and non-weightbearing. Other potential indications are fresh fractures, avascular necrosis, high-risk surgeries more prone to delayed union and nonunion, and Charcot osteoarthropathy.2,3      There are a variety of electrical and mechanical bone growth stimulation modalities available. They include direct current (DC) stimulation, inductive coupling or pulsed electromagnetic fields (PEMF), capacitive coupling (CC), combined magnetic fields (CMF) and low-intensity ultrasound (LIUS). Only direct current stimulation is currently available for implantation into the lower extremity while the other forms of stimulation are available for use externally.      All of the forms of bone growth stimulation work via slightly different pathways but they all reportedly upregulate a number of osteoinductive growth factors, including bone morphogenetic proteins (BMPs), which are normal physiologic regulators of various stages of bone healing. Normal bone homeostasis and remodeling has an exquisite balance between osteoblastic (bone-formation cell function) and osteoclastic (bone-resorption cell function). Bone growth stimulators characteristically improve or accelerate osteoblastic function. Accordingly, tipping the balance toward improved osteoblastic function could be potentially helpful in the management of the Charcot foot.

Rethinking The Pathogenesis Of The Charcot Foot

     The question then as to whether bone growth stimulation can be beneficial in the Charcot foot depends largely upon the actual mechanism of Charcot bone destruction. Recent literature strongly suggests that the process of acute Charcot osteoarthropathy primarily involves an increase in osteoclastic bone resorption activity with minimal to no corresponding increase in osteoblastic activity.4,5      This seems logical given the prior theories of the pathogenesis of the Charcot foot. Two early theories arose to explain the development of the Charcot foot. The “French Theory” espoused that the nutritive trophic regulation of the bones and joints mediated by the spinal cord deprived the bones of nutrition in neuropathic patients, resulting in bone resorption. The “German Theory” advocated that mechanical or repetitive trauma caused the Charcot foot deformity and the associated neuropathy simply allowed it to go unnoticed.      Today, it is clear that neither of these theories entirely explains the development of the Charcot foot. Regardless of the actual cause, it seems plausible today that increased blood flow, with increased osteoclastic activity at the Charcot joint, is responsible for the bone and joint destruction one sees with this condition. Given this point, it follows that decreasing osteoclastic cell activity is likely to help during the acute phase of Charcot foot. The question then becomes whether this presumption is true and whether modalities that increase osteoblastic activity, while having minimal or no effect on osteoclastic activity, can be of any clinical benefit.

A Pertinent Overview Of Charcot Staging

     Eichenholtz divided the Charcot disease process into three clinically and radiographically distinct stages: development, coalescence and reconstruction.6 Stage 1 (the stage of development) represents the acute destructive period, which is typically characterized by profound edema and joint effusions, calor and varying intensities of erythema (often mimicking infection). Radiographs can be negative but more commonly demonstrate soft tissue edema, joint effusions, joint subluxation and formation of bone and cartilage debris (i.e. detritus), and bone fracture or fragmentation. This stage is termed the “acute stage” of Charcot osteoarthropathy.      When it comes to stage 2 (the stage of coalescence), one would note this clinically via the reduced edema, calor and erythema, and radiographically by the absorption of bone and cartilage debris, and healing of fractures. Stage 2 is often called the “subacute stage” of Charcot osteoarthropathy.      Clinicians often refer to stage 3 (the stage of reconstruction) as the “chronic stage” of Charcot osteoarthropathy. Clinically and radiographically, this stage is associated with further repair of the soft tissues and bone with bone remodeling occurring in an attempt to restore joint and osseous stability. It is the early or acute stages of the Charcot foot that are most likely to be amenable to the influences of osteoblastic stimulation or osteoclastic inhibition.

What The Evidence Reveals About Bone Growth Stimulators

     Evidence-based medicine (EBM) has been defined as “the conscientious, explicit and judicious use of current best evidence in making decisions about the care of individual patients. The practice of evidence-based medicine means integrating individual clinical expertise with the best available external clinical evidence from systematic research.”7 The evidence on the use of bone growth stimulators for the management of the Charcot foot is limited but some evidence does exist. No systematic reviews are available on this topic. Most of the papers have looked at the use of external bone growth stimulators as an adjunctive form of therapy in the acute Charcot foot.      In 1987, Bier and Estersohn provided possibly the earliest report on the use of bone growth stimulation for the management of the Charcot foot.8 They reported on three patients, who were each treated with cast and/or Unna boot immobilization, non-weightbearing and pulsed electromagnetic field bone growth stimulation. Using this combination of therapies, the authors reported clinical healing within three to four months.      In a smaller series in 1998, Strauss and Gonya provided two case reports involving the use of low-intensity ultrasound stimulation after Charcot reconstructive surgery.9 In both cases, the surgery involved ankle and subtalar joint arthrodesis with insertion of an intramedullary nail across both joints. Postoperatively, surgeons kept both patients non-weightbearing. Shortly after the surgery, surgeons initiated the LIUS mechanical bone growth stimulation. In one case, they noted a healed arthrodesis after 162 days. In the other case, they noted clinical and radiographic healing after 120 days. The authors concluded, “Adjunct low-intensity ultrasound should be considered in this population based upon its success in other parts of the skeleton and the early success presented here.”      In one of the better reports on this topic, Hanft, et. al., investigated the role of bone growth stimulation as an adjunct in managing the Charcot foot.10 The study included 31 patients. The first 21 subjects were randomized into the study or control groups. All 21 patients had diabetic neuropathy involving their lower extremities, accompanied by clinical and radiographic findings of stage 1 Charcot osteoarthropathy involving the foot and/or ankle.      The investigators immobilized all of the patients with a total contact cast or a fixed ankle walker with a contact molded multi-density thermoplastic insole. All of the patients also received compression stockings to help control the edema present. The researchers also uniformly instructed the patients to decrease their level of ambulation and weightbearing at 50 percent of what they were doing prior to treatment.      The study group received one additional modality, an Orthologic® combined magnetic field bone growth stimulator, which was not given to the control patients. This device was used for 30 minutes daily. After researchers studied and href="/files/photos/ pt1206charcot4.jpg" rel="lightbox">statistically evaluated the initial 21 patients, they enrolled 10 additional patients as study candidates, all of whom received bone growth stimulation.      Researchers examined several areas between the treatment group (21 cases) and the control group (10 cases) including:      • the duration of Charcot osteoarthropathy prior to the start of treatment;      • the patient age;      • the rate of consolidation of insulin-dependent patients with diabetes versus non-insulin dependent patients with diabetes in each group;      • obesity as a factor in consolidation time;      • total contact cast versus fixed walker as a factor in the consolidation time; and      • time to consolidation in patients receiving bone growth stimulation versus those not receiving bone growth stimulation.      The results of the study revealed that the mean time to consolidation for the treatment group was 11.0 weeks versus 23.8 weeks in the control group. This 12.8-week difference between the groups was statistically significant. With the exception of the application of the bone growth stimulation, all the other variables studied had no statistically significant effect on the time to consolidation. The authors also noted that the treatment group had less deformity at the completion of the study than the control group and were able to resume ambulation in less time.

Can Pulsed Electromagnetic Field Bone Growth Stimulation Have An Impact?

     In 2000, Grady, et. al., investigated the use of pulsed electromagnetic field bone growth stimulation in patients with Charcot osteoarthropathy.11 The authors reported on a series of 11 patients who all received PEMF bone growth stimulation in combination with some form of immobilization. Eight patients had stage 1 Charcot osteoarthropathy and three patients had a stage 2 Charcot deformity. The immobilization consisted of either an Equalizer Walker or an Unna boot with a surgical shoe. The patients were allowed to bear weight in their immobilization device.      Every four weeks, radiographs assessed the Charcot deformity. The mean time for radiographic consolidation of the Charcot deformity was 3.5 months among the 11 patients. The researchers continued the bone growth stimulation until there was clinical resolution of edema, erythema and crepitus. They followed the patients in their series for a mean of 18 months with one of the 11 patients having a recurrent acute Charcot episode after nine months.      In 1993, Cohen, et. al., were the first to report the use of an implantable direct current bone growth stimulation as an adjunct in the surgical repair of a nonunion following Charcot midfoot reconstructive surgery.12 More recently, Wang, et. al., described their success using pulsed electromagnetic field bone stimulation following surgical reconstruction of the Charcot foot and ankle with external fixation.13 This is one of the only papers looking at the use of electrical bone growth stimulation following Charcot foot reconstructive surgery.      The authors performed reconstructions in 28 patients with Charcot deformities of mainly Lisfranc’s joint or the ankle joint. In their series, the researchers performed an open or percutaneous tendo-Achilles lengthening, arthrodesis of the involved joints with the use of a hybrid or ring-to-ring external fixator, and application of PEMF external bone growth stimulation immediately postoperatively. The authors noted radiographic consolidation of the correction at a mean of 3.1 months. While they reported consistently good results in their series, the study authors recognized that a larger series would be necessary to support their positive results further.

Current Recommendations: What You Should Know

     What is the bottom line? Current evidence supports the use of electrical or mechanical bone growth stimulation in the acute stages of Charcot foot, but the evidence is still limited. All of the papers report the use of electrical or mechanical bone growth stimulation in the acute stages of Charcot osteoarthropathy or Eichenholtz stage 1 or 2 (i.e. stage of development or early stage of coalescence). There is no current evidence to support the use of bone growth stimulation in the chronic Charcot foot deformity or Eichenholtz stage 3.      Out of the currently available bone growth stimulation devices, the CMF and PEMF stimulators have been the most extensively studied in the Charcot foot, and appear to be the most validated of the electrical bone growth stimulation devices. There are case reports of the use of direct current (DC) bone growth stimulation and mechanical bone growth stimulation (i.e. LIUS) but nothing further is currently available. There are currently no reports regarding the use of the capacitive coupling bone growth stimulation device. Future studies are needed that focus on prospective randomized controlled trials so meta-analyses of these trials can increase the effective study population and result in meaningful, clinically useful guidelines.14      In all situations, the clinician should first clinically and radiographically evaluate the patient with suspected Charcot osteoarthropathy and determine whether a bone growth stimulation device is indicated, appropriate and potentially helpful. One should not expect a bone growth stimulator to correct a malunion nor should clinicians use it as a substitute for immobilization and offloading. In my opinion, once you have determined that a bone growth stimulator is desirable in the management of a patient, the type of stimulator you use is less important.      The non-invasive devices all have different times of application. Often device representatives, in order to promote their device over another device, advertise these application times. Clinicians should recognize that the time of application is highly variable and it does not imply that one device is better than another. With PEMF stimulation, CMF stimulation and LIUS stimulation, generally shorter times have been advocated. Similarly, longer usage times with these devices have shown continued effectiveness but to a lesser degree. DC stimulation and CC stimulation are advocated for use 24 hours a day. These devices have shown improved efficacy with progressively longer periods of use.2      Probably the most important reason for choosing one device over another is availability. Today, insurance approval and reimbursement issues, demographics and ready availability of the different devices are primary factors in choosing which device one uses. If a clinician has developed a good rapport with a particular company or representative, that company or representative will often assist the clinician with these issues and accordingly, the clinician is more likely to use that company’s device.2      Dr. Downey is the Chief of the Division of Podiatric Surgery at Penn Presbyterian Medical Center in Philadelphia. He is a Clinical Professor in the Department of Surgery at the Temple University School of Podiatric Medicine and is a faculty member of the Podiatry Institute. Dr. Downey is in private practice in Philadelphia, Radnor and Doylestown, Pa.



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