A Closer Look At Bone Stimulators For Charcot
- Volume 19 - Issue 12 - December 2006
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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.