Understanding The Benefits Of Electrical Bone Stimulation
- Volume 20 - Issue 12 - December 2007
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Approximately 6 million extremity fractures occur in the United States each year. Five to 10 percent of these fractures will go on to delayed or nonunion. In regard to lost wages and additional treatment for delayed and nonunions, this translates into an annual economic loss to the United States of $3 to $6 billion.
One of the vexing and controversial issues related to the use of electric bone stimulation regards the actual definition of when a delayed or a nonunion occurs. The historic definition of a nonunion by the FDA was that of osseous discontinuity of nine months’ duration in which there has been no evidence of osseous healing for three months. Fortunately, the general consensus today is that one can identify nonunion and delayed unions when there are no demonstrable or progressive signs of healing. This definition allows a much earlier and much more humane approach to the use of electronic bone stimulation.
A Guide To The Evolution Of Electrical Bone Stimulation
The discovery of the relationship between electricity and magnetism launched over 180 years of research into electrophysics and quantum mechanics. Today’s practical applications of this science include everything from the high speed mass storage hard drive to advanced imaging technologies and even a device that positively influences neo-osteogenesis. This device is better known as the electronic bone stimulator.
In the 1950s and 1960s, Fakada and Yasuda theorized that the bending of bone creates a strain that results in electrical streaming potentials within the bone. These studies correlated well with Wolff’s law whereby mechanical loads upon bone are translated into an electrical potential that contributes to the modeling of bone. Currently, the prevailing thinking is that these electrical potentials signal the body to begin the bone repair, modeling and remodeling processes. Application of these loads is known as mechanotransduction and this plays a crucial role in the physiology of many tissues including bone. Mechanical loading can inhibit bone resorption and increase bone formation in vivo.
What You Should Know About The Four Steps Of Mechanotransduction
In bone, the process of mechanotransduction can be divided into four distinct steps: mechanocoupling, biochemical coupling, transmission of signal and effector cell response. In mechanocoupling, mechanical loads in vivo cause deformations in bone that stretch bone cells within and lining the bone matrix and create fluid movement within the canaliculae of bone. Dynamic loading, which is associated with extracellular fluid flow and the creation of streaming potentials within bone, is most effective for stimulating new bone formation in vivo. Bone cells in vitro are stimulated to produce second messengers when exposed to fluid flow or mechanical stretch.
In biochemical coupling, the possible mechanisms for the coupling of cell-level mechanical signals into intracellular biochemical signals include force transduction through various complicated chemical pathways. The tight interaction of each of these pathways would suggest that the entire cell is a mechanosensor and there are many different pathways available for the transduction of a mechanical signal.
In the transmission of signal, osteoblasts, osteocytes and bone lining cells may act as sensors of mechanical signals and may communicate the signal through cell processes connected by gap junctions. These cells also produce paracrine factors that may signal osteoprogenitors to differentiate into osteoblasts and attach to the bone surface. Insulin-like growth factors and prostaglandins are possible candidates for intermediaries in signal transduction.
In the effector cell response, the effects of mechanical loading are dependent upon the magnitude, duration and rate of the applied load. Longer duration, lower amplitude loading has the same effect on bone formation as loads with short duration and high amplitude. Loading must be cyclic to stimulate new bone formation. Aging greatly reduces the osteogenic effects of mechanical loading in vivo. Also, some hormones may interact with local mechanical signals to change the sensitivity of the sensor or effector cells to mechanical load.