Part 4:The Body Electric ... Good News for Mammals ...The Silver Wand

The Body Electric

by Robert O. Becker

Seven 

Good News for Mammals 

Stephen D. Smith was the first to induce artificial regrowth with electricity applied to the limb of a non-regenerating animal. In 1967 Smith, setting forth on his own at the University of Kentucky after his apprenticeship to Meryl Rose at Tulane, implanted tiny batteries in adult frogs' leg stumps. I followed his work eagerly and was elated to hear that he'd gotten the same amount of partial regrowth that had resulted from Rose's salt, Polezhaev needles, and Singer's rerouted nerves. Of all the experiments that have influenced me, this was probably the one that encouraged me the most. 

For a battery that was small and weak enough, Smith had returned to the simple technology of Galvani and Volta. He soldered a short piece of silver wire to an equal length of platinum wire, and put some silicone insulation around the solder joint. He chose these two metals as being the least likely to release ions and produce spurious effects by reacting with the surrounding tissue. When immersed in a frog's slightly saline body fluids, this bimetallic device produced a tiny current whose voltage was positive at the silver end and negative at the platinum end. 

Since our work on frog erythrocytes hadn't yet been published, it was sheer luck that the current from these batteries fell close to the "window of effectiveness" for blastema formation. As Smith later wrote: "It would he nice to be able to say that I had worked out all the parameters in advance, and knew exactly what I was doing, but such was not the case. As so often has happened in the history of science, I stumbled onto the right procedure."

Smith implanted his wires along the bone remnant, with one end bent over into the marrow cavity. The limbs with the positive silver electrode at the cut showed no growth, and in some cases tissue actually disintegrated. The negative platinum ends, however, started regeneration; the new limbs all stopped growing at about the same distance from the device, suggesting that regeneration might have been complete if the batteries had been able to follow along. In 1974 Smith made a device that could do just that, and achieved full regrowth. 

Despite Smith's success, there was no reason to suppose that his method would work in mammals. One researcher had recently noted some regeneration in the hind legs of newborn opossums, but, since marsupials are born very immature and develop in the mother's pouch to a second birth, we suspected that this was merely a case of embryonic regrowth. Most fetal tissues were known to have some regenerative ability while they weren't yet fully differentiated. Richard Goss had shown that the yearly regrowth of deer and elk antlers was true multi tissue regeneration, but this feat seemed too specialized to make us confident about restitution in other mammals or other parts of the body. 

Many thought all such attempts were doomed, because the process of encephalization had progressed much further in mammals than amphibians. All vertebrates were known to have roughly the same ratio of nerve tissue to other kinds of tissue, but in mammals most of the limited nerve supply went into the ever more complex brain, until, as Singer had shown in a recent study, the proportion of nerve to other tissue in rat legs was 80 percent less than in salamander legs. This was well below the critical mass needed for normal regeneration, and we thought it might be impossible to make up the difference artificially.  

Even if we could supply the proper electrical stimulus, we weren't sure there would be any cells able to respond to it. Mammalian red blood cells had no nuclei, so they couldn't dedifferentiate. Based on our work on bone healing in frogs, we suspected that immature red corpuscles in the bone marrow might take over, but perhaps they were programmed to dedifferentiate only for fracture healing. Even if they would respond to an external current, we wondered whether there were enough of them to do the job. 

There was also the problem of complexity. Many regeneration researchers believed that mammalian tissues had become so specialized and complicated that they'd simply outgrown the control system. Maybe it couldn't handle enough data to fully describe the parts needed. If so, any blastema we produced would just sit there, not knowing what to make. 

A First Step with a Rat Leg 

I tested the kind of silver-platinum couplings Smith used and found they delivered several times too much current for ideal dedifferentiation, according to our frog experiments. Joe Spadaro, another of Charlie's grad students, suggested that we put carbon resistors between the two metals, giving us devices of various current levels. 

In 1971, Joe and I amputated the right forelegs of thirty-five rats. We made the cuts through the upper foreleg well away from the elbow so that only the bone shaft, which had long ago ceased growing, would remain at the tip. We used all males, to obviate as many hormonal variables as possible. As controls we treated some of the stumps with no device, or one made of a single metal, or one with the silver positive end facing the stump. We did the actual test on twenty-two of the rats, implanting our batteries with the negative platinum electrode at the wound. We tucked the outer electrode into the marrow cavity and sutured the inner one to the skin of the shoulder. 

We had an answer fast. After three days the stumps of the controls had begun to heal over or even, in the case of the highest-current couplings, die back a little behind the amputation line. But the experimental legs with our medium-current devices, supplying 1 nanoamp, were doing well. In a week, nearly every one had a well-formed blastema and seemed ready to replace the whole limb. 

Since healing is very fast in rats, and because we wanted a uniform sample for our first test, we sacrificed all of the controls and most of the test animals at this time, although we spared a few for a month. We cut  off the entire healing limb, then fixed, stained, and sectioned it for the microscope.

DC STARTS LIMB REGENERATION IN RATS 

I shall never forget looking at the first batch of specimens. The rat had regrown a shaft of bone extending from the severed humerus. At the proper length to complete the original bone there was a typical transverse growth plate of cartilage, its complex anatomical structure perfectly regular. Beyond that was a fine-looking epiphysis, the articulated knob at each end of a limb bone. Along the shaft were newly forming muscles, blood vessels, and nerves. At least ten different kinds of cells had differentiated out from the blastema, and we'd succeeded in getting regeneration from a mammal to the same extent as Rose, Polezhaev, Singer, and Smith had done in frogs.

Slides from some of the other animals were even more spectacular. One stump had two cartilaginous deposits that looked like precursors of the two lower arm bones beyond a fully formed elbow joint. All of the regenerates were bent toward the electrode, and in one the lower humerus had formed alongside the old shaft rather than as an extension of it, but otherwise its structure was quite normal. 

With one exception, slides from longer than a week were less exciting. They seemed to have gotten less organized as time went on. Behind one of these older blastemas, at the end of a nearly unformed ghost of a bone, we found cartilage in a five-fingered shape—this limb had begun to grow a hand. 

In general, though, it looked as if the current had to be of a certain duration as well as a certain strength. This was no less disappointing to us than it was to the Life photographer who visited the lab at that time and wanted before and after shots with a rat playing the piano at the end, but nonetheless we were very pleased. Since the blastemas always formed around the electrodes and since redifferentiation proceeded into organized tissue, we knew the current had stimulated true regeneration, not some abnormal growth. Mammals still had the means for the orderly reading out of their genetic instructions to replace lost parts. We would simply have to learn more exactly the electrical requirements of the whole process, then make devices to supply the proper current at the proper time in the proper place. 

When we published our results, it was hard to shroud our excitement in the circumspect scientific jargon needed. We wrote that we'd activated true, though partial, regeneration with a minuscule direct current and that the marrow cells seemed to be the source of the blastema. I thought this claim was sober enough. Joe and I cautioned that other factors had yet to be studied. Most important, we warned that if such a tiny force could so easily switch on growth, it must be very powerful, and we'd best know it thoroughly before using it routinely on humans, lest we give them unwelcome growths—tumors. 

I felt that, within the constraints of scientific propriety, we'd uttered a rousing call for a big research push to open up the benefits of regeneration to humans. It must have been a whisper, though, for it caused no more ripples than a feather settling on a frog pond. Philip Person, a dental surgeon at the Brooklyn VA hospital and a friend whom I'd known for years, asked me to present our results to the New York Academy of Medicine. Before the academy would permit this, however, it insisted that two experts must visit the lab and look at the actual data. One was Marc Singer, who enthusiastically agreed that we'd really started regeneration in the rat. The other man was totally negative, but he wasn't a specialist in regeneration, so the academy permitted me to speak. 

Singer was one of the few who showed much enthusiasm when I'd finished reading my paper at the meeting. Most of the audience was unresponsive, there were few comments or criticisms To these people, electric growth control was still a vitalistic impossibility, and they seemed unwilling to discuss dedifferentiation. The man who'd visited our lab with Singer complained that the amount of new growth was small. Phil pointed out that it wasn't the quantity but the quality of new tissue that was important, especially in such a short time. Singer, convinced of the paramount importance of the nerves, thought the current might be stimulating them rather than directly causing dedifferentiation, but still thought the experiment was a big step forward. Nevertheless, it wasn't even attempted again until seven years later, when Phil Person himself took on the task; he, and later Steve Smith, confirmed our findings with even better results. 

Meanwhile, buried in the literature we found reports that others had already observed some regeneration in mammals. In 1934 Hans Selye, the famous researcher into the effects of stress, discovered that a rat's limbs could partially regenerate of their own accord when the animal was two to five days old. Five years later Rudolph F. Nunnemacher of Harvard confirmed Selye's observation. Nunnemacher, however, ascribed the growth to a remnant of the epiphyseal plate. The growth-plate cells, he thought, simply might have kept on growing as normal in the adolescent animal. Selye replied that he'd specifically made sure to amputate the limbs high enough to get all of the epiphyseal plate so he could be certain that any growth was regenerative. 

Thus Joe and I found that we'd really just extended the age limit for regeneration in the rat. Indeed, two years later Phil Person showed that even the young adult rats we'd used occasionally exhibited some regrowth, a fact that had puzzled us in a couple of our control animals. So, to be exact, our electrodes had temporarily but drastically boosted the efficiency of the process as it normally waned with age in the rodent. Still, it was the first time that had ever been done in a mammal. 

Childhood Powers, Adult Prospects 

The amputation of a fingertip—by a car door, lawn mower, electric fan, or whatever—is one of the most common childhood injuries. The standard treatment is to smooth the exposed bone and stitch the skin closed, or, if the digit has been retrieved and was cleanly cut, to try to reattach it by microsurgery. The sad fact is that even the most painstaking surgery gives less than optimal results. The nails are usually deformed or missing, and the fingers are too short and often painful, with a diminished or absent sense of touch. 

In the early 1970s at the emergency room of Sheffield Children's Hospital in England, one youngster with such an injury benefited from a clerical mixup The attending physician dressed the wound, but customary referral to a surgeon for closure was never made. When the error was caught a few days later, surgeon Cynthia Illingworth noticed that the fingertip was regenerating! She merely watched nature take its course. 

Illingworth began treating other children with such "neglect," and by 1974 she'd documented several hundred regrown fingertips, all in children eleven years old or younger. Other clinical studies have since confirmed that young children's fingers cleanly sheared off beyond the outermost crease of the outermost joint will invariably regrow perfectly in about three months. This crease seems to be a sharp dividing line, with no intermediate zone between perfect restoration and none at all. 

Some pediatric surgeons, like Michael Bleicher of New York's Mount Sinai Hospital, have become so confident in the infallibility of the process that they'll finish amputating a fingertip that's just hanging by a bit of flesh. A lost one will regenerate as good as new, whereas one that has merely been mutilated will heal as a stump or with heavy scarring. 

Fingertip regrowth is true multi tissue regeneration. A blastema appears and re-differentiates into bone, cartilage, tendon, blood vessels, skin, nail, cuticle, fingerprint, motor nerve, and the half-dozen specialized sensory-nerve endings in the skin. Like limb regeneration in salamanders, this process only occurs if the wound isn't covered by a flap of skin, as in the usual surgical treatment. Illingworth and her coworker Anthony Barker have since measured a negative current of injury leaving the stump. 

Sadly, natural replacement has been accepted only at a few hospitals. Bleicher laments his colleagues' resistance to the evidence: "Mention it to young residents just our of the training program, and they look at you as though you're crazy. Describe it on grand rounds or at other institutions, and they tell you it's hogwash." Nearly all surgeons cling instead to flashier and vastly more expensive yet less effective microsurgical techniques or simple stitches and stunted fingers. 

This discovery and our own research indicated that the potential for at least some artificial regeneration was clearly quite good in young mammals. But what about the ones who needed it most—us older folks whose parts were more likely to be injured or broken down? The answer came unexpectedly several years later, in a way that showed the futility of adhering too rigidly to one's original plan. The scientist must be free to follow unexpected paths as they appear. 

I always expected each of my associates, whether student or established researcher, to follow some independent project unrelated to our work together. In 1979, a young assistant named James Cullen (now a Ph.D. investigator in anatomy at the Syracuse VA hospital) proposed to study what would happen if nerves were implanted into the bone marrow of rats. Jim thought the nerves should induce new bone to form in the marrow cavity. Since the idea seemed logical and the technique might supplement the electrical bone-healing devices we'd developed by then, I encouraged him to go ahead. 

Jim ran into technical problems right away. He could easily dissect the rat's sciatic nerve out of the hind leg, but getting it into the marrow cavity through a hole drilled in the thighbone was like trying to push a strand of limp spaghetti through a keyhole. He resorted to drilling two holes in the femur, passing a wire suture into the outer one, up the femur, and out the hole nearer the hip. Then he looped the wire around the nerve and pulled it into the marrow cavity using the suture. However, after doing a number of these, Jim decided that there had to be a better way. He decided to amputate the rat's hind leg halfway between the hip and the knee. He could then drill a hole into the marrow cavity just below the hip, pass a suture through it, and pull the nerve down the cavity and out the end of the bone remnant. This was much easier and made a better connection of nerve to bone, so Jim prepared a number of animals this way, only to find that the nerve had a disconcerting tendency to pull back, out of the femur. The amputation didn't faze the rats; they used the stump vigorously, and this caused the nerve to retract. 

In those few animals whose nerve had stayed in place, an interesting bone formation had appeared in the marrow cavity. To secure the nerve and look for the same result in other animals, Jim sutured the nerve to the skin that we closed back over the stump. The stitch held the nerve in place, all right, but one animal so treated gave us a totally unpredicted and fascinating result: 

The missing portion of the femur partially regenerated. While this was surprising enough, the most startling fact was that Jim had used a group of surplus rats about six month old. These rats were well into adulthood, when mammals were thought to lose all powers of regeneration except fracture healing. What had happened?

Closer examination revealed that we'd made a hole in the skin when we sutured the nerve to it. The nerve appeared to have grown into contact with the epidermis. One of the requirements for normal regeneration of a salamander limb was a neuro epidermal junction, and it looked as though this had formed spontaneously in our one lucky rat when the two tissues were brought together by surgery. 

We changed the course of the experiment by operating on the other rats to unite the sciatic nerve and epidermis, after scraping away the dermis. We used animals of various ages. The results exceeded our expectations. Even the old rats regenerated their thighbones and much of the surrounding tissue. 

This offered an unparalleled opportunity to find out what it was about the neuro epidermal junction that was so important. We prepared one group of animals with a surgical neuro epidermal junction exactly as before. We prepared a second group the same way, except that we sutured the nerve to the end of the bone, a millimeter away from the hole and with no contact with the epidermis. The first group regenerated, while the second group showed normal rat healing with no growth. The important observation, however, came from electrical measurements we made every day on the stumps. In those animals that formed a neuro epidermal junction, we found electrical potentials following the same curve I'd found in the salamander. The voltage was about ten times as high, but the pattern was exactly the same. In the animals having no neuro epidermal junction, the potentials followed the same curve as in the non regenerating frog. 

We'd discovered that the specific electrical activity that started regeneration was produced by the neuro-epidermal junction, not by the simple bulk of nerve in the limb. My original that the direct current control system was located in the nerves now had to be expanded to include the electrical properties of the epidermis as well. The nerve fibers joined the epidermal cells like plugs into sockets to complete the exact circuit needed for a dedifferentiation current. Furthermore, since the neuro epidermal junction was located over the end of the stump, it continually produced blastemal cells exactly where needed, at the growing tip. This discovery was enormously important, then, because it proved beyond doubt that the electrical current was the primary stimulus that began the regenerative process, and that it could operate even in mammals. 

PRODUCING A REGENERATION CURRENT IN RATS 

Another experiment showed us a formidable obstacle, however. In an additional series of rats we made a neuro epidermal junction, not at the end of the amputation stump, but on the side of the leg. There we measured the same "regenerative" electrical changes, but nothing happened. There was no growth. This meant that there were no sensitive cells at this site—no cells able to dedifferentiate in response to the current. In mammals, it seemed, such cells were found only in the bone marrow, a sparse cell population to serve as a source of raw material, especially in adult animals. 

AN ARTIFICIAL NEURAL EPIDERMAL JUNCTION STARTS REGROWTH IN RATS 

This explained why we never got complete regrowth in any of our rats. The results were typical of an inadequate blastema. There weren't enough sensitive cells in the bone marrow to make a blastema big enough to produce a whole leg. The prospects for full limb regeneration in humans, then, looked very dim—unless we could come up with a way of making other cells electrically sensitive so as to transform them into despecialized blastemal cells. Luckily, while working on a completely different problem described in the following chapter, we stumbled upon a way to do just that.

Part 3 Our Hidden Healing Energy 

Disease is not an entity, but a fluctuating condition of the patient's body, a battle between the substance of disease and the natural self-healing tendency of the body. 

—Hippocrates

Eight 

The Silver Wand 

When Apollo whisked Aeneas off the field of battle before Troy, he healed the hero's shattered thighbone in a matter of minutes. Without a god at the bedside, the process takes three to six months, and sometimes it fails. If the bones didn't knit, the limb formerly had to be amputated after the victim had suffered for a year or more. 

It was only in 1972 that I felt ready to try electrical stimulation of human bone growth in such cases. Zachary B. (Burt) Friedenberg, Carl Brighton, and their research group at the University of Pennsylvania had already reported the first successful electrical healing of a nonunion two years before, but to avoid possible side effects we felt we must duplicate the natural signal more closely than they had, and we didn't know enough until after our work on rat leg regeneration. Like Friedenberg we decided to place a negative electrode between the bone pieces, but using a much smaller current and a silver electrode rather than stainless steel. We thought silver would be less likely to react chemically with the tissue and better able to transmit the electrical current. At that time we were treating a patient whose condition seemed to demand that we try the new procedure. 

Minus for Growth, Plus for Infection 

Jim was in bad shape. Drafted during the Vietnam War, he'd been a reluctant, rebellious soldier. He survived his tour in Nam and was transferred to an Army base in Kansas late in 1970. On New Year's Eve he broke both legs in an auto crash. The local hospital put him in traction, with pins drilled through the skin and bones to hold the pieces together. When he was moved to the base hospital a few days later, all the pins had to be removed due to infection. 

Jim's doctors couldn't operate because of the bacteria, so they had to be satisfied with a cast. Because he'd broken one leg below and the other above the knee, he needed a huge cast called a double hip spica. He was totally encased in plaster, from his feet to the middle of his chest, for six months. By August, his left lower leg had healed, but the right femur showed no progress at all. The quarter-inch holes where the pins had been were still draining pus, preventing surgery. That September he was given a medical discharge and flown to the Syracuse VA hospital. 

When I first saw him, he was still in a large cast, although now his left leg was free. The halves of the right thighbone were completely loose. There was nothing in standard practice to do but leave the cast on and hope. After six more months Jim's hope was just about gone. For a year he'd lain in bed, unable to leave the hospital for even a brief visit home. He vented his rage against the staff, then grew despondent and unable to face the future, which no longer seemed to include his right leg. 

Then Sal Barranco, a young orthopedic surgeon in his last year of residency, was assigned to my service from the medical school. He'd already been a good doctor when he briefly worked with me two years before—smart, hardworking, and really interested in his patients. He took over Jim's care, spent many hours talking with him, and arranged for counseling. Nothing seemed to help. Jim slipped further and further away from us. 

Sal had always been interested in what was going on in the lab. In fact, I'd often tried to interest him in a career of teaching and research, but he preferred surgery and its rewards of helping people directly. In February of 1972, as we were nearing the clinical stage with our bone stimulator, Sal said, "You know, Dr. Becker, you really should consider electrically stimulating Jim's fracture. I don't see anything else left. It's his last chance." 

The problem was that none of Friedenberg patients had been infected. Although Jim's septic pin tracts weren't right at the fracture, they were too close for comfort. If I stirred up those bacteria when I operated to insert the electrodes, the game was lost. Moreover, it was obvious by now that electricity was the most important growth stimulus to cells. Even if it produced healing, no one could be sure what these cells would do in the future. They might become hypersensitive to other stimuli and start growing malignantly later. This was the first time in the history of medicine that we could start at least one type of growth at will. I was afraid of beginning a clinical program that might seize the public's fancy and be applied on a large scale before we knew enough about the technique. If disastrous side effects showed up later, we could lose momentum toward a revolutionary advance in medicine. I decided that if I carefully explained what we proposed to do, with all its uncertainties, and let the patient choose, then ethically I'd be doing the right thing. 

As to the infection, for several years we had been looking for a way to stop growth. My experiments with Bassett on dogs back in 1964 suggested that just as we could turn growth on with negative electricity, so we could turn it off with positive current. If true, this obviously could be of great importance in cancer treatment. Because ours was always a needy program, trying to do more than we had grants for, we couldn't afford the expensive equipment needed to test the idea on cancer cells. We had to settle for bacteria. 

In preliminary tests we found that silver electrodes, when made electrically positive, would kill all types of bacteria in a zone about a half inch in diameter, apparently because of positive silver ions driven into the culture by the applied voltage. This was an exciting discovery, because no single antibiotic worked against all types of bacteria. I thought that if I inserted the silver wire into Jim's nonunion and the area became infected, I could as a last resort make the electrode positive and perhaps save the leg a while longer. Of course, the positive current could well delay healing further or actually destroy more bone. 

I explained all this to Jim and said that, if he wished, I would do it. I wanted him to know the procedure was untested and potentially dangerous. With tears in his eyes, he begged, "Please try, Dr. Becker. I want my leg." 

Two days later, Sal and I operated through a hole in the cast. The fracture was completely loose, with not one sign of healing. We removed a little scar tissue from the bone and implanted the electrode. The part in between the bone ends was bare wire; the rest, running through the muscles and out of the skin, was insulated so as to deliver the minuscule negative current only to the bone. 

The infection didn't spread, and Jim's spirits improved. As I made my daily rounds three weeks later, he said, "I'm sure it's healing. I just know it!" I was still nervous when, six weeks after surgery, it was time to pull out the electrode, remove the cast, and get an X ray. I needn't have worried. Not only did the X ray show a lot of new bone, but when I examined the leg myself, I could no longer move the fracture! We put Jim in a walking cast, and he left the hospital for the first time in sixteen months. In another six weeks the fracture had healed enough for us to remove the cast, and Jim started rehabilitation for his knee, which had stiffened from disuse. 

All the pin tracts, especially the ones nearest the break, were still draining, and Jim asked, "Why not use the silver wire on this hole to kill the infection? Then I'll be all done and won't have to worry anymore about infecting the rest of the bone." I had to agree with his logic. If the hole through the muscle to the outside healed shut, the infection would be more likely to spread within the bone. However, I told him that the positive current might prevent the hole from filling in with bone, making a permanent weak spot there. 

We put in the electrode and used the same current as before, except reversing its polarity. I had no idea how long to let it run, so I arbitrarily pulled it out after one week. Nothing much seemed to have happened. The drainage might have been a little less, though not much; but I was afraid to use the positive current anymore for fear of further weakening the bone. 

Jim left the hospital and didn't keep his next appointment in the clinic. A year later he returned unannounced saying he was just traveling through Syracuse and thought I would like to see how he was doing. He was walking normally, with no pain, placing full weight on the right leg. He said the drainage had stopped a week after he left the hospital and had never recurred. X rays showed the fracture solidly healed and the one pin tract I'd treated filling in with new bone. The pin site on the other leg was still infected, and I said we could treat that in a few days, since we'd improved our technique in the meantime. "No, I have to be moving on," Jim replied. "I don't have a job. I don't know what I'm going to do, but I know I don't want to spend any more time in hospitals." 

Sal had been graduated from the residency program a few months after Jim was discharged in 1973, but before he left he spent all his free time in the lab helping us test the bactericidal (bacteria-killing) electrodes. A few previous reports had mentioned inconsistent antibacterial effects, some with alternating current, some with negative DC using stainless steel, but there had been no systematic study of the subject. We tried silver, platinum, gold, stainless steel, and copper electrodes, using a wide range of currents, on four disparate kinds of bacteria, including Staphylococcus aureus, one of the commonest and most troublesome. 

Soon we were able to explain the earlier inconsistencies: All five metals stopped growth of all the bacteria at both poles, as long as we used high currents. Unfortunately, high currents also produced toxic effects—chemical changes in the medium, gas formation, and corrosion— with all but the silver electrodes. Apparently such currents through most metals "worked" by poisoning both bacteria and nearby tissues. 

Our preliminary observations turned out to be right. Silver at the positive pole killed or deactivated every type of bacteria without side effects, even with very low currents. We also tried the silver wires on bacteria grown in cultures of mouse connective tissue and bone marrow, and the ions wiped out the bacteria without affecting the living mouse cells. We were certain it was the silver ions that did the job, rather than the current, when we found that the silver-impregnated culture medium killed new bacteria placed in it even after the current was switched off. The only other metal that had any effect was gold; it worked against Staphylococcus, but not nearly as well as silver. 

Of course, the germ-killing action of silver had been known for some time. At the turn of the century, silver foil was considered the best infection-preventive dressing for wounds. Writing in 1913, the eminent surgeon William Stewart Halsted referred to the centuries-old practice of putting silver wire in wounds, then said of the foil: "I know of nothing which could quite take its place, nor have I known any one to abandon it who had thoroughly familiarized himself with the technique of its employment." 

With the advent of better infection-fighting drugs, silver fell out of favor, because its ions bind avidly to proteins and thus don't penetrate tissue beyond the very surface. A few silver compounds still have specialized uses in some eye, nose, and throat infections, and the Soviets use silver ions to sterilize recycled water aboard their space stations, but for the most part medicine has abandoned the metal. Electrified silver offers several advantages over previous forms, however. There are no other ions besides silver to burden the tissues. The current "injects" or drives the silver ions further than simple diffusion can. Moreover, it's especially well suited for use against several kinds of bacteria simultaneously. It kills even antibiotic-resistant strains, and also works on fungus infections. 

For treating wounds, however, there was one big problem with the technique. Its effect was still too local, extending only about a quarter inch from the wire. For large areas we needed something like a piece of window screen made of silver, but this would have been expensive and also too stiff to mold into the contours of a wound. 

We'd been doing our clinical experiments with financial support from a multinational medical-equipment company that made our "black boxes," the battery packs with all their circuitry that powered our electrodes. I discussed the problem with the company's young research director, Jack TerBeek, and a few weeks later he came back with a fascinating material. NASA needed an electrically conductive fabric, and a small manufacturing company had produced nylon parachute cloth coated with silver. It could be cut to any size and was eminently flexible. 

It performed beautifully. Although the silver ions still didn't get more than a quarter of an inch from it, we could use it to cover a large area. Hopeful that we might have a cure for two of an orthopedist's worst nightmares—nonunion and osteomyelitis (bone infection)—we studied the positive silver technique in the lab and continued to use the negative electrodes to stimulate bone growth in selected patients. Word spread via newspaper and TV reports. We began getting patients from all over the nation, but we didn't accept many for the experimental program due to my conservative viewpoint. I applied the same criterion as before: Electrical treatment had to be the patient's last chance. 

While slowly gaining experience, we surveyed the literature to stay informed about other people's work. As of 1976, fourteen research groups had used bone stimulators on some seven hundred patients, for spinal fusions and fresh fractures as well as nonunions, all with seemingly good results. 

We'd used our electrical generator on only thirteen patients by then. We were the only ones using silver electrodes, a lucky choice as it turned out; all the others were using stainless steel, platinum, or titanium. We used 100 to 200 nanoamps per centimeter of electrode, while Brighton and most other investigators were using 10,000 to 20,000 nanoamps. The low level approximated the natural current and also minimized the chances of a dangerous side effect. Brighton and Friedenberg had found a danger of infection and tissue irritation when running their high-current electrodes at more than 1 volt. We figured this couldn't happen at our amperage, but just to be sure we built in an alarm circuit to shut off our box automatically if the electrical force rose close to 1 volt. 

By this time we'd also cleared up several more cases of osteomyelitis by reversing the battery and making the silver electrode positive for a day. It looked safe. There was no crossover of effects: When negative, the wire didn't make infectious bacteria grow, and when positive, it didn't destroy bone-forming cells or prevent them from growing when we switched the current to negative. Our confidence in this method grew with one of our most challenging cases, which also forced us to revise our theories.  

Positive Surprises 

In December of 1976 a young man was sent to our clinic for a possible amputation. John was a man of the north woods. Weathered and hard, he faced the problem philosophically. "What's got to be has got to be," he said through tight lips. Three years before, he'd been in a snowmobile accident, breaking his right tibia (shinbone) in three places and also fracturing the fibula, the smaller bone of the lower leg. He'd been treated at a small local hospital, where the broken bones had become infected. He'd undergone several operations to remove dead bone and treat the infection, but the bacteria continued to spread. He came to us with the fracture still not healed and with a long cavity on the front of his shin in which one could see right into the dead and infected bone. He was struggling to walk in a cast extending up to his hip. He was married, with five young children, and his leg was obviously not the only place he was having trouble making ends meet. 

"What kind of work do you do?" I asked him. 

"I trap muskrats, Doc." 

"That's all?" 

"That's all, Doc." 

"How in hell do you manage with that cast on?" 

"I put a rubber hip boot over the cast, Doc." 

Muskrat trapping is hard work, a tough way to make a living even for a man with two good legs. "John, if you have an amputation and wear an artificial leg, you sure won't be able to do that. What will you do then?" 

"I dunno—welfare prob'ly. Prob'ly go nuts." 

"You really like to work in the woods, don't you?" 

"Wouldn't do anything else, Doc." 

"Well, let's get you admitted to the hospital. Something has to be done, and I have an idea that might let you keep your leg." For the first time, John smiled. 

In fighting the infection, the first step was to identify the enemy, the microbes. John's wound was a veritable zoo. There were at least five different types of bacteria living in it. Even with only one kind, osteomyelitis is notoriously hard to treat. Very little blood reaches the bone cells, so both antibiotics and the body's own defense agents are hampered in getting where they're needed. And even if we could get it into the bone, no single antibiotic could fight all of John's germs. Even a mixture would probably create a greater problem than it solved, for  any bacteria resistant to the mix would spread like wildfire when the others competing against them were killed. 

John's X rays were as chaotic as his bacteria cultures—pieces of dead bone all over the place with absolutely no healing—but we had to deal with the infection first. Since we'd have to use positive current for quite a while, I was afraid we'd destroy some of the bone, but I told John that six months after we got the wound to heal over with skin, I would bring him back into the hospital and use the negative current to stimulate whatever was left. I couldn't promise anything and, since I hadn't yet tried the silver nylon on this type of wound, we might run into unexpected problems. But John agreed with me that he had nothing to lose except his leg, which would certainly have to come off if we didn't try my plan. 

A few days later I debrided the wound, removing the dead tissue and all grossly infected or dead bone. There wasn't much left afterward. It was an enormous excavation running almost from his knee to his ankle. In the operating room we soaked a big piece of silver nylon in saline solution and laid it over the wound. It had been cut with a "tail," serving as the electrical contact and also as a sort of pull tab that we could keep dry, outside of the cavity. We packed the fabric in place with saline-soaked gauze, wrapped the leg, and connected the battery unit. 

I watched John anxiously during the first two days. If trouble was going to occur, that was when I expected it. By the third day he was eating well, and the current was beginning to drop off, indicating more resistance at the surface of the wound. Now it was time to change the dressing. We were overjoyed to see that the silver hadn't corroded and the wound looked great. Carefully I took a bacterial culture and applied a new silver nylon dressing. 

The next morning Sharon Chapin, an exceptional lab technician who took an active part in some of the research, showed me the bacterial cultures. The number of bacteria had dropped dramatically. I went to give John the good news and change his dressing again, when I realized that I could teach him to do his own daily dressing changes. They were time-consuming for me, but John had too much time on his hands and was the one most interested in doing the best thing for his leg. It was a nice feeling to teach a muskrat trapper, who bad dropped out of school at sixteen, how to do an experimental medical procedure. He learned fast, and in a day or so he was changing dressings himself and measuring the current, too. By the end of the week, he allowed as how he did a better job than l did. Maybe he did it at that, because by then all of our  bacterial cultures were sterile—all five kinds had been killed. The soft healing tissue, called granulation tissue, was spreading out and covering the bone. In two weeks, the whole base of the wound, which had been over eight square inches of raw bone, was covered with this friendly pink carpet. The skin was beginning to grow in, too, so we could forget about the grafts we thought we'd need to do. 

I decided to take an X ray to see how much bone he'd lost. I could hardly believe the picture. There was clearly some bone growth! We'd been working through a hole in the cast, so I had no idea if the fracture was still loose. Without telling John why—I didn't want to get his hopes up if I was wrong—I removed the cast, felt the leg, and found that the pieces were all stuck together. John watched, and when I was done he lifted his leg into the air triumphantly. It held straight against gravity. His grin opened broader than an eight-lane highway. "I thought you said the bone wouldn't heal yet, Doc!" 

I'd never so much enjoyed being wrong, but I warned John not to get too excited until we were sure the good news would hold up. I put him back into a cast and continued treatment another month, until the skin healed over. By then the X rays showed enough repair to warrant a walking cast. John left the hospital on crutches and promised not to run around in the swamps until I told him it was all right. He didn't come back until two months later. The cast was in tatters, and he walked in without crutches, smiling at everyone. The last X rays confirmed it: Healing was nearly complete, and John went back to the wilds. 

By mid-1978 we'd successfully treated fourteen osteomyelitis patients with the positive silver mesh wire. The funny thing was, in five of them we'd healed nonunions as a "side effect," without any negative current at all. Obviously it was time to revise our idea that negative electricity alone fostered growth and positive inhibited it. 

Andy Marino, Joe Spadaro, and I talked it over. Reducing the DC stimulation technique to its essentials, all you needed was an electrode that wouldn't react with tissue fluid when it wasn't passing current. Since a negative electrode didn't give off ions, any inert metal, such as stainless steel, platinum, or titanium, would work with that polarity. But we knew from our lab work that the situation was very different at the positive pole, where the current drove charged atoms of the metal into the nearby environment. We decided it must be chemical, not electrical, processes that were preventing the bacterial growth at the positive electrode. In that case, maybe polarity was unimportant in growth enhancement. We postulated that, because silver ions were nontoxic to human cells and the electrical aspect was right, we inadvertently grew bone with positive current. This idea turned out to be quite wrong, but we'll get to that story in due time. 

Joe, who was always fascinated by the history of science, now found that none of the contemporary research groups had been the first to stimulate bone repair electrically. We'd all been beaten by more than 150 years. Back in 1812, Dr. John Birch of St. Thomas' Hospital in London used electric shocks to heal a nonunion of the tibia. A Dr. Hall of York, Pennsylvania, later used direct current through electro-acupuncture needles for the same purpose, and by 1860 Dr. Arthur Garratt of Boston stated in his electrotherapy textbook that, in the few times he'd needed to try it, this method had never failed. Because of the primitive state of electrical science then, we didn't know how much current these doctors had used. However, the polarity didn't seem to matter, and they used gold electrodes, which were nearly as nontoxic at the positive pole as silver. 

Realizing that we still didn't know as much as we'd thought about the growth control lock, we continued to ply the silver key. At least seventy patients with bone infections have now had the silver nylon treatment, including twenty at Louisiana State University Medical School in Shreveport, where Andy Marino ended up after the closing of our lab in 1980. In some of our first cases we noticed a discharge exuding from the tissues and sticking to the mesh when we changed the dressings. We thought it was "reactive" exudate—from irritation by the current—until one day when, during a slight delay in the operating room, I sent a sample of it to the pathology lab. It was filled with such a variety of cells that we had to rule out a simple response to irritation. Instead there was a variety of primitive-looking cell types, looking just like the active bone marrow of children. However, the patients were long past that age, and, besides, their marrow cavities were closed off with scar tissue from their unmended and infected bone injuries. We had to consider another source. 

The exudate appeared at the same time as the granulation tissue, which is composed mainly of fibroblasts, ubiquitous connective cells forming a major part of most soft tissues. Since the exudate also contained some fibroblasts, we decided to see if the unfamiliar types had arisen by metamorphosis from them. 

We set up a series of three-compartment culture dishes and placed a standard colony of isolated, pure-bred mouse fibroblasts in each. In one section we put a positive silver electrode, in one a negative electrode, and in the third a piece of silver wire not connected to anything. In cells right next to all three wires, the cytoplasm changed to an abnormal texture in response to ions of dissolved silver, which migrated only about a hundredth of a millimeter. There were no other effects in the control or negative-current chambers. 

Around the positive poles, however, this region was succeeded by an area of great activity for a distance of 5 millimeters on all sides. While doing their job of holding things together, fibroblasts have a characteristic spiky shape, with long sticky branches extending in all directions. In this region where silver ions had been driven by the current, many of the cells had changed to a static, globular form in which mitosis didn't occur. They seemed to be in suspended animation, floating freely instead of adhering to other cells or the sides of the dishes as usual. Mixed among them were many featureless cells with enlarged nuclei, the end products of dedifferentiation. More and more of the rounded fibroblasts turned into fully despecialized cells as the test progressed. Beyond the 5-millimeter line was a border zone with partial changes, followed by a realm of normal, spiky fibroblasts. Dedifferentiated cells normally divide rapidly, but these didn't, perhaps because they were sitting in a plastic dish far removed from the normal stimuli of an animal's body. Within a day after the current was turned off, the cells clumped together into bits of pseudo tissue that looked like the young "bone marrow" we'd seen in the exudate. After two weeks they'd all reverted back to mature fibroblasts, presumably because regular replacement of the nutrient medium had by then washed out all the silver 

To learn more about these astonishing changes, we studied pieces of the granulation tissue itself, taken from patients treated with the silver nylon. We placed the samples in culture dishes and observed them as they grew. Without the silver factor we would have expected a population of slowly proliferating fibroblasts. However, these cells grew fast, producing a diverse and surprising assortment of primitive forms, including fully dedifferentiated cells, rounded fibroblasts, and amoebalike cells. Strangest of all were giant cells that looked almost like fertilized eggs, very active and with several nucleoli. (The nucleolus is a "little nucleus" within the nucleus proper.) When other cells encountered the giant cells, the smaller cells often split open and emptied their nuclei into the giants. After two weeks these diverse cells had coalesced into an amorphous mass of primitive cells closely resembling a blastema, and in another week, as the silver washed out, they'd all become staid, sober fibroblasts acting as though nothing had happened. 

The major difference between the two experiments was that the second one started with cells that had already been exposed to positive silver ions in the human body. Their rapid growth and unspecialized forms suggested that the fibroblasts in the first experiment had in fact been dedifferentiated. It remains to be seen exactly what the various forms do, but it's obvious that in the aggregate they profoundly stimulate softtissue healing in a way that's unlike any known natural process. We ran a controlled study of the healing enhancement on pigs, their skin being physiologically closest to that of humans. Positive silver nylon accelerated the healing of measured skin wounds on the animals' backs by over 50 percent as compared with identical control wounds made on the backs of the same animals at the same time. 

We saw positive silver's life saving potential most clearly in our experience with a patient named Tom in 1979. Tom had had massive doses of X rays for cancer of the larynx, and his larynx later had to be removed. Because of the radiation, the surrounding tissue was helpless against infection, and the skin and muscle of his entire neck literally dissolved into a horrid wound. The ear, nose, and throat doctor treating him begged me to try the nylon, and I agreed after the attending physician got a release signed by the head of his department. After one month of electrified silver treatment, the infection was gone and healing was progressing, the wound healed completely in a total of three months, although Tom soon died from tumors elsewhere in his body. I reported this case at a small National Institutes of Health meeting that same year. One physician, who said he'd never heard of any comparable healing of such a grave wound, was moved to exclaim after seeing my slides, "I have witnessed a miracle!" 

We may only have scratched the surface of positive silver's medical brilliance. Already it's an amazing tool. It stimulates bone-forming cells, cures the most stubborn infections of all kinds of bacteria, and stimulates healing in skin and other soft tissues. We don't know whether the treatment can induce healing in other parts of the body, but the possibility is there, and there may be other marvels latent in this magic caduceus. Just before our research group was disbanded, we studied malignant fibrosarcoma cells (cancerous fibroblasts) and found that electrically injected silver suspended their runaway mitosis. Most important of all, the technique makes it possible to produce large numbers of dedifferentiated cells, overcoming the main problem of mammalian regeneration—the limited number of bone marrow cells that dedifferentiate in response to electrical current alone. Whatever its precise mode of action may be, the electrically generated silver ion can produce enough cells for human blastemas; it has restored my belief that full regeneration of limbs, and perhaps other body parts, can be accomplished in humans. 

Many questions remain, however. We don't know how the changed cells speed up healing or how the silver changes them. We don't know how electrically produced silver ions differ from ordinary dissolved ions, only that they do. They evoke widely different reactions from the fibroblasts, and the cells affected by dissolved ions close to the electrode are prevented from differentiating in response to the electrified silver. Most important is a search for possible delayed side effects. 

These questions urgently need research by some good electrochemists, but the work isn't being done. We were probably lucky we hadn't found this effect in our first round of lab tests on silver electrodes. The Food and Drug Administration let us test the antibacterial technique on selected patients because we found no toxicity and because a few hours a day was enough. To say that the same electrodes run for a longer time could stimulate healing was such a bold claim that permission probably would have been denied. At this point, however, we sorely need enough imagination on the part of research sponsors to follow up these leads in the laboratories, while making the treatment available now to the desperate few who have no other hope. 

The Fracture Market Where does all this leave us in our understanding of electrically triggered bone healing? I'm afraid we're not too much better off than the nineteenth-century doctors who lost this effective treatment because no one understood it well enough to defend it from electro-therapy's opponents. Of course, we have more pieces of the puzzle today, but we still don't have a complete picture of how any of the competing techniques work. 

Besides our low-current silver electrodes, there are two other basic types of bone growth stimulators. Friedenberg and Brighton at first placed their stiff stainless-steel wires through holes drilled into the bone near the break. Now a "semi-invasive" refinement is used in many patients—sticking the electrodes through the flesh into the fracture gap under local anesthetic; several may be needed for a large bone. They're connected to a self-contained battery pack set right into the cast. Friedenberg and Brighton patented their invention, and it's now approved by the FDA and marketed. About three fourths of the groups treating patients use some variation on this theme. 

Australian researchers under D. C. Patterson devised a spiral titanium electrode that's placed into a notch cut in the bone on both sides of the fracture. It's now also FDA approved and marketed. Since this device, battery pack and all, must be implanted and removed in two separate operations, and since the electrode usually must be left behind in the bone, late complications may occur. 

Others have taken a completely different approach, using pulsed electromagnetic fields (PEMF) to induce currents in the fracture area from outside the body. The best-known proponents of this method, Andrew Bassett and electrochemist Arthur Pilla, worked together at the Orthopedic Research Laboratories of Columbia-Presbyterian Medical Center in New York until 1982; Pilla is now at the Mount Sinai Medical Center. They developed a pair of electromagnetic coils sheathed in plastic pads, connected to a book-sized generator that plugs into a wall socket. 

Having experimented with a wide variety of pulsed fields, Bassett and Pilla found four that stimulate fracture healing. The one that works best, which is now also approved and available commercially, is produced by electromagnets driven by alternating current supplied in bursts of pulses. Although it ties the patient to an electrical outlet for twelve hours a day (mostly during sleep, of course), this apparatus completely avoids surgery and its attendant risks. 

The funny thing is that all three methods—low current, high current, and PEMF—seem to work equally well. Since the FDA approved them in late 1979, success rates have stabilized at about 80 percent. As far as the two electrode methods are concerned, I believe some experiments we did in 1977 and 1978 revealed why they both work. When we arranged all the reports in order from lowest current to highest, we found a narrow band of low amperages and a wide band of higher ones that worked, separated by a range in between that failed. We tested various non silver electrodes on animals and found that, at the effective currents, they all produced some electrochemical changes even at the negative pole. Among other products, they created various highly reactive ions called free radicals, essential in cellular chemistry but also destructive in excess. These radicals irritate cells, and, since any continuous irritation stimulates bone-forming cells to lay down new matrix in self-defense, we concluded that the higher-current methods worked primarily by such irritation. Conversely, I believe low-current silver electrodes stimulate bone formation directly—by differentiating the marrow cells and perhaps also by stimulating the periosteal cells. 

At first, PEMF research suggested that the coils worked by inducing in the tissues electrical currents that changed the permeability of cell membranes to calcium. In most nonunions at least a small amount of fracture callus has appeared, consisting of collagen fibers, but for some\ reason it hasn't entered the next stage, in which apatite crystals form on the fibers. Work by Pilla and Bassett suggested that the currents induced by the pulsed fields caused the cells of the callus to absorb large amounts of calcium. Later, when the coils were turned off, they reasoned, the cells dumped this calcium outside among the collagen fibers, and apatite crystals finally formed where they belonged. 

Their experiments raised the hope that other waveforms might regulate membrane passage of other ions or even control DNA transcription and protein synthesis. It seemed these field-induced currents might act as "vocal cords," allowing us to "speak" to the cell nucleus via the membrane, much as sound waves communicate with the brain via the ear. 

PEMF does in fact induce currents—of a type never found normally in the body. Each pulse produces millions of tiny eddy currents briefly flowing in circles. As the magnetic field expands at the beginning of a pulse, the currents circle in one direction; as it collapses, they reverse. However, the latest research has cast doubt on the idea that these currents affect specific cellular processes. Rather, it seems that artificial time-varying magnetic fields directly activate the cells by speeding up their mitotic rate, as discussed in more detail in Chapter 15. 

You may ask, "As long as something works, why quibble about how?" My answer is that understanding how is our best hope for using the tool right, without causing our patients other problems later. By sticking our own neologisms into the cell's delicate grammar, we automatically risk garbling it in unforeseen ways. 

As of now, we're like blind people crossing a minefield. Accelerated mitosis is a hallmark of malignancy as well as healing, and long-term exposure to time-varying electromagnetic fields has been linked to increased rates of cancer in humans. Bassett has discounted potential dangers, saying, "You would experience almost the same field strength by standing under a fluorescent light." However, a fluorescent lamp may well feel like a floodlight to cells that can see nano-amperes of current. One of the main lessons of bioelectromagnetism so far is that less is often more. 

On the other hand, it's too easy to assume that "natural is better." Since it would vindicate our low-current method, I obviously hope it's true, but the fact remains that putting electrodes in a bone is itself a very unnatural act. Stimulation of healing outside the normal limits of the process may incur fewer risks in the end. So far the evidence suggests otherwise, but we don't yet know for sure. That's why I keep emphasizing the need to go slowly, using these contraptions only when all else has failed, until we understand them better. 

The most urgent need is a search for possible malignant effects. As far as I know, I've done the only such research on electrodes to date—one simple tissue culture study without grant support, using some money I saved from our last research project funded by the manufacturer of the battery pack. I proposed more extensive tests to various granting agencies before our lab was closed, but was turned down every time. 

I exposed standard cultures of human fibrosarcoma cells to 360 nanoamps from stainless steel electrodes. I tried it five times, and each time there was a threefold increase in cell population at both electrodes. Even for cancer cells, this is remarkable proliferation for such a short time. To my knowledge, none of the developers or marketers of electrode devices have chosen to duplicate this test or try their own, despite the ease of doing the work and the fact that they have plenty of money. Whatever evidence on this point that may have been presented to the FDA hasn't been made public. After the evaluation panel granted commercial approval, however, several of its members expressed fears that this possibility hadn't been adequately tested. At this time, therefore, I must conclude that high-current electrodes might enhance the growth of any preexisting tumor cells in the electrical path—unlike low-current silver, which when negative had no effect on, and when positive suspended, mitosis of cancer cells in our lab. 

As for PEMF, Bassett and Pilla believe that only cells in a healing process gone awry can "hear" their waveform, so they discount the idea of cancel enhancement from it. They claim to have found no PEMFs that produce or accelerate malignant growth; on the contrary, Pilla and oncologist Larry Norton of Mount Sinai say they've found at least one that The Silver Wand 179 seems to inhibit it in lab animals. This claim is seriously flawed, however, because of the difference between subjecting an entire animal to a magnetic field, and directing the same field to a small area around a fracture (see Chapter 12). Moreover, in 1983, Akamine, a Japanese orthopedic researcher, reported that the pulsed magnetic fields used for bone healing dramatically increased the mitotic rate of cancer cells. The same fields inhibited the return of such "stimulated" cancer cells to a more normal state. Thus PEMF, like high-current treatments, apparently does enhance cancer growth. 

In the last decade or so, electro-biologists have learned a great deal about the effects of time-varying electromagnetic fields (as opposed to steady-state fields) on living tissue. We'll review these discoveries in Chapters 14 and 15. The evidence to date indicates that PEMF works by increasing the mitotic rate of the healing cells, not by altering calcium metabolism. If so, it can't possibly discriminate between bone-healing cells and any other type. It will accelerate the growth of any cellular system that is actively growing; this includes not only healing tissues, but fetal and malignant tissues as well. 

At the present rate of basic research, we won't have direct proof on whether electrical healing stimulators are nurturing seeds of cancer in humans until two or three decades from now. We could find out much sooner by simple experiments on animals having shorter life-spans. Until we have that definitive answer, I contend that all three techniques should remain available as a last resort to prevent loss of limb, but I'm appalled at their increasing use to speed up orthodontics or accelerate healing of fresh fractures. 

Unfortunately, the trend is away from caution. By the time this book is published, tens of thousands of patients will have been treated with the devices, many as a first, rather than last, resort. At a recent orthopedic meeting, I learned that four more companies are hoping to market new models. Several have asked me to advise them, but I haven't found one yet that wants to embark on any serious research. Without such a commitment, I refuse to take part in any battle of salesmen. I never even tried to patent the low-current silver method, because a medical device generally isn't considered patentable if the research that went into it was conducted throughout the scientific community and published for all to read. As I see it, the rush to the marketplace can only spawn jurisdictional disputes and ensure that important findings are kept as proprietary secrets. 

Electrical osteogenesis could be the opening wedge into a new era of medicine. Within a few years, we may know how to use these techniques to repair joint cartilage, or even replace whole joints, and to correct various defects of bone growth. In the further future, we may be able to extend regeneration as needed to nearly all human tissues. For the first time a physician can now direct nature, albeit in a small way, rather than play her helpless servant. We must use this power wisely. We're tapping into the most potent force in all of biology. If we're irresponsible about it, we risk another electrical letdown that could put off medicine's glorious future for many years.

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The Organ Tree 

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