Following his in-depth presentation on bone remodeling and bucked shins (see article #4066 at www.TheHorse.com), David M. Nunamaker, VMD, Dipl. ACVS, Jacques Jenny Orthopedic Surgery Chair at the University of Pennsylvania's New Bolton Center, continued the Milne State of the Art Lecture at the 2002 American Association of Equine Practitioners Convention with a focus on bone properties and fracture treatment in horses.
"Bone is a unique and fascinating material," he began. "People often think of bone as being relatively inert, but I'd like to dispel that concept. Modeling and remodeling can be occurring in the same bone at the same time--bone is always in all stages of remodeling. Bone does not heal, incorporating the scar tissue as seen in most all other tissues--it regenerates itself. It changes its shape and structure based on its use, and if broken can resume 100% of its former strength and function."
Nunamaker described in great detail and with many microscopic views the microstructure and modeling/remodeling processes of bone, beginning with bone composition--which includes osteogenic (bone-building) cells, organic matrix, and mineral. The cells include osteoblasts (which create new bone, are very metabolically active, and participate in matrix mineralization), osteoclasts (which resorb, or break down, bone), and osteocytes. The latter connect with other osteocytes and osteoblasts to cover more than 90% of mature bone matrix, forming a network that controls mineral exchange between bone and blood, and might act as chemical/mechanical transducers to initiate bone modeling or remodeling.
Osteoblasts follow osteoclasts when remodeling, building new bone in the resorbed cavities or depressions on the surface in the wake of osteoclast activity (see image here). "Since bone can only form on surfaces, resorption creates the surface on which the bone forms to replace itself," Nunamaker explained.
"Bone formation and resorption is a vascular phenomenon and does not occur without blood supply," he continued, noting that in the horse no osteocyte is more than 0.3 mm from a blood vessel. "Activation of osteoclasts may be influenced by physical activity and by drugs. For example, many of the non-steroidal anti-inflammatory drugs will decrease bone formation somewhat, and some osteoporosis drugs (used in humans and not yet available for the horse) slow down resorption. As we saw in the first presentation, working horses harder stimulates remodeling in response to particular stresses. The mechanism isn't yet fully understood, but the mechanical effect of stress is changed to a chemical effect that induces remodeling," he added. �Bone resorption will only occur after activation, and may appear in a non-uniform manner. Bone formation rates seem to be independent of physical activity, but can be modified by drugs." He expects that medications for influencing bone growth will hit the market in the next few years.
The new bone laid down will further calcify over time. Bone can be remodeled from within, creating new haversian systems (also called osteons, which can house small blood vessels, see images here), or it can be remodeled on its surface. A gouged appearance on the surface of a bone indicates remodeling. A primary example of surface remodeling for growth is the equine rib; as a foal grows, bone is resorbed from the inner surface of each rib and deposited on the outer surface, "to allow the foal's narrow chest to become the very large adult's chest cavity," Nunamaker explained (see image here).
The organic matrix component of bone consists of mostly collagen (a type of protein) and proteoglycans (protein-polysaccharide compounds) that constitute about one-third of bone's mass. The mineral component of bone, comprising about two-thirds of its mass, is calcium phosphate crystals deposited as hydroxyapatite. The stiffness of bone increases with higher calcium content, but fatigue life decreases (in other words, the stiffer the bone, the less resistant it is to bending and thus lower cycles to failure).
Various densities and porosities are characteristic of different types of bone; cortical or compact bone (the normal outer tubular layer of bone) has a density of about 1.85 g/cm3 and about 5% porosity, while trabecular or cancellous bone (found deeper within bones at ends and some spinal vertebral bodies) has a density of about 0.9 g/cm3 and a porosity of 20% or more. Trabecular bone forms about 20% of bone mass, and has metabolic activity about eight times that of cortical bone. It can compress a bit in response to stress via microfracture within the bone, thus avoiding larger fractures. "It might lose some connectivity, but the basic structure remains intact," Nunamaker explained. "It's Nature's way of maintaining structural integrity in high-load areas."
However, this trabecular bone compression can affect the overlying cartilage and thus hasten arthritis. "Though this phenomenon is not yet fully explained, its existence is well accepted," he said.
Properties of Bone
�Type 1 collagen combined with the mineral gives bone material properties that allow for limited deformation and a certain brittleness,� Nunamaker said of this composite material. �This is why bones bend, then break. The bending is related to the collagen phase, which has a very low modulus (stiffness), and the breaking is related to the mineral phase, that has a high modulus, which allows little deformation (up to 2% strain) before bone failure.
�Bone functions mainly as a support for the body,� he continued. �Bone is strongest in compression and weakest in tension. Bending forces produce tension on the convex (outwardly curved or bent) surface of the bone, hence bones are weak in bending. Torsion (twisting) forces will resolve into tension forces as well, so bones are also weak in torsion. Fatigue failure of bone may occur when bone is repeatedly loaded below its breaking strength.�
Fracture Healing
Different types of bone defects heal differently. For example, holes in a horse�s bone heal by first partitioning into smaller holes that are then filled. Very large holes might never fill in completely, he said. �However, the bone around these will remodel to even out the stresses,� he noted.
For the fracture lines most people think of when they think of broken bones, Nunamaker explained that healing depends on motion and distance between the fragments, which are affected by the strain on the area. Some degree of motion between fragments seems to aid formation of a callus (primary bone mass that is laid down to capture the ends of fragments, then calcifies into solid bone). However, too much motion from large strains prevents union of the fragments.
Following the healing process using plates and screws (in dogs), the new bone is strongest at about 20 weeks, Nunamaker said. However, it then tends to weaken a bit following plate removal from the initial resorption phase of remodeling before becoming even stronger. The same strengthening, weakening, then strengthening process is also seen when a fracture repair plate is removed; he explained that the loss of support of the plate increases stress on the bone, thus causing activation, remodeling, and decreased strength before remodeling. �The bone doesn�t return to its original strength at plate removal until eight to 12 weeks after removal,� he said. �Four to six weeks out is the weakest time.�
Fracture Repair
�Our problems (with fracture repair) in the horse relate to a 1,000-pound animal that is uncooperative and must have immediate full weight bearing to prevent catastrophic sequelae such as laminitis,� he explained. �Infection and pain management are additional significant problems that the surgeon must address with equine patients. Because amputation is not a suitable end result for most equine patients, euthanasia in horses replaces amputation in man.�
Nunamaker took his listeners through more than 30 years of the history of fracture treatment in horses, beginning with Jacques Jenny�s pioneering work using Swiss AO-ASIF (Arbeitsgemeinschaft f�r Osteosynthesefragen, or Association for the Study of Internal Fixation) principles.
�When a horse first stands up after surgery, his first step (on the repaired limb) opens the fracture a bit, then it�s a race between cycles to failure (of the plate) and fracture healing,� he said. Thus, veterinarians have worked hard to refine better fracture repair materials and methods. One of the most widely used has been plate luting.
Plate Luting for Strength
This technique augments rigid plate fixation of a fracture with polymethylmethacrylate (PMMA), an adhesive compound that hardens thoroughly and has sometimes used in hoof repair. The compound is placed between the plate and the bone, and between the screw head and the plate, to improve contact between bone and plate, stability, and fatigue resistance to cyclic loading (see image here).
�Plate luting has been used in our hospital at New Bolton Center to improve the outcome of plate fixation in equine long bone fractures since the 1980s,� said Nunamaker. �With plate luting, the screws were loaded as one and the bone or plate was the usual failure site (rather than individual screws, as is often the case without plate luting). This improvement showed that plate luting could increase the fatigue life of the implants by an order of magnitude (300-1,200%). That meant that the horse could walk on its internal fixation repair three to 12 times longer before implant failure with plate luting than without it. Presently, the use of plate luting is a standard technique in treating long bone fractures with plates. Use it whenever possible.�
Concerns about PMMA�s effect on the healing process of the bone it covers appear to be groundless; Nunamaker cited research that showed no significant difference in porosity of bone under the compound between horses with and without plate luting. �In the horse, plate luting appears to have a great mechanical effect in preserving the internal fixation during cyclic loading (weight bearing) without additional negative biological effects that would influence bone healing,� he said.
He recommended adding an antibiotic to the PMMA, but said that in the event of an infection beneath the compound, removal of the dead bone as well as the PMMA often takes care of the infection.
Nunamaker also discussed new fixation hardware that�s being used in humans, such as threaded screw heads for tighter anchoring of the screw to the plate as well as the bone. This hardware has not yet been used in horses and is quite expensive, although he said, �The concept of mechanically locked screws using a threaded interface between the screw and the plate should provide stronger and more certain stability than plate luting.�
External Skeletal Fixation
The thought of a horse in a �halo� rightfully strikes fear into many owners� hearts because of the potential for further injury as a horse catches the frame on another leg, bucket, etc. However, external skeletal fixation is not indicated for just any equine injury--only those where the horse couldn�t survive any other way.
�These fractures include badly comminuted (shattered) fractures, open fractures, or fractures with �bad skin� (damaged skin due to vascular compromise from bone fragments beneath it),� Nunamaker said. �To date, the results with fractures distal to (below) the carpus (knee) and tarsus (hock) are much better than treatment of proximal (higher) fractures by any transfixation method.
�With a P1 (long pastern bone) fracture, the P1-P2 joint always fuses,� he added. �A fracture involving the fetlock joint can be very problematic, however.�
Continuing his retrospective look at fixation techniques, he described the variable success and risks with pins encased in a plaster or fiberglass cast before going on to describe his work with an open fixator. This device, now in its third iteration, was presented at previous AAEP meetings in its earlier forms. The latest version (Model III) uses two 7.94-mm pins inserted horizontally through the cannon bone and anchored within tapered metal sleeves (new to Model III) to welded vertical supports on either side of the fractured leg for weight bearing (see image here). The vertical supports terminate in a walking plate at the ground, which allows the horse to move around by loading his weight onto the pin/fixator combination rather than the fractured area of the limb. This removal or reduction of weight bearing, along with the near total immobilization provided by gluing the hoof to the walking plate, allows the fractured area to heal with greatly minimized stress and without surgical fracture repair.
�The initial signs are very promising,� Nunamaker said. �You can take a horse that looked like he just wanted to die, and after you put this device on him, he gets right up, walks to his stall, and starts eating.� Also, he said, these horses can be shipped home for convalescence if the owner desires (after a three- to five-day observation period) rather than remaining in the hospital for long periods of time.
Numerical results are not yet available for the Model III fixator, only anecdotal data. However, the few cases that have been treated with this device have had none of the pin failure and new fracture at pin sites that Models I and II had. Out of 26 horses treated with Models I and II fixators, nine survived for a 35% success rate. Nunamaker noted that only two horses of the first 13 treated survived (15%), while seven of the next 13 survived (54%). Problems with Models I and II included fracture of MC3 at the pin site (either during use or during recovery following device removal), pin bending, and frame breakage.
�The loads to bone failure reported were an order of magnitude higher with this new system (Model III) than with the older configuration, and this device can hold about 19 times the horse�s body weight prior to bone failure,� he reported. The evolution of the latest design has involved varying numbers and diameters of pins, as well as different materials for the various components.
Unlike with previous models, �Pin failure has not yet occurred in the Model III fixator,� Nunamaker said. �Pin loosening may be controlled to some extent by periodic tightening of the sleeved pins that is easily accomplished.�
A non-bony advantage to this fixator is that it does not cover skin, allowing easy treatment of any skin injury (from an open fracture, for example). A cast would not allow this.
The device is usually left on for six to eight weeks, at which point the healing fracture is supported to a lesser degree by a cast or Robert-Jones bandage to allow some loading of the bone and promote calcification.
The holes remaining after fixator removal pose a valid concern. �The holes may never completely fill in,� Nunamaker said. �The bone may or may not be as strong as an intact bone without any holes in it. With this in mind, presently treatment of fractures with large-diameter external skeletal fixation pins should be reserved for animals that would not be expected to return to athletic pursuits.�
The Model III external fixator is commercially available through Ron Nash Engineering, Magnolia, Ark., who was heavily involved in the design and testing. It can be purchased for $725, a jig fixture kit (for applying the device and tightening pins) costs $600, and both usually ship within 24 hours (For more information, e-mail rane@magnolia-net.com or call 870/554-2236).
"Pool recovery has been very helpful (with the external fixator)," Nunamaker went on. "The horse wakes up in a sling, in a raft (with descending "sleeves" for the legs; see image here." Thus, any of the horse's sudden movements upon awakening meet only water, avoiding the risk of striking the floor or wall of a recovery stall and thereby undoing the surgeon's work. "This pool recovery system has been a great boon to fracture repair," he added. The fixator is now removed standing to avoid risking injury during another round of recovery from anesthesia.
"Success of fracture treatment has progressed to the point that decisions involving treatment are often related to financial decisions and not to our ability to save the individual's life," he concluded. "Euthanasia should no longer be thought of as a satisfactory treatment."
Disclaimer: Seek the advice of a qualified veterinarian before proceeding with any diagnosis, treatment, or therapy.