Pathophysiology of Bone Healing

Healing of a fracture terminates in the return of the injured bone to its original form.392 The process of fracture healing involves several biologic steps that overlap and interact with each other. Typically, three phases are recognized: inflammatory, reparative, and remodeling.392,393 The inflammatory phase occurs in the initial 2 to 3 weeks after bone fracture, and chemical mediators cause chemotaxis, migration of leukocytes, and vasodilation to the injured area. These mediators protect the injury from infection and stimulate angiogenic factors. Cytokines from platelets aid in angiogenesis and mesenchymal cell growth.392 Granulocytes and macrophages destroy invading bacteria and stimulate cell repair through the release of growth and angiogenic factors. If the inflammatory phase is impaired, fracture healing may be compromised.392

The reparative phase overlaps with the inflammatory phase and may last up to 12 months. This phase attempts to reestablish bone union. Interfragmentary stabilization by periosteal and endosteal callus formation begins if the fractured ends are not immobilized.393 Bony union develops as a result of endochondral and intramembranous ossification.392,393 In the reparative phase, interfragmentary motion may greatly influence fracture healing.

The remodeling phase takes place both during and after the reparative phase. Osteonal remodeling allows for replacement of the necrotic regions of bone. When the bone is loaded, the negatively charged concave surface will attract osteoblasts to add new bone, and the positively charged convex surface will attract osteoclasts to remove bone.392,393 The result is the ability of a fractured bone to straighten itself by creating new bone formation on the concave surface and removing bone from the convex surface.

Repair of a fractured bone with the use of rigid internal fixation will inhibit the naturally occurring callus formation and encourage bone to heal through haversian remodeling. Haversian remodeling requires that a fracture be rigidly fixed, have adequate reduction, and have an adequate blood supply.392,393 Haversian remodeling then functions to revascularize necrotic bone at the fragmented ends of the fracture and bridge interfragmentary gaps. This form of remodeling begins 2 to 3 months after injury.

Fractured bones are often described as healing by primary (direct) or secondary (indirect) intention.389,392,393 Primary bone healing only occurs with complete anatomic reduction and rigid stability. In large animal fracture repair, this is difficult to achieve because of the size of the animal and micromotion at the repair site.389 Secondary bone healing utilizes endosteal and periosteal callus formation, and new bone formed at the fracture site develops after initial formation of fibrous tissue or fibrocartilage.392,393

The rate of bone healing may be decreased if blood supply is inadequate, infection is present, soft tissue damage is extensive, or stability of the bone fragments is inadequate.

Treatment and Prognosis

Treatment options for fractures in large animals include conservative therapy with stall rest and external coaptation (casts, splints) and surgical stabilization with open reduction and internal fixation. It is important to recognize incomplete and stress fractures in order to manage them appropriately with conservative therapy, preventing progression to a catastrophic fracture. The majority of fractures require some form of stabilization for the best chance of a successful outcome. Most horses require surgical stabilization for successful fracture repair. Ruminants are more amenable to successful fracture repair with nonsurgical options.389

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Conservative therapy with stall rest and external coaptation may be successful in some foals and calves with complete, nondisplaced fractures. Young animals have a greater and faster ability to heal bone in a reasonable amount of time, and their body weight is much less than that of a mature animal. In foals and calves, the fracture configurations tend to be simpler, and the surgical implants available for repair are of a suitable strength compared to the animal’s size. Complications in young animals include closure of a physes with fractures in these areas, infection, and angular limb deformities from overuse of the contralateral limb.

In adult animals, it is more common to identify severely comminuted fractures due to the large force needed for bone breakage. Proximal limb fractures in an adult horse are often unable to be successfully treated because severe comminution of the bone occurs, implants are not strong enough to support the bone until it is healed, these horses are less likely to protect the limb, and laminitis formation in the contralateral limb is a common complication. Stall rest with external coaptation alone is rarely associated with a good outcome, and most horses require some form of internal fixation for success. Horses are often required to be athletes, and fracture repair resulting in survival, but not soundness, may be unacceptable. In general, ruminants have a better prognosis for survival than horses because of their less excitable temperament, and complete soundness is often unnecessary for a successful outcome. External fixation may be more successful in ruminants than external coaptation because it provides increased stability and costs less than internal fixation.389 Open fractures in horses greatly decreases the prognosis for survival and may delay the ability to perform internal fixation. In ruminants, open fractures are less common but also carry a poorer prognosis.

Implants used for surgical open reduction and internal fixation methods vary based on the specific bone involved, the animal’s age, the strength of the bone fragments used in the repair, and the surgeon’s preference. Common implants used in large animals include intramedullary (IM) interlocking nails, dynamic compression plates (DCPs), locking compression plates, limited-contact DCPs, screws, wires, pins, and dynamic condylar screw plates. Table 38-6 lists specific treatment options and prognoses.391

Table 38-6 Treatment and Prognosis for Large Animal Fractures

image

HUMERUS

The humeral fracture is often in a spiral or long oblique configuration. In ruminant and equine species, both conservative and surgical treatments have been used. In foals, surgical repair may include the use of IM interlocking nails, DCPs, or IM nails. Prognosis for a closed fracture in a foal is fair to good and depends on configuration, age, and weight.394,395 Humeral fractures in adult horses are not reparable at this time. Conservative treatment may be successful in adult horses with nondisplaced fractures and has been used in small ruminants and foals with acceptable outcomes. Ruminants have a better prognosis in general than equine species.389

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RADIUS

Survival rates for ruminants with radial fractures repaired by external or internal fixation have been reported as 86%.396 Radial fractures in foals repaired with internal fixation have a good prognosis; however, in adult horses the success rate is poor.397 Animals with incomplete fractures that do not progress have a good prognosis for a full recovery.

OLECRANON

There are several different fracture configurations, and the olecranon fracture may be articular or nonarticular. These fractures are common in both young and older horses. Surgical and conservative treatments have been used with success, although internal fixation is the preferred treatment method.398,399 Typically, the fracture is repaired with a DCP applied as a tension band. The prognosis with surgical repair is good, with 62%, 75%, and 87% of horses returning to athletic use, depending on the fracture type.398-400 Conservative treatment has been reported to result in a 73% return to soundness.401

FEMUR

Diaphyseal fractures are more common in calves, whereas proximal physeal fractures are more common in foals.389 Femoral fractures in calves may occur during parturition events. In young calves, these fractures have been repaired by internal fixation and femoral head and neck osteotomies with success. In foals, fracture repair with internal fixation gives the best chance of survival, and the use of IM interlocking nails has shown positive results.402 Femoral fractures in adult horses are not reparable at this time.

TIBIA

Ruminants sustaining tibial fractures have been repaired using splints, external fixators, transfixation pin casts, and DCPs. Fractures repaired with external fixation in adult cattle had a 64% success rate, versus conservative therapy success at 44%.403 Internal fixation is the repair method of choice in horses. Foals have a fair to good prognosis for survival. Adult horses have a poor prognosis for survival because tibial fractures are often open, have limited blood supply, and are often severely comminuted.

METACARPUS/METATARSUS

In cattle, these fractures are common and have a good prognosis when treated with internal fixation, casts, or transfixation pin casts.389 Calves may incur distal physeal fractures after forced extraction during a dystocia, and these may be casted with good success. In horses, cannon bone fractures are frequently open because of a lack of soft tissue coverage. Treatment options include internal fixation with DCPs and screws or transfixation pin casts. One study reported a 67% success rate with surgical repair.404

PHALANGES

In ruminants, fractures of the proximal or middle phalanx are treated with reasonable success by applying a block to the uninjured claw or by cast application. In horses, proximal and middle phalangeal fractures have been treated by internal fixation with screws and DCPs. Prognosis for survival is good, but return to athletic function depends on the degree of osteoarthritis that develops after fixation. One review of proximal phalangeal fractures in racehorses reported that 61% to 75% were able to race.405 Prognosis for comminuted middle phalangeal fractures repaired with proximal interphalangeal joint arthrodesis is 50% for forelimbs and 80% for hindlimbs.389 Severely comminuted fractures may also be treated with transfixation pin casts or the Nunamaker external skeletal fixator. Fractures of the distal phalanx in horses may be successfully treated with surgical fixation, hoof casts, or modification in shoeing, depending on fracture configuration.406

SUMMARY

Animals identified with incomplete fractures should be treated conservatively with stall rest and should be tied to prevent them from lying down if the fracture is at risk of becoming complete (e.g., radius). Animals with stress fractures should be treated conservatively with stall rest and a careful rehabilitation program, with ongoing radiographic evaluation.

Many fractures in large animals are able to be repaired and allow survival of the animal. Prognosis in general is better if the animal is young, it weighs 500 pounds (225 kg) or less, the fracture is closed, appropriate emergency stabilization is implemented, and prompt reduction and stabilization are performed.

SPONTANEOUS FRACTURES IN RUMINANTS

JOHN MAAS

Definition and Etiology

Spontaneous fracture of bone is a syndrome that occurs when underlying bone disease weakens bone(s) to the point where otherwise normally applied stresses result in bone failure. The terms spontaneous fracture and pathologic fracture are synonymous for clinical usage. Fractured bones typically include (1) long bones of the limbs, (2) vertebrae, (3) ribs, and occasionally (4) the mandible or pelvic bones.

Clinical Signs and Differential Diagnosis

Clinical signs of postural deformity, swelling, and lameness are observed, with bone fracture resulting from minimal or no apparent stress. Thorough physical examination often reveals additional fractures that are in the process of healing, particularly of the ribs and long bones. A fracture that occurs in normal bone in response to applied stress is the main differential diagnosis.

Pathophysiology, Epidemiology, and Clinical Pathology

The specific causes of spontaneous fractures in ruminants are varied and include pathologic processes that affect the tensile strength of bone. Although spontaneous fractures are not common, certain disease processes predispose animals to this condition, including (1) tumors affecting individual bones, (2) osteomyelitis, (3) rickets (osteodystrophy) in young ruminants, (4) osteomalacia in adult ruminants, and (5) osteoporosis associated with copper deficiency.

The effect of localized infection or tumor growth is to weaken bone tissue by dissolution of the mineral matrix. More common tumors causing bone weakness and fracture include lymphosarcoma and primary bone tumors in ruminants. Osteomyelitis, as a primary condition or as an extension from septic arthritis, can severely affect the strength of bone over time. Osteomyelitis causing pathologic fractures can be associated with wounds or can occur in diseases such as actinomycosis.

Rickets in young, growing animals occasionally can result in spontaneous fractures of long bones and vertebrae. Osteomalacia in adult ruminants is caused by the same factors that result in rickets in young, growing livestock. As in young ruminants, the cause of osteomalacia is most often a deficiency of phosphorus or vitamin D. Calcium deficiency (primary or secondary), however, can be involved in the pathogenesis. Individual uremic animals may develop osteomalacia and spontaneous fractures from a lack of active vitamin D (1,25-dihydroxycholecalciferol). The pathogenesis of osteomalacia in the adult differs from that of rickets, in that mature and well-mineralized bone is removed and replaced by inadequately mineralized organic matrix. Therefore, radiographic and histologic examination of osteomalacic bone occasionally reveals signs of osteoporosis. Osteomalacia of the metaphysis and epiphysis is less prominent than with rickets. Spontaneous fractures associated with osteomalacia are usually accompanied by pica, skeletal deformities, and hypophosphatemia.

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Copper deficiency can be caused by a lack of adequate dietary copper (primary) or a relative excess of sulfates and molybdenum (secondary), which bind copper and make it unavailable for metabolism, resulting in osteoporosis407 (see Chapter 37). The biochemical mechanism of bony lesions in copper deficiency is unknown; however, lysyl oxidase, a copper-containing metalloenzyme, may be involved. Copper deficiency can be a significant cause of lameness even without spontaneous fractures.408,409 Radiographic and histologic findings in affected bones of lame, copper-deficient ruminants are similar to those seen with rickets.410 Copper-deficient ruminants can also exhibit signs of anemia, achromotrichia, alopecia, diarrhea, poor growth, decreased feed efficiency, osteoporosis, and sudden death. Diagnosis of copper deficiency can be made when serum or plasma copper concentration is less than 0.5 μg/mL (ppm) or when hepatic copper concentration is less than 35 μg/g on a dry-weight basis. Differentiating primary from secondary copper deficiency requires the analysis of diet and water. In my experience with spontaneous fractures associated with copper deficiency, two additional findings are frequently seen: (1) concurrent selenium deficiency and (2) hypophosphorosis with adequate dietary calcium. Syndromes seen in the field may be more complicated than we currently understand.

There are a number of possible causes of spontaneous fractures in ruminants. Factors that might affect a group of animals include dietary deficiencies of phosphorus, calcium, copper, and trace minerals (Se, Mn, Zn); mineral (Ca, P, Mg) imbalances; indoor housing (vitamin D deficiency); protein deficiency (osteoporosis); rapid growth; lactation; and advanced pregnancy. The differentiation of spontaneous fractures from other causes of bone fractures is made by history, physical examination, and identification of one or more associated conditions mentioned previously.

Treatment and Prevention

Treatment of spontaneous fracture is similar to that of common orthopedic problems caused by trauma. In addition, the underlying condition(s) must be corrected. Although the prognosis must be considered guarded or poor, I have examined recovered and ambulatory cattle with multiple healing rib fractures and two healing long-bone fractures. With spontaneous fractures associated with osteomalacia, rickets, and osteoporosis caused by copper deficiency, the animals’ ability to heal is remarkable. Prevention of spontaneous fractures depends on identifying and correcting all underlying problems.

BUCKED SHINS AND STRESS FRACTURES OF THE METACARPUS IN THE HORSE

SUSAN M. STOVER

Definition and Etiology

Bucked shins and stress fractures are the acute and chronic manifestations of disease of the dorsal cortex of the third metacarpal bone. Bucked shins is a painful condition most often involving the middiaphyseal dorsal cortex of 2-year-old and occasionally 3-year-old horses in their first year of race training.

Stress or fatigue fractures are incomplete fractures located in the mid-diaphyseal dorsal cortex and less often in the distal diaphyseal dorsal or dorsolateral cortex. These fractures are seen most frequently in 3-year-old horses but can also affect 2-year-old horses later in the racing season and, with decreasing numbers, older horses.

Bucked shins and stress fractures are occupational diseases of horses in race training. These conditions are more prevalent in young horses training at fast speeds on dirt surfaces than in older horses or horses training on grass surfaces.

Clinical Signs and Differential Diagnosis

A general pattern of clinical signs was observed in one study of 2-year-old thoroughbred horses in race training.411 Bucked shins usually occurred bilaterally. Both metacarpi usually were affected simultaneously, although occasionally one was affected several days before signs were observed in the contralateral metacarpus. In most horses the first clinical indication of bucked shins was a painful response to palpation of the metacarpus. Subtle pain often was found before the detection of an unwillingness of the horse to work at fast speed. Lameness was not necessarily manifested by affected horses.

Pain usually was localized to the dorsal aspect of the middiaphysis or near the junction of the proximal and middle thirds of the diaphysis. Initially, pain was mild and elicited from a diffuse area. With continued training, soft tissue thickness became palpable, and diffuse swelling became visible on the dorsum of the metacarpus. Later, soft tissue thickness and swelling became more focal unless hard work was continued. Approximately 2 to 3 weeks after pain first was detectable, discrete hard swellings could be palpated on the dorsum of the metacarpus. Radiographic abnormalities often are absent in horses with acute bucked shins.412 The dorsal cortex thickens during adaptation to the stresses associated with training,413 but indistinct periosteal proliferation, subperiosteal demineralization,412 or subperiosteal radiolucencies support a diagnosis of bucked shins. Even in the absence of radiographic abnormalities, bone scintigraphy demonstrates a diffuse region of intense radiopharmaceutical uptake in the dorsal cortex of affected horses414 (Fig. 38-43).

image

Fig. 38-43 A, Lateromedial radiograph, and B, lateral scintigram, of the third metacarpal bone of a horse with bucked shins. Although dorsal cortical thickening is present, distinct radiographic changes associated with acute metacarpal disease cannot be detected. However, diffuse exaggerated radiopharmaceutical uptake is demonstrated in the dorsal cortex.

Courtesy P.D. Koblik.

Differential diagnoses include cellulitis, periostitis, and osteitis of traumatic or infectious origin, although these conditions are much less common in the racehorse population. Signs of external trauma or infection (e.g., elevated temperature, wound drainage) may be present with these other conditions.

Incomplete cortical fractures occur approximately five times more frequently in the left than in the right metacarpus.411,415 Left metacarpal fractures occur more often in the mid-diaphysis than in the distal diaphysis; however, in one study a large proportion of right metacarpal fractures occurred in the distal diaphysis.411 Horses with incomplete cortical fractures are more likely to be examined because of lameness of the affected leg(s) than horses with bucked shins. Lameness, which may be marked after activity, usually subsides within a few days.415,416 With chronicity a discrete, hard tissue enlargement is visible and palpable overlying the fracture. Focal pain usually can be elicited by digital palpation of the enlargement.

Incomplete cortical fractures may be detected radiographically; however, not all fractures can be visualized. Fracture lines usually extend in a proximopalmar direction from the periosteal surface of the dorsal cortex at a 30- to 45-degree angle to the dorsal cortical surface (Fig. 38-44, A). Occasionally, fractures extend in a distopalmar direction from the periosteal surface, and less frequently a saucer-shaped fragment is noted within the dorsal cortex. Fractures rarely appear to course completely to the endosteal surface of the dorsal cortex. In the absence of a radiolucent fracture line, a localized periosteal or endosteal reaction is highly indicative of an incomplete cortical fracture. Alternatively, occult fractures may be identified with bone scintigraphy by intense focal accumulation of radiopharmaceutical414 (Fig. 38-44, B).

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Fig. 38-44 A, Lateromedial radiograph, and B, lateral scintigram, of the third metacarpal bone of a horse with an incomplete cortical fracture (arrow) associated with focal, intense radiopharmaceutical uptake.

Courtesy P.D. Koblik.

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Differential diagnoses for stress fractures include traumatic periostitis or osteitis and osteomyelitis. Radiographic findings and clinical signs of external trauma are helpful diagnostically.

Pathophysiology

Bucked shins are believed to result from cumulative microscopic damage within the dorsal cortex of the third metacarpal bone. Microdamage results from excessive strain (i.e., deformation) of young, developing metacarpal bones during training at fast speeds on hard surfaces.

Although third metacarpal bones of 2- to 3-year-old horses have attained adult length, the bone continues to adapt to the increased stresses of race training by enlarging in diameter and replacing intracortical bone through internal remodeling. These processes strengthen the metacarpal bone by increasing its resistance to deformation, decreasing its susceptibility to microdamage with repeated loading, and repairing microdamage. Adaptation usually is completed by 3 to 4 years of age and accounts for the lower incidence of bucked shins and stress fractures in older horses.

If accumulated microdamage with continued training exceeds adaptive and remodeling processes of the metacarpal cortex, bucked shins or chronically incomplete cortical fracture may become clinically and radiographically evident. Because fractures result from accumulation of damage caused by repetitive loading, they are often referred to as “fatigue” fractures. Evidence indicates that the direction of maximum strain on the surface of metacarpal bones changes with a shift from training to racing gaits.417 Because bone adapts by responding to the magnitude and direction of strain encountered, adaptation during training (i.e., trot and slow gallop) is probably different from that occurring during racing (i.e., racing gallop). Thus, metacarpal bones that have adapted to training may not adapt well to the strains of racing and may incur significant microdamage during initial exercise at racing speeds.413

Epidemiology

The incidence of bucked shins in 2-year-old thoroughbred racehorses is approximately 70%,415 occurring most often during the first year of race training. With continued training, horses with cortical microdamage develop stress fractures, which are most common in 3-year-old horses.

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The incidence of bucked shins and stress fractures is lower in quarter horse and standardbred racehorses than in thoroughbreds. The high incidence in thoroughbred horses may be associated with running long distances at the racing gallop.418 Thoroughbred horses are subjected to more high-stress loading cycles than quarter horses running shorter distances or than standardbred horses trotting or pacing. Therefore, thoroughbred horses are more likely to accumulate clinically significant amounts of cortical microdamage.

Necropsy Findings

Bucked shins and incomplete cortical fractures may be found incidentally on postmortem examination of racehorses. Callus may be evident on the periosteal surface. Cross sections of the bone may disclose an incomplete cortical fracture or endosteal bony proliferation. Histologic examination usually reveals an indistinct fracture line characterized by marked bone resorption.419

Treatment and Prognosis

Treatment of bucked shins varies with the degree of pain and the decrease in the performance of affected horses. On palpation, mildly and moderately affected horses exhibit resentfulness and mild soreness, which disappears within 2 to 4 days.420 Training should be continued, but at a slower pace, to promote continued adaptation of bone to the stress of racing and to prevent the accumulation of additional microdamage. In severely affected horses, pain remains evident after 1 week of rest. These horses may require complete rest for a minimum of 3 months before they can be returned to training. After a horse has recovered from bucked shins, the prognosis is good for return to training, although the condition will recur in severely affected horses that were not rested for long enough before their return to training and in horses whose exercise intensity was accelerated too rapidly on return to training.

Many adjunctive therapies, including pin firing, cold therapy, and electrostimulation, also are frequently used. Their effectiveness, however, is difficult to assess without considering concurrent training or rest therapy. Horses with incomplete cortical fractures must be rested for a minimum of 3 to 6 months. Most rested horses show radiographic evidence of bone healing and can be returned to training. Some chronic fractures are refractory to rest alone. Occasionally, returning these horses to light exercise stimulates fracture healing. Alternatively, interfragmentary drilling has resulted in better healing of fractures with fewer adverse effects than lag screw fixation. After interfragmentary drilling and adequate rest (e.g., 3 to 6 months), the prognosis is good for return to racing. Without an apparent relationship to type of treatment, however, incomplete fracture recurs in some horses.

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Prevention

Factors in the prevention of bucked shins and stress fractures include training regimen, racetrack surface, and shoeing. In general, a training program should gradually increase the degree of exercise, allowing time for concurrent bone adaptation, and should subject the metacarpus to similar strains encountered during racing.413 Experimental evidence suggests that the metacarpus would have to encounter the strain associated with racing stress only for short duration a few times per week to stimulate the appropriate adaptive response.421 The effect of exercise on bone adaptation and remodeling is under active investigation. Hard racetrack surfaces are associated with a higher incidence of bucked shins than softer surfaces.422 The stresses and strains incurred by the metacarpus probably can be modified by changing the character of the racing surface or the horseshoe.

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397 Sanders-Shamis M, Bramlage LR, Gable AA. Radius fracture in the horse: a retrospective study of 47 cases. Equine Vet J. 1986;18:432.

398 Swor TM, Watkins JP, Bahr A, Honnas CM. Results of plate fixation of type 1b olecranon fractures in 24 horses. Equine Vet J. 2003;35:670.

399 Swor TM, Watkins JP, Bahr A, et al. Results of plate fixation of type 5 olecranon fractures in 20 horses. Equine Vet J. 2006;38:30.

400 Denny HR, Barr AS, Waterman A. Surgical treatment of fractures of the olecranon in the horse: a comparative review of 25 cases. Equine Vet J. 1987;19:319.

401 Wilson DG, Riedesel E. Nonsurgical management of ulnar fractures in the horse: a retrospective study of 43 cases. Vet Surg. 1985;14:283.

402 McClure SR, Watkins JP, Ashman RB. In vivo evaluation of intramedullary interlocking nail fixation of transverse femoral osteotomies in foals. Vet Surg. 1998;27:29.

403 Martens A, Steenhaut M, Gasthuys F, et al. Conservative and surgical treatment of tibial fractures in cattle. Vet Rec. 1998;143:12.

404 McClure SR, Watkins JP, Glickman NW, et al. Complete fracture of the third metacarpal or metatarsal bone in horses: 25 cases (1980-1996). J Am Vet Med Assoc. 1998;213:847.

405 Holcombe SJ, Schneider RK, Bramlage LR. Lag screw fixation of non-comminuted sagittal fractures of the proximal phalanx in racehorses: 59 cases (1973-1991). J Am Vet Med Assoc. 1995;206:1195.

406 Bertone AL. Fractures of the distal phalanx. In: Nixon AJ, editor. Equine fracture repair. Philadelphia: Saunders, 1996.

407 Suttle NF, Angus KW, Nibet DI, et al. Osteoporosis in copper-depleted lambs. J Comp Pathol. 1972;82:93.

408 Cymbaluk NF, Schryver HF, Hintz HF. Copper metabolism and requirement in mature ponies. J Nutr. 1981;111:87.

409 Smith BP, Fisher GL, Poulos PW, et al. Abnormal bone development and lameness associated with secondary copper deficiency in young cattle. J Am Vet Med Assoc. 1975;166:682.

410 Irwin MR, Poulos PW, Smith BP, et al. Radiology and histopathology of lameness in young cattle with secondary copper deficiency. J Comp Pathol. 1974;84:611.

411 Stover SM. Dorsal metacarpal disease in thoroughbred horses: relationship to the development of the third metacarpal bone. [PhD Thesis]: University of California, Davis, 1987.

412 Norwood GL, Haynes PF. Dorsal metacarpal disease. In: Mansmann RA, McAllister ES, editors. Equine medicine and surgery. ed 3. Santa Barbara, Calif: American Veterinary Publications; 1982:1110.

413 Nunamaker DM. Personal communication. 1987.

414 Koblik PD, Hornof WJ, Seeherman HJ. Scintigraphic appearance of stress-induced trauma of the dorsal cortex of the third metacarpal bone in racing thoroughbred horses: 121 cases (1978-1986). J Am Vet Med Assoc. 1988;192:390.

415 Norwood GL. The bucked-shin complex in thoroughbreds. Proc Am Assoc Equine Pract. 1978;24:319.

416 Richardson DW. Dorsal cortical fractures of the equine metacarpus. Compend Cont Educ (Pract Vet). 1984;6:S248.

417 Nunamaker DM, Butterweck DM, Black J. Fatigue fractures in thoroughbred racehorses: relationship with age and strain. Trans Orthop Res Soc. 1987;33:72.

418 Nunamaker DM. The bucked shin complex. Proc Am Assoc Equine Pract. 1987;32:457.

419 Pool RR. Personal communication. 1987.

420 Arthur R. Personal communication. 1988.

421 Rubin CT, Lanyon LE. Regulation of bone mass by mechanical loading: the effect of peak strain magnitude. Calcif Tissue Int. 1985;37:411.

422 Moyer W, Spencer PA, Kallish M. Relative incidence of dorsal metacarpal disease in young thoroughbred racehorses training on two different surfaces. Equine Vet J. 1991;23:166.

* Bob Rutherford: Personal communication, 1988.

Stormont Laboratories, 1237 East Beamer St, Woodland, CA.

Genetics Lab, School of Veterinary Medicine, University of California, Davis, CA.

* Garamycin Sponge, Essex Chemie AG, Luzern, Switzerland.

Self-tapping infusion bone screw, Mercury Orthopedics, Chesterfield, MI.

Elastomeric pump, Syringe pump, Mila International, Florence, KY, http://www.milaint.com

* Banamine, Schering Plough Animal Health, Union, NJ.

* Modified Ultimate, Nanric, Inc., Lawrenceburg, KY.

Advanced Cushion Support, Nanric.

Therapeutic Equine Products, Indianapolis, IN.