Basic Mammalian Bone Anatomy and Healing

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ORTHOPEDICS 10949194/02 $15.00 .00

BASIC MAMMALIAN BONEANATOMY AND HEALING

Dianne Dunning, DVM, MS, DACVS

To fully appreciate bone anatomy and healing in birds one musthave an understanding of mammalian bone, because avian and mamma-lian skeletal systems have more similarities than differences in structureand function. Both skeletal systems provide a rigid and protective frame-work for most of the soft tissues and internal organs while providing ascaffold for tendon and ligament attachments.4, 15, 18 Additionally, boneserves as an important storehouse for calcium and phosphorus and as asite for fat storage and hematopoiesis.4, 18

BONE COMPOSITION

Bone is a specialized form of connective tissue that consists of amatrix, minerals, and cells. Biochemically, it is a blend of organic (35%)and inorganic (65%) material.4 The inorganic or mineral componentconsists of calcium hydroxyapatite crystals (Ca10[PO4]6[OH]2), which givebone its strength and rigidity and serve as a reservoir for 99% of thebodys calcium, 85% of the bodys phosphorus, and 65% of the bodys

sodium and magnesium.4 The structure and composition of individualbones provide the maximum resistance to mechanical stresses whilemaintaining the least bone mass.25 To accommodate changing mechanicaltresses and the demands of calcium and ion homeostasis, all bones inthe body are in a dynamic state of growth and resorption throughoutlife.2, 4, 18 Avian bones have a higher calcium content (e.g., 16.42% in

From the Department of Clinical Medicine, University of Illinois, College of Veterinary

Medicine, Urbana, IL

VETERINARY CLINICS OF NORTH AMERICA:EXOTIC ANIMAL PRACTICE

VOLUME 5 NUMBER 1 JANUARY 2002 115


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chickens) than do mammalian bones (10%), which may contribute to thethin and brittle nature of avian bones.12, 19, 21 Biomechanical studies inbreeder chickens have revealed that bone density and strength increase

with age, which may be related to increases in inorganic content andcollagen.17

The organic component of bone consists of cells and an extracellularmatrix.2, 4 The cells consist of osteoblasts, osteocytes, and osteoclasts.2, 11

Osteoblast and osteocytes are mesenchymal in origin and are calledosteoprogenitor cells.2, 4, 18, 25 Osteoblasts are immature bone cells that areresponsible for the synthesis and secretion of osteoid, an organic compo-nent of the extracellular matrix of bone.2, 4 Osteoid rapidly undergoesmineralization to form bone.2, 4, 18, 28 The osteoblasts become entrappedwithin the secreted matrix and differentiate into osteocytes. Osteocytes

make up most of the bone cell population in adult animals and areresponsible for the maintenance of the bony matrix. Osteoclasts aremultinucleated cells that are derived from the macrophagemonocytefamily and are involved actively in the resorptive process associatedwith the continuous remodeling of bone.2, 4, 18, 25

The extracellular matrix consists of a ground substance composedof glycoproteins, proteoglycans, and collagen fibers and is mineralized.The glycoproteins and proteoglycans are highly anionic complexes thathave a high ion-binding capacity and are thought to play an importantrole in the mineralization of bone and in the fixation of the calcium

hydroxyapatite crystals to the collagen fibers.14

Type 1 collagen forms thebackbone of the matrix and accounts for 90% of the organic component.4

Osteoblasts deposit type 1 collagen in either a random or lamellarfashion, depending on whether the bone is trabecular or lamellar innature.4 Noncollagenous proteins make up the remainder of the organicmatrix of bone in the form of cell-adhesion proteins, calcium-bindingproteins, mineralization proteins (osteocalcin), enzymes, cytokines, andgrowth factors (Table 1).4 Of these proteins, osteocalcin is the onlyprotein that is unique to bone.4

STRUCTURE OF BONE

There are two types of bone: cortical and cancellous bone. Corticalor compact bone forms the dense walls of the shaft or diaphysis and isthe outer protective covering of all bone.15, 25 Compact bone is made upof columns of bone that are parallel to the long axis of the diaphysealshaft and to the stresses exerted by the normal weight bearing of thebone.4, 14, 18, 19, 25 Each of the columns is composed of concentric layers ofbone, known as lamellae, centered around neurovascular channels re-

ferred to as Haversian canals.4, 14, 18, 19, 25 The neurovascular canals andtheir concentric lamellae are referred to commonly as Haversian system(Fig. 1).4, 14, 18, 19, 25 Between each Haversian system are interstitial lamellae,which further support the infrastructure of cortical bone.4, 14, 18, 19, 25

Haversian canals develop from broad channels lined with osteo-


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BASIC MAMMALIAN BONE ANATOMY AND HEALING 117

Table 1. BONE MATRIX PROTEINS

Protein Class Example Function

Collagen Type 1 Serves as a structuralscaffold2, 18

Cell-adhesion proteins Osteopontin, fibronectin, Mediates cellular adhesivethromboplastin interaction; provides

collagen crosslinks andplatelet aggregation

Calcium binding proteins Osteonectin, bone Mediates calcium bindingsialoprotein

Mineralization proteins Osteocalcin Marker of osteoblasticactivity18

Enzymes Collagenase, alkaline Collagenase catalyzes thephosphatase hydrolysis of peptide

bonds in collagen;alkaline phosphatasecatalyzes the release ofinorganic phosphatefrom phosphoric esters

Growth factors IGF-1, TGF-, IL-6 Control bone cellproliferation,maturation, andmetabolism and act ascellular messengers4

Cytokines Prostaglandin, IL-1, IL-6 Activate proteolyticenzymes important forcture healing18; act ascellular messengers4

Adapted fromContran RS, Kumar V, Collins T: Bones, Joints, and Soft Tissue Tumors. In ContranRS, Kumar V, Collins T (eds): Robbins Pathologic Basis of Disease. Philadelphia, WB Saunders, 1999,pp 12161267; with permission.

blasts. The osteoblasts produce osteoid, which later is mineralized andforms the concentric lamellae. With the deposition of each successivelamellae, the channel narrows and the osteoblasts that become entrapped

in lacunae are called osteocytes, which are arranged in concentric ringswithin the lamella. The osteocytes maintain fine cytoplasmic extensionsto neighboring osteocytes via minute interconnecting channels knownas canaliculi (Fig. 2). The canaliculi provide passages for the circulationof tissue fluid and the diffusion of metabolites and allow rapid commu-nications between osteocytes. Osteocytes are responsible for maintainingcalcium homeostasis via the resorption and uptake of mineralized ma-trix. Calcium levels within the body are influenced directly by a negativefeedback system based on serum calcium concentration and indirectlycontrolled by hormones that are secreted by the parathyroid and thyroid

glands.18, 25There have been limited microscopic studies performed on cortical

bone in birds.13, 19, 2224 Unlike in mammals, mature cortical bone inpigeons contains relatively few Haversian systems.23, 24 Studies haverevealed that the cortical bone is arranged in a circumferential lamellar


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Figure 1. The basic unit of compact bone. Mineralized bone is deposited in concentriclayers around a central canal containing the neurovascular supply of the Haversian system.Intersitial lamellae provide the supportive infrastructure between each Haversian system.(FromRemedios A: Bone and Bone Healing. Vet Clin of North Amer 29:10291044, 1999;with permission.)

pattern in pigeons and a few other species of birds, which may contrib-ute to its brittle nature.23, 24

Cancellous or trabecular (spongy) bone occupies the metaphysis ofall long bones.14, 25 Trabecular bone consists of a network of fine, irregularplates called trabeculae that are separated by intercommunicating spacesfilled with bone marrow and hematopoietic cells.25 The lining of thetrabeculae is covered by endosteum, which contains osteoprogenitorcells.25 Cancellous bone is scarce or nonexistent in certain flat bones of

the skull and pelvis in mammals and birds.4, 15 Furthermore, bones ofthe skull, vertebrae, pelvis, sternum, ribs, the humerus, and sometimesthe femur in birds have minimal trabecular bone owing to their pneu-matic nature9, 14, 19

In immature animals, the medullary cavities of most bones containactive bone marrow, which is responsible for the production of redblood cells. Active bone marrow consists of two main components: asupportive reticulin framework and a system of interconnected bloodsinusoids that drains toward the central vein. Hematopoiesis occurswithin the reticulin framework. Once red cell development is complete

or almost complete, the cells move into the sinusoids and are releasedinto the general circulation. In the adult animal, active marrow is re-stricted to the metaphysis and the medullary cavities of the diaphysisare filled with inactive marrow, which is largely comprised of fat.25

A connective tissue layer called the periosteum covers nonarticular


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Figure 2. Each osteocyte is surrounded by calcified matrix. Long cytoplasmic processesextend between lacunae, which maintain cell to cell contact and provide passages forcirculation of tissue fluid and diffusion of metabolites. (From Remedios A: Bone and BoneHealing. Vet Clin of North Amer 29:10291044, 1999; with permission.)

cortical bone. Muscles, tendons, and ligaments insert into and originatein this dense fibrous connective tissue. A delicate connective tissue layer

called the endosteum covers the inner surface of the medullary cavity.The endosteum and periosteum in mammals contain osteogenic cellsthat are responsible for growth, remodeling, and repair of bone frac-tures.25 In direct contrast to mammals, the endosteum and periosteumin adult birds seem relatively quiescent. In the skeletally mature pigeonhumerus, the periosteum consists of a dense layer of tissue, whichcontains few osteoprogenitor cells. Likewise, avian endosteum containsfew osteospecialized cells. Histomorphometry studies on the pigeonfurther support the lack of biologic activity of the periosteal and endos-teal envelopes, revealing the minimal uptake of fluorescent labeling,

which is an indication of low levels of resorption/formation in theintact bone.24

A layer of hyaline cartilage that is composed of chondrocytes andan extracellular matrix protects the articular surfaces of the epiphysis.25

Hyaline cartilage plays a vital role in the function of articular joints by


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absorbing stresses, distributing mechanical loads, and resisting deforma-tion.

BONE GROWTH AND DEVELOPMENT

Two classes of bone are recognized based on histogenesis: flat bone(ossa plana), which arises from intramembranous ossification,11, 15 andlong bone (ossa longa), which is derived primarily from endochondralossification. Interestingly, the development and growth of long bonesactually involves both types of ossification.15

Intramembranous ossification occurs directly within the mesenchy-mal tissue in specific centers of ossification. Osteoblasts, derived from

primitive mesenchymal cells, begin synthesizing and secreting osteoid,which becomes mineralized. As the osteoid is deposited, the osteoblastsbecome entrapped within lacunae in the matrix; however, they maintaincytoplasmic extensions within canaliculi that allow for cell-to-cell con-tact. Osteoprogenitor cells divide and multiply, producing more osteo-blasts, which continue to lay down additional bone. Progressive boneformation allows the separate centers of ossification to coalesce andfuse. Initially, bone formed by intramembranous ossification appearstrabecular in nature. The randomly arranged configuration of cells, colla-gen fibers, and osteoid are soon remodeled by osteoclasts, allowing the

ordered osteoblastic deposition of compact and trabecular bone.2, 25

In endochondral ossification, mesenchymal cells first differentiateinto cartilage. A small model of the long bone is formed from hyalinecartilage. Then, within the shaft of cartilage, the cartilage cells hypertro-phy and undergo degradation and mineralization.2, 15 This creates whatis referred to as a primary center of ossification.2, 14, 25 Osteoclast-typecells remove the mineralized cartilage, which allows the ingrowth ofblood vessels that carry osteoprogenitor cells.2, 15 Simultaneously, theperichondrium that surrounds the cartilage shaft develops osteogenicpotential and becomes the periosteum.14, 25 The periosteum lays down a

thin layer of bone around the surface of the shaft, and primitive mesen-chymal cells and blood vessels invade the spaces within the shaft afterthe degeneration of the chondrocytes.2, 14, 25 The primitive mesenchymalcells differentiate into the osteoblasts and hematopoietic cells of the bonemarrow.25 The osteoblasts line the mineralized cartilage scaffolding andbegin to produce trabecular bone.25

The epiphyses form separate, secondary centers of ossification, andthe interface between the epiphyses and the shaft of the bone form theepiphyseal plate (also called the growth plate). Long bone growth is thedirect result of continual, rapid proliferation of cartilage at the epiphy-

seal plate, which subsequently mineralizes and is replaced by bone(Table 2). At sexual maturity, most mammals undergo hormonal changesthat result in the cessation of growth and fusion of the growth plate.4, 14, 25

Endochondral ossification in birds is different from that in mammalsin several ways. Although the nomenclature used to describe the zones


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Table 2. EPIPHYSEAL GROWTH PLATE ZONES IN MAMMALS

Zone Cellular Population

Zone of reserve cartilage Consists of hyaline cartilage that isorganized in cellular clusters25

Zone of proliferation Consists of clusters of cartilage cells thatundergo mitotic proliferation25

Zone of maturation Cell division ceases, and the chondrocytesbegin to enlarge25

Zone of hypertrophy and calcification Cellular enlargement continues, and thesurrounding matrix begins to mineralize25

Zone of cartilage degeneration Chondrocytes begin to deteriorate; vascularchannels invade and osteogenic cells setup residence19, 25

Zone of osteogenesis Osteogenic cells differentiate into osteoblastsand begin bone formation25

of the epiphyseal plate varies from publication to publication, there isgeneral agreement to the number of zones (Table 3). The zone of prolifer-ation is relatively wider in many avian epiphyseal plates than it is inmammalian growth plates. Additionally, cells in the zone of hypertrophyare not arranged in orderly columns nor are they invaded systematicallyby vascular channel, which leaves clusters of chondrocytes surroundedby mineralized matrix. Finally, the growth plate in birds is vascularized

by two sets of vessels, from the epiphysis and the metaphysis. Thiscontrasts with the epiphyseal blood supply in mammals, which is sup-plied directly by one vessel from the epiphysis.19

NEUROVASCULAR SUPPLY TO BONE

The basic components of the medullary blood supply are the nutri-ent artery and the proximal and distal metaphyseal arteries. The nutrientartery and metaphyseal arteries anastomose with one another at eachend of the medullary cavity and are responsible for the excellent bloodsupply and healing capabilities of the metaphysis. The nutrient arteryenters the bone along the diaphysis and usually is accompanied by amajor fascial attachment of muscle. It traverses the cortical bone without

Table 3. EPIPHYSEAL GROWTH PLATE ZONES IN BIRDS

Zone Comments

Zone of proliferation Also known as the proliferating and maturing zoneand the proliferating prehypertrophied zoneZone of prehypertrophy Also known as the uncalcified hypertrophic zone and

thehypertrophied zoneZone of hypertrophy Also known as the calcified hypertrophic zone and the

degenerating hypertrophied zone


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arborizing and enters into the medullary cavity. Once in the medulla,the nutrient vessel bifurcates into ascending and descending tributaries,which arborize and penetrate the endosteum. The nutrient and metaphy-

seal arteries provide approximately two thirds of the blood supply oflong bones, with the rest supplied by the muscle attachments of theperiosteum.4, 24, 26

Intramedullary arterial pressure is higher than in the periosteumand maintains the centrifugal flow of blood.26 The afferent vessels enterthe bone and form neurovascular channels known as Haversian canalsorosteons (see Fig. 1). These neurovascular bundles interconnect with oneanother and with the endosteum and periosteum via Volkmanns canals,which traverse the Haversian systems longitudinally. The Haversianvessels supply oxygen and important nutrients to the osteocytes via

canaliculi.18, 25

Venous drainage of blood occurs primarily in a centripetalfashion.18, 26 In mature and immature mammals, the cortex and medullarycavity are drained separately. Medullary venous blood is drained intosinusoids that coalesce into a central venous sinus. The central venoussinus then forms the nutrient vein, which exits the cortex at the samesite as the nutrient artery and drains into the systemic circulation.Cortical venous blood flow is also centripetal, toward the periosteum,where it is drained into periosteal venules then coalesces into largerperiosteal veins before entering the systemic circulation.18

The blood supply in immature bone is similar to that in adult bone,with a few minor exceptions. In immature animals, the periosteal bloodsupply is substantial and is responsible for most of the appositionalbone growth. Once an animal reaches maturity, this abundant bloodsupply atrophies. In all mammals, except for neonatal foals, the physisprovides a barrier that separates the physeal and the epiphyseal bloodsupply. This is an area of active endochondral growth that receives arich vascular supply from a network of vessels called the epiphyseometa-physeal arcade.18

Birds also have an intramedullary blood supply in pneumatic and

marrow-filled bones. As in mammals, the nutrient and metaphysealarteries in birds provide most of the blood supply to the marrow-filledbones (e.g., radius, ulna).24 In the pneumatic bones, such as the humerus,however, the arborization is less extensive.24 Generally, most of theblood supply originates from the medullary cavity, with no appreciableperiosteal circulation present along the diaphysis.24 The lack of periostealcirculation may be attributed to the lack of soft tissue coverage.21 Angio-graphic analysis in pigeons and other species of birds has revealed fewerHaversian systems in the humerus, which may account for its morebrittle nature.24 Additionally, the decreased number of Haversian sys-

tems in birds, with their central vascular channels, suggests a corticalblood supply that is less important in fracture healing and is biologicallyactive.24 Accordingly, the osteon and its accompanying blood vessel mayhave less of a role in bone remodeling and repair.24 As with mammals,immature birds have biologically more active marrow cavities with


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increased vascularization and hematopoietic capacity. Angiographicstudies of immature pigeons have revealed that the intramedullary bloodsupply of the humerus bones is similar to that of the nonpneumatic

bones.24

Lymphatic ducts are present in the periosteum and within themedullary cavity itself.4 The nervous supply to bone is primarily sensory,carrying only afferent impulses of pain to brain.4 Although definitivestudies of the lymphatic and nervous systems to bone have not beenperformed in birds, they are assumed to be similar.

BIOLOGY OF BONE HEALING

Although the biology of bone healing in birds is similar to that inmammals, it often is complicated by the lack of soft tissue coverage, thepresence of brittle pneumatic bones (see Dr. Tullys article for moreinformation on this), and the intense distracting forces of the pectoralflight muscles.22 The rate of fracture healing depends on the displace-ment of the fracture fragments, the amount of damage to the bloodsupply, the presence of infection, and the amount of motion at thefracture site.12

There are essentially two classes of fracture healing: primary (direct)and secondary (indirect). Primary fracture healing occurs in instances

where there is low interfragmentary strain. This usually occurs onlywhen the fracture fragments are reduced anatomically and stabilizedand when the fragments are placed under interfragmentary compression,usually with a dynamic compression plate. In this circumstance, there isdirect formation of lamellar bone across the fracture line and no evidenceof callous formation.1, 11, 16, 18, 20

Depending on the distance between the fracture fragments there aretwo methods of primary healing: contact and gap. Contact healingoccurs when there is a defect of less than 0.01 mm. In this situation, newlamellar bone is formed directly across the fracture line, parallel to the

long axis of the bone. Haversian remodeling is immediate, with osteo-clastic cutting cones crossing the fracture line and bringing perivascularosteoprogenitor cells that differentiate into osteoid-producing osteo-blasts. If the fracture gap is greater than 0.01 mm but less than 0.50 mm,primary bone healing still may occur in the form of gap healing. In gaphealing, endosteal and periosteal cells produce lamellar bone, which isdeposited perpendicular to the long axis of the bone. The perpendicularlamellar bone is remodeled later by Haversian systems into the properlongitudinal orientation.11, 16, 18, 20

Primary healing in birds is preferable but difficult to achieve. Plates

are ideal for promoting primary healing and thus produce the fastestrate of union with the smallest callus, which allows an early return tofunction (Fig. 3).13 Small plating systems are available and lend them-selves well to the avian species. Practices with a high avian case loadshould consider this option because it may provide the best prognosis


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Figure 3. Comminuted femoral fracture owing to gunshot injury repaired by way of a plate-rod combination. (Courtesy of S. Kerwin, DVM, MS, Associate Professor, Louisiana StateUniversity, School of Veterinary Medicine, Baton Rouge, Louisiana.)

for the avian fractures. The disadvantages of plating are the initial costof instrumentation and the learning curve. As mentioned previously,bird cortices are brittle and plate application is technically unforgiving.

Secondary bone healing occurs when there is (1) a lack of rigidinternal fixation and compression, and (2) complex or comminuted frac-tures in which the bony column cannot be reconstructed. This type ofhealing is a common end product of less stable forms of internal fixation(e.g., pin, cerclage), external fixation, and external coaptation with castsor splits. It is also the end product of untreated fractures, which are seencommonly in wild animals and birds and in most cases result in mal-

union of the fracture fragments. The hallmark of secondary bone healingis callous formation, which is directly proportional to the amount ofmotion present between the fracture fragments. Technically speaking,almost all fractures heal via second intention, because it is difficult toeradicate motion completely even with internal plate fixation.1, 10, 11, 18, 20, 22

Secondary bone healing is divided into three phases: the inflamma-


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tory phase, the reparative phase, and the remodeling phase.1, 10, 11, 18, 20, 22

The division between these phases is somewhat arbitrary and there isoverlap; however, for discussion purposes, they are informative. The

inflammatory phase begins immediately after the trauma of afracture.1, 10, 11, 18, 20, 22 In most cases, fractures are associated with animmediate and profound alteration in blood supply to the bone.1, 11, 18, 26

Depending on the kinetic energy associated with the fracture, the medul-lary and periosteal blood supply both may be served. A hematomaforms within the soft tissues and envelopes the fracture fragments.1, 11,18, 26 Disruption of the vascular supply to the bone causes ischemic celldeath and necrosis of the osteocytes at the apices of the fracture frag-ments.1, 11, 18, 26 In response to these vascular changes, the fracture sitebecomes hypoxic and acidotic.1, 11, 18, 26 Inflammatory cells arrive on the

scene and begin the process of phagocytosis.1, 11, 18, 26

Neutrophils are thefirst to arrive, followed by macrophages in 3 to 5 days if infection is notpresent.57 The presence of bacteria and foreign material prolongs theinflammatory phase by weeks to months, depending on severity of theinfection or contamination.57

The vascular system responds to tissue ischemia and inflammationwithin hours of the fracture by enhancing flow to the medullary cavityand periosteum.5, 11, 20 New transient extraosseus blood flow emergesfrom the injured soft tissue adjacent to the fracture site.5, 11, 20 These newblood vessels supply osteoprogenitor cells, which aid in the construction

of the fracture callus.5, 11, 20

The ability of the blood supply to revascu-larize the fracture completely is related directly to whether motion iscontrolled at the fracture site.20

The reparative phase is heralded by the organization of the hema-toma and the formation of granulation tissue. The fracture environmentbecomes more cell friendly, with a gradual shift in the pH toward theneutral or alkalotic range. Mesenchymal cells invade the site from theperiosteum, endosteum, and bone marrow and begin fibrous callusformation, which is mechanically stiffer than the hematoma or the granu-lation tissue. The fibrous callus consists predominately of type III colla-

gen that is produced by fibroblasts during the first week of injury.Mesenchymal cells that are recruited by bone-morphogenic proteinsdifferentiate into chondrocytes and produce a cartilage matrix. In aprocess similar to endochondral ossification, the cartilage callus is re-placed via vascular invasion, cartilage mineralization, and bone forma-tion.1, 11, 18, 20

The remodeling phase is characterized by the slow conversion ofthe bony callus, which is made up of trabecular bone, to compact bone.Osteoclasts resorb the trabecular bone and deposit the lamellar bone ina manner that is biomechanically compatible with the forces acting on

the long bone. This appropriate adaptation of bone to the forces ofweight bearing is known as Wolffs law. Over time, the compact boneof the cortex is restored completely and the medullary cavity is reestab-lished.1, 11, 18, 20

Many growth factors have been shown to influence bone heal-


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g.3, 8, 18 Most of the recent research has focused on several major growthfactors: platelet-derived growth factor, insulin-like growth factor 1, trans-forming growth factor , bone-morphogenic proteins, and fibroblast

growth factor.18

A full discussion of each of these is outside the scope ofthis article, and the reader is referred to several excellent reviews forfurther information.3, 9, 18

FAILURE OF FRACTURE REPAIR

Fracture healing usually is monitored by periodic radiographic reas-sessment. Adelayed unionis defined as the slowed progression of fracture

healing beyond the usual expected timeframe.1, 5, 7

A fracture is termeda nonunion if it does not heal within an expected timeframe and doesnot show radiographic signs of bony activity.1, 5, 7 The causes of delayedunion and nonunion are numerous, but most commonly involve motionat the fracture site, infection, and poor blood supply.1, 5, 7 Other possiblecauses of delayed union or nonunion include metabolic or nutritionaldisturbances, which are seen more commonly in avians than in mam-mals, neoplasia, and advanced age.2, 7, 11, 18

By far the most common cause of failure of fracture repair inmammals and birds is inadequate fixation.1, 5, 7 Inadequate fixation allows

for excessive motion at the fracture site, which impedes vascular inva-sion and angiogenesis.1, 5, 7 A fracture callus is formed; however, it maynot be able to bridge the fracture gap without supplemental support.1, 5,7, 18 Excessive callous formation in birds may inhibit flight function byinterfering with joint mobility and soft tissue adhesions.23 Furthermore,prolonged nonunion may lead to a false articulation between fracturefragments, which is called a pseudojoint.1, 5, 7, 18

Severe soft tissue injury associated with fractures of the distal ex-tremities is also a common impairment to fracture healing. The kineticenergy associated with comminuted fractures often is associated with

severe impairment to the vascular supply, which delays healing, espe-cially if the fracture is not stabilized immediately.23 Posttraumatic osteomy-elitis is defined as inflammation of the bone and most commonly iscaused by bacterial infection, although fungal and viral agents also maybe involved. This condition usually develops after the direct inoculationof bacteria at the time of fracture or during the fracture fixation. Despitethe high incidence of contamination in open and comminuted fracturesin both birds and mammals, osteomyelitis develops in relatively fewcases. Factors that increase the likelihood of infection include excessivesoft tissue injury, periosteal stripping of the muscular attachments to thebone, and inadequate patient preparation before surgery. Fractures canheal in the face of infection, albeit slowly; however, securing fragmentstability is imperative because the combination of motion and infectioncan lead to disastrous results.5, 7


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SUMMARY

The goal of any method of fracture repair should be the early return

to function of the patient with minimum postoperative morbidity. Thisis accomplished most optimally by having a basic understanding of thebiology of bone healing and by being familiar with the musculoskeletalsystem of the species before attempting fracture repair. Applying thefundamental principles of mammalian bone anatomy and physiology tothe bird ensures the best prognosis possible and minimizes postoperativecomplications in the avian patient.

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analysis of the humerus in pigeons. AJVR 57:982986, 199625. Wheater PR, Burkett HG, Daniels VG: Skeletal tissues. In Wheater PR, Burkett HG(eds): Functional Histology: A Text and Colour Atlas, ed 2. Edinburgh, Scotland,Churchill Livingstone, 1987, pp 142160

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University of IllinoisCollege of Veterinary Medicine

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Basic Mammalian Bone Anatomy and Healing