Developmental Biomechanics
`Effect of Forces on the Growth, Development, and Maintenance
`of the Human Body
`BARNEY F. LEVEAU
`and DONNA B. BERNHARDT
`
`The purpose of this paper is to present an overview of growth principles that are
`influenced by mechanical factors. These general principles are followed by some
`biomechanical examples of the growth and development of weight-bearing body
`areas, and examples of growth principles and mechanics related to therapeutic
`applications.
`Key Words: Biomechanics, Child development disorders, Extremities, Fetus, Spinal
`cord.
`
`The growth, development, and main(cid:173)
`tenance of the body is affected by several
`factors including genetics, nutrition,
`drugs, hormones, and mechanical
`forces. Each may work separately or in
`combination to cause normal or abnor(cid:173)
`mal development. Although all of these
`factors can make important contribu(cid:173)
`tions to the formation of the body's
`components, we will address the me(cid:173)
`chanical aspects in this article.
`Forces are constantly acting on the
`body. These forces can affect the size
`and shape of the body parts, especially
`those of the musculoskeletal system.
`Cultural and occupational practices pro(cid:173)
`vide several examples of the effects of
`forces on the body. Several cultures have
`used cradle boards, which flatten the
`children's heads.1,2 Others have re(cid:173)
`stricted the size of women's feet by bind(cid:173)
`ing them. The beauty secret of the Pa-
`daung tribeswoman is based on the pull
`of gravity on brass rings around her
`neck; the gravitational pull gradually
`pushes the clavicles and ribs downward.3
`The result is the appearance of an elon(cid:173)
`gated neck. Hunters and warriors who
`specialized in using a sling developed a
`bent humerus.4 Similarly, a professional
`tennis player may have an enlarged hu(cid:173)
`merus from overuse of the playing arm.5
`Arthritis has been found in the ankles
`of dancers and professional soccer play(cid:173)
`ers.6 The shaping of a child's bones can
`be seen in normal and abnormal growth.
`The deformities of clubfoot and tibial
`
`Dr. LeVeau is Associate Professor, School of
`Medicine, University of North Carolina at Chapel
`Hill, Chapel Hill, NC 27514 (USA).
`Ms. Bernhardt is Clinical Assistant Professor,
`Department of Therapy, Sargent College, Boston
`University, Boston, MA 02215.
`
`1874
`
`torsion are examples of children's prob(cid:173)
`lems that may occur from their having
`been in a poor position in the uterus,
`during sleeping, or while sitting.7,8
`Many physicians have become "ex(cid:173)
`traordinarily impressed" with the im(cid:173)
`portance of mechanical influences on
`the human body as they have noted that
`many aspects of growth, development,
`and maintenance are mechanical.9 Sev(cid:173)
`eral investigators have traced the effects
`of forces on the various skeletal struc(cid:173)
`tures after a child is born,7,8,10,11 others
`have studied forces related to problems
`in adults,12-14 and others have ex(cid:173)
`pounded on the forces that cause de(cid:173)
`formity in the fetus.15-17 Only recently,
`however, have authors reported on me(cid:173)
`chanical aspects involved in the devel(cid:173)
`opment of the embryo.18
`The following sections of this article
`will present some general growth prin(cid:173)
`ciples that are mechanically oriented,
`examples of mechanics
`influencing
`growth and development of selected
`body areas, and examples of growth
`principles and mechanics in therapeutic
`applications. We have termed the study
`of the effects of forces on the musculo(cid:173)
`skeletal system during the entire life
`span developmental biomechanics. By
`understanding these principles and re(cid:173)
`cognizing these and other examples,
`physical therapists will be able to pre(cid:173)
`vent and treat musculoskeletal disorders
`more effectively.
`
`GENERAL GROWTH
`PRINCIPLES
`The general shape of the human body
`depends on the proper development of
`skeletal structures. A deficiency in this
`development leads to gross abnormali(cid:173)
`
`ties in appearance and function.1619
`Most authorities believe that extrinsic
`factors can greatly modify both the ex(cid:173)
`ternal and internal design of bones.20-22
`Wolffs law of bone transformation ad(cid:173)
`dressed this phenomenon in the late
`1800s. The general idea of this law is
`that every change in form or function
`of a bone brings about definite changes
`in the bone's internal and external ar(cid:173)
`chitecture in accordance with certain
`mathematical laws. This law includes
`the principle that bones will increase or
`decrease in their mass according to their
`function.20 Some authors have made
`this law more specific in relation to en(cid:173)
`dochondral
`growth,
`appositional
`growth, and external and internal bone
`form.22-32 By understanding the specific
`reactions of tissues and growth processes
`to loads and by applying principles of
`basic biomechanics, clinicians can help
`direct the normal growth and develop(cid:173)
`ment of the musculoskeletal system.
`They can also use this knowledge to
`prevent deformities or to correct the
`deformities once they have occurred.
`
`EFFECT OF LOADING ON
`TISSUE TYPE
`
`The type and duration of loading can
`influence the type of tissue or articula(cid:173)
`tions being formed. During the process
`of tissue differentiation, forces are im(cid:173)
`portant in determining the type of tissue
`formation.22 In many instances, the type
`of tissue depends on the type of loading
`that occurs. Almost all tissues are sen(cid:173)
`sitive to the loads that are placed on
`them. They respond
`to
`tension,
`compression, shearing, torsion, and
`bending in a manner that contributes to
`their progressive differentiation.20-22
`
`PHYSICAL THERAPY
`
`Petitioner Ex. 1067 Page 1
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`

`
`Generally, chondrogenesis occurs with
`intermittent loading, and osteogenesis
`occurs with continuous loading. Storey
`presented a spectrum of loads from con(cid:173)
`tinuous compression through intermit(cid:173)
`tent loading to continuous tension that
`provided for functional adaptations of
`connective tissue and joints.22
`1. With continuous compression in a
`constant direction, bones become
`connected by bars of cartilage that
`act as shock absorbers and as a flex(cid:173)
`ing system. A synchondrosis is an
`example.
`2. With intermittent compression and
`a range of movement between bones,
`articular cartilage is formed. A path(cid:173)
`ological example is cartilage forming
`in a pseudarthrosis.
`3. With a decreasing magnitude of in(cid:173)
`termittent compression and an in(cid:173)
`creasing amount of tension, sym(cid:173)
`physes are formed.
`4. With intermittent loads of tension
`and compression of equal magni(cid:173)
`tudes along with sliding, condylar
`cartilage develops.
`5. With increasing intermittent tension,
`sutures are formed such as joints in
`the skull.
`6. With continuous tension in one di(cid:173)
`rection, thick collagenous tissue de(cid:173)
`velops into tendons and fascia.
`
`EFFECTS OF LOADING ON
`AMOUNT AND DIRECTION OF
`TISSUE GROWTH
`The magnitude and direction of load(cid:173)
`ing can influence the amount and direc(cid:173)
`tion of tissue growth as well as affecting
`the type of tissues and joints being
`formed. The following principles show
`how loads on the musculoskeletal sys(cid:173)
`tem can exert this influence on tissue
`growth.20,22-25
`
`Effects of Loading on
`Endochondral Growth of Bones
`Once endochondral growth begins,
`functional loads appear to have consid(cid:173)
`erable influence on the final form of the
`bone.22 The epiphyseal plate may react
`in four ways in response to loads: 1)
`growth can increase longitudinally,26 2)
`growth can decrease longitudinally,26 3)
`growth can be deflected by shearing,25
`or 4) torsional growth can occur from
`continual or intermittent twisting.26
`Longitudinal loading. Most epiphy(cid:173)
`seal plates are aligned perpendicular to
`the major
`loads
`that cross
`them.
`
`Volume 64 / Number 12, December 1984
`
`Compression or tension across the epi(cid:173)
`physeal plate, within limits, may stim(cid:173)
`ulate bone growth longitudinally.27,28
`Compression, however, seems to elicit a
`more rapid rate of growth than tension.
`Chondral growth may be accelerated
`with decreased compression, but a cer(cid:173)
`tain amount of compression seems to
`be essential for conversion of cartilagi(cid:173)
`nous tissue into bone.29
`An increase in compression or tension
`outside the normal range of loading in(cid:173)
`hibits chondrocyte mitosis and results in
`retarded or halted growth in length. A
`small increase in magnitude of the load
`can slow growth without stopping it.
`Increased load, however, may even lead
`to bone resorption. The magnitude of
`the load across the growth plate seems
`to be a major factor influencing the rate
`of growth.21,28,30 Stapling across an epi(cid:173)
`physeal plate is an example of using
`compression to retard bone growth.
`Because epiphyseal plates align per(cid:173)
`pendicularly to the time-averaged re(cid:173)
`sultant of the loads across them, the
`direction of growth in these areas may
`be adjusted. An increased compression
`on one side of an epiphysis may slow
`growth on that side, while the normal
`proliferation of cells is occurring on the
`other side. This unequal loading causes
`an angulation of the epiphyseal plate,
`which may lead to further unequal load(cid:173)
`ing. Thus, unequal loading along an epi(cid:173)
`physeal plate can change the direction
`of growth.25,28 Genu valgum and varum
`could occur because of unequal loads
`across the growth plate.
`The duration of applied load is an
`important factor affecting the rate of
`growth.30 Constant compression of great
`magnitude can cause bone atrophy, and
`intermittent compression can cause
`bone growth. A mild constant load can
`produce more overall results on chon(cid:173)
`dral growth than very large, but brief
`and infrequently applied loads.27 Persis(cid:173)
`tent gentle loads (creep) may lead to a
`deformity or correction of a deforma(cid:173)
`tion.15 Casting provides gentle loads
`over a long period of time to correct
`deformities of the lower limb.
`Perpendicular loading. A load applied
`to an epiphyseal plate that is not parallel
`to the direction of growth (perpendicu(cid:173)
`lar to the epiphyseal plate) will deflect
`the growth along the line of the deform(cid:173)
`ing force. As long as the load is main(cid:173)
`tained, new growth will be deflected in
`the direction of the load resulting in a
`lateral displacement of the epiphysis.
`
`The chondral growth gradually yields to
`the shearing component of the load,
`which effectively realigns the direction
`of growth. Depending on the magnitude
`and direction of the load, tilting of the
`epiphyseal plate may or may not oc(cid:173)
`cur.25,27
`Torsional loading. Because the epi(cid:173)
`physeal plate is least resistant to torsion,
`a torsional load will lead to a rotational
`deflection of
`the growth columns
`around the circumference of the epiphy(cid:173)
`seal plate.23 Newly formed bone will
`grow away from the epiphysis in a spiral
`pattern, which gives a torsional change.
`Examples of this effect include normal
`alignment of tibial rotation, a torsional
`deformity of the vertebrae occurring in
`scoliosis, and rotational change resulting
`from the physicians' and therapists' cor(cid:173)
`rection of tibial torsional problems.27
`Gravity may be sufficient to affect
`epiphyseal growth. Muscle forces, how(cid:173)
`ever, are often much greater than those
`of gravity. Joint alignment tends to be
`more influenced by the load caused by
`muscular forces than by the pull of grav(cid:173)
`ity. An imbalance in muscle forces or
`lack of muscle forces secondary to non(cid:173)
`weight bearing may lead to skeletal de(cid:173)
`formation, especially if these abnormal
`forces are applied over a long period of
`time.20,27,28
`
`Effect of Loading on Appositional
`Growth
`Compression and tension. Compres(cid:173)
`sion stimulates appositional growth, and
`lack of compression leads to a reduction
`of bone tissue.27 An increase or decrease
`in tension may produce results in fi(cid:173)
`brous tissues such as tendon and liga(cid:173)
`ments that are similar to those produced
`in bone.33 Increased weight bearing re(cid:173)
`sults in an increase in the thickness and
`density in the tibial shaft.22,27,34 Lack of
`weight bearing, however, resulting from
`factors such as bed rest, immobilization,
`neurological disorders, or space flight, is
`followed by bone atrophy.27 Unused
`bones are usually smaller in size and
`abnormal in shape.35
`Bending. When a bone is bent under
`a load, it modifies its structure by re(cid:173)
`modeling.25,36 The process, however, is
`relative to the normal shape of bone.
`When the surface of a bone becomes
`less concave or more convex, net loss of
`bone occurs as a result of osteoclastic
`activity. The more concave or less con(cid:173)
`vex surface has a net increase of bone as
`
`1875
`
`Petitioner Ex. 1067 Page 2
`
`

`
`a result of osteoblastic activity.24 Frost
`termed this process flexure-drift.25 The
`process appears to be related to electrical
`potentials induced by a piezoelectric ef(cid:173)
`fect when bone is deformed.19,20,37 In(cid:173)
`termittent current seems to be better for
`proper bone formation than a continu(cid:173)
`ous current.37 Hence, intermittent load(cid:173)
`ing of a bone produces better develop(cid:173)
`ment.
`Effects of Loading on Trabecular
`Bone
`The internal structure of bones is de(cid:173)
`veloped to resist the loads they bear. A
`change in the magnitude or direction of
`the loads that produce stress within the
`bone produces a demonstrable change
`in the internal architecture of the
`bone.30,35 The trabeculae are organized
`to provide maximum strength with a
`minimum of material. Compression ap(cid:173)
`pears to be the major load to develop
`trabeculae; however, tension loads can
`also produce trabeculae.30,32 Bony tra(cid:173)
`beculae hypertrophy in response to in(cid:173)
`creased load, but new trabeculae cannot
`appear without a preexisting framework
`to build on. The trabecular system is
`related to forces of both weight bearing
`and muscle pull. Without these loads,
`the trabeculae become thinner and may
`even disappear.19 This reduction of bone
`mass leads to mechanical incompet(cid:173)
`ence.26, 38-42 During about the first four
`or five decades of a normal individual's
`life, the internal replacement and ad(cid:173)
`justment of bone mass is maintained
`according to the mechanical demands
`made upon it. Because mechanical loads
`provide a continual stimulus, the re(cid:173)
`modeling process continues. As an in(cid:173)
`dividual ages, however, the process pro(cid:173)
`ceeds at a slower rate. The bone at(cid:173)
`tempts to maintain maximum density
`in areas of maximum loading.13 Some
`authors, however, have stated that this
`adaptive remodeling loses its effective(cid:173)
`ness and results in an increased bone
`resorption and decreased bone forma(cid:173)
`tion in most people by the age of 35 to
`40 years.42,43 Bone loss can be about 25
`to 30 percent over 20 years44 or between
`0.5 to 1.5 percent each year.43
`
`Effects of Loading on Cartilage
`Cartilage grows within a wide range
`of forces. Constant compression on car(cid:173)
`tilage leads to its thinning, but it may
`regain its thickness if the compression is
`slowly released. When
`intermittent
`
`1876
`
`compression is applied, it becomes
`thicker. Excessive compression causes
`degeneration of cartilage, and absence
`of compression is often followed by atro(cid:173)
`phy. Secondary to either excess or lack
`of compression, congenital deformities
`can cause early appearance of degener(cid:173)
`ative joint disease.22, 35 The main me(cid:173)
`chanical factor causing cartilage degen(cid:173)
`eration appears to be repetitive impulse
`loading, especially from muscle joint
`forces.45, 46 Radin stated that repetitive
`impulse loading for as little as 20 min(cid:173)
`utes each day over a period of several
`months can aggravate the cartilage de(cid:173)
`generation.46 A situation, however, that
`produces chronically increased stress on
`the joint can either be the primary cause
`of degeneration or provide secondary
`changes in the joint.47 Joint degenera(cid:173)
`tion can follow trauma, joint dysplasias,
`subluxations, dislocations, slipped epi(cid:173)
`physes, or segmental torsions.46-52 Once
`the initial lesion occurs, physical activity
`is necessary for the disorder to pro(cid:173)
`gress.53
`
`Effects of Loading on Fibrous
`Tissue
`Soft tissues such as tendons and liga(cid:173)
`ments adapt in tension. They are self-
`aligning and their shape does not need
`to be adapted. Their tissue properties,
`however, are affected by increased or
`decreased loading.13 Intermittent ten(cid:173)
`sion causes collagen tissue to increase in
`thickness and strength. This reaction is
`evident in the ligaments of exercised
`animals.54 Frost termed this response
`the stretch-hypertrophy rule.28 Lack of
`loading on ligaments after immobiliza(cid:173)
`tion, however, decreases their strength
`and ability to absorb energy.55
`Frost also expounded on the stretch-
`creep rule. This rule relates to the creep
`(elongation over time) that occurs
`within the tissue as a tension load is
`applied.28 Many treatment procedures
`use this concept. The use of casting or
`night splints to lengthen tendons in the
`foot is one example. The use of creep
`can be a valuable treatment technique.
`This process, however, takes a pro(cid:173)
`longed period of time. Kite stated that
`casting, using the principle of creep, may
`be preferred to surgery.56 He also warned
`that forced manipulation of the body
`part may cause tearing and resulting
`adhesions in the area. Therefore, knowl(cid:173)
`edge of the advantages and disadvan(cid:173)
`tages of each treatment technique is es(cid:173)
`sential.
`
`Effects of Loading Related to
`Rate of Growth
`The effect of load on growth is directly
`proportional to the speed of growth.
`Any load applied even for a short time
`during the period of rapid growth may
`result in permanent deformity of a
`bone.22 Early fetal growth is extremely
`rapid and reaches a peak around the
`fifth month.57 Later in the fetal period,
`the fetus is exposed to increased extrin(cid:173)
`sic forces such as increased size, de(cid:173)
`creased amniotic fluid, and decreased
`movement. At this time, however, with
`a slowing growth rate and diminished
`plasticity, the fetus becomes increasingly
`able to resist deformation. In general,
`the modification of tissues is achieved
`more easily when they are pliable in
`periods of rapid growth. Rapid growth
`in small bones provides for production
`or correction of angular deformities very
`rapidly. Early correction yields the best
`corrective results.15,17
`
`General Comments
`Without the growth process, correc(cid:173)
`tion of a deformity is almost impossible.
`Incorrect application of loads for correc(cid:173)
`tion during this time, however, may lead
`to other deformities. With appropriate
`management of the deforming forces,
`the adaptive changes may be reversed or
`completely avoided. The problems of
`deformities and their sequelae can be
`greatly reduced if the clinician uses
`knowledge of biomechanical and growth
`principles. The remainder of this article
`provides examples of growth, develop(cid:173)
`ment, and maintenance for weight-bear(cid:173)
`ing areas of the body.
`
`RESULTS OF GROWTH
`PRINCIPLES IN WEIGHT-
`BEARING AREAS
`
`EXAMPLES OF WEIGHT-
`BEARING AREAS
`Spine
`The spine is composed of several
`structures that provide both static and
`dynamic stability. The 24 vertebrae con(cid:173)
`sist of an anterior body that is the pri(cid:173)
`mary weight-bearing area and a poste(cid:173)
`rior arch formed by the pedicles, lami(cid:173)
`nae, transverse processes, spinous proc(cid:173)
`ess, and articular facets.58 The size and
`mass of each vertebra increases from the
`cervical to lumbar area in adaptation to
`
`PHYSICAL THERAPY
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`
`the increasing load from the superin(cid:173)
`cumbent weight. The sacrum is the solid
`bony base of the spinal column. The top
`of these five fused vertebrae forms a 45-
`degree angle with the horizontal plane;
`this angle equalizes the compressive and
`shear forces between the last lumbar and
`first sacral vertebrae. An increase in this
`angle predisposes this area to accentua(cid:173)
`tion of shearing forces, and a diminu(cid:173)
`tion creates elevated compression.59
`
`Spinal longitudinal growth occurs pri(cid:173)
`marily in the vertebral body. Length
`from cervical to lumbar areas is approx(cid:173)
`imately 20 cm at birth and doubles in
`the first year. Growth continues at a
`slow linear rate until the final adult
`length of 60 to 75 cm. The proportion(cid:173)
`ate size of each area of the spine also
`alters with growth. The cervical verte(cid:173)
`brae become relatively smaller, and the
`thoracic vertebrae enlarge in percentage
`of total length. The lumbar area under(cid:173)
`goes little alteration in relative propor(cid:173)
`tions.60
`
`Loads on the spine create both pri(cid:173)
`mary and secondary trabecular systems
`in the vertebrae. The primary system, a
`vertically oriented arrangement through
`the spinal column, develops to sustain
`body weight and is the most resistant to
`atrophy. The secondary systems orient
`in the oblique direction to counteract
`torsion, bending, and shear forces and
`in the horizontal direction to counteract
`tensile muscular pull. These secondary
`systems are the most susceptible to
`atrophic change seen in osteoporosis.61
`
`Viewed from a sagittal perspective,
`the normal spine is lordotic in the cer(cid:173)
`vical and lumbar areas and kyphotic in
`the thoracic and sacral areas. These cur(cid:173)
`vatures result from predictable devel(cid:173)
`opmental changes. At birth, the spine
`has
`two primary posterior convex
`curves. As the infant lifts his head
`against gravity, the lordosis in the cer(cid:173)
`vical area increases. Latent tightness of
`the iliopsoas muscles persisting from fe(cid:173)
`tal flexion, coupled with antigravity
`work by the infant in a prone position
`on flexed or extended elbows, in creep(cid:173)
`ing, or in high kneeling encourage in(cid:173)
`creased lumbar lordosis. Weak abdom(cid:173)
`inal muscles provide little anterior pel(cid:173)
`vic support for the lordotic tendency.
`Thus, the spine develops increased com(cid:173)
`pensatory curvatures that allow close
`approximation to the line of gravity and
`provide inherent stability in all direc(cid:173)
`
`Volume 64 / Number 12, December 1984
`
`tions.58,59 Abnormal or unusual devel(cid:173)
`opmental influences can disrupt the
`normal symmetry and balance of the
`spine, predisposing it to deformity.
`
`One of the more prevalent spinal de(cid:173)
`formities is scoliosis. Although various
`defects in embryological development,
`such as failure of vertebral segmentation
`or undergrowth of chondrification cen(cid:173)
`ters, can produce congenital scoliosis,60
`the majority of scoliosis is caused after
`the embryonic period. The problems of
`muscular imbalance, abnormal muscu(cid:173)
`lar tone, persistent abnormal position(cid:173)
`ing, lack of or abnormal spinal weight
`bearing noted in the various paralytic or
`CNS disorders (eg, poliomyelitis, Werd-
`nig-Hoffman disease, muscular dystro(cid:173)
`phy, myelodysplasia, and cerebral palsy)
`can create an alteration of spinal dy(cid:173)
`namics, which predisposes the spine to
`scoliotic changes.62 The etiology of idi(cid:173)
`opathic scoliosis, the most frequent non-
`neuromuscular variant, remains ob(cid:173)
`scure. The possible causes are asymmet(cid:173)
`rical spindle sensitivity, increase in
`number of slow twitch fibers on one side
`of the spine, positional influences, or
`asymmetrical
`vertebral
`and
`cord
`growth. Any of these causes could create
`abnormal forces during spinal develop(cid:173)
`ment.63,64
`
`Forces of deformation initially affect
`the viscoelastic structures that are most
`susceptible to creep. Ligaments and
`muscles shorten and thicken on the con(cid:173)
`cavity and stretch and eventually relax
`on the convexity. Cartilage degenerates
`secondary to heavy compression on the
`concave side and atrophies secondary to
`stress-reduction on the convex side. The
`disk, compressed on the concavity,
`bulges and demonstrates nuclear migra(cid:173)
`tion toward the convexity. Additionally,
`the disk becomes incapable of maintain(cid:173)
`ing normal vertebral dynamics.62,65
`
`If these changes occur while epiphyses
`are still unfused, bony deformation re(cid:173)
`sults. Compression on the concave side
`causes growth reduction, and minimally
`decreased loading on the convex side
`stimulates overgrowth, which creates
`vertebral wedging. Rotatory alterations,
`begun as a sequela of the lateral deform(cid:173)
`ity, cause distortion of the vertebral ele(cid:173)
`ments and incongruity of the facet
`joints. Rib rotation and lumbopelvic dy-
`synchrony often accompany the verte(cid:173)
`bral distortion.62 The deformation thus
`creates a self-perpetuating system. Creep
`
`with eventual relaxation in combination
`with the force of gravity causes exacer(cid:173)
`bation of the problem. The body at(cid:173)
`tempts to remain balanced over the pel(cid:173)
`vis and frequently develops a compen(cid:173)
`satory curve.
`Similar deformation in an anteropos(cid:173)
`terior direction can occur with kyphosis.
`Postural faults and deficiencies of vas(cid:173)
`cular supply have been implicated in
`addition to the etiologies underlying
`scoliosis as causative factors of thoracic
`kyphosis. Lengthening and weakness of
`posterior viscoelastic elements with
`shortening of anterior elements results.
`Fibrous replacement of disk substance
`secondary to the abnormal pressure
`leads to loss of vertebral mobility. Ex(cid:173)
`cessive anterior pressure interferes with
`anterior vertebral ossification and cre(cid:173)
`ates anterior wedging. The line of gravity
`assists the deforming forces. The spine
`compensates by developing an accen(cid:173)
`tuated cervical or lumbar lordosis.
`A third spinal condition of relative
`importance is represented by spondylo(cid:173)
`lysis or spondylolisthesis. Both condi(cid:173)
`tions have a defect in the laminar area,
`specifically the pars interarticularis, but
`no displacement has occurred in the
`static spondylolysis. Forward slippage of
`the anterior portion of one vertebra on
`the vertebra below characterizes spon(cid:173)
`dylolisthesis. The anatomy of the lower
`lumbar area predisposes this location to
`the highest frequency of slippage.66-70
`Secondary to the normal lumbar lor(cid:173)
`dosis, compressive force is transmitted
`through the neural arch instead of the
`vertebral body. Either a single traumatic
`or continual intermittent force in a hy-
`perextended (hyperlordotic) position
`can pinch the L5 isthmus between the
`L4 articular facet and the upward pro(cid:173)
`jecting sacral process, fracturing the
`weakest point, the pars interarticularis.
`Hence, multiple factors could predis(cid:173)
`pose the area to a hyperlordotic posi(cid:173)
`tion. In addition to congenital birth de(cid:173)
`fects, these factors include any abnormal
`or persistent lumbar lordosis secondary
`to muscular imbalance, abnormal posi(cid:173)
`tion or muscular tone, or tightness of
`the iliopsoas or lumbosacral area. Ad(cid:173)
`ditionally, abnormal or lack of weight
`bearing could produce reduced calcifi(cid:173)
`cation in the lumbar area. Subsequent
`movement superimposed on these con(cid:173)
`ditions of hyperlordosis or decalcifica(cid:173)
`tion can contribute to fracture and slip(cid:173)
`page as a sequela of increased shear
`force.59
`
`1877
`
`Petitioner Ex. 1067 Page 4
`
`

`
`Hip
`
`The adult hip joint is composed of an
`acetabulum that faces outward, forward,
`and downward, and the head of the
`femur that is inclined at approximately
`a 125-degree, neck-shaft angle and an-
`teverted 8 to 11 degrees with the shaft.
`The head of the femur sits deeply in the
`acetabulum and is secured by the la(cid:173)
`bium and strong muscular and ligamen(cid:173)
`tous attachments.71,72 This mature po(cid:173)
`sition is the result of major mechanical
`influences during development on both
`portions of the joint.
`The pelvis is formed from three pri(cid:173)
`mary ossification centers: the ischium,
`pubis, and ilium. These centers con(cid:173)
`verge to form the triradiate cartilage.23
`Endochondral growth in these areas al(cid:173)
`lows the acetabulum to enlarge circum-
`ferentially commensurate with spherical
`growth of the femoral head. The aceta(cid:173)
`bulum, which is the most shallow at
`birth, provides a large range of motion
`but also presents the greatest potential
`for dislocation.73 The normal angle of
`the acetabular roof with the horizontal
`plane is 30 degrees at birth. This angle
`decreases to 20 degrees by 3 years of age
`and remains at this level through ma(cid:173)
`turity.71
`Three growth zones—the longitudi(cid:173)
`nal growth plate,
`the
`trochanteric
`growth plate, and the femoral neck isth(cid:173)
`mus—contribute to development of the
`proximal femur.32 These zones lie on
`the same line at birth. As the child ages,
`the longitudinal plate grows at a more
`rapid rate than the trochanteric plate
`and shapes the angles of inclination and
`declination. At birth, the angle of incli(cid:173)
`nation is 150 degrees with approxi(cid:173)
`mately 40 degrees of anteversion.74 If
`normal compression and tension loads
`are placed on the proximal end of the
`femur, both angles decrease with age to
`adult values.72
`Unless the femoral head is malposi-
`tioned perinatally, the acetabulum and
`femoral head develop congruently.32
`This congruency is essential for proper
`development of both portions.71,75 Ex(cid:173)
`ternal loads guide the development of
`these areas. The most important are
`body weight and muscle tension, applied
`in appropriate magnitude and direction.
`Any abnormality of compressive load or
`incongruity of joint structure will lead
`to bony deformity.32 For example, a
`shallow acetabulum or coxa plana may
`be caused by these abnormal loads.
`
`1878
`
`The trabecular structure of the proxi(cid:173)
`mal femur is a consequence of external
`forces. The two primary systems are the
`principle compressive lines that develop
`from a normal weight-bearing load. The
`secondary systems cross the neck region
`and greater trochanter, developing as a
`sequela of muscular tension. All the tra(cid:173)
`becular systems cross at right angles for
`greatest resistance to compression and
`bending stresses.14
`Abnormal loading or joint incongru(cid:173)
`ity can predispose the hip joint to de(cid:173)
`velopmental abnormalities. A frequent
`deformity
`is congenital dislocation
`(CDH) or subluxation of the hip.26 The
`most probable causes are hereditary,
`mechanical, or multifactorial combina(cid:173)
`tions. Joint laxity has been postulated
`as a genetic problem that can lead to hip
`deformity. Atypical body position in
`utero and the resultant mechanical loads
`may also create hip deformation. Re(cid:173)
`stricted uterine space can trap the fetus
`in a cross-leg or breech position. The
`left hip, which is twice as frequently
`involved as the right, lies against the
`maternal lumbar spine and may be re(cid:173)
`strained for prolonged periods in an ad-
`ducted position.15
`Forces at or briefly following the birth
`process may dislocate the flexible hip
`joint. Because of joint position and
`force, the breech delivery is often fol(cid:173)
`lowed by hip dislocation. As many as 30
`to 50 percent of all children with CDH
`were also breech presentations. At least
`20 to 30 percent of the children who
`were breech deliveries have a diagnosed
`CDH.15 During birth or immediately
`after delivery, the hip may be dislocated
`by passive movement of the relatively
`flexible, unstable hip joint from fetal
`flexion into extension. The hip may re(cid:173)
`locate or remain displaced.26
`Cultural and environmental factors
`may lead to hip instability. Swaddling a
`child tightly in extension with a blanket
`or carrying a child on a cradleboard can
`force extension of the hip and cause
`dislocation. Persistent sleeping or sitting
`with the hip in the extremes of rotation
`may provide deforming forces that
`cause abnormal joint development.26
`The dislocated or subluxed hip in a
`preambulatory child may not appear as
`a developmental problem.26 If the con(cid:173)
`dition is not corrected within a few
`months, however, secondary growth al(cid:173)
`terations and abnormal forces during
`gait can cause serious permanent seque(cid:173)
`
`lae. The magnitude and