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 maintenance 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 abnormal development. Although all of these
factors can make important contributions to the formation of the body's
components, we will address the mechanical 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 provide 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 restricted the size of women's feet by binding them. The beauty secret of the Padaung 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 elongated neck. Hunters and warriors who
specialized in using a sling developed a
bent humerus.4 Similarly, a professional
tennis player may have an enlarged humerus from overuse of the playing arm.5
Arthritis has been found in the ankles
of dancers and professional soccer players.6 The shaping of a child's bones can
be seen in normal and abnormal growth.
The deformities of clubfoot and tibial

torsion are examples of children's problems 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 "extraordinarily impressed" with the importance of mechanical influences on
the human body as they have noted that
many aspects of growth, development,
and maintenance are mechanical.9 Several investigators have traced the effects
of forces on the various skeletal structures after a child is born,7,8,10,11 others
have studied forces related to problems
in adults,12-14 and others have expounded on the forces that cause deformity in the fetus.15-17 Only recently,
however, have authors reported on mechanical aspects involved in the development of the embryo.18
The following sections of this article
will present some general growth principles 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 musculoskeletal system during the entire life
span developmental biomechanics. By
understanding these principles and recognizing these and other examples,
physical therapists will be able to prevent and treat musculoskeletal disorders
more effectively.
GENERAL GROWTH
PRINCIPLES

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

The general shape of the human body

depends on the proper development of
skeletal structures. A deficiency in this
development leads to gross abnormali-

ties in appearance and function.1619

Most authorities believe that extrinsic
factors can greatly modify both the external and internal design of bones.20-22
Wolffs law of bone transformation addressed 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 architecture 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 endochondral
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 development 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 articulations being formed. During the process
of tissue differentiation, forces are important 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 sensitive 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

Generally, chondrogenesis occurs with

intermittent loading, and osteogenesis
occurs with continuous loading. Storey
presented a spectrum of loads from continuous compression through intermittent 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 flexing system. A synchondrosis is an
example.
2. With intermittent compression and
a range of movement between bones,
articular cartilage is formed. A pathological example is cartilage forming
in a pseudarthrosis.
3. With a decreasing magnitude of intermittent compression and an increasing amount of tension, symphyses are formed.
4. With intermittent loads of tension
and compression of equal magnitudes 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 direction, thick collagenous tissue develops into tendons and fascia.
EFFECTS OF LOADING ON
AMOUNT AND DIRECTION OF
TISSUE GROWTH
The magnitude and direction of loading can influence the amount and direction of tissue growth as well as affecting
the type of tissues and joints being
formed. The following principles show
how loads on the musculoskeletal system 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 considerable 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 epiphyseal plates are aligned perpendicular to
the major loads that cross them.
Volume 64 / Number 12, December 1984

Compression or tension across the epiphyseal plate, within limits, may stimulate 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 certain amount of compression seems to
be essential for conversion of cartilaginous tissue into bone.29
An increase in compression or tension
outside the normal range of loading inhibits 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 epiphyseal plate is an example of using
compression to retard bone growth.
Because epiphyseal plates align perpendicularly to the time-averaged resultant 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 loading. Thus, unequal loading along an epiphyseal 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 chondral growth than very large, but brief
and infrequently applied loads.27 Persistent gentle loads (creep) may lead to a
deformity or correction of a deformation.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 (perpendicular to the epiphyseal plate) will deflect
the growth along the line of the deforming force. As long as the load is maintained, 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 occur.25,27
Torsional loading. Because the epiphyseal plate is least resistant to torsion,
a torsional load will lead to a rotational
deflection of the growth columns
around the circumference of the epiphyseal 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' correction of tibial torsional problems.27
Gravity may be sufficient to affect
epiphyseal growth. Muscle forces, however, 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 gravity. An imbalance in muscle forces or
lack of muscle forces secondary to nonweight bearing may lead to skeletal deformation, 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. Compression 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 fibrous tissues such as tendon and ligaments that are similar to those produced
in bone.33 Increased weight bearing results 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 spaceflight,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 remodeling.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 convex surface has a net increase of bone as
1875

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 effect when bone is deformed.19,20,37 Intermittent current seems to be better for
proper bone formation than a continuous current.37 Hence, intermittent loading of a bone produces better development.

Effects of Loading on Trabecular

Bone
The internal structure of bones is developed 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 appears to be the major load to develop
trabeculae; however, tension loads can
also produce trabeculae.30,32 Bony trabeculae hypertrophy in response to increased 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 incompetence.26, 38-42 During about the first four
or five decades of a normal individual's
life, the internal replacement and adjustment of bone mass is maintained
according to the mechanical demands
made upon it. Because mechanical loads
provide a continual stimulus, the remodeling process continues. As an individual ages, however, the process proceeds at a slower rate. The bone attempts to maintain maximum density
in areas of maximum loading.13 Some
authors, however, have stated that this
adaptive remodeling loses its effectiveness and results in an increased bone
resorption and decreased bone formation 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 cartilage 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 atrophy. Secondary to either excess or lack
of compression, congenital deformities
can cause early appearance of degenerative joint disease.22, 35 The main mechanical factor causing cartilage degeneration appears to be repetitive impulse
loading, especially from muscle joint
forces.45, 46 Radin stated that repetitive
impulse loading for as little as 20 minutes each day over a period of several
months can aggravate the cartilage degeneration.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 degeneration can follow trauma, joint dysplasias,
subluxations, dislocations, slipped epiphyses, or segmental torsions.46-52 Once
the initial lesion occurs, physical activity
is necessary for the disorder to progress.53

Effects of Loading on Fibrous

Tissue
Soft tissues such as tendons and ligaments adapt in tension. They are selfaligning and their shape does not need
to be adapted. Their tissue properties,
however, are affected by increased or
decreased loading.13 Intermittent tension 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 immobilization, however, decreases their strength
and ability to absorb energy.55
Frost also expounded on the stretchcreep 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 prolonged 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, knowledge of the advantages and disadvantages of each treatment technique is essential.

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 extrinsic forces such as increased size, decreased 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, correction of a deformity is almost impossible.
Incorrect application of loads for correction 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, development, and maintenance for weight-bearing areas of the body.

RESULTS OF GROWTH
PRINCIPLES IN WEIGHTBEARING AREAS
EXAMPLES OF WEIGHTBEARING AREAS
Spine
The spine is composed of several
structures that provide both static and
dynamic stability. The 24 vertebrae consist of an anterior body that is the primary weight-bearing area and a posterior arch formed by the pedicles, laminae, transverse processes, spinous process, and articular facets.58 The size and
mass of each vertebra increases from the
cervical to lumbar area in adaptation to
PHYSICAL THERAPY

the increasing load from the superincumbent weight. The sacrum is the solid
bony base of the spinal column. The top
of these five fused vertebrae forms a 45degree 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 accentuation of shearing forces, and a diminution creates elevated compression.59
Spinal longitudinal growth occurs primarily in the vertebral body. Length
from cervical to lumbar areas is approximately 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 proportionate size of each area of the spine also
alters with growth. The cervical vertebrae become relatively smaller, and the
thoracic vertebrae enlarge in percentage
of total length. The lumbar area undergoes little alteration in relative proportions.60
Loads on the spine create both primary 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 cervical and lumbar areas and kyphotic in
the thoracic and sacral areas. These curvatures result from predictable developmental changes. At birth, the spine
has two primary posterior convex
curves. As the infant lifts his head
against gravity, the lordosis in the cervical area increases. Latent tightness of
the iliopsoas muscles persisting from fetal flexion, coupled with antigravity
work by the infant in a prone position
on flexed or extended elbows, in creeping, or in high kneeling encourage increased lumbar lordosis. Weak abdominal muscles provide little anterior pelvic support for the lordotic tendency.
Thus, the spine develops increased compensatory curvatures that allow close
approximation to the line of gravity and
provide inherent stability in all direcVolume 64 / Number 12, December 1984

tions.58,59 Abnormal or unusual developmental influences can disrupt the

normal symmetry and balance of the
spine, predisposing it to deformity.
One of the more prevalent spinal deformities is scoliosis. Although various
defects in embryological development,
such as failure of vertebral segmentation
or undergrowth of chondrification centers, can produce congenital scoliosis,60
the majority of scoliosis is caused after
the embryonic period. The problems of
muscular imbalance, abnormal muscular tone, persistent abnormal positioning, lack of or abnormal spinal weight
bearing noted in the various paralytic or
CNS disorders (eg, poliomyelitis, Werdnig-Hoffman disease, muscular dystrophy, myelodysplasia, and cerebral palsy)
can create an alteration of spinal dynamics, which predisposes the spine to
scoliotic changes.62 The etiology of idiopathic scoliosis, the most frequent nonneuromuscular variant, remains obscure. The possible causes are asymmetrical spindle sensitivity, increase in
number of slow twitchfiberson one side
of the spine, positional influences, or
asymmetrical vertebral and cord
growth. Any of these causes could create
abnormal forces during spinal development.63,64
Forces of deformation initially affect
the viscoelastic structures that are most
susceptible to creep. Ligaments and
muscles shorten and thicken on the concavity 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 migration toward the convexity. Additionally,
the disk becomes incapable of maintaining normal vertebral dynamics.62,65
If these changes occur while epiphyses
are still unfused, bony deformation results. 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 deformity, cause distortion of the vertebral elements and incongruity of the facet
joints. Rib rotation and lumbopelvic dysynchrony often accompany the vertebral distortion.62 The deformation thus
creates a self-perpetuating system. Creep

with eventual relaxation in combination

with the force of gravity causes exacerbation of the problem. The body attempts to remain balanced over the pelvis and frequently develops a compensatory curve.
Similar deformation in an anteroposterior direction can occur with kyphosis.
Postural faults and deficiencies of vascular 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. Excessive anterior pressure interferes with
anterior vertebral ossification and creates anterior wedging. The line of gravity
assists the deforming forces. The spine
compensates by developing an accentuated cervical or lumbar lordosis.
A third spinal condition of relative
importance is represented by spondylolysis or spondylolisthesis. Both conditions 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 spondylolisthesis. The anatomy of the lower
lumbar area predisposes this location to
the highest frequency of slippage.66-70
Secondary to the normal lumbar lordosis, compressive force is transmitted
through the neural arch instead of the
vertebral body. Either a single traumatic
or continual intermittent force in a hyperextended (hyperlordotic) position
can pinch the L5 isthmus between the
L4 articular facet and the upward projecting sacral process, fracturing the
weakest point, the pars interarticularis.
Hence, multiple factors could predispose the area to a hyperlordotic position. In addition to congenital birth defects, these factors include any abnormal
or persistent lumbar lordosis secondary
to muscular imbalance, abnormal position or muscular tone, or tightness of
the iliopsoas or lumbosacral area. Additionally, abnormal or lack of weight
bearing could produce reduced calcification in the lumbar area. Subsequent
movement superimposed on these conditions of hyperlordosis or decalcification can contribute to fracture and slippage as a sequela of increased shear
force.59
1877

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 anteverted 8 to 11 degrees with the shaft.
The head of the femur sits deeply in the
acetabulum and is secured by the labium and strong muscular and ligamentous attachments.71,72 This mature position is the result of major mechanical
influences during development on both
portions of the joint.
The pelvis is formed from three primary ossification centers: the ischium,
pubis, and ilium. These centers converge to form the triradiate cartilage.23
Endochondral growth in these areas allows the acetabulum to enlarge circumferentially commensurate with spherical
growth of the femoral head. The acetabulum, 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 maturity.71
Three growth zonesthe longitudinal growth plate, the trochanteric
growth plate, and the femoral neck isthmuscontribute 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 inclination is 150 degrees with approximately 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 malpositioned perinatally, the acetabulum and
femoral head develop congruently.32
This congruency is essential for proper
development of both portions.71,75 External 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 proximal 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 trabecular systems cross at right angles for
greatest resistance to compression and
bending stresses.14
Abnormal loading or joint incongruity can predispose the hip joint to developmental abnormalities. A frequent
deformity is congenital dislocation
(CDH) or subluxation of the hip.26 The
most probable causes are hereditary,
mechanical, or multifactorial combinations. 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. Restricted 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 restrained for prolonged periods in an adducted 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 followed 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 relocate or remain displaced.26

lae. The magnitude and direction of

loads applied to an atypically positioned
hip joint will determine the abnormality
of growth. A shallow or maldirected acetabulum, coxa vara or valga, or abnormal anteversion or retroversion could
result. When the forces of gait are superimposed, early degenerative arthritis
can follow.26,32
The child with cerebral palsy commonly develops various types of hip deformity. Abnormal positioning during
sleeping and sitting are contributory
causes.72,76 Muscular imbalance and
tone abnormalities, especialy in the adductors, iliopsoas, and hamstring muscles, place tremendous potential deforming forces across the developing
hip. Delayed weight bearing alters the
calcification rate, trabecular development, and angular changes of the hip
complex. Weight acceptance in abnormal positions can also create abnormal
force development across the acetabulum and proximal femur. Hence, this
population is subject to coxa valga, femoral anteversion, hip subluxation or dislocation, and hip dysplasia as adolescents or adults.

Knee
Several alignment changes occur at
the knee as development proceeds. In
the adult, the shafts of the femur and
tibia form an angle of 171 degrees secondary to femoral obliquity. This angle
is 180 degrees at birth and progresses to
160 degrees at 3 years of age and 171
degrees by 6 years of age. Therefore,
normal growth proceeds from relative
varus to extreme valgus to normal valgus positioning.10

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 tibial shaft undergoes torsional

changes during growth. Torsion at birth
is 0 degrees but increases to 23 to 25
degrees of external torsion by maturity.
Internal tibial torsion in the adult is,
thus, failure of normal tibial external
rotation.7 Because the epiphyseal plate
is less resistant to torsion, torsional deformities may readily occur if abnormal
forces are present.

The dislocated or subluxed hip in a

preambulatory child may not appear as
a developmental problem.26 If the condition is not corrected within a few
months, however, secondary growth alterations and abnormal forces during
gait can cause serious permanent seque-

The upper end of the tibia undergoes

three further developmental alterations
in alignment. The pull of the hamstring
muscles causes tibial retrotorsion, a natural posterior deflection of the proximal
end of the tibia. Retroflexion, or the
posterior bend of the shaft, is produced
PHYSICAL THERAPY

by the contraction of the gastrocnemiussoleus muscle group. The plateau of the

proximal tibia slants posteriorly about 5
degrees in the adult. This value, called
tibial retroversion, is a reduction in angulation from 27 degrees in the newborn
to 17 degrees at 3 years of age, 7 degrees
at 10 years of age, and 5 degrees by 19
years of age.58
Trabecular systems in both distal femur and proximal tibia originate from
all sides and align perpendicularly to the
articular surface for load resistance. Trabecule also develop in areas of muscular attachment in line with fiber direction to resist tensile forces. The patella
consists of multidirectional trabecular
systems resistant primarily to tension.58
The presence of any abnormal forces
during development can create many
deformities at the knee. Genu recurvatum is a frequent knee deformity noted
congenitally or postnatally. Malposition
in utero with the feet locked in the axilla
or under the mandible, as well as a
breech position, will cause the knee to
develop in extension instead of flexion. 17,29,77 Persistence of tibial retroversion, quadriceps femoris or hamstring
muscle weakness and tightness, or overactivity of the triceps surae muscle can
also create a genu recurvatum.78 Genu
recurvatum developed in utero can result in contracture of the quadriceps
mechanism and anterior capsule; a
small, abnormal, or absent patella; a
lengthened or absent anterior cruciate
ligament; and anterior dislocation of
hamstring tendons so that they act as
knee extensors. The existence of postnatal genu recurvatum, especially in an
ambulatory person, will cause weakening of the posterior joint capsule and
stretching and possibly tearing of the
anterior cruciate and collateral ligaments with resultant rotatory and
anteroposterior instability.
Many possible etiologies of developmental origin have been implicated in
genu varum and valgum. Obesity can
increase loading and create more abnormal mediolateral forces, which alter normal processes of growth. Epiphyseal
damage or avascularity and metabolic
deficiencies can create more deformable
bones that will alter under load. Familial
relaxation or secondary stretching of
collateral ligaments can exacerbate varus or valgus positioning. Muscular imbalance or abnormal tone, especially in
the thigh, can provide abnormal forces
on the developing knee.11

Volume 64 / Number 12, December 1984

Genu varum can specifically be promoted by a persistent prone sleeping

position with the hips and knees flexed
and the tibiae internally rotated. Both
double diapering and straddle carrying
can force persistence of normal varus
positioning.8 Early weight bearing before structures can tolerate the load has
been implicated, as has the absence of
normal tibial external rotation. Genu
varum produces other lower extremity
alterations, including compensatory
pronation, talar adduction, and intoeing. Early onset of osteoarthritis has
been noted in some adults secondary to
the abnormal loading forces.
The presence of genu valgum has
been noted in those patients with excessive external tibial torsion or pronated
feet. Both of these conditions create
forces that exacerbate medial deviation.
Prolonged prone positioning with limbs
flexed and tibiae externally rotated, as
well as "W sitting" with tibiae in external torsion, can predispose the knees to
excessive valgus positioning.10,11 The sequelae of genu valgum can be medial
laxity and rotatory instability secondary
to ligamentous creep. The iliotibial band
will shorten laterally and maintain the
deformity. An increased "Q angle" will
predispose the patella to lateral tracking
and potential chondromalacia. Compensatory rotational deformities of the
foot may occur to keep the sole flat on
the ground.
The most frequent knee disorder is
patellofemoral chondromalacia. Several
developmental problems have been associated with this disorder. As it forms,
the patella conforms to the condyles in
utero because the knee develops in flexion. Any embryological defect in articular cartilage might predispose the joint
to patellofemoral incongruity. A congenitally small patella will provide less
area for dispersion of force. Any abnormality of knee development, either bony
or positional, will create patellar malalignment and irregular trochlear tracking.
Additionally, malposition or malalignment of any portion of the lower
kinetic chain can place abnormal force
on the patellofemoral articulation.78,79
Both overuse and underuse of the knee
have been cited as potential sources of
developmental abnormality. Continual
heavy compression and increased patellofemoral forces in heavy exercise, knee

walking, or ambulation in knee flexion

will cause articular degeneration. Lack
of functional stress in flail, immobile, or
nonambulatory limbs can produce atrophy of articular cartilage.22

Ankle-Foot
The ankle-foot complex undergoes
some very complex developmental realignment in utero. The primitive foot
is initially directed medially and cranially. By the eighth fetal week, the soles
face each other like "praying feet." The
feet are aligned with the leg as no ankle
angulation has yet occurred, so they appear in talipes equinus. Changes in the
talus and calcaneus in the seventh fetal
month drastically alter foot position.
The talus widens as the head begins to
torque. The entire bone shifts laterally
to align with the axis of the foot. These
changes continue postnatally to counterbalance tibial external rotation. The
calcaneus grows broader and longer posteriorly. The angle of the tuber calcanei
with the tibia is reduced from 36 degrees
in the third fetal month to 22 degrees at
birth, 16 degrees in adolescence, and 3.5
degrees at maturity. Concurrently, lower
extremity flexion increases so the feet
are positioned in extreme dorsiflexion
against the uterine wall and appear in
calcaneus position at birth.
The postnatal foot is very elastic with
no longitudinal arches. Muscles and ligaments have not yet developed normal
strength and elasticity. Initial stance
demonstrates a wide base with external
foot position for stability. The feet appear flat and pronated. Gradually, an
arch develops as strength increases. By
2 years of age, the arch is apparent in
weight bearing with a neutral heel position and minimal out-toeing of the
foot.80,81
Growth of the foot is similar in both
sexes until 12 years of age. Half of mature length is achieved in the first year
with a linear annual increase thereafter.
The male foot grows slightly more rapidly during adolescent years so total
length is slightly greater.82
Trabecular development relates both
to compression and soft tissue tension.
The calcaneus has primarily a cortical
structure with few trabeculae that relate
to weight-bearing compression and tensile pull of the triceps surae muscle and
longitudinal arch. The pattern in the

1879

talus demonstrates an arch related to

compression with vertical lines in the
neck area.83
Because of its distal location, flexibility, and late ossification, the foot is very
susceptible to deformities. One of the
most common deformities is metatarus
adductovarus. Several prenatal factors
can contribute to this deformity. Malposition in utero with the feet wrapped
around each other or the body can cause
a varus angulation. Increased mechanical pressure from maternal abdominal
muscle tone, large fetus, or small uterus
and increased hydraulic pressure could
make fetal foot repositioning difficult. A
neuromuscular disorder causing muscular imbalance or paralysis could also
hinder fetal positioning. Postnatal sleeping rotation could create varus deformation.8,11,17 The functional deformations that might result from metatarsus
adductus include widening of the first
two toes, in-toeing or heel eversion, and
foot supination. Talipes equinovarus is
the most frequently diagnosed form of
clubfoot. Malposition in utero or failure
of lower limb rotation has been implicated along with increased pressure and
muscular imbalance. Because of the severity of this deformity, a defect of germ
plasma before the seventh fetal week has
also been postulated as a causative factor. The major problem is talipes
equinus or calcaneus with these bones
overlaying each other. The navicular is
medially displaced on the talus and the
metatarsal shafts adduct. These deformities cause shortening of musculature,
ligaments, and skin medially and posteriorly. The remainder of the bones
rotate medially and mold into abnormal
configurations with deviant articular
surfaces. Compressed vascularity causes
further delay of appearance of ossification centers.17,77 Pes planus, diagnosable
only at 16 to 28 months of age, can
result from primary or secondary developmental abnormality. Shortening of
the first metatarsal, or metatarsus primus varus, can cause a primary pes
planus, as can muscular imbalance and
hypermobility syndromes. Pes planus
also occurs as an adaptive sequela of
genu valgum or torsional deformities.
Theflattened,pronated position creates
a flexible forefoot that can lead to ligamentous creep. A decreased longitudinal bony arch can result from abnormal
compressive loading. Continual medial
loading may also create increasing internal rotation of the first metatarsal. The
1880

reduction of foot stability will require

greater muscular activity for weight acceptance and transfer. The triceps surae
muscle is displaced laterally and is shortened. It becomes an evertor and plantar
flexor, and the tibialis anterior additionally begins to dorsiflex and evert. Both
of these muscles exacerbate the preexisting pronation.81,84
THERAPEUTIC APPLICATION
The preceding clinical problems are
only a few examples of deformities that
can be caused by mechanical forces.
Early recognition of these causative factors are important for prevention or reduction of the degree of the deformity
and disorders through elimination or
counteraction of these forces. Intervention strategies must be accurately directed toward wise and judicious use of
biomechanical and growth principles to
create positive change effectively and
efficiently. Intervention can assume any
of three possible forms: mechanical, surgical, and therapeutic.
MECHANICAL INTERVENTION
Mechanical intervention is primarily
the use of orthotics or positional devices
for correction and maintenance of alignment. These devices use three-point
pressure systems and force couples to
create positive deformation. The principle of creep is used to produce slow
but permanent change over a long period of time.
The use of orthotic devices and serial
casting takes advantage of the plasticity
of tissue and the growth potential of
bony structures. The method of treatment may use corrective forces similar
to those that produced the deformation.9 Modification of footwear, use of
braces such as the Swedish cage or calipers for the hyperextended knee, Pavlik
harnesses for dislocation of the hip, or
serial casting for clubfoot are all examples of mechanical intervention.
SURGICAL INTERVENTION
Surgical procedures also use biomechanical principles as a basis for correction of a deformity. Selective use of
compressive or distractive force can
modify a preexisting condition or reverse deforming forces and prevent
bony molding. Instrumentation or bony

fusion use long-term or permanent stabilizing forces to produce creep and

eventual relaxation of deforming structures.
Surgical intervention may be necessary if conservative measures have not
been successful. This should be done as
soon as the clinical staff establish that
conservative measures are not working.9
Better results from surgery are achieved
if it is performed sufficiently early.85
Early surgical procedures to establish
proper bony alignment will allow mechanical forces to provide more normal
development. Examples of surgical procedures include epiphysis stapling,
which will increase compression across
the epiphysis and retard longitudinal
growth, and osteotomies, which can provide more normal alignment of the affected body part. Surgical procedures
such as joint replacements or arthrodeses may be necessary later as the
patient ages.
THERAPEUTIC INTERVENTION
Therapeutic intervention consists of
any procedure designed to strengthen,
normalize tone and muscular balance,
improve posture and coordination, increase joint or muscle range of motion,
and normalize function. The principles
of growth and biomechanics must be
applied to any therapeutic procedure to
assess how, when, and where it should
be applied. The length of time of application must also be considered, both in
terms of specific technique application
and positional modification. Only
through understanding and application
of these principles can therapeutic intervention be effective in reversing deformation.
Mechanical factors have long been
considered a part in the destruction
process that ultimately leads to joint
deterioration.45-53,86-89 To prevent or delay joint deterioration, trauma should
be avoided and deformities should be
recognized and treated as early as possible. Early gait analysis may help in
recognizing problems before bony destruction takes place.48
The treatment of osteoporosis is still
controversial and poorly understood.40
Prevention or delay of osteoporosis is
the best treatment.41,44 This can be done
in many cases by early strengthening of
the bone. Weight bearing and reaction to
muscle contractions stimulate osteoPHYSICAL THERAPY

blastic activity. Although this bone loss

may be universal, recent literature indicates that physical activity early in life
may prevent bone loss.26,41-43 Continued
physical activity in adulthood may also
prevent or delay the loss of bone mineral.41 In fact, some authors reported
that local bone mass may be increased
in the elderly with proper physical activity.14,41,90 Osteoporosis seems to be rare
in the active individual.44 Weight training can influence increase in bone density.40,43,91,92 Smith and Reddan found
that physical activity for the elderly can
help in prevention and treatment of osteoporosis.14 Early bone atrophy may be

reversed by physical therapy procedures

such as providing weight bearing for two
to three hours daily.90,91
Fractures of vertebrae and the proximal end of the femur are major complications of osteoporosis.44,93,94 Deformities, especially in the spine, resulting
from collapsed vertebrae also occur. Osteoporosis provides little support for internal fixation of fractures and joint replacements.95 Clinicians must be aware
of these complications when they treat
elderly patients. For example, a hip fracture may occur before a patient's fall or
occur during evaluation or treatment.

SUMMARY
This article provides a broad overview
of the growth, development, and maintenance processes that are related to biomechanical principles. It also provides
the major mechanical factors related to
growth and development. By combining
knowledge of these growth factors and
the principles of biomechanics, clinicians should be able to evaluate and
perform prevention and treatment procedures that are being used today. They
should also be able, with some creativity, to devise better procedures for the
future.

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PHYSICAL THERAPY