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A COMPARISON OF THE WEIGHTS
OF THE PELVIC MUSCLES

OF NORMAL AND DYSPLASTIC DOGS

By

.'VF
Susan szfiorowitz

A.THESIS

Submitted to
Michigan State university
in partial fulfillment of the requirements
for the degree of

MASTER OF SCIENCE
Department of Anatomy

1968

ACKNOWLEDGEMENTS

I should like to thank Dr. A1 W. Stinson, my advisor and
committee chairman, for all suggestions and help rendered in
the course of my research and the writing of this thesis. I
sincerely appreciate his time and patience.

I am thoroughly indebted to Dr. Wade Brinker, whose aid
in procurring animals for dissection was invaluable. Appre-
ciation is also felt for his taking the time to serve on my
committee and for offering advice during the writing of this
manuscript.

I should also like to thank Dr. Richard Kociba for
serving as a committee member and for help in the preparation
of this thesis. I am grateful to Dr. M. Lois Calhoun for her
suggestions while preparing this manuscript.

I am.especia11y grateful to Dr. William Heusner for
programming my data and all his help given in the realm of
statistical analysis and mathematical manipulations.

Many thanks to those in the Department of Anatomy whose
brains were picked during my two year sojourn. Appreciation
is extended to Mr. Dave Elliott for his help in collecting my
material, to Reggie Edgerton for his timely help in explaining
how and where to put the numbers and to Judy Vargo for typing

and making this manuscript exist.

II

TABLE

INTRODUCTION . . . . . . .
REVIEW OF LITERATURE. . . .
MATERIAL AND METHODS. . . .
RESULTS AND DISCUSSION. . .

Statistical Analysis

OF CONTENTS

Total Pelvic Muscle Mass . . . .

Action Groups of Muscles . . . .

Individual Pelvic Muscles. . . .

Collateral Observations. . . . .

SUMMARY AND CONCLUSIONS . .
LITERATURE CITED. . . . . .

APPWDIES O O O O O O O O 0

III

Page

12
16
16
16
22
25
29
31
33

38

1.

2.

3.

LIST OF TABLES
Table Page
Animals used.in the study . . . . . . . . . . . . . . 15
Results of statistical analysis and
calculation for relative underdevelopment
in dysplastic dogs for pelvic muscle mass
and action groups . . . . . . . . . . . . . . . . . . 17
Results of statistical analysis and
calculation for relative underdevelopment

in dysplastic dogs for each pelvic muscle . . . . . . 18

IV

1.

2.

3.

4.

5.

LIST OF FIGURES
Figure
Total pelvic muscle mass relative
tobodyweight ............
Action groups of muscle relative
tobodyweight ............
Individual pelvic muscles relative
tobodyweight ............
Amount of underdevelopment in the
total pelvic mass and action groups
of dysplastic dogs relative to normal

50p0Imddog8.............

Amount of underdevelOpment in the individual
pelvic muscles of dysplastic dogs relative

tonormalSOpounddogs...........

Page

20

23

26

24

24

LIST OF APPENDICES
Appendix Page
1. Raw weights of eadh pelvic muscle
for each animal . . . . . . . . . . . . . . . . . . . 38
2. Total pelvic muscle mass and action
groups for each animal relative to
its body weight . . . . . . . . . . . . . . . . . . . 41
3. Individual muscles for each animal

relative to its body weight . . . . . . . . . . . . . 42

INTRODUCTION

The description "congenital dysplasia of the hip joint" has
been adapted by the veterinary profession to depict a condition
in dogs characterized by a failure of the proper development of
the hip joint as a whole. It can be shown radiologically as
varying degrees of failure of prOper fit of the femoral head to
the acetabulum. Clinically, it is Characterized by an abnormal
gait and at necropsy by the reaction of soft and bony tissue to
constant microtrauma implicit in abnormal mObility of the femoral
head (Snavely, 1959).

Reduced to its etymological translation, dysplasia of the
hip simply means "bad form of the hip." Records of a similar
disorder in man date from Hippocrates. The first description of
the malformation in the dog, however, was not made until 1935 by
Schnelle.

During the past three decades there has been much semantic
discussion of the propriety of the name given to the condition
seen in the dog. Congenital does not seem to be applicable since
the joint of the newborn puppy has been shown to be normal in
appearance, both grossly and histologically.

Many other terms have been applied to the condition; these
include congenital dislocation, congenital subluxation, congenital
luxation and acetabular dysplasia.

Hip dysplasia is not Legg—Calves-Perthes disease (asceptic
necrosis) or epiphysiolysis, two other conditions affecting the
hip joint. These conditions occur at different ages and in

different types of dogs than hip dysplasia and are the result

1

2
of interrupted vascular supply to the area of the femoral head
(Wamberg, 1961).

This maldevelopment of the joint seems to be inherited and
affects most of the large breeds of dogs with an incidence of
50 per cent or more (Riser, 1963). Since this involves the
working, hound and sporting groups of dogs, which are still used
in capacities other than pets and whose functioning is disabled
by hip dysplasia, the importance of establishing the etiology
of the condition is evident.

The hip joint is so structured that muscle pull is necessary
to prevent luxation when the joint bears weight. Riser (1963)
determined that the pelvic muscle mass of dysplastic dogs is less
than that of normal animals.

Since one factor in holding the joint in congruity is the
muscle mass of the area, this study was performed to determine
whether the lack of development of the pelvic muscle mass of
dysplastic dogs is general or whether it involves one of the
action groups (flexors, extensors, adductors, abductors) or
whether it involves only individual muscles. With the establish-
ment of the exact muscular components involved, further study

could be directed toward these muscles.

REVIEW OF LITERATURE

Clinical symptoms are present in only twenty to twenty-five
per cent of all radiologically diagnosed dysplastic dogs
(Wamberg, 1961). The first symptoms to appear in puppies are;
clumsiness, swaying of the rear quarters, a slight limp in one
or both hind limbs and an insufficient drive with the rear
quarters. With increasing age further symptoms appear such as
lameness following exercise, difficulty in climbing up and down
stairs, a shorter hind limb stride, pain with pressure over the
hips, sitting with the hind legs extended forward or to the
side rather than under the pelvis on its haunches, incoordinated
gait and a desire to sit (Konde, 1954; Wamberg, 1961 and Mostosky,
1962).

In man, hip dysplasia can be initially diagnosed by the
Ortolani click, which is produced by a manual luxation of the
joint resulting in a clicking noise. During this procedure, one
can feel the femoral head slip in and out of the acetabulum
(Andren and von Rosen, 1958). There is some debate as to
whether this can be done in dogs. Henricson.§£”§1, (1965) claim
to be able to perform this manipulation in dogs under anesthesia
at the earliest age of two weeks. Bardens and Hardwick (1968)
were very enthusiastic about this as a diagnostic aid in pups at
four weeks of age.

Even with the clinical signs, which are not seen with a
great amount of frequency, and palpation, which at best can only
be positive for the more extreme cases of dysplasia, the condition

must be diagnosed radiologically for certain confirmation. Although

3

4
the radiograph is the most accurate diagnostic tool of the
veterinarian, the picture must be taken with extreme caution
and with standard positioning. Lawson (1963), Riser (1962),
Riser and Rhodes (1966) and Whittington ggugl., (1961) considered
the accurancy of positioning and gave directions for the correct
procedure. Age of radiographic diagnosis varies with the
severity of the condition and can be made at four weeks (Mmksic
and Small, 1962), although most suggest six months or older
(Wittington, g; 9_1_., 1961).

There have been two systems worked out to measure the
acetabular depth on radiographs and thus determine the degree of
shallowness that is present. It is the shallowness or the degree
of development of the acetabulum which is diagnostic for hip
dysplasia (Rhodes and Jenny, 1960, and Norberg, as cited by
Olsson 1961b). On the basis of the different degrees of severity
of the pathological changes, Schnelle (1954) set up a grading
system of one to four, representing a range of a slightly poor
fit between the femoral head and the acetabulum.to a very severe
displacement of the head of the femr from the acetabulum.

Since the variations of hip dysplasia affect at least forty
breeds of dogs, it is essential to determine its etiology. The
mode of inheritance was at one time considered to be recessive
(Schnelle, 1954), but more recently workers in the field indicate
this is a misconception. Work done by Faber, Hooff and Verschuer
as quoted by Schales (1956) demonstrated that in man hip dysplasia
is transmitted as a dominant characteristic with irregular

penetrance. After studying the Swedish Army dogs, Henricson and

5
Olsson (1959) postulated an incomplete penetrance of possible
monogenic characters, rather than a simple recessive inheritance.
They further indicate that the incompleteness may be a result of
external environment or the effect of the genetic environment.
Schales (1962) did a thorough genealogical study of dogs and
concluded that in fact canine hip dysplasia is inherited as a
dominant characteristic with irregular manifestation. Hutt
(1967) theorized a polygenic trait caused by cumulative action
of an undetermined nuaber of genes. A common feature of this
type of character is a gradation between extremes of the expression
of a trait, which is characteristic for hip dysplasia. He also
stated that the degree of expression can be influenced by the
environment. Kamen and Gossling (1967) also proposed that the
genetic connotation is complex and multifactorial. Rein (1963)
considered the manifestation of dysplasia as a.phenotype to be
influenced by the presence or absence of an epistatic gene or
environmental factors or both together, thus explaining incomplete
penetrance. She also theorized that inheritance is multifactorial
or polygenic due to the wide variation in severity of the defect.
Bonfors'ggugl., (1964) described the inheritance as autosomal
since there is an equal sex distribution in dogs. He indicated
n (the number of

N’
parental combinations with at least one defective divided by the

the penetrance was according to the formula

total number of litters comprising at least one defective) which
equals sixty percent; or in other words forty percent of the
German Shepherd breed carrying the genetic background for hip

dysplasia are phenotypically normal.

6

Further evidences, other than paper genealogical studies, that
hip dysplasia is inherited are actual reductions of the condition
by planned breeding. Thus, hip dysplasia was eliminated from.a
kennel of Samoyeds (McClave, 1957) and the Swedish Army has also
been able to reduce the incidence by almost one half in their
kennel by selective breeding (Henricson and Olsson, 1959).

Establishment that hip dysplasia is inherited is not generally
contested, but much controversy does arise in determining what
prime etiological factor is genetically carried. Basically there
are three different theories of primary cause:

a. A.congenital malformation of the bones of the joint which

causes dislocation.

b. weakness and laxity of the joint capsule and ligaments
due to a hormonal imbalance and therefore failure to keep
the joint in congruity.

c. Lack of muscle mass for some unknown reason, possibly
disuse strephy or a physiological atrophy, which results
in a failure to hold the joint in place.

Badgley (1949) considered the condition a response to a timing
concept malfunction. He proposed a dynamic concept of a changing
structure with an inherited alteration in the proper timing of
growth or overstimulation leading to faulty develOpment. Although
growth is potentiated intrinsically, extrinsic factors may alter
the intrinsic design.

Hart, as quoted by Innes (1957), is the major proponent of
the theory of a primary defect in the development of the acetabulum,

which he considers as the predisposing cause of hip dysplasia.

7
Schnelle (1959) and Schales (1959) also considered the lesion to
be primarily the result of a faulty deve10pment of the acetabulum.
Paatsamaiggugl., (1966) demonstrated histological and histo-
chemical changes occurring first in the acetabular cartilage and
the epiphysis of the femoral head of dysplastic dogs. Paatsama
and Rissanen (1965) found these changes occurring as early as
three and one half months of age, before the condition was
radiologically seen.

Although Henricsson and Olsson (1959) considered an
acetabular lesion primary, Henricsson g_t_ 51., (1966) reversed
this opinion and stated there is no evidence of a primary
underdevelopment of the acetabulum. Some experimental work
by Smith (1958) indicated that aplasia of the acetabulum is a
result of dislocation rather than the cause. This theory is
based on the fact of experimental dislocation leading to an
acetabular dysplasia (Smith, 1963 and Smith‘ggugl., 1958).
Langenskiold and Laurent (1966) also found that experimental
dislocation is followed by dysplasia. Caffy ggugl., (1956)
studied the normal variation of the acetabular angles of infants
and concluded that the acetabular predislocation theory was not
valid. Andren and von Rosen (1958) also considered the hypOplasia
of the acetabulum to be a result of hip dislocation rather than
the cause.

Chapple and Davidson (1941) and Hofmeyer (1963) emphasized
the fact that the conversion of the cartilagenous acetabulum and
femoral head to bone depends on induced pressure of the two

structures on each other. Therefore, if the femoral head is not

8

closely invested in the acetabular socket the needed stimulus for
ossification is diminished. They concluded that hip dysplasia is
a result of a relaxation or looseness of the soft tissues associated
with the joint, which are incapable of keeping the bones in tight
congruity. Porsyth and Paschall (1963) believed that hip dysplasia
is only one component of an inherited, generalized condition
involving variation in strength and tone of the joint capsule and
supporting structures, which are, in turn, susceptible to forces
applied by weight bearing, muscle pull and an alteration in the
positioning of the bony elements composing the joint in question.

According to Henricson g 31;, (1966) the main feature of
hip dysplasia is a varying degree of laxity of the hip joint
permitting subluxation early in life, therefore giving rise to
skeletal changes. This same theory of relaxation of the joint
capsule was also prOposed by Howorth (1947). The primary cause
of dysplasia is considered by Langenskiold‘ggugl., (1962) to be
a flaccidity of the capsule and ligaments of the hip joint, the
stretched capsule therefore allowing displacement and deformities
of the acetabular socket and femoral head. This dislocation is
only a part of an increased pelvic instability. Somerville (1961)
also considered the pathological changes secondary to a primary
relaxation of the capsule, predicated on maternal hormone
influence.

Andren (1960) stated that the etiology of hip dysplasia is
primarily due to maternal hormones which cause a relaxation of
the capsule and ligaments. Therefore the inherited characteristic

is an increased reaction to maternal hormones and not the

9
dislocation or dysplasia. In 1962 he further stated that hip
dysplasia was only one sign of a general pelvic instability and
that the effect of maternal hormones is specific for all the
tissues of the pelvis. This concept is based on work done by
Andren (1961) and Andren and Borglin (l961a,b) where they found,
by urine analysis, a disordered estrogen metabolism of newborn
children. They also administered large doses of estrogen and
caused a widened symphysis pubis in experimental animals. They
have also induced abnormal 17-B estrogen excretion (which is
diagnostic for dysplastic children) in normal children by
injecting exogenous 17-B estrogen. They conclude that there
is some abnormal enzymatic malfunction in the metabolism of
estrogen.

Zaffaroni (1958) reported that an overdose of estrogenic
hormones in cattle and sheep causes elasticity of the ligaments
which is followed by luxation of the femoral head from.the
acetabulum. Wilkenson (1963) produced hip dislocation in
rabbits by inducing joint laxity with hormones, and also
considers breech malposition as a contributing factor by
stretching the weakened capsule. Mansson and Norberg as quoted
by Riser (1964) treated newborn puppies with relaxin and estrogen
or treated the damuwith relaxin and thus induced dislocation of
the hips in the puppies. Pierce'ggugl., (1964) were able to
induce joint laxity and eventual dislocation of the coxofemoral
articulation by prolonged treatment with estradiol. Pierce and
Bridges (1966) found a lowered capacity to metabolize biologically

active estradiol in animals with inherited hip dysplasia. They

10
considered dysplasia to be secondary to the joint laxity produced
by hyperestrogenism.due to an inherited malfunction of the
enzyme activity involved in estrogen metabolism.

Riser (1963) considered the condition as the result of a
biomechanical imbalance and thus the joint demands a certain
amount of develOpment of the ligaments and muscles of the area
in order to have the needed integrity. He believed the prime
reason for the malformation of the joint was a lack of
develOpment of the pelvic muscle mass. Riser and Shirer (1967)
established a difference in muscle mass between dysplastic and
normal dogs and found that they could differ by as much as fifty
percent. Brookes and wardle (1962), working with human material,
found that unbalanced mscle action alters the shape of bone.

There are others who consider that there is a basic muscle
weakness, but the definition of an exact muscle or group of
muscles that is responsible varies. Bardens and Hardwick (1968)
found the pectineus muscle especially atrophic and suggested a
close look at all the adductor muscles with special attention
given to the muscles innervated by the obturator nerve. Bado
(1961) suggested an insufficiency of the adductor muscles while
Man (1961) believed there is a reduced efficiency of the abductor
muscles. Riser and Shirer (1964) also suggested the abductor
muscles and rotator muscles are most responsible for holding the
joint stable.

Working with normal neonate dogs, Fox (l963a,b) observed an
initial muscle flaccidity at birth, which changed to an increasing

dominance of flexor tone and then to a period of extensor dominance

11
with a balanced tone as the animal matured. Salter g; _a_1_.,
(1963) found that constant extension will lead to dysplasia in
pigs while constant flexion will not. Fox (1964) observed a
longer period of extensor dominance in neonate dogs that proved
to be dysplastic with maturity.

As a conpanion of a lowered mscle mass Riser e_t_ 51;,
(1964) suggested that in those large breeds predisposed to
dysplasia, rapid growth and weight gain during the critical
first four and one half months may injure the soft supporting
tissue. Pierce and Bridges (1966) agreed that the increased
weight and rate of growth may alter the performance of the

weakened articulation, thereby enhancing abnormal development.

MATERIALS AND METHODS

The basis for this research was a litter of purebred Labrador
Retrievers which had been radiographically diagnosed to have
grade four hip dysplasia. These animals had been originally
donated to the College of Veterinary Medicine of Michigan State
University. The litter was comprised of two females and three
males whose weights ranged from 25.0 to 17.1 kg (55.0 to 37.5
pounds). Age at the time of dissection ranged from seven to
nine months.

With these animals as a reference point and proceeding on
the assumption of Riser (1963) that there is a critical weight
of 25 to 30 pounds, such that dogs above this weight will be
prone to dysplasia while dogs below this weight will most likely
be normal, a second group was approximately matched by weight.
Thus, dogs were sought with normal hips whose weight and body
conformation closely approximated the dysplastic group. Five
adult mongrel dogs were obtained from the Departments of
Physiology and Pharmacology. There were two females and three
males in this group also and their weights ranged from 25.0 to
20.4 kg (55.0 to 45.0 pounds).

As a matter of interest and to evaluate a proposal of
Riser (1963) that those dogs below the critical weight should
have a relatively higher pelvic nascle mass than the dysplastics,
five additional mongrel dogs were acquired from the Michigan State
Veterinary Clinic. These were two females and three males
weighing from 9.1 to 7.7 kg (20 to 18 pounds) and whose age

12

13
ranged from approximately six months to adulthood. Table 1
summarizes these groups.
All fifteen dogs had been euthanatized the day of dissection
or one day previously in which case the cadaver was stored in a
cooler. At the time of dissection each animal was skinned at
the pelvis and pelvic limb and any excess fat was trimmed from

the area. The sixteen muscles dissected were as follows:

Quadriceps femoris Iliopsoas

Biceps femoris Superficial gluteal

Adductor magnis et brevis Internal obturator
with adductor longus External obturator

Semimembranosus Deep gluteal

Middle gluteal Pectineus

Semitendinosus Quadratus femoris

Gracilis Gemelli

Sartorius

Determination of which muscles to weigh was made on the basis of a
similar project completed by Riser (1963). According to Miller
$15.21., (1965) who have listed the mscles of the region and their
actions at the hip joint, five action groups of muscles were
composed. Two groups of flexors were made since only one head of
the quadriceps actually is considered to act on the hip. The

groups and their muscles are as follows:

1. Adduction 3. Extension
a. adductor magnus et brevis a. biceps femoris
with adductor longus b. semimembranosus
b. gracilis c. middle gluteal
c. aartorius d. gracilis
d. pectineus e. semitendinosus
f. superficial gluteal
2. Abduction g. deep gluteal
a. biceps femoris h. quadratus femoris
b. internal obturator
c. external obturator 4. Flexion without the
d. deep gluteal quadriceps femoris
e. quadratus femoris a. adductor magnus et brevis
f. gemelli with adductor longus

b. aartorius
c. iliopsoas

l4

5. Plexion with the quadriceps femoris
a. adductor magnus et brevis
with adductor longus
b. aartorius
c. iliopsoas
d. quadriceps femoris

The dissection was carried out on both hind limbs and each
muscle was individually weighed to the nearest tenth of a gram.
In order to calculate the total pelvic muscle mass the muscles
of both limbs were added together and divided by total body
weight.

After the dissection was completed the ossa coxae and the
femurs were disarticulated and boiled to remove any adherring
tissue. The denuded bones were then thoroughly examined to
determine the condition of the hips, especially the mongrel
groups since there had been no radiographs taken to determine

normalcy of these two groups of dogs.

15

Table 1. Animals used in the study.

 

 

 

 

 

 

 

 

 

 

 

“Wei ht

ormal 50 pound 2 female adult 23.0
ormal 50 pound 3 male adult 22.7
zormal 50 pound 4 ‘male adult 22.0
ormal 50 pound 5 female adult 20.4
ormal 20 poundwmflt 9.1
ormal 20 pound 2 adult 8.6
ormal 20 pound 3 months + 8.2
ormal 20 pound 4 months + 8.1
Normal 20 pound 5 months + 47.7
yaplastic 1 months 25.0
ysplastic 2 months 21.6
ysplastic 3 months 19.3
ysplastic 4 months 19.1
splastic 5 female months 17.1

 

 

 

 

16

RESULTS AND DISCUSSION

Statistical Analysis

An analysis of variance was computed to determine whether
there was a significant difference in the relative weights of
the pelvic muscles of three groups of dogs - normal 50 pound
dogs; normal 20 pound dogs; and dysplastic dogs. Analysis was
made on the total weight of the pelvic muscles; the total weight
of each action group (flexors, extensors, abductors and
adductors) and the weight of each individual muscle comprising
the pelvic mass. The raw data used in the statistical analysis
is shown in Appendix 1. The F—test (Guenther, 1964) was used to
determine the existence of any significant difference among the
three groups of dogs.

Since the Pbtest only indicates the existence of a significant
difference, further calculations had to be made. The Tukey method
for multiple comparison (Guenther, 1964) was used to find where
the significant difference among the three groups - normal 50
pound, normal 20 pound and dysplastic - might be. For that data
shwoing no significant F—statistic at the 0.05 level of rejection
of the hypothesis of equal means, the power of the Retest was
computed. The results of these tests are incorporated in Tables

3 and 4.

Pelvic Muscle Mass
The differences among the pelvic muscle mass of the normal
50 pound, normal 20 pound and dysplastic groups is presented in

Graph 1. The Tukey analysis shows there is a significant difference

17

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:H ucoeaoao>oouoocs o>muemou now :oHuoaooAmo one mammfiocm Hooauwfiumum mo mufiomom A.oucoov .m moose

20

Graph 1. Total pelvic muscle mass relative to body weight

15.0
14.0

13.0
12.0
11.0
10.0
' 9.0
3.0

7.0

6.0
5.0
4.0
3.0
2.0

w 1.0
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‘0.

Per cent of total body weight

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Groups of animals measured

5 Normal 50 pound dogs
E Normal 20 pound dogs

I Dysplastic dogs

21

between the pelvic muscle mass of the normal 50 pound and the
dysplastic group (see Table 4). This corroborates the work of
Riser and Shirer (1967) and Riser (1963) that there is a lack
of muscle mass of the pelvic area in dogs with hip dysplasia.

Although a lowered pelvic muscle mass in the dysplastic
animals was shown, further attempts at comparison of values found
in this study with those of Riser and Shirer (1967) proved
futile. The mean values of the pelvic muscle mass of the
dissected dogs in this experiment are lower than those reported
by the above workers. The pelvic muscle mass relative to the
body weight of each animal used is shown in Appendix 3. Table 4
gives the group means.

Since there was interest in Riser's theory of similitude
(1963), the differences between the normal 20 pound and dysplastic
groups and those between the normal 20 pound and normal 50 pound
groups were observed. No significant difference was reported
between the means of the normal 20 pound and dysplastic groups.
Although there was a significant difference between the normal
20 pound and the normal 50 pound groups, the value for the pelvic
muscle mass of the normal 20 pound group was much higher than that
reported by Riser and does not agree with his theory that a dog
of 50 pounds and 24 inches high at the shoulder will have a
pelvic muscle mass three times that of a dog 20 pounds and 12
inches at the shoulder.

Results of this study show a definite decrease in the total
muscle mass of the pelvic area of dogs with hip dysplasia. There
does not seem to be a direct causal relationship between lack of

muscle mass of the area and a biomechanical imbalance.

22

Action Groups of Muscles

The differences in the weights of the action groups of muscles
of the three groups of dissected dogs is shown in Graph 2. The
data shown by this graph indicated that there is a lack of
development as the muscles are grouped according to their action
on the hip joint.

An attempt was made to determine which one of these action
groups was most affected by the underdevelopment. This calculation
was done by taking the difference between the means of the normal
50 pound group and the dysplastic group and dividing the difference

by the mean of the normal 50 pound group i.e. N50 ‘ Dysplastic. It
‘ 50
was not possible to satisfy the requirements for a statistical

test for the significance of the above calculation, therefore only
trends are reported.

The extensor and abductor groups seem to be most affected
(see Graph 5). This work strengthens the suggestions by Riser and
Shirer (1964) and Man (1961) that the abductors may be unduly
affected in the dysplastic animals. This study also indicated that
the extensors, which in the normal animal contributes most to the
pelvic mass, are the moat underdeveloped in the dysplastic animal
and may be an area for further concern.

Since there was some question about the action of the quadriceps
femoris, other than its rectus femoris head, two groups of flexors
were constructed - one containing the quadriceps and one without.
Graph 5 demonstrates what contribution the quadriceps makes to the
flexor group. Graph 4 indicates a lack of development in this

muscle. From both of these graphs it can be inferred that this

x

23

Action groups of muscles relative to body weight.

Graph 2.

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Action groups measured

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24

Graph 4. Amount of underdevelopment in the total pelvic mass and

action groups of dysplastic dogs relative to the normal

50 pound dogs.

 

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Groups measured

muscles of dysplastic dogs relative to normal 50 pound

Graph 5. Amount of underdevelopment in the individual pelvic
dogs.

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*-overdevelopment rather than underdevelopment

25
muscle as a whole is not greatly affected and does not have a

great affect on the act of flexion at the hip.

Individual Muscles of the Pelvic Mass

A general trend of atrophy throughout all of the muscles of
the pelvic area of dogs with hip dysplasia is shown in Graph 3.
With the exception of five muscles, iliOpsoas, external obturator,
deep gluteal, pectineus and quadratus femoris, the statistical
data in Table 3 demonstrates a significant difference between
the normal 50 pound and the dysplastic groups.

The calculation using the formula Meanggo ' :33“ Dys.’ used
an

to determine the lack of development of the action groups, was also
used to find the lack of development occurring in each individual
muscle. Since this data cannot be analysized statistically, the
following is a report of the trend shown.

The progression demonstrated in Graph 4 indicates an extreme
lack of development in the middle gluteal, biceps femoris,
superficial gluteal, semimembranosus and gracilis muscles. These
muscles are involved in the actions of extension or abduction -
the muscle groups which were shown to be affected most by the dysplas-
tic condition. Those three muscles showing the least decrease due
to the dysplasia - deep gluteal, external obturator, and quadratus
femoris - have also shown no significant difference from the normal.

In further examining the data of those muscles which showed no
significant difference, the iliOpsoas and the external obturator
muscles were extremely close to meeting the 0.05 level of rejection.
It is of interest to note that even though a significant difference

was not shown in the external obturator and the deep gluteal muscles,

Graph 3. Individual pelvic muscles relative to total body weight

26

  

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Muscles measured

Normal 50 pound dogs

’3 Normal 20 pound dogs

I Dysplastic dogs

27

  
     
  
      
  

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Muscles measured

Graph 3. (contd.) Individual pelvic muscles relative to total body weight

mm
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550
8.8.”
0
OOH
LfiNU
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28
there was an increase in mass rather than a decrease. Likewise,
there was a significant increase in the gemelli as demonstrated
in Table 3. Thus it is possible that these smaller muscles are
actually increasing in mass as a compensatory reaction to the
general underdevelopment occurring in the dogs with dysplasia.
These three muscles also are included in the abductor action group,
although the general condition of this group is one of a more
extreme lack of development.

An observation made during the dissection of the dysplastic
dogs was the total lack of the samll capsularis coxae muscle.
Even when present in the normal dogs the muscle is only measurable
at the level of .1 grams at most, but its absence may be an
indication that one aspect of the dysplastic condition is in the
muscle tissue itself and not only the result of the general
disorder.

Although Spurrell (1967) admits there is an underdeveloped
condition of the muscles of the pelvic area.which this study
confirms, he suggests it is a result of the dysplasia which he
considers may have some sort of neural cause. Fitzgerald (1961)
also suggests a neural involvement resulting in the atrophy of
the muscles. With the possibility of some sort of neural cause,
Miller 5551., 0.965) was checked for the innervation of all the
muscles of the pelvic area. Special attention was given to those
muscles and action groups which seem to be particularly affected
in accordance with the trend indicated in Graph 4. There is no
one lumbar level that goes to each of these specified muscles or

groups. Since there were five muscles that were not shown to be

29
significantly different, the innervations of these were also
checked and again there is no involvement at one single level.
The three muscles of increased development have no common level

of innervation.

Collateral Observations

During dissection special attention was taken to determine
the condition of the ligamentum.teres or round ligament and the
condition of the joint capsule. In nine of the dysplastic legs
the round ligament was ruptured and the one that was found intact
was present in the 17.1 kg female of seven months of age. Riser
and Shirer (1966) consider the round ligament to be an aid in
the stabilization of the hip joint during the first few months of
life. They do agree with Olsson (1961a) that the absence of the
round ligament is the result of the dysplasia rather than the
cause.

The joint capsules of the dysplastics were much thickened
and looser than those of either of the groups of normal dogs.
This observation is in agreement with those of Snavely (1959),
Howorth (1965) and Massie and Howorth (1951). When the dysplastic
capsules were incised the joint fluid found was viscous, yellow
and was in considerable excess of that found in the normal groups,
which was colorless and the consistency was more watery and thinner.
This observation has also been made by Snavely (1959).

Thus Schnelle (1965) has said that hip dysplasia is part of
a generalized fault or disease of development involving the joint
and its supporting structures. The muscular underdevelopment seen

in this study seems to be only one step in the sequence of

maldevelopment of this area.

30

31

SUMMAR! AND CONCLUSIONS

Dissection of sixteen muscles comprising the mass of the pelvic
area.was performed on three groups of dogs, with a frequency of five
in each group. These groups were normal 50 pound mongrels, normal
20 pound mongrels and dysplastic purebred Labrador Retrievers of
45 pounds. An analysis of variance was calculated to determine
whether there was a significant difference between the pelvic
muscle mass of the normal and dysplastic dogs.

With a confirmation of a significant difference in pelvic mass
between the dysplastic and the normal 50 pound dog further obserb
vation and calculation was made to determine whether there was a
significant difference between the action groups of muscles and
whether there was a significant difference between the individual
muscles of the area in the two groups of dogs.

The data showed that there was a definite underdeveloped
condition and difference between the action groups of dysplastic
dogs compared to those dogs of approximately the same weight with
normal hips. There was a trend implying that there may be an
exaggerated lack of development of the extensor and abductor groups
of muscles.

There was also shown a difference between the individual
muscles of the dysplastic compared to the 50 pound normal. There
was also a trend of exaggerated atrOphy being shown in the biceps
femoris, middle gluteal, semimembranosus, superficial gluteal and
gracilis muscles. These muscles also help make up the already
mentioned underdeveloped extensor and abductor action groups.

There was also an observation of the total lack of the capsularis

32
coxae muscle in the dysplastic dogs. The question of whether
the underdevelopment is due to disuse, neural involvement or a
hormone disorder is point for further study.

It was also seen that the ligamentum teres was ruptured in
nine of the ten dysplastic limbs examined. Upon examination of
the joint capsule as a whole it was seen that there was a
thickening or hypertrOphy of the connective tissue and that the
capsules of the dysplastic animals were stretched and a looser
enclosure of the joint was seen in these animals as compared to

the two normal groups.

33

LITERATURE CITED

Andren, L. 1960. Instability of the pubic symphysis and congenital
dislocation of the hip in newborns. The possible etiological
role of maternal hormones. Acta Radiol. 54:123-128.

Andren, L. 1961. Modern concept of congenital dislocation of the
hip. Cerebral Palsy Bulletin, Suppl. 3:167-169.

Andren, L. 1962. Pelvic instability in newborns with special
reference to congenital dislocation of the hip and hormonal
factors. Acts Radial., Suppl. 212.

Andren, L. and N. E. Barglin. 1961a. A disorder of oestrogen
metabolism as a causal factor of congenital dislocation of
the hip. Acta Orthop. Scand. 30:169-171.

Andren, L. and N. E. Barglin. 1961b. Disturbed urinary excretion
pattern of aestragens in newborns with congenital dislocation
of the hip. Acta Endacr. 37:423-433.

Andren, L. and S. van Rosen. 1958. The diagnosis of dislocation
of the hip in newborns and the primary results of immediate
treatment. Acts Radial. 49:89-95.

Badgley, C. E. 1949. Congenital dislocation of the hip. J. Bone
Jt. Surg. 31A:34l-356.

Bada, J. 1961. The etiology and treatment of congenital dysplasia
of the hip. Proceedings, SacietE International de Chirurgie
Orthopedique et de traumatique. J. Bone Jt. Surg. 43A:
284-288.

Bardens, J. W. and H. Hardwick. 1968. New observations on the
diagnosis and cause of hip dysplasia. vet. Med. Small
Anim. Clin. 63:238-245.

Bonfors, 8., K. Palsson and G. Skude. 1964. Hereditary aspects
of hip dysplasia in German Shepherd dogs. J.A.V.M.A.
145:15-20. '

Brookes, M. and E. N. Wardle. 1962. Muscle action and the shape
of the femur. J. Bone Jt. Surg. 44B:399-4ll.

Caffey, J., R. Ames, W. Silverman, C. Ryder and G. Rough. 1956.
Contradiction of the congenital dysplasia predislacatian
hypothesis of congenital dislocation of the hip through a
study of the normal variation in the acetabular angles at
successive periods in infancy. Pediatrics 17:632-640.

Chapple, C. C. and D. T. Davidson. 1941. A study of the relation-
ship between fetal pasitian and certain congenital
deformities. J. Pediat. 18:483-493.

34

Fitzgerald, H. W. 1961. Etiology and treatment of congenital
dysplasia of the hip. Proceedings, Sacieté International
de Chirurgie Orthopedique et de traumatique. J. Bone Jt.
Surg. 43A:284-2 88.

Farsyth, H. F. and H. A. Paschall. 1963. Genetics of congenital
hip dysplasia. J. Bone Jt. Surg. 45A:l781-1782.

Fax, M. W. 1963a. Conditioned reflexes and innate behavior of
the neonate dog. J. Small Anim. Pract. 4:85-99.

Fax, M. W. 1963b. Development and clinical significance of
muscle tone and posture in the neonate dag. Am. J. Vet.
Res. 24:1232-1238.

Fax, M. W. 1964. Palyarthradysplasia (congenital joint luxation)
in the dog. J.A.V.M.A. 145:1204-1205.

Guenther, W. C. 1964. Analysis of Variance. Prentice Hall Inc.,
Englewaad Cliffs, p. 47-50, 54-57.

Hein, H. E. 1963. Abnormalities and defects in pedigree dogs.
II. Hereditary aspects of hip dysplasia. J. Small Anim.
Pract. 4:457-462.

Henricsan, B., I. Norberg and S. E. Olsson. 1965. Hip dysplasia
in dogs. Nard-Vet-Med 17:118-131 abstracted in Mod. Vet.
Pract. Data and Ref. Lib. 5:132.

Henricsan, B., I. Narberg and S. E. Olsson. 1966. Etiology and
pathogenesis of hip dysplasia. J. Small Anim. Pract.
7:673-688.

Henricson, B. and S. Olsson. 1959. Hereditary acetabular
dysplasia in German Shepherd dogs. J.A.V.M.A. 135:207-210.

Hafmeyer, C. F. B. 1963. Acetabular dysplasia. S. Afr. J. Lab.
Clin. Med. 9:77-80 abstracted in Mod. vet. Pract. Data and
Ref. Lib. 5:87.

Howarth, M. B. 1947. Congenital dislocation of the hip. Ann.
Surg. 125:216-236.

Hawarth, M. B. 1965. The etiology of congenital and infantile
displacement of the hip. Acta Orthap. Scand. 35:212-224.

Hutt, F. B. 1967. Genetic selection to reduce the incidence of
hip dysplasia in dogs. JsAs VsMsAs ”131041-1048.

Innes, J. R. M. 1957. Splay-leg in rabbits-an inherited disease
analogous to joint dysplasia in children and dogs. Lab.
Invest. 6:171‘1860

35

Kaman, C. and H. Gossling. 1967. A breeding program to reduce
hip dysplasia in German Shepherds. J.A.V.M.A. 151:
562-571.

Konde, W. N. 1954. Congenital subluxation of the coxofemoral
joint in the German Shepherd dag. North Ann ver. 27:
595-599.

Langenskiald, A. and L. E. Laurent. 1966. Development of the
concepts of pathogenesis and treatment of congenital
dislocation of the hip. Clin. Orthap. 44:41-49.

Langenskiald, A., 0. Scapia and J. E. Michelssan. 1962.
Experimental dislocation of the hip in the rabbit. J.
Bone Jt. Surg. 44B:209-215.

Lawson, D. D. 1963. The radiographic diagnosis of hip dysplasia
in the dog. Vet. Rec. 75:445-456.

McClave, P. L. 1957. Elimination of caxafemoral dysplasia from
a breeding kennel. Vet. Med. Small Anim. Clin. 52:
241-2430

Maksic, D. and E. Small. 1962. Hip dysplasia: diagnosis. Mod.
vet. Pract. 43:(10)56, (ll)48, (12)62.

Massie, W. K. and M. B. Haworth. 1951. Congenital dislocation
of the hip. III. Pathogenesis. J. Bone Jt. Surg. 33A:
190-198.

Man, H. 1961. Etiology and treatment of congenital dysplasia of
the hip. Proceedings, Sacieté International de Chirurgie
Orthopedique et de traumatique. J. Bone Jt. Surg. 43A:
284-288.

Miller, M. Es, Co Co ChriStensen and H. E. Evms 1965. Anatomy
of the dog. W. B. Saunders Ca., Philadelphia. 231-247.

Mbstasky, U. V. 1962. Hip dysplasia. Popular Dogs 35:28.

Olsson, S-E. 1961a. Control of canine hip dysplasia in Scandi-
navian countries. Adv. Small Anim. Pract. 3:112-116.

Olsson, S-E. 1961b. Roentgen examination of the hip joint of
German Shepherd dogs. Adv. Small Anim. Pract. 3:117-120.

Paatsama, S. and P. Rissanen. 1965. Lesions in hip dysplasia.
Mill. Hosp. 1:168‘1790

Paatsama, 8., P. Rissanen and P. Rokkanen. 1966. Some aspects
of hip dysplasia and coxa plans in dogs. J. Small Anim.
Pract. 7:477-481.

Pierce, K. R., G. H. Bridges and W. C. Banks. 1964. Hormone
induced hip dysplasia in dogs. J. Small Anim. Pract.
6:121-126.

36

Pierce, K. R. and G. H. Bridges. 1966. The role of estragens in
the pathogenesis of canine hip dysplasia. The metabolism
of exogenous estragens. J. Small Anim. Pract. 8:383-389.

Rhodes, W. H. and J. Jenny. 1960. A canine acetabular index.
JOAOVOHOAO 137397.100.

Riser, W. H. 1962. Producing diagnostic pelvic radiographs for
mine hip dysp 188180 JsAs Vans As 1413600-6030

Riser, W. H. 1963. A.new look at developmental subluxatian and
dislocation: hip dysplasia in the dog. J. Small Animn
Pract. 4:421-434.

Riser, W. H. 1964. An analysis of the current status of hip
dysplasia in the dog. J.A.V.M.A. 144:709-721.

Riser, W. H., D. Cohen, S. Lindquist, J. Manssan and S. Chen.
1964. The influence of early rapid growth and weight gain
an hip dysplasia in the German Shepherd dag. J.A.V.M.A.
145:661-663.

Riser, W. H. and Rhodes, W. H. 1966. Producing diagnostic pelvic
radiographs for canine hip dysplasia examination. Anim.
Hosp. 2:167-171.

Riser, W. H. and J. Shirer. 1964. A.new look at canine hip
dysplasia. A.V.M.A. Proceedings Book 1964.

Riser, W. H. and J. Shirer. 1967. Correlation between canine
hip dysplasia and pelvic muscle mass: a study of 95 dogs.
All. J. Vet. Res. 283769-777.

Salter, R., J. Kostuik and J. Schatzker. 1963. Experimental
dysplasia of the hip and its reversibility. J. Bone Jt.
Surg. 45A:l781.

schales, 0. 1956. Genetic aspects of dysplasia of the hip joint.
North Am. vet. 57:476-478.

Schales, 0. 1959. Congenital hip dysplasia in dogs. Vet. Med.
Small Animu Clin. 54:143-148.

Schales, 0. 1962. Hereditary hip dysplasia. Popular Dogs
35:44-46, 75-77.

Schnelle, G. B. 1935. Some new diseases in the dog. Alb Kennel
Gsz. 52:25-26.

Schnelle, G. B. 1954. Congenital dysplasia of the hip (canine)
and sequelae. Proceedings AVMA 91st Annual Meeting:253-258.

Schnelle, G. B. 1959. Canine hip dysplasia. Lab. Invest. 8:
1178-1180.

37

Schnelle, G. B. 1965. Canine hip dysplasia: Qua Vadit veterinarius.
Svensk. Vet. Tidn. 17:523-526.

Smith, W., R. Iretan and C. R. Coleman. 1958. Sequelae of experi-
mental dislacatian of a weight bearing ball and socket in a
young growing animal. J. Bone Jt. Surg. 40A:1121-1127.

Smith, W., C. R. Coleman, M. L. 011x, R. P. Slager. 1963. Etiology
of congenital dislocation of the hip. J. Bone Jt. Surg.
45A:491-500.

Snavely, J. G. 1959. The genetic aspects of hip dysplasia in
dogs. J.A.V.M.A. 135:201-207.

Samerville, E. W. 1961. Etiology and treatment 9f congenital
dysplasia of the hip. Proceedings, Saciete International
de Chirurgie Orthopedique et de traumatique. J. Bone Jt.
Surg. 43A:284—288.

Spurrell, F. A. 1967. Canine Hip Dysplasia. Monograph of the
Univ. of Minnesota, St. Paul.

Wamberg, K. 1961. Kaunen erbliche hfiftgelenksleiden ahne
rantgenuntersuchung klinisch karrect beurteilt warden?
Mh. vet. Med. 16:845-848, abstracted in Mad. Vet. Pract.
Data and Ref. Lib. 5:42.

Wilkenson, J. H. 1963. Prime factors in the etiology of congenital
dislocation of the hip. J. Bone Jt. Surg. 45B:268—283.

Whittingtan, K., W. Banks, W. Carlson, B. Hoerlein, P. Husted,
E. Leonard, P. McClave, W. Rhodes, W. Riser and G. B. Schnelle.
1961. Report of the A.V.M.A. Panal an hip dysplasia.
JOAOVOMOAO 139 3 791-8060

Zaffaroni, A. 1958. Hormones and meat production from livestock.
Recent Pragr. Hormone Res. 14:213.

38

Appendix 1. Raw weights of each pelvic muscle of the 50 pound graup.*

§

 

 

 

 

 

[ 25. O k-, 23.0 k: 22. 7 k; 22. 0k kg. 20.4
It. rt 1

Duadriceps 75.5 273.7 169. 8 165. 8 23.8 225. 27.9 .o. 5. 2 .1
av 274. 6 166. 8 224. 223.1 233.

 

201. 217. 2
-183.417641308134.3 61.812.: 37.1132. 6

179.9 155.0 170.8

 
   

 
     

 

  
 

    
  
       

       
   
 
  
  

 

 

 

 

 

 

 

 

-1453 135.9 109.0 93.2 123.6 126.8 142.3 134.3 126.7 130.
v 138 3 128.4
27.6 117.0 87.1 92.0 6. 0 .
119.6- 89.6 106.2
86.1 31.5 71.0 83.8 79.5
72.3 1
. . .: 2.2 71.1
= 62.0 71.6
. 41.7 39.6 49.0 52.9 39.8 39.3 33.5 .4
. .56.1 40.7 651.9 57.7 53.4
30.9 81.7 39.0 40.5 40.5 46.6 43.0 47.7 .- .
81.3 39.8 43.6 43.2 48. 5
“Pe'{i°1‘t 25. 9 24. 5 16. 2 17. 3 21. 0 20,1 25. 0 23. 0 23. 4 .24..
luteal :

 

 

n
Obturatot a
9 11. 90
i4. gm
7.9 11. 5 412.2
11.9

Ouadratus 7.5 7.5 6.0 5.9 5.0 6.8 0.61)2 .2

 

 

 

 

 

8V 215 61g 9 6.0 69 .3
-melli 2.1 2.5 1.3 1.0 2.0 2.1 1.2 1.4 2. 8 2.
av 2.3 1.2 2.1 1.3 2.8

 

* recorded to the nearest .1 g.
the group is arranged left to right in a progression of decreasing
weight.
av.-average weight of both legs, rt.= right leg, 1f. = left leg

39

 

  

 

  

 

 

 

 

 

 

    
 

 

 

 

 

 

  
   

 

 
  
 

 

   

 

   

 

 

 

 

 

 
 

 

 

 

 

 

 

 

 

   

 

 

 

 

  

 

 

 

Appendix 1. (contd.) Raw weights of each pelvic muscle of the 20
pound group.*
9.1 d5; 3,6 kg. Ig 8.2 kg: 8.1 ks. L—j‘7 kg.
rt. 1f. rt. 1f. rt. ‘f. '* 1f. 't. 1?.
rluadriceps 33.1 52.9 70.0 69.6 65.7 65.9 54.9 33. Md.5 JO.‘
av. 53.0 68.8 65.8 34 49.4
Biceps 37.3 35.8 7.4 68.6 63.1 62.3 50.3 3~.3 36f]
. an. 37.7 68,0 +fig62.8 4&150. 38.”
Adductoxs .2 .O .4 52.2 .6 50.4 .5 «3.6 '3.4 43.5!
av. 39.0 50.7 49.9 33.6 43.2
figmf- ,
membranosus 30.6 28.2 0.7 40.7 43.7 43.0 82.: 32.2 33.7 36.4
av. 29.4 40.7 43.4 12.9 36.1
781881. , .
Gluteal 25.2 24.3 6 32.5 33.9 31.9 23.9 26.4 31.2 34.4
. ' m 24.8 32.9 26. 34.8
’“ml' 22.5 21.5 18.3 18.2 23.0 21wfi
tendinosus
v. 18.3
Gracilis .2 .3.3
419. ‘3.
Sartorius .07 5.7
1:. 15.3
Iliopsoas 18.5 17T2 4.8 23.3 .
+§ av. 14.3 l7.3 17.9 24.6 23.2
.uperflciaf . _
Gluteal 6.7 6.2 0.‘ 3.2 5.7 1.9 5.7
3V. 6.6 5.5 5.8
internal ,
4.6 4.0 4.2 1.; 5.‘ 4.6 4.9
Obtura‘ora.. 3.3 4.1 4.1 3.» 4446 4.6
xternal '
4.1 3.9 3.9 4.4 3.9 4.1 3.3 3.5 3.1 4.3
Obturatora.. 1.0 4.2 4.0 3.: 4.2
ee 3': fl}?
,luteal 3.3 3.6 4.4 4.1 4.2 4.h 4 3 4.t 4.0 3.5
av 25 .3 4,‘ '24 3.8
ectineu> 2.8 2.9 3.3 3 3.7 3.5 H 3. 2.5 2.
61‘. 27.9 M 3,‘ 11‘ 0 7
uadratus '.. 2.) 2.7 3 .Cp2 3.. 3 1 3.0 3
. 3.. 3.4 .3 2.1 7.; 3-9
961110.111 .13 .3 %B :8 j 1.1 7 1.U L
aw. .8 .8 1.0 .8 1.0

 

 

 

* recorded to the nearest .1 g.
the group is arranged left to right in a progression of decreasing

weight
av.=average weight of both legs,rt.= right leg,

 

 

 

1f.= left leg

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Appendix 1. (contd.) Raw weights of each muscle of the dysplastic
group.*
25.0 kg. 21.6ngé:_ 19.3 kg. 19.1 kg. 17.1 kg.
rt. 1f. rt. 1f. rt. If. rr. If. rt. If.
Quadriceps 193.5 207.8 162.7 201.2 161.3 142.3 176.2 171.0 123.0 132.!

av 197.7 182.0 151.8 1’3.n 137:5
Biceps 09.0 110:5 35.0 104.

. . 110.2 9 3
Adductors =26.5 137.6 100.2 103.8 80.1 80.3 04.1 33.3 71.8 97.
! av 132.1 102.0 80.2 98.7 84.5
ngiranosus 95.8 103.1 68.1 86.5 60.6 52.1 69.7 64.5 51.5 72.1

99.5 77.8 56.4 67.1 62.1
65.7 67.8 40.7 56.7 53.7 38.1 52.3 49.3 34.4 40j
66.8 48.7 45.9 50.8 37.6
tendinosus 65.5 69.1 47.3 50.2 43.0 39.6 60.0 54.0 0
67.3 48.8 41.3 57.0
Gracilis 58.5 59.0 36.8 36.6 . .
, av 58.8 36.7 ~32.5
Sartorius 45.6 49. 37.9 43 0 32.6 30.!

av 47.5 40.5 31.4
Iliopsoas 40.0 41.8 30.2 30.4 28.0 24.5
9g' av 40.9 39.3 26.8
G:§:::§°i‘1 11.5 18.9 8.9 14.0 15.5 13.2 1.6 11.0

av 15.2 11.5 14.4 11.3
1nterna1
Obturator 13.2 12.3 9.7 11.2 9.3 8.0 10.5 1 3

1 12.8 10.5 8.7 119.9
:::::::;I 13.8 12.9 12.8 12.0 12.0 11.0 13.9 14.5

13.4 12.4 11.5 14.2
12.5 14.9 11.3 14.9 11.1 10.9 8.? 15.4
13.1 1119, 12.2
13.5 6.0 6.0 5.6 5.7 0.1 5.8
6.0 5.] 6.H
8.2 7.9 5 3 4.8 4.8 7.2 0.5
6.6 4,8 6.0
3.4 3.6 2.9 2.7 3.0 3.0 2.0 2.1
3.2 2.9 2.5 2.3 ]

 

 

 

 

 

* recorded to the nearest .lg.
the group is arranged left to right in a progression of decreasing

weight

av.= average weight of both legs, rt.- right leg, 1f.=1eft 1eg

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