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The Stifles |
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by Fred Lanting |
The knee
is an engineering marvel, extremely complicated and concise, able to move in
multiple combinations of direction, and normally able to withstand considerable
torque forces. The structure is encased in an exquisite joint capsule with
ligaments connecting three large longbones, tendons
running into and over it and connecting bone with muscle, as well as muscle to
muscle via the sesamoids and patella. The capsule is
lubricated by synovial fluid.
The
most common joint disorder in the stifles, other than ruptured cruciate ligaments, is luxated patellas. The patella, or “knee
cap” is a small bone (the body’s largest sesamoid
bone) that seems to “float” outside of a joint. In actuality, it normally is
securely attached to the area and the muscles by means of ligaments and
tendons. It can be considered a
localized ossification center in the tendon
connecting the quadriceps muscle in the upper thigh to the tibia in the lower
leg. You should be able to feel it somewhat above the slight indentation
along the front of your dog’s rear leg, where the breed standards like to refer
to the “bend of stifle”; this is where the upper and the lower thighs meet. In
motion, the patella will normally slide down into a groove between the condyles of the femur. The quadriceps muscle group acts to
extend (straighten) the limb; because the patella is enclosed in the lower
tendon of that muscle group, the knee cap is more in front of the joint
when the muscle is relaxed, and slides upward in front of the lower femur when
contracted. That’s when the major discomfort occurs in dogs with defective
stifles, with the patella missing the center of the
groove in which case it is referred to as being luxated.
Almost all dogs with patellar luxation have some
other structural abnormality related to it; thus, in order to improve the
individual’s life and prevent passing the defect to others, a regime of early
evaluation and detection is important.
The alignment of muscle and
tendon insertions or the relative positions of the leg bones may be such that
the patella is pulled more to one side and hence misses that groove. The
biomechanics are easily described by what we call the “bowstring effect”, in
which the muscle fiber group on one side works better
than the other side, and puts tension on the patellar tendon and associated
bone structures. In so doing, the kneecap is pulled toward the dog’s centerline (medial displacement) and if the force is strong
enough it will slide out of the groove running between the femoral condyles. This wears away the ridge of that “trochlea” so the effect is to slip out of the groove more
easily as time goes on. Meanwhile, the underside of the patella also abrades,
becoming less V-shaped and less likely to stay in the track where it belongs.
In the more severe cases, the abnormal strain on the muscles and joint caused
by forces being misdirected in this manner results in pain. It is usually
considerable and almost always leads to a very noticeable change in gait, such
as skipping or perhaps even a refusal to walk at times. Mild cases can go
undiagnosed by a vet and, to some extent, unnoticed by the owner. Most pups can
be diagnosed only after 4 to 6 months of age. If the luxated
patellar bone is offset toward the centerline of the
dog, the condition is called medial luxation or
displacement. If the bone moves on the “outside”, or away from the centerline, it is called lateral luxation.
A method you can use to keep these terms straight might be to think of the “median
strip” in the middle of a divided highway. Medial patellar luxation is almost undoubtedly inherited.
We
know that in limbs with two bones, such as the lower thigh and the lower
foreleg, there are frequently small differences in the growth rate or eventual
length ratios between tibia and fibula or between ulna and radius. It may well
be that a disruption in growth rate of one of such a pair causes a twist or
misalignment of both hard and soft structures in joints such as the wrist,
elbow, knee, and hock. On the other hand, slightly abnormal muscle-fiber type or ratios might cause more tension on one side
than on another. Some have tried to solve to solve the puzzle of the
chicken-or-the-egg with explanations of one sort, and others have proposed the other.
Whichever happens, and it could be that either is involved in any specific
case, we are more concerned here with the “after-the-fact” condition, and how
it relates to a dog’s gait, health, and value as a show or breeding animal.
Whatever is the reason for a specific abnormality, sometimes all I can do in
this book is describe it. Where possible, I shall try to explain it.
In
some individuals of achondroplastic breeds such as
Bassets and Dachshunds, luxation might be more a
result of “breeder-selected” abnormal shape and position (curvature) of tibia
and femur. The lateral deviation of the distal femur and the medial deviation
of the proximal tibia seem to have similar results as found with luxation caused by muscle abnormalities.
This
is the most common form. Most cases of medial patellar luxation
involve toys and other small breeds, many of which are rather “straight in the
stifle” such as the Shar Pei,
but there may not be more than coincidence in that. Small (Toy and Miniature)
Poodles, perhaps because there are so many of them indiscriminately bred, seem
to be the most “visible” to the casual observer, but there is evidence that
indeed, there is a 4 to 8 times greater predisposition in the miniature and toy
breeds in general, and “the incidence of medial luxations
is high in toy poodles”. Dr. Priester, the same man who did a study on breed, sex, and
other factors in relation to HD, also studied these factors and their
connection to canine patellar dislocation. Medial luxation
in larger dogs is far less common, but does occur.
The
experienced dog show observer can often spot the more severely afflicted dogs,
usually while watching the Pomeranian, Lhasa Apso, Peke,
Four
grades of medial luxation are used to describe the
disorder. Grade 1 is for the dog that usually has a normal condition,
but which can be luxated by minor trauma or pushing
firmly with the thumb and fingers. In Grade 2, the patella can be manually
displaced by adequate finger pressure or can slip out when the leg is fully
extended, though it can be pushed back by the owner or a vet. With the next two
grades it is difficult (grade 3) or impossible (grade 4) to put the patella
back in place. Other signs are progressively worse, too, of course. Older dogs
with Grades 1 or 2 may seem O.K. until a sudden onset that may be triggered
by trauma or arthritic change that the dogs no longer fully tolerate;
nevertheless, it is a genetic problem.
Grade
1 dogs occasionally skip or carry a leg, sometimes only for one stride in a
twenty- or thirty-foot stretch of gaiting. Pain might be barely or not noticed,
even when the cap is luxated slightly with finger
pressure. Grade 2 dogs will more frequently to usually “carry” a leg, and
occasionally bear weight on it; crepitus might be
felt and heard, depending on the dog’s age. Surgery is recommended for Grades 2
to 4, earlier for the worse degrees. In Grade 3, a little weight bearing might
be possible, but there is permanent dislocation; you can push the patella back
into the shallow groove, but it will ride out as soon as you ease up on the
pressure. Most dogs will stand bowlegged or crouched. In Grade 4, the affected
leg will always be carried so that weight is not transmitted to the ground. The
luxation is permanent and surgery will have to
address other surfaces in the joint as well.
When
the patella is displaced toward the “outside”, it is said to be luxated laterally. This condition is not as common,
accounting for less than 24% of patellar dislocations. While it can be found in
any size dog, it is more commonly found in large breeds. Any misalignment in
the quadriceps muscles, the trochlear groove between
the condyles of the femur, the tibia (larger of the
two lower leg bones), and the ligaments early in life will abnormally shape the
cartilage and, as it ossifies into bone, this legacy will solidify. Other puns
aside, though, it has been seen that changing the directions or vectors of the
muscle contraction forces will give unbalanced strains on the growth plates and
other cartilaginous tissues in the young pup, and this means permanent deformities
in the bone structures they will have developed into. It only takes a couple of
weeks of misdirected stresses to produce this permanent deformation.
Coxa valgum, the condition in
which the femoral head is inserted into the acetabulum
at a greater-than-normal angle, tends to force the lower part of the femur
toward the midline, which changes the relative position of the trochlear groove in which the patella should slide without
pressure on one side of the groove or the other. An increase in the anteversion
angle between the femur and the acetabular portion of
the pelvis carries with it a corresponding torsional
force on the whole femur, and another tendency for
medial displacement of the distal femur as well. A vet school professor I
consulted years ago felt that there was a cause-and-effect relationship between
patellar luxation and hip dysplasia,
but admitted there was disagreement on which caused what. Others have mentioned
that lateral luxation can cause deformation of the
femoral head in large, fast-growing breeds.
What
happens when the stifles are brought closer together in this “knock-kneed”
condition known as genu valgum? The dog’s weight is applied unevenly to one
of the femoral condyles, and as the puppy is
subjected to this, the development of the growth plate on that (lateral) side
is inhibited while the medial condyle continues to
grow and ossify normally. The change in
the height of the lateral trochlear ridge, plus the
fact that the patella rides atop it instead of next to it in the groove, makes
for a shallow groove. In addition, if luxation started early, there were little or no
developmental forces to even create a normal groove in the first place. All this presents an easy escape for the
patella into an increasingly bad position. With every step the dog takes, the
abrasion continues, cartilage is destroyed, ligaments are stretched, and pain
probably increases. At almost infinitesimally small
increments, to be sure, but progressively nonetheless.
The
same sort of “bowstring effect” exists as in medial luxation,
but bowing the femur inward instead, and rotating the tibia laterally (outward)
while displacing the developing tuberosity on the
tibia where the patellar tendon is inserted.
The vastus medialis
part of the quadriceps muscle is supposed to act as half of the couple (an
engineering term meaning balanced rotational forces) and insure the patella
rides in the groove and transfers the quadriceps’ force to extend the lower leg
in a straight fashion.
Lateral
luxation of the patella can begin with a hypoplastic muscle called the vastus
medialis. It is the part of the quadriceps muscle
group that is the last to develop and is the first muscle to undergo atrophy
following injury or disuse. Hypoplasia means
underdevelopment, with fewer cells and myofibers, so
the muscle doesn’t stretch properly. It is probably not clinically identifiable
in many or most cases. If it is not working properly, it does not balance the
force of the vastus lateralis,
which is then able to exert too much pull toward the “outside” (laterally). The
vastus lateralis may also
cause or contribute to the femur and tibia being twisted out of alignment with
each other. This compounds the problem, sending the forces of the contracting quadriceps
into a slightly (but importantly) different direction. The whole joint capsule
is abnormally stressed and there is a possibility that a ruptured cruciate ligament so often seen in sporting and working
breeds might be genetically related. Some 15 to 20% of luxated
patella cases have accompanying (or resultant?) cranial cruciate
ligament rupture. It could be that the genes for one muscle’s hypoplasia give cruciate ligament
damage if combined with genes for certain characteristics, and patella luxation if combined with those for other characteristics.
Causes
for lateral patellar luxation are often unproven,
partly because there are so few cases.
Willis in his excellent work on the German Shepherd Dog, says that he
has only seen two cases in the breed, and Priester
reported Saints but no GSDs in his 1972 study,
despite the fact that the latter breed is the most populous in the world and
was one of the five or six most popular breeds in the USA at the time. I hold
the premise that almost everything has a genetic base, and that the reason some
dogs are afflicted by an apparently environmental occurrence is that they are
genetically more susceptible than others, be it rupturing a cruciate
ligament, having gastric volvulus, heat stroke, or
whatever. However, the low incidence makes it hard to convince some people.
Just how such a genetic weakness is expressed, that is, its etiology
and pathogenesis, can easily and understandably be a point of disagreement.
Thus, such “causes” have been proposed as estrogen
imbalance or trauma while in the uterus; both have been pretty much discounted
as possibilities.
In
lateral luxation, the lateral condyle
of the femur, because its growth plate has been subjected to excess pressure
and growth has been altered, is misshapen. The trochanteric
ridge is lower, sort of like riding on one of those compact spare tires, and
the trochlear groove is more
shallow. Thus the patella does
not have a nice, deep, secure groove to ride in, and it is easy to pull it out
of normal direction, especially since the force to one side is so persistent
(every time the dog flexes or extends the knee). The groove becomes even more shallow due to wearing away faster than the dog can
rebuild with new cells. Still, symptoms of lateral luxation
usually are slower to develop than medial luxation
signs. The dog may be over 5 years old by the time clinical signs of Grade 1 or
2 appear. The affected dog may be knock-kneed, cowhocked,
or toed-out, but then, many non-affected dogs may show these traits, so do not
base a diagnosis on those alone. In sudden-onset cases involving both rear limbs at once (perhaps brought on by strenuous
exercise), the dog might not be able to stand and the condition may appear to
be a neurological disorder.
Surgical
correction (not cure) generally is aimed at re-establishing or creating a
deeper groove and repositioning the muscle vectors. If surgery is postponed,
osteoarthritis may be a problem of varying severity, with osteophytes
and a thickened, swollen knee joint capsule making correction more difficult.
Steroids are often prescribed (they are as commonly resorted to as Valium for adult humans or Ritalin for kids) but given the
dangerous and unpleasant side-effects of such medication, your best recourse is
probably surgery, which sometimes is very extensive. Since patellar luxations are progressive, the earlier you detect and
treat, the greater the success will be.
It’s part of my usual soapbox to point toward genetic
origins for almost everything, and this is no exception. Noted geneticist
Frederick Hutt flatly said of patellar luxation, “It is inherited and polygenic”. However, as Olmstead says, the heredity of
lateral patellar luxation is difficult to
substantiate because the condition does not occur as often as, say, HD or many
other more frequently seen orthopedic disorders.
While the role of trauma is easy to see, the “primary pathophysiology”
is not. Just how and why the genes express themselves in luxated patellas, whether
medially or laterally, is not all that clear. But perhaps it need not
be, as long as we follow the wise breeder’s rule: don’t breed defective dogs,
whatever the defect or supposed cause.