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Treatment for the Dysplastic Dog |
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INTRODUCTION
I am frequently approached by people who have bought “the love
of their lives” or a show or working-prospect puppy, only to find out it does
not have what most responsible fanciers would call “breedable”
hips. I am asked what should or could be done about it. Nearly half of the
inquiries include a potential litigious situation, since the pup was bought
with an assumed “guarantee” (seldom any or anything worth the paper it’s on).
In those cases, all I can do is tell them that I am available as an expert
witness in court cases, but they should first try other means of forcing the
seller to “make good”. I don’t want to get involved in arguments between seller
and buyer outside of court (there are too many).
In
this article, I intend to give you a picture of what I feel are the three best
surgical repair methods and the non-surgical alternative to dealing with HD in
the dog, especially puppies. The younger the pup, the more successful most
surgical operations are likely to be. An orthopedic
surgeon friend once described it to me perfectly: he said that with very young
puppies, you could break all their bones, throw them into a bag and shake them,
and they will heal. As dogs get older, healing and natural repair take longer
(old people’s and dogs’ bones may not heal or fuse at all) and there is a lot
more degenerative joint disease (DJD, arthritis, “deposits”) that cause
inflammation and restrict motion.
TOTAL HIP REPLACEMENT
Femoral head and
neck excision (removal) is usually limited to smaller dogs, though I know of a
few Golden Retrievers who have managed quite well with that procedure. Muscles
and ligaments take over in a partial way and form a “false hip joint”. It is
used when simpler, less-invasive methods have not been satisfactory. Replacing the femoral head and the acetabulum with prostheses (man-made body parts) is
considered another “last resort” salvage procedure, and once was recommended
when the dog was too poor a candidate for the other treatments, yet the owner
did not want to choose euthanasia. It became the chief surgical procedure in
later years. Other salvage procedures restrict joint movement or remove the
joint entirely, but a hip prosthesis can allow resumption of quite
normal function, usually without any pain at all. People have been getting
“artificial hips” since the early 1960s, although the very first total hip arthroplasty was performed in 1891 with an ivory ball and
socket and nickel-plated screws. Dogs have been benefiting from the procedure
for many years, and much more successfully after technical improvements around
1974.
While the major
reason for hip replacement is to treat disabling HD, other disorders can also
benefit: Legg-Calvé-Perthes
disease, permanent dislocation from trauma, bad fracture of the femoral head
and neck, hereditary or environmental defects in union of bone centers, and excision arthroplasties
that have failed to solve the problem. Any candidate should be at least ten
months old or the bone remaining may “outgrow” the size of the implanted
prosthesis. Recently a “telescoping” femoral component was proposed that would
lengthen as the pup’s leg continued to do so.
While small dogs may reach skeletal maturity faster, or be close to
their ultimate size earlier than large dogs, they are not as good candidates
because their bones are too small to accommodate present synthetic parts. Dogs
of very small size (under about 35 lbs) may do better with alternative
treatment. Older dogs might be good candidates, if they still have enough of
bone in the pelvis where the synthetic socket must be placed, and as long as
owners realize the cost/benefit relationship. It wouldn’t make sense to implant
a prosthesis if the dog was near the end of its
natural lifespan or was suffering from some other ailment that might require
euthanasia in the near future.
One major producer
of hip prostheses for dogs made two sizes of prostheses, large and medium,
which means that the percentage of bone and marrow removed will vary a little
from one dog to the next, but not much. The endoprosthesis,
which replaces the femoral head and neck, has a long stem that is inserted into
a reamed hole in the diaphysis, the femoral
shaft. A polyethylene plastic cup
replaces the worn and shallow acetabulum. Another manufacturer introduced a promising
modular total hip, and a third company introduced two advances on the type of
implant. The femoral part of their cemented prosthesis is often made of cobalt
chrome (a tantalum alloy may be better) and the acetabular
part is at least partly UHMW (ultra-high-molecular-weight) polyethylene. In the
non-cemented version, the acetabular part could be
titanium coated with hydroxyapatite (the form of
calcium phosphate of which bone is made). Some companies offered a cementless approach, also. Improvements are continually
being proposed by one company after another, and the corporate identity keeps
changing through mergers and takeovers, so the picture by the time you read
this is probably different than it was.
Here is one method
could even be outdated by the time you read this, but helps you to understand
the general procedure. After the dog is made ready, the muscle layers incised,
and joint capsule opened, the head of the femur is cut off at an angle corresponding
to the angle of the prosthesis. The acetabular bed is
prepared by another reaming process and several anchor holes are drilled in the
depression. Then, in one method, polymethylmethacrylate
cement (similar to the well-known “super” glues) is mixed with a powder and
possibly antibiotics, and injected into these holes and the cup until level
with the new rim. The prosthetic cup is positioned very carefully, as wrong
angles or poor seating can result in dislocations and failure. Similarly, the
shaft of the femur is filled with the glue before the femoral prosthesis is
inserted. The excess cement that is squeezed out on insertion of the prosthesis
is removed and the remaining cement gradually hardens, during which time it
emits some heat from the chemical reaction of curing. This heat has been suspected of slightly
damaging some adjacent tissue, especially that of the sciatic nerve. But, with
care and experience, this damage is minimized and minor enough that the dog
returns to normal nerve function during convalescence. Later methods have done
away with the need for the methacrylate cement.
The first month
after surgery requires that activity be very limited, and very little more is
allowed during the second postoperative month to prevent dislocations before
the muscles and ligaments heal, although in many cases, the dog is walking on
the day of surgery! If a dog passes the eighteen-month “milestone,” the
prosthesis should last the rest of its life. Of course, there may be
complications in some individuals, but the number has decreased markedly and is
probably below 5% now. Most complications are dislocations and loosening of the
acetabular component, but these can be almost
completely controlled by careful positioning of the cup and proper care of the
patient in the first few postoperative months. Infections present fewer (less
than 1% failure rate) but perhaps more disastrous complications, and are
treated by removing the cement and prosthesis and starting over again. These
dogs do not recover hip function as fully as those who don’t need a repeat
procedure.
Bilateral
replacement is said to be necessary in about one fifth of the dogs undergoing
this procedure. Most dogs put more weight on their “good” new hip, by rotating
the pelvis slightly, in order to take the strain off the defective hip. In
either case, bilateral or unilateral replacement, a dog with a new hip or two
can return to almost completely normal activity, including some obedience
jumping, jogging with the owner, and other play or work. However, if expected
to do more work than guard the front porch and play, the dog should be put on
an exercise program of gradually increasing demands. Recovery is graded
as excellent if there is normal activity and no pain, good if some stiffness
occurs after much work/exercise or prolonged rest, fair if there is still mild
lameness and continued reduced weight bearing, and poor if there is continued
and marked lameness. Recent results
indicate that about 95% of these surgeries are excellent or good.
For a while,
the major difficulty with THR was that the potion that was cemented or
pressure-fit into the hole drilled in the femur would come loose. Improvements
in design, surface, and techniques have reduced such problems tremendously. At
the Canine Total Hip Replacement annual conference held in 2000 in San Diego,
Dr. Gail Smith, chief of surgery at Penn, presented research data on a
biocompatible, porous tantalum lattice that is also osteoconductive
(allows bone growth into its crevices and pores), called Hedrocel.
Tantalum is a rare metal element, inert and thus quite non-reactive with body
tissues or other chemicals. It offers application for orthopedic
implants of various forms, and especially for bone ingrowth
into structural implants such as total hip replacements. It is also being used
as a trochanteric spacer to change angles and
force/moment patterns in the hip, somewhat like the way a wedge driven into a
saw-cut will cause a tree to lean in the desired direction. Bone ingrowth enables the body (with the surgeon’s help) to fix
or attach an orthopedic implant device to bone. Bone
cells growth into the “pores” of the metal implant. In the study reported on at
PELVIC OSTEOTOMY AND OTHER PROCEDURES
A variety of other
surgical techniques have been developed to treat HD, some of which do not seem
to offer any improvement over the more commonly used procedures. Basically, you can cut the femur or cut the
pelvis. First, we’ll look at procedures on the femur, but even before that,
let’s review a few terms. When you see the ending “-otomy”,
it refers to the act of separation by cutting: pectinotomy
is the (scalpel) cutting of the pectineus muscle,
while femoral or pelvic osteotomy is the (saw)
cutting of bone in femur or pelvis. The ending “-ectomy”
means cutting and removing, so a pectinectomy
is the removal of a length of the muscle so it doesn’t grow back together, and ostectomy is the cutting off and discarding of a portion of
bone. Osteotomy, as in the next examples, usually
involves cutting bone (os-) and then allowing or
helping it to grow back together in a different shape or angle. The form “my-”
refers to muscle, so you will easily see the difference between tenectomy and myectomy (tendon
vs. muscle).
Varus osteotomy
is an attempt to improve the angle of inclination so that the femoral head is
better covered by the hip socket. A different osteotomy
on the femoral neck changes the anteversion angle.
This procedure is not always necessary, but unless it is performed, those dogs
with the largest angles have the least satisfactory results with pelvic osteotomies. Both of these operations involve cutting the
top section of the femur from the rest of the shaft, rotating it into a
different position, then refastening the pieces
together. Sometimes this cutting is done in three different planes to improve
the fit of the ball into the socket.
Femoral osteotomy in treating osteoarthritis
of the hip joint has been described as occurring as early as 1894. This
procedure, the TPO, shelf-building techniques, and other methods all are aimed
at improving the coverage by the dorsal acetabular
rim (or replacing it) — this part of the acetabulum
is what supports most of the dog’s weight on the femoral head. If femoral anteversion is around forty-five degrees, a pelvic osteotomy will not be enough to correct for the severe
internal rotation of the limb and a femoral osteotomy
needs to be done as well. The angle of anteversion
that is considered “normal” has not been established, but most believe anything
greater than forty degrees is excessive.
An intertrochanteric osteotomy is
the cutting of the shaft between the “shoulder” (the greater trochanter) of the femur and the lesser trochanter
in order to change the angle at which the femoral head is seated in the acetabulum. A trochanter is a
natural elevation or process of bone. The operation gets its name from where
the saw cut is made, between the two trochanters on
the femur — one “bump” is shoulder-like and the other is located below the
femoral head. Another operation that is sometimes performed involves cutting
off the greater trochanter and moving it lower on the
shaft so that it won’t rub against the acetabulum in
its new position. An intertrochanteric osteotomy is also often performed when the pelvis is cut
and repositioned. Schrader says, “Caudal transplantation of the trochanter should be avoided because it causes internal
rotation of the hip”. By this is meant
moving it toward the tail. He also recommended that for best results it not be
moved too far down the shaft of the femur, either.
Another procedure
to treat HD is to lengthen the femoral neck to seat the head more firmly into
the acetabulum. This is a simple approach, but it
does not mean that the surgery is simple. According to Slocum and DeVine, a very short neck can contribute to the head
falling out of the socket. Results are not promising if the acetabulum
has filled with new bone or if the osteoarthritic
deposit of bone around the head and cup is too much. Slocum performs femoral
neck lengthening if surgery on the pelvis doesn’t correct enough of the laxity,
but Smith (Chief of Surgery at the
Triple Pelvic Osteotomy
A triple pelvic osteotomy, TPO, is a very popular reconstructive or salvage
procedure among surgeons, in which the pelvis is cut in three locations to
rotate the center portion, where the acetabulum is located. Surgical rotation of part of the pelvis
on its axis been investigated in man at least since the late 1950s. By 1969 it was being tried in dogs. The first
prerequisite is that the dog have enough useful joint
surface to offer a deeper fit once the acetabulum has
been repositioned to give better coverage of the femoral head. It would do no
good if the cartilage or acetabular rim were
excessively worn, for} the purpose of this realignment of acetabulum
and femoral head is to improve congruity) not rebuild the structure.
Much of the
professional literature omits the word “triple” but the procedure is basically
the same. To prepare for pelvic osteotomy, the dog is
examined to see if it is a good candidate. This includes checking for Ortolani sign, good radiographs, and normal pre-op blood
work. A pectinectomy is performed first, then a section of the pubis is removed and reserved for use
in making a bone graft for the ilium. Next, an
incision is made over the ischiatic tuberosity, and the ischium is
exposed and cut. The third cut is made in the ilium,
after which a stepped and twisted metal plate is affixed to the bone on both
sides of the cut, the amount of twist being determined during the preoperative
exam. The reserved piece of pubis is cut up into small bits and used in this
area as bone grafts to help strengthen the new structure.
While intertrochanteric and pelvic osteotomies
reduce laxity and improve congruity, these must be done early, as soon as
laxity and pain are noticed, so that beneficial bone remodeling
can occur. This is best accomplished early in life. Most successful pelvic osteotomies are performed on dogs between the ages of six
and ten months. One study reported first-year success rates of 68-84%. If the
dog is much older, the bones will not heal as fast and the joint is likely to
be changed by osteophytes, an eroded acetabular rim, and other changes.
In earlier years,
pelvic osteotomies sometimes rotated the acetabular section too far, which allowed the acetabular rim to grate against the femoral neck during
movement. Other complications, while not frequent, can still occur: the newly directed compressive forces on the
growth plate and epiphysis sometimes result in a necrosis similar in some
respects to Legg-Calvé-Perthes disease and in growth
disturbances in both the femoral head and neck.
Gait abnormalities often persist, though of a different nature than
before the surgery, and are usually more noticeable in dogs with very little
rear angulation or tarsal hyperextension. Often,
patients seemed more stiff legged and straight in the stifle after having a
pelvic osteotomy. Mobility may have to be sacrificed,
in part, for stability.
Is pelvic osteotomy for your dog?
Perhaps. TPO has become the next-preferred
surgical approach after total hip replacement. Pelvic osteotomy
is perhaps more a preventive, rather than a reconstructive or salvage,
technique; the benefits of preventing further deterioration have not been fully
documented to everyone’s satisfaction. The “catch” is that if owners wait until
they see signs of osteoarthritis, it is possible that some dogs may have too
much remodeling or osteophyte
growth to be ideal candidates for the surgery. Fewer
than a third of dogs with “excessive” laxity do not develop osteoarthritis by
an average age of 28 months, so that means most affected dogs are probably
candidates for some sort of treatment. It may be TPO is right for your
young dog. If you have a younger dog, though, perhaps the next, more recent
procedure is the best yet.
JUVENILE PELVIC SYMPHYSIODESIS
Late in 2000,
another new but less invasive surgical procedure recommended for puppies
determined to be at risk for developing DJD was introduced. It is called
“juvenile pubic symphysiodesis” (JPS), and currently
appears to be optimally performed on pups that are 12 to 20 weeks old.
Obviously, such at-risk pups can best be identified during PennHIP
evaluation of laxity and early bone changes. Dr. Kyle Matthews of NC State
originated the idea, and Drs. Tass Dueland, Allison Patricelli, and
Chess Adams, with other members of the University of WI-Madison research team
developed the technique in dogs. They all strongly suggest “neutering” (orchidectomy or ovariohysterectomy)
be done while the patient is under anesthesia. The
pubic portion of the pelvis is between the left and right halves and is toward
the lower “front” in standing bipedal animals and on the rear belly side in the
dog standing on all fours, where the process of pelvic growth is about the last
to occur. A small ventral and approximately midline incision is made, the very
short symphysis (analogous to the growth plates you
are already familiar with) is cleared of soft tissues, and an electric scalpel
is used to cauterize the pubic portion of the pelvic symphysis.
What this operation does is cause premature closure of the medial
pubic physes. This junction of the two halves is fibrocartilaginous in the middle with hyaline cartilage to
each side, the natural precursor to ossified bone at this age. Since the medial
pubic symphysis is hyaline cartilage, which plays a
major role in growth of the pubis, a cessation or slowing of growth there
allows the continued growth elsewhere to rotate the pelvis and therefore the
hip joint. Thus, the acetabula become rotated, a
similar effect to that produced by TPO; this results in better coverage of the
femoral heads. The Wisconsin experience to date shows, in most cases, that if
the surgery is performed at the appropriate age, hip joint laxity improves (is
reduced) as shown by Ortolani-positive hips becoming Ortolani-negative, and PennHIP
distraction indices improving with time. Collaborative clinical case
investigations are underway at
OTHER SURGERY
The above descriptions do not intend to
imply that there are not other approaches. Surgeons are always trying to
develop improved techniques. At the 1998 Veterinary Orthopedics
Society meeting a technique called “DARthroplasty”
was introduced and suggested for a pool of dogs similar to those looked at by
Penn and by Barr et al. Based on the data from the more conservative
approaches, Smith’s group suggested it be “given ‘investigational’ status until
further scientific studies with appropriate controls” could determine the
efficacy compared with that of the non-surgical treatments.
CONSERVATIVE MANAGEMENT
A study carried
out at
Radiography
revealed 73% to have severe HD as evidenced by subluxation
and 80% had grade one or two secondary degenerative changes described as “periarticular new bone formation.” Not all dogs lasted the
length of the study, but seventy percent were followed; the mean age at
follow-up was four and one-half years. Three dogs were destroyed between the
ages of ten and twelve months because of continued dysplasia
problems, but the information on them was included in the statistical study.
Two had pectineal muscle surgery after entering the
program and one of these, operated on at twelve months, improved over the next
few months in the program. The other was operated on at five years of age when
lameness returned after being absent in early-to-mid adulthood (it had had
signs as a pup when it entered the program). In this dog, the pectinectomy was disappointing when the dog was reexamined six months postoperatively.
At the time
of initial follow-up, nearly half of the study dogs had no hind-limb gait
abnormality (observed without being stressed) and 28% had slight or
intermittent abnormalities such as a swaying action of the hips. Eighteen
percent had moderate abnormalities, and in 6% the problems were considered
severe and continuous. When difficulty in getting to their feet from a sitting
position was evaluated, 18% had slight problems, 26% had noticeably more
trouble, and 56% had no difficulty. Normal exercise amounting to an average of
three miles per day was given to 72%, while owners restricted exercise in 28%
of the dogs.
About 90% of the
nineteen dogs later returned to the veterinary school for clinical and x-ray
examination showed either a slight sway or no gait abnormality at all. A couple
had obvious lameness and several showed pain when the hips were forced into an
extended position beyond what they would do themselves. Several also had crepitus or crepitation, that condition
of a grating or grinding noise in the joints which indicates bone or cartilage
is scraping instead of sliding noiselessly on a cushion of synovial
fluid. About one fifth of the dogs had restricted rear stride and more had some
degree of muscle atrophy around the hip joint. Without heavy exercise, 63%
showed no discomfort, even when limbs were forcibly extended, and 80% had a
normal range of movement. In 72% of the cases, owners reported normal tolerance
to exercise.
Some of the
radiological findings reported in that study do not totally agree with findings
elsewhere, but these researchers felt that as dysplastic
dogs matured, the degree of laxity stayed pretty much the same, but osteophyte formation increased most rapidly between six and
eighteen months of age, and then not as fast thereafter.
The results
of the British study appear, at first, to be startling, but this is because for
so many years we have been focusing on surgical treatments, with only lone
voices calling for restraint. This emphasis is understandable, for if Rover has
pain now, the owner wants his pain relieved now (and for life).
In the days before we had much or any knowledge of HD, the disorder was
attributed to other causes in the persistent cases, but a great many of the
afflicted dogs grew out of the worst symptoms as their skeletons stopped
growing and the joints ceased remodeling. The British
report on conservative management was, in a way, a return to pre-HD-awareness
days.
Spontaneous
improvement in hind-limb problems was attributed to healing of the microfractures (which most feel is the primary cause of
pain), increased stability through less mobility via remodeling
(filling in the joint space with bone deposits), and a thickening of the joint
capsule due to prolonged and repeated irritation of the connective tissue. It
is possible the adult dog can withstand pain better than the young pup. If 76%
of dogs, such as found in this study, can be considered to have acceptable,
long-term function of the hind limbs without anything beyond normal care, the
owner of a pup with dysplasia should carefully weigh
the option of conservative management.
A more recent
study report appeared in an abstract entitled “Non-surgical Management of
Severe Hip Dysplasia: Long-term Results” and authored
by Smith, Fordyce, and Gregor of the
MEDICATION
The use of
medication is included in conservative management in most instances. You might
do nothing in the case of the dog with little or no physical symptoms except to
let him grow through the most difficult period — those fast-growth months. Most
dogs with mild HD are free of outward signs after they reach skeletal maturity
(when the physes are ossified and no further growth
changes take place in the joints and bone ends) and before they reach an age
when the effects of arthritis build to a noticeable level. The effects are highly variable. Some dogs will
not show much sign of movement restriction until a couple years or so before
their natural lifespan ends; others have earlier degenerative joint symptoms by
three to six years of age. If you decide not to use treatment in young dogs,
you might also decide to just let the dog “live with” its disability later or,
if there is some pain, give him occasional analgesics such as buffered or
coated aspirin, some of the newer nonsteroidal
anti-inflammatory drugs (NSAIDs), or other medication
prescribed by your veterinarian. But remember, every drug has side
effects. Use only enough medication to
relieve the worst of the pain and give your dog a rest from the effects as
often as you and your vet decide. Many NSAIDs, like
aspirin, cause bleeding or ulcers in the stomach and small intestine, and have
other undesirable effects; they should be used only for short periods of time
and in carefully controlled dosages. Many are very slow to be eliminated by the
body, and overdose by accumulation can thus be a danger.
Acetaminophen and
ibuprofen have become over-the-counter home remedies, but the former has shown
to be toxic to dogs (worse for cats) and the latter has its own drawbacks for
pets. Some vets prescribe phenylbutazone (“bute”), some meclofenamic acid. The former depresses bone marrow
formation, where red blood cells develop and mature. Carprofen
(one brand name is Rimadyl™) is a more effective
anti-inflammatory agent than aspirin or phenylbutazone,
and apparently reduces crepitus, increases stride length formerly restricted by pain, and
has less gastro-intestinal irritation. As with any medication, some users
blamed it for bad effects, and the popular press and Internet carried many a
panic message for a while. This happens so frequently, that wise owners take
these scares with a grain of salt. There have been a few cases of liver
or other complications, though.
Carprofen is a carboxylic acid related to ibuprofen, ketoprofen, and naproxen — NSAIDs
that you may be familiar with from a tour of your own medicine cabinet. They block production of prostaglandins, providing analgesic and
anti-inflammatory effects.634 Side effects are relatively low. At
the end of 1998, fellow science writer John Cargill told me about a Rimadyl™ vs. EtoGesic™ (carprofen vs etodolac)
comparison using force plate analysis. Force plate testing tells you how much
weight a dog will put on each limb when standing.
Most medications
you are familiar with rely on reduction of inflammation, and the above are
examples. Corticosteroids are in a class of one of the most over-prescribed
medicines that human and animal doctors shove down throats or into
bloodstreams, the other being the antibiotics. In both cases, it is often a
defensive technique, like the M.D. who takes a lot of radiographs more to
“cover his tail” in case of litigation than to find out anything more than he
can with a simpler exam and questions. Steroids such as methylprednisolone,
prednisone and dexamethasone mimic
naturally-generated body chemicals such as cortisone and adrenaline; most have
serious side-effects such as suppression of the immune system, depression of
the adrenal glands’ function, stomach ulcers, capillary rupture and bleeding
just under the skin, other cardiovascular problems, skin becoming brittle, and
increases in appetite and thirst. Doctors Peltier601 and McIlwraith600
have also suggested that corticosteroids can inhibit proteoglycan
synthesis and thus disrupt the cartridge matrix in articulating joints. Proteoglycan is necessary to provide stiffness and other
properties to the matrix. The conclusion is that steroids are not appropriate
for long-term management, although they may be needed for a short time in the
acute stage of many complaints including HD. I once had a bitch that required a
shot of prednisone every 28 days or so, otherwise her atopic-allergy-initiated
scratching and chewing would become intolerable. She also developed heavy
phlegm which she tried to combat by eating anything “scratchy” such as sand,
dried pine needles, debris, and even the part of the fiber-glass
curtains hidden from our view, behind the couch! I am sure the steroids
contributed to her mesenteric bleeding many years later after an operation for
gastric torsion, and her death a few months later.
DMSO, dimethyl sulfoxide, is a chemical
with many uses. It has a long history as an industrial solvent, and almost as
long as a “horse liniment”, giving warm relief to aching muscles and joints.
For years it was a “hot seller” in all sorts of stores for human use in
treating similar pain, and had a relatively short period of use in treatment of
dogs’ aches in hip and other joints and muscles. One big risk is that it is
such a potent solvent, that it apparently dissolves and carries through the
otherwise-protective skin barrier and into the bloodstream, many microorganisms existing on the surface.
One fairly recent
development in drug therapy is polysulfated glycosaminoglycan (PSGAG, one name is Adequan™),
a “natural” compound already in use in equine practice. PSGAG was developed mainly for use in the
horse, but in 1987 an article in a professional journal introduced Adequan to the veterinary community as an experimental drug
for dogs and the news quickly spread through part of the dog breeding community
as well. It is almost a duplicate of the GAGs
naturally produced by the canine body along with vitamin C. Six weekly
injections are supposedly sufficient, in most cases to relieve much of the
symptoms of HD (lameness, Ortolani’s sign, etc.) for
an undetermined length of time.
The drug is
chemically very similar to the mucopolysaccharides of
cartilaginous tissue, which has been described earlier. In fact, many have now
substituted the word glycosaminoglycan for the word mucopolysaccharide. Dr. Joe Alexander, dean of the
veterinary school at Oklahoma State University, describes it as “a potent proteolytic enzyme inhibitor [which] diminishes or reverses
the processes which result in the loss of cartilaginous mucopolysaccharides”.
These processes he speaks of include the synthesis of prostaglandins and
interleukins; the drug may also inhibit the release of, and aid in the
scavenging of, free radicals (damaging ions) as well as inhibit the effects of lysosomal (body-cell‑dissolving) enzymes. Apparently,
it stimulates synthesis of sodium hyaluronate or hyaluronic acid, which with glycosaminoglycan
is the main component of the synovial membrane’s
boundary lubricant; it lowers synovial protein level,
and increases the viscosity of the synovial fluid
much like oil additives are supposed to protect your car’s engine. Some
researchers believe that it slows or even inhibits secondary (arthritic)
degeneration that accompanies HD. The drug apparently also inhibits white blood
cell (neutrophil) activity and the action of
“complement”, which is part of the immune response collection of macromolecules
and chemicals.
One idea is that
it stimulates chondroblast (cartilage-producing
cells) activity and synovial fluid production.
Stepped up production of cartilage may or may not rebuild some abraded or eburnated, worn-thin connective tissue in the joints. While
increased synovial fluid may on the surface seem to
be at odds with Smith’s hypothesis that excess synovial
fluid pressure is a prelude to HD, it may be that once a joint is
deformed by HD, it needs that extra lubricant.
Time will tell
whether PSGAG can be used safely in place of painkillers such as aspirin, which
only cover up some of the discomfort but do nothing in regard to repairing or
protecting the cartilage. Except for some pain response apparently related to
cold weather, Adequan is promoted as being free of
unwanted side effects, with a possible reason given that since it occurs in the
body, any excess is metabolized or excreted. However, there is a possibility
that dogs with frank or subclinical von Willebrand’s Disease or hemophilia,
who are on “blood thinners” or who have infections
might be poor candidates for injectable PSGAG
treatment.
Adequan is currently being used with
variable success, appearing to ease discomfort in a number of joints.
Currently, it appears that some dogs tend to build tolerance to PSGAG, so the
beneficial effects may decrease over a period of time. Perhaps by the time you
read this, some long‑term studies will have been completed that would
lend more confidence to Adequan’s current promise.
In the early
1990s, a cooperative study by Cornell, the Universities of Pennsylvania and
North Carolina, the Ralston Purina Company, and a Swedish pathology lab
indicated that the development of HD could be suppressed somewhat by altering
the concentrates of positively-charged electrolytes in the diet and hence in
the synovial fluid. It was recommended to decrease
meat and bone meal with their high sodium and potassium levels, and partially
substitute more rice and corn gluten meal to boost the chloride level. Still
more work is needed to develop data. If corn meal or corn oil (or other
vegetable oils) are used in greater amounts, I recommend supplementation with
Vitamin E, regardless of health condition.
NUTRITION OR MEDICATION?
There are
several products on the market, some called “nutraceuticals”
because of their hybrid drug/nutrient activity; examples are Glyco-Flex™ and Cosequin™, which
are being touted as beneficial to the dog with HD, supposedly by improving the lubricity in the joints. The former is a preparation from
the green-lipped mussel, brewer’s yeast, and alfalfa; it provides protein, GAGs, amino acids, chelated
minerals, vitamins, and enzymes. The latter is glucosamine,
chondroitin sulfate, and
manganese ascorbate (a combination of vitamin C and
the mineral). Glucosamine (if it indeed has any
lasting benefits) seems to be much more effective if given by injection rather
than orally (enterally). This also seems to be true
of some vitamins, such as B and A. But many people and their dogs find benefits
by ingesting them. Anecdotal testimonials vary from enthusiasm to the statement
that the dog no longer responds to them as it first appeared to. Shark
cartilage and similar health-food approaches have no proven benefit yet, and
feeding chicken necks/wings/joints may please your dog’s palate, but while they
may contribute to a glossy coat and other healthy appearance, it does not seem
to have any real, verifiable value in regard to relieving joint discomfort. For
further reading on the proven products above, read the bibliographic references
given by Dog World writer, John Cargill.
NUTRITION AND ITS ROLE IN TREATMENT
Even
among those who attempt to use and follow precepts of science and logic, there
will be emotion-based decisions and courses of action. Take for example ideas
relating to canine hip joint integrity. Only a few ostrich-brained relics are
still sticking their heads in the sands of ignorance and avoidance, claiming HD
to be simply or mostly an environmental problem. Even among the ranks of the
cognoscenti, however, there are those who hang onto the hope of a “magic pill”
approach. Vitamin C or seaweed or chicken joints or anything else that comes
along with the false promise of an easy, mystical or non-understandable (or
rationalized) way out of the suffering that severe HD can bring — any of these
approaches are emotional roads purported to lead to the goal of better
dogs. But their proponents have
unintentionally or ignorantly twisted the road signs to make you think they are
accurately pointing to the same destination. Only the hardcore of those who
want the easy ways out are today avoiding the logical, science-supported fact
that HD is essentially a genetic disorder and can only be finally dealt with by
selecting breeding partners. You can sometimes ease the life of one afflicted
by modifying the environment through nutrition, bedding, temperature, etc., but
you cannot change the genes.
Since nutrition is a subject with many myths and opinions, I
perhaps should skirt it or treat it in a separate article. But since it
apparently has some therapeutic nature, it should be mentioned here, too. It is
thought that Vitamin E not only works synergistically with C to combat stress,
but even more, helps the body to get rid of metabolic and neuro-synapse
waste products and thus reduce pain. The value of vitamin E in relief of pain
and the support of general well-being has been fairly
well researched. It is not only an intracellular antioxidant, but it also has
other functions, including metabolism of arachidonic
acid, which is a precursor to prostaglandins, which play an extremely important
role in pain management. In this respect, it and other antioxidant vitamins do
something similar to what the steroidal drugs do: inhibit prostaglandins and cyclooxygenase in the “arachidonic
cascade”. An article in the journal VetMed
many years ago gave evidence of its use, synergistically with adequate
selenium, in alleviating HD and other joint pain.
The best
application of a nutritional approach to treatment of HD is very simple: get
the weight off. Excess weight and stress from activity make the dysplastic joint deform and wear faster. To allow the dog’s
cartilage to change to bone before you deform it with overnutrition
and work, keeping it slim will be the kindest deed you can offer your dysplastic pet. Overfeeding truly can be “killing with
kindness”, which really is not kind, but cruel.
Fred Lanting's latest book:
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