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Canine
Hypertrophic Osteodystrophy (HOD)
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Hypertrophic Osteodystrophy
HOD
Hypertrophic Osteodystrophy
Veterinary & Aquatic Services Department,
Drs. Foster & Smith, Inc.
Hypertrophic Osteodystrophy
(HOD) is a bone disease that usually affects young, rapidly growing, large
breed dogs. The disease has several names including skeletal scurvy, Moller-Barlow's
disease, osteodystrophy II, and metaphyseal osteopathy. The disease produces
severe lameness and pain and usually affects multiple limbs. The cause
of the disease is currently unknown.
Who gets hypertrophic osteodystrophy?
HOD is a disease of young, rapidly growing dogs. It usually strikes
puppies between the ages of 3 to 6 months. It is primarily a disease of
large or giant breeds of dogs, although there can be exceptions to this
rule. As with most of the young, large breed bone disorders, it affects
males more commonly than females. There does not appear to be an increased
incidence in any one large or giant breed. There does not appear to be a
strong inherited or genetic link.
What are the symptoms of hypertrophic osteopathy?
Dogs that are stricken with HOD often show symptoms of mild to moderate
painful swelling of the growth plates in the leg bones. It most commonly
affects the ends of the radius, ulna, (long bones from the elbow to the
wrist) and tibia (long bone from the knee to the hock). The dogs may show
lameness and a reluctance to move. They may be lethargic and refuse to eat.
A fever may come and go rising as high as 106 degrees. The disease usually
affects both legs at the same time. The symptoms may wax and wane and resolve
on their own or if the fever is very high for long periods and the bony involvement
severe, the dogs may suffer permanent structural damage or even die.
How is hypertrophic osteodystrophy diagnosed?
Diagnosis is based on the history, symptoms, physical exam showing pain
and swelling at the growth plates, and with x-rays. The x-rays will show
a thin radiolucent (dark) line at the metaphysis (growth plate) in the end
of the ulna, radius, or tibia. Bony inflammation and bone remodeling may
also be seen at these sites. Occasionally, there may be involvement and changes
in the skull and teeth. Dogs often have a fever and occasionally a high
white blood cell count.
What is the treatment?
The treatment is generally supportive. Since this is a very painful
condition anti-inflammatories and painkillers such as buffered aspirin
or carprofen (Rimadyl) are given. (Do NOT give your cat aspirin unless
prescribed by your veterinarian.) In addition, the animals are usually given
a broad-spectrum antibiotic. Strict rest on a comfortable warm bed is recommended.
Feeding a nutritious, highly palatable food will help to encourage some
dogs to eat. In severe cases steroids may need to be given to control the
pain, but because of the possibility of this being a bacterial disease their
use may be contraindicated due to their immunosuppressive qualities. Vitamin
C is often supplemented though its benefit may be questionable.
What causes it and how is it prevented?
The prevention lies in understanding what causes this disease. Unfortunately,
there is currently no agreement on the cause of this disease. One possible
cause may be a bacterial infection. The bony changes and high fever support
this possibility. The difficulty in obtaining a bacterial culture from the
site and the sometimes-poor response to antibiotic therapy may fuel the
argument against this possible cause.
Another suspect in the disease is vitamin C. It has been shown that
dogs with this disease show very similar symptoms and bony changes as people
with scurvy (vitamin C deficiency). In addition, these dogs often have a
lowered blood vitamin C level. However, dogs synthesize their own vitamin
C and do not have a nutritional requirement for this vitamin. In several
studies and in practice, feeding affected dogs high doses of vitamin C does
not always alter or cure the disease. Some researchers therefore speculate
that the low blood level of vitamin C may be a result of the disease, not
the cause.
Another possible cause of the disease may be nutritional. It has been
suggested that several bone diseases in young puppies are linked to an
excess of protein and calories in the diet leading to the development of
these problems. The studies have not been done that confirm this, though
many owners of large and giant breed puppies are currently feeding a diet
lower in fat and protein to try to encourage moderate steady growth instead
of rapid growth. It is possible that this disease may be caused by several
factors. At this time, however, we do not know the cause or how to prevent
it. Hopefully future studies will give us more information on the cause and
prevention of this painful and debilitating disease.
References and Further Reading
Bloomberg, M; Taylor, R; Dee, J. Canine Sports Medicine and Surgery.
W.B. Saunders Co. Philadelphia, PA; 1998.
Brinker, W; Piermattei, DL; Flo, GL. Handbook of Small Animal Orthopedics
and Fracture Treatment. W.B. Saunders Co. Philadelphia, PA; 1983.
Ettinger, S. Textbook of Veterinary Internal Medicine. W.B. Saunders
Co. Philadelphia, PA; 1989.
Copyright
© 1997-2007, Foster & Smith, Inc. All Rights Reserved.
C 2006 Drs. Foster and Smith, Inc.
Reprinted as a courtesy and with permission from PetEducation.com (
http://www.PetEducation.com)
On-line store at
http://www.DrsFosterSmith.com
Free pet supply catalog: 1-800-323-4208
reprinted with kind permission from Josie Pitterle Article Reprint Coordinator
Drs. Foster and Smith
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HYPERTROPHIC
OSTEODYSTROPHY (HOD)
By Fred Lanting
The pup the Smiths bought
was a very promising individual with a great pedigree. Here, they hoped,
was the foundation of their successful showing and breeding future. But
in a matter of a couple of weeks, a previously unnoticed cow hocked condition
developed and worsened. They shrugged this off, having heard that dogs with
"extreme" rear angulation sometimes develop loose hock action between 2
and 6 months of age. The pup will outgrow it, they thought.
But in another month the pup was acting sickly, evidencing an uncharacteristic
listlessness. Rectal temperature showed a fever, and because the pup had
intermittent diarrhoea, it was started on antibiotics. It had already been
routinely treated for worms even though there were no eggs or spores in
recent stool checks. After another week the pup “went down” with partial
paralysis in the rear, and had very weak (slanted) pasterns with splayed
feet and swollen “wrists” or carpal-foreleg joints.
There followed a succession of treatments: Mediprin™, Bufferin™, Prednisolone™,
antibiotics, Vitamin D, calcium gluconate, Vitamin C, and more. Sometimes
it seemed one course of action was working when suddenly the condition
would worsen. Months of worry, pity, temporary relief of pain, nursing care,
and assistance passed before the pup pulled out of this perplexing condition.
Never did it attain the stature and weight of most others of its breed
and line, nor did it lose its cow hocked stance and gait, although it finally
gained normal health.
Many variations on the above theme have been played by a frustrating
and painful disease known as HOD, which stands for hypertrophic osteodystrophy.
Hyper- means excessive, and -trophy or -trophic refers to growth, so the
name describes an abnormal and excessive growth of bone (os-) in certain
locations. Since this excessive growth does not usually occur as much around
the shaft, but certainly at the area of the metaphysis, the term “metaphyseal
osteopathy” had at one time been suggested. It has also been called Osteodystrophy
I and/or II, Barlow's or Moeller-Barlow's disease, skeletal scurvy, and just
Vitamin C deficiency at one time or another, although some of these terms
are misleading or inaccurate.
BREED, SEX, AND AGE CORRELATION
Once thought to be strictly a problem in giant breeds, HOD is also
seen in large and medium size breeds, including Setters, Labrador Retrievers,
Doberman Pinschers, Weimaraners, Pointers, German Shepherd Dogs, Collies,
Boxers, Basset Hounds, Great Danes, and Borzoi. Probably the greatest occurrence
has been reported in Irish Setters. It appears that early rapid growth
rate is a factor as it is in the case of hip dysplasia and panosteitis,
but size of the individual does not appear to play any role. Several years
ago the Irish Setter and the German Shepherd Dog were two of the breeds
most seen with HOD but while the incidence truly is higher in the Irish
Setter, the inclusion of the GSD in 1979 may be mostly because of its greater
numbers rather than a high percentage or incidence in this breed.
One Greyhound, 20 months old, was diagnosed in Sydney, Australia as
suffering from HOD, but because of its untypical age and breed, it may
possibly have been something else. One group of researchers in 1975 gave
the age range as 3 to 8 months, and a 1990 textbook gave 2 to 8 months,
and may have included rare early incidents such as the 1973 Australian
study that reported an 8-week old pup having had the symptoms for 2 weeks
before being presented at the clinic. A 4-year Norwegian compilation of
26 affected dogs indicated that slightly less than half of the cases are
diagnosed between 13 and 15 weeks of age, and an equal percentage spread
out between 15 and 24 weeks of age. The first half is at approximately the
age at which distemper and hepatitis (and many others, in some cases) vaccines
are given to most dogs, which may give rise to speculation about challenges
to the immune system. In that same study, twice as many males were afflicted
as females, which ratio has been noted elsewhere by breeders. It has been
shown that females are generally more able to handle stresses.
CLINICAL SIGNS
A description of symptoms should be prefaced by the warning that any
one or several can be evident in other diseases as well, and either some
or all can be present in the disorder discussed here. It may reappear three
or four times, and in this respect it is a little like panosteitis. In a
few cases, serious multiple relapses have been noted, enough to warrant
euthanasia for relief of the pain. Recovered dogs may have radiographic evidence
of residual bone change, or may have frank limb deformities.
In addition to the foregoing example of the Smith's dog, HOD's clinical
signs (symptoms) can include a clear discharge at the eyes, bowing of
the foreleg below the elbow, and turned out ("east-west") front feet.
There may be depression, pain (even in the jaws), lameness, reluctance
to stand, and anorexia (loss of appetite and weight), with painful joint
swelling at the distal metaphyseal regions of the long bones. Although most
physical signs are in the distal radius/ulna (pastern area), they are also
seen in the distal tibia (hock area). Fever might not be manifest in the
early stages of the disease. Diarrhoea often, but not always, precedes
the joint episodes by a couple of days to a couple of weeks. Usually the
severe pain in the lower area of the leg, where either the pastern or the
hock begins, typically gives the dog anything from a stiff gait to slight
or severe. Extremely adducted pasterns, often described as “soft” or “down”,
are very characteristic of HOD. Carpal subluxation, in which the dog stands
and walks on its pasterns, is an extreme example of being down at the
pasterns, and the similarity is known by breeders who have fed very high
energy, high protein foods. HOD, inherited carpal subluxation, and panosteitis
share the similarity in that they are all much worse when such diets are
consumed. Death is not unknown but fairly rare, and preventable.
RADIOGRAPHIC SIGNS
Correct diagnosis is best made by X-ray film examination along with
observation of the clinical signs (symptoms). As young leg bones grow,
the end sections are continually changing in composition between cartilage
and bone. A short distance from the ends, in the metaphyseal region, is
a transverse line of cells known as a growth plate. In order to make the
bone increase in length, you'll remember, cartilage near the end of the
shaft is replaced by bone cells while bone in the epiphysis is transformed
to cartilage at the growth plate. Meanwhile, cartilage on the far end of
the epiphysis ossifies and is itself added to by simple cell division growth.
The greatest change occurs in the distal end of the lower leg, where growth
is apparently most rapid in the breeds with medium or long legs.
Radiographically, early signs include a small and irregular radiolucent
(clearer) line in the metaphysis just above and parallel to the growth
plate and separated from it by a relatively dense band. It’s most easily
seen in the lower end of the forearm. In some advanced cases much proliferation
of new bone (“calcium deposits”) appears around the metaphysis. This mineralization
does not appear to be firmly attached to the cortical bone, but lies on
the surface of the periosteum. The longer the condition persists, the further
up the limb this ossification of the tissue of the periosteal cuff proceeds.
In the worst stages, this new bone will be incorporated with the cortical
bone, the hard, dull, dense bone beneath the periosteum. If it goes this
far, some remodelling and permanent change will occur. Radiographic evidence
may also be seen elsewhere on the bone, at some distance from the joint
most affected, and soft tissue swelling may also be evident.
When HOD strikes, the metaphysis becomes generally denser and thus
more opaque to X-rays, and usually becomes more enlarged; in the growing
pup it already is normally wider in proportion to the shaft than it is in
the adult. The epiphysis and growth plate largely retain normal appearance,
but the radiolucent line is quite noticeable in the increased radio dense
end of the metaphysis closest to the growth plate. Because the opaque appearance
is sometimes irregular, granular, and discontinuous, some investigators
in the 1960s felt these signs to indicate either a separate disease or a
variant of HOD which they called “hypertrophic osteodystrophy type II”.
Almost all of us now realize that the use of the term osteodystrophy-II
is superfluous as a description of a supposedly different disorder, because
early cases of HOD eventually develop new bone growth in and around the surface
of the bones.
As the disorder advances, or in dogs suffering from a more severe
form or phase, the enlargement of the end of the ulna above the epiphysis,
and the bony calcium deposits that form on the outside of the periosteum,
are preceded or accompanied by haemorrhage beneath as well as outside the
periosteum, and blood cell infiltration into the bone itself.
The periosteum is the tough, smooth, elastic white covering of bones,
and it serves as a point of attachment for other connective tissues such
as ligament, cartilage, and the fascia of muscles. The ossification shows
up on the radiograph as a billowy or beaded opaque deposit separated from
the metaphysis by a translucent line at the periosteum. The swelling resulting
from such haemorrhage and bony growths is often very warm and always painful.
Such deposits are not usually found in areas of slower growth, such as the
proximal metaphysis of the radius and ulna, but can be quite massive on
the distal end in just a couple of weeks after symptoms commence. As the
disease runs its course and the patient recovers, the mineralization outside
the periosteum is gradually resorbed and the radiographic appearance of
the metaphysis resumes normal shape and density. At the same time, body temperature
has returned to normal, lameness begins to subside, and appetite returns.
While repair and remodelling are usually complete, there are some cases
in which distortion of the diaphysis and residual osteophytes can remain.
HAEMATOLOGIC AND HISTOLOGICAL INDICATIONS
A higher than normal level of white blood cells (primary infection
fighters) is often an indication of the presence of a viral or bacterial
agent, and in HOD there is sometimes a high leukocyte count in bones as
well as in the blood. However, biochemical analysis and haematologic tests
are not very fruitful in this disease, even though neutrophilia, lymphocytopenia,
and monocytosis may be findings during the late or active stages; these probably
reflect stress and inflammation, and are effects rather than causes. Blood
tests can show mytosis, an increase in a certain type of leukocyte, and
anaemia to a slight degree. Chemical analysis discovers low serum ascorbic
acid (vitamin C), but to implicate a deficiency of this vitamin would be
a mistake. The reduced serum level often found is now considered a secondary
change rather than a causal factor. Besides, microscopic changes in bone
in these patients are different than those in hypovitaminosis C (deficiency).
See discussion of vitamin C below.
The most noticeable histologic changes are seen in the metaphysis,
specifically in the nature of its spongy bone. Here the pathologist can
find microfractures in the trabecular bone, necrosis, osteomyelitis, and
other bone defects. That dense band I mentioned earlier is a result of excess
calcification spreading from the cartilage lattice of the primary spongiosa,
and from abnormal trabecula cell growth. Upon necropsy, he can also confirm
what the radiologist has seen, the ossification of the periosteum and nearby
soft tissues.
NUTRITION
By 1957 it was obvious that dietary vitamin D increase was not effective,
and in fact by the mid-1960s breeders were warned against mineral overloading
(calcium supplements in the diet). Yet even in the 1980s and to a lesser
extent the 1990s, calcium supplementation occasionally had still been prescribed
for HOD! It is part of human nature to rest on what we've been told rather
than practice continuing education, since “the world is too much with us”,
so don't be surprised if your vet hasn't kept up on everything and especially
on things not as necessary to his daily practice. HOD doesn't show up
frequently enough to warrant that much attention, but the orthopaedic specialist
who gets referrals from many vets may more easily identify its symptoms.
To be fair, one must also acknowledge the report of one study that
involved supplementing the diets of young large breed dogs with minerals
and vitamins A and D at three times the NRC recommendations. These dogs
had no differences in growth rates, radiographs, or blood chemistry. But
I feel the preponderance of evidence leans toward the previous view, that
there is considerable risk to many dogs in supplementing in that way, especially
those breeds or families that may have a genetic predisposition to HOD.
Most who have studied HOD now conclude that it is probably some sort
of a metabolic disorder, and many if not most believe also that the tendency
to fall prey to owners' practices of over supplementation and over nutrition
is genetic. An imbalance of minerals, protein, and vitamins interferes
with normal deposition of calcium phosphate (bone) and turnover of cartilage
which lead to the physical, visible changes. If a high protein, high calorie/energy,
and highly palatable diet producing over nutrition is indeed a candidate
for cause, the process possibly traces its route through excess calcium,
hypercalcemia, hypercalcitonism, hypoparathyroidism, and retarded bone resorption.
The body reacts to excess calcium by lowering the level in the blood (excretion,
deposition) but it goes too far into hypocalcemia because of the persistent
hypercalcitonism. As you learned in the chapter on nutrition, this condition
arises because excess dietary calcium stimulates the gut to secrete more
gastrin.
On the other hand, some investigators remain sceptical because hyperthermia
(fever), which is a reliable sign in most diagnosed cases, was not recorded
in the experimentally over nourished dogs in the main nutrition study,
and certain histologic and radiographic signs found in HOD cases “in the
field” were not seen in the experiment dogs. Further, HOD does occur in
some dogs on dietary intake that would not be considered over nutrition
under current guidelines.
Vitamin C
Even researchers who once felt that HOD in the late form may be associated
with deficient vitamin C will admit that the vitamin theory was controversial
and that the response to vitamin C therapy was variable. Clinical signs
similar to those of scurvy (frank vitamin C deficiency) have been reported
in young dogs but no direct link was firmly established by that work. Later,
a Finnish team at the vet school in Helsinki published a poorly founded
one-page anecdotal report of two cases they diagnosed as being HOD. The undated
and unidentified copy of “Scurvy as a cause of HOD in two young dogs” that
I received from a vitamin supplement salesman in Finland had poorly documented
references but quoted, among other sources, work by Kivirikko as stating
that insufficient vitamin C resulted in the failure to biosynthesize collagen.
The deduced chain of events was given as disappearance of collagen bundles,
and cartilage becoming thin and watery in appearance. They concluded that
the livers of young pups become stressed by the vaccines against distemper,
hepatitis, and other viral disorders, and since the liver is where most of
the dog's vitamin C comes from, the shots temporarily disrupt the natural
in-situ synthesis of this vitamin. They also implied that larger, fast-growing
breeds required more ascorbate/vitamin C than their livers could make to
keep up with the enormous amount of collagen production needed. Respected
nutritionists have debunked this work, and one I won't name here (but I have
in personal correspondence) gives it the name of a famous rodent created
by Walt Disney.
Many people with some degree of hypochondria imagine themselves as
having a particular disease or group of ailments, based on the descriptions
of the symptoms common to them. Similarly, some people see what they think
are indications of disorders in their dogs, jump to conclusions, and make
a diagnosis, often erroneously. It is a normal thing for many breeds, especially
the giant and some of the other large breeds, to have somewhat "knobby"
carpal joints, so this should not lead one to a supposition of HOD. On the
other hand, it would be exercising wisdom not to over-feed or supplement
with vitamins A or D and calcium.
The great vitamin C controversy is far from over, as can be seen by
the frequent resurrection of “scientific studies” which have little or
no basis, but represent a “magic pill” answer for the hopeful producers
and readers of club newsletters and magazines who are careless about what
they promote or believe. These articles are resurrected in greater frequency
than the independent return of HOD.
Man has apparently benefited from very large doses of this vitamin
during times when the body is under stress as a result of viral and other
infections, but most animals make their own ascorbate (vitamin C). Newborn
puppies synthesize their own even when the colostrum and bitch milk have
elevated vitamin C levels, and relatively large doses of the vitamin sometimes
have little effect on either the production rate of self-synthesized serum
ascorbate or on the course of certain diseases such as HOD, hepatitis, kennel
cough, etc. Vitamin C salesmen usually claim the doses were not large enough.
HOD is associated with retardation of bone resorption and by excessive
bone formation, and is linked to excessive dietary carbohydrates and protein.
That is its only relationship or similarity to HD, as much as we can tell.
Vitamin C deficiency as a factor in causing HOD is highly unlikely, and
vitamin C supplementation can only make HOD worse, according to University
of Liverpool researcher Dr. David Bennett.
The measurement of ascorbate or ascorbic acid is difficult and often
inaccurate, as it is very unstable. I remember the frustration I encountered
when finding this to be true in graduate work, in my organic chemistry
lab. Therefore, I don't get excited when I read reports of ascorbic acid
measurements in blood and urine in connection with HOD.
Extra vitamins C and A can enhance calcium absorption from the intestine,
and more calcium certainly is not what you want when a dog is suffering
from "calcium deposits". Because of the report of low serum ascorbate (vitamin
C in the bloodstream) some work was undertaken at Cornell which contradicted
the suggestion to supplement, and found that large doses failed to give
consistent results. This was in agreement with Bennett’s work. Those researchers
at Cornell claimed the earlier studies supporting the use of vitamin C were
uncontrolled and the results equivocal. Some dogs in the Cornell investigation
had a temporary remission, others were totally unaffected.
More about diet
The effect of diet as a causative factor may be equivocal, but there
is no doubt that excessive calcium supplementation can greatly exacerbate
the pain and radiographic signs. As a general rule, stay away from calcium/vitamin
D additions to the food, since it not only makes the HOD worse, it contributes
to the severity of other orthopaedic and systemic disorders as well. Even
ad libitum feeding of high-nutrient density, balanced dog food without
extra calcium has resulted in experimentally induced HOD. If a growing dog
eats all it wants of a "good" dog food, it can absorb more calcium than
is beneficial compared to a pup on a restricted diet. Keep your puppies
on the thin side, and you can avoid some health problems.
Use a high quality, but not high energy (calorie) dog food, don't
feed more than the dog needs or wants in a short mealtime, and don't supplement
with Vitamins C or D or calcium if HOD is known in your breed, unless your
nutrition expert veterinarian prescribes these for some specific reason.
Certainly don’t supplement if the symptoms of HOD appear. It would probably
be wise to switch the HOD patient's diet to a lower calorie, lower protein
food as quickly as you can without causing diarrhoea. Make sure it has
a low enough calcium level to satisfy your veterinarian (whom you've already
asked to confer with perhaps a specialist in the veterinary teaching hospital
at the university.)
CAUSE
The cause of HOD is unknown. This is the message that comes out of
all the work done so far, and the picture is unlikely to get any better
until there is sufficient information and controlled studies to yield some
scientific conclusions. One veterinarian/breeder published in the newsletter
of the Irish Setter Club of America a questionnaire in which he sought
answers to some 32 questions designed to uncover a connection with another
disease, diet, or genetics. Almost no one responded, although Irish Setter
publications had carried a number of tear-jerker case histories and warnings
about HOD. Apathy will certainly hinder the fight. Perhaps some group will
find the interest and the contributions, and fund sufficient research to
solve the HOD enigma. But then, I had expressed the same hope in 1980.
I once suspected a viral agent might have been directly connected
with HOD, but no evidence has come to light to support that, although
further work is needed before we can exclude microbial infections. It now
appears HOD is quite possibly a result of nutritional and immunological
forces acting in dogs, most of who may be genetically at risk. Familial
relationships have been claimed in anecdotal reports gleaned from discussions
I've had with many breeders. Most cases are diagnosed at approximately the
age at which distemper vaccine (at least, the “adult shots”) is administered,
and many have shown initial symptoms one to six weeks after vaccination.
The fact that fever accompanies other signs, and the additional history of
diarrhoea frequently preceding the onset of pain are indications that if
a virus or bacteria is not a direct causative agent in genetically susceptible
dogs, it is possible that an inactivated, killed, or modified live virus
somehow upsets the dog's immune system. Immune response is related to the
function of many endocrine glands that produce hormones, and hormones have
been identified as playing a part in mineral absorption and joint development.
Too tenuous a thread for you to follow with credulity? Understandable. That's
why I present it only as an idea to run up the flagpole. If nobody ever
salutes, there's no harm done. In humans, measles vaccine has caused bone
disease surprisingly similar to canine HOD. Nearly every dog fancier knows
of the similarity between measles and distemper viruses, the former being
commonly used in a modified version to immunize very young puppies against
distemper before the pups are completely weaned. Incidentally, there is some
suspicion that human multiple sclerosis is related to canine distemper virus,
though it is an unproven theory as yet.
An attempt to induce HOD in healthy dogs by transferring the disease
from affected dogs was planned in Norway and partially completed, but with
somewhat disappointing results. Blood was transfused from a dog in the
acute stage of HOD to healthy dogs of different breeds, and some developed
distemper and died! Their blood donor had been vaccinated against distemper
and hepatitis one week before it had shown signs of HOD. Other dogs died
after receiving blood from another HOD afflicted donor, but none of that
dog's recipients developed signs of HOD. Interestingly, there was an epidemic
of distemper in the area at the time, but less than 3 years after that,
HOD had almost disappeared, with only two dogs being diagnosed for it since
the 26 cases at the clinic in 1976. Could whatever causes HOD be transmitted
in the blood and also cause distemper? Could some individuals challenged
with either virulent distemper virus or modified viral vaccine comes down
with HOD, and others get distemper?
Why does HOD seem to come and go, like consecutive bad years for dog
ticks or cicadas, followed by a respite for a few or several years? That
is hard to answer, and any attempt is speculative. HOD could be a single
disease with one or more causes, or it could be a syndrome. You remember
that means a collection of symptoms, and that there could be up to several
disease “events” going on at one time. Your dog with HOD might have a copper
deficiency, a diet too high in protein and calories, a microbial infection,
a challenged immune system, or any combination of these and other processes
going on at once. That HOD seems to come in “waves” lends credence to the
multiple-cause hypothesis.
TREATMENT OF HOD
Penicillin, streptomycin, sulfa, and other antibiotics, and a host
of analgesics (“pain killers”) such as aspirin preparations, Mediprin™,
and others have been administered with no reliable beneficial or conclusive
results. Steroids and other medications were given to no avail as far as
the primary lesion was concerned. Because of spontaneous remissions and
unforeseen worsening or relapses, the success or value of any treatment
will continue to be elusive. Remission and drug use are probably coincidental
in almost all cases. As in the case of panosteitis, it appears that in most
cases the dog will get better whether or not it is treated at all, and regardless
of diet except for the harmful addition of calcium, vitamin D, and possibly
vitamin C. Some owners reported apparent improvement with one choice one
time, and then did not repeat their success the next time. It may be wisest
to treat symptoms conservatively and assume we have another self limiting
disorder in HOD afflicted dogs, with TLC (tender loving care) and patience
the best tools at your disposal.
The difference in this conservative management approach to HOD compared
to panosteitis is that the complications in HOD may be very serious. The
dog may not die from the HOD itself, whatever the cause may prove to be.
This is similar to the situation in human medicine wherein the patient does
not die of the AIDS virus directly but of the complications it brings on,
such as cancer or disorders in the lung, heart, and other organs and systems.
Therefore, medical management of HOD should be directed toward halting
the diarrhoea, lowering the fever, getting rid of parasites, and relieving
whatever pain you can. Symptomatic treatment might make the difference between
losing your dog and saving him, but death is such a rare consequence that
the owner is cautioned not to go overboard on treatment. Don’t try to eliminate
all symptoms, in other words, or the remedy might be worse than the disease.
At present, the only generally recognized treatment prescribed is purely
symptomatic: relief of pain through buffered aspirin or sometimes corticosteroids.
Some few of the many owners I have corresponded with have been positive that
if they had not treated the symptoms such as appetite loss, diarrhoea, etc.,
they would have lost their pups. Most people who have studied this disorder
agree that the best you can do is give the dog rest, aspirin if the dog
is obviously in pain, and a diet not excessive in protein or energy. In
the worst cases, the dog might have to be force fed or given fluid therapy
to prevent dehydration, and other symptom oriented treatments.
DISORDERS WITH SIMILAR SIGNS
Besides reading the following short comments about disorders that
could conceivably be mistaken for HOD, it would be a good idea to read
more about them in works dealing with other miscellaneous disorders. Your
vet will be especially careful to avoid a poorly exposed or focused radiograph,
as the wrong diagnosis otherwise could easily be made.
Panosteitis usually occurs in older pups than does HOD, and is less
severe with a zero fatality risk in itself. Moeller-Barlow's Disease was
once thought to be a separate problem with less fever associated with
it than HOD, according to some reports but most now believe it to be the
same lesion. The signs of HOD resemble those of scurvy in humans, and radiology
shows features of both clinical rickets and scurvy. Osteodystrophy-II,
mentioned earlier, is probably a stage in the progression of HOD, beyond
which some individuals never go before recovering. Hypertrophic pulmonary
osteoarthropathy also has periosteal new bone formation at the distal ends
of the extremities, but it is almost always accompanied by lung disease,
and the osteophytes are more in the wrist and hock than in the long bones.
Legg-Calvé-Perthe's disease and hip dysplasia involve the proximal
end of the femur and is usually a problem just in toy breeds. OCD of the
shoulder and knee (stifle) and some elbow disorders can give somewhat similar
clinical signs, but are readily identifiable radiographically.
Another, very similar disorder is hypertrophic osteopathy or hypertrophic
osteoarthropathy, again characterized by osteophytes on the outside of
the ulna, radius, and other long bones, usually worse at the distal ends
near the pastern or hock. How this differs from HOD is not so much in radiographic
and direct visual appearance, but in age of onset, recommended treatment,
and probably the cause. While HOD strikes puppies in a certain age range,
this disorder affects dogs of all ages, most often adults.
Fungal infection
Sometimes bony involvement of long bones caused by Blastomyces will
cause radiographic shadows with similarities to HOD, but this fungal disease
may also show up as skin lesions around the distal end of the limb section
where the apparent increase in bone density is found on film. It shouldn't
be difficult to differentiate between them.
Multiple Cartilaginous Exostoses
Yet another condition with radiographic similarities to HOD is found
in humans, cats, horses, and dogs. This is also known as osteochondromatosis,
hereditary multiple exostosis and, in Britain, diaphyseal aclasis. It
is seen mostly on ribs, vertebrae, and the long bones, although it has
been seen on every bone except the skull. Because the growth, a gross exostosis,
seems to involve mostly the metaphyseal area (near the growth plate at the
ends of the long bones), it can be mistaken for HOD.
Polyarthritis
The name suggests the problem: arthritic inflammation in several locations.
This disorder can be classified as erosive or non-erosive, but both types
can mimic HOD upon cursory observation, especially in that they can produce
swelling at the carpus and tarsus (pastern and hock), but also in other
symptoms. Where HOD usually occurs between 3 and 5 months, this disorder's
onset is more typically between 9 and 10 months of age.
CONCLUSION
HOD is an orthopaedic disease seen in medium, large, and giant breeds,
more common in some than others. There may be several causative factors
including heredity, infection, and possibly vaccines, with contributing
factors being both genetic susceptibility (“weakness”) and calcium supplementation
or unlimited/excessive feeding of pups resulting in mineral overloading
as an intensifier of pain and abnormal bone growth.
As in the case of panosteitis, the disease appears to be self limited
and transient, independent of treatment. Although there are rare deaths,
probably due to “complications”, most pups outgrow HOD within one to a
few months. The fatality rate is too erratic to reliably measure. In some
reports it has been 25-35% (almost certainly inflated via poor statistics
and diagnoses) and in others it was less than 4%. In every case, it is
traumatic because of the pup's pain and the owner's helplessness and frustration.
Multiple relapses are not uncommon, and the same bones can be affected
more than once. Extraperiosteal calcification is slowly resorbed and radio
density of the affected limbs returns to normal or nearly so. Some individuals
are left with permanently bowed forelegs because the ulna has grown at
a different rate than the radius (as is the case in some elbow dysplasias),
and some are cow hocked for life. Most, however, endure and survive the
effects of HOD without permanent damage.
The author has had years of experience as a conformation judge for
AKC, SV, UKC, and many other registries, and regularly trains his dogs in
schutzhund, trying to live up to the title of his book “The Total German
Shepherd Dog” (available from www.Hoflin.com).
He consults as a behavioural analyst and training coach, and gives seminars
on training, canine anatomy & gait, as well as orthopaedic problems (he
is the author of the book on HD). Lectures can be scheduled by contacting
him at mailto:Mr.GSD@Juno.com
The above information is simply informational.
It's intent is not to replace the advice of a veterinarian nor to assist you
in making a diagnosis of your pet. Please consult with your own veterinarian
for confirmation of any diagnosis. Your pets life may depend on it.
