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 cowhocked 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 diarrhea, 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 cowhocked 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
other, 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. Diarrhea 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 remodeling 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 more dense 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-radiodense 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
hemorrhage 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 hemorrhage 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 remodeling are usually complete, there are some cases
in which distortion of the diaphysis and residual osteophytes can
remain.
HEMATOLOGIC 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 hematologic 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 anemia
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
orthopedic 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 overnutrition 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 overnutrition 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 skeptical 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 overnutrition 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 orthopedic 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 diarrhea. 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 whom 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 diarrhea
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 come 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
diarrhea, 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, diarrhea, 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 orthopedic 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 both 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 radiodensity 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 cowhocked for life. Most, however, endure and survive the effects of
HOD without permanent damage.
The author has had years of experien