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 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
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
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
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
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
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.
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Copyright 2001 Fred Lanting, Canine Consulting. Mr.GSD@juno.com. All rights reserved. Please
view his site Real GSD.
NOTE: A well-respected AKC
and Schaferhund Verein
judge, Mr. Lanting has judged in more than a dozen
countries, including the prestigious FCI Asian Show hosted by Japan Kennel
Club, the Scottish Kennel Club, a Greyhound specialty in