Growth-Associated Bone
Disorders in the Dog
What are "growing pains"?
"Growing pains" are symptoms most often affecting medium, large, and giant
breeds of dog: those breeds that are usually subjected to rapid growth periods
within their first year of development. Symptoms of pain and lameness can be
the result of any trauma to bones, joints, or the supporting soft tissues, but
often they are caused by specific diseases of the bone.
During normal growth and
development, cartilage growth precedes bone formation. The cartilage grows and
becomes calcified. Vessels from the bone marrow invade this calcified layer of
cartilage. Some of the calcified cartilage is reabsorbed, but some remains and
is used as a framework for the bone.
In instances of bone
disease, one or more of these steps is interrupted and the formation of bone
ceases or causes a defect if bone formation continues. Exposure of
incompletely formed or abnormally formed bone to pressure and tension
resulting from movement causes symptoms of pain and lameness.
It is important to
understand that "growing pains" are a symptom and do not constitute a
diagnosis. For proper treatment of bone disease and prevention of further bone
damage leading to secondary complications of osteoarthritis, it is essential
that the underlying cause of pain and lameness be identified.
How are bone disorders
diagnosed?
There are multitudes of
disorders that may present symptoms of joint pain and lameness in growing,
active dogs. Observation of clinical symptoms and physical examination alone,
therefore, are not sufficient to accurately diagnose growth-associated
disorders.
Survey radiography (x-ray
imaging) is often reliable for the identification and differentiation of many
bone and joint disorders. Often, however, particularly in the early stages of
disease, radiographic evidence of bone changes associated with a disease
process may be minimal or absent despite clinical symptoms. Additionally, some
joint abnormalities are not clearly discerned by conventional x-rays.
Therefore, in the presence of significant pain and lameness despite negative
findings on x-ray, computed axial tomography (CT) or magnetic resonance
imaging (MRI) is often successful in detecting bone and joint abnormalities
that are overlooked by survey radiography. Additionally, CT and MRI are
considered invaluable for pre-operative planning in cases where corrective
surgery is indicated.
Another approach that may be
used alone or in combination with diagnostic imaging is the laboratory
collection and analysis of joint fluid from the effected limb. This method may
be helpful in confirming presence of joint disease even in the absence of
detectable disease by imaging techniques. Additionally, joint fluid analysis
will discern between inflammatory and non-inflammatory joint disease, as well
as detect presence of a bacterial infection. However, a major limitation of
joint fluid analysis is that it is unable to differentiate between one
inflammatory or non-inflammatory disorder and another
What causes bone disorders?
There is no single factor
that has been identified in causing any of the various bone diseases, rather,
certain "risk factors" are attributed to increased occurrence of these
disorders in dogs. Size is widely considered a predisposing risk factor. Dogs
of large and giant breeds undergo a more rapid growth phase during their first
year of development putting them at greater risk for skeletal abnormalities.
Excessive calcium supplementation and rapid weight gain are also considered
risk factors, however, evidence supporting a role of other nutritional factors
such as high protein or carbohydrate diets is not as strong. Additionally,
clinical data suggests that the role of nutrition in the development of the
various skeletal diseases is more of a modulating effect. In other words,
controlling for nutrition alone will not prevent these diseases, rather
nutritional management may lessen the severity of disease in those dogs
predisposed by other factors such as size, genetics, trauma or as of yet
unknown causes.
What are some of the common bone
disorders affecting dogs?
The most common bone
disorders affecting growing dogs will be described here. The disorders have
been divided into two groups: 1) those in which one or more stages in the
construction of bone is interrupted and 2) those affecting the actual
formation of bones and joints.
Disorders of Bone Construction
Osteochondritis Dissecans (OCD):
This disorder occurs when calcification does not follow cartilage growth. The
cartilage continues to grow, becomes thicker than normal, and vessels from the
bone marrow are unable to penetrate. Under these conditions, bone formation
does not proceed and cracks and crevices form in the abnormally thickened
cartilage. Fragments of cartilage eventually detach from the underlying
cartilage and become lodged within the affected joint. Affected joints, listed
from most to least commonly involved, are the shoulders, knees, elbows, hocks,
and rarely the joints of the spinal column. Males have a higher risk than
females for developing OCD.
Age of onset: 4-12 months
Cause: Several factors are
indicated in the development of OCD including nutrition, rapid growth, joint
conformation and genetic predisposition. In regard to genetic predisposition,
certain instances of OCD are suspected of being inherited as a polygenic trait
since common OCD lesions are frequently found among littermates. This is
particularly the case in elbow dysplasia. OCD is also suspected of playing a
role in the development of certain hip dysplasias, but it is not known with
certainty whether the presence of OCD lesions is a cause or effect of the
various changes taking place within the hip joint.
Symptoms: OCD presents as
persistent, mild to moderate lameness that usually progresses in severity over
time. Symptoms are most obvious immediately after rest periods when the dog
first attempts to get up and walk. Joint swelling may or may not be evident,
however, hyperextending the affected joint will almost always elicit an
unmistakable, often vocal, pain response from the dog. Though lameness may
only appear to present on one side (unilateral), asymptomatic OCD will usually
be found in one or more joints of the opposite extremity (bilateral).
Diagnosis: Survey radiography is
often reliable for identifying lesions associated with OCD. Though
free-cartilage in the joint-space is not consistently evident on x-ray, bone
irregularities and widening of the joint-space are consistent with a diagnosis
of OCD. In advanced cases, evidence of degenerative joint disease may also be
observed on the x-ray.
Treatment: Treatment for OCD may
be non-surgical or surgical. Conservative treatment includes weight control
and exercise limitation combined with administration of non-steroidal
anti-inflammatory drugs [NSAIDs] (ex. buffered-aspirin, carprofen, or etodolac)
to reduce pain and inflammation, and chondroprotective drugs (ex. polysulfated
glycosaminoglycans, glucosamine, or chondroitin sulfates) to limit cartilage
damage and degeneration. Surgical treatment now commonly utilizes arthr oscopy,
a microsurgical procedure that is minimally invasive, to remove loose and
diseased cartilage. Clinical data suggests that both conservative and surgical
methods have been effective for treatment of OCD. No long-term follow-up to
compare dogs treated by either approach, however, has yet been conducted. Dogs
treated by either method eventually do develop progressive osteoarthritis. In
light of significant improvement observed in dogs treated surgically compared
to untreated dogs, many orthopedic specialists consider surgery to be the
primary treatment for OCD. Surgical intervention is strongly indicated when
non-surgical treatment fails to produce improvement in symptoms within 6-8
weeks or radiographic evidence suggests that lesions are becoming more severe
despite conservative therapy.
Prognosis: Mild to moderate OCD
lesions may heal spontaneously with 4 to 6 weeks of crate rest and leash
walking. More severe OCD lesions or those occurring in dogs whose owners are
unable to enforce exercise restriction usually require conservative or
surgical therapeutic intervention to reduce secondary and long-term
complications associated with osteoarthritis. Untreated, advanced lesions or
those that do not respond to conservative therapy usually require surgical
intervention to inhibit progression of debilitating disease.
Hypertrophic Osteodystrophy (HOD):
When calcified cartilage fails to be penetrated by vessels from the bone
marrow, the unvesiculated tissue dies. Excess mineralization takes place
resulting in calcium deposits at the affected sites. The radius and ulna bones
of the forelimbs and the tibia bone of the hind limbs are all affected in dogs
with HOD. Males and females are equally at risk for developing HOD.
Age of onset: 3-6 months
Cause: Results from early
studies suggested improper nutrition in the form of over-supplementation
leading to imbalance of the calcium:phosphorous ratio or dietary deficiency of
vitamin C as factors contributing to the development of HOD. Though
overnutrition is still one factor accepted as playing a role in HOD, vitamin C
deficiency has been ruled out as a contributing factor. Additionally, there is
evidence to support a viral or bacterial infectious agent, as well as
immunizations with multivalent vaccines (see:
Orthopedic Disease (Vaccine-induced Hypertrophic Osteodystrophy; HOD) in "Vaccines,
Infectious Diseases and the Canine Immune System") as playing a role in
this disorder.
Symptoms: Lameness associated
with HOD comes on suddenly, lasting for 2-3 weeks at a time with symptoms
recurring throughout cycles of growth. Pain occurs in all four limbs at the
same time, therefore, the dog is reluctant to move and will spend most of the
time laying down. When the dog does stand up, he may stand with his back
arched and all four limbs tucked under his body. Intermittent fevers
(sometimes above 104° F), lethargy, and loss of appetite are other symptoms
associated with HOD. Bone swelling and conformational abnormalities may also
occur in advanced cases of HOD. Examples of the latter would include
hyperextension of joints (such as "double-jointed hock") and angular
deformities in the bones of the lower limbs.
Diagnosis: Survey radiographs
are reliable for identifying bone abnormalities associated with HOD. Extensive
evidence of irregular, new bone formation along the shafts of the bones, bone
thickening at the ends of the bone shafts, and swelling of the surrounding
soft tissue are the most common findings on x-ray. Additionally, areas of
mineralization are sometimes observed. An important note in the diagnosis of
HOD is that these radiographic lesions should appear on more than one limb,
otherwise a differential diagnosis of osteomyelitis, a bone infection caused
by bacteria or fungi, must also be considered. Osteomyelitis occurs when
infectious microorganisms gain access to the bone commonly through bite wounds
or other penetrating wounds. Symptoms and radiographic lesions of
osteomyelitis are common with those of HOD.
Treatment: Correcting
nutritional imbalance, through discontinuation of supplementation and
reduction of caloric intake, is usually the first step in providing treatment
for HOD. Though administration of vitamin C (ascorbic acid) was once a common
therapy for HOD, other clinical findings contraindicate the use of vitamin C
in the treatment of HOD since it was found to inhibit the normal process of
bone resorption. Thus, administration of vitamin C may further exacerbate
abnormal bone development associated with HOD. To date, the most effective
therapies include administration of corticosteroids and antibiotics.
Prognosis: Unfortunately, dogs
diagnosed with HOD do not respond consistently to therapy, therefore,
long-term prognosis remains guarded.
Panosteitis: This disorder
occurs when the normal process of bone degeneration and resorption fails to
occur. As a result, there is an excess formation and thickening of bone. This
condition most commonly affects the long bones of either the front (humerus)
or hind (femur or tibia) limbs. Males have a higher risk than females for
panosteitis.
Age of onset: 4-18 months
Cause: The inflammatory process
responsible for panosteitis is poorly understood, however, overnutrition and
rapid growth are factors widely accepted as playing roles in the development
of this disorder.
Symptoms: Panosteitis is
characterized by a sudden onset of intermittent lameness that may last for a
few days or several weeks with the possibility of recurrence throughout cycles
of growth. The lameness may be mild to moderate, may shift from one limb to
another, and is unaffected by rest or exercise. Applying pressure to the
bone-shaft of the affected limb usually produces an evident pain response.
Lethargy and loss of appetite may also occur. In dogs with frequent recurrence
or persistence of symptoms, there may be muscle atrophy of the affected limb.
Diagnosis: Radiographic evidence
of panosteitis will be absent in early or mild cases of the disorder. In more
advanced or moderate cases, areas of increased bone density within the shaft
of the affected bone will be evident on x-ray.
Treatment: Corticosteroids,
buffered-aspirin or non-steroidal anti-inflammatories may be used to reduce
pain but have not otherwise been reported to noticeably influence the course
or outcome of the disease.
Prognosis: Panosteitis resolves
itself and symptoms usually cease by the time the dog reaches 18-24 months of
age.
Structural Disorders of Bone and
Joint Formation
Elbow Dysplasia: Elbow dysplasia
is a broad term used to describe an improper formation of the elbow joint
often presenting with persistent, progressive symptoms and leading to severe
arthritic inflammation (osteoarthritis) and eventual degeneration of the
joint. Four forms of elbow dysplasia have been identified and include 1)
ununited anconeal process (UAP), 2) fragmented medial coronoid process (FMCP),
3) osteochondritis dissecans (OCD) of the medial condyle of the humerus, and
4) incongruity (IC). OCD of the elbow joint occurs as a result of abnormal
bone construction and therefore, is described in detail in the prior section
of this article. Structural abnormalities of the elbow joints include UAP,
FMCP, and IC. These disorders have been attributed to asynchronous growth of
the radius and ulna (the lower bones of the front limbs equivalent to the
forearm bones of humans). When one of these bones grows more rapidly than the
other at the end of the bone shaft composing the joint of the elbow, there
occurs abnormal weight bearing on the opposite bone. This increased stress
increases risk for abnormal bone formation, fragmentation of cartilage, and
erosion of joint cartilage. UAP is believed to occur when the radius grows
longer than the ulna. FMCP has been attributed to increased length of the ulna
compared to the radius. IC occurs when there is abnormal alignment of the
bones of the elbow joint because of asynchronous bone growth. Therefore, IC
often occurs concurrently with UAP and FMCP. Other possible causes for these
disorders include absence in the development of normal curvature of the ulna (UAP);
delay in the steps leading to bone ossification which increases risk for
cartilage fragmentation (FMCP); and malformation of the area of the ulna
involved in formation of the elbow joint (IC).
Age of onset: 4-5 months
Cause: It is widely believed
that structural bone abnormalities occur secondary to the abnormalities in
bone formation described in the previous section of this article. As such,
factors including rapid growth, improper nutrition, and genetic traits that
predispose to formational abnormalities also increase risk for structural
abnormalities. In terms of nutritional factors, it has been found that
nutritional management alone will not completely prevent risk of structural
bone abnormalities. Nutrition does, however, have a direct effect on frequency
and severity of occurrence in genetically predisposed dogs, particularly
during rapid periods of growth. Clinical evidence now strongly supports
incidence of elbow dysplasia as being inherited as a polygenic trait in a
number of breeds including the Labrador Retriever, Bernese Mountain dog,
Rottweiler, German Shepherd dog and Bassett Hound. The fact that frequency of
elbow dysplasia has now surpassed frequency of hip dysplasia in some breeds
further supports the idea that clinical screening and controlled breeding are
necessary to reduce incidence of elbow dysplasia in the breed populations.
Symptoms: In the early stages of
the disorders, all four conditions have the same symptoms: stiff gait during
the first few minutes after rest. Eventually, front limb lameness is presented
as a slightly stiff, stilted gait. The dog will hold his elbows close to his
chest. A painful response is often observed when the elbows are extended or
flexed. In advanced cases where degeneration of the joint has begun, swelling,
muscle atrophy and joint crepitus is often observed.
Diagnosis: Survey radiography is
capable of detecting elbow dysplasia associated with UAP as early as 4-5
months of age when symptoms are first noted. Radiographic abnormalities
produced by the other disorders are often rarely discernable and when they
are, they are usually not observable until 8 months of age. In clinical
comparisons, CT and MRI provided a more sensitive and accurate means for
diagnosing UAP, FMCP, and OCD than conventional x-rays. Radiographs are rarely
useful for diagnosis of IC, therefore, CT or MRI is also recommended for
assessment of IC. Bone scans and joint tap, though not definitive diagnostic
techniques for elbow dysplasia, may assist in identifying a source of lameness
to either the bone, joint or soft tissue. In the absence of definitive lesions
by diagnostic imaging techniques, arthroscopy is often utilized to observe the
affected joint for the purpose of identifying occult joint disease.
Treatment: Surgery is widely
considered the best option for elbow dysplasias associated with UAP and OCD.
Dogs treated early in the course of the disease when there is only minimal
osteoarthritis exhibit the best long-term outcome in terms of reduction of
symptoms and restoration of activity. However, despite surgical intervention,
most of these dogs will develop progressive osteoarthritis and likely require
long-term therapy with non-steroidal anti-inflammatories and/or
chondroprotective drugs. Clinical data on the surgical treatment of FMCP has
thus far demonstrated no significant gains over non-surgical treatment for
this condition. Treatment alternatives to surgery include rest, weight
reduction, low-impact exercise, and drug therapy with non-steroidal anti-inflammatories
and/or chondroprotective drugs. No comparison studies between surgical and
non-surgical treatment for IC has yet been conducted. When surgical
intervention is selected, arthroscopic surgery to correct bone malalignment
has proven a successful surgical option.
Prognosis: Progression of
disease and outcome of treatment is dependent upon the individual dog. In
general, dogs diagnosed with elbow dysplasia are expected to exhibit a fair to
good outcome. Secondary osteoarthritis is an expected complication of elbow
dysplasia. Despite this, both non-surgically and surgically treated dogs
adjust to their disease through self-limitation of activity while still
leading functional lives. Working dogs, however, may be significantly limited
in their performance ability. Likewise, dogs with severe, progressive
osteoarthritis or joint degeneration refractory to drug treatment may become
significantly debilitated.
Hip dysplasia (HD): Hip
dysplasia is a term widely used to describe any one of a number of conditions
that bring about abnormal formation of the hip joint eventually resulting in
mild to severe osteoarthritis and joint degeneration. The primary cause of hip
dysplasia is attributed to muscle laxity during growth. During this period,
the pelvic muscles must hold the ball of the thighbone (femur) into the socket
of the pelvis (acetabulum) for proper formation of the joint. If muscle tone
is inadequate, or if bone growth proceeds at a faster rate than muscle
development, the femoral head pulls away from the acetabulum, a process known
as subluxation. Subluxation leads to abnormal wear and erosion of the joint
cartilage. As a result, there is flattening of the femoral heads and shallow
development of the acetabula. This improper fit of the ball and socket of the
joint creates additional friction and cartilage erosion that leads to
secondary osteoarthritis.
Age of onset: 8-12 months;
earlier in severe cases. Some afflicted dogs may never show clinical symptoms.
Cause: Like elbow dysplasia,
there is no one factor considered responsible for the development of HD.
Considerable evidence suggests a polygenic basis for inheritance of HD with
certain risk factors playing a substantial role in degree of expression. These
risk factors include size, muscle mass, growth rate, overnutrition,
electrolyte imbalance, and hormonal influences during gestation. Clinical
evidence suggests a strong correlation between muscle laxity and development
of HD independent of environmental factors. Therefore, a new method for
screening breeding stock, the PennHip distraction index (DI) has been proposed
as a more accurate means than the Orthopedic Foundation for Animals (OFA)
method. This is because the PennHip method entails an objective measurement of
muscle laxity in comparison to the OFA’s subjective evaluation, in which
results may be dependent upon a number of external variables, for predicting
genetic predisposition for HD.
Symptoms: Symptoms of HD vary
from dog to dog. Early signs are usually observed as abnormalities in the
dog's gait: the dog may exhibit a swaying gait when walking and may "bunny
hop" on the hind limbs when running. Many cases of severe HD exhibit very few
clinical signs. Many dogs compensate for hind limb abnormalities by shifting
most of their body weight to the front end. As a result, dogs showing few
clinical symptoms may develop increased shoulder musculature ("loaded
shoulders") while hind limb musculature remains under-developed. As damage to
the joint progresses and secondary osteoarthritis sets in, symptoms of
stiffness and lameness may present.
Diagnosis: Survey radiography is
usually accurate for the diagnosing HD in dogs presenting with clinical
symptoms. However, HD may occur concurrently with a number of other skeletal,
muscular and neurological disorders. Often a dog presenting with recent
symptoms of hind limb lameness and indications of advanced hip osteoarthritis
on radiographs will be found to have lameness associated with knee ligament (cruciate
ligament) disorders rather than HD upon closer scrutiny. Therefore,
radiographic evidence of HD alone is not sufficient to conclude that symptoms
are directly associated with HD, and a complete physical exam and history of
the dog is required to rule out other disease processes. In terms of genetic
selection against HD, x-ray only demonstrates actual appearance (phenotype) of
hips at one given point in time, therefore, there are limitations to this
method's predictive value in terms genetic assessment for HD (see
"Canine Hip Dysplasia: Are Breeders Winning the Battle?").
For example, many dogs that pass radiographic OFA standards for absence of HD
at two years of age may go on to develop HD later in life and therefore,
should still be considered genetically predisposed to HD. Measurement of
muscle laxity as early as 4 months of age using the PennHip DI score has been
clinically shown to provide an accurate predictive assessment for dogs with
low risk (DIŁ 0.4) for HD or dogs with high risk (DI > 0.7) for developing HD
sometime within their lifetimes. Scores between 0.4 and 0.7 at this age,
however, are less reliable for predicting risk and require reassessment of DI
at 6 to 12 months of age.
Treatment: Treatment of HD is
dependent on several factors and may be conservative or surgical. In deciding
upon the course of treatment, factors to consider include the dog's tolerance
and/or ability to adapt to the disorder, rate of progression of osteoarthritis
and joint degeneration, and cost for treatment. Many dogs are capable of
living normal lives despite HD provided that they are allowed to choose their
own level of activity. Improvement and even disappearance of symptoms is
common. In such instances, moderate exercise is encouraged to prevent muscle
atrophy that may contribute to further subluxation, possible dislocation, and
more rapid progression of joint degeneration. Forced, sudden activity or
jumping should be discouraged. Non-surgical therapy includes administration of
non-steroidal anti-inflammatories and/or chondroprotective drugs. Surgical
intervention is usually indicated in cases of gross malformation or where
joint degeneration proceeds at an accelerated rate resulting in severe
disability. There are several surgical procedures that have been developed for
the treatment of HD. Direct clinical comparisons of long-term outcome for each
method, however, have not been conducted. Despite this, clinical reports on
the various methods indicate a positive response to surgical intervention in
terms of slowing joint degeneration, increasing activity tolerance and/or the
reducing symptoms. The simplest of these procedures, pectineus tendonectomy,
entails severing the pectineus tendon of the leg thereby releasing tension on
the hip joint. This allows for greater abduction in weight bearing and
alleviation of symptoms in some HD-afflicted dogs. This method, however, does
not inhibit progression of joint degeneration, and therefore, may not be the
best procedure for treating dogs exhibiting accelerated joint-degeneration.
Pelvic osteotomy is another method aimed at reducing stress on the hip joint.
This procedure depends on repositioning the acetabulum so that it provides
support to the leg bone and thus prevents subluxation. This is usually
accomplished by rotating the acetabular roof over the femoral head. High
success rates have been reported for long-term outcome on dogs treated by this
procedure. Additionally, recovery time is brief, and because dogs can undergo
surgery on both hip joints at the same time, secondary complications related
to stress on the untreated hip during recovery are not problematic. A third
method, resection arthroplasty, entails complete removal of the femoral head
to alleviate the source of pain. This procedure, however, has its limitations
particularly in larger dogs where it was found that the weight of these dogs
caused the top of the bone shaft (from which the femoral head was excised) to
hit against the pelvis during exercise and produce another source for pain and
symptoms. Therefore, in larger dogs that had originally undergone this
surgical treatment in the past, a second surgery to improvise muscle support
to the initial surgical site was required to correct this problem. The fourth
procedure, total hip arthroplasty, entails fitting and insertion of an
artificial hip joint. Drawbacks to this procedure, include high cost and
increased risks for secondary complications. Additionally, concern has been
raised about long-term functional life of the prosthesis and the potential for
cement disease: issues that plague hip replacement in human medicine. Despite
these issues, total hip arthroplasty is widely considered to be the best
treatment for HD in regard to long-term patient outcome and control of joint
degeneration.
Prognosis: Dogs afflicted with
HD showing mild to moderate evidence of joint degeneration are considered to
have a good prognosis with either conservative or surgical treatment methods.
Often, severity of joint degeneration may not be evident by observing symptoms
alone, however, and joint deterioration may progress in the absence of
clinical symptoms. In cases demonstrating significant progression of joint
disease, it may be anticipated that at some point, these dogs may not be
sufficiently managed by conservative therapy alone. Surgical intervention then
becomes a viable option for restoring normal function and activity.
Preventing Growth-Associated
Bone Disorders
The key to prevention of the
various growth-associated bone disorders lies in the attempt to control for
both genetic and environmental risk factors that may increase susceptibility.
As discussed earlier in this article, proper nutrition of growing puppies in
the form of restricted feeding through avoidance of high-calorie diets and
oversupplementation are steps in prevention from an environmental perspective.
Another potential method for reducing incidence in dogs known to be at higher
risk for developing growth-associated skeletal disorders may be through
administration of preventative drugs. Much clinical research has focused
recently on the use of disease-modifying osteoarthritis drugs (DMOADs), also
called chondroprotective drugs, that claim to prevent, reduce or reverse the
degeneration of cartilage resulting from joint abnormalities. From a genetic
standpoint, in cases of bone disorders suspicious or known to have genetic
transmittance, selective breeding to eliminate affected dogs from the gene
pool is one step in reducing occurrence in future generations. Several methods
for genetic screening have been developed specifically for this purpose.
Drugs for the Prevention and
Treatment of Osteoarthritis Related to Skeletal Disorders
By the time symptoms of bone
disorders occur, changes in the cartilage have already taken place.
Non-steroidal anti-inflammatory drugs (NSAIDs) may help to quickly improve
pain and inflammation secondary to cartilage damage and erosion. Some evidence
suggests that they may also slow down the processes related to cartilage
degeneration. Buffered aspirin is probably the most widely used NSAID.
However, long-term use of aspirin, itself, has been implicated in damaging
cartilage in both normal and diseased joints. Though this finding should not
deter use of aspirin for short-term therapy of symptoms, because many dogs
with joint disease may require long-term administration of therapy, aspirin
would not be considered a suitable treatment option in such cases. Carprofen
(Rimadyl) and etodolac (Etogesic) are alternative NSAIDs to aspirin that have
been approved for use in dogs for the treatment of osteoarthritis. These two
drugs may have some positive protective properties without the detrimental
effects on cartilage. Piroxicam, another NSAID, may also be a potential
candidate for treating dogs with osteoarthritis, however, clinical data
supporting a protective effect on cartilage has not been consistently
demonstrated. As with many drugs, some dogs treated with NSAIDs may develop
mild to severe reactions following drug administration. Potential
complications associated with administration of these drugs, as well as signs
and symptoms that would indicate an adverse drug reaction should be discussed
with the attending veterinarian.
Complex sugars are another
class of drugs that have been recognized for their efficacy in treating and
possibly even preventing degenerative joint disease. Polysulfated
glycosaminoglycan (PSGAG), the major component of which is chondroitin
sulfate, is a DMOAD and has been used in Europe since the 1960s. One form of
this drug, Adequan, has recently been approved for use in dogs in the United
States. Research indicates that this drug not only biochemically interacts
with cartilage and other tissues of the joints, but also increases
concentration of joint lubricant. In a study exploring a potential
prophylactic effect for PSGAG, young dogs predisposed to HD and administered
PSGAG demonstrated significantly better hip joint conformation than untreated
dogs. However, subsequent clinical trials to examine the beneficial effects of
PSGAG in dogs, in terms of reducing symptoms and slowing joint degeneration,
have demonstrated no significant impact on disease progression. Despite this,
because clinicians have observed improvements in dogs on an individual basis,
some recommend early prophylactic treatment with PSGAG for dogs with high risk
for disorders such as OCD, elbow dysplasia and HD. Additionally, some
orthopedic surgeons will treat dogs with PSGAG beginning 7 to 10 days after
joint surgery. Health complications have been reported for PSGAG and are
mostly related to the potential for serious side-effects when PSGAG is
administered to dogs with a history of bleeding disorders, shock or
hypersensitivity.
Neutraceuticals of PSGAG are
available without prescriptions. These products are not in the same purified
and/or modified form as their federally controlled counterparts. For example,
neutraceuticals do not contain the direct-acting molecules that are PSGAGs,
but rather may contain a precursor to the active form of the drug. Therefore,
a neutraceutical molecule must undergo a biochemical reaction once absorbed by
the body to become active and effective. This requirement can produce much
limitation on extent of effectiveness. Because of this, however, these
products are considered nutritional supplements and do not require approval
for use. Common PSGAG-like neutraceuticals include Glycoflex and Cosequin.
These drugs appear relatively safe with no toxic side-effects, however, there
is no evidence to date that suggests they biochemically interact with the
joint tissue or increase cartilage integrity as found with PSGAGs. Nor have
clinical trials with proper controls been conducted to substantiate claims for
improvement of joint symptoms in dogs treated with these neutraceuticals. In
absence of scientific evidence to support benefits of use in dogs with joint
disease as well as the high cost of these neutraceuticals, clinicians
recommend that if improvement of symptoms is not observed 6-8 weeks after
treatment is started, treatment should be discontinued and alternative
therapies considered.
Pentosan polysulfate (PPS)
is another complex sugar classified as a DMOAD. PPS is currently undergoing
pre-clinical testing in dogs in the United States but has not yet been
approved for clinical treatment of dogs. PPS interacts with joint tissues
similar to the biochemical mechanisms observed for PSGAG and, similarly
decreases cartilage degeneration associated with osteoarthritis. In one study,
dogs diagnosed with elbow dysplasia were treated with either PPS or surgery.
No difference in long-term functionality was observed between the two groups,
but in short-term comparisons, the PPS group's functional improvement occurred
sooner following the onset of treatment compared to the surgery group. Despite
these promising results, further studies with PPS are required to substantiate
its clinical benefits in dogs. Complications associated with PPS are few but
include potential for development of blood clots.
Hyaluronan is a slow-acting
drug that provides long-term benefits related to pain relief and restoration
of function. Pre-clinical testing to determine potential benefits for human
patients was conducted in canine models for osteoarthritis. As such, results
from these studies suggest that hyaluronan may have clinical benefits for use
in dogs. Though clinical trials using hyaluronan to treat osteoarthritis in
horses have been conducted, no such trials have been conducted in dogs at the
time this article was written.
Control Through Genetic
Selection
Many breeders, concerned
with the physical "soundness" of purebred dogs, have attempted to reduce
incidence of skeletal diseases within their breeds' populations. With the
knowledge that many developmental bone and joint disorders are genetically
transmitted, methods for screening afflicted dogs and eliminating them from
the breeding pool have been devised in the hopes of reducing incidence of bone
disorders and increasing genetic soundness of future progeny. However, there
is strong evidence suggesting that joint disorders such as elbow and hip
dysplasias are polygenic: conditions caused by more than one gene. As with all
polygenic traits, environmental factors significantly influence the degree of
expression and rate of progression of these disorders. These factors are
likely responsible for the difficulty encountered when screening breeding
stock and applying results to evaluate genetic risk.
Certification of breeding
stock through the Orthopedic Foundation for Animals (OFA) is currently the
most widely used screening method for elbow dysplasia and hip dysplasia.
Radiographs of elbows and hips are taken by the breeder's/owner's veterinarian
and then submitted to the OFA for review by experts in the field of canine
orthopedics. Dogs found to be clear of elbow and/or hip dysplasia will receive
OFA number certification in the elbow and/or hip dysplasia registry. For OFA
number certification in the hip dysplasia registry, dogs must be at least two
years of age at the time the radiograph is taken. Between two and five years
of age is the best time for OFA review. Below two years of age it is often
difficult to draw the line between what is normal and abnormal in the
developing hip joint, and above five years of age, primary arthritis of old
age may be impossible to differentiate from slight hip dysplasia. Though the
OFA should be viewed as one valuable tool in the control of hip dysplasia,
limitations for this method have been identified and suggest why OFA
certification alone over the past several decades has not assured freedom of
risk for HD in recent generations.
The Wind-Morgan program is
another genetic screening method, specifically for Labrador Retrievers, that
has gained much popularity. In addition to radiographs of elbows and hips,
this program also reviews and assesses shoulders, knees, and hocks: other
sites frequently predisposed to genetically transmitted joint diseases. This
method is proving to be invaluable, particularly for detecting lesions in
joints not routinely screened by the OFA. However, like the OFA, the
Wind-Morgan evaluation is also based on radiographic appearance of the joint
at a particular point in time. Because many joint disorders are not always
evident on radiograph, as well as the finding that joint appearance does not
necessarily correlate with genetic risk for transmitting joint disorders,
Wind-Morgan may have the same limitations as reported for OFA.
A more recent and upcoming
method of screening specifically for hip dysplasia is the PennHip method. This
method uses the distraction index (DI) to measure muscle laxity as an
indicator for risk of hip dysplasia independent of factors such as degree of
disease expression and rate of progression. The DI measurement is based on the
observation that increased muscle laxity in the hip joint is associated with
increased subluxation and joint abnormalities. Therefore, dogs with more
muscle laxity are genetically at increased risk for developing and passing-on
hip dysplasia to offspring even in the absence of radiographic evidence of
joint disease. Dogs with DI scores equal to or less than 0.3 are considered at
no risk for developing HD throughout their lives. The greater the dog's score
is above 0.3, the greater the risk for developing HD. Since average DI scores
for many breeds may be well above 0.3, particularly in the large and giant
breeds, this method is not advocated for elimination of dogs from a breeding
program. Rather, selecting individuals with the lowest DI scores in each
generation for breeding has been observed to significantly improve hip
conformation within only a few generations. Therefore, the PennHip method used
alone or together with either the OFA or Wind-Morgan methods, may provide the
best outlook for control of HD in future generations (see
"Canine Hip Dysplasia: Are Breeders Winning the Battle?").
References:
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Olsson SE. Pathophysiology,
morphology, and clinical signs of osteochondrosis in the dog. In: Bojrab, MJ,
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Schrader SC. Differential
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Schrader, SC. The use of
the laboratory in the diagnosis of joint disorders of dogs and cats. In:
Bonagura, JD, ed: Kirk's Current Veterinary Therapy XII. Philadelphia: W.B.
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Schulz KS, Payne JT,
Aronson E. Escherichia coli bacteremia associated with hypertrophic
osteodystrophy in a dog. J Am Vet Med Assoc., 199:1170-1173, 1991.
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Schwarz, PD. Canine elbow
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Smith, GK and McKelvie, PJ.
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