Hypertrophic Osteodystrophy (HOD)
S. Gary Brown, D.V.M., D.A.C.V.S.
Irish Setter Health Committee Member
This is a revised version of the article by Dr. Brown on HOD. Please note that he has changed the protocol for treatment. This article was taken from the Irish Setter Club of America, Inc. Memo To Members, JUNE 2001.
Hypertrophic Osteodystrophy (HOD) is a developmental disease in large breed dogs (commonly the Great Dane, Alaskan Malamute, and Irish Setter.) This disease usually begins between the ages of 3 months to 5 months of age. HOD is often sporadic and can vary in intensity although at times several dogs from one litter may be affected. There are questions about the heritable nature of the disease but no answers from an organized study have been documented.
Most of the affected animals are first presented because of lameness or reluctance to walk. There are often fevers of 104 - 104.2 degrees F and anorexia (refusal to eat). These signs usually get progressively worse. Over days the metaphyseal regions of the long bones (the area next to the growth plate, but towards the mid bone, not the joint) will be tender to digital pressure, slightly swollen and warm to the touch (using the inside of the wrist.) More adversely affected animals will be systemically ill. The fevers and anorexia will continue, and weight loss comes quickly if the affected animal is not treated.
This disease is bilateral (both sides) and often will effect the metaphyses of front legs as well as rear legs. Symptoms can be episodic and are often relentless. Reports of responses to various treatments can be traced to dogs with episodic disease and varying degrees of severity. This information is anecdotal at best. Early on the metaphyseal area becomes swollen and very painful. It is in this metaphyseal area that HOD exerts its major pain and produces radiographic changes. The distal radial /ulnar metaphysis (above the wrist joints) are the most commonly affected sites, although the metaphyses of all long bones are certainly susceptible. Therefore, it is not uncommon to see clinical disease and radiographic changes in the metaphyses of many long bones in the body. There are severe inflammatory changes going on in the metaphysis and resultant changes in the local blood flow. This change can disturb normal cartilage growth and development of the adjacent growth plate (physis). The resulting interference in the cartilage transformation into bone (endochondral ossification) can be seen as finger-like at times, extending up into the metaphyseal marrow cavity. The result can be premature slowdown or early growth plate disruption, resulting in shorter bone length or even curvature. This, is more common in the Great Dane than the Irish Setter (in my experience). The usual microscopic changes, which are seen in the metaphysis are inflammation, hemorrhage, necrosis (cellular death), microfractures and remodeling of the bone. Periosteal new bone (a thin sleeve of bone around the outside of the cortex) can occur as the result of inflammation.
The cause of HOD remains unknown, however, there are many speculations. The autoimmune nature of this is currently under investigation at one university. Vira1 causes (even Canine Distemper) have been implicated, although they just might be one more kind of stress precipitating HOD. Vitamin C deficiency has been thought to be a cause, however, there is neither documentation nor scientific reason for this in the dog. Vitamin C therapy has not met with much success. Excessive amounts of dietary protein and high caloric intake have been implicated, scientific support for this is also lacking. However, over nutrition does play an important role in Osteochondrosis. An infectious origin has been proposed, and there are reports where hematogenous (blood borne) bacteria have been noted to produce florid radiographic changes in the metaphyses which perhaps could be confused with HOD. Therefore, if not careful, hematogenous or osteomyelitis (bone infection) could possibly be confused with HOD. A good radiologist should be able to differentiate this. Documentation of the use of possible blood cultures, to isolate bacteria, in HOD cases has not been reported. Therefore documentable cases of actual infections have been few. For most cases, the cause is still unexplained.
Diagnosis is usually clinical, and later confirmed by radiographic examination. In the very early stages there is point tenderness in the metaphysis. One week later we see radiographic changes. This is represented by a radiolucent line, parallel and immediately adjacent to the growth plate. This line represents bone necrosis and reabsorption of some of the microspicules of bone. This metaphyseal region may remain mildly affected throughout the course of the disease if well treated, or may show early irregular widening if there is some alteration in the growth plate and its endochonral ossification. The periosteal new bone formation may form a collar around the bone, localized to the inflamed metaphysis, or it can be rather extensive and extend several centimeters toward the mid bone. On occasion, severe involvement can affect the growth plate, often the distal ulna, resulting in lateral bowing deformities of the front legs.
Remember, to make this diagnosis you need the classic metaphyseal point tenderness, and the zone of necrosis parallel to the growth plate (lucency) and usually the metaphyseal periosteal new bone. These radiographic changes appear 7-10 days after the onset of symptoms, ie: fever, lethargy and metaphyseal pain.
In all cases of true HOD, treatment is begun by anti-inflammatory doses of Prednisone. The initial dose is 2 mg/kg/day for 7 days. The dose is halved weekly for one month. The last week*s dose may need to be extended for a fifth week. One should always cover with clindamycin or clavamox and use antacids like Tagamet or Pepcid for 3-4 weeks. We*re using glycoflex-plus or synovi-msm as a second anti-inflammatory. Some dogs can*t come off the prednisone without a return of mild symptoms. These cases get 5 mg total every other day for a long time; if necessary until the end of adolescence. In two cases like this their size ended up just as large as their littermates and the wrists were not thickened. Furthermore, their coats did not suffer.
Mild cases are not difficult to treat, whereas the more severely affected animals require more aggressive care. Those animals that are not treated early on require IV fluids and electrolytes, nutritional support, and tremendous nursing care to arrive at a successful result. On occasion, parenteral nutrition is needed for a severely affected animal. Pharyngostomy tubes have been used for liquid food administration.
If well treated with anti-inflammatories, the need for pain medications can be greatly reduced to the use of other oral medications such as Torbutrol, being careful not to suppress the dog*s appetite.
Recurrence after a month or so can also happen. Start back with 1 mg/kg/day of Prednisone for a week. Half the dose for the second week and probably give 5 mg every other day long term. Cover with antibiotics for the two weeks when you restart the Pred.
Dogs which have been treated solely with Rimadyl (r) have mostly not done well at all. The prognosis for mild cases can have a good prognosis. Severe cases are more difficult. Lately we have seen more effective treatment for the severely affected cases with the above regimen.
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