does anyone know how long it CAN take to "get over" h.o.d. ?

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.

http://www.workingdogs.com/doc0018.htm

http://www.workingdogs.com/doc0046.htm

http://www.vetinfo.com/dencyclopedia/dehod.html

I think whether they fully recover or not depends on the severity, but I am not sure, read the links I posted.