by Bobbie Kelley

Khan, a 4-month old Kuvasz puppy from our first litter (1985), had been in his new home for one month. I received a call from the concerned and anxious owner. The puppy, lethargic for a couple of days, now wouldn't rise, exhibiting excruciating pain all over. His hind legs had no strength. There was high fever, lack of appetite, and diarrhea. The veterinarian, uncertain of the diagnosis at first, treated Khan symptomatically for fever and pain, and prescribed a precautionary antibiotic. A radiographic and blood work-up was ordered. Over the next several months, the clinical signs would subside and flare up again episodically, showing a recurring pattern. Each relapse was often more severe than the last. The initial symptoms were so generic that proper diagnosis was difficult. Within several weeks of the onset of symptoms, however, diagnosis was simplified by the physical changes that occurred. Enlargement of the ends of the long bones (appearing as swollen joints), weakened pasterns, splayed feet, and stunting of the long bone growth were seen. The associated pain kept the pup relatively inactive, and when movement was required, his gait was restricted and mincing. Radiographs taken at this stage confirmed the problem: HYPERTROPHIC OSTEODYSTROPHY (H.O.D.) (1).


Perhaps no other juvenile orthopedic disorder in dogs causes such intense pain. There is no known cure; one can only attempt to ease the suffering with anti-inflammatory medications and analgesics. Some puppies show gradual improvement over the course of several months and eventually recover fully, although some permanent stunting or bowing of the long bones may occur. Others get progressively worse and either succumb or are euthanized. Other than providing supportive care, the owner is relatively helpless, as the outcome of the disease seems independent of the treatment (2,3,4,5). Time drags as the owner waits, day by day, to see if the puppy will improve or worsen. Hopes soar as the pup seems to feel better, only to plummet at the next relapse. Khan's suffering ended at six months of age, when prolonged anorexia, dehydration, and fever caused by the HOD claimed his life. As breeders, our nightmare was far from over. By then, in Khan's litter of eleven puppies, two other confirmed (and one other suspected) cases of H.O.D had been diagnosed.


The cause of H.O.D. remains unknown (2,6,7). Hindered by a lack of research dollars available to study such a rare disease, veterinary researchers are unable to agree on the cause of H.O.D. A review of the scientific literature since the 1930's reveals that the cause of H.O.D. may be one or perhaps a combination of the following: genetics, nutrition, infection, trauma, autoimmune disease, hormone imbalance, or reaction to vaccination (1,2,5,6,8). Among affected puppies, there is little that can be pointed to as a common denominator.

Genetics Seen only occasionally in the canine population, some breeds are more commonly afflicted with H.O.D., namely Great Danes, Boxers, Irish Setters, Weimaraners, and several other large, fast-growing breeds (1,4,5,6). The disease is sporadic, usually affecting only isolated puppies in a particular litter or line. However, there are reports of family clusters, entire litters, or significant numbers of littermates being affected (1,3). Some breeders have experienced consistently high percentages of pups with H.O.D. in related litters, suggesting genetic influences. This was the case in our own breeding program. Khan's dam produced two litters before she was spayed; 3 of 11 pups (27%) from the first litter and 3 of 8 (38%) in the second litter had H.O.D. An unaffected litter-sister to Khan was bred once, and 3 of 9 (33%) had HOD. By contrast, three unrelated bitches of ours have produced 26 puppies, none affected, raised with similar nutrition and management. These observations are suggestive of recessive genetic mechanisms. Yet when researchers twice bred two littermate Great Danes that had H.O.D. in puppyhood, two normal, unaffected litters were produced (8). Other breeders produce only one or two isolated cases from years of repeat breedings and/or line breedings of closely related individuals. These data raise questions about the genetic mode or transmission. It is unknown whether complicated genetic mechanisms result in a predisposition to the development of H.O.D. in certain individuals (1,2,5).

Nutrition H.O.D. has occurred in puppies oversupplemented with vitamins, minerals (calcium), protein, and calories. It is well documented that overfeeding highly palatable diets free-choice promotes bone growth abnormalities (1,2,6). But experimental oversupplementation has not been shown to consistently reproduce H.O.D. in test puppies (1). Litters of puppies all fed and supplemented in the same way may have only one or two of the pups affected with H.O.D. Overnutrition may be an exacerbating factor but is probably not a direct cause, as pups in all nutritional states have been affected (1,2). Vitamin C deficiency has also been postulated to cause H.O.D.; the radiographic appearance of HOD in dogs is similar to human scurvy. But the studies are controversial and inconclusive at best, and there is no substantiated evidence to support Vitamin C deficiency as a cause of H.O.D. (1,6,7,9). Dogs synthesize their own Vitamin C; however, it has been suggested that certain breeds of dogs may be predisposed to faulty Vitamin C metabolism. Since puppies with H.O.D. rarely improve with dietary correction or Vitamin C therapy, the association between nutrition and H.O.D. is inconsistent (1,2,4,7).

Infected puppies with H.O.D. commonly have high fever, diarrhea, and sometimes upper respiratory signs. There is suppurative inflammation within the metaphyses of the long bones, and often an elevated white blood cell count (1,7,8). The systemic clinical signs and the bilaterally symmetric inflammatory response seen histologically has led some investigators to look for an infectious agent as the culprit (1,5). To date, no causative organism has been found in H.O.D.- afflicted dogs, and attempts to transmit the disease from affected to unaffected dogs have been unsuccessful (1,5). Yet, some human diseases act in the same way; congenital syphilis in humans looks very similar radiographically to H.O.D. in puppies, and the causative microorganism in syphilis disappears from tissue very early in the course of the infection (1). More studies of infectious agents as a cause of H.O.D. are warranted.

Various other theories on the cause of H.O.D. have been suggested, and these include trauma (overuse, overexercise), autoimmune disease, calciotropic hormone imbalance, and reaction to vaccination (1,5,8). We have noticed in our own experience (in all but one case) that the initial onset of symptoms occurred within 48 hours of the pup's final distemper vaccination. Whether this is a correlation, or simply coincidental with the typical age of onset of HOD (4 months of age), remains unknown.


Although as yet not considered by breeders to be a predominant disease in Kuvaszok, the tally of owners and breeders who have experienced the problem is surprisingly high. When one looks at the number of Kuvaszok affected relative to the Kuvasz population, and compares this with the occurrence of H.O.D. in the general dog population, there appears to be a disproportionately high occurrence in our breed. Regardless of the specific cause of HOD, there may be an underlying genetic predisposition for an animal to demonstrate the disease, thus explaining why some breed lines display the disease more often than others. Because of this possible heritability, until the cause of H.O.D. is verified, it would be prudent to cull affected lines from breeding, so that H.O.D does not become any more prevalent in the breed than it is already.


There has been an unfortunate tendency among breeders to minimize the problems encountered in their breeding programs, and to be reluctant to discuss them objectively. But when puppies are dying after a long-suffering illness, it is time to bury our egos. This is not simply a mild juvenile orthopedic problem which the dog, or surgery, can compensate for as in the case of the more commonly observed hip dysplasia (H.D.) and osteochondrosis (O.C.D.). While H.D. and O.C.D. are certainly problems of concern in our breed, they are normally not life-threatening. Though H.O.D is usually referred to as self- limiting and rarely terminal, five of the nine H.O.D-affected puppies we have produced (56%) have died from H.O.D or its complications. Breeder apathy will not only impede research efforts at understanding H.O.D, but because of the limited gene pool among Kuvaszok, could result in the proliferation of affected and carrier animals.

In 1978, Dr. R. P. Wright, a veterinarian and breeder of Irish Setters, attempted to collect information from setter breeders and owners through their breed newsletter. Similarly, I attempted to compile information following the 1992 publication of an earlier version of this article in several Kuvasz newsletters. A team of veterinary researchers at the University of Florida was ready to assist me with this effort, and a private foundation had committed $30,000. We sought to compile information and conduct studies of affected puppies, with the goal of determining the cause, and thereby perhaps developing a treatment for H.O.D. Despite heart-wrenching stories of gorgeous puppies of distinguished breeding being crippled or dying from H.O.D., breeder and veterinary cooperation was minimal (5). I was unable to maintain the interest of the University or the private foundation with the paucity of data collected. Despite our disappointing progress in understanding H.O.D., I maintain a personal file on H.O.D., and I invite any of you with firsthand knowledge of H.O.D. to send me your case histories and pedigrees. Maybe someday they will prove useful.


1. Bellah JR. Hypertrophic osteodystrophy. In, Bojrab MJ, ed. Disease Mechanisms in Small Animal Surgery, WB Saunders, Philadelphia, pp. 858-864, 1993.

2. Alexander JW. Hypertrophic Osteodystrophy. Canine Practice 5:48-52, 1978.

3. Woodard JC. Canine hypertrophic osteodystrophy, a study of the spontaneous disease in littermates. Vet Pathol 19:337-354, 1982.

4. Bookbinder PF. Hypertrophic osteodystrophy: cause unknown, cure still unknown. Interview in: Cornell University Animal Health Newsletter 8:7, Dec. 1990.

5. Lanting FL. Hypertrophic osteodystrophy (HOD). In, Lanting FL. Canine Hip Dysplasia and Other Orthopedic Problems. Alpine Pubs., pp 183-195, 1981.

6. Sinibaldi KR. Hypertrophic osteodystrophy. In, Bojrab MJ, ed. Pathophysiology in Small Animal Surgery, WB Saunders, Philadelphia, pp. 670- 676, 1981.

7. LaCroix JA. Juvenile orthopedic diseases. AKC Gazette, p. 62, Nov. 1980.

8. Bellah, JR. Personal communication, 1991.

9. Teare JA, Krook L, Kallfelz FA, Hintz HF. Ascorbic acid deficiency and hypertrophic osteodystrophy in the dog: a rebuttal. Cornell Vet 69:384-401, 1979.

Copyright c 1996, by Bobbie Kelley. Copies may be made, provided proper attribution is given.