Hypertrophic osteodystrophy

Last updated

Hypertrophic Osteodystrophy (HOD) is a bone disease that occurs most often in fast-growing large and giant breed dogs; however, it also affects medium breed animals like the Australian Shepherd. The disorder is sometimes referred to as metaphyseal osteopathy, and typically first presents between the ages of 2 and 7 months. [1] HOD is characterized by decreased blood flow to the metaphysis (the part of the bone adjacent to the joint) leading to a failure of ossification (bone formation) and necrosis and inflammation of cancellous bone. [2] The disease is usually bilateral in the limb bones, especially the distal radius, ulna, and tibia. [3]

Contents

The Weimaraner, Irish Setter, Boxer, German Shepherd, and Great Dane breeds are heavily represented in case reports of HOD in the veterinary literature, but the severity of symptoms and possible etiology may be different across the breeds. For example, familial clustering of the disease has been documented in the Weimaraner, but not in other breeds. [4] The disease in the Weimaraner and Irish Setter can be particularly severe, with significant mortality observed in untreated dogs. The classical age of onset is typically 8 to 16 weeks of age, with males and females equally affected.

Speculated causes of HOD

Causes have been speculated to include decreased Vitamin C uptake, increased vitamin (other than C) and mineral uptake, and infection with canine distemper virus(CDV). [1] [5] [6] Decreased Vitamin C uptake has been dismissed as a cause, but excessive calcium supplementation remains a possibility. [7] There is no evidence over-feeding is a significant cause. [8] In Weimaraners, recent vaccination with a modified live vaccine has been a suspected cause, partly because HOD often presents immediately after a vaccination, and partly because of the autoimmune nature of the disorder. The canine distemper vaccination in particular has been a suspected causal factor due to the significant number of overlapping symptoms observed between systemically affected HOD puppies and dogs suffering from distemper, [9] but to-date, no definitive linkage has been demonstrated. [10] The cause of canine HOD largely remains unknown. However, because of the familial clustering, HOD in the Weimaraner is suspected to have a genetic, or partly genetic, origin.

Clinical features

Figure 2: Characteristic roaching in 4-month-old Weimaraner puppy with HOD. HOD Roaching Weimarner 2010-12.jpg
Figure 2: Characteristic roaching in 4-month-old Weimaraner puppy with HOD.

A primary characteristics of the condition is lalameness. This is generally due to the swelling of the metaphysis of the long bones that is observed. Other bones may be affected, particularly the ribs, the metacarpal bones, the mandible, and the scapula. [11] [12] [13] Lameness may present as mild limping or more severely as a reluctance or inability to stand. In some breeds and/or individuals, the stance of an HOD puppy as observed from behind has sometimes been described as “cow-hocked.” Shaking of limbs and a reluctance to put full body weight on the front legs is often observed. Sometimes the puppy will exhibit a characteristic “roaching” or arching of the spine when standing (see Figure 2).

Lameness is accompanied by pain upon palpation of affected bones, warmth in the limb as felt by the inside of the clinician's wrist, depression, and loss of appetite. Limb involvement is usually bilateral, typically involves the distal radius and ulna, and may be episodic. There is evidence to suggest that most dogs recover after one episode, but some relapse. [3] [11] Dogs suffering systemic manifestations of the disorder often have poorer prognoses. Systemic manifestations include fever, multiple body organ inflammation, nasal (nose) and ocular (eye) discharge, diarrhea, hyperkeratosis of the foot pads, pneumonia, and tooth enamel hypoplasia (many of these symptoms overlap with symptoms of CDV). [11] [12] [13] [14] Early diagnosis must be based on clinical signs, so prior to diagnosis other disorders should be ruled out (e.g., nutritional bone disease, and osteochondrosis).

Radiographic features

Figure 3: X-Ray image of HOD presentation in 4-month-old Weimaraner puppy. Note "moth-eaten" appearance of metaphyses. Hypertrophic Osteodystrophy Weimaraner XRay 2010-12-27.jpg
Figure 3: X-Ray image of HOD presentation in 4-month-old Weimaraner puppy. Note "moth-eaten" appearance of metaphyses.

Diagnosis relies on clinical signs and characteristic changes in radiographic images of the metaphyses. Bone changes can be observed on radiograph, and the disorder may progress to actual angular limb deformity. In the early stage of the illness, the metaphyseal area on X-ray may be observed to have an uneven radiolucent zone parallel to the physis with a thin band of increased radiodensity directly bordering the physis. Early stage radiographic changes have sometimes been described as having a "moth-eaten" appearance (see Figure 3). As the disease progresses, the radiolucent line may disappear and radiodensity may increase in the affected area as the body attempts to repair damage. Relapses can cause new radiolucent lines. This area is often followed by a dark line at the metaphysis, which may progress to new bone growth on the outside of that area. This area represents microfractures in the metaphysis and bone proliferation to bridge the defect in the periosteum. [7]

Treatment

Treatment options have been controversial. Mild illness is often successfully treated with pain medication (usually NSAIDs) and supportive care. Dogs presenting with severe, systemic symptoms not responding to NSAID treatment require more intensive treatment. The Weimaraner and Irish Setter American Kennel Club (AKC) parent clubs advocate the use of immunosuppressive doses of corticosteroids, supplemented with antibiotics and antacids (to compensate for the decreased thickness of the stomach's mucosal lining as a result of the corticosteroids and to decrease the possibility of forming stomach ulcers). [15] [16] More severe cases that are not recognized and treated early often require IV fluids, electrolytes, nutritional support, and significant nursing care to achieve successful results. AKC parent clubs have supported research into the genetic causes of HOD, and have reported fairly good success using this protocol, saving many puppies from unnecessary suffering, deformity, and death.

NOTE: Supplementation of Vitamin C is contraindicated due to an increase in calcium levels in the blood, possibly worsening the disease. [17]

Breeds at increased risk for HOD

Related Research Articles

<span class="mw-page-title-main">Canine distemper</span> Viral disease affecting some mammals

Canine distemper virus (CDV) is a viral disease that affects a wide variety of mammal families, including domestic and wild species of dogs, coyotes, foxes, pandas, wolves, ferrets, skunks, raccoons, and felines, as well as pinnipeds, some primates, and a variety of other species. CDV does not affect humans.

<span class="mw-page-title-main">Gastric dilatation volvulus</span> Medical condition in dogs

Gastric dilatation volvulus (GDV), also known as gastric dilation, twisted stomach, or gastric torsion, is a medical condition that affects dogs in which the stomach becomes overstretched and rotated by excessive gas content. The word bloat is often used as a general term to mean gas distension without stomach torsion, or to refer to GDV.

<span class="mw-page-title-main">Weimaraner</span> Dog breed

The Weimaraner is a German breed of hunting dog of medium to large size, with history going back at least to the nineteenth century.

Renal osteodystrophy is currently defined as an alteration of bone morphology in patients with chronic kidney disease (CKD). It is one measure of the skeletal component of the systemic disorder of chronic kidney disease-mineral and bone disorder (CKD-MBD). The term "renal osteodystrophy" was coined in 1943, 60 years after an association was identified between bone disease and kidney failure.

<span class="mw-page-title-main">Dog health</span> Health of dogs

The health of dogs is a well studied area in veterinary medicine.

<span class="mw-page-title-main">Canine parvovirus</span> Contagious virus mainly affecting dogs

Canine parvovirus is a contagious virus mainly affecting dogs and wolves. CPV is highly contagious and spreads from dog to dog by direct or indirect contact with their feces. Vaccines can prevent this infection, but mortality can reach 91% in untreated cases. Often, treatment involves veterinary hospitalization, and Canine parvovirus infects other mammals, including foxes, wolves, cats, and skunks. Felines (cats) are also susceptible to panleukopenia, a different strain of parvovirus.

Panosteitis, sometimes shortened to pano among breeders, is an occasionally seen long bone condition in large breed dogs. It manifests with sudden, unexplained pain and lameness that may shift from leg to leg, usually between 5 and 14 months of age, earning the nickname "growing pains. " Signs such as fever, weight loss, anorexia, and lethargy can also be seen. The cause is unknown, but genetics, stress, infection, metabolism, or an autoimmune component may be factors. It has also been suggested that rapid growth and high-protein food are involved in the pathogenesis. Whole blood analysis may show an elevated white blood cell count; this finding lends support to the theory that panosteitis is due to an infection.

Malignant histiocytosis is a rare hereditary disease found in the Bernese Mountain Dog and humans, characterized by histiocytic infiltration of the lungs and lymph nodes. The liver, spleen, and central nervous system can also be affected. Histiocytes are a component of the immune system that proliferate abnormally in this disease. In addition to its importance in veterinary medicine, the condition is also important in human pathology.

Canid alphaherpesvirus 1 (CaHV-1), formerly Canine herpesvirus (CHV), is a virus of the family Herpesviridae which most importantly causes a fatal hemorrhagic disease in puppies less than two to three weeks old. It is known to exist in the United States, Canada, Australia, Japan, England and Germany. CHV was first recognized in the mid-1960s from a fatal disease in puppies.

Craniomandibular osteopathy, also known as lion's jaw, is a developmental disease in dogs causing extensive bony changes in the mandible and skull. In this disease, a cyclical resorption of normal bone and replacement by immature bone occurs along the inner and outer surfaces of the affected bones. It usually occurs between the ages of 3 and 8 months. Breeds most commonly affected include the West Highland White Terrier, Scottish Terrier, Cairn Terrier, and Boston Terrier. It is rare in large-breed dogs, but it has been reported. Symptoms include firm swelling of the jaw, drooling, pain, and difficulty eating.

Hypertrophic osteopathy is a bone disease secondary to cancer in the lungs.

Granulomatous meningoencephalitis (GME) is an inflammatory disease of the central nervous system (CNS) of dogs and, rarely, cats. It is a form of meningoencephalitis. GME is likely second only to encephalitis caused by canine distemper virus as the most common cause of inflammatory disease of the canine CNS. The disease is more common in female dogs of young and middle age. It has a rapid onset. The lesions of GME exist mainly in the white matter of the cerebrum, brainstem, cerebellum, and spinal cord. The cause is only known to be noninfectious and is considered at this time to be idiopathic. Because lesions resemble those seen in allergic meningoencephalitis, GME is thought to have an immune-mediated cause, but it is also thought that the disease may be based on an abnormal response to an infectious agent. One study searched for viral DNA from canine herpesvirus, canine adenovirus, and canine parvovirus in brain tissue from dogs with GME, necrotizing meningoencephalitis, and necrotizing leukoencephalitis, but failed to find any.

Wobbler disease is a catchall term referring to several possible malformations of the cervical vertebrae that cause an unsteady (wobbly) gait and weakness in dogs and horses. A number of different conditions of the cervical (neck) spinal column cause similar clinical signs. These conditions may include malformation of the vertebrae, intervertebral disc protrusion, and disease of the interspinal ligaments, ligamenta flava, and articular facets of the vertebrae. Wobbler disease is also known as cervical vertebral instability (CVI), cervical spondylomyelopathy (CSM), and cervical vertebral malformation (CVM). In dogs, the disease is most common in large breeds, especially Great Danes and Doberman Pinschers. In horses, it is not linked to a particular breed, though it is most often seen in tall, race-bred horses of Thoroughbred or Standardbred ancestry. It is most likely inherited to at least some extent in dogs and horses.

Progressive retinal atrophy (PRA) is a group of genetic diseases seen in certain breeds of dogs and, more rarely, cats. Similar to retinitis pigmentosa in humans, it is characterized by the bilateral degeneration of the retina, causing progressive vision loss culminating in blindness. The condition in nearly all breeds is inherited as an autosomal recessive trait, with the exception of the Siberian Husky (inherited as an X chromosome linked trait) and the Bullmastiff (inherited as an autosomal dominant trait). There is no treatment.

<span class="mw-page-title-main">Vaccination of dogs</span>

Vaccination of dogs is the practice of animal vaccination applied to dogs. Programs in this field have contributed both to the health of dogs and to the public health. In countries where routine rabies vaccination of dogs is practiced, for example, rabies in humans is reduced to a very rare event.

<span class="mw-page-title-main">Canine degenerative myelopathy</span> Progressive disease in dogs

Canine degenerative myelopathy, also known as chronic degenerative radiculomyelopathy, is an incurable, progressive disease of the canine spinal cord that is similar in many ways to amyotrophic lateral sclerosis (ALS). Onset is typically after the age of 7 years and it is seen most frequently in the German shepherd dog, Pembroke Welsh corgi, and boxer dog, though the disorder is strongly associated with a gene mutation in SOD1 that has been found in 43 breeds as of 2008, including the wire fox terrier, Chesapeake Bay retriever, Rhodesian ridgeback, and Cardigan Welsh corgi. Progressive weakness and incoordination of the rear limbs are often the first signs seen in affected dogs, with progression over time to complete paralysis. Myelin is an insulating sheath around neurons in the spinal cord. One proposed cause of degenerative myelopathy is that the immune system attacks this sheath, breaking it down. This results in a loss of communication between nerves in lower body of the animal and the brain.

<span class="mw-page-title-main">Cancer in dogs</span>

Cancer is the leading cause of death in dogs. It is estimated that 1 in 3 domestic dogs will develop cancer, which is the same incidence of cancer among humans. Dogs can develop a variety of cancers and most are very similar to those found in humans. Dogs can develop carcinomas of epithelial cells and organs, sarcomas of connective tissues and bones, and lymphomas or leukemias of the circulatory system. Selective breeding of dogs has led certain pure-bred breeds to be at high-risk for specific kinds of cancer.

<span class="mw-page-title-main">Sebaceous adenitis</span> Skin disease

Sebaceous adenitis in an uncommon skin disease found in some breeds of dog, and more rarely in cats, rabbits and horses. characterised by an inflammatory response against the dog's sebaceous glands, which can lead to the destruction of the gland. It was first described in veterinary literature in the 1980s.

Autoimmune skin diseases occur when the immune system of an infected animal attacks its own skin. In dogs, autoimmune skin diseases are usually not detected until visible symptoms appear, which differs from detection in humans who are able to verbally express their concerns. Genetics, nutrition, and external environmental factors all collectively contribute to increasing the probability an autoimmune skin disease occurring. The severity of symptoms varies based on the specific disease present and how far it has progressed. Diagnosis often requires the onset of visible symptoms and for a biopsy to be performed. For many diseases, the condition itself cannot be cured, but a veterinarian can prescribe medications and other forms of treatment to help manage the symptoms of the dog.

References

  1. 1 2 Thrall, Donald E. (1994). Textbook of Veterinary Diagnostic Radiology (2nd ed.). W.B. Saunders Company. ISBN   0-7216-3143-6.
  2. ↑ "Hypertrophic Osteodystrophy". The Merck Veterinary Manual. 2006. Retrieved 2007-02-06.
  3. 1 2 Miller C (2001). "Hypertrophic osteodystrophy in a Great Dane puppy". Can Vet J. 42 (1): 63–6. doi:10.4141/cjas62-009. PMC   1476419 . PMID   11195528.
  4. ↑ Abeles, V, Harrus, S, Angles, JM, Shalev, G, Aizenberg, I, Peres, Y and Aroch, I. (1999). "Hypertrophic osteodystrophy in six Weimaraner puppies associated with systemic signs". Vet Record. 145 (5): 130–134. doi:10.1136/vr.145.5.130. PMID   10466830. S2CID   25786721.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ↑ Baumgartner, W., Boyce, RW, Aldinger, S, Axtheim, MK, Weisbrode, SE, Krakowka, S and Gaedke, K. (1995). "Metaphyseal bone lesions in young dogs with systemic distemper virus infection". Vet Microbiol. 44 (2–4): 201–209. doi:10.1016/0378-1135(95)00013-Z. PMID   8588314.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ↑ Baumgärtner W, Boyce RW, Weisbrode SE, Aldinger S, Axthelm MK, Krakowka S (1995). "Histologic and immunocytochemical characterization of canine distemper-associated metaphyseal bone lesions in young dogs following experimental infection". Vet. Pathol. 32 (6): 702–9. doi: 10.1177/030098589503200612 . PMID   8592806.
  7. 1 2 Wehrenberg, Aaron; Elkins, A.D. (Sep 2006). "Juvenile Orthopedics". Veterinary Forum. 23 (9). Veterinary Learning Systems: 22–28.
  8. ↑ Ettinger, Stephen J.; Feldman, Edward C. (1995). Textbook of Veterinary Internal Medicine (4th ed.). W.B. Saunders Company. ISBN   0-7216-6795-3.
  9. ↑ Abeles V, Harrus S, Angles JM, et al. (1999). "Hypertrophic osteodystrophy in six weimaraner puppies associated with systemic signs". Vet Rec. 145 (5): 130–134. doi:10.1136/vr.145.5.130. PMID   10466830. S2CID   25786721.
  10. ↑ Crumlish P, Sweeney T, Jones B, Angles J (2006). "Hypertrophic osteodystrophy in the Weimaraner dog: lack of association between DQA1 alleles of the canine MHC and hypertrophic osteodystrophy". Vet J. 171 (2): 308–13. doi:10.1016/j.tvjl.2004.11.015. PMID   16490714.
  11. 1 2 3 Grondalen, J. (1976). "Metaphyseal osteopathy(hypertrophic osteodystrophy) in growing dogs. A clinical study". J Small Anim Pract. 17 (11): 721–735. doi:10.1111/j.1748-5827.1976.tb06936.x. PMID   1003929.
  12. 1 2 Woodard, J.C. (1982). "Canine hypertrophic osteodystrophy. A study of the spontaneous disease in littermates". Vet Pathol. 19 (4): 337–354. doi: 10.1177/030098588201900401 . PMID   6806967. S2CID   3109992.
  13. 1 2 Watson, A.D.J., Blair R.C., Farrow, B.R.H.; et al. (1973). "Hypertrophic osteodystrophy in the dog". Aust Vet. J49 (9): 433–439. doi:10.1111/j.1751-0813.1973.tb06853.x. PMID   4777208.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ↑ Crawford, M.A.; C.S. Foil (1989). "Vasculitis: Clinical syndromes in small animals". Compend Contin Educ Pract Vet. 4: 400–415.
  15. ↑ http://www.weimclubamerica.org/breeders_ed/columns/january2009.pdf [ bare URL PDF ]
  16. ↑ "Archived copy" (PDF). Archived from the original (PDF) on 2010-12-16. Retrieved 2011-02-28.{{cite web}}: CS1 maint: archived copy as title (link)
  17. ↑ Bennett, David; Clements, Dylan J. (2004). "Letters to the Editor". Journal of the American Veterinary Medical Association. 225 (1): 29. doi:10.2460/javma.2004.225.28. PMID   15239461 . Retrieved 2006-05-11.
  18. ↑ LaFond E, Breur G, Austin C (2002). "Breed susceptibility for developmental orthopedic diseases in dogs". J Am Anim Hosp Assoc. 38 (5): 467–77. doi:10.5326/0380467. PMID   12220032.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.