Friday, December 4, 2020

3884. Hypertrophy osteopathy in dogs and human

 

Hypertrophic osteodystrophy

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Hypertrophic Osteodystrophy (HOD) is a bone disease that occurs in fast-growing large and giant breed dogs. 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]

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[edit]

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[edit]

Figure 2: Characteristic roaching in 4-month-old Weimaraner puppy with HOD.

A primary characteristics of the condition is lameness. 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 and ocular 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] Because early diagnosis must be based on clinical signs, to the extent possible, other disorders should be ruled out (e.g., nutritional bone disease, and osteochondrosis).

Radiographic Features[edit]

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[edit]

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[edit]


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Hypertrophic Osteopathy

Hypertrophic osteopathy (Marie's disease) is typified by palisading periosteal new bone, which appears to be perpendicular to the cortices and irregular in outline in the acute stage. It affects principally the diaphyseal and metaphyseal regions of long bones and spares the joints. In the early stages, very soft exposures must be used to avoid overexposing this relatively radiolucent bone. 


Later the margins of the new bone become more opaque and smoother, and the distinction between the original cortex and the new bone becomes less obvious. These bony lesions develop secondary to a tumor, abscess, or other lesion in the thorax or abdomen, or in association with diffuse granulomatous disease. The bony lesions may regress and model if the primary lesion can be identified and successfully treated.

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https://radiopaedia.org/articles/hypertrophic-osteoarthropathy

HUMAN CONDITION - JOINTS


Hypertrophic osteoarthropathy

Dr Keshav Kulkarni and Assoc Prof Frank Gaillard◉◈ et al.

Hypertrophic osteoarthropathy (HPOA) is a syndrome characterized by periosteal reaction of the long bones without underlying bone lesion. There are a broad range of manifestations, although typically there is symmetrical involvement of the appendicular skeleton. Accompanying abnormal soft tissue proliferation is variable and may result in clubbing of the fingers and toes.

Hypertrophic osteoarthropathy is largely considered a secondary phenomenon, and nearly always (95-97% of cases) occurs in the setting of a wide variety of other cardiopulmonary, gastrointestinal, endocrine, hematologic, and inflammatory conditions 5. When associated with cancer, it is considered a paraneoplastic syndrome. A primary form, pachydermoperiostosis, is due to a heritable genetic mutation that results in similar clinical manifestations, although tend to have more soft tissue findings 5.

Hypertrophic osteoarthropathy has been given various names including Pierre-Marie syndrome, Bamberger syndrome, osteoarthropatia hypertrophica, Mankowsky syndrome, and Hagner syndrome.

"Hypertrophic osteoarthropathy" may refer to either the primary or secondary syndrome, although general usage implies the secondary form, given the rarity of primary hypertrophic osteoarthropathy (also known as pachydermoperiostosis).

"Hypertrophic pulmonary osteoarthropathy" specifically refers to hypertrophic osteoarthropathy in the setting of a lung disease, and not from other intrathoracic processes such as mediastinal or pleural disease 5.

Hypertrophic osteoarthropathy has a variable clinical presentation, ranging from asymptomatic morphologic and radiographic findings to pain accompanying the changes of the fingers and toes 5.

The primary form of hypertrophic osteoarthropathy is due to mutations in the genes encoding 15-hydroxyprostaglandin dehydrogenase and solute carrier organic anion transporter family member 2A1, resulting in abnormal accumulation of prostaglandin E2 5.

Although the cause of secondary hypertrophic osteoarthropathy is not established, a similar mechanism involving abnormally elevated levels of circulated hormones has been proposed as a potential etiology. Alternatively, neurogenic etiology has been proposed 5.

Associated disease states include:

Typically seen as long bone metaphyseal and diaphyseal smooth periosteal reaction.

With disease progression, periostitis becomes more prominent or multilayered and extends to the epiphyses 1.

  • symmetric linear increase in tracer accumulation along diaphyseal and metaphyseal surfaces of long bones 4

  • tram-track sign

The success of treatment depends on whether the hypertrophic osteoarthropathy is due to a primary or a secondary cause.

Most success and rapid regression of hypertrophic osteoarthropathy is achieved in cases where the underlying cause is identified and treated;  such as in lung tumor treated by surgical resection, radiotherapy and/or chemotherapy.

The results are less successful in the presence of metastatic disease.

In primary hypertrophic osteoarthropathy (or in cases where the underlying condition could not be treated), symptomatic relief can be obtained by use of NSAIDs, corticosteroids or bisphosphonates 6,7.

General imaging differential considerations include:

Consider the differential for a smooth periosteal reaction.

On bone scintigraphy, differentials include:

  • normal variant
    • lateral cortices of the tibiae often appear with a symmetric linear uptake 
  • shin splints
    • can appear similar, but confined to the tibiae
  • chronic venous insufficiency 
    • can cause symmetrical periosteal uptake
    • usually confined to the lower extremities below the knees

Lymphedema on its own is not known to cause hypertrophic osteoarthropathy.

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