Panosteitis is a self-limiting orthopaedic condition found in dogs during the growth period. The lesions occur exclusively in the diaphyseal and metaphyseal regions of long bones, usually affect several bones, may migrate from one site to another and are prone to relapse. The condition is characterized by bone marrow fibrosis, endosteal proliferation and, occasionally, a periosteal reaction. The first report of panosteitis in veterinary literature was made in 1951 by Gratzl, who described the pathology in 14 German Shepherd dogs and a Scottish Terrier. Despite the name, the condition does not indicate a primary disorder of bone, but rather a disease of the adipose bone marrow (yellow bone marrow) with secondary involvement of bone.
AETIOPATHOGENESIS
Although the aetiopathogenesis of panosteitis is still not clear, numerous hypotheses, corroborated and validated to various degrees, have been published in the veterinary literature. The first was put forward by Gratzl in 1951 who suggested that panosteitis is a purulent haematogenousosteomyelitis. However, pathogenic microorganisms have not been isolated from microbiological cultures of bone marrow from affected dogs. No virus has ever been documented. In 1969, Sprinkle proposed that the disease was related to excessive oestrogen levels and later, in 1972, Kaastrom suggested that panosteitis is due to a parasite; here again, researchers were unable to isolate any parasite responsible. In 1975, Van Sinkle hypothesised that the disease has a genetic basis, given the high incidence in German Shepherd dogs (86%). Some years later, high levels of calcitonin were considered a possible cause.
More recently, Hazewinkel and Tryfonidou examined the possibility that large quantities of growth hormone could trigger panosteitis. By increasing osteoblastic activity, growth hormone would result in reduced modelling of nutrient foramina and, consequently, lead to oedema of the bone marrow cavity. According to the rigid compartment theory proposed by Schawalder in 2002, the cause of the oedema in the bone marrow cavity could be an excess of water soluble proteins in the diet. The pathogenesis starts with the death of adipose tissue in the bone marrow close to the nutrient foramina of long bones. Osteoblasts and fibroblasts begin to proliferate inside the bone marrow cavity, the endosteum and sometimes also the periosteum. Microscopically, osteoblastic activity has been seen in the final stages of panosteitis.
EPIDEMIOLOGY
Panosteitis is found mainly in medium-sized, large and giant dog breeds during the growth period with a greater prevalence in males, German Shepherd dogs and Dobermanns. The onset is usually between 4 and 8 months of age but the disorder can present later, in dogs up to 1 year of age or over. Panosteitis is rarely found in adult dogs. It most frequently affects the German Shepherd, Dobermann, Basset Hound, Saint Bernard, Bernese Mountain Dog, Spaniels, Retrievers, Rottweiler, Dalmatian, Dogue de Bordeaux, Shar Pei and others.
CLINICAL SIGNS
The lameness which always accompanies panosteitis can have an acute or hyperacute onset, with intense pain on deep palpation of the involved bone. The front legs are more usually affected, in particular the ulna (42%), followed by the radius (25%), the humerus (14%), femur (11%) and tibia (8%). The lameness is rarely associated with systemic symptoms but when present these are anorexia, lethargy and hyperthermia.
DIAGNOSIS
An orthopaedic examination will locate the site or sites of pain which will may then be confirmed to be associated with lesions by X-ray. However, the severity of the clinical profile is not always reflected by the X-ray findings or at least there is not a temporal relationship between the two. In the case of evident lameness without clear X-ray signs, it could be useful to repeat the X-ray after 1 or 2 weeks, especially if the lameness is of recent onset. It is not uncommon for X-rays to show a still silent focus of enostosis or previous lesions which are healing. It is, in any case, advisable to take X-rays of several bone segments. In the initial stages of disease, X-rays show a modest increase in bone radio-opacity or radiolucency of the bone marrow cavity near a nutrient foramen. This is followed by an increase in the radio-opacity of the bone marrow (Fig. 1A and B), the presence of radiodense lines, attenuation of the cortico-medullary contrast and loss of the bone trabeculation. In the intermediate stages of the disease, there is an increase in intramedullary radio-opacity and endosteal coarseness associated, rarely, with a periosteal reaction. Late signs are the disappearance of the radio-opaque areas and endosteal coarseness, and the persistence of medullary sclerosis with an increase in bone trabeculation (Fig. 2). Not infrequently, the enostosis can be associated with other orthopaedic diseases found in growing dogs, such as forms of elbow dysplasia, (Fig. 3), osteochondritisdissecans of the humeral head, hip dysplasia, cranial cruciate ligament rupture and osteochondritisdissecans of the hock.
TREATMENT
The therapeutic approach to panosteitis is symptomatic and exclusively medical, being based on the use of anti-inflammatory drugs (corticosteroids and non-steroidal anti-inflammatory drugs [NSAIDs]). Corticosteroids act directly on the intramedullary oedema promoting protein catabolism in the peripheral tissues. The inhibitory effect on the action of osteoblasts and on the synthesis of bone matrix, together with osteoclastic stimulation, help to correct the bone alterations typical of this disease. Corticosteroids also have a notable anti-inflammatory action. Unlike cortisone, aspirin and other NSAIDs bind irreversibly to cyclo-oxygenase and thromboxanesynthase, resulting in a longer duration of effect which persists until new enzymes are produced by endothelial cells and the platelets are replaced. This could explain why acetylsalicylic acid and other NSAIDs can produce good results in some subjects who do not respond to cortisone therapy. The doses described in veterinary literature for acetylsalicylic acid vary from 10 to 25 mg/kg every 12 hours. However, in the light of the numerous side-effects of aspirin in dogs, the recommended dose is the lowest found to be effective, which is usually 5 mg/kg every 24 hours. The recommended doses of the other NSAIDs are those indicated for each one of them. Schawalder proposed a new treatment, benzopyrone, which would act by reducing the amount of protein in the bone marrow cavity; the recommended dose is 2-4 mg/kg every 24 hours. This effect on proteins is similar to that of glucocorticoids, but since benzopyrone has no analgesic or anti-inflammatory action, its effectiveness in panosteitis would confirm Schawalder’s hypothesis of the aetiopathogenesis of the disease.
PROGNOSIS
The prognosis of panosteitis is excellent, given the self-limiting nature of this condition. It is, however, essential to inform the owner of the protracted course of the disorder as well as the possibility of cyclical recurrences and shifting lesions.
Suggested readings
- Gratzl E. “Die eosinophile panostitis der junghunde (osteomyelitis der jungen schaferhunde)” Wiener Tierarztliche Monatsschrift 38: 629-670, 1951
- Sprinkle T.A. and Krook L. “Hip dysplasia, elbow dysplasia and “eosinophilic panosteitis”. Three clinical manifestations of hyperestrinism in the dog?” Cornell Vet, 60(3): 476-90, 1970
- Kaastrom H. et al “Panosteitis in the dog. A radiographic, scintimetric and trifluorochrome investigation” Acta Radiol Suppl, 319: 15-23, 1972
- Van Stickle D. “Canine panosteitis” in “Selected orthopedic problems in growing dogs” Monograph, South Bend, American Hospital Association, 20-28, 1975
- Tryfonidou MA et al “Growth hormone modulates cholecalciferol metabolism with moderate effects on intestinal mineral absorption and specific effects on bone formation in growing dogs raised on balanced food” Domestic Animal Endocrinology 25(5): 155-174, 2003
- Schawalder P. “Canine panosteitis, an idiopatic bone disease investigated in the light of a new hypothesis concerning pathogenesis. Part I” Schweiz Arc Tierheilkd, 144(3): 115-130, 2002
- Schawalder P. et al “Canine panosteitis, an idiopatic bone disease investigated in the light of a new hypothesis concerning pathogenesis. Part II” Schweiz Arc Tierheilkd, 144(4): 163-173, 2002
- Hazewinkel H.A.W. “Calciotropic hormones and bone metabolism” in ed Rijnberk A. “Clinical endocrinology of dogs and cats” Dordrecht, The Netherlands: Kluwer Academic Publischers, 177-198, 1996
- Hazewinkel H.A.W. “Skeletal disease” in “The Warton book of clinical nutrition of the dog and cat” Willis ed, 395-425, 1994
- La Fond E. et al “Breed susceptibility for developmental orthopedic diseases in dogs” J Am An Hosp Assoc 38(5): 467-477, 2002
- Sebestyen P. “What is your diagnosis? Panosteitis in a 4 year old spayed female german sheperd” J Am Vet Med Assoc 212(4): 493-4, 1998
- Montgomery R. “Miscellaneous orthopaedic diseases” in Slatter “Textbook of small animal surgery” ed. Sauders 3rd ed, 2252-2253, 2002
- Villa E., Mortellaro C.M. “Enostosi una patologia in cerca d’Autore: stato dell’arte a mezzo secolo dalla prima segnalazione” Tesi di laurea, Dipartimento di Scienze Cliniche Veterinarie, Facoltà di Medicina Veterinaria, Università degli Studi di Milano, 2007
- Demko J., Mc Laughlin R. “Developmental orthopedic disease” Vet Clin North Am Small Anim Pract 35(5): 1111-35, 2005