Sie sind auf Seite 1von 5

Vol.18, No.

January 1996

Continuing Education Article

FOCAL POINT 5 Because spontaneous recovery
from panosteitis usually occurs 12 to 18 months after diagnosis, an alternative diagnosis should be sought if lameness is still present at this time. Treatment is supportive. University of Wisconsin

Peter Muir, BVSc, MVetClinStud, PhD Richard R. Dubielzig, DVM Kenneth A. Johnson, MVSc, PhD

s Panosteitis is a common idiopathic bone disease of young dogs. s Affected dogs usually have acute, shifting lameness secondary to bone pain. s Panosteitis is one of several idiopathic bone diseases that are characterized by excessive bone remodeling and osseous proliferation. s Although the cause of panosteitis is unknown, the published literature suggests an infectious source.

anosteitis is one of a group of idiopathic canine bone diseases that are characterized by osseous proliferation and excessive bone remodeling.13 Other diseases in the group include hypertrophic osteodystrophy4,5 and craniomandibular osteopathy.6,7 In this article, we consider panosteitis; a companion article to be published subsequently will discuss hypertrophic osteodystrophy.

CLINICAL FEATURES Young, large-breed dogs that are 6 to 18 months of age are typically affected by panosteitis. Occasionally, middle-aged dogs are affected, usually German shepherds.3 Other terms used to refer to the condition include eosinophilic panosteitis and enostosis (endosteal proliferation of new bone). These terms have been used because tissue inflammation is usually absent and peripheral eosinophilia (although not a consistent finding) was found in approximately half of affected dogs in one study.2,3,8 Panosteitis is a common orthopedic disease worldwide.2,9,10 It usually affects the diaphysis of long bones. The proximal ulna, distal humerus, central radius, proximal and central femur, and proximal tibia are the most commonly affected regions; the metacarpal bones and pelvis may also be involved. Affected dogs are often male. Panosteitis has a higher incidence in German shepherds than in other breeds. Other commonly affected breeds are Great Danes, Doberman pinschers, golden retrievers, Labrador retrievers, and basset hounds.2,3,8,9 Lameness is usually of sudden onset, may vary from mild to severe, and may not be associated with a history of trauma. Bouts of severe lameness with minimal weight bearing usually last 2 to 3 weeks. Various long bones may be affected during the course of the disease. Lameness typically has a cyclic or recurrent pattern or may shift to another limb. Pain is usually elicited by deep palpation of affected bones. Dogs with panosteitis can become systemically ill and exhibit pyrexia, tonsillitis, and elevated white blood cell counts,13,9,11 but these clinical signs are not always identified (see the box). Because panosteitis is a common orthopedic disorder of young dogs, patients should be carefully evaluated for other juvenile orthopedic diseases (e.g., shoulder and elbow osteochondrosis or hip dysplasia) that may be present concurrently.3 All painful regions of affected limbs should be radiographed.

Small Animal

The Compendium January 1996

Figure 1A

Figure 1B

Figure 1C

Figure 1(A) Lateral radiographic view of a middle-phase panosteitis lesion in the humerus. Focal radiodensities are present

in the medulla, and there is associated endosteal roughening (arrows). (B) Lateral radiographic view of the elbow. An ununited anconeal process (curved arrow) and middle-phase panosteitis lesions (straight arrows) are evident. (C) Lateral radiographic view of the thoracic limb. A middle-phase panosteitis lesion in the proximal ulna and osteochondrosis of the humeral head are evident (arrows).

RADIOGRAPHIC FEATURES High-quality radiographic technique is necessary to appreciate the subtle bone changes that occur in panosteitis lesions that are present when clinical lameness commences. If there is uncertainty concerning the radiographic diagnosis, additional radiographs should be taken two or three weeks later, when changes should be more obvious. There is no relationship between the severity of clinical signs and the radiographic appearance of the bone lesions.3,9,11 The radiographic signs of panosteitis can be divided into three phases.2,3 During the early phase, a subtle, poorly marginated, and occasionally granular increased radiodensity is evident in the medullary canal; medullary blurring and loss of corticomedullary contrast result. In the middle phase, an obvious patchy or mottled

increase in radiodensity is apparent in the medullary canal; the radiodensity may approach that of cortical bone. The changes are often centered around the nutrient foramen. Endosteal roughening and an accentuated, coarsened trabecular pattern may be visible. Periosteal and endosteal new bone formation usually develops such that cortices may appear thickened and indistinct in affected areas (Figure 1). In the late phase, the medullary canal regains a more normal appearance and the patchy radiodensities disappear as the lesions are gradually remodeled (during a period of 2 to 3 months).

HISTOPATHOLOGIC FEATURES Panosteitis is characterized by excessive bone remodeling. Initially, the normal hemopoietic and fatty marrow tissue is replaced with fibrous tissue. This response


The Compendium January 1996

Small Animal

is not usually inflammatory and corresponds with the phase of increased medullary density and corticomedullary blurring that is radiographically evident. Bone remodeling is generally evident in the cortex and medulla of an affected region. The degree of remodeling may vary among affected bones in a dog. Bone resorption and new bone formation increase.12 Woven bone is formed in the fibrous tissue, which contains increased numbers of fibroblasts, osteoblasts, and osteoclasts. Endosteal new bone formation is usually most prominent and may be disseminated throughout the diaphysis. It leads to the formation of short, thick, woven-bone trabeculae, which protrude into the marrow cavity and may virtually obliterate the medullary canal (Figure 2). These changes correspond Figure 2B with the phase of the dis- Figure 2A ease in which a mottled Figure 2(A) Postmortem lateral radiographic view of a panosteitis lesion in the proximal increased density is radio- ulna of a dog. (B) The corresponding gross specimen, sagittally sectioned. Focal endosteal graphically apparent in the new bone formation is evident in the region of the nutrient foramen. medullary canal. Periosteal new bone forOriginally, it was suggested that the condition was a mation may be evident and consists of radially oriented form of bacterial osteomyelitis.15,16 In one study, however, new bone trabeculae and secondary osteonal remodelnecropsy examination of 18 affected dogs failed to identiing of the cortex. Cortical bone may be replaced with fy a bacterial pathogen.1 Panosteitis was successfully transnew woven bone (especially in the region of the nutrimitted from affected dogs to healthy dogs by intraent foramen), which may appear radiographically as a medullary inoculation of bone marrow. Characteristic zone of decreased density. As cortical remodeling conradiographic signs of panosteitis developed in inoculated tinues in response to the localized disease, porosity may bones after 2 to 3 weeks, and these changes were associatbe dramatically increased by the regional acceleratory ed with lameness. The delay coincides with the intervals phenomenon as specific osteonal remodeling fronts adbetween episodes of relapse that are clinically evident in vance longitudinally through the cortex.1,3,811,13,14 many dogs. Transmission was accomplished more readily CAUSE in male dogs. In one male, lesions also developed in a The cause of panosteitis is currently unknown. Since bone that was not inoculated. Bacteria were not isolated the disease was first described in the 1950s, various from inocula, and disease transmission was accomplished possibilities have been considered. with or without filtration to remove most bacteria.1

Small Animal

The Compendium January 1996

These findings are conpanosteitis. Although pansistent with the hypothesis osteitis is idiopathic, future Possible that viral infection of bone investigations should involve Clinical Signs is part of the cause of panfurther virologic studies. osteitis. 2 Furthermore, the of Panosteitis TREATMENT AND secondary clinical findings Peripheral eosinophilia PROGNOSIS of pyrexia, tonsillitis, and Mild to severe lameness Panosteitis is usually selfleukocytosis reported in some of sudden onset limiting; spontaneous reaffected dogs 13,9,11 might Pain during deep palpation also indicate systemic viral covery occurs after several of affected bones infection. weeks. Improvement is more Pyrexia Metabolic disease,3 genetgradual in some dogs, and Tonsillitis ic disease, 13 parasitism, 12 lameness may persist for sev Elevated white blood cell counts hyperestrinism,17 and hemeral months.3 Lameness may 18 Concurrent shoulder and elbow osteochondrosis ophilia have been suggestshift from one leg to another Concurrent hip dysplasia ed as causes of panosteitis; every few weeks during this there is scant evidence of period. Relapses are possible. any of these causes. A genetBouts of the disease are usuic or infectious cause would be supported by the facts ally approximately 1 month apart.3 Spontaneous recovery from panosteitis usually occurs 12 to 18 months after that (1) sequential litters bred from the same sire and diagnosis (at the latest); therefore, an alternative diagnodam may be affected with panosteitis1 and (2) offspring from affected dams may subsequently develop panossis should be sought if lameness is still present at this teitis.3 In an experimental colony of 8-week-old Gertime. man shepherds, which were raised in confinement and Treatment of patients with panosteitis is supportive. vaccinated against canine distemper virus and infecThe activity of affected dogs should be restricted. Analtious canine hepatitis, all 12 dogs developed panosteitis gesics should be administered as necessary1,3; we recom11 mend oral buffered aspirin (10 to 20 mg/kg every 8 within 140 days of the onset of the study. Although panosteitis is prevalent in German shepherds, it has hours). Because of the possible infectious cause, we do been described in many breeds; a purely genetic cause not recommend corticosteroid medication for prolonged thus is unlikely. periods. Although intense cortical remodeling and inVirus infection of bone has been identified in hucreased cortical porosity are present in many lesions, mans,19 cats,20 and dogs.21,22 Infection of all bone cell pathologic fracture is not a recognized complication.12 The prognosis for patients with panosteitis is good. types with canine distemper virus has been demonstrated in experimentally infected dogs.23 Publication of the first descriptions of panosteitis in the 1950s coincided with the time that vaccination of dogs with live canine About the Authors distemper virus became prevalent.24 Persistent canine Dr. Muir is currently affiliated with the Department of Surgidistemper virus infection for several months occurs in cal and Radiological Sciences, School of Veterinary some dogs, even in the present of serum antibody25; Medicine, University of California, Davis, California. When postvaccinal canine distemper virus infection of dogs this article was written, he was with Dr. Johnson in the Dehas also been described.26 If canine distemper virus in partment of Surgical Sciences and Dr. Dubielzig, Departvaccine does infect canine bone cells, attenuation of the ment of Pathobiological Sciences, School of Veterinary virus during vaccine manufacture may prevent active Medicine, University of Wisconsin, Madison, Wisconsin. virus replication in bone cells but allow transcription into messenger RNA.27 Attempts to isolate an infectious agent from dogs afREFERENCES fected with panosteitis have been unsuccessful.28 Evi1. Zeskov B: A contribution to eosinophilic panosteitis in dogs. Zentralbl Veterinarmed 7:671680, 1960. dence that suggests a viral cause of panosteitis can be 2. Barrett RB, Schall WD, Lewis RE: Clinical and radiographic summarized as follows: (1) transmission experiments, features of canine eosinophilic panosteitis. JAAHA 4:94 (2) localization of canine distemper virus in the bone 104, 1968. cells of dogs, (3) the self-limiting nature of the disease, 3. Bohning RH, Suter PF, Hohn RB, Marshall J: Clinical and (4) association with live canine distemper vaccination, radiologic survey of canine panosteitis. JAVMA 156:870 883, 1970. and (5) clinical signs of systemic illness in dogs with

The Compendium January 1996

Small Animal

4. Meier H, Clark ST, Schnelle GB, Will DH: Hypertrophic osteodystrophy associated with disturbance of vitamin C synthesis. JAVMA 130:483491, 1957. 5. Grondalen J: Metaphyseal osteopathy (hypertrophic osteodystrophy) in growing dogs. A clinical study. J Small Anim Pract 17:721735, 1976. 6. Riser WH, Parkes LJ, Shirer JF: Canine craniomandibular osteopathy. J Am Vet Rad Soc 8:2331, 1967. 7. Watson ADJ, Adams WM, Thomas CB: Craniomandibular osteopathy in dogs. Compend Contin Educ Pract Vet 17(7):911922, 1993. 8. Cotter SM, Griffiths RC, Leav I: Enostosis of young dogs. JAVMA 153:401410, 1968. 9. Stead AC, Stead MCP, Galloway FH: Panosteitis in dogs. J Small Anim Pract 24:623635, 1983. 10. Johnson KA, Allan GS: Panosteitis in a cocker spaniel dog. Aust Vet J 58:153155, 1982. 11. Burt JK, Wilson GP: A study of eosinophilic panosteitis (enostosis) in German shepherd dogs. Acta Radiol 319:713, 1972. 12. Kasstrom H, Olsson S, Suter P: Panosteitis in the dog. A radiographic, scintimetric and trifluorochrome investigation. Acta Radiol 319:1523, 1972. 13. Frost HM: Intermediary Organization of the Skeleton. Boca Raton, FL, CRC Press, 1986. 14. Tandy J, Haywood S: A case of panosteitis. Vet Rec 100: 287289, 1977. 15. Baumann R, Pommer A: Die chronische Osteomyelitis der jungen Schaferhunde. Wien Tierarztl Wochenschr 38:670 676, 1951. 16. Gratzl E: Die eosinophile Panosteitis der Junghunde. Wien Tierarztl Wochenschr 38:629670, 1951.

17. Sprinkle TA, Krook L: Hip dysplasia, elbow dysplasia and eosinophilic panosteitis. Three clinical manifestations of hyperestrinism in the dog. Cornell Vet 60:476490, 1970. 18. Grondalen J, Sjaastad O, Teige J: Enostosis (panosteitis) in three dogs suffering from hemophilia A. Canine Pract 16: 1014, 1991. 19. Silverman FN: Virus diseases of bone. Do they exist? Am J Res 126:677703, 1976. 20. Hoover EA, Griesemer RA: Bone lesions produced by feline herpesvirus. Lab Invest 25:457464, 1971. 21. Boyce RW, Axthelm MK, Krakowka S, Weisbrode SE: Metaphyseal bone lesions associated with canine distemper virus infection. Proc Annu Meet Am Coll Vet Pathol:126, 1983. 22. Axthelm MK, Krakowka S: Immunocytochemical methods for demonstrating canine distemper virus antigen in aldehyde-fixed paraffin-embedded tissue. J Virol Methods 13: 215229, 1986. 23. Mee AP, Webber DM, May C, et al: Detection of canine distemper virus in bone cells in the metaphyses of distemperinfected dogs. J Bone Miner Res 7:829834, 1992. 24. Appel M: Canine distemper virus, in Virus Infections of Carnivores. Amsterdam, Holland, Elsevier, 1987, pp 133159. 25. Appel M: Pathogenesis of canine distemper virus. Am J Vet Res 30:11671182, 1969. 26. Hartley WJ: A post-vaccinal inclusion body encephalitis in dogs. Vet Pathol 11:301312, 1974. 27. Mee AP, Gordon MT, May C, et al: Canine distemper virus transcripts detected in the bone cells of dogs with metaphyseal osteopathy. Bone 14:5967, 1993. 28. Turnier JC: A case study of canine panosteitis: Comparison of radiographic and radioisotopic studies. Am J Vet Res 39:3540, 1978.