3. small Anim. Pract. (1975) 16, 495-513.

Polyostotic cystic bone lesions in a dog

C . B. C A R R I G , * R . R . P O O L AND J. M. M c E L R O Y
Departments of Radiological Sciences (Carrig) and Pathology (Pool) School of Veterinary
Medicine, University of California, Davis, CA 95616, and Ocean Avenue Veterinary Hospital
(McElroy) 1001 Ocean Avenue, San Francisco, CA 94112

ABSTRACT
The clinical, radiological, and pathological features of' a polyostotic cystic
bone lesion in a 9-month-old Doberman Pinscher are described. T h e patient
was diagnosed as having nutritional secondary hyperparathyroidism at
6 weeks of age and after dietary correction it remained clinically normal
until 9 months when there was sudden left hind-limb lameness due to a
pathological fracture through a cystic lesion in the distal femur. Radio-
graphy revealed additional cystic structures in the metaphyses of the left
radius, and left and right tibia. Pseudofractures were associated with two
of the cystic lesions.
I n some areas the cysts were crossed by trabeculae and in others there
were bony ridges on the inner cystic wall. The cavities were lined with
flesh-coloured fibrillar material which formed a lacy network extending into
cavities. Histologically, multiple small cysts were present adjacent to the
larger cavities noted radiographically. The secondary spongiosa and the
metaphyseal periosteum were the major abnormal tissue sites. T h e small
cysts appeared to arise in a n oedematous and congested metaphyseal spon-
giosa. The cysts were accompanied by small foci of intense osteoclasis but
unattended by compensatory bone production, and the consequent
possibility of pseudofractures is a n important clinical consideration. Earlier
reports demonstrated that resolution of the lesions will follow surgical
drainage and curettage of the cystic cavity. Of six cases of polyostotic cystic
bone lesions observed in the dog, five were in the Doberman Pinscher
breed.

* Departments of Small and Large Animal Surgery and Medicine, College of Veterinary
Medicine, Michigan State University, East Lansing, Michigan 48823.

495
496 c. B. CARRIG et al.

INTRODUCTION
Cystic bone lesions have been reported infrequently in the dog (Huff & Brodey,
1964; Nutt, 1967; Carrig & Seawright, 1969; and Jubb & Kennedy, 1970). They
can be monostotic (involving only one bone) (Rothman & Schnelle, 1949; Riser,
1958; Owen & Walker, 1963; Nutt, 1967; Riser, 1968 and Carrig & Seawright,
1969) or polyostotic (involving more than one bone) (Gourley & Eden, 1954; Huff
& Brodey, 1964; Riser, 1968 and Carrig & Seawright, 1969). They have been
reported in five Doberman Pinschers (Huff & Brodey, 1964; Riser, 1968 and
Carrig & Seawright, 1969) and a breed predisposition has been suggested by Car-
rig & Seawright (1969). An association between cystic bone lesions and subperi-
osteal cortical defects was recorded by Carrig & Seawright (1 969).
This report describes the clinical, radiological, and pathological features of a
polyostotic cystic bone lesion in a 9-month-old male Doberman Pinscher.

CLINICAL FINDINGS
At 6 weeks of age the patient was unwilling to walk. It had been fed an all-meat
diet since it was weaned at 4 weeks of age. Extreme thinning of the cortices was
noted in radiographs of the hind-limbs and pelvis. The metaphyses were radio-
dense, but the density did not extend as far from the growth plates as is normally
seen. The growth plates appeared radiographically normal. A diagnosis of nutri-
tional secondary hyperparathyroidism was made and the diet was changed to a
balanced commercial puppy food. The pup showed rapid improvement and ap-
peared clinically normal for the next 7 months.
At 9 months of age the dog was presented with a sudden non-weight bearing
lameness in the left hind leg of 2 days' duration. There was no history of unusual
trauma to the animal. No superficial 1esions.were noted. The dog was in good
bodily condition and appeared alert. Palpation of the left hind leg elicited abnor-
mal movement, cre'pitus, minimal pain reaction and moderate soft tissue swelling
in the region of the distal femur. There was also a noticeable enlargement of the
distal left radius, which was not painful upon deep palpation.
Radiographs were taken of the pelvis, right and left radius and ulna, right and
left tibia and left femur. The dog was subsequently euthanatized and a radio-
graphic survey of the skeleton performed.
Results of the examination of a venous blood sample were PCV 38%, WBC
15,000 (Neutrophils 63 %, lymphocytes 19%, monocytes 18%). Plasma values
were: total protein 7 4 mg%, phosphorus 5.2 mEq/L; calcium 5.3 mEq/L; SGOT
15 IU/L; alkaline phosphatase 54 IU/L, creatinine phosphokinase 2.9 IU/L.

RADIOLOGICAL FINDINGS
The degree of mineralization appeared adequate in unaffected bones and the
 U
0
FIG. 1. Distal lefr radius of 9-month-old Doberman Pinscher with polyostotic v s t i c bone lesions. (A) Lateral and (B) anteroposterior radio- 0
graphs of distal radius and ulna showing cystic lesion in distal half of the left radius. Note expansion of the shaft of the
radius and extreme thinning of the cortices. A pseudofracture is present in the antero-medial radial cortex (arrows). A periosteal
reaction is evident adjacent to the pseudofracture and this probably represents callus formation a t this site. (C) Gross specimen
following saggital section through distal radius. Note the two main compartments of the cystic lesion and the fine fibrillar material
lining the cystic cavities. (D) Radiograph of gross specimen shown in Fig. 1(C). Note the fine bone trabeculae traversing the prox-
imal cyst cavity and the ridges on the inner wall of the cavity which probably represents unresorbed remnants of previous bony
partitions across the lesion. (E) Radiograph of 2mm thick slab of distal radius. Note that the growth plate and metaphyseal bone
adjacent to it are apparently unaffected by the cystic structures. Multiple small cystic structures can be visualized in the diaphys-
eal region adjacent to the junction of abnormal diaphysis with normal appearing diaphysis.
498 c. B. C A R R I G etal.
cortices were ofnormal thickness. Abnormalities were noted in the left radius, right
radius, left femur, left tibia and right tibia.

Lejl radius
A cystic lesion was present in the distal half of the left radius, extending from
just proximal to the distal growth plate to the mid-diaphyseal region (Fig. lA,
B). There was expansion of the bone and thinning of the cortices over the lesion.

FIG.2. Distal right radius. (A) Radiograph of distal radius and ulna. Notice smoothly
outlined defect in posterior aspect ofdistal radius (arrows).Thisappears to be an exagger-
ation of the cut-back zone normally seen in this region of the radius. (B) Gross specimen
illustrating the defect in the distal radius.

Bony trabeculations were evident within the lesion. A radiolucent line (pseudo-
fracture) could be seen running transversely across the middleofthe lesion. Asmall
zone of periosteal new bone was noted adjacent to this pseudofracture (Fig. 1A).
The posterior cortex of the radius just above the growth plate appeared to be
completely resorbed.

Right radius
The radiographic appearance of the right radius appeared normal except for a
 POLYOSTOTIC LESIONS I N A DOG 499

smoothly outlined defect located in the posterior cortex, just proximal to the distal
growth plate (Fig. 2A). The defect appeared to be an exaggeration of the normal
remodelling activity which is usually seen in this area. There was no periosteal
reaction adjacent to the defect.

FIG. 3. Leftfemur. There is a large cystic lesion situated in the posterior aspect of the
distal femoral metaphyseal region. An oblique, comminuted fracture is present running
through the cystic lesion.

Lgt femur
An oblique, comminuted fracture with slight anterior displacement and 1.5 cm
overriding was present in the distal metaphyseal region. The fracture was pre-
disposed to by a 6 cm x 3 cm radiolucent cystic lesion situated just proximal to the
distal femoral metaphysis (Fig. 3 ) . There was a minimal zone of increased bony
density surrounding the lesion. Soft tissue swelling was noted, and the popliteal
lymph node was enlarged (3 cm x 2 cm).
 500
c . B.
CARRIG
etai.

FIG.4. Proximal right tibia. (A) Lateral and (B) anteroposterior radiographs of right distal femur and proximal tibia.
There is a large cystic lesion situated in the posterior aspect of the proximal tibial metaphyseal region. Notice that the
posterior cortex of the tibia is completely resorbed. A cystic lesion is present in the cortex of the tibia (arrow). The right
femur is radiographically normal. (C) Gross specimen of horizontal section through proximal right tibial metaphysis.
The major cystic structure can be identified (a). Another cystic structure in the remaining cortical bone is seen. The
smaller cystic structure contains blood tinged fluid. (D) Radiagraph of specimen shown in Fig. 4(C) demonstrating that
multiple cystic structures are present in the cortical bone (arrows).
 POLYOSTOTIC LESIONS I N A DOG 50 1

L ~ and
t right tibias
Both tibias had similar lesions present in the proximal metaphysis (Fig. 4):
8 x 3 x 3 cm lesions were present in both posterior metaphyseal regions. There was
a minimal sclerotic zone surrounding the lesions and the posterior cortices were
completely resorbed. A radiolucent line (pseudofracture) was present in the lesion
in the left tibia. Defects were also present in the cortices of the tibia (Fig. 4B).

Hip joints
The acetabula appeared of normal depth. There was a minor degree of mal-
articulation of the left femoral head and this was probabl'y related to the fracture of
the left femur. There were no degenerative changes noted in the hip joints.

BACTERIOLOGICAL FINDINGS
Fluid from the left radial and right tibia1 lesions was cultured aerobically and
anaerobically. There was no detectable growth.

PATHOLOGICAL FINDINGS
Gross and microscopic findings : fresh tissues from the lesions in the left femur and
tibia were fixed in 10% neutral buffered formalin. Both radii and ulnae and the
right tibia were examined in an unfixed, frozen form. Sections from these frozen
bone specimens were subsequently fixed in 10% neutral buffered formalin. Histo-
logical sections from the frozen material were of sufficient quality to permit micro-
scopic interpretations.

L$t radius
The lesion in the left radius was a double-chambered cystic structure occupying
the distal half of the bone (Fig. 1C) . The proximal half of the radius appeared
normal. The larger anterior-proximal compartment was separated from the pos-
terior-distal compartment by a 3 mm thick layer ofspongy bone. This compartment
extended from 12 mm proximal to the distal growth plate to the middle of the
radial diaphysis. The pear-shaped, smaller, posterior-distal compartment extended
from a broad floor, located 2 mm proximal to the distal growth plate to a n apex
25 mm in a proximal direction along the posterior side of the diaphysis. Both cham-
bers contained approximately 5 ml of a clear, straw-colored fluid. Walls of the
lesions were lined by a flesh-colored delicate fibrillar material which formed a lacy
network extending into the cavities. Well defined bony trabeculae traversed the
anterior-proximal chamber while vestigal trabeculae formed ridges on the inner
walls of the two chambers.
A thin, delicate collagenous membrane lined by large, polygonal, multi-
nucleated giant cells formed the wall of both cystic structures. That portion of the
radial cortex in contact with the cyst wall was porous. The rarefied cortex was
502 c . B. C A R R I G et al.

composed of fenestrated plates of lamellar bone without osteon formation. Trabe-

culae of primary bone emerging from the growth plate immediately beneath the
distal cystic lesion were separated from the cyst wall by loose oedematous connective
tissue. These trabeculae were uniform in width, and similar in size and orientation
to those forming the spongiosa in adjacent metaphyseal areas uninvolved with
cystic structures.
The periosteum of the distal radius was more fibrous than osteogenic and osteo-
clastic activity was more pronounced than was appositional bone growth. The
morphological appearance of the entire distal radial growth plate was normal and
seemingly unaffected by the cavities in the metaphysis.

Right radius
The defect in the distal metaphyseal region which was noted radiographically,
appeared as a fibrotic area in the posterior metaphyseal cortex of the distal radius

FIG.5 . Defcct in the posterior metaphysis of the distal right radius. Irregular resorption of the
posterior cortical surface (PC). Residual bony spicules have concavities on their borders
identical with Howship’s lacunae (H). Spicules are set in a fibrovascular stroma (FS)
which is continuous with the fibrous periosteum (FP). H & E x 40.

(Fig. 2B). No cyst-like lesion was present. Microscopically, the outer surface of the
posterior metaphyseal cortex was formed of irregular bony spicules with faceted
edges having the characteristic silhouettes of Howship’s lacunae (Fig. 5). These
spicules were set in a radially oriented, dense, fibro-vascular stroma which was
continuous with the fibrous periosteum.
 POLYOSTOTIC LESIONS IN A DOG 503

Rilht tibia
The tibial lesion had multiple compartments which were partially separated by
prominent bony ridges (Fig. 4C, D). Five ml of blood tinged fluid were present in
the lesion. Walls of the compartments contained less of the fragile, shaggy,
fibrillar network than did the left radial lesions. The proximal and distal portions
of the posterior metaphyseal compartment were examined microscopically.
The proximal portion of this cystic lesion began approximately 2 mm beneath
the proximal growth plate where there was one major centrally placed compart-
ment and several small, adjacent and more peripherally oriented cavities (Figs.
4C, D, & 6). All cysts were lined by a similar delicate fibrillar membrane. Con-
tinuity between cysts was not determined. Cysts were confined within the region

FIG.6 . Posterior quarter of a transverse section through the right tibia. Taken approximately 2mm
distal to the proximal growth plate it shows the proximal end of the major cystic lesion
(M) in the proximal tibia and two smaller cavities (S). A delicate membrane lines the
chambers (L). Central metaphyseal spongiosa derived from endochondral ossification
(C). Irregular, peripheral cancellous bone (P) laid down by a fibro-osseous stroma (FS)
which is continuous with the fibrous periosteum (FP). Cystic degeneration of stroma
(D).H & E x 9.
of the metaphyseal spongiosa which arose from the growth plate by endochondral
ossification. While much of the spongiosa was replaced by the cystic lesions, the
bony trabeculae that were present were of normal thickness for this location when
compared to a control dog of similar age. These trabeculae were composed of
lamellar bone. The peripheral metaphyseal spongiosa forming the outer surface of
the posterior tibial cortex was remarkably different in that the bony trabeculae
were numerous, small, irregular in shape, and were composed of woven bone.
5 04 c . B. CARRIG etal.

Trabeculae arose in an uneven pattern from a collagenous matrix which in places

underwent cystic degeneration in the absence of giant cells. The abnormal peri-
pheral spongiosa was deposited by cells of a fibro-osseous stroma which was
continuous with the fibrous periosteum. I n the growing dog this region is typically
a site of bone resorption in the funnelization process of a long bone.
I n the distal portion of the posterior metaphyseal compartment the rust-
coloured appearance of the cyst wall and fluid in the cavity suggested the presence
of minor hemorrhage. Bone was absent in the site of the posterior tibia1 cortex.
The outer wall of the posterior compartment was formed by a thickened fibrous
periosteum and adjacent muscle mass. Microscopically, (Fig. 7) the cyst wall was
lined with eosinophilic amorphous material adhered to a thin collagenous layer
containing numerous distended blood vessels. I n turn, this layer was supported by

FIG.7 . Posterior cortex of the proximal righf fibia at the distal end of the cystic lesion in the
metaphysis. Amorphous lining of the cystic structure (A). Distended vessels in a thin
col!agenous layer (V). Bony spicules (B) forming by osseous metaplasia in the thickened
fibrous periosteum (P). H & E x 40.

the fibrous periosteum in which irregular spicules of bone were forming by

osseous metaplasia. The cyst wall was not very cellular. A few multinucleated giant
cells accompanied by macrophages containing hemosiderin were present in the
vascular layer.

Left tibia
The intact bone was not available for gross examination but sections of lesions in
 POLYOSTOTIC LESIONS I N A D O G 505
this bone were available for microscopic examination. Multiple cystic lesions (Fig.
8) were present in the proximal metaphysis with the largest compartment filling
the posterior half of the metaphysis and extending proximally to within 2 mm of the
growth plate. Two smaller cavities occurred in the inner one-third of the anterior
proximal metaphyseal spongiosa. The wall of the larger of the two small cavities
(Fig. 9) closely resembled the wall of the major compartment. The cyst wall was
composed of a relatively dense fibrovascular membrane randomly studded on the

FIG.8 . Anterior third of a longitudinal section through the proximal lefi tibia. Epiphysis (E),
growth plate (G), and primary spongiosa of the metaphysis (S) are normal. Major cystic
lesion (Ml). Larger of the two smaller chambers (M2). Smallest cystic lesion (M3). Focus
of intense osteoclastic activity (M4). Rarefied anterior cortex (C). H & E x 9.

inner surface with multi-nucleated giant cells. Adjacent metaphyseal trabeculae

were being removed by osteoclastic activity. The marrow spaces of the spongiosa
were filled with an oedematous and fibrillar connective tissue containing distended
vascular channels. T h e wall of the smallest cystic lesion (Fig. 10) had more
numerous multinucleated giant cells on the surface and perhaps less connective
tissue in its walls than the larger lesions. Osteoclastic destruction of adjacent
E
506 c. B. C A R R I G etal.

FIG. 9. Larger of the two small cyctic lesions in the proxal metaphyseal spongiosa of the left tibia.
Fibrovascular wall of the cystic structure has a fewrnultinucleated giant cells on the inner
surface. Osteoclastic resorption occurs inadjacent trabecular bone. Oedernatous, reactive
connective tissue fills the marrow spaces. H & E x 50.

FIG. 10. Smallest ystic lesion in the spongiosa of the proximal left tibia. Numerous multi-
nucleated giant cells line the surface of fibrovascular wall. Osteoclasia is intense on the
surfaces of the adjacent secondary spongiosa. H & E x 50.
 POLYOSTOTIC LESIONS I N A D O G 507

spongiosa appeared more intense. Otherwise, walls of the lesions were similar.
Two minute (less than 0.5 mm diameter), highly vascular foci of intense osteoclas-
tic activity without compensatory bone formation occurred in the metaphyseal
spongiosa unassociated with the cystic lesions (Figs 8, 1 1, 12). Vessels in these sites
were distended with blood. Marrow spaces were oedematous and contained
extravasated erythrocytes, some of which were within macrophages. Mitotic
figures were present in some of the spindle cell population of the stroma. Osteo-
clasts of varying sizes appeared to be forming from large mononuclear cells in the
stroma.
The growth plate and primary spongiosa of the proximal tibia were unaffected

FIG. 1 1. Focus of intense osteoclasia in the spongiosa of the proximal lejt tibia. Resorption of an
area.of secondary spongiosa without bone replacement is evident. Hypermia and extra-
vasation of erythrocytes occurs in marrow spaces filled with fibroblastic and osteoclastic
connective tissue elements. H ti E x 110.

(Fig. 8 ) . The secondary spongiosa was composed of lamellar bone and showed a
change in compactness and orientation which related to the position of the meta-
physeal cavitations. The cortex was rarefied and congested. Highly vascularized
508 c. B. CARRIG etal.

fibrous tissue filled abnormally numerous longitudinally oriented resorption

cavities in the cortical bone. Osteoclastic activity was also present on the periosteal
surface of the cortex.

L$l femur
Only sections of formalin-fixed bone were available for examination. T h e outer
cortical surface of the distal diaphysis was covered by a 12 mm thick covering of
dense connective tissue. The cortex was porous, and a dark rusty coloured shaggy
membrane lined the inner cortical surface. Microscopic examination showed a well
organized callus supporting a cortex rarefied by numerous resorption cavities
(Fig. 13). The external callus was composed primarily of cartilage in the sub-
periosteum undergoing endochondral ossification along the surface of the original

FIG.12. Higher magnification of site of intense osteoclasia shown in Figure 11. Fibrillogenesis ( F ) ,
phagocytosis of erythrocytes and unidentified granular material by macrophages (M),
and numerous large mononuclear and binuclear cells (L) with the nuclear appearance
. and cytoplasmic staining properties of osteoclasts (0)is seen. H & E x 290.
cortex. The internal callus was formed primarily of cancellous woven bone an-
chored to an irregular inner cortical surface. The inner border of the internal callus
blended into haemorrhagic granulation tissue which contained remnants of a
fibrocellular membrane similar to the one found in the other cystic lesions. As the
major disruption of the left femur occurred only 2 days prior to euthanasia, it is
apparent that previous microfracture of the wall of the cystic lesion, without
displacement, occurred which caused the changes seen histologically in the left
femur.
 P O L Y O S T O T I C L E S I O N S IN A D O G 509

FIG.13. Anterior cortex of the distal diaphysis of the leftfemur. External callus (E) composed
of cartilage with ossification occurring along the cortical surface (0).Rarefied cortex
with numerous resorption cavities (R). Internal callus of cancellous bone (I) applied to
an irregular inner cortical surface. Haemorrhagic granulation tissue (T) covers the
surface of the internal callus. Remnants of the wall of the cystic lesion (C) in the distal
femur. H & E x 19.

DISCUSSION
The differential diagnosis of cystic bone lesions includes bone cyst, aneurysmal
bone cyst, ganglionic cystic defect, post-haematoma cysts, neuro-fibromatosis,
fibrous dysplasia, non-ossifying fibroma, hyperparathyroidism and enchondro-
matosis (Huff & Brodey, 1964; Aegerter & Kirkpatrick, 1968; Kambolis PI al.,
1973).
No lesions have given rise to greater confusion in terminology than those in which
cysts and fibrous tissue are formed within a bone (Wiles & Sweetnam, 1965). These
con-&tions can be classified as solitary bone cysts, monostotic fibrous dysplasia or
polyostotic fibrous dysplasia. The term ‘fibrous dysplasia’ emphasizes the one
common feature of all these conditions, namely, the replacement of bone by fibrous
tissue which may contain areas of cystic degeneration, but does not convey a
precise concept of any such lesion. A more precise understanding of the nature of
these lesions awaits the discovery of the aetiology and studies of their histogenesis
(Wiles & Sweetnam, 1965). Fibrous dysplasia is a disturbance in postnatal intra-
medullary bone maintenance where normal bone undergoing physiological lysis is
replaced by an abnormal proliferation of fibrous tissue (Aegerter & Kirkpatrick,
1968). Further, that the so-called solitary unicameral bone cyst, which occurs at the
510 c. B. CARRIG et al.

ends of the large cylindrical bones of the extremities in the growing skeleton, is
the only purely cystic lesion of bone; other cyst-like lesions should be designated as
areas of liquefaction necrosis rather than cysts because they are merely areas of
degeneration in proliferative processes (Aegerter & Kirkpatrick, 1968).
Accordingly, it was previously suggested that these cystic bone lesions in the dog
be designated fibrous dysplasia until a more precise understanding of the histo-
genesis is obtained (Carrig & Seawright, 1969). The pathogenesis and biological
behaviour of cystic bone lesions in the dog can be determined only by studying a
number of such lesions in varying stages of development (Huff & Brodey, 1964).
The inadequate nutrition that the puppy of this report received up to 6 weeks of
age, resulting in secondary hyperparathyroidism at that age, would suggest that a
nutritional basis could be involved in the aetiology of the lesions. I n man, cystic
lesions sometimes occur in haemophiliacs (Aegerter & Kirkpatrick, 1968) and it
has been suggested that an extravasation of blood into the metaphysis of a young,
growing bone could be involved in other cystic lesions of bone (Aegerter & Kirk-
patrick, 1968). Cystic lesions have been produced in the bones of rabbits by injec-
tion of partially haemolyzed, acidified blood (Cottier, 1952). Whether trauma to
the weakened bones of the puppy of this report at 6-8 weeks of age led to micro-
fracture and haemorrhage in the metaphyseal regions is uncertain. However,
several known facts would tend to negate this possibility: (a) There was no evi-
dence of demineralization of the skeleton at 9 months of age, (b) in other reported
cases (Carrig & Seawright, 1969) no suggestion of poorly balanced or deficient
diets were involved, (c) the multiple location of the lesions in the dog of this report
and in other reported cases (Huff & Brodey, 1964; Riser, 1968; Carrig & Sea-
Wright, 1969), (d) cystic bone lesions are rarely seen, whereas nutritional problems
are encountered frequently in young dogs and cats, (e) the presence of pseudo-
fractures, which are not symmetrically located within the skeleton, would suggest a
non-nutritional aetiology (Paul & Juhl, 1967) and (f) of the six cases of polyostotic
cystic bone lesions reported in the dog, five have occurred in Doberman Pinschers
(Table 1). This would suggest a breed predisposition (Carrig and Seawright,
1969).
The straw colour of the cystic fluid would rule out a diagnosis of aneurysmal
bone cyst. Although the cystic lesion in the right tibia did contain blood-tinged
fluid it has been reported that only minimal trauma is necessary to cause haemor-
rhage in cystic structures in bone (Cohen, 1960). It is probable that the
haemorrhage present in the cystic lesion in the right tibia resulted from some recent
trauma to the area and was not involved in the aetiology.
I t has been suggested (Nutt, 1967) that the locular radiographic appearance of
these canine cystic bone lesions is due to the presence of ridges on the medullary
surfaces of the cyst wall and not to bony partitions traversing the cystic cavity. I t
can be seen from this case that both ridges and partitions of bone are responsible
for the locular appearance. The ridges present on the medullary surface appeared
to be unresorbed remnants of previous bony partitions across the lesion.
 POLYOSTOTIC LESIONS I N A DOG 51 1
TABLE
1. Cystic bone lesions in the dog

Breed Age Sex Monostotic Polyostotic Reference

Great Dane 8 mos M + Rothman & Schnelle (1949)

Bull Mastiff x 6 mos M + Gourley & Eden (1954)
Weimaraner 15 mos M + Riser (1958)
Irish Wolfhound 6 mos * + Owen & Walker (1963)
Doberman Pinscher 9 mos M + Huff & Brodey (1964)
German Shepherd 12 mos * + Nutt (1967)
Doberman Pinscher 10 mos M + Riser (1968) pers. comm.
German Shepherd 12 mos * + Riser (1968) pers. comm.
Doberman Pinschert 5 mos F + Carrig & Seawright (1969)
Doberman Pinschert 7 mos F + Carrig & Seawright (1969)
Doberman Pinscher t 7 mos M + Carrig & Seawright (1969)
Doberman Pinscher 9 mos M + Carrig, et al. (1975 present
report)

* Not recorded. t Siblings.

Although the pathogenesis of cystic lesions in bone was not resolved in the
present case, certain impressions were gained from microscopic examination of
affected tissues which may help in understanding the development of polyostotic
cystic bone disease in dogs. It appears that the growth plates and the primary
spongiosa of bones with cystic lesions are not involved in the disease process.
Secondary spongiosa and the metaphyseal periosteum are the major tissue sites
affected.
In addition to major cystic lesions in bone, identically structured microcysts,
one less than 1.5 mm in greatest dimension, evolved in a congested and oedematous
metaphyseal spongiosa. Microcysts were accompanied by even smaller foci of
intense osteoclastic bone destruction unattended by compensatory bone production.
Without osseous repair it is conceivable that the latter foci may undergo cystic
degeneration as they enlarge.
The histological appearance of the cyst walls in the case of this report was
similar to that previously reported (Carrig & Seawright, 1969). However, no
tissue resembling fibrous dysplasia of man, as was reported in curetted material
from cystic lesions in other Doberman Pinschers (Carrig & Seawright, 1969) was
found in this case. Only in the broadest sense could the disease in this case be
termed fibrous dysplasia with cystic degeneration.
Failure to maintain secondary spongiosa had a corresponding abnormality in
the metaphyseal periosteum. I n bones in which cystic structures partially or
completely bridged the metaphyseal cortex, the periosteum covering this site was
effectively non-osteogenic, or produced a meagre fibro-osseous periosteal response
in which cystic degeneration sometimes occurred. The metaphyses of all bones
examined histologically showed a thickened fibrous periosteum. These periosteal
512 c. B. C A R R I G et al.

changes appeared to be an exaggeration of normal remodelling activity which is

often pronounced in the metaphyses of immature bones in breeds with long slender
limbs. I n the right distal radius this resulted in the increased size of the cut-back
zone noted radiographically. It is of interest to note that the limits of the posterior-
distal cystic lesion in the left radius of the dog of this report, and those in other
reported cases (Rothman & Schnelle, 1949; Huff & Brodey, 1964; Nutt, 1967;
Carrig & Seawright, 1969) closely correspond to the shape of the exaggerated cut-
back zone in the right radius of this dog. This suggests that these particular lesions
may have arisen from a cystic degeneration of abnormal fibrous periosteum in this
region.
Pseudofractures, or Looser’s zones, are transverse fissure-like defects that extend
part way or completely through the bone. They are infractions of bone in which
osteoid is formed in the defect, but with failure of calcium deposition so that a
fissure defect is present on the roentgenogram (Paul & Juhl, 1967). They usually
occur at points of stress (Aegerter & Kirkpatrick, 1968) and are probably similar
to chronic fatigue fractures and develop in bone that is incapable of withstanding
the stresses placed upon it (Paul & Juhl, 1967). I n man, pseudofractures are seen
associated with osteomalacia, Paget’s disease, fibrous dysplasia and osteogenesis
imperfecta (Paul & Juhl, 1967 ;Aegerter & Kirkpatrick, 1968).Inosteomalacia, the
pseudofractures are usually bilateral and symmetrical (Paul & Juhl, 1967). I n
the reported cases of cystic bone lesions in the dog, pseudofractures have been
noted (Carrig & Seawright, 1969) or present in photographs of roentgeno-
grams accompanying the case reports (Huff & Brodey, 1964; Nutt, 1967).
There was no tendency for the pseudofractures to be bilaterally symmetrical in
these cases.
Pseudofractures can proceed to fractures with displacement of the bone frag-
ments (Paul & Juhl, 1967). I n the case of this report it was not determined whether
a pseudofracture predisposed to the fracture of the left femur; however, pseudo-
fractures were present in the left radial and left tibia1 lesions. The histological
evidence of callus formation in the left femur of the case of this report would sug-
gest that microfractures without displacement had occurred in the wall of the
cystic lesion prior to the major disruption of the bone. The periosteal reaction
associated with the pseudofracture in the left radius would indicate that a micro-
fracture had occurred at this site also. Pseudofractures were present in bones which
subsequently underwent pathologic fracture in two reported cases in the dog (Huff
& Brodey, 1964; Nutt, 1967). Thus, when pseudofractures are seen on the roent-
genogram, consideration should be given to supplying additional support to the
affected limb to prevent pathological fracture.
Although treatment was not attempted in the case of this report, it has been
shown that resolution of these cystic bone lesions will result following surgical
drainage and curettage of the cyst wall (Rothman & Schnelle, 1949; Huff &
Brodey, 1964; Carrig & Seawright, 1969). Healing of a fracture through a cystic
bone lesion was reported following immobilization with a Steinman intramedullary
 POLYOSTOTIC LESIONS IN A DOG 513

pin ( H u f & Brodey, 1964). Resolution of a lesion in one dog occurred without
surgical intervention (Gourley & Eden, 1954).

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