PALLIATIVE IRRADIATION OF SCOTTISH FOLD

OSTEOCHONDRODYSPLASIA

MADELEINE HUBLER, DR. MED. VET., MATHIAS VOLKERT, DR. MED. VET.,BARBARA KASER-HOTZ, PROF. DR. MED. VET., SUSI ARNOLD, PD DR. MED. VET.

This report describes palliative irradiation as treatment for Scottish Fold osteochondrodysplasia. A 3-year-old

female spayed Scottish Fold cat suffering from osteochondrodysplasia was referred to the Veterinary Teaching

Hospital, University of Zurich. Based on the breed, history, clinical signs, radiographic findings, and the

histologic diagnosis of a biopsy specimen, Scottish Fold osteochondrodysplasia was confirmed. To control the

exostoses leading to inflammatory processes and pain, radiotherapy was initiated as palliative treatment. This

was successful in relieving the clinical signs within a few weeks. The short- and long-term results after ra-

diotherapy are presented and discussed with a comparable human disease, the plantar heel spur, which also

responds well to radiotherapy. Veterinary Radiology & Ultrasound, Vol. 45, No. 6, 2004, pp 582–585.

Key words: palliative treatment, radiotherapy, Scottish Fold osteochondrodysplasia.

Introduction

SCOTTISH FOLD OSTEOCHONDRODYSPLASIA is a hereditary

disease affecting bone growth and the formation of

articular cartilage and leads to progressive skeletal de-

formities at the distal extremities and tail. Initially it was

thought to affect only cats homozygous for the folded ear

(Fd) gene, which is inherited as an autosomal dominant

trait.1 Later, several reports described similar, but less se-

vere lesions occurring in heterozygous cats (Fd/fd), but

with a later onset and varying signs of skeletal disease such

as progressive lameness, stiff and stilted gait, reluctance to

jump or sometimes without ambulatory problems.2–5 Be-

cause the underlying disease is a genetic defect, the ther-

apies in use mainly aim at reducing the clinical signs and

accompanying pain. Pentosane polysulfates subcutaneous-

ly or complex glycosaminoglycans per os were used with a

reduction in lameness and discomfort in some cats.2 In one

cat a surgical approach, including staged bilateral os-

tectomies and pantarsal arthrodeses of both hindlegs, re-

solved the lameness.3 In the latest report the same result

was achieved with only the surgical removal of the tarsal

exostoses.5 The present report describes palliative radio-

therapy in a Scottish Fold cat affected by Scottish Fold

osteochondrodysplasia.

Case History

A 3-year-old neutered female cat with folded ears was

presented to the Veterinary Teaching Hospital, University

of Zurich, for evaluation of a progressive swelling of the

left and right tarsus. The cat had a slightly stiff gait in the

hindlegs for less than 1 month before presentation and

could no longer climb trees. The mother was a Scottish

Fold and the father a Chartreux. There were three litter-

mates, one with folded and two with straight ears.

The cat was bright and alert and had grossly thickened

tarsi (Figs 1 and 2). By palpation, which caused no pain, the

right tarsus was more swollen and had a greater decrease in

range of motion. On the plantar aspect of the tarsus and

metatarsus of both hindlimbs new bone formation was

present, extending from the proximal calcaneus to the

proximal metatarsus. Along the dorsal, lateral, and medial

aspect of the tarsi no further swelling was noted. Radio-

Fig. 1. Three-year-old female spayed Scottish Fold cat at presentation.

Dr. Volkert’s current address is the private surgery of Dr. Med. Vet. G.Klaus, 4410 Liestal, Switzerland.

Address correspondence and reprint requests to Barbara Kaser-Hotz,Prof. Dr. Med. Vet., at the above address. E-mail: bkaser@vetclinics.unizh.ch

Received October 24, 2003; accepted for publication February 25, 2004.doi: 10.1111/j.1740-8261.2004.04101.x

From the Section of Small Animal Reproduction, (Hubler, Volkert,Arnold), and Section of Radiology and Radiation Oncology (Kaser-Hotz), Department of Small Animals, Faculty of Veterinary Medicine,Zurich University, Winterthurerstr. 260,8057 Zurich, Switzerland.

582

graphs were made of both distal hindlegs. On the dorsal

aspect of the right tarsus periosteal, new bone proliferations

were present, extending from the proximal os tali to the

proximal metatarsus. On the dorsal aspect of the talus and

at the intertarsal joints osteophytes were visible (Fig. 3). On

radiographs of the left tarsus there were similar, but milder

changes and on radiographs of both carpi no degenerative

changes were present. A biopsy taken from the bony pro-

liferation by the referring veterinarian was submitted for

histopathologic examination; results were compatible with

osteochondrodysplasia. The breed of the cat, history, clin-

ical signs, and radiographic findings were consistent with

the histological diagnosis of osteochondrodysplasia.

To decrease the new bone formation, which eventually

will lead to reactive inflammation and progressive ankylos-

ing arthropathy, radiotherapy was initiated as a palliative

treatment. Over 2 weeks the cat was irradiated in six frac-

tions of 1.5Gy each, on a Monday–Wednesday–Friday

schedule. The radiation used was 30-MeV electrons. The

radiation source was a Betatron.� For radiotherapy, the cat

was anesthetized with intravenously injected propofolw (in-

duction dose: 7mg/kg, maintenance: 0.5mg/kg/min). The

cat was positioned on its back with both hindlegs positioned

in the air and fixed to a rack. The irradiated field included

the whole tarsal area of both hindlegs and extended from

the tibia to the distal ends of the metatarsi. A single beam

was directed in a plantaro-dorsal direction and both tarsi

were irradiated in the same field. The Dmax was 100% at 1-

mm depth and no bolus was used. The entire depth and

circumference of both tarsi received 100% of the dose.

After six radiotherapy sessions the cat had no side effects

and went home in a good condition. The referring veterin-

arian re-examined the cat at regular intervals over the next

2 years and according to the owner the cat had no ambu-

latory problems and was now able to climb trees 1 month

after completion of radiotherapy. Twenty-eight months af-

ter therapy radiographs were repeated. On both hindlegs

there were no signs of further bone proliferation. The ex-

ostoses had strikingly smooth surfaces and a less opaque,

but more homogenous, structure. The talocrural joint

space of the more severely affected right hind limb was

narrowed and the proximal intertarsal joint was almost

completely fused. At the distal intertarsal and tarsometa-

tarsal joints ankylosis was almost complete with no effect

on the cat’s locomotion. Additionally, within the previous

Fig. 2. Right hindleg with pronounced swelling on the plantar aspect ofthe tarsus and metatarsus.

Fig. 3. Radiograph of the right tarsus (medio-lateral view) before radi-ation therapy.

�BBC, Switzerland.wDisoprivan, Fresenius Pharma (Schweiz) AG, 6370 Stans,

Switzerland (induction dose: 7mg/kg, maintenance: 0.5mg/kg/min).

583RadiationTherapy in a Scottish Fold CatVol. 45, No. 6

radiation treatment field a few new bony proliferations

were evident at the proximal plantar end of the metatarsal

bones (Fig. 4). On radiographs of the left leg there was only

minor new bone formation at the tarsal joint. The joint

spaces were still intact and without apparent changes.

Discussion

The trait for forward folded ears (Fd) originated as a

spontaneous mutation, in 1966, in a female British short-

hair, the founding cat of the Scottish Fold breed.1 Genetic

studies using breeding experiments revealed an autosomal

dominant inheritance.1 Additionally, it became evident

that cats homozygous for the gene (Fd/Fd) developed a

progressive skeletal disease, including a short thickened

and inflexible tail and deformities of the distal extremities

early in their lives. At the age of 7 weeks radiographic

changes are already apparent: there are distorted met-

aphyses and widened physes of the metacarpal and met-

atarsal bones. Similar but milder changes are seen at the

phalanges. This results in a reduced growth of the affected

bones, leading to shortened extremities and short, thick-

ened vertebrae of the tail with widened endplates.1 Histo-

logically the pathological changes of the affected bones are

mainly located at the growth plates and the neighboring

metaphyses. The growth plates have defective bone for-

mation with disordered chondroblast proliferation and ir-

regular groups of cells, which finally results in a disturbed

enchondral ossification with insufficient mineralization.

During growth the extremities become deformed and the

affected joints are abnormally stressed, resulting in degen-

erative joint diseases and periarticular new bone formation

at sites of ligamentous attachment to bone and joint cap-

sules.2 The extensive investigation of Scottish fold cats, in-

cluding pedigree analysis2 demonstrated clearly that not

only the homozygous, but also the heterozygous carriers

are affected to some degree by this osteochondrodysplasia.

The therapeutic approach in cats with clinical signs is solely

aimed at reducing the impaired locomotion and the ac-

companying pain. The use of pentosan and glyco-

saminoglycan preparations only helps in some cats2 and

surgical therapies3,5 indeed resolved the lameness, but they

are rather invasive procedures. It was therefore decided in

the presented cat to use a minimal invasive treatment, ra-

diotherapy, to stop the excessive bone formation and to

suppress the inflammatory process.

For this cat a low dose regimen of six fractions (1.5Gy)

was chosen. This fractionation schedule was arbitrarily

based on information for plantar heel spur radiation in

human medicine6–8 and was purely palliative with the aim

to stabilize the skeletal changes. The underlying problem

itself is incurable. In addition, we wanted to spare the

normal tissue. The achieved result, namely the suppression

of bony proliferation, and therefore a pronounced slowing

down of the osteochondrodysplasia, is promising, espe-

cially when compared with the more invasive surgical

methods.3,5 There was no posttreatment necessary and

long-term success was good. On radiographs made 28

months after radiotherapy there was just a minimal in-

crease of the exostoses.

A comparable and well-known disease in humans is the

plantar heel spur, an original disease of the ‘‘Calcaneodynie

syndrome,’’ which irritates the whole osseous and tend-

inous system of the heel in its function. Because the etio-

logy of the plantar heel spur is still controversial, the aim of

treatment is primarily to eliminate the accompanying irri-

tations.8 Beside local and systemical medical treatment

with antiphlogistic and analgetic substances, physical ther-

apy and inner soles are the preferred therapeutic approach-

es for the plantar heel spur. It is often refractory to medical

therapy, but has responded well to radiotherapy which is

well established in European countries.6–8 The primary

goal of radiotherapy in affected people is the control of

inflammation, which is responsible for the subjective pain

of the patient. In one prospective study8 three different

dose concepts were compared with a variable number of

fractions and different total radiation dose. Group A

(n¼ 72 heels) received 12-Gy total radiation in three frac-

tions per week and two series (6� 1Gy/series) separated

by 6 weeks; group B (n¼ 98 heels) received 3-Gy total ra-

diation in ten fractions of 0.3 -Gy (n¼ 50) or 5Gy

(10� 0.5Gy) (n¼ 48) with conventional fractionations in

one series. At the end of therapy 75% of group A and 77%

of group B had a subjective pain relief of 80–100%. A

delayed response after 4 weeks or subjective pain relief of

less than 80% was observed in 25% (group A) and 24%

(group B), respectively. On long-term evaluation complete

pain relief was achieved in 67% (group A) to 71% (group

B) of the treated patients, with no significant difference

between the three radiation protocols. However, prognos-

Fig. 4. Radiograph of the right tarsus (medio-lateral view) 28 monthsafter radiation therapy.

584 Hubler et al. 2004

tic factors for complete pain relief were short duration of

pain symptoms prior to therapy and acute pain symptoms

prior to radiotherapy.

The clinical presentation of the Scottish Fold osteo-

chondrodysplasia and the onset of clinical signs in our cat,

as well as the good response to radiotherapy, are somewhat

similar to the human heel spur problem.6–8 Because os-

teochondrodysplasia results in degenerative joint disease and

periarticular new bone formation leading to inflammatory

processes, it explains the good response to radiotherapy in

our cat. Therefore, the palliative radiotherapy offered an ef-

fective and minimally invasive treatment for this Scottish

Fold osteochondrodysplasia, if the degree of the skeletal

changes, including degenerative joint diseases, is not too ad-

vanced. Because in cats heterozygous for the folded ear (Fd)

gene, the age at onset of clinical signs (6 months–6 years), as

well as the severity of changes and rate of progression, is

considerably variable, palliative radiotherapy should be eval-

uated individually for each case. When the skeletal changes

are not too advanced, and there is a good clinical response to

radiotherapy, a second irradiation could be considered if

clinical signs reoccur. Although the result of palliative radi-

otherapy was quite promising in this Scottish Fold cat, the

maintenance of this breed should be discouraged2 as cats

heterozygous for the folded ear gene are also affected by this

osteochondrodysplasia sometime during their lifetime.

REFERENCES

1. Jackson OF. Congenital bone lesions in cats with fold-ears. Bull FelAdvis Bur 1975;14:2–4.

2. Malik R, Allan GS, Howlett CR, et al. Osteochondrodysplasia inScottish Fold cats. Aust Vet J 1999;77:85–92.

3. Mathews KG, Koblik PD, Knoeckel MJ, Pool RR, Fyfe JC. Res-olution of lameness associated with Scottish Fold osteodystrophy followingbilateral ostectomies and pantarsal arthrodeses: a case report. J Am AnimHosp Assoc 1995;31:280–288.

4. Partington BP, Williams JF, Pechman RD, Beach RT. What is yourdiagnosis? Scottish Fold osteodystrophy. J Am Vet Med Assoc1996;209:1235–1236.

5. Simon D. Osteochondrodysplasie bei einer Scottish-Fold Katze.Tierarztl Prax 2000;28:107–110.

6. Basche ST, Drescher W, Mohr K. Ergebnisse der Rontgenstrahlen-therapie bei Fersensporn. Radiobiol Radiother 1980;21:233–236.

7. Schafer U, Micke O, Glashorster M, Rube C, Prott F-J, Willich N.Strahlentherapeutische Behandlung des schmerzhaften Fersenbeinsporns.Strahlenther Onkol 1995;171:202–206.

8. Seegenschmiedt MH, Keilholz L, Stecken A, Katalinic A, Sauer R.Radiotherapie beim plantaren Fersensporn. Indikation, Technik, klinischeErgebnisse bei unterschiedlichen Dosiskonzepten. Strahlenther Onkol1996;172:376–383.

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