S. Sulficar1, Anse Vellappally, N. Madhavan Unny1, Sudheesh S. Nair1 and S. Ajithkumar2
1Assistant Professor, 2Professor & Head, Department of Teaching Veterinary Clinical Complex,College of Veterinary
& Animal Sciences, Kerala Veterinary and Animal Sciences University,Mannuthy, Thrissur-680651.
[Received: 09.6.2018; Accepted: 15.4.2019]
{DOI 10.29005/IJCP.2019.11.1.001-004}


Three Neopolitan Mastiff littermates aged three months were presented to the Teaching Veterinary Clinical
Complex, Mannuthy with the history of puppies being recumbent for past 5 days of presentation. Anamnesis revealed
the occurrence of high fever and diarrhoea one week before. On examination the puppies were found to be recumbent
and cachectic with firm swellings on the carpal and stifle joints. Radiographic findings were suggestive of periosteal
reactions and soft tissue swellings around the metaphyses of long bones pertaining to the features of hypertrophic
osteodystrophy (HOD). Two separate treatment strategies were adopted for the three puppies. The male puppy was
treated with corticosteoroid and antibiotic while other two female puppies were treated with antibiotic therapy alone.
An uneventful recovery was observed in case of male puppy on 3rd day suggesting the effectiveness of corticosteoroid
therapy and later the same treatment was adopted to other puppies which also showed complete recovery.
Keywords: Hypertrophic Long bones, Osteodystrophy (HOD), Periosteal reactions.

Hypertrophic Osteodystrophy or Metaphyseal Osteopathy is a developmental skeletal abnormality in fast growing heavy dog breeds occurring at 2-8 months of age. The disease manifestations include anorexia, depression, fever, symmetrical lameness, recent diarrhoea, warm and painful enlargements of the metaphyses of long bones
(Abeles et al., 1999). The severity of acute onset of lameness varies from mild limping to complete reluctance to stand or walk (Miller 2001). The underlying etiolgy of the disease is unknown, although there are reports of
several factors like oversupplementation of vitamins and minerals, infectious agents like Escherichia coli (Schulz et al., 1991), high calcium diet (Abeles et al., 1999) and Canine Distemper virus vaccination (Baumgärtner et
al., 1995) also contribute to the pathogenesis. This paper describes the successful medical management of HOD in three Neopolitan Mastiff littermates with corticosteroid therapy followed by NSAIDS in tapering doses along
with antibiotic.

Case History and Observations
Three non-ambulatory, dull and depressed Neopolitan Mastiff littermates aged three months with considerable muscle wasting were presented at TVCC, Mannuthy. All the three puppies exhibited firm and swollen carpal joints with pain on palpation. The male puppy in addition had a swollen stifle joint that elicited pain on palpation. Past
history revealed diarrhoea and high fever before one week, followed by acute onset of lameness that progressed to recumbency. The puppies had normal appetite and were maintained on cooked chicken and rice along
with pelleted grower food and calcium supplementation.


The haematological parameters of the three puppies were alike with mild leucocytosis and anaemia. The serum
biochemical profiles were also within the normal range, except for the higher concentrations of phosphorus and alkaline phosphatase but cannot be confirmed and may also be attributed to the hyperphosphataemia and elevated alkaline phosphatase routinely detected in juvenile animals.

Radiography of medio-lateral view of hind limbs suggested early signs of periosteal reactions on the distal extremities of femur and tibia giving a typical radiolucent appearance with elevated periosteal linings of
these long bones (Fig.1). Osteolytic changes consistent with HOD were observed on the ventro-median view of hip joint (Fig.2). Increased radiolucency was evident on the distal extremity of radius along with soft tissue swelling on carpal joint(Fig.3).

Two different treatment regimen was adopted for the three littermates. The male puppy ( puppy1) was administered a single dose of Methyl prednisolone acetate @ 1mg/kg on day 1, followed by a tapering dose of Meloxicam @ 0.2mg/kg on day 2 and 0.1mg/kg on day 3 under the protective coverage of antibiotic Ceftriazone – Tazobactam @ 20mg/kg for 3 days. Other two female puppies (puppy 2 & puppy 3) were maintained on antibiotic alone for 3
days without any corticosteroids. Proton pump inhibitor, Pantoprazole @ 1mg/kg were administered to all the three puppies to prevent any gastrointestinal disturbances. An uneventful recovery was made by the male

puppy on day 3, while no improvement was observed in case of other two female puppies and was still found to be recumbent. The female puppies later underwent the same corticosteroid therapy and meloxicam regimen and started normal ambulation at day 2 of treatment, suggesting the effectiveness of corticosteroid and NSAIDS for the condition. After discontinuing the above treatment, on a review after one week the puppies showed normal ambulation and neurological and orthopaedic examinations revealed satisfactory results. Pain was elicited only on
palpation of hip joint and manipulation of carpal and stifle joints were well tolerated. Oral medication consisting of
rimadyl@5mg/kg OD and tablet combination of glucosamine hydrochloride 500mg, chondroitin sulphate 400mg, manganese sulphate 5mg, Boswellia serrata 50mg, Withaniasomnifera 50mg and vitamin C 12.5mg@ 1 tab BID were prescribed as follow up therapy. Dietary regulation was made by advising a Ragimillet based diet.

This paper describes the rare case of hypertrophic osteodystrophy in three Neopolitan Mastiff littermates of its kind. The response to corticosteroid therapy suggests the presence of an underlying inflammatory process triggering the progress of the disease and dampening of this process restricted the expression of disease as also reported by Abeles et al. (1999). Radiographic appearance of a radiolucent line just above the physes referred to as double physeal line
is a predominant finding in HOD as also recorded by Hill et al. (2015), although it may not be evident in all stages of the disease. The treatment methodology is conservative and non-specific aimed at managing the pyrexia
and bone repair using steroids or Non Steroidal Anti Inflammatory Drugs (NSAIDS) as also suggested by Safra et al., (2013) and Hill et al. (2015). The studies so far on HOD propose a good prognosis for mildly affected puppies and a guarded one for the severely affected ones.

Abeles, V., Harrus, S., Angles, J.M., Shalev,  G., Aizenberg, I., Peres, Y.and Aroch, I. (1999). Hypertrophic Osteodystrophy in six Weimaraner puppies associated with systemic signs. Vet. Rec., 145: 130-134.

Baumgartner, W., Boyce, R.W., Alldinger, S., Axthelum, M.K., Weisbrode, S.E., Krakowka, S. and Gaeoke, K. (1995).
Metaphyseal bone lesions in young dogs with systemic canine distemper virus infection. Vet. Microbiol., 44: 201-209.

Hill, M., Scudder, C.J., Glanemann, B. and Drees, R. (2015). Hypertrophic osteodystrophy in a dog imaged with CT.
Vet. Rec. Case Reports, 3: e000155.

Miller, C. (2001). Hypertrophic osteodystrophy in a Great Dane puppy. Can. Vet. J., 42: 63-66.

Safra, N., Johnson, E.G., Lit, L., Foreman, O., Wolf, Z.T., Aguliar, M., Karmi, N., Finno, C.J. and Bannasch, D.L. (2013). Clinical manifestations, response to treatment and clinical outcome for Weimaraners with hypertrophic
osteodystrophy:53 cases (2009-2011) J. Am. Vet. Med. Assoc., 242: 1260–1266.

Schulz, K.S., Payne, J.T. and Aronson, E. (1991). Echerlichia colibacteremia associated with hypertrophic
osteodystrophy in a dog. J. Am. Vet. Med. Assoc., 199: 1170-1173.

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