Abstract
We would like to thank Dr Foster for her constructive letter regarding a report about Idiopathic hypertrophic osteopathy in a cat from Ocarino et al, published in Journal of Feline Medicine and Surgery (2006)
The purpose of this letter is to elucidate the questions asked by Dr Foster and to enrich the discussion about this disease whose aetiopathogenesis still is obscured.
The manuscript of Ocarino et al (2006) mentions that there are few reports on hypertrophic osteopathy (HO) in cats in the literature, but it does not conclude that there are only four cases diagnosed. In the introduction of our paper, we did not try to accurately determine the number of published cases of HO in cats, although we agree it is very important. Our purpose was to present a case that was different from all the other HO cases reported in cats available in the main search websites. It may be difficult to accurately determine the number of cases of certain pathology in an animal species, with the risk of omitting a report. This happens because many journals are not available in the main search websites, such as pubmed. As Carr 1971, Richards 1977 and Nafe et al, 1981 were not mentioned by Ocarino et al, and were mentioned by Dr Foster. Furthermore, books, although classic, are not always available, which makes it difficult to cite them.
At necropsy, the animal reported by Ocarino et al (2006) did not present with extraskeletal changes. As we know HO may be associated with extraskeletal lesions (in the lungs, bladder, oesophagus, heart, adrenal among others) (Mandel 1975, Randolph et al 1984, Santos et al 1998, Becker et al 1999, Anderson et al 2004), this animal's necropsy was thorough, with a detailed macroscopic evaluation of all organs. Due to the absence of macroscopic extraskeletal lesions, we opted for a histological evaluation of organs that are more commonly affected in association with HO. Moreover, pathologies such as inflammatory and neoplastic processes, frequently diagnosed in association with HO, are characterised by clear macroscopic changes (Brodey 1971, Van de Watering et al 1972, Ndikuwere and Hill 1989, Masegi et al 1994). The absence of lesions associated with HO allows diagnosing primary or idiopathic hypertrophic osteopathy. Ocarino et al (2006) opted for the idiopathic terminology. Until then, idiopathic HO had only been reported in the human (Bhate et al 1978) and equine species (Mair et al 1996).
Regardless the study of Ocarino et al, not mentioning the exact number of HO cases in cats, there is no doubt that it differs from the others. Furthermore, Dr Foster's observations regarding HO causes in cats, reaffirms this is the first report of idiopathic HO in cats. We hope that the study of Ocarino et al (2006) is not just one more HO report but that it alerts clinicians that HO in cats may be primary. This report together with other reports on idiopathic HO in the human (Bhate et al 1978) and equine species (Mair et al 1996) show that the disease's genesis may be more complex than it was thought before.
We would like to thank Dr Foster for her observations and JFMS for the opportunity of replying.