Know Your Pathology: Avian Osteopetrosis

Avian osteopetrosis is an infection that can reach epidemic proportions. Caused by the action of the avian leucosis virus group, which belongs to the family Retroviridae, that stimulates the proliferation of osteoblasts in chickens, this leaves characteristic evidence on the skeleton (Brothwell, 1993: 41) that is visible macroscopically to the archaeozoologist, such as thickening of the metatarsals, symmetrical thickening of the long bones, and changes in other parts of the skeleton which are similar but not as pronounced (Biltz and Pellegrino, 1965: 1365). This proliferative growth of immature bone fails to become fully mineralised even after the growth of new bone subsides and a new phase of osteogenesis becomes evident (Biltz and Pellegrino, 1965: 1376).

Chemical and histological analysis of avian osteopetrotic bone from modern chickens has shown the disease to be characterised by (Biltz and Pellegrino, 1965: 1374-1375):

  1. An increase in total bone mass caused by overproduction of bone and resulting in hypermineralisation;
  2. Decreased hydrated-bone density reflecting an increase in water content and an increase in vascularity or porosity;
  3. A decrease in the apparent densities of dry bone, mineral, and organic fractions;
  4. A decrease in the degree of mineralisation or dry-bone density

Avian osteopetrosis has many similarities with human osteopetrosis and infantile cortical hyperostosis, all manifesting distinctive histological features and presenting similar appearances in x-rays. Chemical evidence of disturbance of maturation in avian osteopetrotic bone also accords well with histological evidence of a similar defect in humans with the condition (Biltz and Pellegrino, 1965: 1375). The study of avian osteopetrosis, therefore, presents an opportunity to not only study such a condition in chickens, but may also be helpful in understanding the disorder in other species (Biltz and Pellegrino, 1965: 1375). Besides humans and birds, the condition has been described in an inbred herd of rabbits, where the condition was caused by an inherited lethal factor that was present at birth (Marks et al., 1986), as well as cattle and rodents (Smith and Ivanyi, 1980: 523), and dinosaurs (Campbell, 1966).

However, whilst human osteopetrosis (Albers-Schonberg disease) and avian osteopetrosis appear to have some common characteristics, it has been argued by some authors (Simpson and Sanger, 1968: 278-279) that the two are fundamentally different. In humans, the disease is hereditary, whilst the avian disease is caused by a virus. In humans, the problem is a failure to remove the primary spongiosa underneath the epiphyseal plate and there is no excess proliferation of periosteal bone. It has therefore been suggested that the disease in humans results from an imbalance between the formative and resorptive mechanisms.

A crude attempt to construct the historical geography of avian osteopetrosis (Brothwell, 2002: Fig. 2) demonstrates, albeit tentatively, that the leucosis virus was established in some chicken flocks in South East England by Roman times, and there is growing evidence for osteopetrosis by the post-Roman period, possibly over a wider area. There are potential sources of the infection in other parts of the Roman Empire as the condition has been identified at the Roman castellum at Velsen in the Netherlands (Prummel, 1987) and in the Lower City at Troia (Fabis, 1997).

Whilst currently infrequently reported in archaeological material, this may be due to either small sample size or a failure to recognise the early stages of the condition. The variable incidence of whole or complete chicken bones in the archaeological record also makes it difficult to determine the prevalence in Gallus populations. However, as the virus causes bone changes in only a small proportion of infected birds, even one incidence of pathology may indicate a notable infection within the flock (Brothwell, 2002: 318). It can, therefore, provide evidence for the conditions in which the stock were kept.

References:

Biltz, R. M. and Pellegrino, E. D. 1965. Avian osteoporotic bone: A correlation of its chemical composition with its roentgenographic and histological appearance. Journal of Bone and Joint Surgery 47-A (7): 1365-1377.

Brothwell, D. 1993. Avian osteopathology and its evaluation. Archaeofauna 2: 33-43.

Brothwell, D. 2002. Ancient avian osteopetrosis: the current state of knowledge. Proceedings of the 4th Meeting of the ICAZ Bird Working Group Kraków, Poland, 11-15 September 2001. Acta zoologica cracoviensia 45 (special issue): 315-318.

Campbell, J. G. A dinosaur bone lesion resembling avian osteopetrosis and some remarks on the mode of development of the lesions. Journal of the Royal Microscopical Society 85 (2): 163-174

Fabis, M. 1997. A case of infectious disease among domestic fowls of Troia IX. Sonderdruck aus Studia Troia Band 7. Verlag Philipp von Zabern: Mainz an Rhein.

Marks, S. C., Seifert, M. M. F., and Fox, R. R. 1986. The osteopetrotic rabbit: general and skeletal features of a new outbred stock. Bone 7: 359-364

Prummel, W. 1987. Poultry and fowling at the Roman castellum Velsen. Palaeohistoria 29: 183-201

Simpson, C. F. and Sanger, V. L. 1968. A review of avian osteopetrosis: comparisons with other bone diseases. Clinical Orthopaedics 58: 271-281

Smith, R. E. and Ivanyi, J. 1980. Pathogenesis of virus-induced osteopetrosis in the chicken. Journal of Immunology 125 (2): 523-530.

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One response to “Know Your Pathology: Avian Osteopetrosis

  1. Pingback: Life before death :: Tangled Bank #94 :: December :: 2007

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