Osteoarthritis as a complication of artificial environment: the Cavia (guinea pig) story
- Arthritis Center of Northeast Ohio, Youngstown, OH 44512; Department of Medicine, Northeastern Ohio Universities College of Medicine, Rootstown, OH 44272; Department of Biomedical Engineering, University of Akron, Akron, OH 44242; The Carnegie Museum of Natural History, Pittsburgh, PA 15213; and University of Kansas Museum of Natural History, Lawrence, KS 66045
- Correspondence to:
Professor B M Rothschild, Arthritis Center of Northeast Ohio, 5701 Market Street, Ohio 44512, USA
- Accepted 12 March 2003
Osteoarthritis (OA) has been variously described as a phenomenon of aging or a mechanically derived process,1–3 perhaps a simplification. Animals caught in the wild seldom (about 1%) have any evidence of OA, in contrast with captured animals (be they colony or cage raised).4–6 Removal of an animal from its natural habitat is associated with a 10-fold increase in the prevalence of OA, whether the animals were zoo or colony raised.4–6 This is clearly not a simple issue of lifespan, as the distribution of affected joints (for example, knee, shoulder), is different in wild-caught and captive samples.4–6
It has been suggested that Cavia, the guinea pig, is a possible exception.7–9 Analysis in those studies was based on captive guinea pigs. The contribution of an artificial environment to the propensity to develop OA was therefore explored by examination of wild-caught and captive Cavia skeletal collections for evidence of OA.
The skeletons of captive and wild-caught Cavia (guinea pigs) were examined macroscopically in the collections of the museums and universities of North America: American Museum of Natural History (AMNH), New York City; Cornell University (CU), Ithaca, NY; Field Museum of Natural History (FMNH), Chicago, IL; Kansas University Museum of Natural History (KU), Lawrence; McClung Museum, University of Tennessee (MMNH), Knoxville; Michigan State University (MSU), East Lansing; Museum of Comparative Zoology, Harvard University (MCZ), Boston, MA; National Museum of Natural History (NMNH), Washington, DC; Southern Methodist University (SMU), Dallas, TX; University of Colorado Museum (OS), Boulder; San Noble Oklahoma Museum of Natural History (OMNH), Norman; University of New Mexico, Albuquerque (MSB) and University of Wisconsin Zoological Museum (UWZM), Madison, WI. OA was defined by the presence of distal femoral, proximal tibial, and patellar osteophytes.10 Captive versus wild-caught status and sex were obtained from the museum/university specimen acquisition records. χ2 and Fisher exact tests were used to determine the statistical significance of differences in the prevalence of OA.
There was no evidence of osteophytes in any of 74 Cavia (guinea pigs) caught in the wild from Bolivia, Brazil, Uruguay, Paraguay, Argentina, or Venezuela. Tibial osteophytes were found in 41/44 captive specimens (fig 1), independent of cage or colony status. This difference in prevalence of OA was highly significant (χ2=71.83; p<0.00001; Fisher exact test p<00001). Sex ratios were 1:1 in both wild-caught and captive specimens.
OA in Cavia (guinea pigs) was limited to captive animals. Animals caught in the wild were free of OA. The perspective that OA is common in guinea pigs7–9 seems derived from the artificial housing/testing environment of the test subjects, rather than any inherent susceptibility of the species. As the prevalence in captive animals was independent of cage or colony (for example, zoo) status, and zoos have been quite attentive to natural diet, maintaining nutritional balance and assuring appropriate exercise levels, there is little evidence that the propensity to OA could alternatively be blamed on diet, weight, or activity. The similar prevalence of OA in caged and colony raised animals indicates that this is not simply a “cage phenomenon”, but rather a consequence of captivity habitats. Previous genetic attributions in captive guinea pigs7–9 are intriguing. Assessment of significant genetic differences between wild-caught and captive guinea pigs is necessary. It seems imperative to determine whether the same loci are present in animals caught in the wild, which do not develop OA, as are found in captive guinea pigs, or whether the latter have different loci owing to artificial environmental factors.
This study confirms previous perspectives4–6 that OA is essentially a disease of an artificial environment. As human habitation has removed itself so far from the natural environment, it is perhaps not surprising that OA has become a common problem in humans today.