Abstract

Dental disease due to osteoclast over‐activity reaches epidemic proportions in older domestic cats and has also been reported in wild cats. Feline osteoclastic resorptive lesions (FORL) involve extensive resorption of the tooth leaving it liable to root fracture and subsequent tooth loss. The aetio‐pathogenesis of FORL is not known. Recent work has shown that systemic acidosis causes increased osteoclast activation and that loci of infection or inflammation in cat mouth are likely to be acidotic. To investigate this, we generated osteoclasts from cat blood and found that they formed in large numbers (∼400) in cultures on bovine cortical bone slices. Acidosis caused an increase in the size of cells—in cultures maintained up to 14 days at basal pH 7.25, mean osteoclast area was 0.01 ± 0.003 mm2, whereas an 8.6‐fold increase was observed in cells cultured between 11 and 14 days at pH 7.15 (0.086 ± 0.004 mm2). Acidosis caused a modest increase in the number of osteoclasts. Exposure to pH 6.92 exhibited a 5‐fold increase in the area of bone slices covered by resorption lacunae (∼70% bone slice resorbed). In line with this finding, significant increases were observed in the expression of cathepsin K and proton pump enzymes (both approximately 3‐fold) that are key enzymes reflective of resorptive activity in osteoclasts. These results demonstrate that acidosis is a major regulator of osteoclast formation and functional activation in the cat, and suggest that local pH changes may play a significant role in the pathogenesis of FORL. J. Cell. Physiol. 213: 144–150, 2007. © 2007 Wiley‐Liss, Inc.

Highlights

  • The consensus is that Feline osteoclastic resorptive lesions (FORL) is not related to caries lesions or to periodontal diseases

  • We examined the effect of altering pH on the in vitro development and resorptive activity of feline osteoclasts and found that large numbers of osteoclasts of great size developed from peripheral blood monocytes under acidic culture conditions and that these were highly active in in vitro bone resorption

  • Peripheral blood mononuclear cells (PBMCs) were cultured with Macrophage Colony Stimulating Factor (M-CSF) (25 ng/ml) and Receptor Activator of NFkB Ligand (RANKL) (30 ng/ml) and examined over a 14 day culture period

Read more

Summary

Introduction

The consensus is that FORL is not related to caries lesions or to periodontal diseases. Many factors have been implicated, such as dietary texture, mechanical stress, dietary deficiencies, excessive vitamin A intake, periodontal disease, developmental tooth defects, breeding, and local and systematic viral disease (e.g. FCV, feline calicivirus; FcoV, feline coronavirus; FeLV, feline leukemiavirus; FHV, feline herpesvirus; FPV, feline parvovirus) (Reiter and Mendoza, 2002, for review) None of these have been definitively proven to be the direct cause of tooth resorption; compared with other species, little is known about the biology. We examined the effect of altering pH on the in vitro development and resorptive activity of feline osteoclasts and found that large numbers of osteoclasts of great size developed from peripheral blood monocytes under acidic culture conditions and that these were highly active in in vitro bone resorption We conclude that these innate characteristics could account for the pathology of FORL in the absence of other causative factors, and for the apparent rarity of this disease in other species such as humans

Methods
Results
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.