Relationship between articular cartilage damage and subchondral bone properties and meniscal ossification in the Dunkin Hartley guinea pig model of osteoarthritis

Abstract

Objectives: To describe the age-related changes of articular cartilage, subchondral bone morphology, and stiffness. Furthermore, to investigate whether subchondral bone histological and mechanical properties and meniscal histological properties are related to articular cartilage damage in the Dunkin Hartley guinea pig model of osteoarthritis (OA).

Methods: Forty male Dunkin Hartley guinea pigs aged 2, 6, 9, and 12 months were studied. The right stifle joints and the left menisci were embedded undecalcified and the tibial articular cartilage and subchondral bone and the menisci were examined using histology. The stiffness of the left tibial subchondral bone was determined with indentation testing.

Results: The Osteoarthritis Research Society International (OARSI) grade of the osteoarthritic cartilage lesions of the medial (p < 0.001) and lateral (p < 0.001) condyle and the ossification of the medial (p < 0.001) and lateral (p < 0.001) meniscus increased significantly with age and was significantly more pronounced at the medial condyle than at the lateral condyle. The grade of the osteoarthritic cartilage lesions was significantly correlated (r  =  0.78, p < 0.001) with the meniscal ossification, weakly correlated (r  =  0.34, p < 0.007) with the subchondral bone plate thickness, and not correlated with the subchondral bone density (r  =  −0.010, p  =  0.94) and the subchondral bone stiffness (r  =  −0.13, p  =  0.30).

Conclusion: The meniscal ossification observed in Dunkin Hartley guinea pigs may play an important role in the pathogenesis of OA in these animals.

Acknowledgements

We are grateful for the excellent technical assistance of Jytte Utoft, Institute of Anatomy, University of Aarhus. Heidi Meldgaard Jensen and Henriette Mikkelsen, Institute of Anatomy, University of Aarhus, are thanked for their help with handling the animals. Merete Fischer, Institute of Anatomy, University of Aarhus is thanked for linguistic revisions of the manuscript. This work was kindly supported by the Danish Rheumatism Association (233-1210-26.09.05); the Michaelsen Foundation; the Novo Nordisk Foundation; Aarhus University Research Foundation; The Foundation for Promotion of Medical Science; Helga and Peter Korning's Foundation; and Kong Christian den X's Foundation.