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Objectives: Osteoarthritis (OA) is an age-related disease that results in chronic pain and disability for millions of Veterans. The pathogenesis and progression of OA has been shown to be regulated by mechanical loading of the joint.1 In particular, we have proposed that the degeneration of articular cartilage in OA is promoted by cyclic octahedral shear stress and inhibited by cyclic hydrostatic compressive stress.2 OA can be considered as the final stage of endochondral ossification of the skeleton, and therefore has many biological processes in common with those of bone growth and development. The objective of this study is to determine if our views on the mechanobiological regulation of osteoarthritis can be extended to describe and predict the response of growth plates (physes) to variations in joint loading.
Methods: A 2D, plane stress, finite element model of a generic long bone with a growth plate was generated. Four different joint compressive loading distributions were applied and, for each case, hydrostatic and octahedral stress were determined in the growth plate. The hypertrophic region (growing region) of the growth plate consisted of the three rows of cartilage elements directly above the interface with diaphyseal bone. The growth rate in this region was calculated using an assumed biological growth rate that was modulated by the mechanobiological growth contributions of hydrostatic compression and octahedral shear stress.
Results: With no loading the bone grew at a constant biological growth rate and the growth front progressed evenly across the physis. With a moderate compressive load across joint surface, growth was promoted and the growth front progressed further than without loading. Under a severe compressive load, however, growth was inhibited and the growth front progressed less than without loading. Under a linearly increasing moderate compressive load across the joint surface, growth was promoted the most where the load was the highest. This resulted in a growth differential across the physis. The hypertrophic zone grew more on one side than on the other, and the bone began to curve. With a linearly increasing severely compressive load, growth was inhibited the most where the load was the highest and the bone curved in the other direction. These results are consistent with clinical findings of the normal and abnormal growth of bones in children.3, 4
Conclusions: We have found that the same mechanobiological principles that are associated with OA also govern the growth of the physis. These findings support the view that the endochondral ossification process, whether it is in growth and development or osteoarthritis, is promoted by octahedral shear stress and inhibited by hydrostatic compressive stress. These findings establish a mechanobiological framework for clinical treatment for the management of OA within the context of principles used for the treatment of other conditions of cartilage growth, development and degeneration.
References: 1) Carter et al. (1987) Acta Orthop Scand 58:611; 2) Carter et al. (1987) CORR 219:237; 3) Frost (1990) Anat. Record 226: 423; 4) Pauwels (1980) Biomechanics of the Locomotor Apparatus. Berlin, Springer-Verlag.
Acknowledgments: Department of Veterans Affairs Rehabilitation R&D Center (Palo Alto, CA), Stanford Graduate Fellowship to S.J.S., and National Science Foundation Fellowship to S.J.S.