A hypothetical mechanism for the stimulation of osteonal remodelling by fatigue damage.

This paper presents a theory describing mechanisms by which repetitive stress initiates remodelling in compact bone. The theory is based on the observation that the lamellar structure of osteons arrests and traps microcracks produced by cyclic loading. Debonding of an osteon by a crack may produce changes in the Haversian canal wall adjacent to the crack which initiate a new secondary osteon. The repair of damaged areas by secondary osteons prevents the accumulation of microdamage due to repetitive loading and protects compact bone from fatigue failure.