Increased intracortical remodeling following fatigue damage.
We previously demonstrated that microcracks occurred in common with resorption spaces more often than expected by chance, and proposed that fatigue damage initiates remodeling events. However, it was possible that cracks accumulated at sites of preexisting resorption spaces and did not initiate new remodeling. The goal of this work was to determine whether osteonal remodeling follows the accumulation of microcracks, as expected if microcracks are responsible for initiation of bone remodeling, or if it precedes microdamage accumulation. A three-point bending load was applied to the left limb of 13 dogs for 10,000 cycles at 2 Hz with 2500 microstrain on the cranial radial surface. The right limb was loaded in the same manner eight days later, and the dogs sacrificed immediately after the second loading episode. A nonloaded groups (n = 7) was used as an external control. Radii were strained en bloc for microdamage; parameters related to bone resorption, microdamage accumulation, and the association of damage and resorption were collected. The data demonstrate a significant increase in new remodeling events subsequent to the generation of microdamage. This temporal relationship between microcracks and resorption spaces is inconsistent with the hypothesis that cracks localize at sites of preexisting resorption spaces. This demonstrates that bone remodeling occurs preferentially in fatigue-damaged regions, and supports a direct cause and effect relationship between the initiation of microdamage in bone and its repair.
Mori
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S
Department of Orthopaedic Surgery, University of the Ryukyus Hospital, Okinawa, Japan.
Burr
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DB
D000818:Animals; D016723:Bone Remodeling / Q000502:physiology*; D001862:Bone Resorption / Q000473:pathology / Q000503:physiopathology*; D004285:Dogs; D005221:Fatigue / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D011885:Radius Fractures / Q000473:pathology / Q000503:physiopathology*