In vivo matrix microdamage in a naturally occurring canine fatigue fracture.

Greyhound central tarsal bone (CTB) from animals with (n = 11) and without CTB fatigue fracture (n = 15) was examined histologically for the presence, numerical density, and morphology of in vivo microdamage. Complete fracture of the right CTB is a common occurrence during dog racing, because this is the outside limb when running counterclockwise on a circular or oval track. The CTB consisted of both remodeled cortical bone and inner trabecular bone. Thickening and coalescence of trabeculae were observed, particularly dorsally and medially, causing reduction or elimination of the marrow void spaces. A band of tightly packed transverse osteons was also observed adjacent to the concave proximal joint surface. Typical linear microcracks were most often seen in remodeled cortical and trabecular bone and were often observed adjacent to vascular channels. In contrast, ultra-microcracking, represented by diffuse staining with basic fuchsin, was consistently observed in the plantar process around the attachment site for the plantar ligament complex. Dog status (fractured or intact) and side (left or right) both had a significant effect on microcrack density and microcrack surface density (p < 0.05). Microcrack density and microcrack surface density were increased in the right (fractured) CTB from greyhounds with CTB fracture. There was also a trend for side to have a significant effect on microcrack length, with microcrack lengths being higher in the right CTB of both intact and fractured dogs. These data support the general hypothesis that fatigue fracture occurs because of ongoing cyclic stresses after induction of reparative remodeling. Development of methods for biomechanical testing of small cuboidal bones should allow investigation of relationships between accumulation of loading cycles and bone weakening because of microdamage.