Stress Fracture and Functional Bone Adapation

Stress or fatigue fractures are a common problem affecting running athletes.  In racing Greyhounds and racing Thoroughbreds, stress fractures occur at high strain sites in the skeleton, are typically site-specific, and arise in heavily adapted bone.  Repetitive loading of bone induces accumulation and coalescence of fine linear microcracks in compact bone.  Functional adaptation to this type of loading includes a modeling response, principally through periosteal new bone formation, and site-specific remodeling which is targeted to the removal of microcracks.  Although the pathogenesis of stress fracture is not fully understood, development of such a fracture likely represents a failure of functional adaptation.  Importantly, osteoporotic fractures likely arise by a similar imbalance between induction and repair of skeletal microdamage.

Our long-term goal is to obtain a fundamental understanding of the mechanisms that regulate functional adaptation of bone.  Functional adaptation of bone is thought to be a local mechanically regulated maintenance and repair mechanism sustained by living cells that minimizes fracture risk and bone mass.  Our research has confirmed that central tarsal bone fractures in racing greyhounds and condylar fractures in racing Thoroughbreds are stress fractures.  In Thoroughbreds, condylar fractures arise from microcracking of the joint surface of the distal end of the cannon bone.  Microcrack initiation is site-specific within the condylar grooves of the fetlock joint and is associated with progressive endochondral ossification of the joint surface of the distal end of the cannon bone.  These changes in the subchondral plate likely represent adaptive responses to racing and training; microcracking is likely a consequence of joint overload.  Our research has also shown that functional adaptation is likely regulated, at least in part, by a neuronal mechanism, which may enable cross-talk between different bones of the skeleton.  With further understanding of the regulatory pathways that control skeletal adaptation, there is the promise that the adverse affects on the skeleton of common pathological bone diseases, such as stress fracture and osteoporosis, can be more effectively inhibited or prevented.

Figure .  Photograph of an oblique frontal calcified bone section through the palmar distal region of the distal end of a Mc-III bone, from a 3-year-old Thoroughbred gelding.  Regions-of-interest across the joint surface were:  (1) Lateral condyle; (2) Lateral condylar groove; (3) Sagittal ridge; (4) Medial condylar groove; (5) Medial condyle.  These regions were established by identifying the point that was equidistant from the tip of the sagittal ridge and the bottom of the condylar groove as the interface between the condylar groove and sagittal ridge regions.  The same distance abaxial from the bottom of the condylar groove determined the interface between the condylar groove and the condyle regions.  Sclerosis of the subchondral bone can also be seen, which is centered on the axial part of the lateral and medial condyles (black arrowheads).  Bulk-stain with basic fuchsin, bar = 10 mm.  The hyaline articular cartilage has been removed by digestion with 0.1M NaOH.		Figure.  Photomicrograph of an oblique frontal calcified bone section through the palmar distal condylar groove region of the distal end of a Mc-III bone from a 5-year-old Thoroughbred stallion.  Multiple stained microcracks can be seen within the calcified cartilage in the medial condylar groove region (white arrowheads).  Microcracking is co-localized with in-growth of blood vessels from the subchondral plate into the calcified cartilage.  Resorption spaces were often co-localized with microcracks that penetrate into subchondral bone (white arrows).  Short microcracks can also be seen within the calcified cartilage layer in this lateral condylar groove region.  Bulk-stain with basic fuchsin, bar = 200mm.  The hyaline articular cartilage has been removed by digestion with 0.1M NaOH.