Background Proximal sesamoid bone (PSB) fracture is the most common fatal injury in Thoroughbred (TB) racehorses in the United States. Epidemiological and pathological evidence indicates PSB fracture is likely the acute culmination of a chronic stress‐related process. However, the aetiopathogenesis of PSB fracture is poorly understood. Objective To characterise bone abnormalities that precede PSB fracture. Study design Two retrospective case‐control groups of PSBs from TB racehorses with, and without, unilateral biaxial PSB fracture. Methods Proximal sesamoid bones were harvested post‐mortem from TB racehorses subjected to euthanasia for unilateral biaxial PSB fracture (cases) or causes unrelated to PSB fracture (controls) while racing or training. The fractured medial PSB (FX‐PSB) and contralateral intact medial PSB (CLI‐PSB) from racehorses that sustained PSB fracture, and an intact medial PSB (CTRL‐PSB) from racehorses that did not have a PSB fracture were collected as case and control specimens. Study 1 distributions of morphological features were compared among case and control groups using visual examination, photographs, radiographs and histology of whole PSBs and serial sagittal sections (10 FX‐PSB, 10 CLI‐PSB and 10 CTRL‐PSB). Study 2 local bone volume fraction and mineral densities were compared among case and control PSBs using microcomputed tomography (9 FX‐PSB, 9 CLI‐PSB and 9 CTRL‐PSB). Results A focal subchondral lesion characterised by colocalised focal discoloration, radiolucency, osteopenia, low tissue mineral density and a surrounding region of dense cancellous bone was identified in most case horses but not in controls. This subchondral lesion was found in a slightly abaxial mid‐body location and was bilaterally present in most case horses. Main limitations The post‐mortem samples may not represent the spectrum of abnormalities that occur throughout the development of the subchondral lesion. Lateral PSBs were not examined, so their contribution to biaxial PSB fracture pathogenesis is unknown. Conclusion Abaxial subchondral lesions are consistent with pre‐existing injury and likely associated with PSB fracture.

Medial proximal sesamoid bones (PSBs) from Thoroughbred racehorses that did (Case) or did not (Control) experience unilateral biaxial PSB fracture were evaluated for bone volume fraction (BVF), apparent mineral density (AMD), tissue mineral density (TMD), and microdamage in Case fractured, Case contralateral limb intact, and Control bones. A majority of Case bones had a subchondral lesion with high microdamage density, and low BVF, AMD, and TMD. Lesion microdamage and densitometric measures were associated with training history by robust linear regression. Exercise intensity was negatively related to BVF (0.07 ≤ R2 ≤ 0.12) and positively related to microcrack areal density (0.21 ≤ R2 ≤ 0.29) in the lesion; however, in an undamaged site, the relationships were opposite in direction. Regardless of location, TMD decreased with event frequency for both Case and Control, suggesting increased bone remodeling with exercise. Measures of how often animals were removed from active training (layups) predicted a decrease in TMD, AMD, BVF, and microdamage at regions away from the lesion site. A steady‐state compartment model was used to organize the differences in the correlations between variables within the data set. The overall conclusions are that at the osteopenic lesion site, repair of microdamage by remodeling was not successful (e.g., lower bone mass, increased damage, and lower mineralization) but that in regions away from the lesion remodeling successfully controlled damage (e.g., higher bone mass, less microdamage, and lower mineralization).

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In clinical practice, decisions must be made about whether and how to convert to newer technologies. To address this issue, two separate studies were conducted. We evaluated the relationships between results of lumbar spine measurements using two dual photon absorptiometry (DPA1 and DPA2) instruments and one dual energy X-ray (DXA) instrument with the same subjects (49 volunteers), and also in 65 patients who were measured on the DPA1 and DXA machines. Second, we measured the lumbar spine and the proximal femur in three groups of 12 female volunteers three times on one instrument within 1 week. We purposely simulated a busy clinic setting with different technologists, older radioactive sources, and a heterogeneous patient group. The comparison study indicated a significant difference between the mean bone density values reported by the machines, but the results were highly correlated (R2 = 0.89-0.96). The short-term precision errors (coefficients of variation) differed among the instruments, ranging from 1.3% (DXA of the spine) to 5.1% (DPA1 of the spine), and in the femoral neck, 2.3% and 2.4% (DXA and DPA1, respectively) versus 3.5% by DPA2. This study emphasizes the differences between instruments, the potential for greater error in busy clinic environments, and the apparent superiority of dual energy X-ray absorptiometry under these less than ideal conditions.

Focal bone lesions are often found prior to clinically relevant stress-fractures. Lesions are characterized by low bone volume fraction, low mineral density, and high levels of microdamage and are hypothesized to develop when bone tissue cannot sufficiently respond to damaging loading. It is difficult to determine how exercise drives the formation of these lesions because bone responds to mechanical loading and repairs damage. In this study, we derive steady-state rate constants for a compartment model of bone turnover using morphometric data from fractured and non-fractured racehorse proximal sesamoid bones (PSBs) and relate rate constants to racing-speed exercise data. Fractured PSBs had a subchondral focus of bone turnover and microdamage typical of lesions that develop prior to fracture. We determined steady-state model rate constants at the lesion site and an internal region without microdamage using bone volume fraction, tissue mineral density, and microdamage area fraction measurements. The derived undamaged bone resorption rate, damage formation rate, and osteoid formation rate had significant robust regression relationships to exercise intensity (rate) variables, layup (time out of exercise), and exercise 2–10 months before death. However, the direction of these relationships varied between the damaged (lesion) and non-damaged regions, reflecting that the biological response to damaging-loading differs from the response to non-damaging loading.