Abstract: Functional adaptation of bone normally protects the skeleton from fracture during daily activity. Accumulation of microcracking and loss of osteocytes have been implicated in the regulation and initiation of targeted (reparative) remodeling of bone and, in certain situations, the development of fatigue or stress fracture. We performed a histologic study of the dorsal cortex of the mid-diaphysis of the third metacarpal (Mc-III) bone of Thoroughbred racehorses after bones were bulk-stained in basic fuchsin and transverse calcified sections were prepared. The Thoroughbred racehorse is an extreme athlete whose Mc-III bone experiences particularly high cyclic strains during training and racing. A group of non-athletic horses was also included in the experiment. The following variables were quantified: activation frequency (Ac.f); bone formation rate (BFR); resorption space density (Rs.N/T.Ar); microcrack density (Cr.Dn); microcrack mean length (Cr.Le); microcrack surface density (Cr.S.Dn); osteocyte density (Ot.N/T.Ar; Ot.N/B.Ar); and bone volume fraction (B.Ar/T.Ar). Ac.f and BFR were estimated using a mathematical algorithm. Using confocal microscopy, bones were examined for fine microcracks, diffuse matrix injury, and disruption of the osteocyte syncytium. Low values for Cr.Dn (#/mm2) were found in both groups (0.022+/-0.008 and 0.013+/-0.006 for racing Thoroughbreds and non-athletic horses, respectively). There was no significant relationship between Cr.Dn and Ot.N/T.Ar; Ot.N/B.Ar, B.Ar/T.Ar, and Ot.N/T.Ar; Ot.N/B.Ar, and remodeling (Ac.f, Rs.N/T.Ar) and Ot.N/T.Ar; Ot.N/B.Ar. Intense remodeling of the Mc-III dorsal cortex was found in the racing Thoroughbreds (Ac.f 12.8+/-7.4 #/mm2/year; BFR 31.5+/-15.6%; Rs.N/T.Ar 0.19+/-0.09 #/mm2) and was significantly increased compared with non-athletic horses. Overall, remodeling was weakly correlated with Cr.Dn (r2=0.15, P<0.05). Subtle matrix injury, not detectable by bright-field microscopy, was particularly evident adjacent to resorption spaces in Thoroughbred bone. In non-athletic horses, disruption of the dendritic cell processes of osteocytes associated with cement lines and interstitial fragments was more evident. Taken together, these findings suggest that site-specific (targeted) induction of remodeling during functional adaptation of bone in a high-strain skeletal site is not dependent on accumulation of microcracking or loss of osteocytes. We hypothesize that athleticism can directly influence bone turnover in this extreme athlete through pathways that do not involve classical linear microcracks.
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The study investigates the ability of bone to adapt and repair itself under stress, particularly focusing on racehorses who experience high strain on their bones during training and racing. The results suggest that stress-induced bone remodeling and repair do not necessarily depend on accumulated microcracking or loss of osteocytes, suggesting alternate pathways for bone repair in highly athletic organisms.
Research Method
The researchers conducted a histological study of the dorsal cortex in a specific part (mid-diaphysis) of the third metacarpal bone in Thoroughbred racehorses. This bone tends to experience high stress during training and racing.
The bones were stained and sectioned, and variables related to bone health and stability were quantified. These variables include activation frequency, bone formation rate, resorption space density, microcrack density, osteocyte density, and bone volume fraction.
The study also included a group of non-athletic horses for comparison.
Confocal microscopy was used to examine fine microcracks, diffuse matrix injury, and disruption of the osteocyte syncytium.
Findings
The study found low levels of microcrack density in both groups of horses. There was no significant relationship found between microcrack density and several measured variables, including osteocyte and bone volume fraction, or between microcrack density and remodeling activity.
Intense remodeling of the dorsal cortex was observed in the racing Thoroughbreds, which was significantly increased when compared with non-athletic horses.
Remodeling was weakly correlated with microcrack density.
In Thoroughbred horses, subtle matrix injury adjacent to resorption spaces was observed, while disruption of osteocyte processes was more evident in non-athletic horses.
Conclusion
The research suggests that site-specific bone remodeling in response to functional adaptation at high-strain skeletal sites is not dependent on the accumulation of microcracks or the loss of osteocytes. This suggests other pathways might be responsible for stress-induced bone repair and remodeling.
Overall, this research suggests that athleticism might directly influence bone turnover in athletes via pathways that do not involve accumulation of classical linear microcracks.
Cite This Article
APA
Da Costa Gómez TM, Barrett JG, Sample SJ, Radtke CL, Kalscheur VL, Lu Y, Markel MD, Santschi EM, Scollay MC, Muir P.
(2005).
Up-regulation of site-specific remodeling without accumulation of microcracking and loss of osteocytes.
Bone, 37(1), 16-24.
https://doi.org/10.1016/j.bone.2004.12.016
Comparative Orthopaedic Research Laboratory, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA.
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