Abstract: Failure of functional adaptation to protect the skeleton from damage is common and is often associated with targeted remodeling of bone microdamage. Horses provide a suitable model for studying loading-related skeletal disease because horses are physically active, their exercise is usually regulated, and adaptive failure of various skeletal sites is common. We performed a histologic study of the navicular bone of three groups of horses: (1) young racing Thoroughbreds (n = 10); (2) young unshod ponies (n = 10); and (3) older horses with navicular syndrome (n = 6). Navicular syndrome is a painful condition that is a common cause of lameness and is associated with extensive remodeling of the navicular bone; a sesamoid bone located within the hoof which articulates with the second and third phalanges dorsally. The following variables were quantified: volumetric bone mineral density; cortical thickness (Ct.Th); bone volume fraction, microcrack surface density; density of osteocytes and empty lacunae; and resorption space density. Birefringence of bone collagen was also determined using circularly polarized light microscopy and disruption of the lacunocanalicular network was examined using confocal microscopy. Remodeling of the navicular bone resulted in formation of transverse secondary osteons orientated in a lateral to medial direction; bone collagen was similarly orientated. In horses with navicular syndrome, remodeling often led to the formation of intracortical cysts and development of multiple tidemarks at the articular surface. These changes were associated with high microcrack surface density, low bone volume fraction, low density of osteocytes, and poor osteocyte connectivity. Empty lacunae were increased in Thoroughbreds. Resorption space density was not increased in horses with navicular syndrome. Taken together, these data suggest that the navicular bone may experience habitual bending across the sagittal plane. Consequences of cumulative cyclic loading in horses with navicular syndrome include arthritic degeneration of adjacent joints and adaptive failure of the navicular bone, with accumulation of microdamage and associated low bone mass, poor osteocyte connectivity, and low osteocyte density, but not formation of greater numbers of resorption spaces.
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This research explores the changes in the navicular bone of horses due to intense physical activities and presents findings about the effects of such changes to the bone structure. It studies how these changes can lead to diseases and other health issues in horses.
Objective of the Research
The primary objective of this research was to understand the failure of functional adaptation in the skeleton which is often associated with targeted remodeling of bone microdamage. This study also seeks to understand changes observed in the navicular bone of horses, specifically the effects of high-activity pursuits such as horse racing on the bone structure.
Methodology
The research utilized a histologic study of navicular bones from three groups of horses: young racing Thoroughbreds, young unshod ponies, and older horses diagnosed with navicular syndrome, a common cause of lameness due to extensive remodeling of the navicular bone.
The researchers quantified various variables such as volumetric bone mineral density; cortical thickness; bone volume fraction, microcrack surface density; density of osteocytes and empty lacunae; and resorption space density. They also examined the disruption of the lacunocanalicular network and the birefringence of bone collagen using appropriate microscopy techniques.
Observations and Findings
Remodeling of the navicular bone brought about the formation of transverse secondary osteons, and bone collagen was similarly oriented. In horses with navicular syndrome, remodeling resulted in the formation of intracortical cysts and the development of multiple tidemarks at the articular surface.
Further, these changes brought forth significant levels of microcrack surface density, a low bone volume fraction, low osteocyte density, and deteriorating osteocyte connectivity. The study also noted an increase in empty lacunae in thoroughbred horses.
The study did not find an increase in resorption space density in horses diagnosed with navicular syndrome. This could mean that while the disease may affect bone density and structure, it may not necessarily lead to bone loss.
Conclusion
Based on their findings, the researchers suggest that the navicular bone may experience habitual bending across the sagittal plane due to the high physical activity involved in horse racing.
This kind of cumulative cyclic loading can lead to arthritic degeneration of nearby joints and the adaptive failure of the navicular bone. There is also a corresponding increase in microdamage, low bone mass, poor osteocyte connectivity, and a drop in osteocyte density; nonetheless, there is no creation of a higher number of resorption spaces.
Cite This Article
APA
Bentley VA, Sample SJ, Livesey MA, Scollay MC, Radtke CL, Frank JD, Kalscheur VL, Muir P.
(2007).
Morphologic changes associated with functional adaptation of the navicular bone of horses.
J Anat, 211(5), 662-672.
https://doi.org/10.1111/j.1469-7580.2007.00800.x
Comparative Orthopaedic Research Laboratory, School of Veterinary Medicine, University of Wisconsin--Madison, Madison, WI 53706, USA.
Sample, S J
Livesey, M A
Scollay, M C
Radtke, C L
Frank, J D
Kalscheur, V L
Muir, P
MeSH Terms
Animals
Bone Density
Bone Diseases / pathology
Bone Diseases / physiopathology
Bone Remodeling
Breeding
Horse Diseases / pathology
Horse Diseases / physiopathology
Horses
Microscopy, Confocal
Microscopy, Fluorescence
Osteocytes / cytology
Osteocytes / pathology
Physical Conditioning, Animal
Tarsal Bones / anatomy & histology
Tarsal Bones / pathology
Tarsal Bones / physiopathology
Tarsus, Animal / anatomy & histology
Weight-Bearing
References
This article includes 30 references
Bentolila V, Boyce TM, Fyhrie DP, Drumb R, Skerry TM, Schaffler MB. Intracortical remodeling in adult rat long bones after fatigue loading.. Bone 1998 Sep;23(3):275-81.
Burr DB, Forwood MR, Fyhrie DP, Martin RB, Schaffler MB, Turner CH. Bone microdamage and skeletal fragility in osteoporotic and stress fractures.. J Bone Miner Res 1997 Jan;12(1):6-15.
Burr DB, Hooser M. Alterations to the en bloc basic fuchsin staining protocol for the demonstration of microdamage produced in vivo.. Bone 1995 Oct;17(4):431-3.
Burr DB, Stafford T. Validity of the bulk-staining technique to separate artifactual from in vivo bone microdamage.. Clin Orthop Relat Res 1990 Nov;(260):305-8.
Colopy SA, Benz-Dean J, Barrett JG, Sample SJ, Lu Y, Danova NA, Kalscheur VL, Vanderby R Jr, Markel MD, Muir P. Response of the osteocyte syncytium adjacent to and distant from linear microcracks during adaptation to cyclic fatigue loading.. Bone 2004 Oct;35(4):881-91.
Mullender MG, Tan SD, Vico L, Alexandre C, Klein-Nulend J. Differences in osteocyte density and bone histomorphometry between men and women and between healthy and osteoporotic subjects.. Calcif Tissue Int 2005 Nov;77(5):291-6.
Noble BS, Peet N, Stevens HY, Brabbs A, Mosley JR, Reilly GC, Reeve J, Skerry TM, Lanyon LE. Mechanical loading: biphasic osteocyte survival and targeting of osteoclasts for bone destruction in rat cortical bone.. Am J Physiol Cell Physiol 2003 Apr;284(4):C934-43.
Ogino S, Sasho T, Suzuki M. Origin of osteoarthritic knee pain: immunohistochemical analysis of subchondral bone – second report. Trans Orthop Res Soc 2007;53:0134.
Shibakawa A, Yudoh K, Masuko-Hongo K, Kato T, Nishioka K, Nakamura H. The role of subchondral bone resorption pits in osteoarthritis: MMP production by cells derived from bone marrow.. Osteoarthritis Cartilage 2005 Aug;13(8):679-87.
Tomlin JL, Lawes TJ, Blunn GW, Goodship AE, Muir P. Fractographic examination of racing greyhound central (navicular) tarsal bone failure surfaces using scanning electron microscopy.. Calcif Tissue Int 2000 Sep;67(3):260-6.
Vashishth D, Verborgt O, Divine G, Schaffler MB, Fyhrie DP. Decline in osteocyte lacunar density in human cortical bone is associated with accumulation of microcracks with age.. Bone 2000 Apr;26(4):375-80.
Verborgt O, Gibson GJ, Schaffler MB. Loss of osteocyte integrity in association with microdamage and bone remodeling after fatigue in vivo.. J Bone Miner Res 2000 Jan;15(1):60-7.
Barbe MF, Jain NX, Massicotte VS, Popoff SN, Barr-Gillespie AE. Ergonomic task reduction prevents bone osteopenia in a rat model of upper extremity overuse. Ind Health 2015;53(3):206-21.
Jain NX, Barr-Gillespie AE, Clark BD, Kietrys DM, Wade CK, Litvin J, Popoff SN, Barbe MF. Bone loss from high repetitive high force loading is prevented by ibuprofen treatment. J Musculoskelet Neuronal Interact 2014 Mar;14(1):78-94.
Barbe MF, Gallagher S, Massicotte VS, Tytell M, Popoff SN, Barr-Gillespie AE. The interaction of force and repetition on musculoskeletal and neural tissue responses and sensorimotor behavior in a rat model of work-related musculoskeletal disorders. BMC Musculoskelet Disord 2013 Oct 25;14:303.