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IN-DEPTH: RACING-RELATED LAMENESS


Fig. 1. Transverse cut thorough the right hind metatarsus of a 3-year-old Thoroughbred shows the original yearling shin marked by the curved arrow. The newly formed bone dorsal to the original metatarsus marked by the open arrow has been formed in response to training. Note the clearly demarcated cement line where growth stopped and bone made in response to training was re-initiated. Ideally, training would begin before growth stopped to minimize the demarcation between the bone of two different ages because this leaves an area of differing maturity, density, and stiffness of bone until the cement line is remodeled.


respond to increasing demand by becoming osteo- blasts and initiating bone formation. When not used, these cell populations atrophy.9 Therefore, it is ideal to initiate training at the end of growth before the cell populations and supporting blood supply atrophy after growth, so they can be con- verted to the tasks of bone modeling and adaptation of the skeleton to training with as little interruption in the bone formation process as possible. This is desirable because of the economy of converting the blood supply and cell populations from one job to the next without significant “retooling,” but it is also advantageous to have a homogeneous bone struc- ture without the distinct interfaces (cement lines) of markedly different ages of bone that are created when bone formation stops for a time, then is re- initiated due to changing stimuli (Fig. 1). Definitive “cement lines” are sources of stress concentration until the normal remodeling process eliminates them and homogenizes the bone cortex.10 Bone-lining cells become osteoblasts under the biomechanical stimulus that exercise creates. Os- teoblasts do not make bone directly; they make the proteinaceous precursor of bone called osteoid, which contains the collagen matrix component of bone. The osteoblast then excretes the mineral component, which forms the crystalline mineral hy-


The extreme number of cyclic loads that must be withstood by the racehorse requires localized adap- tation between bones and within the same bone to withstand these loads.5,6 The most extreme exam- ples of this occur in the dorsal cortex of the meta- carpus/metatarsus and the posterior cortex of the tibia.6 These cortical bone sites literally double or triple their cortical thickness on the heavily loaded cortex to enable the bone to withstand the cyclic loads that are produced by high-speed racing and training, but the trans cortex remains virtually un- changed (Fig. 1). There are basically two cell populations that in-


crease or decrease the size of the skeleton and re- model the skeleton to better withstand exercise: the osteocyte and the osteoclast populations.7,8 The osteocyte, which is the mature osteoblast en- cased in the bone matrix, is the permanent cell of bone. “Bone-lining cells” are the osteoblast source cells and are present within the medullary cavity and on the periosteal surface of bone. Growing bones have high populations of bone-lining cells un- til the end of growth, when the cells are no longer needed. These quiescent cells are able to quickly


droxyapatite, Ca10(PO4)6(OH)2, within the osteoid matrix to form bone. The osteoblast eventually surrounds itself and becomes entrapped by the bone it produces, becoming an osteocyte.11 Though an osteocyte is trapped within the bone, it is far from isolated from the other osteocytes and the external environment because osteocytes maintain communi- cation with other cells and the supporting blood supply by means of multiple cytoplasmic dendrites that lie within the numerous bone canaliculi.9 The dendrites interconnect with other osteocytes, with the vessels of the Haversian canal circulatory sys- tem of bone, and the periosteal surface of the bone. Osteocytes are capable of adding to or subtracting


from bone mass by adding bone or reabsorbing bone from the walls of their lacunae and canalicular spaces.3 Therefore, they can increase or decrease the density of the bone per unit of volume of bone tissue. Bone formation and dissolution must go on at low levels continuously to make calcium available to the body as needed to maintain the circulating calcium levels, should the ingested calcium be insuf- ficient to supply these needs. It can be accelerated or decelerated as needed with physiologic demands. Calcium ingested in the diet and calcium excreted in the urine are the macro-sources of calcium acquisi- tion and excretion, but the stability of the narrow physiologic range of serum calcium requires the sta- bility of the bone’s supply of calcium to fine tune systemic calcium levels. The ions in flux during the process of increasing or decreasing bone density as bone is added or subtracted from the intra-osseous canalicular spaces produce the body’s readily avail- able calcium ions.9


AAEP PROCEEDINGS  Vol. 59  2013 413


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