IN-DEPTH: RACING-RELATED LAMENESS


new bone containing living osteocytes. This raises the question of whether the mechanism of stimulat- ing remodeling is actually the loss of the inhibition of the BRU that a living osteocyte may produce. Training is the next most powerful stimulus for


bone modeling and remodeling. Exercise trumps all hormonal and metabolic stimuli for bone remod- eling, and its effect on bone lasts for years.6,17 The micro-damage, stimulated by exercise, causes over- compensation by the bone through the modeling and remodeling process, strengthening the bone mass and changing its shape to prevent the micro-damage from occurring in subsequent exercise sessions. If the exercise is then increased, the bone is over- loaded again and over-repairs again, further strengthening and modeling the bone to neutralize the load. This stepwise stimulus of hypertrophy by “overload” then “over-repair” is the basis for training in all tissues. The bone’s ability to respond to training is, how-


ever, not an unlimited resource. There is a maxi- mum rate of response that the bone can generate. It takes time for the osteocytes to increase the den- sity of the existing bone and for the osteoblasts to change the size of the bone. The “art” of training is to use the hypertrophy response to produce a con- tinually stronger athlete, without progressing too rapidly for the bone to adapt, causing injury. The question is often posed “Why is the horse so


prone to injury and lameness?” The answer is not so much that the bone is weak but that the other sys- tems are so strong. The heart and circulatory sys- tem are so highly developed that they can adapt rapidly to nearly any level of sequentially increasing exercise that they encounter. Bone is more limited.18 Overload in excess of repair results in structural damage, injury, and eventually, pain.10 Pain is demonstrated as lameness. Lameness is the shift- ing of weight from one limb to another to avoid loading of the painful limb. This makes the horse asymmetric and then often precipitates a secondary additional lameness. Few horses performing at high levels are compromised by a single minor lame- ness. It is often the second or the third painful area that creates the decline in form. A horse will pro- tect and demonstrate lameness on the most painful limb until that pain is relieved by treatment or diagnostic anesthesia. The horse will then protect the next most painful site. Progressive elimination of one lameness at a time until the horse is sound is the best way to determine all of the sites of pain. It is often not the most painful lameness that is the original and therefore most important lameness site. Treatment of the secondary lameness alone is prone to failure because the inciting lameness is still present and the secondary lameness will re-occur. The key or underlying lameness must be identified and treated as well if the horse is to regain sound- ness. This is the “art” of lameness treatment that must be combined with the “science” of understand-


ing the mechanism of pain in bone and how the primary problem can be treated without endanger- ing the horse or its performance capabilities over the long term. Lameness is a sign of a problem, not the problem itself. This concept is difficult for some owners and trainers to grasp. Pain in bone and the resultant lameness is a sign


of damage and results from instability, hyperten- sion, or invasion of sensitive structures such as the periosteum, ligaments, or joints by the structural damage. Pain results in lameness, therefore lame- ness must be properly regarded as a sign of a prob- lem, not the problem itself, to correctly interpret and treat it. Veterinarians should be well equipped to help the client with the understanding and inter- preting of this normal response to training. Trainers often regard lameness as “the problem”


rather than a sign of a problem. This understand- ing is difficult for some and should be the purview of the veterinarian to understand the cause and treat the cause rather than only the symptom of the prob- lem. Treatment of the symptom rather than the cause is often only temporarily effective, often dam- aging in the long term, and can be dangerous if pain indicating progressive structural damage is elimi- nated without regard to its cause. What causes lameness in the racehorse? The most common causes are cyclic loading, load accumula- tion, plastic deformation, and structural damage to the bone.10,19 Joint inflammation and overload of tendons and ligaments is frequently a secondary sequela.20 Bone is very good at adapting to gradual changes


in loading levels or loading types, but this adapta- tion is work-specific and dictated by the biomechani- cal load the bone receives. Julius Wolff described this a century ago, and the adaptation of bone to specific needs has come to be known as “Wolff’s Law,” which states “bone is laid down where strength is needed and removed where strength is unnecessary.”13 Few animals carry this to the ex- treme of the training horse. The overload/over-re- pair cycle literally molds the racehorse skeleton (Fig. 1). The bone can take two actions when faced with


the increased need for strength dictated by exercise. It can change the material make-up of the existing bone volume, or it can change the size and shape of the bone to better resist the loads. Changing the material make-up occurs by adding bone mass per unit bone; filling in trabecular, canalicular, and la- cunar space with more osteoid and hydroxyapatite to increase density increases the amount of osseous mass in the same volume of bone. Bone can also change its shape to neutralize the applied stress by adding bone as occurs in the dorsal cortex of the metacarpus/metatarsus and the caudal tibia.18 With the use of the same amount of material, chang- ing the shape of a material from a rod to the cylinder doubles the strength of the structure in resistance to


AAEP PROCEEDINGS  Vol. 59  2013 415


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