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548   Chapter 4


            fractures that are not treated surgically. Most of these   (2‐ and 3‐year‐old) racehorses and discovered that many
            joints develop significant OA and restricted range of   horses have increased size and number of vascular chan-
  VetBooks.ir  nosis is poor due to the loss of suspensory support and   more than two irregular vascular channels had a
                                                               nels without lameness.
                                                                                       Yearling Thoroughbreds with
            joint motion. If both sesamoids are fractured, the prog-
                                                                                   37,38
                                                               decrease in number of race starts and earnings at 2 and
            only should be considered for salvage of valuable breed-
            ing stock or in horses of great sentimental value.  3 years of age.  This supports the idea that remodeling
                                                                            85
                                                               is a normal response to training and that only if the
            SESAMOIDITIS                                       stresses  exceed, the  bones’  capability  to  strengthen
                                                               would microfracture and bone damage occur. Although
              Sesamoiditis is observed frequently in racing horses   radiographic vascular changes of bone remodeling were
            and hunters and jumpers between 2 and 5 years of   not  associated  with  sesamoid  fracture,  the  vascular
            age. 60–62,89  The condition is characterized by pain associ-  structures course along known lines of fracture in adult
            ated with the proximal sesamoid bones and insertions of   racehorses. The sesamoid bones have an extensive sen-
            the SL that result in lameness. The pain is thought to   sory nerve supply that may explain bone pain associated
            result from inflammation at the interface of the SL with   with trabecular bone injury. 26,27  Concurrent suspensory
            the proximal sesamoid bones. 62,89  Concurrent SL branch   branch injury may also contribute to the palpable pain
            disease should be suspected in these horses. A significant   and lameness in affected horses. 34,58,71
            relationship between the presence of sesamoiditis and
            the subsequent development of SL injuries has been doc-  Clinical Signs
                    71
            umented.  Evidence of sesamoiditis suggests a 5 times
            greater risk for developing injuries to the SL branch   Symptoms of this condition are similar to those
            with the onset of training.  Pain, heat, and inflamma-  caused by fracture of the sesamoid bone. In the early
                                   58
            tion can usually be clinically detected at the insertion of   stage, minimal swelling is observed, but increased heat
            the SL during the active stages of the disease process, but   may be felt over the abaxial surface of the sesamoid
            marked  lameness  and  limitations  on  performance  can   bone(s). As the disease progresses, visible enlargement of
            also occur without any clinically detectable signs. 22,37  the soft tissues overlying the palmar/plantar surface of
              Radiographs can  reveal a range of  changes from   the fetlock can be seen as fibrosis of/around the injured
            accelerated early remodeling response in the bones   SL becomes apparent. On palpation, pain withdrawal
            (increased size and number of vascular canals) to marked   can usually be elicited by placing pressure over the
            proliferation of bone along the abaxial margin of the   abaxial surface of the sesamoid bones. In more advanced
            sesamoid and increased bone density of the sesamoid.   cases, pain may be elicited by applying pressure over the
            The SL and the DSLs may also be affected and show   branches of the SL. The horse will also likely be positive
            calcified areas. The increased bone production is thought   to distal limb flexion.
            to result from inflammation from tearing of the attach-  At exercise, the lameness varies considerably and
            ments of either the SL or the DSLs. Young Thoroughbreds   depends on the acuteness of the injury and its degree. In
            with more severe radiographic signs of sesamoiditis are   general, the lameness is most evident during the first
            thought to be at increased risk to develop future suspen-  part of exercise and is more exaggerated when the horse
            sory branch injuries.  However, it is also possible to see   is exercised on hard surfaces. Perineural and/or intra-
                             58
            radiographic changes indicating chronic sesamoiditis in   synovial anesthesia is used infrequently to diagnose this
            sound performing horses, suggesting that some horses   condition.  Horses  respond  to  a  low  four‐point  nerve
            heal the injury and regain suspensory strength. 37  block, but not to an intra‐articular fetlock block, locat-
                                                               ing the lameness to the periarticular structures.
            Etiology
                                                               Diagnosis
              Any unusual strain to the fetlock region may produce
            sesamoiditis. Most commonly in racehorses, hunters,   The radiologic changes of true sesamoiditis have
            and jumpers, it can affect any type of horse. It is caused   been described as bony changes on the abaxial surface
            by increased stress to the attachment of the SL to the   or basilar region, increased number and irregularity of
            sesamoid bones. Injury to the DSLs may also occur at   the vascular channels, and increased coarseness and
            their attachment to the basilar portion of the sesamoid   mottling of the bone trabeculation (Figure  4.130). In
            bones.                                             acute cases, radiographs may have to be taken approxi-
              The sesamoid bones have a substantial intraosseous   mately 3 weeks after onset of the condition to deter-
            blood supply that enters the midportion of the bone   mine whether bony changes will occur on the sesamoid
            through multiple abaxial channels that correspond to   bones. The condition may also occur with tenosynovi-
            the channels that enlarge in sesamoiditis, indicating   tis, fracture of the sesamoid bones, and injury to the SL
            bone remodeling. This may represent the initiation of   from which it must be differentiated. Careful radio-
            the remodeling response to bone stress of training, or it   graphic interpretations of the mottled trabecular pat-
            may reflect an increase in blood flow due to inflamma-  tern seen in the proximal sesamoid bone are necessary
            tion and injury to the SL, or both.  The sesamoid bones   to differentiate a fracture. Incomplete fracture can be
                                         94
            undergo intense remodeling in response to training,    differentiated from these coarse vascular canals because
                                                          107
            and the progression of radiographic changes correlates   the fracture usually extends to the abaxial surface and
            to bone response to remodeling and injury.         the vascular canals do not. In addition, fracture lines
              Interestingly, several studies have categorized the   frequently run at different angles than the vascular
            radiographic changes in sesamoid bones of young    channels.
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