Page 878 - Adams and Stashak's Lameness in Horses, 7th Edition
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844   Chapter 7




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             A                                                      B
            Figure 7.50.  Flexed lateral to medial radiograph (A) and   femoropatellar joint. The osteochondroma was a loose body within
            arthroscopic view (B) of an osteochondroma within the   the joint and was likely contributing to joint effusion in this horse.

            develop a blood supply, and grow to form osseous   Osteodystrophia Fibrosa (Nutritional Secondary
            masses. These may or may not cause a clinical problem,   Hyperparathyroidism)
            but will often lead to persistent synovial effusion. The
            dorsal aspect of the fetlock and the femoropatellar joint   Osteodystrophia fibrosa or nutritional secondary
            appear to be particularly susceptible to osteochondroma   hyperparathyroidism is a generalized bone disease
            formation (Figure 7.50).                           caused primarily by a dietary calcium deficiency in the
                                                               face of phosphorus excess.  Due to awareness and sen­
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                                                               sitivity about the condition, it is rarely seen today. It
                                                               occurs in all equids, although the horse is more suscepti­
            Tumoral Calcinosis (Calcinosis Circumscripta)
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                                                               ble than its relatives.  It is most common in horses being
              Tumoral calcinosis is the formation of calcified,   fed cereal and cereal by‐products such as bran (diets
            granular, amorphous deposits in the subcutaneous tis­  high in phosphorus and low in calcium), hence the name
            sues that induce a fibrosing granulomatous reaction.    “bran disease.” Addition of legume hay, which is high in
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            The deposits usually occur in the subcutis near joints   calcium, to the diet can usually prevent the disease. 18,72  It
            and tendon sheaths. 22,34  It occurs infrequently in the   is also  seen in  horses  grazing plants  high in oxalates,
            horse although it may be more common than is actually   which chelate the calcium and interfere with the absorp­
            recognized.  The etiology of the condition is unknown.   tion of calcium. Horses in Queensland, Australia, devel­
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            Affected horses are usually presented for unsightly   oped osteodystrophia fibrosa when grazed on tropical
            swellings that are  becoming  progressively  larger, and   grasses.  A subclinical form of the disease may also
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            lameness is uncommon.  The swellings are firm and   occur but is difficult to diagnose because the clinical
            painless, and the skin is usually intact and movable over   manifestations are subtle.
            the swellings. The most common location for tumoral   The underlying pathogenesis in osteodystrophia
            calcinosis lesions is the lateral aspect of the stifle, lateral   fibrosa is defective mineralization of bone. The diet high
            to the fibula, and beneath the aponeurosis of the biceps   in phosphorus leads to increased absorption of phos­
            femoris and lateral crural fascia. Of 18 cases reported   phorus and elevation  of serum  phosphate levels. This
            in the literature, lesions occurred over the lateral sur­  tends to lower serum calcium and stimulate the parathy­
            face of the tibia close to the femorotibial joint in 16   roid glands to increase secretion of parathyroid hor­
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            horses.  Radiographically, the lesions are characterized   mone. Parathyroid hormone increases activation of
            by radiopaque calcified deposits. On cut surface of the   remodeling, leading to resorption of bone. With bone
            lesions, there is a honeycomb‐like appearance with a   resorption there is a compensatory replacement with
            calcareous, gritty deposit enclosed in a dense fibrous   fibrous tissue.   This causes poorly mineralized bone
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            capsule.                                           that is eventually replaced with cellular connective tis­
              The treatment for calcinosis circumscripta is surgical   sue. Horses of both sexes and all ages are susceptible.
            excision.  This  should  be  performed  only  in  cases  in   Lactating mares and foals appear to be at increased risk
            which lameness can be directly attributed to the lesion.   to develop osteodystrophia fibrosa.
            The lesion may be so firmly attached to the stifle joint   The classic form of osteodystrophia fibrosa is called
            capsule that it is impossible to dissect it free without   “bighead” because of the predilection of the jaws and
            opening the joint. Therefore, surgical excision of these   flat bones of the skull to respond to parathyroid hor­
            lesions should be performed cautiously.            mone.  The classic clinical signs of the disease include a
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