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Bones are dynamic organs, growing and continually remodeling throughout life. The specific cells of bone are osteoblasts, osteocytes and osteoclasts. It has been postulated that osteoblasts are derived from mesenchymal stem cells called osteoprogenitor cells. It has recently been proven that osteoclasts originate in bone marrow and probably represent members of the mononuclear phagocyte system.
The intercellular component of bone is called osteoid or matrix. Osteoid is typical of a connective tissue matrix in many ways. It consists of an amorphous ground substance and a fibrillary component. The fibrillary component is composed primarily of collagen fibers with an admixture of precollagenous reticular fibers. The collagen found in bone contains large amounts of hydroxyproline, thus increased urinary excretion of this amino acid tends to be indicative of increased collagen degradation subsequent to increased bone resorption. The amorphous ground substance of osteoid is an extracellular and interfibrillar material common to all connective tissues. The origin of this substance is unknown, but its production is probably regulated by osteoblasts. In general, osteoid matures and acquires an affinity for minerals over a period of approximately 8 days.
Bone growth or development occurs through intramembranous bone formation and through endochondral bone formation. In intramembranous bone formation, fibroblastic-appearing cells of the inner layer of the periosteum gradually differentiate into osteoblasts and subsequently osteocytes. This results in osteogenesis in the form of layers along the periosteal surface. (Flat bones, such as the bones of the skull, develop almost exclusively by intramembranous bone formation. This type of bone formation is also responsible for the new growth along the periosteal surface of the shafts of long bones.) Endochondral bone formation is responsible for the increase in the length of long bones. This process takes place at the diaphyseal end of the epiphyseal cartilage. (There is an interstitial proliferation of cartilage which is used as scaffolding for the formation of bone.)
The majority of the important skeletal diseases are metabolic in origin. They represent imbalances in bone exchange, imbalances in the sites and ratios of activity of the osteoblasts and osteoclasts acting on bone surfaces to produce or remove bone tissue, and /or imbalances in the activity of osteocytes in regulating the mineral homeostasis of osteoid.
The complexity of the process by which the skeleton is formed provides ample opportunity for developmental anomalies. Thus developmental errors which are ultimately expressed and detected in the osseous skeleton may actually be primary abnormalities of primitive mesenchyme, cartilage, or bone. This is true because the skeleton develops in mesenchyme, which in most areas, is progressively converted into cartilage to form a model for bone formation. Bone anomalies may be localized or generalized and most generalized developmental disturbances of bone are considered to be reflections of a primary cartilaginous disorder which qualifies them as chondrodystrophies. In addition, most are inherited conditions and thus the term chondrodysplasia is more accurate.
Chondrodysplasias are characterized by disproportionate body growth. The defect usually involves abnormal interstitial (endochondral) bone growth and results from abnormal development of epiphyseal, articular and basocranial cartilages. In many cases intramembranous (appositional) bone growth is normal. In affected animals, the limbs, cranial base, and vertebral column are extremely short and the limbs are usually abducted and very thick. The soft tissues, primarily the muscles, are of normal volumes and therefore are excessive as they relate to the skeleton. The epiphyses are enlarged and mushroom shaped due to arrested interstitial growth along with normal appositional growth. The cranium becomes enlarged and dome-shaped. (Endochondral growth occurs primarily in the intersphenoid, sphenooccipital, and interoccipital subchondroses, thus these cartilages grow via interstitial proliferation and premature cessation of growth of these subchondroses leads to premature synostosis with consequences for the remainder of the skull.) Actually, enlargement of the skull (dome-shaped, etc.) is related to the fact that the brain continues to grow, and there is a tendency for hydrocephalus to develop in chondrodysplasia fetalis. The more commonly reported inherited chondrodysplasias include chondrodysplasia of the Dexter type, chondrodysplasia of the Telemark type, chondrodysplasia of the brachiocephalic type, chondrodysplasia of the dolichocephalic type, all in cattle and several chondrodysplasias in dogs.
Microscopically, osteochondral junctions are characterized by the presence of chondrocytes which are arranged in an irregular fashion (chondrocytes do not form the palisades which are the normal preliminary to provisional calcification).
The Dexter breed of cattle are heterozygous for an incompletely dominant autosomal gene that causes chondrodysplasia. In the homozygous state, the trait is lethal. Fetuses that are homozygous (d/d) for the trait (Dexter "bulldog" calves) are severely deformed and are usually aborted before the seventh month of gestation.
In Telemark cattle (a Norwegian breed), chondrodysplasia fetalis is transmitted as a recessive character (the heterozygous parents are phenotypically normal). Grossly, the dwarf calves are characterized by dome-shaped heads, brachygnathia, cleft palate, protruded tongue, short neck, and short limbs. It is characteristic of the Telemark type of chondrodysplasia that the affected calves are phenotypically uniform. These calves are usually born alive but die shortly thereafter. A similar autosomal recessive chondrodysplasia has been reported in jerseys; however, the affected calves are more variable phenitypically and some survive beyond the early postnatal period.
Chondrodysplasia of the short-headed type is the designation applied to the form of dwarfism which commonly occurs in beef producing breeds in the United States. This form of dwarfism is both anatomically and genetically complex. There are three recognized manifestations or forms.
7.3.4.1 The brachycephalic
Form (short-headed dwarf) is characterized by an extremely short and broad head. In affected cattle, the forehead bulges and the jaws are shortened (the mandible is slightly longer than the maxilla). The eyes are protruded and displaces laterally. The vertebrae are compressed in their longitudinal dimension. There is premature synostosis of the basocranial synchondrosis. The cerebellum is compressed and the heart is rounded.
7.3.4.2 The dolichocephalic
Form (long-headed dwarf) is considered to be another expression of this same complex. this form of dwarfism is characterized by extreme elongation of the head in proportion to the body size as a whole. The elongated head tapers to a rather fine muzzle. In general, the affected animals are unthrifty, they grow very slowly, and they tend to be slightly larger than those with the brachycephalic form.
7.3.4.3 The compact and/or compressed
forms of chondrodysplasia are characterized by phenotypically normal individuals with proportionately reduced body size. This is considered primordial dwarfism. Selection for this type of dwarfism is responsible for the wide dissemination of the genes for chondrodysplasia.
Several chondrodysplasias have been reported in dogs as well. These syndromes, each of which is inherited, include pseudoachondroplastic dysplasia in poodles, multiple epiphyseal dysplasia in beagles, chondrodysplasia in Alaskan malamutes, and chondrodysplasia in Norwegian elkhounds.
Osteopetrosis or metaphyseal dysplasia is characterized by a failure of removal of primary spongiosa. This condition primarily involves bone of endochondral origin. Cartilage does not disappear, as it should in normal bone development, but it persists and becomes calcified and is eventually surrounded by osteoid which also becomes calcified. Therefore the outer dimensions of affected bones are increased and the marrow cavities are reduced or completely obliterated. Osteopetrosis has been reported in most domestic species and in humans and it is considered to be hereditary (the condition is rare in humans and in animals). Osteopetrosis occurs with some frequency in birds where it is considered to be a form of the leukosis complex.
Osteogenesis imperfecta refers to any of several inherited connective tissue diseases characterized by increased fragility to bones. It has been reported in humans and there have been reports of similar syndromes in calves and lambs. There have also been reports of osteogenesis imperfecta in dogs but most have been traced to nutritional imbalances and are not true examples of this disease. Most cases are characterized by thin cortices and widened marrow spaces but a few are characterized by thick cortices and narrow marrow cavities. (These are probably representative of different syndromes.) The bones are very brittle and sometimes calluses are noted at birth. (This is indicative of fractures occurring in utero.) Most affected calves are stillborn but a few are born alive. Those born alive are usually unable to stand and those can stand or are helped to stand are usually very ataxic. Fractures as well as hypermobility of joints contribute to the inability or unwillingness to stand and walk. Other clinical findings include bluish discoloration of the sclera, pinkish discoloration of the teeth, increased fragility of the teeth. Histopathologic lesions exist mainly in the form of marked reductions in the amount of bone deposited on the cartilaginous scaffolding.
So-called crooked calf disease is characterized by a wide spectrum of anatomical malformations. However, malformation of the limbs, especially the forelimbs, is the most common alteration. The limb abnormalities consist of contracture and arthrogryposis with disordered growth of joints and shortening and rotation of bones. Scoliosis, kyphosis, brachygnathia, and cleft palate are also common manifestations. The etiologic mechanism has not been completely elucidated; however, the condition has been associated with ingestion of wild lupines and poison hemlock by pregnant cows and by feeding rations deficient in manganese. The condition has been reported most frequently in the western U.S.
"Contracted foals" refers to a congenital alteration characterized by torticollis, scoliosis, asymmetry of the skull, and varying severities of flexion of the distal limbs. The cause is unknown but foals with this syndrome have been aborted as early as the third month of gestation. This suggests that the defect could develop in the cartilaginous model of the skeleton.
Malformations of the limbs are common and a wide variety may occur. Localized chondrodysplasias are frequently observed; in fact, this is actually a feature of certain breeds of dogs. The defect is usually in the distal limb bones, resulting in the type of dwarfism that characterizes such breeds as the Dachshund and Basset Hound (in some breeds, such as the Pekinese, there is chondrodystrophy of the limbs as well as basocranial chondrodysplasia; breeds such as the Boxer and Boston Terrier are characterized by basocranial chondrodysplasia alone).
Terms that you may encounter in reference to abnormalities of the limbs include
Abnormal curvature of the vertebral column has been reported in a number of species. The term scoliosis refers to a lateral deviation of the spine whereas kyphosis refers to a dorsal curvature or deviation of the spine (hump-backed). Lordosis refers to a ventral curvature or deviation of the spine. Hemivertebrae refers to malformations in which there is only partial development of vertebrae. This condition may be clinically silent or, in extreme cases, the spinal cord is compressed. Spina bifida refers to an absence of the dorsal portion of the vertebrae. There are various forms of the defect; these forms are based primarily on the severity of the condition. In animals, spina bifida is seen most frequently in Manx cats.
The principal causes of metabolic bone diseases are deficiencies and/or imbalances of dietary calcium, phosphorus, and vitamin D, resulting in osteodystrophies. (It is important to note that these are acquired conditions.) The specific interrelationship between calcium, phosphorus and vitamin D are complex and have not been completely elucidated.
A deficiency of calcium alone (hypocalcemia) causes hyperparathyroidism with the development of osteodystrophia fibrosa or osteoporosis (or both). Calcium deficiency alone is not the usual cause of rickets or osteomalacia. A deficiency of vitamin D is the classical cause of rickets in growing animals and osteomalacia in adults. The principal effect of vitamin D is to enhance or facilitate intestinal absorption of calcium and phosphorus. However, there is evidence to suggest that vitamin D is also necessary for the transfer of calcium ions across cell membranes. The initial process in the mineralization process is the concentration of phosphate in the bone matrix; then calcium, which has a great avidity for phosphate, is deposited. Thus, phosphorus deficiency retards mineralization but calcium deficiency does not (because calcium is transferred from serum to bone even to the extent of producing hypocalcemic tetany).
There are four basic diseases of bone that traditionally have been accepted as having metabolic pathogenesis. These are osteoporosis, rickets, osteomalacia, and osteodystrophia fibrosa (fibrous osteodystrophy). As is common throughout medicine, the pathogeneses for these conditions is discussed as though the typical cases were clear and uncomplicated when the truth is that most of these diseases are really not so simple. Simplified versions of the pathogenetic mechanisms are important in the development of an understanding of these conditions, but it is equally or more important to understand that the actual cases that we encounter will often be complicated combinations of the aforementioned diseases. In addition, the lesions observed vary depending on the stage at which the disease is encountered. These situations make diagnosis of these conditions difficult. Diagnosis of the resulting osteodystrophies must be based primarily on histopathologic criteria. Bone ash and serum analysis will generally not allow separation of the various diseases.
Rickets is a disease of growing animals, characterized by a failure of adequate deposition of calcium salts in the matrixes of bone and cartilage, resulting in an excess of poorly mineralized osteoid and cartilagenous matrix. Abnormalities occur in both endochondral and membranous bone formation. Vitamin D deficiency is the classical cause of rickets in young animals and children; however, we must add that a deficiency of phosphorus can also cause rickets. The basic function of the active form of vitamin D is to help maintain normal serum levels of calcium, which is necessary for normal bone mineralization.
-- Vitamin D can be derived from dietary sources or from 7-dehydrocholestrol in the skin. Regardless of the source, cholecalciferol is transported in the blood to the liver, where it is converted to 25-hydroxycholecalciferol. The 25-hydroxycholecalciferol is then transported to the kidneys, where under certain circumstances, it is further hydroxylated to form 1, 25-dihydroxycholecalciferol. This form is considered to be the active form of vitamin D or the antirachitic agent and its primary effect is to enhance the absorption of calcium and inorganic phosphate in the small intestine. Calcium homeostasis is also influenced by the release of parathormone from the parathyroid glands. The interaction between parathormone and 1,25-dihydroxycholecalciferol is complicated. However, parathormone is necessary for the synthesis of 1,25-dihydroxycholecalciferol by the kidneys. (It should be noted that the kidneys do not always convert 25-hydroxycholecalciferol into 1,25-dihydroxycholecalciferol; for example, when serum calcium and inorganic phosphate concentrations are within normal limits, 25-hydroxycholecalciferol is converted into 24,25-dihydroxycholecalciferol, which is a relatively inactive metabolite). Thus, the factors necessary for the kidneys to convert 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol appear to be twofold:
The essential skeletal changes in rickets consist of:
Grossly, rickets is characterized by enlargement of the ends of long bones and by enlargement of the costo-chondral articulations. The epiphyseal cartilage is abnormally wide (this can be observed when a long bone is sawed longitudinally). In severe cases, bones are abnormally soft and can often be cut with a knife. Bones of limbs may become permanently bent under the weight of the animal's body resulting in "bow-legs" and other skeletal abnormalities. In bones of the skull which form in membranes, excessive osteoid is deposited but not calcified. Growth at the base of the skull (endochondral bone formation) is subject to the same inhibitions as is growth at any other osteochondral junction. Therefore, the cranium appears more done-shaped and the fontanels remain open.
Microscopically, rickets is characterized by an increase in the depth of the zone of proliferating cartilage/epiphyseal plate. This cartilage grows in an unorganized manner. In addition, there is a failure of provisional calcification of cartilage and excessive uncalcified osteoid.
Rickets is often complicated by fibrous osteodystrophy. In fact, the fibrous connective tissue proliferation listed among the essential features of rickets might actually represent this change. In addition, since all bones in an individual don't mature simultaneously, it is conceivable to have rickets and osteomalacia occurring at the same time.
Clinically, pain and muscle weakness may be manifested (the abdomen may be pendulous, "pot-bellied"). Pathologic fractures may occur, and the serum alkaline phosphatase levels are elevated. In long standing cases, the parathyroid glands undergo hypertrophy (hypocalcemia, regardless of the cause, will lead to secondary hyperparathyroidism).
Some vitamin D refractory forms of rickets have been reported, including vitamin D resistant rickets and vitamin D-dependent rickets. These are inherited syndromes in which rickets develops in animals or humans in absence of uremia or malabsorption and with adequate dietary vitamin D.
Osteomalacia refers to a failure of mineralization of bone matrix, resulting in softening of bone in adult animals after endochondral bone growth has ceased. The condition is similar to rickets in many respects; however, the changes tend to be confined to defects in membranous bone formation. (In rickets, there are abnormalities in both membranous and endochondral bone formation.) Therefore, in osteomalacia, there are abnormally large amounts of uncalcified osteoid on the surfaces of bone, and extensive resorption of mineral deposits in bones that are already formed.
The cause of osteomalacia is a continued or prolonged negative balance of vitamin D or phosphorus. It should be remembered, endochondral bone growth is no longer in progress in the adult; thus, endochondral or epiphyseal bone changes are absent or minimal. The condition occurs most commonly in cattle in which it is due to a deficiency of phosphorus.
Grossly, there is irregular thickening of bones along the diaphysis. However, affected bones are soft and easily cut. The trabeculae of the spongiosa are affected first; later, bone is reabsorbed from the haversian canals and from beneath the endosteum. Recent fractures and/or calluses are common. When osteomalacia is well developed, the marrow cavity is enlarged and the cortex is thin and spongy. Microscopically, the changes are characterized by active resorption of bone and by the presence of excessive osteoid.
As was noted in the discussion of rickets, fibrous osteodystrophy sometimes complicates osteomalacia and rickets.
Fibrous osteodystrophy (also referred to as "osteodystrophia fibrosa" and "osteitis fibrosa cystica" is a disease of bone that develops subsequent to advanced hyperparathyroidism (excessive parathyroid hormone is secreted in response to declining serum levels of calcium). The disease is characterized by:
If primary or secondary hyperparathyroidism results in continuous and excessive action of parathormone on bone, fibrous osteodystrophy develops. The increased secretion of parathormone causes rapid osteoclastic resorption and exuberant growth of fibrous connective tissue in bone. Secondary hyperparathyroidism is actually the most common cause of fibrous osteodystrophy in animals; hypocalcemia is the stimulus for the increased activity. In summary, those factors that result in hypocalcemia (decreased dietary calcium, large excess of phosphorus, etc.). may cause hyperparathyroidism and subsequent fibrous osteodystrophy. It should be remembered that excessive parathormone inhibits the proper mineralization of osteoid even in the presence of hypercalcemia. If cases of rickets or osteomalacia are complicated by hyperparathyroidism, fibrous osteodystrophy may occur.
Fibrous osteodystrophy associated with secondary hyperparathyroidism is the most important osteodystrophy in domestic animals. (A large proportion of the osteodystrophies diagnosed as rickets and/or osteomalacia are most likely manifestations of secondary hyperparathyroidism). In general, growing animals are most severely affected because their requirement for calcium is high and growth rate is rapid. In horses, cattle, pigs and sheep, fibrous osteodystrophy occurs most commonly when the diet consist of grain or grain by-products; whereas in dogs and cats, diets of meat and liver are usually incriminated. In monkeys, the condition usually occurs when the diet consist exclusively of fruit.
Fibrous osteodystrophy is a generalized disease, but the changes are most severely expressed in the bones of the face and mandible. Grossly, affected bones are deformed, soft, and easily incised with a knife. Microscopically, the haversian canals are enlarged and osteoclasts line the receding bone. The space formally occupied by calcified bone is ultimately replaced with fibrous connective tissue: The proliferating fibrous connective tissue may undergo cystic degeneration (probably due to inadequate blood supply). Parathyroid hyperplasia may be recognized on gross and/or microscopic examinations. Radiographs show generalized demineralization of bone.
Nutritional secondary hyperparathyroidism occurs when the diet consist almost exclusively of meats which are very high in phosphorus and low in calcium (beef heart, etc.). The resulting hypocalcemia leads to hyperparathyroidism with excessive secretion of parathormone. Subsequently, the excessive parathormone leads to generalized fibrous osteodystrophy.
The disease is quite fulminating in cats and puppies (experimentally, young kittens placed on a diet of beef hearts and distilled water develop hypocalcemia in 5 to 7 days). Grossly all bones are soft and friable with increased susceptibility to fractures. There is very little new osteoid deposited and calluses are poorly formed. Clinically, there is hypocalcemia and hyperphosphatemia.
Nutritional secondary hyperparathyroidism occurs when the diet contains excessive phosphorus in proportion to calcium. Thus, hyperparathyroidism occurs indirectly by virtue of the ability of hyperphosphatemia to decrease the serum concentrations of ionized calcium. (Actually, the amount of calcium in the diet may be adequate or it may be low and the serum calcium concentrations may be normal or high). This condition in the horse is commonly referred to as "bran disease" or "Miller's disease", and it occurs when the diet consist almost exclusively of cereal or cereal by-products. There is demineralization of all bones in the body, but head and facial bones are most prominently involved. Thus, the characteristic feature of this disease is swelling of the head, face, and jaws (BIG HEAD).
Nutritional secondary hyperparathyroidism is usually related to a deficiency of vitamin D3 in their diet or to a lack of exposure to ultraviolet radiation or sunshine (in New-World monkeys, vitamin D2 is relatively ineffective in promoting intestinal absorption of calcium). In addition, the condition may be caused /or aggravated by food high in phosphorus and low in calcium. The disease occurs almost exclusively in New World monkeys and it is characterized by facial deformities, reluctance to move, bending of bones, and multiple fractures.
Fibrous osteodystrophy is commonly due to secondary hyperparathyroidism which occurs subsequent to chronic renal disease. The kidney lesions result in retention of inorganic phosphate in the blood (hyperphosphatemia). The hyperphosphatemia causes an imbalance in calcium-phosphorus homeostasis which induces hyperparathroidism. Excessive secretion of parathormone causes mobilization of calcium from bones (parathormone, however, cannot induce the excretion of inorganic phosphate via the kidneys because of the renal insufficiency). The net result is generalized demineralization of bones in long standing cases.
In renal secondary hyperparathyroidism, all bones of the body are demineralized, but those of the jaws and head are especially soft and pliable. The teeth are loose and fractures may occur during routine physical examination. Affected dogs will usually exhibit the signs associated with uremia. (It should be remembered that the role of the kidneys in producing the active form of vitamin D may be important in the pathogenesis of this syndrome).
Osteodystropic changes in bones may also be associated with vitamin D toxicosis and fluoride poisoning.
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Osteoporosis is a condition characterized by a decrease in bone mass with enlargement of bone spaces and increased fragility of affected bones. It essentially refers to atrophy of bone and the word osteopenia is sometimes used as a synonym. It can arise due, primarily, to a lack of osteoid or minerals and causes for its development are quite variable. This condition reflects and imbalance between the rate of bone formation and the rate of bone resorption favoring resorption. The commonly incriminated causes of osteoporosis include malnutrition, deficiencies of calcium and phosphorus, disuse, malabsorption associated with intestinal parasitism, and senility. (It is important to reemphasize that though simple pathogenetic mechanisms are discussed, uncomplicated causes of this condition are rare.)
Grossly, in advanced cases, there is a marked reduction in cancellous bone and thinning of the cortices of compact bone with enlargement of the marrow cavities. These changes are evident in radiographic studies as well. Various types of fractures are common in animals suffering from this condition. Histologically, there is a reduction in the numbers of trabeculae and possibly evidence of abnormal activity of osteoblasts, osteocytes, or osteoclasts. In some cases, increased osteoclastic activity along vascular channels (Haversian canal's) in cortical bone causes lengthwise intracortical resorption. Evaluation of bone ash may provide information as to the matrix-mineral relationship and thus help to characterize the cause.
Necrosis of bone (osteonecrosis) occurs when bone is deprived of its blood supply (fractures, inflammation, etc.). Necrotic bone may remain white in color or it may be brown. In the acute stages, it is quite difficult to differentiate necrotic bone from normal bone since discoloration takes place rather slowly. The earliest recognizable change in necrotic bone is a dull and dry appearance of the periosteum. Microscopically, necrotic bone is characterized by death and disappearance of osteocytes (presence of empty lacunae).
A relatively common location for osteonecrosis in animals is the head of the femur. Osteonecrosis in this location is often the result of a slipped capital femoral epiphysis or it may represent what is known as Legg-Calve-Perthes disease. Slipped capital femoral epiphyses have been reported in most domestic species and the suggested pathogeneses mostly involve trauma.
Legg-Calve-Perthes disease is also characterized by osteonecrosis (necrosis) of the femoral head. It has been reported in dogs, mainly small terrier breeds, and it must be distinguished from slipped capital femoral epiphysis. There is speculation that the pathogenesis involves occlusions of venous return from the femoral head.
Navicular disease in horses can result from any of several mechanisms including navicular bursitis, stress fractures, bacterial infections, and ischemic necrosis. In the case of ischemic necrosis, the suggested pathogenesis involves occlusion of arterioles entering the sesamoid bone.
Inflammation of bone (osteitis) is always confined to the vascular connective tissue of bone (periosteum, medullary cavity & the connective tissue of the haversian & Volkmann's canals). A progressive inflammatory process will involve all 3 sites.
Osteitis - refers to inflammation of bone.Periosteitis - refers to inflammation of the periosteum.
Osteomyelitis - refers to inflammation of the medullary cavity.
The mineralized component of bone does not undergo inflammation in the traditional sense. Actually, the mineralized component undergoes secondary changes (degeneration, necrosis, resorption, & regeneration) when the vascular connective tissue of bone is inflamed.
Osteitis is a rather common condition in animals. It may be hematogenous in origin, or it may develop following trauma or subsequent to inflammation of soft tissue overlying bone. Hematogenous metastasis begin in the medullary region. Subsequently, such an inflammatory process may spread in all directions (reaching the periosteum via the haversian and Volkmann's canals of cortex). Many organisms are capable of causing inflammation of bone.
Actinomycosis is a chronic suppurative and granulomatous disease in which inflammation and necrosis are prominent features. The disease is caused by Actinomyces bovis and it occurs in cattle, horses, swine, dogs, and cats. In cattle, the classical lesion is so-called "lumpy jaw" in which there is necrosis and inflammation of the mandible, maxilla, or other bony tissues of the head and face; metastasis of infection seldom occur. Lesion consists of abscesses, fistulous tracts, inflammation, connective tissue proliferation, and granulomas. Organisms occur in colonies (located in pus) and these colonies are referred to as "sulfa granules". The sulfa granule colonies are yellowish-white and they may be be visible to the naked eye. Internally, the sulfa granules consist of tangled masses of filamentous, gram-positive organisms with a peripheral rim of closely packed, club-shaped bodies. Evidence suggest that Actinomyces bovis is obligatory parasite on the mucous membranes of oral pharynx.
In swine, A. bovis may occur in a variety of tissues, but it is of primary importance as an infection of the mammary gland. In horses, A. bovis is commonly recovered from cases of "poll-evil" and "fistulous withers".
Bone fractures occur when bone yields to stress of short duration. The term "traumatic fracture" is used when fractures occur in bones which are initially normal, whereas the term "pathologic fracture" is used when fractures occur in bones that have been structurally altered (by neoplastic diseases, inflammation, etc.).
Healing of fractures occurs as follows. There is hemorrhaging from the fractured ends of the bone. This blood clots and essentially seals the fracture site. Within a few days, a fibrovascular stroma invades this clot and forms the soft tissue callus. Later, osteoprogenitor cells, originating in the periosteum, proliferate and invade the soft tissue callus. These cells initially form cartilage and once the callus is largely cartilaginous with bone spicules it is referred to as a provisional callus or procallus. As the vascular network increases in the procallus the cartilage is converted to bone by endochondral ossification. Once the healing process is nearly complete then remodeling of the bone takes place in an attempt to recreate the original contour of the bone.
Primary skeletal neoplasms occur with frequency, but secondary tumors are rare. Most skeletal neoplasms occur in dogs. The important primary tumors include osteogenic, chrondrogenic, and giant cell tumors.
Osteogenic sarcomas occur rather frequently in dogs, but they are less common or rare in other animals. These tumors arise from osteoblasts or primitive multipotent cells and occur most frequently along the ends of long bones of the limbs and ribs. Generally, osteogenic sarcomas are highly malignant and they metastasize early and rapidly. However, some tumors of the ribs in adult dogs may persist for months without scopic appearance. Slow growing tumors elaborate considerable amounts of osteoid with the formation of bony spicules; these tumors are hard and firm. Highly malignant and rapid growing tumors are soft and quite vascular. Microscopically, osteogenic sarcomas are characterized by the presence of proliferating osteoblasts (the proliferating cells may resemble a fibrosarcoma) with osteoid deposition.
Chondromas and chondrosarcomas of the skeleton are rare in animals. Chondromas consist of well-defined or well-differentiated cartilage, whereas chondrosarcomas is the malignant chondrogenic tumor (refer to page 197 of your textbook).
Hypertrophic osteoarthropathy is an non-inflammatory, non-neoplastic proliferation of new bone commonly associated with neoplasms or chronic inflammations of the lungs. Primary and metastatic neoplasms of all types as well as both chronic suppurative and granulomatous inflammations of the lungs have been incriminated (however, the bone lesions may exist without the presence of lesions in the lungs). The proliferation of new bone occurs initially and most severely in sites where the periosteum is free of tendenous insertions; however, endosteal lesions may also occur. The condition has been recorded most frequently in the dog and the long bones are commonly involved. The new bone may be deposited very rapidly ( width of the cortex may be doubled in a few weeks). The exact etiologic mechanism is unknown, however, several mechanisms have been postulated.
Craniomandibular osteopathy is a non-inflammatory, non-neoplastic lesion which affect the mandible, temporal and occipital bone, primarily. The condition occurs in Scottish Terriers and West Highland White Terriers. The cause has not been completely elucidated, but the condition probably has a genetic basis. The earliest lesions are observed around the 8th month of life and there are alternating episodes of proliferation and repair resulting in irregular thickening of involved bones. Lesions are usually bilateral trabeculae are affected. Resorption of normal bone and osteoid deposition are prominent features. The new osteoid deposits are poorly mineralized.
Diarthritic joints are subject to a wide variety of injuries and infections. The basis components of these joints are
Articular capsules and ligaments are poorly supplied with blood vessels, and these structures have a limited capacity for repair following injury. Synovial membranes play an important role in the production of synovial fluid. Synovial fluid is basically a protein free dialysate to which hyaluronate is added by synovial cells. The articular cartilage is diarthritic joints is hyaline cartilage. In young animals, it is smooth, bluish in color, and semi-transparent, whereas in older animals it is yellowish and opaque.
Arthritis refers to inflammation of the interarticular structures of joints. The condition is most often due to infection. Microorganisms may enter joints via direct extension or by way of the blood stream. Hematogenous polyarthritis occurs with frequency in animals (especially in large domestic species) and organisms initially invade the synovial layer of the articular capsule.
Acute inflammation of the joints is usually serous, fibrinous, or purulent. Serous arthritis is characterized by distention of the joint capsule with clear, watery fluid; the synovial membranes become hyperemic and the tissue surrounding the affected joints are often edematous and hot. The cause is usually trauma with involvement of a single joint. Purulent arthritis is characterized by the accumulation of pus; the condition is usually severe and destructive. This type of arthritis is commonly associated with "naval ill" of foals, lambs, and calves (early cases usually appear as serofibrinous). There are numerous organisms capable of producing arthritis Chronic arthritis may develop subsequent to the acute disease.
Chronic erysipelas in swine is manifested as either an arthritis or endocarditis or both. The chronic lesions are causes by localization of organisms which may occur as a sequelae to an acute septicemia or as a sequelae to a mild or important systemic infection. The arthritis is usually characterized by excessive fluid and hyperplasia of the synovial membrane; there is an fibrous connective tissue over articular surfaces. Also, erosion of articular cartilage is a common finding.
Glasser's disease of swine is an acute systemic disease caused by Hemophilus influenza suis; the condition is characterized by a fibrinous polyarthritis as well as a fibrinous meningitis and polyserositis. In general, the diseases is acute, the course is short, and there is rapid response to antibiotic treatment.
Glasser's disease occurs chiefly in pigs from about 5 to 12 weeks of age and stress is an important predisposing factor. Grossly, there is a serofibrinous polyarthritis which is most severe in the atlanto-occipital articulation and in the larger joints of the limbs. There tends to be a fibrinopurulent exudate in the meninges; the meninges are usually cloudy. A serofibrinous exudate develops on the membranes lining the body cavities (pleura, pericardial sac, peritoneum, etc.).
In field cases,H. suis is difficult to isolate or culture and it may be necessary to make a diagnosis on the basis of typical signs and lesions. MYCOPLASMA HYORHINIS is capable of producing a syndrome nearly identical to that of Glasser's disease caused by Mycoplasma hyorhinis is subacute to chronic in duration and treatment is not successful. Also, brain lesions are rare. (Brain lesions are quite common in Glasser's).
Arthropathy refers to degenerative diseases of joints and it is primarily a problem of aging (older) animals. The condition is usually associated with multiple and minor injuries to joints, and lesions develop slowly enough to allow for some functional compensation. (However, degenerative joint lesions may begin early in life, progress rapidly, and result in severe pain or locomotor disturbances.)
The primary pathologic changes are in the articular cartilage; defects may appear as grooves, or large areas of denudation may occur. Spicules or small nodules of bone may develop along the articular margins. (You should be able to differentiate arthropathy from arthritis).
Alterations of the vertebral column often involve its articulations. They may be degenerative or inflammatory in nature and they may involve intervertebral discs or vertebrae or both. There are several terms used to refer to problems involving the vertebral column including: spondylosis which refers to a degenerative disease of the vertebral column, spondylitis which refers to inflammation of a vertebrae, discospondylitis which refers to inflammation of an intervetebral disc and a vertebrae. Ankylosing spondylitis/spondylosis is a syndrome characterized by osteophyte development on the ventral or lateral aspects of adjacent vertebral bodies with eventual bridging of the intervertebral joint.
Degeneration of the intervertebral discs is a form of arthropathy that occurs frequently in certain breed of dogs. (Please refer to your handout on the Central Nervous System).
Acute injuries to joints include sprains, subluxations, and luxations: these are due to traumatic injuries which are single, sudden, and severe. (Multiple and minor traumatic injuries to the joints are discussed under degenerative arthropathy.) In acute injuries, the joints are forced to move beyond the limits of elasticity of their ligaments. The synovial tissues, capsular tissues, capsule, and ligaments may be stretched, lacerated, or torn. (PLEASE REVIEW YOUR GENERAL PATHOLOGY NOTES ON THIS SUBJECT).
Osteochondritis dissecans is a traumatic lesion which is characterized by "flaking defects" of juvenile articular cartilage. The condition occurs primarily in the shoulder joints in immature larger breeds of dogs (also, a similar flaking defect of juvenile cartilage occurs commonly in pigs which are calcium deficient). The lesions in articular cartilage may be mild, or portions of the cartilage may be completely detached. There is evidence to suggest that the lesions over the humerus occur when the articular cartilage is subjected to excessive compression by the posterior rim of the glenoid cavity, when the joint is fully extended. Affected dogs or may not exhibit clinical signs.
7.16.8.1 HIP DYSPLASIA IN DOGS
Dysplasia of the hip is an apparent congenital condition which occurs in young dogs of larger breeds. The main feature of hip dysplasia is "looseness" of the joints which is due to a congenital or inherited lack of strength. At birth, the hip joints appear normal; shortly after birth, dysplasia begins to develop if the femoral head fails to maintain full contact with the acetabulum. (At this time the femoral head and most of the acetabulum are still cartilaginous and the shapes of these parts are easily altered.) Grossly, varying degrees of shallowness of the acetabulum occurs (minor defects are best observed via X-ray examination). Likewise, the head and neck of the femur exhibit varying degrees of deformity. The head becomes broad and flattened, and the neck becomes more aligned with the long axis of the femur. In severe cases, subluxation, arthropathy, etc. may occur.
7.16.8.2 UNUNITED ANCONEAL PROCESS
This condition is considered to be a fusion defect affecting the ossification areas of the elbow. Studies suggest that the anconeal process develops as a secondary ossification process; normally it should fuse to the proximal ulnar shaft by 4-5 months of age. The presence of ununited anconeal process is abnormal after this age (4-5 months of life). The condition can readily be diagnosed via radiographs if the elbow is flexed. Traditionally, ununited anconeal fragments are removed via surgery.
Gout is the disease that occurs when uric acid and urate crystals are deposited in tissues subsequent to defective purine metabolism. The condition occurs primarily in humans and in birds. Gout in birds is characterized by the presence of urates in joints and visceral organs (articular & visceral of gout). The exact pathogenic mechanism is unknown; however, the condition occurs most commonly in laying flocks. Affected birds become dull and listless, and eventually die. Grossly, the articular from is characterized by enlarged and swollen joints; when affected joints are incised, and uric acid crystals exudes. In the visceral form, a white, flake-like material (uric acid crystals) covers abdominal and thoracic organs).
Perosis in birds (slipped tendon) is an anatomical deformity of the leg bones of young chickens, turkeys, and other birds. The condition is considered to be caused by a manganese deficiency (also, any one of the following vitamins may be responsible for the condition - choline, nicotinic acid, pyridoxine, biotin, folic acid). Perosis is characterized by swelling and flattening of the hock joints. Oftentimes, this is followed by slipping of the achilles tendon from its condyles. One or both legs may be affected.
Riboflavin deficiency in chicks is characterized by "curling of the toes" (curled paralysis). This deficiency is denoted by softening and swelling of the peripheral nerves (especially the brachial & sciatics). In poults, riboflavin deficiency is characterized by a severe dermatitis of the feet and shanks.
Based on the knowledge and skills gained from your study of the skeletal system, you should be able to provide appropriate answers for the following questions. Please review the instructional material (2x2 slides, etc.) as needed.
121. How would you characterize osteochondritis dissecans?
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SLIDE 1: EQUINE BONE (gross): OSTEOPETROSIS - This is an example of osteopetrosis in an aborted equine fetus. The primary spongiosa was not removed and the cartilage was calcified. Note the complete absence of the marrow cavity; the marrow cavity consisted of calcified cartilage and osteoid. If this animal had been born alive, would you expect to observe severe myelothistic anemia with extramedullary hematopoeisis?
SLIDE 2: BOVINE BODY (gross): CROOKED CALF DISEASE - This is an example of "crooked calf disease" with severe contraction of the tendons resulting in distortion of the limbs. In this calf, the involvement is most severe in the hind limbs. (Discuss the gross alteration associated with this syndrome. Discuss possible etiologic mechanisms. Define the following: scoliosis, kyphosis, lordosis, brachygnathia, and endochondral bone formation.)
SLIDE 3: BOVINE LIMB (gross): PEROMELIA - This 2 day old calf was born with the condition observed in this slide. Note the absence of the distal portion of the limb. The owner of this calf requested euthanasia.
SLIDE 4: BOVINE VERTEBRAL COLUMN (gross): KYPHOSCOLIOSIS - This is an example of kyphosis & scoliosis; the spine is twisted and distorted. (PLEASE DEFINE KYPHOSIS & SCOLIOSIS).
SLIDE 5: BOVINE VERTEBRAL COLUMN (gross): HEMIVERTEBRAE - This is an example of the malformation commonly referred to as hemivertebrae. Observe the partially developed vertebrae. Some are triangular
SLIDE 6: CANINE BODY (gross): SPINA BIFIDA - Slides # 6 & 7 are different views of the same condition. In this slide, note the hump-backed appearance (kyphosis). Also, observe the skin defect along the dorsal aspect of the "hump".
SLIDE 7: CANINE BODY (gross): SPINA BIFIDA - This pup was born with the defect observed in this slide. Note the absence of the dorsal portion of the vertebrae as well as an absence of the skin and musculature in the affected area. (What is an "meningocele"?)
SLIDE 8: CANINE CERVICAL VERTEBRAE (gross): CANINE WOBBLER SYNDROME - Note the malformed cervical body of C7. In addition, the intervertebral discs between C6 and C7 and between C7 and T1 are disintegrated and there is evidence of necrosis of the associated vertertebral bodies.
SLIDE 9: BOVINE BONES (gross): CONGENITAL PORPHYRIA - Congenital porphyria was discussed in your General Pathology course and you should review any pertinent notes. This condition is actually characterized by a metabolic defect in porphyrin metabolism. (This is not a primary bone disease.) The abnormal porphyrins formed are deposited in dentine and bone resulting in an abnormal discoloration. In congenital porphyria, there is a metabolic defect in the synthesis of "ferroprotoporphyrin" which is the normal heme pigment. This error results in the release of free protoporphyrin, uroporphyrin III which accumulate in serum and tissue. In this slide, observe the abnormally discolored bone and compare with the normal bone.
SLIDE 10: BOVINE BONES (gross): CONGENITAL PORPHYRIA - This is a cross section of an affected bone and a normal bone; note the discoloration. In cattle, this disease is believed to be inherited as a simple Mendelian recessive trait, whereas in swine and cats it is believe to be inherited as a dominant characteristic.
SLIDE 10: BOVINE BONES (gross): CONGENITAL PORPHYRIA - In congenital porphyria, affected bones and teeth elicit a strong reddish fluorescence with ultraviolet light. This is a useful aid to a clinical or postmortem diagnosis. In this slide, note the fluorescence with ultraviolet light; compare the normal and abnormal bones.
SLIDE 11: BOVINE TEETH (gross): CONGENITAL PORPHYRIA - Observe the reddish fluorescence of the teeth under ultraviolet light. Remember, except for its photosensitizing effect, this disorder is clinically harmless.
SLIDE 12: This slide is the same as slide 11.
SLIDE 13: BOVINE BODY (gross): RICKETS - This 3-month-old calf was crippled and unable to stand without assistance. Observe the abnormal posture - front legs out-stretched, etc. as well as the swollen joints. (How would you define rickets? Why would you expect to observe abnormalities in both endochondral and membranous bone formation in cases of rickets? Briefly, give the process by which the antirachitic factor is formed from cholecalciferol found in the serum. What is considered to be the basic cause of rickets in animals? What is the antirachitic factor or agent? What are the effects of the antirachitic agent on the small intestine and on bone? What effects do parathormone have on serum levels of calcium and inorganic phosphates? What are the basic differences between rickets and osteomalacia? What lesion(s) would you expect to observe in cases of rickets which would not be prominent in cases of osteomalacia?
SLIDE 14: BOVINE BONES (gross): RICKETS - This is an example of a long-standing case of rickets. There was a deficiency of vitamin D with subsequent hypocalcemia. At necropsy, multiple pathologic fractures were observed. Many of the bones could be cut easily with a sharp knife. In this slide, compare the normal and abnormal bones; note the very thin cortex. (What characteristic changes would you expect to observe in the involved bone on microscopic examination? What are pathologic fractures? Why would you expect pathologic fractures to occur in this animal? Why does rickets occur in cases of vitamin D deficiency?)
SLIDE 15: BOVINE BONE (gross): RICKETS - This is a case of rickets complicated by fractures. (Please describe the changes observed in this slide.)
SLIDE 16: DUCK BEAK (gross): RICKETS - Also refer to slide #17. This duck had an advanced case of rickets characterized by a very soft and pliable beak as well as soft bones and swollen joints as observed in this slide. The beak would bend with slight pressure.
SLIDE 17: DUCK LIMBS (gross): RICKETS - This is the same duck as denoted in slide #16; observe the markedly swollen joint. (Why would you expect the joints to be swollen or enlarged in cases of rickets?)
SLIDE 18: CHICK RIBS (gross): RICKETS - In this chick, rickets was characterized by severe changes involving the costo-chondral articulations as well as pathologic fractures of the ribs. Observe the nodular and distorted ribs. (What does the term "rachitic rosary" mean to you?)
SLIDE 19: FELINE BONE (gross): FIBROUS OSTEODYSTROPHY - This bone was taken from a cat that was fed a diet high in phosphorus and low in calcium; note the fragile and soft cortex and the pathologic fracture along the middle one-third.
SLIDE 20: CANINE HEAD AND NECK (gross): FIBROUS OSTEODYSTROPHY - This is a dog that was fed a diet which had a high protein content. Note the rubbery consistency of the maxilla evident in the ability to twist it around its long axis.
SLIDE 21: CANINE HEAD (gross): FIBROUS OSTEODYSTROPHY - Notice the ease with which the maxilla of this dog can be pushed laterally. This dog had chronic renal disease and renal secondary hyperparathyroidism.
SLIDE 22: CANINE THYROID AND PARATHYROID GLANDS (gross) - Notice the markedly enlarged parathyroid gland in the tissue nearest the ruler. It is enlarged to 3 or 4 times its normal size.
SLIDE 20: EQUINE VERTEBRAE (gross): OSTEONECROSIS (BONE NECROSIS) - This is an example of bone necrosis that occurred subsequent to a traumatic experience; there was also damage to the spinal cord. Compare the necrotic and normal bone; note the discoloration. Observe the necrotic tissue attached to the dorsal aspect of the spinal cord. What clinical signs would you expect to observe in the live animal? How would you differentiate necrotic from normal bone on gross examination? What is Legg-Calve-Perthes disease?
SLIDE 21: CANINE BONE (gross): OSTEONECROSIS (NECROSIS OF BONE) - This is an example of bone necrosis associated with a neoplastic disease (osteogenic sarcoma). Observe the thin and necrotic cortex (note the arrow). In addition, the proliferation of "new" bone is quite prominent.
SLIDE 22: BOVINE FEET (gross): OSTEONECROSIS (NECROSIS OF BONE) - This cow had a condition commonly referred to as "foot-rot". Please name the bones observed in this slide. Can you identify the necrotic bone? Briefly, discuss the cause(s) and lesions of "foot rot" in cattle.
SLIDE 23: BOVINE LIMB (gross): OSTEITIS (ACTINOMYCOSIS) - The lesion observed in this slide developed subsequent to the invasion of bone by Actinomyces bovis. A fistulous tract and granulomatous lesions occurred in soft tissue overlying the involved bone.
SLIDE 24: BOVINE MANDIBLE (gross): OSTEITIS/OSTEONECROSIS (ACTINOMYCOSIS) - Note the inflamed and necrotic bone in this cow with actinomycosis.
SLIDE 25: BOVINE MANDIBLE (photomicrograph): OSTEITIS (ACTINOMYCOSIS) - Observe the well-defined tangled masses of organisms (A. bovis)
SLIDE 26: BOVINE:= MANDIBLE (photomicrograph): OSTEITIS (ACTINOMYCOSIS) - This is a close-up of slide #24. Observe the masses of organisms as well as the inflammatory cells.
SLIDE 27: CANINE FACE (gross): OSTEITIS/OSTEONECROSIS (CRYPTOCOCCOSIS) - This is an example of necrosis and inflammation of bone associated with the invasion of bone by cyptococcal organisms.
SLIDE 28: CANINE VERTEBRAL COLUMN (gross): FRACTURE OF BONE - This spine of this dog was fractured subsequent to the lodgment of a pellet. A young man received a rifle for Christmas and this dog was used for target practice. Note the fracture adjacent to the arrow.
SLIDE 29: EQUINE VERTEBRAL COLUMN (gross) FRACTURE OF BONE - This horse fractured its neck while attempting to jump a fence during a severe thunderstorm. Observe the fracture as well as the compressed spinal cord.
SLIDE 30: CANINE VERTEBRAL COLUMN (gross) FRACTURE OF BONE - This healing vertebral fracture occurred subsequent to an automobile accident; the dog survived for a period of time following the accident because of good nursing. Observe the fractured bone protruding into the vertebral canal resulting in spinal cord compression.
SLIDE 31: EQUINE LIMB (gross): FRACTURE OF BONE - Observe the linear fracture in the joint region; this foal was kicked by its mother.
SLIDE 32: DUCK SKULL (gross): FRACTURE OF BONE WITH SOFT TISSUE DAMAGE - This is an example of fracture with subsequent repair. What is a callous?
SLIDE 34: CHICKEN LIMB (gross): OSTEOGENIC SARCOMA - This osteogenic sarcoma is characterized by proliferation of new bone as well as destruction of bone.
SLIDE 35: CHICKEN LIMB (gross): OSTEOGENIC SARCOMA - This is the same bone demonstrated in slide #34; observe the proliferation of new bone as well as necrotic and hemorrhagic tissue over the cut surface.
SLIDE 36: CANINE LIMB (gross): OSTEOGENIC SARCOMA - Observe the neoplastic mass along the end of this long bone.
SLIDE 37: CANINE LIMB (gross): OSTEOGENIC SARCOMA - This is a close-up view of slide #36.
SLIDE 38: CANINE BONES (gross): HYPERTROPHIC OSTEOARTHROPATHY - These bones are from a dog that had a massive bronchiogenic carcinoma; observe the massive proliferation of new bone over the cortex. Clinically, th legs were markedly enlarged and the animal had difficulty walking.
SLIDE 39: BOVINE JOINT (gross): SUPPURATIVE ARTHRITIS - The calf had a severe suppurative umbilical infection subsequent of E. coli infection; organisms lodged in all major joints resulting in a polyarthritis. Observe the purulent exudate and the thickened synovial membranes. What organisms are oftentimes associated with suppurative arthritis in the horse, in the pig? Discuss the routes by which microorganisms may reach the major joints.
SLIDE 40: PORCINE JOINT (gross): SUPPURATIVE ARTHRITIS - This is a across-section of a joint, observe the purulent exudate.
SLIDE 41: CAPRINE BODY (gross): CHRONIC ARTHRITIS - This goat developed chronic arthritis subsequent to the acute disease. Prior to euthanasia, the animal was unable to walk on the front feet. Treatment and good nursing care were unsuccessful. Note the manner in which this goat had to walk. Also, refer to slide #42.
SLIDE 42: CAPRINE JOINT (gross): CHRONIC ARTHRITIS - This hip joint is from the goat denoted in slide #41. Note the dull appearing and roughed femoral head; also observe the tissue damage around the affected joint.
SLIDE 43: CANINE JOINT (gross): CHRONIC ARTHRITIS/HIP DYSPLASIA - Chronic arthritis in this dog developed subsequent to a condition known as "hip dysplasia" (a German Shepherd dog). Note the articular cartilage as well as the chronic changes of the synovial membrane. Also, a joint "mouse" can be observed.
SLIDE 44: CHICKEN JOINTS (gross): MYCOPLASMAL ARTHRITIS - This bird had a chronic respiratory disease caused by Mycoplasma gallisepticum. Subsequently, organisms localized in the joints resulting in a severe synovitis.
SLIDE 45: PORCINE JOINTS (gross): ARTHRITIS (ERYSIPELAS) - The joints are from pigs with arthritis associated with swine erysipelas. Observe the markedly swollen joints. What lesions would you expect to find in the heart of these pigs? Describe the skin lesions that you would expect to find in pigs suffering from erysipelas.
SLIDE 46: PORCINE JOINT (gross): ARTHRITIS (ERYSIPELAS) - Observe the marked changes in the articular tissue; especially in the synovial membrane. What changes do you observe in the articular cartilage?
SLIDE 47: CANINE JOINT (gross): DEGENERATIVE ARTHROPATHY - This 12-years old German Shepherd developed pain in the front and rear limbs over a 3 to 4 year period. Note the grooves as well as erosions of the articular cartilage in this stifle joint.
SLIDE 48: CANINE JOINT (gross): DEGENERATIVE ARTHROPATHY - This joint is from the same dog denoted in slide #47. In addition to the changes involving the articular cartilage, note the presence of bony spicules along the articular margins.
SLIDE 49: PORCINE: VERTEBRAL COLUMN (gross): DISCOSPONDYLITIS - Note the accumulation of a whitish material between and around these vertebral bodies. This material is pus and this is consistent with an abscess of the intervertebral disc and the vertebral bodies.
SLIDE 50: BOVINE VERTEBRAL COLUMN (gross): SUPPURATIVE SPONDYLITIS - Note the accumulation of a whitish material in the vicinity of the spinal canal. The definitive diagnosis in this case was "Necrobacillosis".
SLIDE 49: CANINE VERTEBRAL COLUMN (gross): INTERVERTEBRAL DISC PROTRUSION - The protruded discs in this dog resulted in severe damage to the spinal cord. Please note the protruded discs as well as the hemorrhage along the spinal cord.
SLIDE 50: CANINE VERTEBRAL COLUMN (gross): INTERVERTEBRAL DISC PROTRUSION - The protruded disc in this dog resulted in severe damage to the spinal cord. Please note the protruded discs as well as the hemorrhage along the spinal cord.
SLIDE 51: PORCINE:
SLIDE 51: CANINE HUMERUS (gross): OSTEOCHONDRITIS DISSECANS - This is the humerus from a German Shepherd that exhibited mild signs of lameness in the front limbs. Note the partial and complete separation of articular cartilage in the bones denoted in this slide.
SLIDE 52: CANINE HUMERUS (gross): OSTEOCHONDRITIS DISSECANS - Note the detached articular cartilage; trauma is considered to be the primary cause.
SLIDE 53: CANINE HIP JOINT (gross): DYSPLASIA OF THE HIP JOINT - This dog developed signs of hip dysplasia around 5 months of age. Subsequently, secondary changes developed (such as arthritis, synovitis, etc.). In this slide, you should be able to observe the flattened and deformed head of the femur. In addition, the acetabulum was quite shallow. (What is a joint mouse?)
SLIDE 54: CANINE ULNA (gross): UNUNITED ANCONEAL PROCESS - Observe the normal and the separated anconeal process in this 6-month old dog. This was an incidental finding at the time of necropsy; actually the dog died subsequent to canine distemper.
SLIDE 55: CHICKEN FEET (gross): ARTICULAR GOUT - This bird has a condition known as articular gout; there is heavy deposition of uric acid in the joints resulting in enlargement of the feet.
SLIDE 56: CHICKEN FEET (gross): ARTICULAR GOUT - Please compare the normal and abnormal feet. Note the marked difference in size.
SLIDE 57: CHICKEN FOOT (gross): ARTICULAR GOUT - Note the thick, white material over the incised surfaces of the joint (deposition of uric acid crystals).
SLIDE 58: PARAKEET BODY (gross): ARTICULAR GOUT - Note the deposition of uric acid crystals associated with several joints.
SLIDE 59: CHICKEN BODY (gross): PEROSIS - Observe the abnormal position of the legs; this bird had difficulty walking; also note the curled toes.
SLIDE 60: CHICKEN BODY (gross): PEROSIS - In this bird, the achilles tendon was displaced; note the manner in which the abnormal leg is held; enlarged joints are prominent.
SLIDE 61: CHICKEN BODY (gross): CURLY-TOE PARALYSIS - Note the position of the toes; this chick was unable to walk and had to rest on its hocks.
