Pathology

Question 1

Answer 1

Polydactyly- increased number of digits

Question 2

Answer 2

Amelia- absence of a limb

Question 3

Answer 3

Kyphosis (hump)

Question 4

Chondrodysplasia

Answer 4

Disorder of endochondral ossification

Both physis (metaphyseal growth plate) and/or Articular Epiphyseal Complex (AEC) is involved.

Mostly genetic defects or undetermined cause.

Question 5

Articular Epiphyseal Complex

Answer 5

The zone of endochondral ossification beneath the articular cartilage in growing animals. The AEC is composed of a layer of articular cartilage and a subjacent layer of growth (epiphyseal) cartilage. The growth cartilage is present only in immature animals, and its structure and function is similar to that of the physis (growth plate).

Question 6

Answer 6

Texel Chondrodysplasia. Short. Characteristic wide-based stance. Normally euthanized or not allowed to have progeny.

Question 7

Answer 7

Texel chondrodysplasia. Erosion of femur head cartilage. The animals also have tracheal collapse and dyspnoea.

Question 8

Answer 8

Spider lamb syndrome. Deformity of hind limbs.

Question 9

Answer 9

Spider lamb syndrome. Abnormal ossification centers in the olecranon (left) and supraglenoid tubercle of the scapule (right). All joined.

Question 10

Answer 10

Brachiocephalic snorter dwarfism

Bulldog calves.

Question 11

Answer 11

Chondrodysplasia. Shortened legs with normal body. Irregularly thickened physes in the distal radius and proximal humerus in an affected pup. The lessions can be confused with rickets. Can be selected for (Dachsund)

Question 12

Osteochondrosis

Answer 12

Joint disorder. It’s a dysplasia affecting growth plates. Articular epiphyseal complex and less involvement of the metaphyseal growth plate. Focal failure of endochondral ossification.

Picture: in a growing animal if you have a lack of vascular supply in the articular cartilage you can end up with necrotic cartilage. So it won’t undergo hypertrophy. Necrotic cartilage will be retained and vascular invasion will not occur. Focal problem but it disrupts old cartilage.

**Lack of avascular supply therefore necrosis, and disruption of enchondral ossification- will affect later vascular invasion as well**

Question 13

Name and cause?

Answer 13

Osteochondrosis.

Genetic defect, trauma, rapid growth, others?

Question 14

Answer 14

Osteochondrosis. The cartilage extending to the epiphysis is from epiphyseal cartilage that has failed to undergo endochondral ossification and retained cartilage has been converted to bone.

Question 15

Answer 15

Osteochondrosis with the erosion of the articular cartilage (osteochondrosis dissecans).

Question 16

Answer 16

Osteopetrosis

Defective osteoclastic function. Poor remodeling of primary spongiosa (mineralized cartilage matrix). Medullary cavity filled with spongy bone. Increased bone fragility.

Trabecular grows down to the diaphysis and not remolded by osteoclasts. CONE SHAPED LESION IN A BONE. Grayish discouloration.

Question 17

Answer 17

Osteopetrosis. Primary trabeculae are retained and fill the entire medullary cavity. Retained straight undremodeled trabeculae containing cartilaginous cores fill the medullary cavity.

Question 18

Answer 18

Osteoporosis. Calcium deficiency causes osteoporosis. Reduced amount of qualitatively normal bone. Imbalance between bone formation and bone resorption in favour of the latter. Bone is normal but there isn’t enough.

Picture: The cortices, reduced density of cancellous bone and serous atrophy of medullary fat. The latter suggests either starvation or malabsorption e.g. parasitism or Johne’s disease.

BIG PROBLEM in SHEEP due to starvation. Bone marrow looks abnormal and trabecular bone at the end looks abnormal as well.

Question 19

Answer 19

Trabecular bone is not normal. Severe case of osteoporosis in a sheep. This is what happens when you keep loading the weight. So the reinforcement bars form if the animal is able to produce some bone.

Question 20

Causes of Osteoporosis

Answer 20

1. Nutrition deficiencies- Vit C def (cofactor in enzymes for the production of collagen), Hypoproteinaemia, Copper def (cofactor in enzymes for the production of collagen), **Calcium def**, low Calcium, high phosphorous diets, phosphorous def, hypervitaminosis A, GI parasitism

**Excess phosphorous diets can cause hypocalcium- which can cause osteoporosis. Not enough phorsophorous will cause osteoporosis by istelf though.

2. Endocrine disease- hyperadrenocorticism, sex hormone deficiency

Question 21

Wolff’s Law

Answer 21

Use it or lose it.

Bone adapts and remodels in response to the mechanical demands placed upon it. According to Wolff’s law, it is deposited at sites where it is required and resorbed where it is not. For example, trabeculae in the metaphysis and epiphyses of long bones are aligned in directions which reflect the compressive forces associated with weight bearing.

Question 22

Answer 22

Growth arrest line & Osteoporosis. Usually an indication that physeal growth ceased then recommended on several occasions probably due to starvation.

Question 23

Answer 23

Osteoporosis- excessive porosity of trabecular bone and pathological fracter. Because of it’s greater surface area, trabecular bone disappears more rapidly than cortical bone in animals with osteoporosis. Vertebral bodies are particularly susceptible.

Question 24

Rickets/ osteomalacia

Answer 24

Defective mineralization of physeal cartilage at sites of endochondral ossification.

Vitamin D or P deficiency.

(Vitamin D enhances absorption of P (Phosphorous) and Ca from small intestine. Stimulates the release of P and Ca from bone (resorption). Enhances P resorption in the kidney). AIM OF VIT D: Hypercalcaemia (Ca in the blood)

** sunlight is key.

Question 25

Answer 25

Rickets. Vitamin D deficiency. Ca and P crystals cause precipitation of minerals into the trabecular bone. So without Vitamin D- unmineralized cartilage- DOES NOT TRANSFORM INTO TRABECULAR BONE. THICKENED GROWTH PLATE with NO trabecular bone. Osteoblasts and osteoclasts- reach the metaphyseal plate to do their job but without the mineralization- therefore they become disordered but still undergo hypertrophy. So it basically becomes jumbled.

Question 26

Answer 26

Rickets. Enlarged costrochondral junction (on the side) because it is disorganized. Metaphyseal plate is not as it should be. \* Difficult to distinguish rickets from chondrodysplasis (?)

Question 27

Answer 27

Rickets. Irregular thickening of rapidly growing physes. Enlarged costrochondral junctions.

Question 28

Answer 28

Fibrous osteodystrophy. Widespread osteoclastic resorption of bone and replacement by fibrous connective tissue. Primary, secondary, and nutritional hyperparathyroidism. Parathyroid hormone is essential for bone formation. Potent stimulator of osteoclastic bone resorption. Bone: Potent stimulator of osteoclastic bone resorption. In the Kidney: Increases resorption of Calcium. Increases excretion of Phosphorous. Promotes conversion of vitamin D into its active metabolite.

Question 29

Primary hyperparathyroidism and Secondary Hyperparathyroidism

Answer 29

Problem with parathyroid gland. For example, a tumour. Produces excess parathyroid hormone. Therefore bone resorption. Secondary parathyroidism. Also causes excess PTH and therefore osteoclastic bone resorption. Why not osteoporosis? With increase in parathyroid hormone. Transformation of bone marrow stem cells into fibroblasts and therefore you have excess fibroblast production. USUALLY with Fibrous Osteodystrophy, it is CHRONIC problem. MORE SEVERE. YOU CAN HAVE BOTH.

Question 30

Answer 30

Replacement of maxillary bone with fibrous tissue. Aka "Big Head" The disease is usually nutritional in origin with excess phosphorous. A diet rich in bran. "Bran disease" Not the same in other species.

Question 31

Answer 31

Cortical bone is okay but trabecular bone is affected. Swollen jaw.

Question 32

Answer 32

Fibrous osteodystrophy. Bilateral swelling of maxillae. In a dog it is caused by renal disease. Renal secondary hyperparathyroidism. Much worse when renal failure occurs early when the skelton is still forming.

Question 34

Answer 34

Chronic fluorosis. Toxic osteodystrophies. Black discolouration of teeth as a result of toxicosis during odontogenesis and the periosteal exostoses of the metatarsals.

Question 35

Answer 35

Osteomyelitis Haematogenous - Bacteraemia or Septicaemia- bones are highly vascularized. Calves and foals Direct Implantations- wounds, fractures. Penetrating trauma. Local infections- From adjacent tissues e.g. arthritis.

Question 36

Osteomyelitis pathogenesis

Answer 36

Bones are highly susceptible to bacteraemia and septicaemia because bacteria lodge in the metaphyseal capillaries. Peculiar vascular supply in the bone. Usually complicates inflammation- which you already have... thrombosis and infarction too.

Question 37

Answer 37

Osteomyelitis- spread of infection The loop is where the bacteraemia spread, cause problems.

Question 38

Answer 38

Embolic Osteomyelitis. Younger more susceptible (LOOPS) Severe cases detatchment of the growth plate. You can see the spread of infection. Vessels are not as numerous as in the growing bone and without vascular loops- so in adult animals they are less susceptible. FOALS ARE MOST SUSCEPTIBLE particularly if they have salmonella. Difficult to fix because antibiotics do not reach the bone easily. Severe issue in foals. Rim of active hyperaemia borders the pale region. Pale region in the metaphysis extending downward to the top middle border represents suppurative inflammation and necrosis. A fissure is a result of bone lysis caused by the infection.

Question 39

Answer 39

Embolic (suppurative) osteomyelitis.

Question 40

Answer 40

Osteomyelitis. Bacterial inflammation has destroyed the physis and has extended into the periosteum and joint cavity.

Question 41

Answer 41

Suppurative osteomyelitis. Distinct pale white foci adjacent to the growth plate. Septic infacts with slight red zone of inflammation around them. SEQUESTRUMS Usually Streptococcus equi.

Question 42

Answer 42

Mandibular osteomyelitis. Lumpy Jaw. Cavitated lesions in the mandible caused by inflammation. Regional LNs are concurrently affected.

Question 43

Answer 43

Osteosarcoma. Most common in dogs. Most common in the distal femur. Predisposing factors: weight, big large breeds, load bearing, poor prognosis (usually micro metastysis around- amputation is usually the way to go followed by chemotherapy but often only gives them a year)- usually die in 2-3 months Osteosarcoma - some production of osteod (woven bone)- if you don't have osteod in histological section you cannot make the diagnosis. The osteo sarcoma lyses and replaces normal bone. Reactive periosteal new bone formation- large area of haemorrhage (arrows) and necrosis (asterix)

Question 44

Answer 44

Ossifying fibroma. Well differentiated fibrous tissue with scattered spicules of woven bone lined by osteoblasts.

Question 45

Answer 45

Chondrosarcoma. Widespread white foci within the mass are areas of mineralization. Can destroy and replace normal bone structure.

Question 46

Answer 46

Lymphoma.

Question 47

Answer 47

Multiple myeloma. Multifocal lytic lesions are typical of plasma cells myeloma. Cancer of the bone marrow.

Question 48

Answer 48

Hypertrophic (pulmonary) osteopathy- Marie's disease Tumour in the thorax is usually the cause. Production of new bone in the digits (periosteum). Hypertension in the capillaries of the digits caused by the tumours in the thorax (not well understood this is just a theory).

Question 49

Luxation vs. subluxation

Answer 49

Complete dislocation and partial dislocation (subluxation)

Question 50

Answer 50

Osteogenesis imperfecta (an inherited type I collagen defect). Abnormal joint laxity.

Question 51

Answer 51

Piglet with congenital arthrogryoposis. One or more joints are hyperextended or hyperflexed due to underdevelopment of the skeletal muscles and their tendons. The joint capsule may also be abnormally tight.

Question 52

Answer 52

Severe chronic degenerative joint disease of the hip joint, with severe fibrous thickening of the joint capsule.

Question 53

Answer 53

Structure of synovial membrane- well vascularized and there is no basement membrane beneath the synociocytes (which produce and turnover synovial fluid)

Question 54

Synovial fluid

Answer 54

Viscous \*due to glycoprotein content, clear, and colourless (slightly yellow in horses) \* low total nucleated cell count- some lymphocytes, monocytes/ macrophages, with a few synoviocytes; neutrophils comprise less than 10% of nucleated cells. \* Lubricates joints and nourishes articular cartilage-- CHIEF SOURCE IN ADULT ANIMALS (in young animals, diffusion from blood vessels in the epiphyseal growth cartilage and subchondral bone aids)

Question 55

Answer 55

Cat with a synovial sarcoma- the cell of origin of this tumour is the synovioblast, the cell from which synoviocytes is derived from in health

Question 57

What is this showing the structure of? What is it mainly made up of? What maintains the matrix?

Answer 57

Articular cartilage. 70-80% water. Proteoglycans with water. Matrix molds itself so underlying subchondral bone gets a more evenly distributed load. \*\* Withstands compressive forces during weight bearing and shear forces during motion. \*\*Chondrocytes maintains the matrix- new collagen; new proteoglycans and degrading the stuff they made previously. Constantly in flux. Health of the matrix and collagen fibres and water content.... depends on health of chondrocytes.

Question 58

What happens to articular cartilage in an adult?

Answer 58

Chondrocyte mitotic activity is minimal in adults and teh cellularity decreases with age. It becomes yellow-tinged, opaque and superficially roughened, and has reduced elasticity

Question 59

What are the two growth plates and what do they do?

Answer 59

Metaphyseal growth plate- at the metaphysis- remnants from endochondral ossification. Articular epiphyseal complex (AEC)- articular cartilage overlies and merges with the epiphyseal growth cartilage

Question 60

What is the AEC?

Answer 60

E= epiphysis M= metaphysis P= physis or growth plate AC= Articular cartilage EGC = epiphyseal growth cartilage (blood vessels within it and the fact that it is not clearly demarcated from the overlying AC) \* AEC is both AC and EGC

Question 61

What pathology is this? If the split propagates through the overlying healthy articular cartilage, what is it called then?

Answer 61

Split in the epiphyseal growth cartilage (underlying the articular cartilage) because of OSTEOCHRONDROSIS. If the split propagates through the overlying healthy articular cartilage, the disease is known as OSTEOCHONDRITIS DISSECANS (OCD).

Question 62

Answer 62

Osteochondritis dissecans (OCD) Flaps of articular cartilage developing over humeral heads.

Question 63

In mature animals, what prevents diffusion of nutrients from bone marrow to the chondrocytes of the articular cartilage?

Answer 63

In mature animals, subchondral bone prevents diffusion of nutrients from bone marrow to the chondrocytes of the articular cartilage. Articular cartilage is dependent on nourishment from the synovial fluid.

Question 64

In young animals, where are they receiving nourishment from?

Answer 64

Chondrocytes of articular cartilage receive nourishment from both the synovial fluid and via blood vessels in the underlying epiphyseal growth cartilage.

Question 65

What causes decreased thickness in articular cartilage?

Answer 65

Overloading and underloading

Question 66

Answer 66

Osteodystrophia fibrosa (metabolic bone disease). Subchondral bone collapse and invagination of articular cartilage of the humeral head.

Question 67

What are the two types of injury and healing that occurs in the structures shown here?

Answer 67

Superficial cartilage lacerations or defects. Above the blue line (aka tide mark) can heal fairly well. Adjacent living chondrocytes can go into mitosis- can make new cartilage matrix and new glycosaminoglycans. BUT if deep cartilage injury- into the subchondral bone that involves the tidemark, the mineralized zone of cartilage or the subchondral bone also stimulate transient replicative and synthetic activity by adjacent chondrocytes. Granulation tissue (called pannus in this case)-- red grainy appearance-- grows up from subchondral bone to fill defect. The fibrocartilaginous "scar" may persist indefinitely and does not perform as well as the original articular cartilage when subjected to mechanical loading.

Question 68

What is this? Where is it derived from?

Answer 68

Pannus in severe degenerative joint disease (DJD) Pannus is derived from bone marrow spaces in subchondral bone AND synovium (line joint cavities, bursae, and tendon sheaths- SYNOVIAL MEMBRANE)

Question 69

What is synovium?

Answer 69

A thin, outer, fibrofatty connective tissue layer which is rich in blood vessels, lymphatics and nerves and which merges with fibrous joint capsule. It liines joint cavities, bursae, tendon sheaths. \*the synovial membrane\*

Question 70

What are synoviocytes? What are the two types?

Answer 70

Type A cells- phagocytic and APCs Type B cells- akin to fibroblasts and produce hyaluronan and matrix components such as collagen, they can also release enzymes capable of degrading cartilage and bone.

Question 71

Answer 71

Pannus can lead to fibrous or bony AKYLOSIS of joints- this pig's stifle joint has undergone fibrous ankylosis.

Question 72

Answer 72

Bony ankylosis of the second and third phalanges and the navicular bone in a horse.

Question 73

Answer 73

Loss of proteoglycans, so too much water. Actually softer. Chondromalacia- articular cartilage matrix degeneration. If the animal keeps moving the joint after chondromalacia- it starts to wear.

Question 74

Answer 74

Fibrillation of the cartilage. Continued wear of softened articular cartilage (chondromalacia- loss of proteoglycans, proportional increase in water content) may result in grooving of the cartilage

Question 75

What causes fibrillation and eburnation? What are they?

Answer 75

Chondromalacia may progress to fibrillation (grooves) of the cartilage and eventually to loss of cartilage and exposure, thickening and polishing of the underlying subchondral bone (= eburnation).

Question 76

Answer 76

Severe Degenerative Joint Disease (DJD) with eburnation of subchondral bone

Question 77

Answer 77

Femoral heads from dogs with chronic hip dysplasia. Severe DJD with eburnation of subchondral bone.

Question 78

Answer 78

Synovial villous hyperplasia and hyperaemia in a pig with septic arthritis

Question 79

Answer 79

Periarticular osteophytes in chronic joint disease.

Question 80

Answer 80

Periarticular osteophytosis-- in chronic DJD

Question 81

Answer 81

Synovial chondromas/ osteochondromas- transitional zone of the synovium. Despite their name, these are metaplastic rather than neoplastic.

Question 82

Answer 82

Joint mice. Due to chronic arthritis (Caprine Arthritis- Encephalitis- CAE- viral infection). Can also get soft joint mice that are soft- blood clots, fibrin coagula, detached synovial villi \* Just cartilage fragments or osteophytes break free and interfere with joint movement \* In OCD (osteochondritis dissecans) common.

Question 83

Answer 83

Subchondral bone cysts. Often in horses. Most often due to osteochondrosis but sometimes due to damage to the articular cartilage and/or subchondral bone.

Question 84

Answer 84

Subchondral bone cysts.

Question 85

Answer 85

End stage joint due to DJD

Question 86

What is sometimes regarded as the primary lesion in DJD?

Answer 86

Sclerosis (stiffening) of the subchondral bone plate- predisposing the articular cartilage to injury. If DJD is due to secondary to metabolic or nutritional disease of the underlying bone, the subchondral bone may collapse rather than become sclerotic and eburnated.

Question 87

What can lead to DJD? What are the two types?

Answer 87

Virtually any insult that structurally damages the articular cartilage of subchondral bone or the supporting structures of joints can lead to DJD. \* Primary DJD- no apparent predisposing cause- older animals- accumulated minor wear and tear injuries on joints \* Secondary DJD- predispoign cause- obesity, exercise, injury

Question 88

Answer 88

Distal femurs of an old cow. Chronic DJD of the stifle joints.

Question 89

Answer 89

Horse- hip joint with acute trauma. Rupture of the ligament of the head of the femur and haemarthrosis.

Question 90

What happens with permanent or chronic luxation?

Answer 90

necrosis- cells of the articular cartilage will die off, matrix will disappear, peranent luxation- bone end could end up being covered by collagen or fibrocartilage from pannus. If there is a lot of movement- periosteal bone growth (new spurs).

Question 91

What is haemarthrosis?

Answer 91

Bleeding into joints- from trauma, neoplasia, or inflammation. Repeated bleeds (coagulopathies. e.g. haemophilia A or B)-- iron positive charge, glycosaminoglycans negative charge-- if you have too much free iron, it neutralizes the charge which mucks up the synovial barrier- so seepage of plasma proteins including fibrinogen... \*\* therefore accelerated journey with DJD

Question 92

What is the source of pain in joint injuries?

Answer 92

Damaged synovium, subchondral bone, joint capsule, ligaments, and overlying soft tissue. \*\*No nerves (no blood vessels, no lymphatics) in articular cartilage\*\* (minus some rodents)

Question 93

Answer 93

Congenintal arthrogryposis (crooked joints) and torticollis \* arthrogryposis- hyperextension or hyperflexion of one or more joints due to a CNS or PNS insult that causes inadequate muscle development in utero

Question 94

Answer 94

Congenital contracted tendons (can improve)

Question 95

Answer 95

Carpal subluxation

Question 96

Answer 96

Congenital lateral luxation of the patella (usually medial in small dogs)- not disuse atrophy of skeletal muscles

Question 97

Answer 97

Bilateral hip dysplasia and lateral subluxation of the femoral heads. Lack of conformity between the femoral heads and the acetabula- laxity and subluxation of the coxofemoral joints- DJD (one theory growing bony structure faster- so doesn't grow the ligaments and tendons to hold everything into place properly)

Question 98

Answer 98

6 month old German Shepherd- chronic degeneration of cartilage due to hip dysplasia. (could be osteochrondrosis- but you would need histo to prove it)

Question 99

Answer 99

Infectious polyarthritis due to bacteraemia \*\* particularly common in young livestock \*\* haematogenous spread to the joints- umbilical infections; resp. tract infections; GIT infections (basic E. coli)-- it would go everywhere, not just joints

Question 100

Answer 100

Osteomyelitis of the metaphysis and epiphysis (it has undermined the overlying articular cartilage)- bacteria might extend from focus into adjacent joint cavity.

Question 101

Answer 101

Fibrinous (left) vs. suppurate (right) exudate from infected synovial joints \* Pyogenic- Staphylococcus.

Question 102

Answer 102

Coagulated fibrin in joint cavities in septic arthritis.

Question 103

Answer 103

Severe septic suppurative arthritis with copious blood stained pus in the joint cavity.

Question 104

Answer 104

Rhematoid arthritis- rare in dogs. IgG, IgM, or IgA auto-antibodies directed against Fc region of the IgG--\> persistent immune complex deposition in the synovium--\> complement activation--\> chemotaxis of leukocytes--\> release of cytokines and lysosomal enzymes--\> severe joint damage.