Pathology Flashcards
Polydactyly- increased number of digits
Amelia- absence of a limb
Kyphosis (hump)
Chondrodysplasia
Disorder of endochondral ossification
Both physis (metaphyseal growth plate) and/or Articular Epiphyseal Complex (AEC) is involved.
Mostly genetic defects or undetermined cause.
Articular Epiphyseal Complex
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).
Texel Chondrodysplasia. Short. Characteristic wide-based stance. Normally euthanized or not allowed to have progeny.
Texel chondrodysplasia. Erosion of femur head cartilage. The animals also have tracheal collapse and dyspnoea.
Spider lamb syndrome. Deformity of hind limbs.
Spider lamb syndrome. Abnormal ossification centers in the olecranon (left) and supraglenoid tubercle of the scapule (right). All joined.
Brachiocephalic snorter dwarfism
Bulldog calves.
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)
Osteochondrosis
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**
Name and cause?
Osteochondrosis.
Genetic defect, trauma, rapid growth, others?
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.
Osteochondrosis with the erosion of the articular cartilage (osteochondrosis dissecans).
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.
Osteopetrosis. Primary trabeculae are retained and fill the entire medullary cavity. Retained straight undremodeled trabeculae containing cartilaginous cores fill the medullary cavity.
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.
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.
Causes of Osteoporosis
- 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.
- Endocrine disease- hyperadrenocorticism, sex hormone deficiency
Wolff’s Law
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.
Growth arrest line & Osteoporosis. Usually an indication that physeal growth ceased then recommended on several occasions probably due to starvation.
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.
Rickets/ osteomalacia
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.
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.
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 (?)
Rickets. Irregular thickening of rapidly growing physes. Enlarged costrochondral junctions.
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.
Primary hyperparathyroidism and Secondary Hyperparathyroidism
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.
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.
Cortical bone is okay but trabecular bone is affected. Swollen jaw.
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.
Chronic fluorosis. Toxic osteodystrophies. Black discolouration of teeth as a result of toxicosis during odontogenesis and the periosteal exostoses of the metatarsals.
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.
Osteomyelitis pathogenesis
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.
Osteomyelitis- spread of infection
The loop is where the bacteraemia spread, cause problems.
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.
Embolic (suppurative) osteomyelitis.
Osteomyelitis. Bacterial inflammation has destroyed the physis and has extended into the periosteum and joint cavity.
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.
Mandibular osteomyelitis. Lumpy Jaw. Cavitated lesions in the mandible caused by inflammation. Regional LNs are concurrently affected.
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)
Ossifying fibroma. Well differentiated fibrous tissue with scattered spicules of woven bone lined by osteoblasts.
Chondrosarcoma. Widespread white foci within the mass are areas of mineralization. Can destroy and replace normal bone structure.
Lymphoma.
Multiple myeloma. Multifocal lytic lesions are typical of plasma cells myeloma. Cancer of the bone marrow.
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).
Osteogenesis imperfecta (an inherited type I collagen defect). Abnormal joint laxity.
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.
Severe chronic degenerative joint disease of the hip joint, with severe fibrous thickening of the joint capsule.
Structure of synovial membrane- well vascularized and there is no basement membrane beneath the synociocytes (which produce and turnover synovial fluid)
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
What is this showing the structure of?
What is it mainly made up of?
What maintains the matrix?
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.
What is the AEC?
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
What pathology is this? If the split propagates through the overlying healthy articular cartilage, what is it called then?
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).
Osteochondritis dissecans (OCD)
Flaps of articular cartilage developing over humeral heads.
In mature animals, what prevents diffusion of nutrients from bone marrow to the chondrocytes of the articular cartilage?
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.
In young animals, where are they receiving nourishment from?
Chondrocytes of articular cartilage receive nourishment from both the synovial fluid and via blood vessels in the underlying epiphyseal growth cartilage.
Osteodystrophia fibrosa (metabolic bone disease). Subchondral bone collapse and invagination of articular cartilage of the humeral head.
What are the two types of injury and healing that occurs in the structures shown here?
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.
What is this? Where is it derived from?
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)
Pannus can lead to fibrous or bony AKYLOSIS of joints- this pig’s stifle joint has undergone fibrous ankylosis.
Bony ankylosis of the second and third phalanges and the navicular bone in a horse.
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.
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
What causes fibrillation and eburnation? What are they?
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).
Severe Degenerative Joint Disease (DJD) with eburnation of subchondral bone
Femoral heads from dogs with chronic hip dysplasia.
Severe DJD with eburnation of subchondral bone.
Synovial villous hyperplasia and hyperaemia in a pig with septic arthritis
Periarticular osteophytes in chronic joint disease.
Periarticular osteophytosis– in chronic DJD
Synovial chondromas/ osteochondromas- transitional zone of the synovium. Despite their name, these are metaplastic rather than neoplastic.
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.
Subchondral bone cysts. Often in horses. Most often due to osteochondrosis but sometimes due to damage to the articular cartilage and/or subchondral bone.
Subchondral bone cysts.
End stage joint due to DJD
Distal femurs of an old cow.
Chronic DJD of the stifle joints.
Horse- hip joint with acute trauma. Rupture of the ligament of the head of the femur and haemarthrosis.
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
Congenital contracted tendons (can improve)
Carpal subluxation
Congenital lateral luxation of the patella (usually medial in small dogs)- not disuse atrophy of skeletal muscles
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)
6 month old German Shepherd- chronic degeneration of cartilage due to hip dysplasia. (could be osteochrondrosis- but you would need histo to prove it)
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
Osteomyelitis of the metaphysis and epiphysis (it has undermined the overlying articular cartilage)- bacteria might extend from focus into adjacent joint cavity.
Fibrinous (left) vs. suppurate (right) exudate from infected synovial joints
* Pyogenic- Staphylococcus.
Coagulated fibrin in joint cavities in septic arthritis.
Severe septic suppurative arthritis with copious blood stained pus in the joint cavity.
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.
