Bone and Joints 2

Question 1

What is rickets and how does it present

Answer 1

-Rickets is the failure of EO: failure to mineralize cartilage/bone undergoing EO
-It presents as animals being stif/lame, limbs may “bow” as they are poorly mineralized and soft, affects growing animal (growth retardation)

Question 2

What is osteomalacia and how does it differ from rickets

Answer 2

-Osteomalacia occurs during periods of bone turnover/remodeling when P or vit D deficient. Osteoid deposited at that time goes unmineralized, making bones soft, fragile, and deformed
-It differs from rickets because it is in adults (growth ceased) so centers of EO are not affected

Question 3

What causes fibrous osteodystrophy and what are the 2 forms

Answer 3

-Increased PTH causing osteoclastic resorption and fibrous tissue replaces
-The two forms are primary hyperparathyroidism form and secondary hyperparathyroidism form

Question 4

What are the two forms within the secondary hyperparathyroidism form of fibrous osteodystrophy

Answer 4

-Nutritional and renal forms

Question 5

What is the pathogenesis of the nutritional form of fibrous osteodystrophy, and what are some causes

Answer 5

Pathogenesis: decreased serum Ca causing an increase in PTH leading to more resorption than formation. This high remodeling rate means that the lamellar bone that is resorted is replaced by weaker woven bone.
Causes: diets low in Ca and high in P (High P in diet exacerbates low Ca as interferes with absorption). These diets include all meat diets in dogs and cats, diets high in bran with low uality roughage in horses, poorly balanced grain rations (low in Ca or vit D) in pigs, low Ca diets (fruits and veg) in reptiles

Question 6

What is the pathogenesis of the renal form of fibrous osteodystrophy and what is an example

Answer 6

Pathogenesis: Associated with chronic renal failure. Reduction in functional nephrons leads to a decreased GFR causing reduced P excretion (hyperphosphatemia). This results in increased P, decreased Ca, and increased PTH. This leads to a higher rate of resorption than formation, leading to weaker fibrous tissue replacing lamellar bone

Question 7

What are some examples of toxic osteodystrophies

Answer 7

-Lead: interferes with osteoclastic resorption band of increase bone density (osteosclerosis) in metaphysis- ‘lead line’
-Fluoride: cattle/sheep. Bones exhibit periosteal hyperostosis (new bone formation). Also affects teeth- defective enamel
-Vitamin A: cats that consume high quantities of bovine liver longterm, deforming cervical sponylosis- osteophyte formation around cervical vertebrae leading to ankylosis

Question 8

What is osteonecrosis and what age and breed of dogs are most affected

Answer 8

-Osteonecrosis is necrosis ischemia to the femoral head secondary to venous obstruction leading to infarction within the femoral head. Resorption of this necrotic bone leads to collapse of the epihysis/articular cartilage.
-Young small terries and poodles ages 4-8 months are most affected (called Legg-Calve-Perthes disease)

Question 9

What is osteomyelitis

Answer 9

Inflammation of the bone, often involving additional bone necrosis/removal/new bone formation

Question 10

What bacteria and fungi can cause osteomyelitis and how are they introduced into the bone

Answer 10

Bacteria: Staph aureus, T. Pyogenes, salmonella
Fungi (less commonly): Blastomyces dermatitidis, Coccidoies immitis, cryptococcus neoformans
Methods of introduction: compound fracture, extension from surrounding tissue/joint, hematogenously

Question 11

What are some consequences of osteomyelitis

Answer 11

-Lack of drainage causing persistent bacteria leading to pathological fractures and discharging sinus tracts
-Isolated fragments of necrotic bone surrounded by exudate (sequestrum)
-Exudate surrounded by collar of reactive bone which is created to try to contain inflammatory process (involucrum)

Question 12

What is craniomandibular osteopathy (Lion jaw) and what breeds/ages of dogs are more affected

Answer 12

-Bilateral symmetrical new periosteal and endosteal bone formation with irregular thickening of mandibular rami, occipital/temporal bones, tympanic bullae (dense spikes new bones)
-WHWT, Scottish and Cairn terriers, Great Danes, boxers between 4-7 months. Doesn’t happen in cats

Question 13

What is an osteochondroma

Answer 13

-Benign dysplasic exostosis arising from the surface of bone adjacent to physics or subarticular growth cartilage
-Arise in young animals and enlarge until skeletal maturity
-Once bone growth ceases cartilage cap replaced by bone

Question 14

What is the pathogenesis and most common locations of osteochondromas

Answer 14

-Pathogenesis: physeal cartilage “pinched off” and grows laterally- ectopic/dysplastic endochondral bone growth. May undergo malignant transformation and become a chondrosarcoma or osteosarcoma
-Location: variable, commonly metaphases of long bones, pelvis, ribs, scapula, vertebrae, lesions in some locations interfere with action of ligaments/tendons and don’t seem to reabsorb

Question 15

What are the types of bone neoplasia

Answer 15

-Osteomas: uncommon, benign, usually on head (jaws/nasal sinuses of horses, sheep and cattle)
-Osteosarcomas: neoplastic osteoblasts form bone and/or osteoid, if cartilage also produced: chondroblastic or combined osteosarcoma, can arise from central or surface locations

Question 16

Where do 80% of osteosarcomas occur and what is “away from elbow, around the knee”

Answer 16

-80% occur in the central metaphyses
-Away from elbow =proximal humerus, distal radius
-Around the knee= distal femur, proximal tibia

Question 17

Are osteosarcomas more likely in the forelegs or the hindlegs, and do they cross the joint cavities

Answer 17

-Tumors in forelegs are twice as common as in hindlegs
-They do not cross joint cavities

Question 18

Where do 20% of osteosarcomas occur

Answer 18

-In the axial skeleton: skull, ribs (esp costochondral junction), vertebrae, and pelvis

Question 19

What do osteosarcomas look like grossly and microscopically

Answer 19

-Gross: growth rapid and painful, irregular grey white lobules fill medullary cavity and destroy cortical bone leading to new bone formation (Codmans triangle)
-Microscopically: pleomorphic cells producing osteoid, islands of eosinophilic osteoid produced by malignant osteoblasts

Question 20

What is the metastatic outlook, prognostics, and radiology of central/medullary osteosarcomas

Answer 20

-Metastasis: aggressive local invasion, early pulmonary metastases, easy access to blood through loose endothelial junctions of bone marrow sinusoids
-Prognostics: median survival time following limb amputation 3-4 months, less aggressive in cats so prognosis somewhat better
-Radiology: new bone formation on periosteal surface, “sunburst”

Question 21

How do surface/peripheral/periosteal osteosarcomas differ from central/medullary

Answer 21

-Generally slower growing/less aggressive than central/medullary type
-Arise from osteogenic layer of periosteum
-Still invade cortex and can eventually metastasize

Question 22

Describe multilobular tumor of bone (particular to skull of dog)

Answer 22

-Lobulated, solitary, smooth contoured, immovable
-3-7 cm diameter
-Slow growing, locally invasive
-Mature dogs of med/large breeds
-late pulmonary metastasis

Question 23

How are osteosarcomas and granulomatous osteomyelitis different

Answer 23

-Similar on radiographs
-Osteosarcomas:do not cross joints, generally one large mass, abruptly transition to normal bone
-Granulomatous osteomyelitis: May cross joints, may be several regions affected, more gradual transition to normal bone