Skeletal Diseases Flashcards
Osteoblasts
Bone formimg cells that produce the organic matrix (single nuclei)
Osteocytes
In lacunae
Regulates minute to minute Ca flux with osteoblasts
Osteoclasts
Bone removing cells (multinucleate)
Restores bone by secreting H+ and metalloproteinases
____________ is up inhibitor of osteoclasts
Calcitonin
Endochondrial ossification
Bone forms and replaces a cartilage model
Osteoclasts bone resorption
Activation of osteoblasts —> resorption of lamina limitans —> exposure of mineralized tissue for osteoclasts —> attachment of osteoclast and resorption
What stimulates osteoclast activity?
PTH
Tension on bone
IL1, IL6, TNFa, PGE2a, RANK, Ligand
Deformities/ anomalies of development
Abnorm. Modeling into appropriate shape
Inadequate growth during development
Defective endochondral ossification @ physis of articular- epiphyseal complexes
Genetic and acquired
Types of chondrodysplasia and skeletal dysplasia
Dwarfism
Angular deformities (foals and sheep)
Amelia/ hemimelia
Skull/ mandible abnormalities (prognathism, brachygnathism, chiari malformation)
What causes chondrodysplasia and skeletal dysplasia?
Genetic defects
Teratogens (veratrum californicum and thalidomide)
Nutritional abnormalities (iodine deficient goiter in foals)
Osteochondrosis (dissecans)
Focal defect in endochondral ossification
Articular- Epiphyseal (AE) complex —> OCD
Disease of animals bred to rapid long bone growth
Lesions associated with OCD
Plug of necrotic cartilage
Defect/ flap of articular cartilage
Uneven joint surface and subchondral bone
OCD pathogenesis
Premature vessel closure —> AE ischemia —> cartilage necrosis —> necrotic cartilage breaks free into joint
Loss of bone
Osteoclastic resorption exceeds bone production
Diffuse: osteoporosis and osteopenia
Focal: bone lysis
Hyperostosis
↑ amount of bone production
Caused by compression, periosteal/ endosteal injury
Osteosclerosis
Abnormally dense bone due to failure of osteoclasts (↓ # and activity of osteoclasts)
Osteopetrosis
Diffuse osteosclerosis
Marble bone disease
Defective osteoclast bone resorption (no trabeculae)
Fractures
Fx through the physis results in premature closure
Fx healing → callus formation
Remodeling
Osteoporosis
Atrophy of bone (& mineralized cancellous bone)
↑ resorption than formation
Causes: lack of vit. D
What causes osteoporosis?
Normal aging, malnutrition, excess Vit. A, deficiencies of Ca and P, disuse, parasitism, declining estrogen
Gross lesions associated with osteoporsis?
↑ fragility
Reduction in cancellous bone and thinning of cortices of compact bone
Enlargement of marrow cavities
Histo lesions associated with osteoporosis?
Reduction in #s of trabeculae
Abnormal activity of osteoblasts and osteoclasts
Osteopenia
↓ in bone density and mass with no CS
Osteomalacia
Softened bone (membranous bone formation)
In adult animals
Excessive bone resorption + unmineralized osteoid
Deficient in Vit. D or calcium
Rickets
Softened, bowed bones (endochondral and membranous bone)
In juvenile animals
Failure of deposition of Ca salts in the matrixes
Deficient in Vit. D or calcium
Rickets pathogenesis
Chondrocytes proliferate and don’t mature and degenerate → cartilage retained and widens growth plate
Gross lesions of rickets
Enlargement of ends of long bones and costo-chondral articulations
Epiphyseal cartilage wide
Bones soft (severe)
Fibrous osteodystrophy (FOD)
Prolonged hyperparathyroidism
↑ osteoclastic resorption of bone
Deposition of immature fibrous tissue, IM and periosteal
What causes Fibrous osteodystrophy?
Any mechanism that ↓ serum Ca: low dietary Ca, high dietary P, Vit. D deficiency, chronic renal failure
Toxic osteodystrophies
Hypervitaminosis A and D
Lead intoxication
Lesions associated with Fibrous osteodystrophy
Diffuse osteoclastic bone resorption
Proliferation of fibrous tissue in bone
Nutritional FOD
↓ dietary Ca or ↑ dietary P
↓ Vit. D → ↓ serum Ca → ↑ PTH
Species affected by nutrional FOD
Horses with high bran diet (High P) → big head disease
Dogs, reptile with all meat diet (high P)
Reptiles with all fruit diet (low Ca)
Renal FOD
↓ TGFR → ↑ serum P (can’t excrete) → ↓ D3 production ↓ serum Ca →↑ PTH → secondary soft tissue mineralization (nephrocalcinosis)
Fibrous osterodystrophy is associated with __________
Parathyroid adenoma (check the kidneys and parathyroid glands!!)
Gross effects of FOD
Bone pliable
Changes in bones of face and mandible (thickened)- in horses and dogs
Microscopic effects of FOD
Haversian canals enlarged
Osteoclasts line receding bone
Spaces OG with calcified bone now have fibrous CT
Hypovitaminosis D
Physeal chondrodystrophy (Rickets)
Osteomalacia
FOD
Osteonecrosis
Death of bone cells and medullary tissue
Due to ischemia, bacterial toxins, heat and cold
Necrotic bone in situ until osteoclastic removal
Osteitis
Inflammation of the bone
Periosteitis
Inflammation of the periosteum and medullary cavity
Osteromyelitits
Inflammation of the medullary cavity and bone
Parts of the joint capsule
Fibrous layer, loos fibrovascular layer and synoviocyte layer
What makes up the articular cartilage?
Chondrocytes
Collagen matrix
Proteoglycan/ GAG matrix
Water
___________ is the nutritional source for chondrocytes
Synovial fluid
Chondromalacia
Thinning and fibrillation of cartilage due to matrix loss
↑ wear and tear due to loss of lubrication
Eburnation
Subchondral bone hyperstosis
↑ focal compression on subchondral plate due to loss of cartilage and abnormal joint loading
Joint response to inflammation
Synovial villi hypertrophy
↑ synovial fluid volume
↓ synovial fluid viscosity
Fibrinous exudate
Neutrophil-rich exudate
Neutrophil enzymes → cartilage erosion
Septic artritis in more than one joint
