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Endochondral Ossification involves
Cartilage template
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In Endochondral Ossification, centers of ossification develop with:
Vascularization
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Major growth of long bones occurs at
metaphyseal growth plates (Physes)
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Mineralization of cartilage matrix occurs so that:
vascular ingrowth can occur, bringing in osteoclasts and developing osteoblasts
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primary trabeculae (spongiosa) on histo are
thin seams of pink osteoid deposited on the mineralized cartilage spicules
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Woven Bone is:
Primary spongiosa produced very rapidly
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Lamellar Bone is modelled
deeper in the growth plate; produced from woven bone and inner cartilage spicules
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Lamellar Bone is more organized,
less cellular and stronger than woven bone
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Where can woven bone be found
Trabecular (cancellous) or Compact (osteonal) bone
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A "tide line" of mineralization anchors articular cartilage into the subchondral bone when
the epiphyseal growth plate begins to close
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Loss of overlying cartilage due to DJD results in
sclerosis (thickening) of Subchondral Bone
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Intramembranous ossification occurs without
cartilage template
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Intramembranous bone formation occurs
within a cellular mesenchyme from which osteoprogenitors and osteoblasts develop
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Compact Bone is predominantly found
in the cortex of long bones and bears the brunt of forces on the diaphysis
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which type of bone surrounds a haversion canal
well organized concentric lamellae of compact bone
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Trabecullar bone consists of
interconnected struts that distribute forces
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Where is trabecular bone concentrated?
within epiphysis and metaphyses
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Trabecular bone serves as reserve for
Calcium and Phosphorus
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Which type of bone is preferentially resorbed when minerals are needed?
Trabecular
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Lamellar bone can be both
Trabecular and Compact; characterized by nice alignment of well-mineralized collagen fibers; it is much stronger than woven bone
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After insult, what kind of bone is laid down first?
woven bone is produced and can be present within both compact and trabecular bone. It will later be modeled (during “quiet, restful times”) to lamellar bone.
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Woven bone is
Produced faster, inherently weaker, less organized/ more cellular, and present in compact bone and trabecular bone
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Defects in bone formation can have different consequences depending on
location; I.e. Palatoschisis exposes nasal cavities and results in aspiration pneumonia
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Equine Wobbler's Syndrome
disease results from malformations of the cervical vertebrae. These are irregular bones with multiple centers of ossification that involve both endochondral ossification (facets, vertebral bodies) and intramembranous bone formation (laminae, transverse processes, etc). Can compress spinal cord if severe enough
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Osteochondritis Dessicans (OCD)
Dissecting cartilage flap, results in 1)Much more severe joint instability2)Much more inflammation (exposure to the well-vascularized subchondral bone -> blood/serum/fibrin, non-suppurative inflammatory cell exudation)3)More rapid and advanced DJD (degenerative osteoarthritis = degenerative joint disease)
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Osteochondrosis
lesion characterized by roughened articular cartilage
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Joint Mouse
OCD lesion can fragment away from the bone, leading to a free-floating osteochondral fragment
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Pathogenesis of OCD
The defect in endochondral ossification will -> a FOCAL retained cartilage core-> results in a “weak point” in the articular epiphyseal complex and can result in cartilage degeneration and the formation of a fissure -> dissecting cartilage flap
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Difference b/w Osteochondrosis and osteochondritis dessicans
with Osteochondritis dissecans, there is formation of a dissecting cartilage fissure/flap
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During Growth, Disorders of Bone resorption result in a
Growth Retardation Lattice
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Growth Retardation Lattices
an osteosclerotic bone dz that results in increased bone density
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Acquired Causes of Growth Retardation Lattices
Defects in Osteoclast Resorption:Acquired:InfectiousBVD and CDV -> kills osteoclasts -> retained primary trabeculaeToxicLead -> kills osteoclast ->retained primary trabeculae, “lead line”
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Congenital causes of Growth Retardation Lattices
Congenital:Osteopetrosis (autosomal recessive mutation in black angus cattle) -> defect in osteoclasts -> entire medullary cavity is filled with mineralized primary trabeculae
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Osteoporosis
Caused by Calcium deficiency, Protein Calorie Deficiency, Disuse Atrophy, Chronic Glucocorticoid excess
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Osteopenia
DECREASED BONE DENSITY OF MASS (structure of bone is normal, AMOUNT of bone is REDUCED)
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Osteoporosis Definition
CLINICAL SYNDROME of REDUCED BONE MASS manifested by BONE PAIN and PATHOLOGIC FRACTURESResults in THINNING and INCREASED POROSITY of bone (Trabecular >> Osteonal bone).
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With Osteoporosis, what happens to osteoblasts and trabeculae
Trabeculae are thin and sparse; osteoblasts are flattened rather than plump and polygonal in regions of new bone formation
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Important causes of Rickets and Osteomalacia
Failure of mineralization due to Vit. D Deficiency, Phosphorous Deficiency
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Sites affected by Rickets and Osteomalacia In Young animals:
1) Cartilage growth plates- sites of Endochondral Ossification2) Sites of bone turnover modeling: immature woven -> lamellar bone remodeling: normal continual physiologic turnover
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Sites affected by Rickets and Osteomalacia In mature animals
Growth plates have closed, so only sites of bone turnover are affected; clinical signs of pain and pathologic fractures take longer to develop and manifest; exception= layer hens due to constant demand for Ca
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Because you cant mineralize cartilage growth plates or sites of new bone formation due to deficiencies, Rickets results in
1. FLARED METAPHYSES2. PATHOLOGIC FRACTURES AND BOWING OF LIMB BONES 3. LARGE SEAMS OF UNMINERALIZED OSTEOID DEPOSITED ON BONE TRABECULAE (and within osteonal canals)4. RETAINED CARTILAGE TOUNGES AT GROWTH PLATES
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rickets and renal dz
Vit D production is lost, thus young animals in renal failure can develop rickets and fibrous osteodystrophy
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Fibrous Osteodystrophy
Persistent Elevation in PTH; Renal fail -> high phosphorous; Nutritional dietary excess -> high phosphorous; primary causes less common
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Pathogenesis of renal fibrous osteodystrophy
Chronic Renal Failure -> Retained PO4 -> CaPO4 crystallization -> decreased iCa levels -> detected by PT glands -> production of PTH and bilateral PT hyperplasia -> stimulation of OCL bone resorption -> fibrous replacement due to decreased OB bone formation and differentiation of mesenchymal cells to fibroblasts (instead of OB)
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appearance of jaw with fibrous osteodystrophy
thick and pliable with wiggly teeth- rubber jaw
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Other signs apparent FO
accompanying signs of uremia; sublingual ulcers, uremic mineralization of pleura and endocardium, bilateral parathyroid gland hyperplasia, shrunken, firm, pitted kidneys
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Fracture repair Part 1
Tearing of the periosteum & displacement of fracture ends with adjacent soft tissue trauma;Hemorrhage with hematoma & clot formation by fibrin polymerization
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Frature Repair Part 2
1)Impaired blood flow -> Necrosis of fracture ends2)Release of cytokines & growth factors by platelets & macrophages within the blood clot (TGF-B, BMP, PDGF) & necrotic cells from damaged tissue 3) Proliferation of undifferentiated mesenchymal cells (stem cells) and granulation tissue (new capillaries embedded within a loose structural network of fibrous tissue)
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Fracture Repair Part 3 (within 3 days)
Differentiation of mesenchymal stem cells into osteoblasts Metaplasia of granulation tissue to cartilage and boneFormation of woven bone and primary fracture callus Establishment of the primary fracture callus can take up to 4-6 weeks Consists of extensive periosteal and endosteal woven bone with periosteal vessels Low O2 tension will result in hyaline cartilage formation -> later undergoes endochondral ossification
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Articular fractures can heal with good return to fxn and minimal DJD with:
minimally displaced fractures, with good sx anatomic reductions and healing
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What may occur from fractures that have poor vasculature, are infected, or are severely displaced with excessive motion
Osteomyelitis and sequestra, fibrous non-union, and/or degenerative osteoarthritis
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what is a sequestrum
dead bone fragment
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Osteomyelitis
Inflamm. of bone most likely due to:Bacterial infxn: Coliforms, Salmonella, Strep zooepidemicus (neonates) Actinomyces bovis, Staphylococcus auereus, etc (adults)Fungal infxn: Coccidioides immitis, Blastomyces dermatitidis, Aspergillus, Candida
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Infections in bone can result in
infection of joint (and vice versa)
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Most common routes of entry in neonates
Umbilicus, Resp. Tract, GI Tract
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In Lg Animal Neonates, septic arthritis and osteomyelitis are:
fairy common and typically occur within growth plates, easily entering joint
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Lumpy Jaw
Caused by Actinomyces Bovis- Pyogranulomatous osteomyelitis with osteoproliferation and osteolysis; aggressive bone infxns can resemble neoplastic processes
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Diskospondylitis
infection of the intervertebral disk and vertebral bodies; typically result from prostatitis and Brucella infection (dogs, pigs)
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Degenerative Osteoarthritis
often final pathway for:infectious arthritis, Malarticulations from fractures or OCD, non-infectious inflamm. arthritis
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Imp't features of Chronic Degen. arthritis (from OCD lesion)
Cartilage thinning, erosion, and ulceration -> EBURNATION (when there is bone on bone contact) and “polishing”Subchondral bone sclerosis and lippingPeriarticular osteophytosisSynovial membrane villous hyperplasiaJoint capsular fibrosis
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Canine Hip Dysplasia
Genetic predisposition in German Shepherd (and some other large breeds of) dogsResults in increased coxofemoral joint laxity -> Degenerative osteoarthritis (DJD) and hindlimb lameness
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Cardinal Signs of DJD (coxofemoral joints)
Loss of joint space from cartilage atrophy, erosion and ulcerationFlattening of the femoral head & shallow acetabular cupsSubchondral sclerosis and “lipping”Periarticular osteophytosis
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Ankylosis
self-fusion of a joint; can occur from chronic, severe DJD
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**Osteosarcoma
most common primary bone tumor in the appendicular skeleton of large and giant breed dogsAgressive neoplasm with rapid progression and met.
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Osteosarcoma characterized by:
1)Osteolysis2)Osteoproliferation3)Production of mineralized or non-mineralized bone matrix (osteoid) by neoplastic osteoblasts 1 and 2 can be seen on X-ray; 3 requires histopath
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