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110 Cards in this Set
- Front
- Back
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What are the three cell types in bone tissue within an extracellular matrix?
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Osteoblasts, Osteocytes and Osteoclasts
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What are osteoblast?
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Derived from bone marrow stromal cells
produce a protein called osteoid stimulated by vitamin D estrogen and calcitonin |
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What are osteocytes?
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Line the surface of bones or entrapped within bone lacunae
actively involved in the mineral resorption (osteocytic osteolysis) stimulated by parathyroid hormone |
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What are osteoclasts?
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Multinucleated cells derived from hematopoietic progenitor cells that also give rise to monocytes
resorption of bone (osteoclastic osteolysis) cellular activiety dependent on PTH vit D calcitonin negative feedback and cytokines IL-1 IL6 TNF and PGF2a |
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What appositional growth?
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An increase in size by addition of new tissue or similar material at the periphery of a particular part or structure
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What is interstitial growth?
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Growth originating in different centers with a structure or an area, characteristic of tissues formed of nonrigid materials
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What are the zones of endochondral ossification?
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Zone of normal cartilage,zone of proliferation,zone of hypertrophic and calcifying cartilage, zone of ossification
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What is seen with zone of normal cartilage?
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Reserve cartilage
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What stimulates the zone of proliferation and what does that cause?
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Stimulated by GH -> somatomedins which stimulates chondrocytes to mitotic divisions
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What is seen in the zone of ossification?
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Osteoid of woven bone is laid down on calcified cartilage spicules, cartilaginous scaffolding
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What are the two main morphologic types of bone?
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Cancellous (trabecular) bone compact (cortical) bone
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What is cancellous (trabecular) bone?
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the spongy bone of the medullary cavity
formed by a three-dimensional lattice of interlacing spicules or trabeculae (< 30% density). The spaces between these spicules contain the bone marrow |
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What is compact (cortical) bone?
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forms the dense walls of the diaphysis
The compact bone has high density ( > 30% density). |
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What is an Osteon Unit?
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Structure provides strength against compression
Occurs throughout life Is bone removal followed by replacement Occurs in response to stresses on bone Is normally a balanced process |
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What is Woven bone?
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Woven bone is immature bone present during fetal development or in the early stages of bone repair. The collagen fibers in woven bone are randomly distributed and microscopically have a crisscross pattern (woven).
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What is Lamellar Bone?
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Lamellar bone is mature bone present in normal adult stages. The collagen fibers in lamellar bone are perfectly arranged in a parallel pattern
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What are biomechanical properties of bone?
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2/3 hydroxyapatite and 1/3 type and osteoid (type--1 collagen, glycoproteins, hormones)
Mineral: rigidity, strength, resists compression Collagen: minimal flexibility to resist bending Woven bone: mechanically inferior; bone of fetus and injury Lamellar bone: strong bone of adult: modeling; remodeling |
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What part of embryogenesis is bone derived from?
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Mesoderm
Somites Dermatome Myotome Sclerotome Lateral plate mesoderm |
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What are the type of bones are there?
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Flat
long sesamoid short irregular |
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What are the regions of long bone?
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Epiphysis
Diaphysis Physis Metaphysis |
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What are the done surfaces of bone?
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Articular surface
Perichondrium Periosteum Endosteum |
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What is Wolff's Law?
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Bone will adapt to applied forces
disuse = bone lose Over use = bone gain |
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What is Hyaline and Fibrocartilage?
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supportive connective tissue of mesenchymal origin
no innervation and no regeneration no blood supply hyaline type 2 fibrocartilage type 1 permeable weight bearing yet flexable |
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What is Articular cartilage?
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Lacks a perichondrium
Supplied nutrition by joint fluid and underlying subchondral bone Slippery (low frictional forces) Appositional and interstitial growth Supports soft tissues, growth of bones |
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What does anisotropic mean?
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Exhibits dissimilar properties in resisting loads delivered from different directions
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Where is the majority of Ca liberated from bone?
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The majority of calcium is liberated from trabecular bone
Up to 20% maybe produced by osteocytic osteolysis Storage and management site of hematopoietic tissues |
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How is phosphate involved with bone?
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Important component of bones & teeth, important element of cell membrane & organelles
Inorganic phosphate is involved in pH regulation and energy storage and metabolism The physiologic mechanisms for phosphate homeostasis are the same as those for calcium In hypocalcemia or when the Ca:P ratio is changed Ca:P product Ca is immediately transferred from bones to the extracellular pool Tight dependence on plasma calcium may explain why nutritional, renal & hormonal imbalances often result in bone disease |
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How does parathyroid hormone affect bone?
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causes osteoblasts to release OSF (RANK-L) and resultant osteolysis
Estrogens and androgens have critical regulatory effects including inhibition of bone resorption IL6 and IL11 are important in decreasing bone mass in estrogen deficiency |
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How does Calcitonin affect bone?
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stimulates bone formation via inhibition of osteoclastic action
Insulin is important in matrix synthesis and cartilage formation Glucocorticoids have a catabolic effect through both activation of osteoclasts and inhibition of osteoblasts |
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What are some hormonal effect on bone?
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ILGF is key in bone formation and maintaining bone mass
TGFb is important in bone remodeling PDGF is a potent stimulator of bone formation |
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What are ways to clinically asses bone?
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bone biopsy
tetracycline labeling radiographs Densitometry |
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What scheme is used for coming up with differentials?
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Damnit V
or vitamin d and b |
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What are some examples of vascular bone diseases?
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Septic and aseptic necrosis
Legg-Calve-Perthes Disease Infarcts of bone (coagulative necrosis) Bone reaction to injury Panosteitis |
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What is aseptic necrosis?
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Usually associated with bacterial emboli in young animals (see picture for septic infarcts of the metaphysis)
It is the result of bone ischemia and infarction Microscopically characterized by empty lacunae with little inflammation Aseptic necrosis of the femoral head is an important entity in small breed dogs (Legg-Calve-Perthes disease) |
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What is Legg-Calve-Perthes Disease?
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Necrosis of the femoral head is a result of idiopathic disruption of a major portion of the blood supply to the capital epiphysis with subsequent ischemic necrosis
Common in miniature dog breeds; rare in cats 4 to 11 months of age, no sex predisposition due to ischemia |
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What is bones reaction to injury?
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Necrosis (osteosis)
Grossly: Softening, discoloration. Histologically: Empty lacunae, resorption Possible sequelae to bone necrosis: Necrosis > resorption > woven bone > mature bone Necrosis > resorption > woven bone > scar (callus) Necrosis > sequestrum (no resorption). Necrosis > resorption > inflammation >proliferation (exostosis). |
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What is sequestrum bone necrosis?
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A piece of necrotic bone isolated from the remaining viable bone
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What is involucrum bone necrosis?
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A dense collar of bone surrounding a piece of necrotic bone isolated from the remaining viable bone (sequestrum)
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What are examples of infections and inflammatory diseases of bone?
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OSTEITIS, OSTEOMYELITIS, PERIOSTEITIS, PANOSTEITIS
Etiology: Bacterial, mycotic, viral, parasitic Course: Generally chronic, progressive Route of entry: Hematogenous, extension, penetration Types: Destructive (osteolytic) or productive (sclerosis) Examples of Specific Forms of Osteomyelitis in Domestic Animals |
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What is Lumpy Jaw?
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an infectious disease caused by actinomyces bovis
an bacterial osteomyolysis Soil-born organism penetrates through injured oral mucosa and extends deep into the bone where it causes a chronic proliferative pyogranulomatous osteomyelitis difficult to treat, animals are often sent to slaughter |
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What is Hematogenous osteomyelitis?
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a disease commonly in farm animals following bacteremia or septicemia.
Most common in neonates secondary to OMPHALOPHLEBITIS Often bacterial emboli lodge in metaphysis hairpin capillary loops or epiphyseal vessels of long bones. Frequent bacteria isolated from septic osteomyelitis include Salmonella spp., Actinobacillus pyogenes, Staphylococcus aureus, Fusobacterium necrophorum and other pyogenic organisms |
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What is Septic Spondylitis?
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These infections are important in young foals where 70% of foals with joint -ill (Septic arthritis) also have septic osteomyelitis
Septic osteomyelitis in the vertebrae (spondylitis) occurs commonly in pigs and sporadically in other species Tail biting/docking incriminated in pathogenesis of spinal abscesses in pigs and lambs Vertebral infections eventually vertebral fractures, spinal meningitis, myelitis. Posterior paralysis is frequent sign of septic spondylitis Grossly, the ventral bodies of affected vertebrae are swollen. Cut section reveals mucopurulent exudates (spinal abscesses) Common in snakes (due to salmonella) |
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What are examples of bone osteitis?
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Bone diseases caused by viruses are uncommon & not important in domestic animals.
The following viruses are reported to affect the bone in domestic animals: CAV-1 (K9 adenovirus-1) (Canine hepatitis) Canine Morbillivirus (Distemper) Feline Leukemia Virus Bovine Virus Diarrhea (BVD). Lesions in other organs caused by these viruses are more relevant, clinically and pathologically, than those present in bones. |
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What is an example of parasitic periosteitis?
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Hepatozoon americanum is a tick-borne apicomplexan protozoan
Found in dogs throughout much of the southeastern U.S. Granulomatous inflammation with intracytoplasmic parasites within macrophages Prominent features of disease is cardiac myositis Periosteal exostosis, intratrabecular fibrosis, increased osteoblastic and osteoclastic activity that begins in proximal bones of the limbs and spares distal bones of the limbs. |
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What is Panosteotisis?
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Nonfatal, self-limiting, painful disorder primarily of young
Shifting leg lameness Dogs (6-18 mos mos), esp. male German shepherd pups (75%) Induces a diaphyseal enostosis of major long bones Early lesions are centered on nutrient foramina and arterial vasculature that leaks protein-rich edema fluid Edema stimulates reticular cells of marrow to proliferate, form fibrous tissue, woven bone, organize edema fluid |
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What is a tension force?
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Force that stretches or exerts pull on a bone surface produces a fracture line transverse to the pull-transverse fracture
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What is a compression fracture?
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Compression: Force that compresses a bone surface produces a fracture line longitudinal to the force force-longitudinal fracture
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What is a Bending fracture?
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Produces a long transverse (tension) fracture line and short (spike) longitudinal (compression) fracture line
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What is a Torsion fracture?
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Produces a spiral fracture line. Tight spiral (load load-bearing + twist) vs Loose spiral(nonweight-bearing or pulling while twisting)
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What is a low energy fracture?
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Energy sufficient to break bone but is delivered at low rate, e.g. incomplete, green green-stick or two-fracture fragment.
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What is a high energy fracture?
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: Energy delivered at high rate of loading resulting in multiple fracture fragments in which most fragments maintain their blood supply and are incorporated in the healing process, e.g. hit by car.
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What is a very high energy fracture?
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Energy delivered at very high rate of loading, e.g. by a gunshot wound, in which many shattered fragments have lost their blood supply and soft tissue is macerated.
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What are they types of salter-harris fractures?
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Type I
A transverse fracture through the hypertrophic zone of the physis. Type II A fracture through the physis and the metaphysis, but the epiphysis is not involved in the injury. Type III A fracture through the physis and the epiphysis. Type IV The fracture passes through the epiphysis, physis, and metaphysis. Type V A compression or crush injury of the epiphyseal plate with no associated epiphyseal or metaphyseal fracture. Type VI: This is a rare injury and consists of an injury to the perichondral structures Type VII: This is an isolated injury to the epiphyseal plate Type VIII: This is an isolated injury to the metaphysis, with a potential injury related to endochondral ossification Type IX: This is an injury to the periosteum that may interfere with membranous growth |
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What are the ways of repair for fractures?
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Simple or hairline fractures often heal by primary intention (repair).
Displaced or comminuted fractures often heal by secondary intention (repair). For primary repair there must be good opposition and stabilization. |
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What is a consequence of non union of bone?
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a false joint
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What is an example of toxic osteodystrophy?
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Lead poisoning interferes with osteoclastic activity.
Osteoclasts and renal proximal tubule epithelium with contain typical acid-fast inclusions. Damages bone marrow and causes release of erythroid precursors Lesions are subtle and consist of increased bone density in the metaphyses |
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What is Osteofluorosis?
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Osteofluorosis due to chronic ingestion of high concentration of fluorides present in water, plants, rocks of some geographical regions.
Only herbivorous animals affected Fluorosis interferes with the normal metabolism of bones and teeth, particularly in fetuses and growing animals. Must be > 2,500 p.p.m. to affect bones in cattle. Growing bones (metatarsal, mandibles, the pelvis) become thickened due to excessive periosteal ossification. Also produces rickets-like lesions in bones, and a notable softening and discoloration of teeth, referred to as odontofluorosis. Soft, black teeth with excessive wear & tear of occlusal surfaces characterize Odontofluorosis. |
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What is hypervitaminosis A?
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A causes toxic osteodystrophy in cats, and to a lesser extent in calves & piglets.
Mature cat on a liver diet (low Ca: high P) and supplement high in Vitamin A in any animal Thick pelvic bones osteopenia and coarsening of cancellous bone Double cortex formation Pathogenesis of hypervitaminosis A is poorly understood High levels of retinoid & other vitamin A metabolites stimulate osteoblastic activity. In kittens kittens: : ↑↑Vit A kills chondrocytes of physes resulting in premature closure of growth plates. In adults adults: : ↑↑Vit A kills chondrocytes in fibrochondrocytes fibro--cartilage of insertions. Dying chondrocytes undergo endochondral ossification and enthesophyte formation in elbows and scapula |
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What is hypervitaminosis D?
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Vitamin D maintains serum calcium at optimal levels
Increasing intestinal absorption of calcium (and phosphorus) enhancing parathyroid-hormone dependent renal tubular resorption of calcium (and excretion of phosphorus) and PTH dependent mobilization of calcium from bone Required for mineralizing osteoid to form bone Sources of intoxication: Iatrogenic; excessive dietary supplementation Ingestion of 1,25-dihydroxycholecalciferol-glycoside (most active form of vitamin D3) containing plants, including Solanum malacoxylon, Cestrum diurnum, and Trisetum flavescens Cholecalciferol rodenticide intoxication—Metastatic calcification Excess vitamin D is stored mainly in fat and is released as the fat is metabolized Mainly affects long bones especially Thickened sclerotic metaphyses; loss of metaphyseal spongiosa extending into diaphysis |
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What is the consequence of Veratrum californicum?
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Ewe ingests skunk cabbage on day 14 of gestation
Collapse of cranial midline formation Prolonged gestation Pituitry produces ACTH due to fetal stress hypertrophy of fetal adrenal increased secretion of fetal cortisol which would act on the placenta reduced progesterone & increased estrogen thereby promoting the synthesis & release of PGF2a, which sensitizes the uterus to oxytocin followed by parturition. (See slide 13 for PGF2a effect). Usually still born or do not live long |
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What is Osteochondromatosis?
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anomaly
May be solitary Congenital, autosomal dominant hereditary disorder in horses and dogs (Hereditary Deforming Chondrodysplasia) Described in horses, dogs, mice, and cats Occurs in young animals and humans, and mature cats Irregular endochondral ossification Development of exostoses ceases with bone development Occur adjacent to growth plates in long bones, ribs, scapula and pelvis; intratracheal reported in young dogs |
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Regarding metabolic bone disease what can affect the production of the bone matrix (osteoid)?
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Deficiency or excess
vitamins A C D Ca P F Pb nutritional |
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Regarding metabolic bone disease what can affect the mineralization of bone?
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PTH,estrogen, thyroid adrenal etc
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Regarding metabolic bone disease what can affect resorption of bones?
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toxic lead or fluoride
decreased inhibitions of estrogens and androgens disuse atrophy |
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What are the best-known metabolic bone diseases?
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Osteoporosis
Osteomalacia Fibrous Osteodystrophy |
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What is osteoporosis?
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Osteoporosis: (syn. bone atrophy cf. osteopenia). The basic problem in osteoporosis is a negative balance between the formation and resorption of bone leading to reduction of bone mass.
A simple definition of osteoporosis is "there is little bone, but what bone there is, is chemically normal." (cf. osteopenia = reduction in bone mass but makes no inference as to its quality). It is difficult to evaluate osteoporosis grossly unless it is a rather severe case. Grossly, there is reduction in the thickness of cortical bone and reduced number of trabeculae in cancellous bone. Causes include starvation, parasitism, chronic wasting diseases, Ca and Cu deficiencies, hyperadrenocorticism, and prolonged administration of steroids, physical inactivity (disuse atrophy of bone) and senility. |
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What is a corticosteroid?
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The protein-mobilizing or catabolic effect of cortisol
is apparent on its effect on bone metabolism: decreased development of cartilage interruption of growth and inhibition of formation of new bone. In adrenalectomized animals: diminished absorption of glucose & Ca from the GIT. |
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What is osteomalacia?
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Osteomalacia (softening of bones in grown animals) It is a failure in the calcification of osteoid during the normal remodeling of bone associated primarily with Vitamin D or P deficiencies.
Unmineralized osteoid is resistant to osteoclastic activity and accumulates in the bones. The bones are soft and deformed. Histologically, there is accumulation of unmineralized osteoid. Pathological fractures are common sequelae to osteomalacia. Etiology of osteomalacia is similar to that of rickets in that deficiencies of P & vit. D are major contributors. |
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What is Osteodystrophia Fibrosa?
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It is a metabolic bone disease characterized by increased osteoclastic resorption of bone and replacement by fibrous connective tissue.
It results from prolonged and excessive secretion of a parathyroid hormone (PTH) (hyperparathyroidism) which could be primary or secondary. Commonly associated with diets rich in P & low in Ca |
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What is Primary hyperparathyroidism?
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Primary hyperparathyroidism is caused by active parathyroid adenomas and is rare in domestic animals.
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What is secondary hyperparathyroidism?
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Secondary hyperparathyroidism is the most common and can be classified as nutritional or renal. The fundamental mechanism is a reduced concentration of calcium in the plasma with a relative increase in phosphorus. Nutritional hyperparathyroidism results from a low-calcium/high phosphorus diet. In renal hyperparathyroidism, there is failure to eliminate P in the urine, which causes hyperphosphatemia
excessive PTH bone reabsorption through osteoclastic activity. Bones, particularly cranial, become swollen, soft (loose teeth), deformed & prone to pathological fractures. |
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What is Osteodystrophia Fibrosa. Dog (Rubber Jaw)?
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Osteodystrophia Fibrosa. Dog (Rubber Jaw).
In dogs this disease is commonly associated with chronic renal disease (secondary hyperparathyroidism due to renal failure). Renal osteodystrophy is due to the inability of the kidneys to excrete P. Excess P in blood and a relative reduction of blood Ca++ (hypocalcemia) activate parathyroid glands to secrete PTH. This hormone is hypercalcemic since it removes Ca++ from bones via osteoclasts (osteoclastic osteolysis) and osteocytes (osteocytic osteolysis). PTH also increases absorption of Ca++ in the intestine. In addition, animals with renal disease are unable to activate Vitamin D3 in kidneys. bone is replaced with fibrous connective tissue |
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What is Hypertrophic (pulmonary) osteoarthropathy (HPO)?
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A condition sporadically reported in dogs
Recently, enhanced exposure of peripheral tissues to VEGF and/or COX2-derived PGE2 could have a role in HPO pathogenesis Although speculative, three observations support the possibility of a role for COX2-derived PGE2 in HPO pathogenesis. Patients are refractory to high-dose narcotics, yet it was extremely sensitive to the COX2 inhibitor rofecoxib. Prostaglandins are rapidly inactivated in the lung, but masses could allow shunting and prolong prostaglandin half-lives, extending both the duration and range of biological activity Finally, the measured levels of urinary PGE-M correlate with clinical signs Interestingly, tumors of the urinary bladder and ovaries have also been associated with HPO. Most of the long bones and rarely flat bones show thickening due to bone proliferation of the cortices (hyperostosis) usually leaving the articular surfaces free Bone changes are always bilaterally symmetrical characterized by multiple focal to coalescing osteophytes that affect primarily the appendicular skeletons. |
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What is Craniomandibular osteopathy ("Lion jaw")?
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Craniomandibular osteopathy ("Lion jaw") is a localized bone disease of unknown etiology in dogs. It is mainly seen in West Highland White and Scottish Terriers. Lesions affect only the head, are bilaterally symmetrical, & self-limiting. Affected dogs have a swelling of the temporo-maxillary region. Grossly and radiographically, there are proliferative changes in the temporal, maxillary, mandibular & occipital bones causing bony bridging on the periosteal surface.
Disease apparent at 4 to 7 months of age and can regress. Mastication painful & difficult. Muscles of the skull atrophic due to disuse |
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What is Rickets?
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softening of bones in young, growing animals
metabolic bone disease of complex etiology affecting growing bones. Pathogenesis: deficient calcification of osteoid & cartilaginous matrices (endochondral ossification) bones become soft and the areas of endochondral ossification appear swollen as in rachitic rosary (costochondral joints) especially in human beings. Causes: multi-factorial but generally involves deficiencies of vitamin D or phosphorus. Rickets is commonly found in animal housing facilities where there is little sunlight, or in areas where the soil is deficient in phosphorus. |
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What is hypovitaminosis C?
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scurvy
Scorbutic osteoarthropathy Nonhuman primates (except some prosimians), guinea pigs, some bats, and several species of birds and fish Ascorbic acid is required by fibroblasts and osteoprogenitor cells for the formation of collagen, dentin and osteoid Hallmarks of scurvy are capillary hemorrhage and lack of bone deposition Disease is most severe in young, growing animals Swollen joints/enlarged costochondral junctions (scorbutic lattice) Pathogenesis: Lack the enzyme L-gulonolactone oxidase, which is required for L-gulonolactone conversion to L-ascorbic acid. Physeal cartilage is deformed and mineralized Insufficient production of osteoid by osteoblasts Decreased absorption of cartilaginous matrix Overgrowth of cartilaginous matrix extends into the metaphysis Calcified cartilage scaffold is weak, microfractures and hemorrhages result from mechanical forces Grossly looks similar to Rickets with hemorrhaging at the articular sites |
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What is Hypertrophic osteodystrophy (HOD)?
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Metaphyseal osteopathy – Double physeal line
Inflammatory bone disease of unknown etiology that primarily affects young large breed dogs (usually 3-6 months of age), high incidence in Weimaraner dogs Nutritional etiology suspected Hypovitaminosis C Nutritional imbalance Copper deficiency Infectious; canine distemper viral RNA in bone cells of several HOD cases All fast-growing bones are susceptible, but the distal radius and ulna are usually most severely affected. Bones distal to the carpus and tarsus are usually spared. Inflammation results in necrosis of primary spongiosa and osteoblasts Inflammation and necrosis results in metaphyseal infarction and separation from the physis Periosteal proliferation and subperiosteal new bone formation thought to compensate for weakened metaphysis |
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What is Amelia?
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Absence of a limb or limbs.
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What is Hemimelia?
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Absence of the distal half of a limb or limb(s).
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What is Phocomelia?
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Absence of proximal portions of the limb(s) [seal].
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What is Peromelia?
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Absence of distal portions of the limb(s)
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What is Micromelia?
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Small limbs
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What is Syndactylia?
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Fusion of digits
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What is Polydactylia?
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Supernumerary digits.
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What is Polymelia?
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More than four limbs
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What is Lordosis?
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Ventral deviation of a vertebral column.
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What is Kyphosis?
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Dorsal deviation of a vertebral column.
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What is Scoliosis
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Lateral deviation of a vertebral column.
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What is Kyphoscoliosis?
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Dorsolateral deviation of a vertebral column.
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What is Chondrodysplasia (chondrodystrophia fetalis)?
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is characterized by a defective endochondral ossification that results in disproportionate (shortlegged) dwarfism.
It is most frequently seen in cattle (Angus, Hereford) and dogs (Alaskan Malamute). In chondrodysplasia, membranous (appositional growth) is normal but endochondral growth is impaired resulting in disproportionate growth of the skeleton. There are lethal and non-lethal forms of the disease |
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What is Osteopetrosis?
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Osteopetrosis (petros=rock) an inherited disease in which defective osteoclasts fail to reabsorb and remodel the fetal bone (primary spongiosa) in increased bone density with concurrent reduction of medullary spaces. Since there is no space for the bone marrow to grow, animals with osteopetrosis often exhibit aplastic anemia.
Osteopetrosis sporadically occurs in dogs, pigs, sheep horses and cattle (Angus), as well as in human beings. On cut surface, bones with Osteopetrosis appear diffusely solid. Paradoxically, affected bones have a notable propensity for pathological fractures. causes an aplastic anemia |
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What is Congenital Cortical Hyperostosis of Pigs?
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a generalized deformity
affects long bones and is characterized by exaggerated periosteal (appositional) bone growth. Affected limbs swollen because of excessive deposition of radiating trabeculae on the periosteal surface & edematous because of blockage of lymphatic circulation. Most piglets with congenital cortical hyperostosis are born dead or die within hours. The joints are normal. |
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What are Angular limb deformities?
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a localized deformity
Angular limb deformities are important in horses and characterized by lateral deviation of the distal portion of one or more limbs (more during the lab) Sometimes this problem is present at birth, while in others it develops later in life. Pathogenesis includes malposition in utero, joint laxity, hypothyroidism (congenital goiter), trauma (ischemia or reduced blood supply), malnutrition, and defective endochondral ossification. |
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What is Hypoplastic Dens: Atlanto-axial instability?
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Most commonly seen in small breed dogs due to congenital abnormalities or large breed dogs with traumatic fracture of the dens (odontoid process)
There are six ossification centers in a normally formed Dogs with an instability exhibit clinical signs prior to one year of age Signs can range from pain to tetra-paresis or death, with the majority of animals resisting ventral neck flexion on physical examination |
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What is Articular cartilage?
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The surface of a normal joint should be smooth, moist, and glistening with a bluish color (esp. in young animals). The articular cartilage is formed by type II collagen and proteoglycans, & it lacks blood and lymphatic vessels and nerves, has a poor capacity for regeneration and therefore necrosis of the cartilage (chondromalacia) remains generally unrepaired.
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What types of joints are there?
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Fibrous joint
cartilaginous joint synovial joint |
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What is a fibrous joint?
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Bones or cartilages united by fibrous tissue. There-are three main types of fibrous joints: 1. Sutures (cranial sutures). 2. Syndesmosis (tibia-fibula) and 3. Gomphosis (i.e., tooth-socket)
Synarthroses |
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What is a cartilaginous joint?
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Bones or cartilages united by hyaline cartilage (i.e., costochondral joints) or fibrocartilage (i.e., pelvic and mandibular symphysis)
Amphiarthrosis |
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What is a synovial joint?
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These types of joint unite two bone ends covered by articular cartilage and all surrounded by a thick articular capsule. Examples of synovial joints are those in the appendicular skeleton and vertebral joints.
Diarthrosis / True joints |
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What is a synovial fossa?
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These are bilateral depressions not covered by cartilage. The function of synovial fossae is not known but it may be involved in the lubrication of the joint. Not present at birth, synovial fossae appear in the first few months of life. Inexperienced persons may mistake synovial fossae as articular lesion.
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What is Synovial fluid?
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It is a clear, viscous, colorless or slightly yellow fluid produced by synoviocytes; it has low cellularity and low protein content. Its main functions are to reduce friction (lubrication) & to nourish the articular cartilage.
Synovial fluid notably increases in many joint diseases and this is called a synovial effusion. In inflammatory joint diseases the synovial fluid becomes turbid (cloudy) because of an increase in protein content and the presence of leucocytes |
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What is an Articular Capsule?
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This is a thick sack of connective tissue that covers the entire joint and provides additional joint stability. A thin synovial membrane internally lines the articular capsule. In chronic arthritis the articular capsule often becomes thickened due to fibrosis and the deposition of exudate.
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What is a Synovial membrane?
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It is a thin membrane with discrete villi superficially lined by a continuous layer of highly specialized cells called synoviocytes. There are two main types of synoviocytes: Synoviocytes type A have phagocytic activity; while synoviocytes type B are responsible for the production of the synovial fluid. Both types of synoviocytes proliferate rapidly in response to injury (reactive hyperplasia).
When injury is severe and chronic, synovial villi become elongated and covered with hyperplastic synoviocytes (synovial villous hyperplasia). Hyperplasia is best observed by placing the synovial membrane under water. |
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What are the joints reaction to injury?
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Fibrillation: It is an early degenerative change of the articular cartilage due to
(a) loss of proteoglycans (b) the unmasking of collagen fibers & (c) increased water content in chondrocytes. Fibrillation is the equivalent of a superficial erosion of the cartilage. Affected cartilage becomes dull with a yellowish discoloration taking a characteristic ground-glass appearance. |
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What is Eburnation?
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This is the complete loss (ulceration) of articular cartilage, which is generally accompanied by a thickening of the subchondral bone (osteosclerosis). Exposed bone surfaces take an ivory-like appearance (hard and polished). It is a permanent lesion since lost cartilage cannot be repaired
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What are Joint Mice?
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This is a conventional term used to describe viable and often growing fragments of cartilage floating free in synovial fluid. The formation of joint mice occurs when pieces of degenerating cartilage detach from the subchondral bone. Joint mice are commonly seen in degenerative joint diseases particularly in "Osteochondrosis dissecans."
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What are Osteophytes?.
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These are multiple bone outgrowths derived from chondrification of fibrous tissue. (Osteophytes are mainly found in the junctions of cartilage with periosteum or along the insertions of synovial capsules to the bone
Formation could start 3 days after injury but is only detected grossly around 2 weeks and radiographically in 5 weeks. If the source of injury ceases, osteophytes no longer grow but remain as multiple periarticular spurs of bone causing variable degree of joint deformity. The process of osteophyte formation is known as osteophytosis. It is not a specific lesion and occurs in degenerative and inflammatory joint diseases. |
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What is the synovial membrane response to injury?
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ViIlous hyperplasia/hypertrophy: A common but non-specific reaction of synovial membrane to persistent injury 'velvety" appearance (particularly if immersed in water) due to the formation of tonguelike synovial villi covered with hyperplastic synoviocytes.
In some chronic cases (infectious arthritis), there are also aggregates of lympho-plasmacytic cells around the synovial blood vessels. In chronic intra-articular hemorrhage, the synovial membrane takes on a tan color due to the deposition of hemosiderin pigment (pigmented synovitis). |
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What is Capsular Fibrosis?
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This is thickening of the capsule due to the proliferation of connective tissue and deposition of exudate.
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What is Pannus?
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This is the formation of granulation on the synovial membrane. Granulation tissue often undergoes chondral or osseous metaplasia (osteophytes - joint mice) and may lead to fixed joint (ankylosis).
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