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64 Cards in this Set
- Front
- Back
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What are the 5 steps of general bone formation?
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1. Osteoblast differentiate
2. Deposit matrix 3. Calcification 4. Primary bone laid down as trabeculae 5. Replaced (by secondary bone), removed (to form bone marrow), or converted (to primary compact bone by compaction) |
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What are Mesenchymal cells
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MSCs, are multipotent stem cells that can differentiate into a variety of cell types[1], including: osteoblasts (bone cells), chondrocytes (cartilage cells) and adipocytes (fat cells).
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What is osteoid?
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It is the unmineralized, organic portion of the bone matrix that forms prior to the maturation of bone tissue
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What are the steps in Intramembranous Ossification. (6 steps)
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1) Is the differentiation of mesenchymal cells into osteoblasts
2) the formation of a primary center of ossification. 3) The osteoblasts deposit osteoid, which eventually calcifies. 4) As the osteoblasts become surrounded by the mineralized matrix, spicules form and the osteoblasts become osteocytes. 5) Spicules will fuse and give rise to compact bone OR the fusion will be less pronounced and will give rise to spongy bone. 6) Blood vessels and differentiating mesenchymal cells (osteoclast precursor cells) will aid in the formation of the marrow. |
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What is the difference between Intramembranous Ossification and Endochondral Ossification
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Intramembranous Ossification does not use cartilage, Endochondral Ossification needs cartilage
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What does Intramembranous ossification contribute to?
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To the growth of short bones and the thickening of long bones
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Describe the steps in the development of a long bone.
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1) A bone collar forms produced by intramembranous ossification within the perichondrium of the cartilage foundation that resembles the eventual long bone. ( perichondrium is renamed periosteum).
2) The chondrocytes under the bone collar degenerate, the cartilage calcifies. 3) Blood vessels penetrate the bone collar bringing osteoclast precursor, Osteoprogenitor, and mesnchymal cells. 4) Osteoblasts develop and begin depositing bone on the calcified cartilage forming the primary center of ossification (endochondrial ossification). 5) Osteoclast-like cells resorb the calcified cartilage 6) The primary center of ossification continues to expand and osteoclasts resorb bone forming the marrow cavity which grows towards the epiphyses. 7) Eventually, blood vessels and osteoprogenitor cells penetrate the epiphyseal cartilage forming secondary centers of ossification. (not necessarily simultaneous) 8) Growth is radial at the secondary centers of ossification. 9) The growth plates eventually disappear and the epiphyseal and metaphyseal trabeculae fuse. |
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What bones in the body grow by endochondrial ossification.
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Bones of the base of the skull, the vertebral column, the pelvis, and the extremities
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Where can bone cartilage be found?
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a) outer surface of the epiphyses of long bones
b) epiphyseal growth plate of developing bones. |
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What does the growth plate connect
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a. epiphysis to the diaphysis.
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What is the cartilage at the epiphyses
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a. It is articular cartilage, a special type of hyaline cartilage.
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Describe the characteristics of articular cartilage
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It is a special type of hyaline cartilage
b. It is not covered by a perichondrium. c. Its collagen fibers are arranged in overlapping arches, called Benninghof arcades, which are thought to provide strength and resiliency to the joint. |
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What are Benninghof arcades?
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Its collagen fibers are arranged in overlapping arches in articular cartilage of the epiphyses.
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Does Articular cartilage contribute to bone elongation
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No
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Name the 5 zones of cartilage at the growth plate.
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a. The resting zone
b. The zone of proliferation c. The zone of hypertrophy d. The zone of calcification e. The zone of ossification |
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Newly formed bone spicules during bone growth contain a central region of ....
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of calcified cartilage surrounded by primary bone.
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During the development of a long bone, the epiphyseal plates are displaced from
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the middle of the diaphysis
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How do bones widen?
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Bones widen by the APPOSITION of bone formed by osteoblasts derived from the periosteum.
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Describe the resting zone of cartilage at the growth plate.
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The resting zone (closest to the epiphysis) is characterized by a small number of chondrocytes arranged randomly in the hyaline cartilage and are quiescent.
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9) When does longitudinal growth stop, and what happen to the epiphysial plates?
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When the epiphyseal plates close, at about age 20
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Describe the zone of proliferation of cartilage at the growth plate.
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The zone of proliferation is located below the resting zone. The chondrocytes are actively undergoing mitosis and are arranged in columns parallel to the long axis of the bone driving the longitudinal growth of long bones.
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Describe the zone of hypertrophy of cartilage at the growth plate.
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The chondrocytes mature they eventually accumulate glycogen and undergo Hypertrophy.
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Describe the zone of calcification of cartilage at the growth plate
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The matrix between the chondrocytes calcifies and is reduced to thin septa.
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Describe the zone of ossification of cartilage at the growth plate
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Osteoclast-like cells destroy the horizontal septa allowing osteoblasts to deposit bone on the surface of the vertical calcified septa.
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Define bone modeling
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change the amount and shape of bone
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Define bone remodeling
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replace old bone with new bone; no change in amount or shape
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How much of the body’s calcium is stored in bone?
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99%
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What is the yearly turnover rate for the body’s calcium?
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18%
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Pertaining to calcium what is the rapid method of metabolizing?
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transference of ions from hydroxyapatite
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Pertaining to calcium what is the slow method of metabolizing?
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hormonal regulation
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What is the key regulator of calcium and phosphate homeostasis and bone turnover?
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Parathyroid hormone (PTH) secreted from the parathyroid gland
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How does PTH effect calcium metabolism when blood-calcium levels are low.
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a) It acts indirectly via the active form of vitamin D (produced in kidney) to increase absorption in the gut .
b) In the kidney it increases re-absorption of Ca and prevent re-absorption of phosphate (to increase concentration of Ca) b) In bone, PTH binds to receptors on the cell surface of osteoblasts and stimulates them to produce RANKL & M-CSF, and block OPG production. |
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What is Osteoprotegerin, what does it do. How is it effected by PTH?
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a) Osteoprotegerin (OPG), which is produced and secreted from osteoblasts, blocks the maturation of osteoclast precursor cells. It binds to RANKL on osteoblasts, thereby preventing the interaction between RANKL and RANK.
b) PTH inhibits OPG production. The balance between OPG and RANKL determines the amount of bone resorption. |
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What is RANKL?
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a) Receptor for activation of nuclear factor kappa B ligand
b) It is an integral plasma membrane protein of osteoblasts c) It binds directly to RANK on the cell surface of osteoclast precursors and promotes their maturation. The cells actually touch since both RANK and RANKL are membrane proteins. |
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What is M-CSF
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a) macrophage colony-stimulating factor
b) M-CSF is a secretory protein. c) M-CSF stimulates the proliferation of osteoclast precursor cells. |
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Where is calcitonin produced?
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a) parafollicular cells of thyroid
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How does Calcitonin effect bone metabolism?
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a) inhibits matrix resorption and therefore lowers calcium blood levels.
b) decreases ruffled border of osteoclasts, which have receptors for calcitonin. |
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How does excess/deficiency of Thyroid hormone effect bone metabolism?
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Receptors on both Osteoblasts and osteoclasts
a) excess causes accelerated bone turnover resulting in a weakening of bone because it does not have time to mineralize correctly. b) deficiency results in slower bone turnover. |
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How does Growth hormone (somatotropin) effect bone metabolism?
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a) Indirectly stimulates proliferation, secretion, and maturation of chondrocytes in the growth plate without allowing the fusion of growth plates.
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How does Estrogen effect bone metabolism? (general) (4)
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a) It stimulates bone formation and inhibits resorption.
b) During puberty estrogen causes closure of epiphyseal plate. c) In adults, it maintains bone mass. d) Both osteoblasts and osteoclasts have estrogen receptors |
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How does Estrogen regulates bone turnover?
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a) by stimulating production of negative regulators (TGF-β) and attenuating production of positive regulators (cytokines) of osteoclast precursors.
b) When estrogen levels decrease in postmenopausal women TGF-βlevels decrease and cytokine levels increase resulting in more osteoclast activity and greater bone resorption. |
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Which cells in bone produce TGF-β
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It is made by osteoblasts and osteoclasts.
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How does TGF-β effect bones(3)?
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TGF-β is a negative regulator and it
a) blocks differentiation of osteoclast precursors into osteoclasts b) inhibits the activity of osteoclasts c) promotes apoptosis of osteoclasts |
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Which cells in bone produce cytokines?
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Marrow cells & osteoblasts make important cytokines in this pathway
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How do cytokines effect bones?
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Cytokines are positive regulators in this pathway and stimulate the differentiation of osteoclast precursors into osteoclasts = greater bone resorbtion.
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What functions does Vitamin C have with collagen?
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It is a reducing agent required for proline hydroxylation and proper collagen
formation. Vitamin C maintains prolyl hydroxylase in an active form, probably keeping its iron in reduced ferrous state. |
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a) What is Osteogenesis imperfecta (OI) a disorder of?
b) What is the genetic basis behind it? c) Which type of OI is fatal? |
a) It is a genetic disorder of type I collagen synthesis leading mainly to changes in skeleton. Spontaneous fractures, skeletal deformity
b) Mutations in one allele of either a1 and a2 collagen genes lead to defects in type I collagen, deletions of all or part, Or single changes of glycine c) 7 types of OI have been characterized of which type II is fatal |
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What is Osteopetrosis?
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It is a rare genetic disorder characterized by increased skeletal density resulting from a defect in osteoclast function (lessruffled border).
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What is Scurvy?
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It is a metabolic disorder that results from a dietary deficiency of vitamin C. Lack of vitamin C leads to thin growth plates and shafts that are prone to fractures and to skin lesions.
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What is Osteoporosis? What two ways is it treated?
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a) It is a metabolic disorder that is characterized by a decrease in bone mass (especially trabecular) caused by decrease in bone formation and/or increase in resorption. Both mineral and matrix are lost.
b) Estrogen treatments can retard the bone loss. c) Osteoporosis can be treated with bisphosphonates, which are stable analogs of pyrophosphoric acid. |
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What are the steps of Fracture repair?
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1. formation of blood clot
2. removal of damaged bone by macrophages 3. proliferation of osteoprogenitor cells 4. simultaneous endochondral and Intramembranous ossification 5. primary bone unites to form bone callus 6. normal activity remodels bone callus 7. primary replaced by secondary bone |
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How do Bisphosphonates help with OI?
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a) Bind calcium phosphate
b) Inhibit formation of calcium phosphate crystals c) Inhibit crystal dissolution d) ***Inhibit bone resorption by osteoclasts by inhibiting vesicular trafficking e) Promote apoptosis of osteoclasts f) Inhibit osteoblast production of osteoclast stimulating activity |
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Define bone mineralization.
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The formation and deposition of hydroxyapatite on bone.
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What are matrix vesicles pertaining to bone formation?
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They are vesicles that contains the nascent hydroxyapatite crystals.
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What is the key enzyme in the process of bone mineralization?
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Tissue nonspecific alkaline phosphatase (TNAP)
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What does Tissue nonspecific alkaline phosphatase (TNAP) do in relation to bone mineralization?
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a) Removes pyrophosphate (PPi)
b) Produces orthophosphate (Pi) |
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How does pyrophosphate (PPi) effect bone mineralization?
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It is an inhibitor of the bone mineralization process.
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How is orthophosphate (Pi) significant in the process of bone mineralization?
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It is the substrate for the formation of hydroxyapatite crystals.
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Where can Tissue nonspecific alkaline phosphatase (TNAP) be found?
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a) free floating
b) surface of matrix vesicles c) surface of osteoblasts |
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What type of process is bone mineralization?
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A physical chemical process.
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What pathways are there for bone mineralization?
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a) Matrix vesicle dependent (TNAP on the surface)
b) Matrix vesicle independent pathway (free floating TNAP) |
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Where can nucleation occur for bone mineralization?
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de nova (without a foundation) or they can be deposited on a nucleation site.
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What are the steps to hydroxyapatite formation?
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TNAP converts pyrophosphate to phosphate which combines with calcium to form hydroxyapatite.
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What is the source of phosphate for the process of hydroxyapatite formation.
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Nucleotide triphosphates (NTP) are the source for both pyrophosphate and phosphate.
a) PC-1 converts NTP to pyrophosphate (don't need to know enzyme) b) TNAP hydrolizes NTP to phosphate |
