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16 Cards in this Set
- Front
- Back
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What the composition of Bone?
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Inorganic (calcified) - calcium phosphate & hydroxyapatite
Organic: 1. Proteoglycans - GAGAs 2. Multiadhesive glycoproteins - osteonectin serves as glue b/w collagen and hydroxyapatite crystals; sialoproteins contain osteopontin and sialoprotein I and II Bone-specific, vit-K dependent proteins: osteocalcin - captures calcium from circulation then attracts and stimulates osteoclasts in bone remodeling protein S - assists in removal of cells undergoing apoptosis Matrix gla-protein - helps in development of vascular calcificaitons growth factors and cytokines: -growth factors, bone morphogenic proteins (BMPs), IL1 and IL6 -Bone morphogenic proteins-7 (OP-1) used to induce bone growth after bone surgery |
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What are the parts of bone structure?
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Periosteum:
-has outer dense collagen layer an inner cellular osteoprogenitor (osteogenic) layer -Sharpey fibers (type I collagen) attach periosteum to bone surface -distributes blood vessels to bone Endosteum: -Osteoprogenitor cells and osteoblasts bone is composed cells and ECM (type I collagen) called osteoids which become mineralized by deposition of calicum hydroxyapatite Osteoblasts and Osteocytes --> osteoprogenitor cells Osteoclasts --> monocytes |
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What do each of the bone cells do?
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Osteoblasts:
-Basophilic cuboidal cells -secrete alkaline phosphatase (ALP), signal osteoblast activity and can be blood marker for cancer -stimulated by vit D, calcitonin, estrogen -possess receptors for PTH Osteocytes: -mature bone cells in own lacunae -maintain calcium level -have cytoplasmic processes called canaliculi which nourish osteocytes with nutrients and metabolites -maintain communication with each other by gap junctions Osteoclasts: -large, multinucleated -located in howship lacunae which represent areas of bone resorption -maintain blood calcium homeostasis by response to PTH and calcitonin |
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What is the RANK-RANKL mechanism?
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Transcription factor in Osteoclasts
Receptor Activator of Nuclear Factor K B Interacts with RANKL which is on stromal cells and osteoblasts RANK-RANKL mechanism is essential for osteoclast maturation During inflammation T lymphocytes produce RANKL which increase bone resorption These pathways can be blocked by Osteoprotegerin (OPG) produced mainly by osteoblast |
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What is seen under the electron microscope in osteoclasts?
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1. Ruffed Border
-site of active bone resorption with ATP dependent pumps -microvilli secrete organic acids that dissolve mineral component -lysosomes destroy osteoid matrix 2, Clear Zone -actin on both sides -cell to cell adhesion (integrin receptors) 3. Vesicular Zone -exocytotic vesicles transfer lysosomes to howship lacunae -endocytotic vesicles transfer degraded bone products from howship to interior of cell |
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What happens in Bone resporption?
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osteoclasts attach to surface of bone by integrins
produce HCl by proton pump and chloride channels to keep an acidic environment in the Howship's lacunae osteoclasts secrete Tartrate resistant acid phosphatase (TRAP) and cathepsin K (cysteine protease) to increase acidity and decalcify surface of bone resorb residues and release into CT capillaries |
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What are the different types of bones?
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Flat bones - skull bones
Long bones - limbs -periphery has dense CT, central has spongy bone marrow -also called trabecular, cancellous, and spongy -articular surfaces have articular cartilage (hyaline cartilage) -layer from superficial to deep: periosteum --> sharpey fibers --> compact bone -> endosteum (osteoprogenitor cells) Short bones - hands and feet Irregular bones - Vertebra, ethmoid bone Primary (immature) or woven: -replaced and remodeled by secondary bone except for tooth sockets and near suture in skull bones Secondary or lamellar bone: -all bones in adults -has regular osteons -has osteocytes in lacunae -calcified matrix is arranged in layers |
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What is compact bone?
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consist of concentric bony layers (lamellae) around a central canal containing blood vessels and nerves
neurovascular channels = haversian canals Haversian canals + concentric lamellae = Haversian system the neurovascular bundles connections with one another and the endosteum and periosteum are called volkmann's canals osteon = central canal + all concentric lamellae + canaliculi |
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What are Osteons?
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organizing feature of compact bone
contain: Haversian canal - nerves, blood vessels, lymphs Volkman's canal - connect adjacent haversian canals Lamellae - collagen deposition in concentric layers Interstitial lamellae - located between haversian systems and remnants of remodeled haversian systems Circumferential lamellae - surrfaces of diaphysis Lacunae - occupied by osteocytes and a little ECM Canaliculi - exchange between osteocytes and blood capillaries Cement line - outer boundary of osteon |
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What are Hyperparathyroidism and Paget's disease?
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Hyperparathyroidism:
-increase in erosive activity of osteoclasts leading to destruction of bone and brown tumors -symptoms of hypercalcemia -predisposition to fracture Paget's disease: -unknown cause -excessive osteoclastic activity followed by excessive osteoblastic activity -new bone is woven bone -elevated osteocalcin levels |
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What is Endochondral and Intramembranous Ossification?
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Endochondral:
-long bones, vertebrae use cartilage model which is replaced by bone, called cartilage bones -begins as hyaline cartilage -primary center develops before birth at mid of diaphysis --> epiphysis -initial bone collar of primary center is by intramembranous followed by blood vessels penetrating into cartilage model leading to endochondral -secondary (after birth) develop at epiphysis Intramembranous Ossification: -mesenchymal (primary ossification centers) --> osteoblasts which secrete osteoid -osteblasts trapped --> osteocytes; this area where they are trapped are called trabeculae -fusion of trabeculae produce spongy bone as blood vessels invade are and undifferentiated mesenchymal cells give rise to bone marrow -periosteum and endosteum come from mesenchyme that doesnt undergo ossification -mitotic activity of mesenchymal cells give rise to osteoprogenitor cells |
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What are the Zones of the Epiphyseal growth plate?
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Reserve:
-randomly arranged inactive chondrocytes Proliferation: -rapid mitosis, rows of isogenous cell groups Cell hypertrophy and maturation: -chondrocytes enlarged Calcification: -chondrocytes die, cartilage becomes calcified Ossification: -osteoblasts make bone matrix on calcified cartilage, this becomes resorbed |
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What are the roles of vitamins in bone formation?
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Vit D - absorption of calcium in intestine
Vit C - necessary for collagen (scurvy) Vit A - deficiency leads improper bone formation; excess leads to early epiphysis closure PTH - osteoclast stimulator, excess PTH leads to calcium deposition in arterial walls as well as constipation due to excessive water absorption in GIT Calcitonin - produced by parafollicular cells of thyroid gland, eliminates the ruffled border of osteoclasts, prevents the release of calcium Growth Hormone - stimulates growth of epiphyseal plates, excess causes pituitary gigantism and acromegaly |
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What happens in bone fractures?
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1. Hematoma formation
-damaged blood vessels produce a localized hemorrhage with formation of a blood clot 2. Fibrocartilaginous callus formation -blood clot, cells, and damaged bone matrix removed by macrophages -periosteum and endosteum respond with intense proliferation of osteoprogenitor cells 3. Bony callus formation -irregularly formed trabeculae of primary bone temporarily unites extremities of fractured bone 4. Bone remodeling -primary bone is resorbed and replaced with secondary bone as fracture heals |
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What are the layers of a diarthroses joint?
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External (fibrous) - layer of dense CT
Internal (synovial) capsular layer: Type A - intensely phagocytic, many lysosomes and sparse RER Type B - resemble fibroblasts with well developed RER; secrete synovial fluid |
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What are some bone diseases?
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Osteogenesis Imperfecta:
-abnormal synthesis of type I collagen -abnormally thin sclera due to deficiency in type I -easy bruising, involvement of inner and outer bones of ear produce deafness Osteoporosis: -imbalance between osteoclast and osteoblast activity -found in postmenopausal women due to low estrogen (inhibits formation of cytokines --> osteoclasts) Rickets: -due to insufficient dietary calcium or vit D -wide osteoid seams are apparent Osteomalacia: -rickets of adults Osteopetrosis: -congenital disease due to deficiency of cathepsin K, carbonic anhydrase II, and proton pump proteins -in XRay bones appear dense but are fragile and break easily -obliterates bone marrow cavitiy leading to anemia Osteosarcomas: -common at lower femur, upper tibia, and upper humerus |
