Cell Functions- Bone

kms013's version from 2015-09-25 23:08


Question Answer
What are the types of bones?Long, short, seasmoid, flat, irregular
Osteoblastcreating bone; syntehsize and secrete organic components of bone matrix
bonespecialized CT composed of calcified ECM
Calcificationmatrix vesicles concentrate Ca and PO4 and form hydroxyapatite crystals
osteoidlayer of new material produced by osteoblasts b/w osteoblast and pre-existing bone layer
bone lining cellsinactive osteoblasts represent most of the flattened BLC in botht he endosteum and periosteum
Osteocytefound in cavities called lacunae b/w bone matrix layers called lamellae with cytoplasmic processes extending into small canaliculi b/w lamellae
lacunaebarrier w/i matrix of bone with cytoplasmic processes extending into small canaliculi
canaliculiconnections b/w lacunae; a way to transport nutrients b/w one cell layer to another; this is usually diff. due to calcification of bone
osteoclastvery large, motile cells with multiple nuclei and play a major role in matrix resorption during bone growth and remodeling; has ruffled border
ruffled borderin active osteoclasts, it is the surface against the bone matrix that is folded into irregular projections surrounded by cytoplasm rich in actin filament; it is the site for adhesion to the matrix; creats zone for bone reabsorption; have receptors for PTH and calcitonin
bone matrixstill CT, just not watery substance like cartilage; 35% organic (collagen and proteoglycans); 65% inorganic (calcium phosphate--hydroxyapatite); layered down by osteoblast; demineralized will maintain shape but it is flexible; osteonectin-- calcium binding glycoproteins; the organic matter embedded in the calcifed matrix includes type I collagen, proteoglycan aggregates, and bone-specifi multiadhesive glycoproteins such as osteonectin;; osteonectin and the phosphatases released in matrix vesicles by osteoblasts promote calcification of the matrix; decalcified bone is usually acidophilic due to its high collagen content
endosteumcovers the trabeculae of bone matrix of each individual trabeculae; single layer of cells; this also goes aroudn the central canals too, explained in creation of bone; internal surfaces of bone covered by this tissue layers with bone-forming cells
periosteumexternal surfaces of bonecovered by this tissue layer with bone forming cells; what is holding neurovascular component (this causes pain); organized much like perichondrium; most outer layer, glues just to a bone tendon bone surgery as opposed to other surgeries; contains osteoblasts and menchymal cells called osteoprogenitor cells--osteoblasts; bon themselves are not innervated; outer fibrous layer
Perforating (sharpeys) fiberswhat holds the periosteum to bone: tendon links to these to bone
compact (cortical) bone80$ bone mass; dense area on outside of bone; what we touch
osteonrefers to complex concentric lamellae surrounding small canal
concentric lamellaecircular layers surrounding a central canal
central canalwhere vasculature resides along with nerves, loose CT and endosteum
Perforatin canalstransverse canal that allows nutrients to go from one central canal to another
interstitial lamellaeresidual of destroyed osteon via osteoclasts but theres some bone is left while a new osteon is layed down; this is b/w osteons (rings)
cement linethe outer boundary of each osteon is this more collagen-rich layer
spongy (cancellous/trabecular) bone20% of bone mass; deeper areas with numerous interconnecting cavities; inside of bone that is porous and you can feel ridges
trabeculaeinerconnecting rods or plates of bone; like scaffolding; spaces filled with marrow and blood vessesl; covered with endostum; oriented along stress
lines of stressyou see this in the head and neck of femur; adds support; consists of several lamellae (thin-sheets) with osetocytes located in lacunae between them
bone remodelingcontinuous throughout life and involves a process of bone resorption/formation; in compact bone, remodeling resorbs parts of old osteons and produces new ones; normal cells--OC eats bone--OB comes in with new material--- makes new osteon; reabsorption phase- 2-4 wks; formation phase 4-6 months; fracture only needs formation phase; resorption--OC eating, 2-4 weeks; reversal--OB builds osteoid synthesis..formation-- 4-6 months
osteopetrosisbone reabsorption is decreased and bone formation is increased; petrosis = stone; normal is = ; over calcification of bone (xrays show very large dense bone)
osteopenialosing bone mass
osteoporosisbone reabsorption is greater than bone formation
wolff's lawstress theory; you can modify bone structure by increasing stress or putting stress on it; adaptation to stressors on bone; disuse-- remodeling goes down, remodeling goes away; overuse/overload-- makes more bone and/or fractures-- increases modeling...OsGoodsloughter-- tendon is being avulsed and bone build bone to tie down bone
woven bonenonlamellar and characterized by random disposition of type I collagen fibers and is the first bone tissue to appear in embryonic development and in fracture repair; forms quickly but less strenght than lamellar bone
osteogenesisbone development
intramembranous ossificationwhere osteoblasts differentiate directly from besenchyme and begin secreting osteoid; takes place in the membranes of mesenchymal cells; example-- frontal, parietal, occipital, temporal, mandible, maxilla; FLAT bone development; matrix forms shell; vascularized; fibroblast bring in osteoblast; then they move away from vasculature
eondochondral ossificationeverything else!! In which a preexisting matrix of hyaline cartilage is eroded and invaded by osteoblasts, which then begin osteoid production
fetal hyaline cartilage model1. fetal cartilage model develops 2. cartilage calcifies and a periosteal bone collar forms around diaphysis 3. primary ossiication centers forms in the diaphysis
bone cartilageproduced by osteoblasts that form within periosteum; loop around mid part of bone
primary ossification centerhappens in diaphysis; in center of bone
diaphysisin shaf of bone
secondary ossification centerin the epiphysis
epiphysestop and bottom part of bone separated bythe epiphyseal plate; is formed bone in the same way with primary ossification center; metaphysisi-- b/w diaphysis and epiphysis
epiphyseal platedoes not change size until last steps and produces bone at same rate of cartilage
resting zoneconsists of hyaline cartilage with typical chondrocytes; at very top; made of hyaline not much going on; just hyaline cartilage, cartilage is resting
proliferative zonesight of mitosis producing chondrocytes; under or highly influenced GH; cohondrocytes begin to divide rapidly and form columns of stacked cells parallel to the long axis of the bone
hypertrophic cartilage zonecells are slowing down in numbers but are spreading out and producing more matrix; contains swollen degerative chondrocytes whos cytoplasm has accumulated glycogen; this hypertrophy compresses the matrix into thin septa b/w the chondrocytes
calcified cartilage zone further away from blood; begin producing hydroxyappatate crystals; loss of the chondrocytes by apoptosis is accompanied by calcification of the septa of cartilage matrix by the formation of hydroxyapatitie crystals
ossification zonecells becoming osteofied and true bone to trabecular bone and continue to grow as destined; bone tissue first appears
growth in bone lenghtepiphyseal plates stays same distance apart until it begins to close; growth in lenght of long bone occurs by proliferation of chondrocytes in the epiphseal plates; at the same time, chondrocytes in the diaphyseal side of the plate hypertrophy, their matrix becomes calcifed and the cells dies. osteoblasts lay down a layer of new bone on the calcified cartilage matrix; because te rates of these two opposing event (proliferation and destruction) are approximately equal, the epiphyseal plate does not change thickness; istead; it is displaced away from the middle of the daphysis, resulting in bone growth.
growth in bone lengthepiphyseal plates stays same distance apart until it begins to close
growth in bone widthappositional growth
fracture repairbleeding causes inflammation at area is red and inflammed; but cleaning out abnormal and also bring in progenitor cells and lay down new bone-- they make osteoblasts
reactive fracture repairis inflammation phase #1
reparativewoven bone is layered down (#2)
remodelinghard callus (takes months) to better alignement (#3-4)
Horomone Influences1.GH- Apit increases bone growth and everything metab, muscle growht, etc. 2. TH- metabolic precursor for body 3. PTH increase calcuim reabsorption- puts into blood stream 4. calcitonin- decrease calcium -- puts in bone
dwarfismlow HGH levels; treat by giving HGH
agromegalyincrease adults onset of HGH; big hands, long mandible ; bone growth has happened so not ex hiehgt but increased in other characteristics
bone scanstracers in body (radioactivity) goes to bone with increased metabolism or hemopoetic activity; look for tumor
dexa scanlooks for bone desnity
female athelete triadeating disorders (no food) amenorrhea (low blood nutrients) osteoporosis (from no nutrients--- stress fracture) Adolescent girls (gymnist, runner, etc)