Cartilage Handout Flashcards
locations of hyaline cartilage
nasal, costal, laryngeal, tracheal, bronchial, endplate of bones
locations of elastic cartilage
auricular, external auditory meatus, auditory tube, laryngeal, epiglottis
locations of fibrocartilage
intervertebral disk, symphysis, articular disks, tendon insertions
synovial joints contain what cartilage?
specialized type of hyaline cartilage: articular cartilage
chrondrocytes
cartilage cells, produce cartilage matrix. oval/round, basophilic cytoplsm. also secrete enzymes that can degrade CM. maintain integrity of CM.
cartilage matrix components
fibers, ground substance, noncollagenous multiadhesive glycoproteins
fibers
give mechanical stability to ground substance, predominant type in CM is cartilage-specific collagens
type II collagen
predominant isoform of cartilage-specific collagens.
cartilage collagens
type II, IX, X and XI. type VI is at periphery of chondrocyte (link btwn chondrocyte and cartilage matrix)
type II
most abundant of cartilage-specific collagens, mech stability for matrix
type IX
stabilizes type II, facilitating collagen fibril-proteoglycan interaction
type X
assoc w hypertrophic regions in cartilage where it organizes collagen fibrils into a 3D lattice
type XI
regulates type II fibril size
ground substance
hydrated gel: water, ions, proteoglycans (predominant component of CM)
aggrecan
predominant proteoglycan monomer
multimolecular proteoglycan aggregates
formed by aggrecan monomers bound to central hyaluronate backbone. dense negative charge, keeps them expanded. H20 and Na attracted to neg charges hydrates the CM
noncollagenous multiadhesive glycoproteins
components of CM. small regulatory and structural proteins that influence interactions btwn chondrocytes and ECM. chondronectin, tenascin and anchorin CII. markers of cartilage turnover and degeneration.
isogenous groups or cell nests
clusters of chondrocytes.
lacunae
space w/in CM that chondrocytes occupy
chondroclasts
multinucleated cells that degrade calcified cartilage. derived from monocytes, similar to osteoclasts. can give rise to tumors.
hormones affecting sulfated GAG synthesis by chondrocytes
increase synthesis: growth hormone, thyroxin, testosterone. decrease synthesis: cortisone, hydrocortisone, estradiol
perichondrium
outer part = fibrous connective tissue, type I collagen, secreted by fibroblasts (contains capillary plexus, nerves & lymph). inner part = flattened chondrogenic cells, can become chrondroblasts
becoming a chondrocyte
once a chondroblast surrounds itself w cartilage matrix, it becomes a chondrocyte
chondroblasts derivation
in embryo, derived directly from mesenchyme
nourishment of cartilage
nourished by diffusion thru CM. needs to be hydrated. some water is loosely bound, allowing diffusion. chondrocytes have a high metabolic rate. CM has no lymph or nerve endings.
3 types of cartilage
hyaline (most common), elastic, fibrocartilage
LM characteristics of hyaline cartilage
homogenous matrix. pericellular matrix surrounds chondrocyte, buffer btwn cell and territorial matrix. interterritorial matrix between lacunae- thick collagen fibers, most of the proteoglycan.
specialized types of hyaline cartilage
articular cartilage: covers articular surface. arrangement allows them to distribute compressive forces. no perichondrium (smooth surface).
also epiphyseal plates.
tidemark
boundary btwn mineralized deep zone and 3 unmineralized zones above it. thick band of mineralized matrix.
elastic cartilage
yellowish. chondrocytes are randomly distributed within matrix, hyaline-like matrix surrounds chondrocytes. perichondrium present.
fibrocartilage
white, opaque b/c type I collagen. linear arrangement. no perichondrium.
2 ways cartilage can grow
interstitial growth (expands from within, in young cartilage w/ more matrix plasticity, imp w/ epiphysial cartilage & long bone growth) AND appositional growth (growth from surface)
appositional growth mech
inner layer of perichondrium contains chondrogenic cells which can become chondroblasts that express SOX 9. secrete CM and become enclosed w/in it, and as a result new cartilage is added to surface of existing cartilage element.
age related changes to cartilage
affects matrix org, mechanical props & chondrocyte fxn. can get fibrillation, ulceration, chondromalacia.
degenerative changes in articular cartilage
arthritis. OA (progressive loss of articular cartilage that can’t be repaired) vs RA (inflammatory rxn vs synovium of join, chronic, can lead to destruction of joint. IL-1 and TNF-a cause degradation of core protein w/in proteoglycan aggregates)
repair of articular cartilage
injury not extending across tidemark doesn’t heal due to lack of influx of chondrogenic cells, fibrin clot or growth factors. if injury extends into bone, repair is incomplete & doesn’t restore normal composition/mechanical properties to CM
intervertebral discs & degenerative changes
decrease in water d/t decrease in water content in nucleus pulposis & fewer proteoglycans bind water. size of aggrecan molecules decreases. nucleus becomes firm. tears appear in annulus fibrosis. increased probability of mech failure, disk herniation.
mineralization of cartilage
CM loses resilience, can occur as a result of aging or pathological change. stiffen matrix, cause loss of resilience.
