tissue adaptation

basic structure of the ECM

• fibroblasts in most connective tissue

• GAG polysaccharide chains (repeating dissacharides)

• GAGs which covently bond to proteins- proteoglycans

• fibrous proteins such as collagen

• proteoglycans form a gel like substance where fibrous proteins are embedded which resists compressive forces, allow diffusion

glucosaminoglycans

• structure

• branched or unbranched

• hydorphobic or hydrophilic

• how do they withstand compression

• unbranched polysaccharide chains

• repeating disaccharide chains

• hydrophilic

• porous gels (hydrated) filling up most of the extracellular space

• attract cations so water in by osmosis- turgor- withstand compression

collagen

• how many polypeptide chains

• how many forms

• triple stranded helical structure

• 3 polypeptide chains

• 29 forms

elastin

• hydrophobic or hydrophilic

• what is the precursor molecule

• how does the precursor form elastin

• highly hydrophobic protein

• precursor is tropoelastin

• tropoelastin is secreted into the extracellular space and assembled into elastic fibres close to the plasma membrane, which then cross link

• coiled

• stretch and recoil

tendon

• collagen

• proteoglycans

• elastin

• tenocytes

ligament

• fibrocytes

• ecm

• lower collagen, more proteoglycan

• elastin

cartilage

• which collagen

• which is the predominant proteoglycan

• other molecules

• how much percent of water

• chondrocytes

• type ii collagen mostly

• proteoglycan predominantly chondrotin sulphate

• hyaluoran

• 68 percent water

• regional variation

ecm of bone

• what gives rigidity and compressive strength and where is this deposited?

• which gives tensile strength and elasticity

• hydroxyapatite gives rigidity and compressive strength

• this is deposited on collagen fibres

• load bearing

• inorganic

• type i collagen gives tensile strength and flexibility, elasticy, structural organisation, organic

what is mechanical loading

• ecm turnover is triggered by mechanical loading

• involves cell signalling

• loading increases synthesis of new ecm proteins and degrading enzymes

• loading can alter the molecular conformation of proteins changing how enzymes bind and degrade (change in collagen type and organisation)

• tissue properties influence how they degrade eg stiffness

wolffs law

• increase in loading causes architecture of spongy bone to strengthen and cortical layer strengthening whilst decrease causes bones to weaken and bone tissue to be resorbed

intramembranous ossification

• what do mesenchymal cells become and what is secreted

• what forms in this area

• what aggregates

• what happens and what is trapped as a result

• what turns into what

• wht surrounds blood vessels and what is formed

• what is formed on the outside

• multipotent mesenchymal cells become osteoblasts which secrete osteoid

• blood vessels form in the area

• osteoblasts aggregate in the ossification centre

• osteoid matrix becomes calcified and hardens trapping osteoblasts

• ostoeblasts turn into osteocytes

• osteoid surrounds blood vessels forming cancellous bone

• mesenchymal cells on the outer surface of newly formed bone forms the periosteum

endochondral ossification

• what do mesenchymal cells differentiate into

• what happens to them

• what is formed

• what forms around it

• what happens to the cells and what does this form

• what happens within and what does this allow

• what change occurs and what is brought over

• what is deposited and what does this lead to

• what does this form and what is brung in as a result

• what structure does this form

• mesenchymal cells differentiate into chondroblasts that secrete ECM

• chondroblasts become encased forming chondrocytes

• forms a hyaline cartilage model

• perichondrium forms around it

• chondrocytes increase in size and some burst releasing cell contents triggering calcification

• chondrocyte cells die within the calcifying matrix forming cavities for osteoblasts to move into

• perichondrium changes to periosteum. it contains blood vesels containing nutrients which diffuse into the cartilage precursor and bring osteoblasts

• osteoblasts deposit bone around the diaphysis preventing nutrients from diffusing into the hyaline cartilage leading to chondrocyte death at the centre

• this forms cavities where blood vessels can penetrate bringing in osteogenic cells

• this forms the medullary cavity, osteoblasts begin depositing bone into the spaces which is the primary ossification centre

• secondary ossification centres develop in each end of the long bone

• thin cartilage called the epiphyseal growth plate develops between primary and secondary

• chondrocytes in the plate continue proliferating and also forms new cartilage which turns into bon

• in adulthood chondrocytes in the grwoth plate stop dividing until the physis itself ossifies. then cartilage is only found at the articular surface of joints.

nutritional and hormonal influences

• which 2 salts and what do absorption of these depend on

• vitamins

• which hormones are needed for calcium metabolism regulation

• which hormones for bone growth

• dietary calcium and phosphate salts

• absorption depends on calcitriol (a hormone only made in the presence of vitamin D )

• Vitamins C, A, K, and B12

• calcitonin and parathyroid hormone - calcium metabolism regulation

• insulin, growth hormone, thyroxine- bone growth

• oestrogen- growth plate closure (also testosterone) osteoblast activity

supericial tangential zone

85% collagen; collagen fibres orientated tangential to surface.

Greatest ability to resist shear stresses

middle transitional zone

Transition between the shearing forces of surface to compression forces in deep layer; collagen arranged obliquely;

composed largely of proteoglycans

deep radial

Collagen fibers attached radially (vertical) into the tidemark - distributes loads and resists compression; high PG content

regions