MS1 terms - exam 2

bone biomechanical functions

1. protect internal organs
2. provide rigid kinematic links
3. provide attachment points for muscles
4. facilitate muscle action and movement

bone organic extracellular matrix

mostly type I collagen and ground substance - 30% of weight; high content of inorganic mineral salts (calcium and phosphate) - 60% of weight; water - 10%

* mineral provides mechanical rigidity and load-bearing strength
* organic matrix provides elasticity and flexibility

bone remodeling

continuous removal of discrete packets of old bone, replacement of these packets with newly synthesized proteinaceous matrix, and subsequent mineralization of the matrix to form new bone; begins before birth and continues until death; 2-3% each year

bone balance

difference between old bone reabsorbed and new bone formed during remodeling

* periosteal BB: very mildly positive
* endosteal and trabecular BBs: mildly negative

factors affecting biomechanical behavior of bone

1. mechanical properties
2. direction of loading
3. geometric characteristics
4. rate of loading
5. frequency of loading

anisotropy of bone

exhibits different mechanical properties when loaded differently

tension

usually seen in bones with large proportion of cancellous bone (ie. pulling out on both ends); under these forces, the structure lengthens and narrows; transverse fractures; debonding of osteons at cement lines

compression

equal and opposite loads are applied toward the surface of the structure (ie. pushing in on both ends); fractures commonly seen in vertebrae; oblique fractures; the most tolerated stress in bones

shear

load is applied parallel to surface of the structure; happens during compression and tension along the neutral axis; greatest shear occurs when angle of force applied is 45 degrees; causes crack along the neutral axis of bone and most often seen first in cancellous bone; the further the bone is from the center of axis, the more shear stress is experienced; the least tolerated stress of bone

bending

loads are applied in a manner that causes the bone to bend about an axis, subjected to a combo of tension and compression; 3-point vs. 4-point; bone can withstand compression better, so a fracture will happen first on the side of tension (the weaker side)

boot top fracture

occurs without stabilization of muscle contraction; muscle contractions prevent fractures since they are stronger than compression and tension forces

torsion

twisting around axis; shear stresses around entire structure proportional to the distance from the neutral axis; max shear stresses act on planes parallel and perpendicular to the neutral axis, while max tensile and compressive stresses act on a plane diagonal to the neutral axis

torsion fractures

fractures first in shear (crack parallel to neutral axis), then fractures along the greatest tensile stress path

combined loading

regular activity includes multiple loads across a period of time

viscoelasticity

fluid and solid like properties; all biologic material; material behavior is time or rate dependent

viscoelasticity of bone

bone will fracture with less stress if load is applied at a slower rate; damage will be greater with higher loading rates (more energy)

fatigue under repetitive loading

resistance to fatigue greater in compression than tension; not only depends on magnitude of application and number of repetitions, but number of reps within a given time

factors that lead to stress fractures

1. most common in tibia, metatarsals, navicular, fibula, and calcaneus
2. amenorrheic athletes have a 1.5-3x risk
3. rapid increase in frequency, mileage pace, or terrain (reps x load)
4. lack of rest after long period of activity

area moment of inertia of bone

for a given bone length, the wider the outer bone, the more resistant to bending stress

wolff’s law

remodeling of bone is influenced and modulated by mechanical stresses → long bones can change shape to accommodate stress placed on them; bed rest causes a 1% decrease of bone mass per week

mechanotransduction

forces applied to the body signal a cascade of events to make changes at the cellular level; control of cell metabolism via response to mechanical stimuli

* mechanocoupling: mechanical trigger
* cell-cell communication: communicate the loading message thru tissue
* effector response: cellular response to correct alignment

osteoprogenitor

stem cells of bone derived from primitive mesenchymal cells; form a population of stem cells that can differentiate into the more specialized bone-forming cells; make up the deep layer of the periosteum that invests the outer surface of bone and endosteum

osteoclast

only cell known to be able to resorb bone; controlled by hormonal and cellular mechanisms; function in groups termed “cutting cones” that attach to bare bone surfaces and, by releasing hydrolytic enzymes, dissolve the inorganic and organic matrices of bone and calcified cartilage

osteoblast

builds new bone; synthesize and secrete both collagen and non-collagenous proteins; upregulated by increased force through their region bone

osteocytes

mature osteoblasts trapped within the bone matrix; from each one, a network of cytoplasmic processes extends through cylindrical canaliculi to blood vessels and other ones; involved in remodeling behavior via cell-to-cell interactions in response to local environment

modeling

process by which bones change their overall shape in response to physiologic influences of mechanical

mechanosensation

function of the osteocyte-osteoblast cell syncytium

mechanostat theory

optimal length and window of use exists! modeling and remodeling effects on bone strength and mass: disuse window, adapted window, mild-overload window, and pathologic window

bone loading maintenance

low reps with high loading OR high reps with low loading

bone phases of healing

1. early inflammation - hematoma formation
2. repair stage - soft callus and hard callus formations
3. late remodeling - bone remodeling

revascularization

fracture healing requires a blood supply for successful repair; osteoblast and chondrocytes promote the invasion of blood vessels and transforms the avascular cartilaginous matrix into a vascularized osseous tissue

prostaglandins

group of physiologically active lipid components in almost every tissue that mediate the inflammatory process with hormone-like effects; enzymatically derived from COX1/2

inflammatory cells in bones

macrophages, monocytes, and lymphocytes; results in the formation of granulation tissue, ingrowth of vascular tissue, and migration of mesenchymal cells

fibroblasts role in inflammation

infiltrate the bone to lay down a stroma to help support vascular ingrowth

soft callus

fibrin-rich granulation tissue forms between fracture ends both at endochondral and periosteal sides; cartilaginous tissue forms a soft callus which gives the fracture a stable structure; dependent on recruitment of MSCs from surrounding peripheral blood; very weak in first 4-6 weeks

hard callus

ossification response occurs subperiostally directly adjacent to the distal and proximal ends of the fracture and forms a bridge of woven bone between the fracture fragments; provides some stability but does not restore biomechanical properties of normal bone

remodeling of bone

healing bone is restored to its original shape, structure, and mechanical strength; hard callus becomes a lamellar bone with a central medullary cavity via osteoclast/blast activity; occurs slowly over months to years and is facilitated by mechanical stress placed on bone (axial loading); adequate strength reached in 3-6 months

successful remodeling of bone requires:

1. adequate blood supply
2. gradual increase in mechanical stability

stiffness

stress / strain

effects of aging on bone

1. decreased toughness/stiffness
2. thinning of cancellous and cortical bone
3. decreased bone mineral density
4. thinning trabeculae

safe fall strategies

1. increase time of fall to decrease force magnitudes
2. decelerate by flexing joints and engaging muscles; engaging more muscles also neutralizes force
3. move COM towards site of impact to help distribute load

tendon functions

1. attach muscle to bone
2. transmit tensile of the muscle load to bone
3. proprioception - GTOs

ligament functions

1. connect bone to bone
2. augment joint stability
3. prevent excessive mobility
4. guide joint motion
5. proprioception - mechanoreceptors

tenocytes

specialized fibroblast cell of tendons (20%); produce and degrade extracellular matrix in response to mechanical load

extracellular matrix of tendons

80% of tendon composed of up to 70% water; dry weight composed of collagen (mostly type I), elastin, proteoglycans, and proteins

rounded fibroblast

ligament cells (20%) that produce and degrade extracellular matrix in response to mechanical load

extracellular matrix of ligaments

80% of ligament that contains about 70% water; dry weight comprised of collagen (type I), elastin, proteoglycans, and proteins

paratenon

tendon sheath with 2 layers to assist in gliding

epitenon

synovial like membrane of tendons prominent in areas of high friction

blood supply and innervation of tendons

1. blood: only 1-2% of extracellular matrix; derived from vessels at perimysium or periosteal insertion
2. innervation: proprioceptive and nociceptive

blood supply and innervation of ligaments

1. blood: sparse supply; epiligament continuous with periosteum where blood is obtained
2. innervation: prioprioceptive and nociceptive

tendon insertion into bone

1. zone 1: collagen fibers
2. zone 2: fibrocartilage
3. zone 3: mineralization of fibrocartilage
4. zone 4: cortical bone

hysteresis

energy loss caused by repetitive loading of a tendon

load relaxation

specimen is stretched to constant length; initial rapid decrease in stress and then more slowly

creep

specimen placed under constant load for a period of time; length initially increases rapidly then more slowly

factors that affect biomechanical behavior

1. maturation/aging
2. pregnancy/postpartum
3. mobilization/immobilization
4. comorbidities (metabolic influences)
5. pharmacological agents

ligament failure

1. loads for clinical knee test
2. physiologic activity
3. microfailure
4. complete rupture

injury to tendons

mechanisms: high stress, high strain, or both; related to cross-sectional area of tendon; amount of force due to contraction

injury to ligaments

mechanisms: high stress, high strain, or both; fast rate: ligament failure, slow rate: bone failure

tendon/ligament repair

1. inflammation: up to 3 days; hematoma forms, platelets degranulate, phagocytosis of necrotic material, and fibroblasts migrate to the area; NSAIDs may interfere
2. proliferation day 3 - week 6: increased migration of fibroblasts, synthesis of type III collagen increases, repair of callus, laying of scar tissue; fibroblasts resorb collagen and produce new collagen at same time, then orienting collagen more longitudinally according to tension forces
3. remodeling: biomechanical strength is increasingly restored; more cross-linking in long axis; collagen III replaced by collagen I but not completely

final properties of tendons/ligaments post-injury

rarely achieve biomechanical properties of pre-injured state; final tensile strength 30% less; heal at slower rate due to hypovascularity and hypocellularity; some don’t heal much at all on their own (ex/ ACL)

ACL reflex functions

joint stability and muscular inhibition

ligamento-muscular reflex

prevent joint distraction and reduce stress on the ACL → create stability in joint thru co-contraction; some inhibitory effects → protect ligaments by reducing force in the muscles that stress them

optimal loading

a certain amount of mechanical load is crucial for tendon healing, however the right amount and timing have not yet been defined, knowing that over- and under-stimulation can have adverse effects

mechanical load

fibroblasts respond to mechanical stresses by regulating expression of ECM; load leads to upregulation of collagen mRNA expression and increased growth factor concentrations; correlation of increased activity and tendon/ligament cross-sectional area; under- vs over- stimulation

articular cartilage functions

1. distribute joint loads over a wide area
2. allow relative movement of opposing joint surface with minimal friction and wear

AC composition

chondrocytes and ECM (collagen, PGs, and water)

chondrocytes

AC cells that make up less than 10% of volume; manufacture, secrete, organize, and maintain ECM; no cell-cell connections but respond to growth factors, mechanical loads, forces, and hydrostatic pressures; limited capacity for replication

chondrocyte regions

1. pericellular: primary role is signal transduction upon load-bearing
2. territorial: protect cartilage cells from damage; basket-like network around chondrocytes
3. interterritorial: largest region; contributes most to biomechanical properties of AC

AC collagen

mostly type II; fibrous ultrastructure; zonal pattern of fiber distribution (layered); fibers strong in tension but weak under compression

* superficial zone: in contact with synovial fluid, integrity essential to protect deeper layers, woven parallel to surface, densely packed and flat-shaped chondrocytes, and resists shear stress
* middle zone: 40-60% of volume, collagen oriented obliquely, chondrocytes are round and low density, and first line of protection to compression
* deep zone: thicker fibers, lowest water content, chondrocytes stacked perpendicular to bone surface, highest PG content, and greatest protection against compression
* tidemark: calcified layer of fibrils that anchors AC to bone

proteoglycans (PGs)

large protein polysaccharide molecule composed of GAGs bound to a protein core; GAGs are ratio of chondroitin (CS) and keratin (KS)

aggrecan PGs

elastic molecules that make up 90% of mass and give ability to resist compression; extremely high capacity to attach to hyaluronan molecules

non-aggregating PGs

10% of mass; may represent degrading aggrecans

water in AC

80% of AC mass with most of concentration on the surface; up to 70% may be moved with compressive force → controls mechanical behavior and allows lubrication of joint; essential to health of AC by permitting gas, nutrient, and waste product movement between chondrocytes and surrounding synovial fluid

AC during joint loading

1. joint loading
2. deformation of matrix
3. deformation of chondrocyte and response


1. remodeling of ECM
2. increase of hydrodynamic/osmotic pressure → resulting swelling pressure and mechanical response

viscoelasticity of AC

biphasic!


1. creep: viscoelastic material subjected to constant load; slow, progressively increasing deformation


1. when loaded, fluid is forced out until equilibrium
2. fluid reabsorbed when load is removed
2. stress relaxation: viscoelastic material subjected to constant deformation; rapid, high initial stress, followed by slow, progressively decreasing stress


1. apply constant deformation and assess load on tissues
2. water seeps out of tissue or redistributes throughout AC

permeability

controlled by PGs, the measure of ease with which fluid flows through porous membrane for a given period; AC has porous membrane but the fluid is very viscous → low permeability

* rapid loading: little time for fluid exchange
* slow/prolonged loading: time for fluid flow and tissue deformation to occur

joint lubrication

joints serve as area of contact between bones; in synovial joints, goal is movement; coefficient of friction of joint = .001; allows for very little wear of AC surface

AC lubrication theories

1. fluid film: thin layer of lubricant causing bearing surface separation; squeeze film (perpendicular surfaces moving toward each other) or hydrodynamic (fluid “wedge” formed)


1. low loads and/or oscillate in magnitude when contacting surfaces are moving at high speeds
2. boundary: single monolayer of lubricant molecules absorbed on each bearing surface; plays larger role in sustained heavy loading


1. high load, low speed, long duration

AC metabolism

avascular and devoid of nerves; nutrition derived solely from flow of fluid in and out of tissue supplied thru the synovial fluid; motion and compression are stimuli necessary to facilitate fluid flow and maintain tissue health

AC synthesis/degradation

driven by cytokines released by chondrocytes that then bind to cell surface receptors; can enhance or slow chondrocyte division and matrix synthesis/degradation and can inhibit/promote their mutual effects; cytokines may act synergistically or additively; anabolic effects: growth factors to balance the catabolic effects

degradation dysfunction

release of proteolytic enzymes that break down aggrecan and type IX collagen; imbalance in regulation of promotor and inhibitor leads to cartilage damage (ex/ arthritis)

hypotheses on AC degeneration

1. low capacity to repair and regenerate
2. progression of AC failure relates to: magnitude of stresses, total number of sustained stress peaks, changes in intrinsic molecular structures, and changes in intrinsic mechanical properties
3. inflammation
4. aging

effects of aging on AC

1. strength of weight-bearing AC decreases after the third decade of life
2. matrix composition changes and altered activity of chondrocytes → decreased chondrocyte response to stimuli, aggrecan size reduced, and type II collagen damage

intrinsic AC repair

stop degradation; fills in depleted pericellular regions through clonal chondrocyte proliferation and increase in matrix synthesis

end-stage AC degeneration

eroded cartilaginous tissue with denuded bone-plate regions; cracks in subchondral plate; formations of subchondral bone cysts as a result of focal resorption

extrinsic repair of AC

help at later stages than intrinsic; vascular supply of bone marrow allows for this type of repair; newly formed tissue covering boneplate is mechanically suboptimal fibrocartilage

altered stress pattern

increased stresses cause decreased capacity to produce fluid film lubrication → results in surface to surface contact

mechanical degredation

1. fatigue wear: accumulation of microscopic damage within bearing materials under repetitive stressing
2. interfacial wear: interaction of bearing surfaces


1. adhesion: bearing surfaces come in contact (no lube)
2. abrasion: soft material scraped by harder material

influence of exercise on OA

may improve symptoms by improving joint stability; but if significant malalignment, increased strength could be detrimental; neuromuscular control?

microfracture

surgical intervention that capitalizes on properties of AC extrinsic repair; release of multipotent stem cells from bone marrow

surgical interventions for AC degeneration

1. cartilage regeneration
2. synthetic replacement
3. biological replacement

anisotropy of tendons/ligaments

can take more stress along long axis (tensile forces), ligaments more-so than tendons

tendon responses to different stimuli

1. loading: anabolic response; increased synthesis, increased CSA, and increased stiffness
2. unloading/inactivity: catabolic response; decreased synthesis and decreased stiffness
3. aging: slight catabolic response; decreased cell #, decreased synthesis, and decreased stiffness
4. injury: anabolic response (inflammatory); decreased cell #, increased synthesis, and increased CSA

modifiable risk factors for injury

1. internal: malalignment, neuromuscular control, skills, body mass, nutrition
2. external: training surface, weather conditions, footwear, equipment

how to prevent overuse injury

1. only increase one variable at a time
2. only increase one aspect of distance, time, or intensity by 10% a week
3. ensure adequate time for recovery within training schedule
4. keep a training log and follow the schedule
5. monitor HR, weight, and sleep quality

continuous passive motion

improves motion and biological properties of AC compared to immobilization and intermittent active motion; mechanisms: clearing of inflammatory and waste products, increased movement of nutrients thru the synovium, but not necessarily uptake of nutrients of the AC

functional scoliosis

curves reduced by sitting; possibly due to pelvic imbalance or one leg being bent or shorter

structural scoliosis

adolescent idiopathy; curvature does not change with movement/positional change

posture LOG

runs directly thru mastoid process/external meatus, slightly posterior to greater trochanter, slightly anterior to knee joint, and anterior to lateral malleolus