Tissue Mechanics - Cartilage - PDF

Summary

This document presents a detailed analysis of articular cartilage, covering its anatomy, physiology, and mechanics. The text explores the four zones within the cartilage, the roles of proteoglycans, and how the structure of the cartilage supports movement by reducing friction of opposing surfaces during loading and unloading.

Full Transcript

ARTICULAR CARTILAGE Zakariya H. Nawasreh, PT, MSc, PhD ARTICULAR CARTILAGE  Hyaline cartilage  70-85% water by weight  10-30% Type II Collagen  8-10% Proteoglycans (PGs)  More than other connective tissue  It’s really important in cartilage!  Avascular a...

ARTICULAR CARTILAGE Zakariya H. Nawasreh, PT, MSc, PhD ARTICULAR CARTILAGE  Hyaline cartilage  70-85% water by weight  10-30% Type II Collagen  8-10% Proteoglycans (PGs)  More than other connective tissue  It’s really important in cartilage!  Avascular and no nerves  Articular cartilage purposes:  Distributes joint loads and decreases stress at joints  Reduce friction between joint surfaces  Cartilage is smoother than glass on glass ANATOMY  Forms a relatively thin covering on the ends of articulating bone  Has a smooth, firm, resilient, and low friction surface  Resilient: ability of an object to rebound form the surface of other object (tennis ball)  Comprised of cells secreting extracellular matrix with collagen and elastin  Chondrocytes  Type II collagen fibers  Collagen fibers gives cartilage its tensile strength  Significant water content in matrix but still is a stiff gel ANATOMY: FOUR ZONES ZONE 1: SURFACE TANGENT LAYER  Region closest to the joint surface (size is 10-20%)  High collagen fibers oriented parallel to joint surface  To distribute the load all over the joint surface  Withstand shear forces  Decreases friction of opposing joint surface  Low permeability  Low Proteoglycans (PGs) content ZONE 2: MIDDLE LAYER TRANSITIONAL STRATUM  Transitional Stratum  Randomly oriented loosely coiled fibers 0  Permits deformations  More isotropic layer as fibers are oriented randomly in 3D  Helps absorb forces on joint surface  Higher number of PGs  More water ZONE 3:MIDDLE LAYER RADIATE STRATUM  Radiate Stratum  Fibers oriented more perpendicular to the surface  Fewer collagen fibers  Highest content of PGs ZONE 4: DEEP LAYER  Collagen fibers oriented vertically or radially related to the joint surface  Collagen fibers penetrates into the tide marker and into classified cartilage  Calcified Cartilage  Beginning of Bone  Tide mark does not permit water to pass PROTEOGLYCANS (PGS) IN ARTICULAR CARTILAGE  Negative charges, flexible  Negatively charged proteoglycan tend to Repel each other  Extremity hydrophilic (high affinity to water)  Osmatic swilling pressure: expanding outward  The expansion is resisted by the tensile restraint provided by the collagen fibers  In rest: collagen fibers in tension due to water content and negatively charged proteoglycan that repel each other DURING LOADING  Under compression  ↓ Volume = ↑ Pressure  Causes fluid to flow out into joint space through pores in Zone 1  Fluid does not travel horizontally  PGs becomes less saturated  Becomes more hydrophilic  Collagen becomes compressed and less permeable  Increases collagen stiffness of the cartilage  The increased in loading rate:  Rapid loading increases the collagen stiffness  Slow loading no increased in stiffness leads to outflow of fluid  Fluid flow occurs rapidly and will stop when the pressure in the cartilage reaches equilibrium with the applied load DURING UNLOADING  Fluid flows back into the cartilage after the motion or compression ceases  Permeability ↑  Stiffness ↓  PGs become more saturated  Hoop Stress or circumferential stress, a normal stress in the tangential direction  The hoop stress is the force exerted circumferentially (perpendicular to the axis and the radius of the object) in both directions on every particle  stress remains unchanged if the stressed object is rotated about some fixed axis.  tensile stress in Zone 1 caused by PGs & H 2 0 compression in collagen network  Cyclic loading & unloading is good  Cartilage rehydrates  Nutrients get into cartilage PHYSIOLOGY  Hyaline cartilage has no blood vessels and nerves  Nourishment only comes from fluid flow into and out of tissue during the loading/ unloading process  Free flow of fluid:  Essential for the health of cartilage  Acts as an aid for reducing friction  Cartilage was built to be loaded in compression not in tension:  If cartilage is loaded in tension it breaks (causes tear) IMMOBILIZATION  After prolonged immobilization hyaline cartilage degenerates  ↓ Motion = ↓ Fluid Flow = ↓ Nutrition  This leads to  Loss of cartilage thickness  Cartilage softening or fissuring  Loss of cartilage thickness leads to pressure point necrosis  Conversely, prolonged high compressive loading completely cuts of f fluid flow also reducing nutrition DEGENERATION  The thin layer of hyaline cartilage will deform subchondral bone under compression A. Normal joint covering, B. Fragmentation and thinning of cartilage, C. Patchy loss of cartilage exposing subchondral bone, D. Extensive cartilage loss, cystic degeneration of underlying bone and osteophyte formation INJURY  Cartilage injuries do not repair on their own  Due to minimal blood supply  Microfracture surgery  Small holes drilled into subchondral bone  Stimulates blood into injury site which brings nutrients to cartilage surface  Rehab limitations  New cartilage is fragile  Partial weight bearing for up to 5 weeks  Running after at least 12 weeks BIOMECHANICS OF ARTICULAR CARTILAGE BIOMECHANICAL BEHAVIOR OF ARTICULAR CARTILAGE Intrinsic material properties and resistance to flow of solid matrix define interstitial fluid pressurization. Interstitial fluid pressurization influences:  Load-bearing capacity  Lubrication capacity LUBRICATION OF ARTICULAR CARTILAGE  Lubrication processes limit wearing of cartilage  Fluid-film lubrication:  Uses film of lubricant causing a bearing surface  Load is supported by pressure developed in fluid-film  In dynamic activity fluid squeeze out from the area between surfaces  Depends on viscosity, shape of the surface, and the joint surfaces  Boundary lubrication:  Surfaces protected by absorbed layer of boundary lubricant  Lubricrin that is absorbed to joint surface  Prevents surface to surface contact or decrease friction LUBRICATION OF ARTICULAR CARTILAGE Mixed lubrication  Combination of fluid-film and boundary lubrications:  Temporal coexistence of both at distinct locations  Boosted lubrication: shift of fluid-film into cartilage results in concentrated gel (Hyaluronic)  Prevent direct contact between joint surfaces ROLE OF INTERSTITIAL FLUID PRESSURIZATION IN JOINT LUBRICATION  Fluid-film lubrication contribution is transient because of rapid dissipation of fluid-film thickness by joint loading.  When interstitial pressurization is high, friction coef ficient is low.  As creep equilibrium is reached, friction coef ficient is high: fluid squeezed out  Ef fective friction coef ficient decreases with:  Increasing rolling and sliding joint velocities  Increasing joint load DAMAGE OR WEARING OF ARTICULAR CARTILAGE Is unwanted removal of material from solid surfaces by mechanical action. Can be: Interfacial wear:  Bearing surfaces come into direct contact, with no lubricant film separating them. Fatigue wear:  Accumulation of microscopic damage within the bearing material under repetitive stressing  Overuse injury: long standing/ running without resting Wear due to synovial joint impact loading WEAR OF ARTICULAR CARTILAGE (CONTINUED) Once collagen-PG matrix is disrupted it can induce: Further disruption of collagen-PG matrix due to repetitive matrix stressing Increased “washing out” of PGs due to violent fluid movement and thus impairment of articular cartilage’s interstitial fluid load support capacity Gross alteration of normal load carriage mechanism in cartilage, thus increasing frictional shear loading on the articular surface HYPOTHESES ON THE BIOMECHANICS OF CARTILAGE DEGENERATION  Cartilage failure progression relates to:  Magnitude of imposed stresses  Total number sustained stress peaks  Changes in intrinsic molecular and microscopic structure of collagen - PG matrix  Changes in intrinsic mechanical property of tissue  This is associated with decreased cartilage stif fness and increased cartilage permeability. FUNCTIONAL TISSUE ENGINEERING OF ARTICULAR CARTILAGE  Cartilage has poor healing capacity.  Tissue engineering is:  Incorporating an appropriate cell.  This cell will grow fabricated tissues.  These tissues will be used for repair and replacement of damaged or diseased tissues and organs.

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