CPMS Biomechanics Tissue Mechanics III Cartilage 2022 PDF

Summary

This document covers the function, physiology, and composition of cartilage, its biomechanics and mechanical properties, modes of mechanical failure, joint lubrication, and the etiology of osteoarthritis related to mechanical factors. It also discusses cartilage types, composition, structure, mechanical behavior under tension and compression, viscoelasticity and lubrication methods.

Full Transcript

Biomechanics & Surgery: Tissue Mechanics III Cartilage n Function, physiology and composition of cartilage n Biomechanics of cartilage – mechanical properties – Viscoelasticity n Readings: – Optional/Recommended: Association Between Friction and Wear in Diarthrodial Joints Lacking Lubricin: Jay et a...

Biomechanics & Surgery: Tissue Mechanics III Cartilage n Function, physiology and composition of cartilage n Biomechanics of cartilage – mechanical properties – Viscoelasticity n Readings: – Optional/Recommended: Association Between Friction and Wear in Diarthrodial Joints Lacking Lubricin: Jay et al, 2007 on D2L Vassilios G. Vardaxis, Ph.D. Cartilage: Objectives At the completion of this topic the students should be able to: – Describe the structure and composition of cartilage in relation to its mechanical behavior – Examine the material properties of cartilage, what they mean physically, and how they can be determined – Describe modes of mechanical failure of cartilage – Describe the current state of understanding of joint lubrication – Describe the etiology of osteoarthritis in terms of mechanical factors Vassilios G. Vardaxis, Ph.D. Cartilage types n articular (or hyaline) – most predominant in the body (diarthrodial joints, growth plates) n fibrocartilage – intervertebral disks, mandibular condyles, meniscus n elastic cartilage – epiglottis, eustachian tube Vassilios G. Vardaxis, Ph.D. Cartilage: Composition Cartilage Reading #s: Vassilios G. Vardaxis, Ph.D. Water - 65%-85% ww Collagen - 75% dw Proteoglycan - 20%-25% dw Hyaline Cartilage: function n n n articular (or hyaline) cartilage covers bone surfaces within the joint capsule “fluid-filled, wear-resistant bone surface” basic functions: – – – – – – Supports / transmits loads across mobile surfaces distributes joint loads over a wider area (stress reduction) Stabilize and guide joint motion lines the ends of bones (prevents wear) lubrication reduces friction coefficient (0.0025) despite common belief does not serve as a “shock absorber” n very thin n capacity negligible compared to muscles and bones Vassilios G. Vardaxis, Ph.D. Hyaline Cartilage: composition n n Water Chondrocytes (~1% dw) – Produce collagen and proteoglycans as needed – Release enzymes to breakdown aging components n Organic matrix – dense network of fine collagen fibrils that are imbedded in a concentrated solution of proteoglycans (PGs: protein + sugar) – Collagen: most abundant protein in the body – Proteoglycan: large protein-polysaccharide molecule Protein core with attached glycosaminoglycans (GAGs) GAGS - mainly two types: n n CS – Chondroitin Sulfate KS – Keratan Sulfate Vassilios G. Vardaxis, Ph.D. Hyaline Cartilage: structure Chondrocyte distribution (shape & arrangement) Water 80% Water contains free mobile cations (Na+, K+, Ca2+) that influence the mechanical and physicochemical behavior of the cartilage Transfer nutrients from the synovial Water 65% fluid Vassilios G. Vardaxis, Ph.D. Hyaline Cartilage: structure n Collagen orientation – – – n parallel to the surface on the superficial layer oblique in the middle layer perpendicular to the surface in the deep zone Proteoglycan content – increases from surface till the middle zone and diminishes towards the deep zone Vassilios G. Vardaxis, Ph.D. Hyaline Cartilage: structure n Collagen Orientation No perichondrium – Absence of fibrous and chondrogenic layers – No ready source of primitive fibroblasts n Superficial zone – – – n densely packed collagen fibrils organized parallel to articular surface oblong chondrocytes n Deep zone – Middle zone – – – fibers more or less randomly arranged greater fiber diameter round chondrocytes Vassilios G. Vardaxis, Ph.D. n Cells arranged in columns along the radial direction Calcified cartilage and subchondral bone – large fibers from the deep zone anchor into this region Hyaline Cartilage: structure n Water – – – – proteoglycans can hold water up to 50 times their weight 70% of the water is bound to proteoglycans remaining 30% bound to collagen inorganic ions such as Ca, Na, Cl and K are dissolved n balance fixed charges on proteoglycans and generate swelling pressure Vassilios G. Vardaxis, Ph.D. Hyaline Cartilage: Composition Components are arranged in a way that is maximally adapted for biomechanical functions n Proteoglycan + collagen – Form structural networks of significant strength and are the structural components that support the internal mechanical stresses that result from external loads Vassilios G. Vardaxis, Ph.D. Cartilage: Collagen Creates a framework that houses the other components of cartilage Majority is Type II collagen Provides cartilage with its tensile strength Vassilios G. Vardaxis, Ph.D. Cartilage: Proteoglycans Each subunit consists of a combination of protein and sugar: Long protein chain Sugars units attached densely in parallel Subunits are attached at right angles to a long filament Produce macromolecules: the proteoglycan aggregate Vassilios G. Vardaxis, Ph.D. Cartilage: Composition n n water contains dissolved inorganic salts tissues with high proteoglycan content – – – – high water content low hydraulic permeability high compressive stress damage to proteoglycans will result in increased water mobility and impaired mechanical function Vassilios G. Vardaxis, Ph.D. Cartilage: Mechanical Behavior n interaction between chemical and mechanical factors – High concentration of (GAGs) CS and KS in solution at physiological pH – High concentration of fixed negative charges that create strong intra-, inter-molecular repulsive forces – This forces tend to extend and stiffen the PGs – Osmosis requires discharge or attraction of counter-ions for electroneutrality è Results in swelling pressure è Develops tension on the collagen network (pre-stress) even in the absence of external load è External load è deformation è internal pressure increases è liquid tends to flow out of the tissue è PG concentration increases è osmotic swelling pressure increases and resistance to compression is achieved. Vassilios G. Vardaxis, Ph.D. Cartilage: Mechanical Behavior Anisotropic due to inhomogeneous distribution of collagen and PGs Examples Knee Lateral Condyle Knee Patellar Groove COMPRESSIVE AGGREGATE MODULUS 0.70 0.53 PERMEABILITY COEFFICIENT 1.18 2.17 Permeability - The rate of flow of a liquid or gas through a porous material. Vassilios G. Vardaxis, Ph.D. Cartilage: Tensile Force 1. Toe region: collagen fibrils straighten out and un- “crimp” 2. Linear region: that parallels the tensile strength of collagen fibrils: collagen aligns with axis of tension 3. Failure region: Vassilios G. Vardaxis, Ph.D. Cartilage: Under Tension Collagen fibers stretch along the axis of loading Tensile loading is generated by the intrinsic stiffness of collagen fibers Tensile modulus (stiffness) is a measure of resistance to tensile loading and depends on: Density of collagen fibers Orientation of collagen fibers Type or amount of collagen cross linking Tensile modulus is flow independent Tensile modulus varies 5-25 MPa depending on: Location of joint surface (high or low weight bearing region) Depth of specimen Orientation of specimen relative to the joint surface Vassilios G. Vardaxis, Ph.D. Cartilage: Compressive Force Uniaxial (confined compression) and indentation configuration Permeability decreases in an exponential manner as function of both increasing applied compressive strains and increasing applied pressure Vassilios G. Vardaxis, Ph.D. Articular cartilage shows nonlinear strain dependence and pressure dependence The decrease of permeability with compression acts to retard rapid loss of interstitial fluid during high joint loadings Cartilage: Under Compression Volumetric changes and time-dependent viscoelastic behaviors occur due to fluid exudation and redistribution Load distribution, recovery due to unloading and transport of large solutes depend on: Exudation Imbibition Flow of the interstitial fluid The very low permeability (k) the matrix to fluid flow create Energy dissipation, through High fluid pressure Very high drag forces between fluid and solid matrix Mechanism of protection of the cartilage solid matrix from stresses and strains associated with normal joint loading Vassilios G. Vardaxis, Ph.D. Cartilage: Shear Force Vassilios G. Vardaxis, Ph.D. Cartilage: Swelling pressure 1. Each sugar has one or two negative charges, so collectively there is an enormous repulsive force within each subunit and between neighboring subunits 2. This causes the molecule to extend stiffly out in space 3. Each proteoglycan requires a mobile counter-ion (e.g. Na+) to maintain electroneutrality 4. The negative charges make the molecules extremely hydrophilic and cause water to be trapped within 5. This property gives articular cartilage its resiliency to compression Vassilios G. Vardaxis, Ph.D. I Cartilage: Swelling pressure The swelling pressure is balanced by stresses generated within the collagen-proteoglycan solid matrix and stresses from joint loading At equilibrium cartilage is in a state of pre-stress Hydration - Swelling effects are recorded by means of tissue weight change Less than 3% weight change in healthy human cartilage Significantly greater ~30% in the degenerate cartilage This helped develop the prevailing hypothesis: “maintenance of the integrity of the collagen and proteoglycan network in cartilage is important in governing the normal swelling behaviors of articular cartilage” Vassilios G. Vardaxis, Ph.D. I Cartilage: Viscoelasticity Time dependent response of a tissue subjected to a constant load or a constant deformation Creep & Stress Relaxation The viscoelastic behavior of the cartilage is caused by: the interstitial fluid flow the macromolecular motion the intrinsic viscoelastic behavior Vassilios G. Vardaxis, Ph.D. Cartilage: mechanical tests F Porous Metal Cartilage Impermeable walls n Confined compression: creep test – – – creep is controlled by the exudation of fluid through the porous platen movement of fluid controlled by the hydraulic permeability k equilibrium deformation controlled by the intrinsic compressive modulus of the specimen Vassilios G. Vardaxis, Ph.D. Cartilage: Creep test Rate of creep is determined by the rate at which fluid may be forced out of the tissue This, in turn, is governed by the permeability and stiffness of the porouspermeable collagenproteoglycan solid matrix For 2-4 mm human or bovine articular cartilage it takes 4 to 16 h to reach creep equilibrium (c). Vassilios G. Vardaxis, Ph.D. Cartilage: Stress relaxation The sample is compressed to point B and then maintained over time (points B to E) Increase stress to reach end of compressive phase Fluid redistribution allows for relaxation phase (points B to D) and matrix deformation Equilibrium is reached at point E Vassilios G. Vardaxis, Ph.D. Cartilage: Loading rate Stress – strain relationship changes with strain rates Vassilios G. Vardaxis, Ph.D. Fluid-film lubrication method A thin fluid-film lubricant causing bearing surface separation n The load is supported by the pressure developed in the fluid-film n ~ 20 micrometers –Hydrodynamic n Non-parallel surfaces move tangentially –Squeeze-film n Bearing surfaces move perpendicularly Vassilios G. Vardaxis, Ph.D. Lubrication depends on the physical properties of the lubricant (viscosity) and the bearing material (stiffness & geometry) DMU: Division of Physical Therapy Foundational Sciences, Block II Boundary lubrication n single layer of boundary lubricant reduces friction and prevents wear Boundary lubrication exists as a complimentary mode of lubrication Jay et al (2007), showed that friction is coupled with wear at the cartilage surface in vivo. They imply that acquired lubricin degradation occurring in inflammatory joint diseases predisposes the cartilage to damage. Vassilios G. Vardaxis, Ph.D. DMU: Division of Physical Therapy Foundational Sciences, Block II Combination lubrication (Mixed) Both lubrication modes appear to function in the human joints The effective mode depends on the applied loads and the relative velocity of the bearing surfaces Severe loading è Boundary lubrication Low or oscillating magnitude of load è Fluid-film lubrication Vassilios G. Vardaxis, Ph.D. DMU: Division of Physical Therapy Foundational Sciences, Block II Cartilage: Friction coefficient Cartilage is subjected to enormous range of loading conditions and sustains minimum wear Vassilios G. Vardaxis, Ph.D. Cartilage: OA - Mechanical Model Damage to cartilage based on disruption of the mechanical environment of the joint. Surgery on periarticular structures or abnormal joint load Knee: Surgical resection of one or combination ACL, MCL, Meniscus Foot: Abnormal foot structure (flat feet, high arches) Common affected joints: Tibiotalar, talocalcaneal, talonavicular, calcaneocuboid, 1st matatarsophalangeal Repetitive impulse loading – Loading rate Altered kinematics (immobilization, instability) Cartilage affected by OA Becomes less stiff in compression and sheer (decreased stiffness) Fluid flows easier through the tissue (increased permeability) Larger amount of deformation Greater rate of deformation In Summary: Alterations in the normal pattern of joint loading/motion has been linked to OA predisposition and may be caused by a variety of factors such as immobilization, joint instability, overuse, trauma, surgery, injury, or obesity. Vassilios G. Vardaxis, Ph.D. Cartilage: OA – Inflammatory Model Long considered “wear and tear” disease However, progress in molecular biology in the 1990s led to this model Inflammatory mediators may initiate and perpetuate the OA process Source of mediators: Local or Systemic (Adipose tissue à blood stream à subchondral bone à joint cartilage) Berenbaum 2013 There is a direct link between mechanics and inflammation: Mechanoreceptor signaling Vassilios G. Vardaxis, Ph.D.

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