Lecture 3
Diarthroses / Synovial Joints
Articulating ends are covered in hyaline cartilage (1-5 mm) – ends of long bones /
chicken bones

Avasular, aneural, and without lymphatics
What does this tell you immediately about hyaline or articular cartilage?

Function
 Distribute loads
 Allow for movement
Composition

Cellular – chondrocytes (10% of volume) – manufacture, secrete, and
maintain organic matrix

Extracellular Matrix

Organic – collagen (type II) (10-30% of weight) in proteoglycans (3-10%
of weight)

Water (most abundant component), inorganic salts, glycoproteins, lipids
(60-87%)
Collagen fibers offer little resistance to compressive forces.
Highly organized  stiffness and tensile strength (most important mechanical property)
Structural components of articular cartilage  collagen and PG along with water
Isotropic – material properties of a substance are the same regardless of direction of
loading
Ansiotropic – material properties differ with direction of loading
Hyaline cartilage is ansiotropic:
1. Collagen arrangement
2. Cross link density
3. Collagen/PG interaction
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Fluid is extremely important to hyaline cartilage. Why?
1. Permits diffusion of gases, nutrients, wastes  SYNOVIAL FLUID
2. Important to the structural organization of collagen  load bearing
/mechanical behavior
What effects of dehydration have on the hyaline cartilage?
Water – 80% concentrated near the surface and 65% concentrated in deep zone
Most of water is extracellular and is free to move when loaded
Collagen-PG Interaction  resist compression
1. Plays direct role in organization of the extracellular matrix
2. Important to the mechanical properties of AC
Biomechanical behavior is biphasic:
1. Fluid phase (water and inorganic salts) – “water soaked sponge”
2. Solid phase (collagen and PG)
Highly and variably stressed tissue – forces at the joint surface range from 0 to > body
weight
Nature of Articular Cartilage (viscoelastic material)
Creep (constant load) – rapid initial deformation  slow(time dependent)  deformation
(creep)  equilibrium
This creep is caused by the exudation of interstitial fluid  resistant to compressive
forces.
Creep to Equilibrium
Deformation
Time
Once compressive stress balances (=) with the applied stress  NO fluid
flowEQUILIBRIUM
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Stress Relaxation - result of fluid redistribution
Stress continuously decays until equilibrium is reached
Peak Stress
Stress
Equilibrium
Time
Behavior of AC under Tension (uniaxial)
Stress
Toe Region
Linear Region
Strain
Toe Region – Alignment of collagen fibers
Linear Region – Stretching of the collagen fibers
Cortical Bone in Tension
Stress
Strain
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Alteration of tensile properties is due to :
1. Alteration of molecular structure of the collagen fibrils
2. Alteration of fibers in the network (ansiotrophy)
3. Alteration in collagen fiber cross linking  fibrillation
Collagen cross link alteration  fibrillation  OA  deterioration of tensile properties
of the collagen-PG solid matrix.
Disruption of the collagen network is a key factor to early OA
Loosening of collagen network  increased swelling
Behavior of AC in pure shear
Stiffness in shear is result of collagen or collagen-PG interaction and not PG
Synovial Fluid
Functions:
1. Lubrication
2. Reduce friction
3. Nutrition



Plasma-like
High in hyaluronate  lubrication to reduce friction
Lubricin – has an affinity for AC - cartilage lubrication
Viscous – ability to resist loads that produce shear
Viscosity is inversely related to the velocity or rate of shear
 Fast movements  decreased viscosity less resistance to motion
 Increased temperatures  decreased viscosity  less resistance to
motion
Hyaluronate is responsible for the viscosity in synovial fluid
At least 2 pharmaceutical companies produce a synthetic-like synovial fluid
Types of Lubrication of AC
1. Boundry – lubricin (glycoprotein) has an affinity for the load bearing surfaces of the
AC effectively forming a layer of lubrication that reduces friction.
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2. Hydrostatic (weeping) – a film of lubricant is maintained thru compressive loading
which causes an increase in fluid and an increase in pressure “lubrication on
command”
3. Hydrodynamic – a wedge of fluid is formed when non-parallel surfaces slide over
each other
4. Squeeze film – pressure is created in the fluid film by bearing surfaces that are
perpendicular to each other – squeeze the film out
5. Elastohydrodynamic – thickness of protective film is maintained by elastic
deformation of AC
6. Boosted – pools of lubricant are trapped in undulations that result from elastic
deformation
What is the key to almost all of these lubrication theories? Movement and loading and
fluid
Wear of AC
Wear – removal of material from solid surfaces thru mechanical action.
1. Interfacial –wear due to interaction of bearing surfaces (no lubricant)
 Adhesive – bearings come in contact – surface fragment adhere to
each other  tearing
 Abrasive – hard surface scrapes a soft surface
Probably rare but may occur in degenerated joint
2. Fatigure – wear due to bearing deformation under load.

Microscopic damage due to repetitive stressing
1. Disruption of collagen-PG solid matrix due to repetitive stress
2. PG washout – mass exudation and imbibition of interstitial fluid which
washes PG’s out of matrix
3. Rapid application of heavy loads preventing adequate stress relaxation
 reduced fluid redistribution
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Cartilage Degeneration
1.
2.
3.
4.
Magnitude of imposed stresses
Total number of sustained stress peaks
Changes in collagen-PG matrix
Changes in mechanical properties of the tissue
Loosening of collagen network  PG expansion  tissue swelling  decrease in
stiffness and increase in permeability  altered cartilage function
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Biomechanics of Tendons and Ligaments
Ligaments (joint capsules)
1. Augment the mechanical stability of joints
2. Guide joint motion
3. Prevent excessive motion
Tendon
1. Attach muscle to bone
2. Transmit tensile loads from muscle to bone
Dense connective tissue (parallel-fibered collagenous tissues)
 Sparsely vascularized
Cellular (fibroblasts) – 20 %
Extracellular (80%)
(70% of this is water/ 30% is solids –collagen, ground substance, elastin)
collagen content is approx 75% of solids and is greater in tendons
extremity tendons – solid material maybe 99% collagen
Ligamentum flavum – has highest content of elastin
Functions to:
 protect spinal nerve from impingement,
 preload motion segments,
 provide intrinsic stability to the spine
Paratenon (tendon)
 sheath of areolar tissue around tendon
 protects and enhances gliding in tendons
Tendons and Ligaments are viscoelastic
Tendons


sustain high tensile forces
flexible
Ligaments
 pliant and flexible
 strong and inextensible/inelastic
Damage to these structures is affected by:
1. rate of impact
2. amount of load
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Tendon
Load
Deformation
Ligamentum Flavum
Load
Deformation
ACL Ligament Injury
Microfailure
Physio Loading
Load
Complete
Failure
Clinical
Test
Joint Displacement
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Viscoelastic –
Creep – constant load
Treatment of deformities – serial casting, bracing (scoliosis)
Factors that affect mechanical properties
1. Maturation – up to 20 - # and quality of cross-links increases  increased tensile
strength and increase in collagen fiber diameter (hypertrophy)
WHY?
2. Aging – collagen content decreases  decrease in stiffness, strength and ability to
withstand deformation
3. Pregnancy and postpartum – tensile strength and stiffness in tendons decreases
4. Physical training –
 increases tendon tensile strength and ligament-bone interface strength
 ligaments become stronger and stiffer, collagen fibers increase in diameter
5. Immobilization
 Decrease tensile strength of ligaments , more elongation, less stiff
 Decrease in cross-links
 After 8 weeks of immobilization it took 12 months to recover strength and
stiffness values
6. NSAIDS
 Increased tensile strength possibly due to increased cross-linkage
7. Local injection of cortizone
 Alters collagen organization in tendon – random versus parallel
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