Ligament, Meniscus, Articular Cartilage Injuries

Front 1

talk about Ligaments:

Back 1

*Bone to bone attachments, typically across a joint
*Have built in laxity at low tension
*Become more stiff at higher tension
*Very strong and stiff when compared to other connective tissue, eg. skin
*Passive/ static function
-Stabilize (often work in pairs)
-Guide joint motion (kinematics)
-Proprioception

Front 2

talk about Multiple or paired ligaments:

Back 2

*Critical for joint stability and kinematics
*Primary and secondary stabilizers
-Redundancy between ligaments to share load carrying function

*Joint motion combination of translations and rotations determined by interaction of ligament forces, joint contact forces, externally applied forces, and muscle activity

Front 3

Ligament Gross Anatomy: Classification and naming:

Back 3

-Bony Attachment coracoacromial
-Relation to joint collateral
-Relation to other ligament cruciate
-Gross shape deltoid
-Less distinct capsular

Front 4

gross/ microscopic appearance of ligaments:

Back 4

*Gross- uniform band-like connective tissue, little apparent complexity

*Microscopic- intricate amalgam of collagen, extra-cellular matrix proteins and a diverse population of cells

Front 5

Back 5

ligament

Front 6

Ligament composition:

Back 6

*Biphasic- solids, fluid
*Collagen

*Ground Substance
-Composite material
-Water 60-70%
-Proteoglycans, glycoproteins and non-collagen proteins
-Binds collagen fibrils to form fascicles
-Matrix supports cells, vessels, nerves, and lymphatics
-Allows some sliding motion between fibrils

Front 7

Type I Collagen:

Back 7

*Major structural protein of tendon and ligament
*All alpha chains are composed of repeating triplets of polypeptides, glycine-x-y (most common is glycine-proline-hydroxyproline)

*Proline molecule geometry forces the alpha chain into a left-handed helix (2º structure)
*Collagen molecule: Three alpha chains form a long right handed triple super-helix (3º structure)
*4° structure-microfibrils organized in staggered array that aligns oppositely charged amino acids
*Spiral and stacked configuration gives tensile strength

Front 8

Ligament Histology:

Back 8

*Collagen microfibrils, subfibrils, fibrils closely packed, parallel bundles oriented in a longitudinal pattern

*Collagen fibrils embedded in matrix of ground substance, including water and proteoglycans

Front 9

Ligament fibers:

Back 9

*Longitudinal fascicles (20-400 µm)
*Fascicle collagen has an organized sinusoid waveform (crimp)
*Crimp responsible for initial non-linear stiffness in response to stress

Front 10

Ligament Histology of fascicles:

Back 10

*Fibroblasts arranged in long parallel rows in the spaces between collagen fibrils within fascicles

*Cells have extensive thin cytoplasmic processes that extend between collagen fibrils

*Fascicles bound together by endotenon (loose connective tissue)

Front 11

Ligament cells:

Back 11

*Fibroblasts- differentiated by nuclear shape and presence of a lacunar space
-Fusiform-spindle shaped
-Spheroid
-Ovoid
*Not uniformly distributed, associated with crimped collagen fibers
*Varied response to tensile and compressive stress, injury
*Express actin isoform

Front 12

Biomechanics of ligament structures:

Back 12

*Response to tensile load similar among collagenous soft tissues with characteristic stress- strain curves

*Dependent upon anatomic features, crimping, and biochemical bonding between collagen structural subcomponents

*High tensile strength due to Type I collagen

Front 13

Stress-Strain Curve for ligaments:

Back 13

*Curve depicts mechanical properties of the ligament structure
*Stress=load applied to material
*Strain=change in length of material (deformation)
*toe, linear, and yield/failure regions

Front 14

Toe Region:

Back 14

*Ligament stretches; straightening of crimped fibrils
*More pronounced in ligament v. tendon
*Decreases with age because the amount of crimp decreases

Front 15

Relationship b/t crimp and stress-strain curve:

Back 15

Front 16

Linear Region:

Back 16

*“Working” region for physiologic stress
*Slope=stiffness of the structure
*Stiffer tissue has greater slope

Front 17

Yield and Failure region:

Back 17

*Irreversible changes (failure) or permanent stretching of the tissue; non-recoverable deformation
*This is what occurs with injury

Front 18

Viscoelasticity:
creep-
stress (load) relaxation-
hysteresis-

Back 18

*Creep
progressive deformation of a viscoelastic structure with time as the amount of load remains constant

*Stress (Load) Relaxation
progressive decrease in load with time as the deformation of the structure remains constant

*Hysteresis
Energy stored in a viscoelastic material when a load is given and then relaxed.

Front 19

Viscoelasticity:

Back 19

*Elongation depends upon rate and history of force application

*Increased rate of loading
becomes stiffer
sustains a higher load to failure
stores more energy before failure

*Increased history of loading
Repeated loading and unloading (i.e. stretching) shifts stress-strain curve to right (becomes less stiff)
Effectively adapts to and dissipates tissue stresses

Front 20

Ligament Preconditioning:

Back 20

*Long periods of inactivity (hours) soft tissues imbibe additional fluid
*1st few applications of force to tissue extrude the extra fluid
*1st few cycles after inactivity show greater stiffness
*Following warm-up behavior of tissue becomes more repeatable

Front 21

Mechanical Regulation of Connective Tissue Homeostasis:

Back 21

*Envelope of function
-Dye, Arnoczky

*Theory that describes a range of tissue loading that is compatible with homeostasis
*Physical stress↔ Biologic response

*Mechanotransduction
-Cytoskeleton displacement initiates a cascade of gene expression activating catabolic or anabolic responses

*Fibroblasts are programmed to sense a certain amount of strain (set point) and are capable of generating an internal tensional homeostasis

Front 22

Relationship b/t mechanical load and gene expression:

Back 22

Front 23

Tissue Overload:

Back 23

*Cumulative trauma-failure under strain or tensile overload

*Repetitive stress in the ligament exceeds the metabolic tolerance of this structure, failure occurs at a cellular level

*Narrows the functional envelope and makes tissue prone to injury

*Cell death happens first!

Front 24

Ligament Homeostasis:

Back 24

*Uniform microvascularity originating at attachment sites

*Provides oxygen and nutrition for cells
-Krebs cycle (aerobic)
-Pentose phosphate shunt (aerobic)
-Glycolysis (anaerobic)

*When stressed and avascular, damage from normal activities accumulates (fatigue) and the ligament is at risk for rupture

Front 25

Ligament Tensile Overload:

Back 25

*Cellular damage increases with strain and precedes structural failure (red regions= cell death; green=normal)

Front 26

Knee Ligaments:

Back 26

Front 27

Ligament Injury:

Back 27

*Damage to ligament = sprain

*Injury results from excess tensile load causing collagen fiber failure

*Mechanism of injury may be direct (eg. contact), indirect (eg. twisting) trauma or repetitive

*Allows joint surfaces to partially (subluxate) or completely (dislocate) disengage

Front 28

Ligament Injury grades:

Back 28

*Grade I-mild sprains, overstretching without disruption

*Grade II-moderate sprains, gross tears and hemorrhage, continuity maintained

*Grade III-complete disruption of ligament
eg- ACL, MCL

Front 29

Back 29

*Ligament Injury
*Single tensile load, micro-structural collagen failure, 250x

Front 30

Extra-Articular Ligament Healing:

Back 30

*Healing analogous to healing and repair process of other vascular tissues

Phase 1-inflammation
Phase 2-matrix and cellular proliferation
Phase 3 and 4-remodeling and maturation

Front 31

Back 31

Ligament Healing
Phase 2-matrix and cellular proliferation

Front 32

Back 32

Ligament Healing
Phase 3 and 4-remodeling and maturation

Front 33

Medial Collateral Ligament Tears:

Back 33

Extraarticular ligament
Excellent blood supply for healing
Majority treated non-operatively

Front 34

Back 34

Front 35

Intra-Articular Ligament Healing:

Back 35

*Torn ligament does not spontaneously heal
*Unable to form fibrin clot, support humeral response, ligament ends retract
*Requires replacement to restore ligament function (if symptomatic)

pic is ACL; can't heal on its own

Front 36

Back 36

*Lubricin distribution in the torn human anterior cruciate ligament and meniscus

Front 37

ACL Tears:

Back 37

*Intra-articular/ synovial ligament
*Poor healing potential
*Causes knee instability or “giving out”
*Can lead to meniscus tear and secondary osteoarthritic changes
*Typically surgically reconstructed in younger active patients

top- torn ACL
bottom- ACL graft

Front 38

Ligament Summary:

Back 38

*Important for joint function, stability, and kinematics
*Collagen fibers (Type I) provides tensile strength
*Biphasic structure results in viscoelastic behavior and allows ability to adaptation to physiologic stresses
*Dynamic and active tissue, undergoing constant remodeling in response to stress
*Varied intrinsic and extrinsic healing capabilities after injury

Front 39

Articular Cartilage:

Back 39

*Hyaline cartilage
-Avascular
-Aneural
-Alymphatic
-Varied thickness

Front 40

Back 40

Articular Cartilage

Front 41

where do we have articular cartilage?
traits/functions?

Back 41

-Synovial joints
-Low friction articulation
-Load bearing
-Shock absorption
-Extremely resilient

Front 42

Articular Cartilage Collagen:

Back 42

*Predominantly type II (90-95%)
Unique to hyaline cartilage
Forms cross banded fibrils
Provides tensile strength
Fiber density/orientation has zonal variation
Traps glycoprotein aggregate

*Types II,VI,IX,X,XI
Stabilize fibril meshwork
Binds chondrocytes
Mineralization

Front 43

Back 43

Front 44

Proteoglycan Aggregate:

Back 44

*Hyaluronate backbone in articular cartilage
*~300 aggrecan molecules attached via link protein (bottlebrush appearance)
*Large negative charge due to carboxyl and sulfate groups attract cations
*Donnan osmotic pressure effect
*Hydrophyllic- Water content has a major influence on the biomechanical properties

Front 45

Articular Cartilage Metabolism:

Back 45

-Despite a lack of blood supply, there is considerable chondrocyte metabolic activity
-Cells respond to mechanical, electrical, and chemical stimuli

Front 46

Effects of Joint Motion on articular cartilage:

Back 46

*Joint motion and loading serve as the principal stimulus to cartilage cells

*Required to maintain normal composition, structure, and mechanical properties

*Excess (overload) or insufficient (immobilization) loading alters nutrition, and results in a change in the balance of synthesis and degradation

Front 47

Articular Cartilage Biomechanics and Response to Loading:

Back 47

*Biphasic: water capable of flowing through the solid matrix
*Flow dependent/ independent viscoelastic behavior

Front 48

Meniscus Cartilage Anatomy:

Back 48

*Main function is to protect the articular cartilage
*Semicircular
*Wedge x-section
*Conforms tibia-femoral articular surfaces
*Attached peripherally to capsule, tapers to free edge in joint

Front 49

Meniscus vasculature:

Back 49

*Relatively avascular
*Peri-meniscal plexus within capsule and synovium
*Penetrate 10- 30% of the meniscus width

*Tears within the red zone have the
potential to heal with repair, symptomatic white zone tears are removed

Front 50

Meniscus Cartilage Ultrastructure and Biochemistry:

Back 50

*Fibrocartilage

*Cells
-Fibrochondrocyte
-Fibroblast
-Surface cells

*Matrix
-Water
-Collagens
-Proteoglycans
-Glycoprotiens

Front 51

medial vs lateral meniscus:

Back 51

Medial
Larger
More firmly attached to capsule (less mobile)
transmits 50% of force
*A tear here isn't quite as bad

Lateral
Covers larger amount of plateau surface area
More mobile
transmits 70% of force

Front 52

Meniscus Collagen Framework:

Back 52

-hoop fibers

Front 53

fibroblasts, Fibrochondrocytes, and surface cells in meniscus:

Back 53

*Fibroblast
Peripheral meniscus
Cytoplasmic projection
Responds to tensile loads

*Fibrochondrocyte
Central meniscus
Round/ oval
Pericellular matrix
Synthesize collagen

*Surface cell
Fusiform
Express actin isoform
Migrate to injury region

Front 54

Meniscus Cartilage Function:

Back 54

Load bearing
Shock absorption
Joint stability
Joint lubrication
Proprioception

*Load bearing
Protects articular cartilage
Efficiently dissipates stress on joint surface
Meniscectomy results in increased stress over a smaller surface area

Front 55

how does meniscus provide joint stability?

Back 55

*Joint stability
*Wedge shape= chock block
*Increased MM stress with ACL removal/tear (increased MM tears with chronic ACL tear)
*Increased AP translation with medial menisectomy, ACL tear

Front 56

Meniscus tears:

Back 56

*Occur with knee trauma and instability
*Symptoms of joint pain, swelling, locking and instability
*Tear increases load on articular cartilage and late osteoarthritis
*Most have poor healing potential
*Treatment goal= preserve functional meniscus with repair, partial menisectomy, replacement

Front 57

Meniscus healing:

Back 57

*Stable, peripheral tears result in formation of a fibrin clot and a typical healing inflammatory cascade
*Unstable and avascular tears have poor healing potential

*Fusiform superficial zone cells do respond to injury
-Alpha smooth muscle actin
-Migrate to meniscus wound

*Healing in the avascular region can be stimulated with the addition of blood flow, fibrin clot, PRP, growth factors..

Front 58

Describe the Limited potential for articular cartilage repair:

Back 58

*Repair = replacement of damaged cells and matrix with new cells and matrix

*Lack of Blood Supply
No hemorrhage, fibrin clot, inflammatory cells, cytokines

*Lack of Undifferentiated cells
No repair cells for migration, proliferation
Limited chondrocyte migration, proliferation

Front 59

Articular Cartilage Injury- how does it happen?

Back 59

*Normal cartilage
-Overload
Traumatic impact
Repetitive activities
Increased load/ stress

*Degenerative Cartilage
Normal loads

Front 60

Types of Articular Cartilage Injury:

Back 60

-Micro-damage to cells, matrix
-Macro-disruption of cartilage alone (chondral fracture)
-Macro-disruption of cartilage and subchondral bone (osteochondral fracture)

Front 61

Articular Cartilage Injury- Micro-damage to cells, matrix:

Back 61

*Single moderately severe impact without tissue disruption
-Matrix
↓ Proteoglycan content
Altered collagen fibril arrangement
↑ Tissue hydration

*Cell
-Chondrocyte injury, death
-Altered anabolic, catabolic function

*Altered Structural Properties- less stiff, more permeable, more susceptible to injury

Front 62

Articular Cartilage Injury- Macro-disruption of cartilage alone, no bone penetration:

Back 62

*Response to Superficial Laceration
Lesions not crossing tide mark do not heal
Fraying/ clefts in superficial layer common
Loss of proteoglycan
Limited chondrocyte proliferation without migration
Defects not filled by new matrix
Progressive injury ensues

Front 63

Articular Cartilage Injury- Macro-disruption of cartilage alone, with bone penetration:

Back 63

*Articular cartilage shearing off subchondral bone
*No blood supply, marrow cells= no healing
*Propagates,"", breaks off (loose body), and leads to progressive wear

Front 64

Articular Cartilage Injury- Macro-disruption of cartilage and subchondral bone (osteochondral fracture):

Back 64

*Injury crosses tide mark into subchondral bone
*Hemorrhage, fibrin clot, inflammation
*Cell migration, proliferation, differentiation
*Chondrocyte-like cells produce ECM (collagen types I and II, proteoglycans)

Front 65

Microfracture Arthroplasty:

Back 65

*Penetrate subchondral bone to recruit pluripotential marrow cells
*Heals with a hyaline / fibrocartilage composite
*Repair tissue sensitive to loads
-Chondral defect often not fully repaired
-Poor bonding to surrounding cartilage
-Early deterioration, fibrillation, loss of cells

*Material properties of cartilage repair tissue inferior to normal articular cartilage
*Despite limitations, repair tissue frequently persists and is functional

Front 66

Natural history- Osteoarthritis:

Back 66

*Early silent phase- no symptoms, normal radiographic studies
*Typically progressive over prolonged time
*Can lead to significant disability with joint failure causing pain, stiffness, and diminished mobility
*Varies considerably by joint and individual

Front 67

Articular and meniscus cartilage summary:

Back 67

*Meniscus and articular cartilage are biphasic and have viscoelastic behavior which allows efficient dissipation of joint stress
*The primary role of the meniscus is to protect the articular cartilage
*Articular cartilage =Type II collagen
*Cellular and matrix disturbance from injury makes cartilage less stiff, more permeable, more susceptible to further injury and wear
*There is limited potential for articular cartilage repair
*Progressive loss of articular cartilage resulting in osteoarthritis can lead to significant disability with joint failure causing pain, stiffness, and diminished mobility

Front 68

Knee Injury Prevention:

Back 68

*Exercise-Flexibility, Strength, Fitness
*Weight loss
*Neuromuscular training
*Bracing
*Rule changes/ enforcement (sports rules)