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68 Cards in this Set
- Front
- Back
talk about Ligaments:
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*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 |
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talk about Multiple or paired ligaments:
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*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 |
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Ligament Gross Anatomy: Classification and naming:
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-Bony Attachment coracoacromial
-Relation to joint collateral -Relation to other ligament cruciate -Gross shape deltoid -Less distinct capsular |
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gross/ microscopic appearance of ligaments:
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*Gross- uniform band-like connective tissue, little apparent complexity
*Microscopic- intricate amalgam of collagen, extra-cellular matrix proteins and a diverse population of cells |
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ligament
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Ligament composition:
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*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 |
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Type I Collagen:
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*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 |
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Ligament Histology:
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*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 |
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Ligament fibers:
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*Longitudinal fascicles (20-400 µm)
*Fascicle collagen has an organized sinusoid waveform (crimp) *Crimp responsible for initial non-linear stiffness in response to stress |
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Ligament Histology of fascicles:
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*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) |
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Ligament cells:
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*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 |
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Biomechanics of ligament structures:
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*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 |
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Stress-Strain Curve for ligaments:
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*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 |
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Toe Region:
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*Ligament stretches; straightening of crimped fibrils
*More pronounced in ligament v. tendon *Decreases with age because the amount of crimp decreases |
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Relationship b/t crimp and stress-strain curve:
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Linear Region:
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*“Working” region for physiologic stress
*Slope=stiffness of the structure *Stiffer tissue has greater slope |
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Yield and Failure region:
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*Irreversible changes (failure) or permanent stretching of the tissue; non-recoverable deformation
*This is what occurs with injury |
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Viscoelasticity:
creep- stress (load) relaxation- hysteresis- |
*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. |
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Viscoelasticity:
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*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 |
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Ligament Preconditioning:
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*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 |
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Mechanical Regulation of Connective Tissue Homeostasis:
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*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 |
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Relationship b/t mechanical load and gene expression:
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Tissue Overload:
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*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! |
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Ligament Homeostasis:
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*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 |
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Ligament Tensile Overload:
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*Cellular damage increases with strain and precedes structural failure (red regions= cell death; green=normal)
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Knee Ligaments:
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Ligament Injury:
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*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 |
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Ligament Injury grades:
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*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 |
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*Ligament Injury
*Single tensile load, micro-structural collagen failure, 250x |
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Extra-Articular Ligament Healing:
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*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 |
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Ligament Healing
Phase 2-matrix and cellular proliferation |
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Ligament Healing
Phase 3 and 4-remodeling and maturation |
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Medial Collateral Ligament Tears:
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Extraarticular ligament
Excellent blood supply for healing Majority treated non-operatively |
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Intra-Articular Ligament Healing:
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*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 |
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*Lubricin distribution in the torn human anterior cruciate ligament and meniscus
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ACL Tears:
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*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 |
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Ligament Summary:
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*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 |
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Articular Cartilage:
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*Hyaline cartilage
-Avascular -Aneural -Alymphatic -Varied thickness |
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Articular Cartilage
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where do we have articular cartilage?
traits/functions? |
-Synovial joints
-Low friction articulation -Load bearing -Shock absorption -Extremely resilient |
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Articular Cartilage Collagen:
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*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 |
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Proteoglycan Aggregate:
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*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 |
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Articular Cartilage Metabolism:
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-Despite a lack of blood supply, there is considerable chondrocyte metabolic activity
-Cells respond to mechanical, electrical, and chemical stimuli |
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Effects of Joint Motion on articular cartilage:
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*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 |
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Articular Cartilage Biomechanics and Response to Loading:
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*Biphasic: water capable of flowing through the solid matrix
*Flow dependent/ independent viscoelastic behavior |
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Meniscus Cartilage Anatomy:
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*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 |
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Meniscus vasculature:
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*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 |
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Meniscus Cartilage Ultrastructure and Biochemistry:
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*Fibrocartilage
*Cells -Fibrochondrocyte -Fibroblast -Surface cells *Matrix -Water -Collagens -Proteoglycans -Glycoprotiens |
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medial vs lateral meniscus:
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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 |
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Meniscus Collagen Framework:
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-hoop fibers
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fibroblasts, Fibrochondrocytes, and surface cells in meniscus:
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*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 |
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Meniscus Cartilage Function:
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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 |
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how does meniscus provide joint stability?
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*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 |
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Meniscus tears:
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*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 |
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Meniscus healing:
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*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.. |
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Describe the Limited potential for articular cartilage repair:
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*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 |
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Articular Cartilage Injury- how does it happen?
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*Normal cartilage
-Overload Traumatic impact Repetitive activities Increased load/ stress *Degenerative Cartilage Normal loads |
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Types of Articular Cartilage Injury:
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-Micro-damage to cells, matrix
-Macro-disruption of cartilage alone (chondral fracture) -Macro-disruption of cartilage and subchondral bone (osteochondral fracture) |
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Articular Cartilage Injury- Micro-damage to cells, matrix:
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*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 |
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Articular Cartilage Injury- Macro-disruption of cartilage alone, no bone penetration:
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*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 |
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Articular Cartilage Injury- Macro-disruption of cartilage alone, with bone penetration:
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*Articular cartilage shearing off subchondral bone
*No blood supply, marrow cells= no healing *Propagates,"", breaks off (loose body), and leads to progressive wear |
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Articular Cartilage Injury- Macro-disruption of cartilage and subchondral bone (osteochondral fracture):
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*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) |
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Microfracture Arthroplasty:
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*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 |
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Natural history- Osteoarthritis:
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*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 |
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Articular and meniscus cartilage summary:
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*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 |
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Knee Injury Prevention:
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*Exercise-Flexibility, Strength, Fitness
*Weight loss *Neuromuscular training *Bracing *Rule changes/ enforcement (sports rules) |