adapted from kapandji extension ivf decreases in size al lig. stretched pl lig. and lig flavum...

Adapted from Kapandji Extension IVF decreases in size AL Lig. stretched PL Lig. and Lig Flavum relaxed Supra and Interspinous Ligs. relaxed Spinous Processes brought together Nucleus Propulsus pulled/pushed forward Anterior Annulus tensed Posterior Annulus compressed Articular Facets compressed, capsules relax Flexion IVF increases in size AL Lig. relaxed PL Lig. and Lig Flavum stretched Supra and Interspinous Ligs. stretched Spinous Processes separate Nucleus Propulsus pulled/pushed backward Anterior Annulus compressed Posterior Annulus tensed Articular Facets unloaded, capsules stretch The Vertebral Motion Segment EXTENSION

MOVEMENTS OF THE SPINE Functional motions Normal and typical motions Usually occurs diagonal or oblique to cardinal planes Non-functional motions Motion in one of the cardinal planes Usually used for evaluation Notepack: page 21

Vertebral Sagittal Plane Rotational FLEX & EXT Notepack: page 22 Source Gary Gorniak, PT, PhD

Vertebral Frontal Plane Rotational SIDE BENDING Notepack: page 22 Source Gary Gorniak, PT, PhD

Vertebral Transverse Plane Rotational TWIST Notepack: page 23 Source Gary Gorniak, PT, PhD

Vertebral Combined Motion Kinematics Notepack: page 23 Source Gary Gorniak, PT, PhD Note: TOTAL ROM is not the sum of segmental ROMs

The Intervertebral Discs LOADS: 80% DISC *** 20% POSTERIOR STRUCTURES (JOINTS, LAMINA) *** WWTIVDD? 1.Bind vertebral bodies 2.Permit movement between vertebra 3.Transfers loads from one vertebra to another

Annulus Fibrosus 6 10+ circular rings of fibrocartilage Collagen fibers in layers surrounding nucleus pulposus are arranged loosely Collagen fibers in the outer layers are densely packed and run obliquely between the vertebral bodies Collagen fibers in the outer-most 1-2 layers have a crossing herringbone pattern which makes these layers strong in resisting tension WHAT FORCES COULD BE RESISTED BY THE ANNULUS ALONE? Posterior 65 to 70 0

Nucleus Pulpulsus Pulp-like gel located in the mid to posterior part of the disc. 70-90% water thickened with large branched proteoglycans, type II collagen, elastic fibers, and non- collagen proteins. (collagen mesh in a mucoprotein gel) Functions: Force transmitter Equalizes unit stress in all directions to the annulus fibrosus Absorbs and retains water Nutrition conduit

Nucleus Propulsus lies central to slightly posterior Nucleus Propulsus lies more posterior Disc Structure in the Different Vertebral Regions Nucleus Propulsus central to slightly posterior 2/3 1/3 1/2

REGION FLEXIONEXTENSION SIDE BEND RIGHT ROTATION RIGHT ATLANTO OCCIPITAL ROC and LOC roll anteriorly and glide posteriorly ROC and LOC roll posteriorly and glide anteriorly ROC and LOC roll right and glide left ROC moves slightly back and LOC moves slightly forward ATLANTO AXIAL RF and LF of Atlas moves forward on Axis facets RF and LF of Atlas moves backward on Axis Atlas slides right RF of Atlas moves back and LF moves forward C2/3 T2/3 RF and LF slide up and forward RF and LF slide down and back RF slides down and back and LF slides up and forward RF slides down and back and LF slides up and forward THORACIC T3/4 T11/12 RF and LF slide up RF and LF slide down RF slides down and LF slides up RF distracts and LF compresses and acts as fulcrum LUMBAR RF and LF slide upRF and LF slide down RF slides down and LF slides up RF distracts and LF compresses and acts as fulcrum Cervical Kinematics Notepack: page 26

OA Joint Complex Lateral Flexion I.A.R. White & Punjabi (1990) 3-7 0 RIGHT Rectus Capitis Lateralis LEFT Occiput on Atlas R Lateral Flexion Without Restraining Ligaments 5 0 Lateral OA Flexion: White and Panjabi 1990 Lateral Flexion Restrained by Alar Ligament

Posterior Longitudinal Ligament & Tectorial Membrane Cruciform Ligament

Loads on the Cervical Spine OA Joint: highest in full flexion lowest in full extension Facing Forward, Slightly Retracted Correct Posture Extended Flexed INCREASING LOADS LEAST GREATEST FOR JOINTS C7-T2

DENS Flexion IVF increases in size Anterior Longitudinal Lig. relaxed Posterior Longitudinal Lig. and Lig Flavum stretched Ligamentum nuchae stretched Spinous Processes separate Nucleus Propulsus pulled/pushed backward Anterior Annulus compressed Posterior Annulus tensed Articular Facets unloaded, capsules stretched C2 SLIDE EXTENSION SLIDE C3 SLIDE C7 SLIDE Extension IVF decreases in size Anterior Longitudinal Lig. stretched Posterior Longitudinal Lig. and Lig Flavum relaxed Ligamentum nuchae relaxed Spinous Processes brought together Nucleus Propulsus pulled/pushed forward Anterior Annulus tensed Posterior Annulus compressed Articular Facets compressed, capsules relax

Osteokinematics of the Thoracic Spine

Extension IVF decreases in size AL Lig. stretched PL Lig. and Lig Flavum relaxed Supra and Interspinous Ligs. relaxed Spinous Processes Impact Nucleus Propulsus pulled/pushed forward Anterior Annulus tensed Posterior Annulus compressed Articular Facets Impact, capsules relax Flexion IVF increases in size AL Lig. relaxed PL Lig. and Lig Flavum tensed Interspinous Ligament stretched Spinous Processes separate Nucleus Propulsus pulled/pushed backward Anterior Annulus compressed Posterior Annulus tensed Articular Facets unloaded, capsules stretched FLEXION EXTENSION T6 T7 T6

The Mechanics of Lumbar Rotation Segmental Rotation Minimal segmental rotation !!! Contralateral facet impacts Ipsilateral facet gaps + capsular stretch. Nucleus Pulposus is compressed Shear stress on annulus Left Axis

Lumbar Lateral Flexion*** Segmental Lateral Flexion Ipsilateral Vertebral Tilting Ipsilateral Annulus Compression Contralateral Annulus Tension Nucleus pulled/pushed contralaterally Ipsilateral IVF narrowing, contralateral enlargement Contralateral superior facet: upward slide and decreased compression Ipsilateral superior facet: downward slide and increased compression Contralateral Transverse Lig tension, slack on ipsilateral COUPLING: ROTATION AND IPSILATERAL SIDE BENDING ** IAR

TRUNK SIDE BENDING 1.Ipsilateral quadratus lumborum, erector spinae and abdominal muscles initiate trunk side bending. 2.Gravity then pulls the trunk further laterally (increasing the ipsilateral side bending). 3.Erector spinae, Quadratus Lumborum, Gluteus Medius on contralateral side contract eccentrically to control the rate and the amount of gravity produced ipsilateral side bending. 4.Return to an erect posture is produced by concentric activity of the Erector Spinae and Quadratus Lumborum on contralateral side. Ipsilateral side

Arthrokinematics (Opening) STAGE 1 (EARLY PHASE) Notepack page 42 STAGE 2 (LATE PHASE) SLIDE TRANSLATION Condyle and Disc Move Together Condyle Rotates Relative to Inferior Disc Surface

Arthrokinematics (Opening) EARLY PHASE During the initial 0 to 20 mm of opening (range: 11-25 mm) Condyles Rotate, (spin), anteriorly on the disks. Disks stay in place Notepack page 42

Arthrokinematics (Opening) LATE PHASE: STAGE 2 During terminal opening: (during the time when the jaw continues to open past the initial 20 mm) Condyles and Discs together Translate Anteriorly over the articular eminences with concurrent anterior rotation Superior Lamina stretches, (which helps to control forward disc displacement) Inferior Lamina tenses Jaw opening up to 40-50mm

Arthrokinematics (Closing) Initial Phase of Jaw Closing ( starts from the period of full opening, (~40-50mm), until approximately 11-25mm of opening). 1. Condyles and Discs together Translate Posteriorly over the articular eminences with concurrent posterior rotation Superior Lamina recoils, (which helps to pull the disc back posteriorly into the glenoid fossa). Inferior Lamina relaxes Eccentric control of Lateral Pterygoid controls posterior disk translation.

Arthrokinematics (Closing) Terminal Phase of Jaw Closing ( starts from the period of approximately 11-25mm of opening (mandibular depression) until full closure-0 mm). 1. Condyles rotate, (spin) posteriorly on the disks. 2. Superior and inferior lamina are relaxed 3. Disk remains within the glenoid fossa.

Muscles Acting on the Mandible IL = ipsilateral CL = contralateral

Trabecular or Cancellous bone Biomechanically an Internal Scaffolding Network Notepack page 83-84 Support with Light Weight Transmit Forces to Shafts

Cortical Bone The outer dense shell (5-10% porosity) Complex network of cylindrical units of laminated bone (osteons) and interstitial bone Osteons 2-3 mm long and about 0.2-0.3 mm in diameter Run parallel to the long axis of a bone

Bending of Bone about an Axis Tensile forces/strains on the convex side Compression forces/strains on the concave side

Bending of Bone about an Axis *** STRESSES ARE HIGHER AT THE SURFACES OF THE BONE (cortical bone) AND LOWEST NEAR THE NEUTRAL AXIS Neutral Axis of a Long Bone

Why? Because bone structure is dissimilar longitudinally vs. transversely. BONE IS STRONGEST AGAINST COMPRESSIVE FORCES/LOADS AND WEAKEST AGAINST SHEAR FORCES/LOADS OVERALL: From Nordin & Frankel. 2001

Keys to Biomechanical Behavior of Bone Behavior is affected by: 1.Intrinsic mechanical properties (compact vs spongy) Flexibility & resilience from its collagen (tensile strength) Rigidity & strength from its minerals & water 2.Loading mode (GRFs, muscle contraction) 3.Geometry (size, shape, and x-sectional area) 4.Direction of loading (anisotrophic characteristics) 5.Rate of loading 6.Frequency of loading Note: There is a biomechanical distinction between the mechanical behavior of bone tissue as a material and the mechanical behavior of a whole bone as a structure

General General Mechanics of Long Bones 1.Long Bones with smaller diameters, (x-sectional areas), resist tensile stresses better than thicker diameter bones. 1.X-sectional: longitudinal ratios (wall to lumen ratios) 2.Differences in collagen alignment 2.Bones with larger diameters, (x-sectional areas), resist compressive forces much better than bones with thin diameters. 3.Thin bones deform during bending, tension, and torsion with greater magnitudes over thick bones. 4.Both spongy and compact bone are weaker with tensile forces compared to compressive forces.

General Mechanics of Long Bones 5. Total bending is a function of the length of a bone, (longer bones have a greater magnitudes of bend vs. smaller). 6.Total strength of long bones during bending is a function of x- sectional area, (thicker bones are stronger > thinner bones). (Consider both compression and tension forces with bending ) 7.Overall 7.Overall: compact bone is stronger in compression, tension, and shear than spongy bone.

Mechanical Properties of Bone Compression/Tension Compact Bone: 1.Stiffer, (HIGHER Youngs Modulus), vs. cancellous 2.Stronger vs. cancellous 3.Resists compression > tension (> shear) Notepack page 93 Spongy Bone Bone tissue as a material.

Mechanical Properties of Bone Compression/Tension Cancellous Bone: Less stiff, (LOWER Youngs Modulus), vs. cortical Weaker vs. cortical Resists compression > tension Notepack page 93 Bone tissue as a material.

Long Bones Mechanical Response to Tensile Forces (forces directed away from a bones surface) Tensile Strength, (amount of stress at failure) Greater in thin long bones > thick long bones Tensile Strain (amount of strain at failure) Greater in thin long bones > thick long bones Notepack page 94

Long Bones Mechanical Response to Compressive Forces (equal and opposite forces directed towards a bones surface) Compressive Strength, (amount of stress at failure) Greater in thick long bones > thin long bones > Compressive Strain (amount of strain at failure) Greater in thin long bones > thick long bones Notepack page 95

Long Bones Mechanical Response to Bending Forces (forces directed at bending a bone about an axiscombo of tension and compression) Bending Strength, (amount of stress at failure) Greater in thick long bones > thin long bones > Bending Strain (amount of strain (bend) until failure) Greater in thin long bones > thick long bones Notepack page 96

Long Bones Mechanical Response to Torsion Forces (forces that cause a torque within the bone) Torsion Strength, (amount of stress at failure) Greater in thick long bones > thin long bones > Torsion Strain (amount of strain at failure) Greater in thin long bones > thick long bones Notepack page 97

Fractures / Failures of Long Bones Site of a fracture is dependent on: Type of forces applied. The distribution of spongy and compact bone in the areas where forces are applied. Example: epiphyses and tuberosities are prone to compressive fractures > shafts of long bones Due to increased amounts of spongy bone and decreased amounts of compact bone!

Fatigue of Bone Under Repetitive Loading Factors Leading to Fatigue Fractures, (microfractures) 1. Repetitive low loads (cycles) 2. The number of load applications cycles per unit of time. 3. Muscle fatigue (inability to absorb some of the energy)

Bone Fracture Healing Unorganized calcified osteoid secreted by Osteoblasts Osteoblasts Osteoclasts 6 weeks 18-24 weeks Extremely weak, unable to resist bending or torsion forces Macrophages

BONE IS ADAPTABLE AND MODIFIABLE!!!! Bone formed on Soft Tissue Bone resorbed/formed at the same site Bone formed on existing bone

thoracic >cervical) Compressi">

Vertebral Bones COMPACT BONE SHELL CANCELLOUS BONE CORE COMPRESSIVE FORCES Strength related to vertebral size, (lumbar > thoracic >cervical) Compressive loads shared by Cortical Shell < Trabecular Core

Compressive Loading Strength Breaking Strength: Lumbar > Thoracic > Cervical Adapted from White and Punjabi 1990

Vertebral Compressive/Tensile Strength and Aging 1.With age: tensile properties decrease 10-20% 2.With age: decreasing compressive properties Breaking load decreases 50% Strength decreases 45% Strain decreases 40% 1. Gadek, A et al 2001 Compressive strength is related to the trabecular structure 1

1. Straightening of Relaxed (Wavy) Fascicles 2. Nerve Gliding In relation to interfacing tissues Example: median nerve ulnar nerve Internally, (interfascicular) 3. Nerve elongation (this occurs via the elastic properties of its collagenous connective tissue) 4. Intraneural Blood Flow Changes Decreased Blood Flow > 8% elongation of a nerve Complete Arrest of Blood Flow at 15% elongation of a nerve Peripheral Nerve Responses to Tensile Forces

Blood Flow Responses to Compression within a Peripheral Nerve Reduction in Venous Flow at 20 30 mm Hg Inhibition of Axonal Transport 30 50 mm Hg Inhibition of Blood Flow 30 50 mm Hg Complete Loss of intraneural blood flow 50 70 mm Hg

Compressing a PN Circumferentially Adapted from Nordin & Franken 2001

The Edge Effect of Circumferential Compressive Forces EDGE OF COMPRESSION

ARROWS DEPICT DIRECTION AND MAGNITUDE OF NERVE FIBER DISPLACEMENT CIRCUMFERENTIAL PRESSURE ON A NERVE INITIALLY CAUSES DISPLACEMENT/DAMAGE OF NERVE FIBERS TOWARDS THE PERIPHERY (EDGES) OF THE COMPRESSION = damage

Compressing a PN Laterally Caused by: A force that squeezes a nerve against underlying: 1. Bone 2. Dense CTs, fibro- osseous tunnels. 3. An abnormal dense mass (tumor). Cross-sectional deformation of the nerve from circular to elliptical Mechanical damage to axon membranes directly under the lateral contact areas. Increased hydrostatic pressure.

Key Points Regarding Compression of a P.N. Generally larger fibers are usually affected first > thinner fibers Larger fibers undergo a relatively greater amount of deformation > thinner fibers at a given pressure Clinically we often see the signs of larger fiber damage first (large fibers carry motor function and proprioception while thin fibers are ones that tend to mediate pain, temperature)

Sustained Sustained Neural Compression Increased Hydrostatic Pressure Neural Ischemia (Arterial and Venous) Neural Edema Neural Fibrosis Loss of Intraneural mobility Loss of Extraneural mobility Direct Mechanical Damage Peri & Epineuriums

PROGNOSIS for Compressive Forces (Magnitude and Duration) Good Prognosis: low magnitude of force for short durations. Fair Prognosis: high magnitude of force but only for a short duration. Fair Prognosis: low magnitude of force for a long duration Poor Prognosis: high magnitude of force for a long duration

DISLOCATION OF THE NODES OF RANVIER STRUCTURAL ALTERATIONS IN THE MYELIN SHEATH STRUCTURAL ALTERATIONS IN THE AXONS ORGANELLES FOCAL SEGMENTAL DEMYELINATION FIBROTIC CHANGES IN THE NEUROMUSCULAR JUNCTION Leads to CHRONIC Blunt INJURY

Nerve Regeneration Nerve Regeneration** Axon degenerates Myelin breaks down Macrophages clean up **Each injured AXON Crush or Cut Injury 1 millimeter a day of re-growth

Stress Strain Curve (example: Hypothetical ACL Ligament) TOE REGION ELASTIC REGION COMPLETE FAILURE PERMANENT DEFORMATION PHYSIOLOGIC RANGE PLASTIC REGION

Straightening of Collagen Fibers Scanning Electron Micrographs of Collagen Fibers Knee Medial Collateral Ligament) Unloaded (non-stretched) collagen fibers Loaded (stretched) collagen fibers WHY WOULD LIGAMENTS & TENDONS BECOME STIFFER AS STRAIN INCREASES?

Youngs Modulus (of Elasticity) (the slope of the LINEAR ELASTIC ZONE Y/X --- a.k.a. stiffness) MaterialModulus of Elasticity (N/mm2) Stainless Steel 200,000 Titanium Alloy 100,000 Polyethylene 1000 Cortical Bone 18,000 Trabecular Bone 90 Female ACL 1 199 Male ACL 1 308 Patellar Tendon 2 ( 6 months post ACL repair) 135 (- 66%) Yamada H 1970 Chandrashekar 2005 Burks RT 1990 POLYETHYLENE TRABECULAR BONE x y

Viscosity Application of a continuous force to a fluid body..the body will continually deform.and we call this flow The resistance to flow/shear is called viscosity (HINT: Think of it as the internal friction of a liquid)

Viscoelastic Materials A material that seems to have both fluid and solid properties A viscoelastic material displays both viscous and elastic characteristics when undergoing deformation (examples: tendons and ligaments) SOLID FLUID V

Viscoelasticity (when stress-strain curves change as a function of time) Definition: time-dependent material behavior where the stress response of the material depends on both: the amount of strain applied RATEthe strain RATE at which it was applied! Most biological tissues are viscoelastic!

Ex: Ligaments and Tendons Functionally Behave Elastically and with Viscous Properties Notepack page 46 Viscous FlowElastic Deformation

Time Dependent Viscous Effects and Time Dependent Behaviors of Tissues (via the reorganization of collagen and PGs) 1.Deformation Creep Response The tendency of a solid material to slowly move or deform permanently under the influence of stresses, (constant load). 2.Deformation Stress Relaxation Response The tendency for a material held at constant length to experience a decreased magnitude of stress (tension) Notepack page 62

Creep a time dependent deformation Length Application of Constant Load Notepack page 62 Record Length Constant Load Applied Load Tendon or Ligament Time 0

Tensile Load Time Specimen Held at a Constant Length Load Relaxation a time dependent deformation Record Tension Notepack page 62 Deformation Constant Deformation Stress Relaxation 0 Tissue Fixed at Constant Length

Types of C.T. Deformation Strain Stress Viscoelastic Deformation Elastic Deformation Stress Strain Plastic Deformation Notepack pages 48-49

Energy Lost as Heat/Molecular Rearrangement (Elastic Hysteresis) No Energy Loss Energy Loss Notepack page 46 different Loading and unloading occur on different stress-strain paths Elastic

Resilience vigorously The property of a tissue to absorb energy when it is elastically deformed and then, upon unloading to have this energy vigorously recovered. Example: a rubber band shows a fairly high degree of resilience. R = W W W Notepack page 48 Clinical Application Clinical Application: Tendons have the ability to release the energy from being stretched. W = work

Tissue Damping The property of a tissue to absorb energy and the rate and amount of energy that is dissipated when the tissue is elastically deformed. The energy is not recovered directly back to the tissue Opposite of Resilience Viscoelastic materials have properties of damping, they are slower to recover their original shape or length vs. purely elastic materials Strain Memory Foam D = 1 Resilience 0 Stress

Strength of a Tissue Strength is the magnitude of the force needed to break a material. Stress (N/m2) Magnitude of Stress at the point of COMPLETE FAILURE Strain 0

Toughness of a Tissue Stress Strain TOUGHER STRONGER Rambo The amount of energy per volume that a material can absorb before rupturing/failing. Toughness measured by considering the total area under the stress strain curve Which is Stronger, Which is Tougher?????? 0 0

Fragility vs. Toughness Failure TOUGH FRAGILE Toughness is not necessarily equal to strength How much energy a material will absorb before it fails or fractures???

Brittle vs. Ductile How much a material will plastically deform before it fails or fractures??? Not necessarily related to strength! 0

The Effects of Aging on Tissue Mechanics (combined properties in general) Yamada 1970

Hydrated proteins Proteoglycans GAGS, (the carbohydrate portion) 1.Hyaluronan (synovial fluid, cartilage) 2.Chondrotin Sulfate (cartilage, tendons, ligaments, nucleus propulsus) 3.Dermatan Sulfate (skin, bvs, tendons, fibrocartilage, ligaments) 4.Keratan Sulfate (bone, cartilage, nucleus propulsus, annulus propulsus) Glycoproteins Interfibrillar Matrix ** of C.T. ** PROVIDES SOME OF THE VISCOELASTIC PROPERTIES IN LIGAMENTS AND TENDONS

ACL TENSILE LOADING Joint Instability + Pain Anterior Drawer Test Some pain Slight weakening But NO CLINICAL JOINT INSTABILITY, No Permanent Deformation Strain (%) Complete Failure

Physiological Responses of Tendon and Ligament to Stress* Increased tensile stress leads to: (via mechanical, chemical, or electrical signals?) 1.Addition of collagen fibrils, (increased metabolic production from fibroblasts)?? 2.Increases in covalent bonding between collagen molecules. Clinical Application: Following injury or post surgical repair, small amounts of tensile forces stimulate fiber orientation and collagen production (potentially increasing its strength)????

Physiological Response to Injury in a Ligament/Tendon Day 2-4: Cellular Stage Clot forms (erythrocytes, inflam. cells) Macrophages and fibroblasts invade the damaged area (remove debris and begin synthesis of a new CT matrix) Fibroblasts produce type III collagen Union is weak and fragile, ruptures with very low tensile stresses (stretching) Notepack page 64 Application: Protection from tensile forces

Physiological Response to Injury in a Ligament/Tendon Day 5-21: Fibroplasic Stage Matrix and Cellular proliferation stage Scar is very cellular, (macros, mast, fibroblasts) Continued increase in collagen synthesis but now also degradation as collagen remodeling just begins towards the end of this phase. Collagen fibrils beginning to enlarge Notepack page 64 Using what you have learned!!! How would you rehabilitate the LCL of the knee with respect to AROM during this phase????????? Application: Ideal time to begin low tensile ROM Low tensile stresses helpful

Physiological Response to Injury in a Ligament/Tendon Day 21-60: Consolidation Stage Remodeling of collagen fibrils organization Gradual in # of fibroblasts and macrophages Union is progressively stronger Collagen fibrils increasing in diameter and more densely packed, fibroblasts slow collagen proliferation Increasing cross links as tissue is now becoming more stable and less responsive to treatment that aims to effect collagen organization Notepack page 64 Application: Progressively increase tensile forces via AROM/PROM Repetitive low tensile stresses remain helpful

Physiological Response to Injury in a Ligament/Tendon Day 60-360: Maturation Stage Primary strength from type I collagen. Tissue appears only slightly disorganized and hypercellular. Tissue is stable and union is stable. Poor ability to modify tissue therapeutically. Application of adequate stresses increases fibril density and covalent collagen cross linking. Application: More aggressive but progressive increase tensile forces via AROM/PROM/Exercises **** IN THE EARLY PART OF THIS PHASE TISSUE IS STILL NOT ABLE TO RESIST EXCESS TENSILE LOADS.

Collagen Production and Tensile Strength Notepack page 65 C o l l a g e n R e o r g a n i z a t i o n INJURY

Physiological Responses of Tendon and Ligament to Stress* Increased tensile stress leads to: (via mechanical, chemical, or electrical signals?) 1.Addition of collagen fibrils, (increased metabolic production from fibroblasts)?? 2.Increases in covalent bonding between collagen molecules. Clinical Application: Following injury or post surgical repair, small amounts of tensile forces stimulate fiber orientation and collagen production (potentially increasing its strength)????

Physiological Response to Injury in a Ligament/Tendon Day 5-21: Fibroplasic Stage Matrix and Cellular proliferation stage Scar is very cellular, (macros, mast, fibroblasts) Continued increase in collagen synthesis but now also degradation as collagen remodeling just begins towards the end of this phase. Collagen fibrils beginning to enlarge Notepack page 64 Using what you have learned!!! How would you rehabilitate the LCL of the knee with respect to AROM during this phase????????? Application: Ideal time to begin low tensile ROM Low tensile stresses helpful

Aggregating hydrophillic PGs interspersed in an interfibrillar collagen matrix attract large volumes of H 2 0 into the cartilage matrix (+ PGs stiffen from negative repulsive actions of GAGS) Influx of H20 increases osmotic pressure and subsequently expands the interfibrillar matrix Expansion is resisted by tensile strains of the collagen matrix Ability of Cartilage to Resist Compressive Deformation

CREEP time Displacement equilibrium FLUID PHASE of ARTICULAR CARTILAGE Notepack: page 73 After a constant load is applied fluid WATER AND NUTRIENTS are extruded out of the cartilage INITIAL LOAD

1.Fluid exudes through pores within the outer cartilage layer 2. Collagen and PGs begin to reorganize, CAN BE QUITE A DRAG!!! With time (4 to 16 hours) equilibrium occurs when compressive stress within the matrix and external load are equal No further fluid flow Continued Initial Viscoelastic Behavior (CREEP of articular cartilage) Notepack page 73

Viscoelastic Behavior (Stress relaxation of articular cartilage) B E C A D STRESS TIME B to E: Fluid, PGs, and Collagen are reorganized Key: This evens out compressive stresses from top to bottom Notepack page 74 A to B: High stresses due to forced rapid efflux of fluid STRESS RELAXATION LOADING CARTILAGE THICKNESS T =

: Lowers viscosity of snovial fluid : Lubricates

Strength: total disc mass: lumbar > thoracic > cervical Strength: per unit of fibrocartilage: cervical = lumbar > thoracic Torsional Intervertebral Discs Torsional Properties Aging: decreases torsional strengths to less than 20% of younger.

Viscoelastic Properties of the IVD IVDs exhibit: (NP > AF) secondary to PGs Creep Relaxation Clinical: 1. Creep occurs slower in healthy vs. degenerated discs. a. Creates increased stress to supporting tissues 2. Discs have only peripheral blood supply and peripheral nerve supply

Regulation of Muscles Extensibility* (The Musculotendinous Unit) (in)Parallel Elastic Components Epimysium, perimysium, endomysium sarcolemma, Titin filaments (in)Series Elastic Components Tendons Contractile Elements SE CE PE *** Quite variable among skeletal muscles due to individual characteristics of PE, SE, and CE Hills Model of Skeletal Muscle bone SE

The Mechanical Ability of a Muscle to Stretch/Elongate is Dependent Upon 1.The amount, the architecture, and make up of its associated CT 2.Its active components (those that create resting tension

Skeletal Fiber Arrangement Muscle fibers can shorten up to 30 50% of their length. Muscles with short fibers and large physiological cross-sectional area, (PCSA), are designed for force production. Muscles with long fibers and small PCSA are designed for producing larger tendon excursions and joint motions with high velocity.

FIBER ALIGNMENT SUMMARY FUSIFORM/PARALLEL FIBERS RUN NEARLY PARALLEL TO THE LONG AXIS OF MUSCLE (+) LONGER MUSCLE FIBERS = GREATER TOTAL MUSCLE SHORTENING, (increased tendon excursion). (+) PARALLEL ALIGNMENT TRANSLATES INTO DIRECT SHORTENING OF MUSCLE APPLIED TO TENDON versus (-) SHAPE LIMITS # OF FIBERS PER UNIT AREA PENNATE FIBERS RUN AT OBLIQUE ANGLES TO THE LONG AXIS OF MUSCLE (-) SHORTER MUSCLE FIBERS = SMALLER TOTAL MUSCLE SHORTENING (+) MORE MUSCLE FIBERS PER UNIT AREA = GREATER FORCE POTENTIAL but: (-) OBLIQUE ALIGNMENT TRANSLATES IN LESS THAN DIRECT SHORTENING OF MUSCLE AND THUS LESS TENDON EXCURSION.

adapted from kapandji extension ivf decreases in size al lig. stretched pl lig. and lig flavum...

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