Atlanto-Occipital Joints
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- Elastic
- Tendon/Ligaments response to rate of stress
- Creep and Load Relaxation
- Tendon and Ligament Injury
- TENDON STRESS STRAIN RELATIONSHIP
- Stress/Strain Properties and Aging
Reticular Fibers- thin, delicate fibers that form lace-like networks around smooth muscle cells, sarcolemma of striate muscle, and endoneurium of peripheral nerves Elastic Fibers-occur at varying quantities in CT and contain the protein Elastin; elastic fibers are abundant in some ligaments, large arteries, the trachea, and the dermis of the skin Connective Tissue Cells
Ground Substance Contains water, GAGs and Proteoglycans GAGs are polymers of disaccharide units
*attach at one end to a protein core and radiate out from core *arrangement forms a proteoglycan monomer *proteoglycan monomers attach to hyaluronic acid to form a proteoglycan aggregate *GAGs produce negative charge over periphery of proteoglycan monomers which repels adjacent negatively charged monomers as they approach which results in increased tissue stiffness *GAGs of proteoglycans are also hydrophilic so they attract and hold water which delivers nutrients to cartilage and produces compressive stiffness of cartilage Major GAGs in CT
Biomechanics of Fibers Collagen -shows very little elongation in tension but bends in compression -greater resistance to shear stress than elastic fibers -structures such as tendons that transmit muscular forces and ligaments that provide joint stability are composed mainly of collagen fibers making them strong and stiff in tension Elastic -less stiff than collagen fibers -easily elongate 1.6-2.0 times when tension is applied
-Toe region: collagen fibers on slack so that small stresses produce great deformation as fibers tighten -Linear/Elastic region: collagen fibers tightening and as they tighten greater stress is needed to produce deformation/strain -Progressive failure: some collagen fibers break and then material is damaged and permanently deformed; small increase in stress results in proportionately large deformation -major failure: most of the collagen fibers are broken and the material is weak and permanently deformed; maintained or decreased stress continues to produce a proportionately large deformation -rupture: all collagen fibers are broken Tendon/Ligaments response to rate of stress As rate of applied tension on a tendon/ligament increases, increased stiffness and decreased elongation result Suggests that elongation of ligaments/tendons is best obtained by applying low force for long durations As magnitude of stress increases with time, tendon/ligament may respond by adding collagen and increasing the number of cross-links which = increased strength Tension on tendons/ligaments at sub-failure levels stimulates fibroblasts to produce new collagen fibers Surgically repaired tendons/ligaments show accelerated healing with tension, increased strength of CT scar at repair site and direction of orientation of collagen fibers along the direction of stress Additional new collagen fibers results in increased thickness and stiffness of that structure Body strengthens tendons/ligaments to match the demands of increased muscle force and increased joint straction that occur with resistive exercise, increased workloads, and with growth Stiffness of collagen in tension changes with temperature- cold makes collagen brittle; heat makes collagen extensible; cold with low tensile loads breaks prematurely/heat with low tension elongate farther than normal before breaking Creep and Load Relaxation -tendons and ligaments are viscoelastic materials and thus show phenomena for creep and load relaxation -creep is an increase in deformation that occurs over time when the load is constant
-high levels of tension applied to tendons and ligaments will not produce failure of all collagen fibers at the same time…there will be microfailure (some collagen fibers fail) -microgailutrs cause some pain and weakness in the tendon/ligament but do not cause instability -where enough collagen is damaged and the tendon passes it’s yield point and there is permanent deformation and noticeable inflammation and joint instability -when all fibers fail= rupture -laxity of ligaments causes hypermobility which creates a joint instability. This can causes subluxation or dislocation. Hypermobility exposes the joint surfaces to abnormal forces which produce abnormal wear and degeneration leading to pain and inflammation at both the joint and the soft tissues associated with movement at that joint.
Tension is important during fibroplasias and consolidation *activates fibroblast production of collagen *controls direction of collagen fiber alignment *produces large collagen bundles *increases scar strength by increasing alignment, amount, size and stability of collagen *increases healing rate and completeness of healing *DAYS 2-21= collagen increases in amount and strength of scar increases *DAYS 21-60= collagen amount levels off and is fairly constant but strength of the scar increases…fiber alignment, large bundles of collagent forming and increase in cross link formation contribute to strength *ligament and tendon replacements may need several weeks before they can be loaded in tension…replacement degenerates initially and then starts to heal. New collagen is produced at this point and tension becomes important to align collagen fibers and strengthen and heal the replacement as in regular tendon/ligament healing. IMMOBILIZATION ~ loss of tissue stiffness and strength ~ 7 weeks of immobilization does not affect ligament or capsule if there is no inflammation ~ if there is inflammation, adhesions and joint involvement occur within 4 weeks of immobilization ~ prevent and quickly elimate joint inflammation when a joint is immobilized AGING Stiffness of tendons/ligaments changes with age Young collagen will elongate more with less force than mature collagen because young collagen is less stiff in tension As collagen matures, strength and stiffness increase because of increased collagen production and cross-link formation Advancing age will decrease tensile strength and elasticity of ligaments/tendons Amount of collagen decrease Number of large bundles of collagen decreases Elastic fibers are damaged Slight until 70 years old (decreases 5% up to 50, another 5% from 50-70, 10% after 70) With aging, these changes are greater for ligaments than for tendons CARTILAGE Typically avascular Chondrocytes lie in lacuna Ground substance contains H2O, proteoglycans and collagen H20 and proteoglycans give cartilage its hardness and its resistance to compression Collagen provides cartilage’s ability to resist tension Compaction of ground substance squeezes water from articular cartilage as it deforms. A s cartilage loses water, proteogylcans are compacted. Repelling negative ionic forces occur among the proteogylcans and the rigidity of the ground substance increases. When articular cartilage is unloaded, proteoglycans draw water back into cartilage and return to it’s pre-loading stiffness. Proteogylcans interact with H2O to produce stiffness so maintenance of proteoglycans is crucial for normal articular cartilage function. Loss of proteogylcans greatly reduces the loading capability of the cartilage.
TENDON STRESS STRAIN RELATIONSHIP TOE REGION- COLLAGEN FIBERS ARE SLACK BUT BEING LOADED IN TESNION AND ALIGNING IN A DIRECTION TO RESIST TENSION LINEAR REGION- COLLAGEN FIBERS ARE STRETCHING AND BECOMING MORE AND MORE TENSE AS STRESS INCREASES FAILURE- COLLAGEN FIBERS BREAK AND CARTILAGE TEARS TYPE II COLLAGEN IN ARTICULAR CARTILAGE IS LESS DENSE AND FIBERS ARE SMALLER THAN TYPE I COLLAGEN OF LIGAMENTS/TENDONS WATER AND PROTEOGLYCANS GREATER IN ARTICULAR CARTILAGE THAN IN LIGAMENTS/TENDONS ARTICULAR CARTILAGE TENDS TO FAIL WITHOUT A YIELD POINT AND PLASTIC REGION Creep and Stress Relaxation Articular cartilage is a viscoelastic material and thus undergoes creep and stress relaxation Creep occurs after initial compression and extrusion of water Further deformation of articular cartilage in time when constant stress is being applied= creep Results from collagen and proteoglycans reorganizing to teach an equilibrium state Load relaxation occurs after initial compression and extrusion of water and when stresses are high toward the surface of the articular cartilage and low at the bottom With deformation of the articular cartilage remaining constant with time, redistribution of water, proteoglycans and reorganization of collagen occurs Even redistribution of stresses from surface to bottom of articular cartilage occurs producing a stress equilibrium state SYNOVIAL JOINT LUBRICATION
ARTICULAR CARTILAGE WEAR
Articular Cartilage Degeneration Fibrillation Early articular cartilage degeneration Result of fraying of collagen fibers in superficial layer Cavitation Cavities form in cartilage between collagen bundles Vertical splitting Cavities deepen, clefts in cartilage Clefts extend as vertical splits from superficial to deep and even to subchondral bone Continued erosion Final stage Cartilage erosion continues in split areas Articular Cartilage Repair
Fibrocartilage (IVD) contains gel like nucleus pulposus surrounded by 8-10 rings of Fibrocartilage innermost rings have loose arrangement of collagen to allow deformation of NP middle rings are dense collagen with fibers running in one direction fiber directions of sequential rings are perpendicular outermost rings are dense and show herrningbone pattern which indicates material is strong in tension and shear tensile strength NP- 3kg/m2 Inner rings- 45kg/m2 Middle rings- 53 kg/m2 Outer rings- 80kg/m2 Menisci Fibrocartilage Superficial collagen fibers are crossed in herringbone pattern to resist tension and shear Deep fibers run circumferentially to strength menisci in anteriorposteriorly direction tension With compression, proteogylcans can resist compression but shear and anterioposterior and med/later tension is resisted by collagen Function Increase surface area for force distribution which decreases unit forms on femoral head and tibial condyles Increase surface area for lubrication of condyles Joint proprioception because anterior and posterior horns are innervated Blood supply Only in peripheral 10-30% in teens and adults Central 70-90% is avascular Poor healing capacity Stress/Strain Properties and Aging Download 180.28 Kb. Share with your friends:
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