Atlanto-Occipital Joints



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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

Collagen producing cells

Fibroblasts

Myofibroblasts

Fibroblasts in CT proper

Chondroblasts/Chondrocytes in cartilage

Osteoblasts in bone

Skeletal muscle cells in skeletal muscle

Smooth muscle cells in blood vessels and some organs


Produce elastic and collagen fibers

Produce glycosaminoglycans which form proteoglycans



Have properties of fibroblasts and smooth muscle

Produce collagen but contain myofilaments

Abundant at sites of inflammation

Involved in wound closing





Ground Substance

Contains water, GAGs and Proteoglycans

GAGs are polymers of disaccharide units
GAGs

*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

Hyaluronic Acid

CT proper, cartilage and synovial fluid

Chondroitin 6 sulfate

Chondroitin 4 sulfate



hyaline and elastic cartilage, bone large blood vessels, and the nucleus pulposus

Dermatan Sulfate

tendon, ligament, Fibrocartilage, nerve, arteries and the dermis

Keratin sulfate

cornea, cartilage, nucleus pulposus and annulus fibrosus

Heparin Sulfate

basal lamina, aorta, lung, liver, smooth muscle, and endoneurium



Types of Connective Tissue Proper

Loose (areolar)

Fibers

Few loosely arranged collagen fibers

Few reticular and elastic fibers



Cells

Fibroblasts, myofibroblasts, macrophages, plasma cells, mast cells, eosinophils, basophils, lymphocytes, fat cells

Locations

Superficial fascia, epimysium, myofascia, papillary layer of dermis, tunica adventia of blood vessels

Functions

Movement of neurovascular bundles during limb and trunk movement

Movement of adjacent muscles to contract individually

Enlargement of blood vessels


Dense Irregular

Fibers

Densely packed collagen bundles arranged in many different directions

Some elastic fibers



Cells

Few fibroblasts

Macrophages



Locations

Dermis of skin, periosteum, perichondrium, joint capsules, capsules around organs, aponeurosis

Functions

Resists multidirectional tensile and shear forces

Stabilizes joints

Protection


Dense Regular

Fibers

Densely packed collagen bundles in parallel rows running in same direction

Cells

Few fibroblasts

Locations

Tendons, ligaments, fascia, aponeuroses

Functions

Transmit unidirectional tensile forces

Stabilizes joints



Elastic Connective Tissue

Fibers

Mostly elastic fibers interwoven among collagen fibers

Cells

Fibroblasts

Locations

Ligamentum flavum, ligamentum nuchael, wall of large arteries, vocal ligaments of larynx

Functions

Dampen high pressure in arteries

Return structures to resting position


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

Tendon/Ligament Stress-Strain Curve

-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

-load relaxation is a decrease in stress over time when the magnitude of the deformation is constant

-both creep and load relaxation are the result of reorganization of the collagen and proteoglycans in the material
Tendon and Ligament Injury

-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.




Days 2-4

Clot forms

Infiltration of macrophages and fibroblasts

Weak and unstable type III collagen produced

Connection is cellular and fragile

Stretching tears connection


Days 5-21

Still cellular

Increased collagen production

High collagen synthesis and degradation

Collagen remodeling

Increase ROM and joint function during rehab

Tension helps direct collagen fiber direction, increase strength of connection and increase rate of healing and completeness of healing



Days 21-60

Well organized collagen

Fibrous rather than cellular

Increased strength of connection

Increased number of stable bonds or cross links

Decreasing tissue response to treatment with time


Days 60-360

Large type I collagen mostly

Connection is mainly collagen

Stable connection

Poor response to treatment


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.




Hyaline cartilage

Fibers: fine network of type II collagen fibers

Cells: chrondrocytes

Locations: costal cartilage, articular cartilage of joints, epiphyseal growth plate, trachea, skeleton of larynx, nasal septum

Elastic cartilage

Fibers: abundance of densely packed elastic fibers interwoven among type II collagen fibers

Cells: chondrocytes

Locations: auricle of ear, epiglottis, Eustachian tube, wall of external auditory canal

Fibrocartilage

Fibers: dense network of type I collagen fibers

Cells: chondrocytes

Locations: menisci (knee, SC, TMJ, etc), IVD, disk at pubic symphysis, tendo-osseous junction




Superficial Tangential zone:

Surface 10-20% of articular cartilage

Collagen fibers parallel to articular surface and tightly interwoven

Tough and durable

Smooth and slippery

Contains proteogylcans within articular cartilage

Middle Zone:

Middle 40-60% of articular cartilage

Collagen fibers arranged randomly and loosely

High concentration of proteoglycans between loosely arranged fibers

Deep Zone:

Bottom 30% of articular cartilage

Larger than in superficial and middle zones

Fibers vertical, perpendicular to surface of bone

Penetrate into subchondral bone

Nutrition:

Articular cartilage is avascular

Nutrition and removal of waste comes from joint loading and unloading

Leave with compression, return with unloading

When superficial zone is damaged, water and proteoglycans are loast and nutrition to the cartilage is decreased





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



Boundary lubrication

Lubricant/Glycoprotein is in surface layer of articular cartilage

With extreme loading conditions, lubricant is extruded to lubricant articular surface

Last method for protection of articular surface when other methods fail


Hydrodynamic lubrication

Used in joints where opposing joint surfaces are not parallel to each other

Synovial fluid drawn between surfaces as opposing articular surfaces move on each other



Squeeze film lubrication

Used in joints where opposing surfaces are parallel to each other

Synovial fluids tend to pool in concave surface of joint and are squeezed out between the joint surfaces when the joint is compressed


ARTICULAR CARTILAGE WEAR



Interfacial wear

Adhesive wear

Chronic inflammation and disease may result in adherence of the opposing joint surfaces

Movement pulls and tears at these adhesive areas causing surface wear


Abrasive wear

Particles of cartilage or bone lying between opposing joint surfaces

Movement compresses particles between joint surfaces and causes abrasion

Crepitus is result of this type of wear



Fatigue wear

Repeated stresses of articular cartilage producing tissue failure with time

Generally occurs with age

Can result from low loads of high reps for a long time as with aging

Also results from high loads of high reps of a short time as with sports or occupations



Impact wear

Rapid , very high impact loading of joint

Few reps involved


Articular Cartilage Degeneration



  1. Fibrillation

    1. Early articular cartilage degeneration

    2. Result of fraying of collagen fibers in superficial layer

  2. Cavitation

    1. Cavities form in cartilage between collagen bundles

  3. Vertical splitting

    1. Cavities deepen, clefts in cartilage

    2. Clefts extend as vertical splits from superficial to deep and even to subchondral bone

  4. Continued erosion

    1. Final stage

    2. Cartilage erosion continues in split areas

Articular Cartilage Repair



Natural repair

Limited due to avascularity

Superficial damage may be repaired but transient (2-3 weeks)

Complete thickness tears extend to subchondral bone- blood from subchondral bone fills split and forms fibrous clot- fibrous scar matures and forms Fibrocartilage-like plug- may last for years


Surgical drilling

Imitates natural repair

Modification would be to draw blood from patient and centrifuge it into firbrous paste and spread it over the cavities and splits in articular cartilage rather than drill holes



Cartilage transplant

Small amount of healthy cartilage and subchondral bone removed from donor site and ground into paste

Natural growth factors are mixed with paste and it’s spread over damaged area

Patient is NWB for 4wks and uses CPM 6hr/day to allow new cartilage to grow and mature

Forms hyaline-like articular cartilage

Good results


Joint lubricants

Hyalgen, orthovisc, synvisc injected into joints for lubrication and to stimulate production of synovial fluid

May also stimulate cartilage growth

Mainly for osteoarthritis

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

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