fracture, lig, capsul blok 8
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Fracture, rupture ligament andcapsul
dr. Rendra Leonas ,Spot, FiCS, (k) spine, M Humkes
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Anatomy of the Bone
A. Anatomical structures• Bones form the skeleton of the
body (frameworked)• Locomotor system and allow the
body to be supported againstgravity and to move and function
in the world.• Bones also protect some body
parts
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B. Physiological organ• Bone marrow is the production
center for blood product• Reservoir of calcium and is always
undergoing change under theinfluence of hormones
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• Bone is not a stagnant organ.• Parathyroid hormone increases
blood calcium levels by leechingcalcium from bone, whilecalcitonin has the opposite effect,allowing bone to accept calcium
from the blood.
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Types of bone tissue
• compact tissue - the harder, outertissue of bones.
• cancellous tissue - the sponge-liketissue inside bones.
• subchondral tissue - the smooth
tissue at the ends of bones, which iscovered with another type of tissuecalled cartilage
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Bone Composition
• Cells – Osteocytes – Osteoblasts –
Osteoclasts• Extracellular Matrix
– Organic (35%)• Collagen (type I) 90%•
Osteocalcin, osteonectin, proteoglycans, glycosaminoglycans,lipids (ground substance) – Inorganic (65%)
• Primarily hydroxyapatite Ca 5(PO4)3(OH)2
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Bone Biomechanics
• Bone is anisotropic - its modulus is dependentupon the direction of loading.
• Bone is weakest in shear, then tension, thencompression.
• Ultimate Stress at Failure Cortical Bone – Compression < 212 N/m 2
–
Tension < 146 N/m2
– Shear < 82 N/m 2
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Bone Biomechanics
• Bone is viscoelastic: its force-deformationcharacteristics are dependent upon the rate of loading.
• Trabecular bone becomes stiffer incompression the faster it is loaded.
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Bone Mechanics
• Bone Density – Subtle density changes
greatly changesstrength and elasticmodulus
• Density changes – Normal aging –
Disease – Use – Disuse
Cortical Bone
Trabecular Bone
Figure from: Browner et al: Skeletal Trauma
2nd Ed. Saunders, 1998.
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Basic Biomechanics
• Bending• Axial Loading
– Tension – Compression
• Torsion
Bending Compression Torsion
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What causes a fracture?
• When outside forces are applied to
bone it has the potential to fail.Fractures occur when bone cannotwithstand those outside forces.Fracture, break, or crack all meanthe same thing.
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FRACTURE
Definition :A fracture, whether of a bone, an epiphyseal plate ora cartilaginous joint surface, is simply a structural break in its continuity.
must be consider :
surrounding soft tissue around the fracture site
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Definition
• Break in the structural continuity of the bone• No More than a crack, a crumpling or a
Splintering of the cortex• Most often the break is compleate• displaced
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Appley; Principles of fracture
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What causes of the pain ?
• The nerve endings that surround bonescontain pain fibers and and these fibersbecome irritated when the bone is broken orbruised.
• Broken bones bleed, and the blood andassociated swelling (edema) causes pain.
• Muscles that surround the injured area maygo into spasm when they try to hold thebroken bone fragments in place, and these
spasms cause further pain. 15
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Descriptions of fractures can beconfusing. They are based on:
• where in the bone the break hasoccurred,
• how the bone fragments are aligned, and• whether any complications exist.• Is open or closed• Next, there needs to be a description of
the fracture line. Does the fracture linego across the bone ( transverse ), at anangle ( oblique ) or does it spiral ? Is thefracture in two pieces or is itcomminuted , in multiple pieces?
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Fracture Mechanics
Figure from: Browner et al: Skeletal Trauma 2nd Ed, Saunders, 1998.
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Fracture Mechanics
• Bending load: – Compression strength
greater thantensile strength
– Fails in tension
Figure from: Tencer. Biomechanics in Orthopaedic
Trauma, Lippincott, 1994.
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Fracture Mechanics
• Torsion – The diagonal in the direction of the applied force is in
tension – cracks perpendicular to this tension diagonal – Spiral fracture 45º to the long axis
Figures from: Tencer. Biomechanics in Orthopaedic
Trauma, Lippincott, 1994.
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Fracture Mechanics
• Combined bending &axial load
–
Oblique fracture – Butterfly fragment
Figure from: Tencer. Biomechanics in Orthopaedic
Trauma, Lippincott, 1994.
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Fracture Mechanics
1. Fracture Callus1. Moment of inertia
proportional to r 4
2. Increase in radius bycallus greatlyincreases moment of inertia and stiffness
1.6 x stronger
0.5 x weaker Figure from: Browner et al, Skeletal Trauma
2nd Ed, Saunders, 1998.Figure from: Tencer et al: Biomechanics inOrthopaedic Trauma, Lippincott, 1994.
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Fracture Mechanics• Time of Healing
– Callus increaseswith time
– Stiffness increaseswith time
– Near normalstiffness at 27 days
– Does notcorrespond toradiographs Figure from: Browner et al, Skeletal Trauma,
2nd Ed, Saunders, 1998.
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Stages of Fracture Healing
• Inflammation• Repair• Remodeling
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Inflammation
• Tissue disruption results in hematoma atthe fracture site
• Local vessels thrombose causing bonynecrosis at the edges of the fracture
• Increased capillary permeability results in a
local inflammatory milieu• Osteoinductive growth factors stimulate
the proliferation and differentiation of mesenchymal stem cells
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Repair
• Periosteal callus forms along the peripheryof the fracture site
– Intramembranous ossification initiated bypreosteoblasts
• Intramedullary callus forms in the center of the fracture site
– Endochondral ossification at the site of thefracture hematoma
• Chemical and mechanical factors stimulatecallus formation and mineralization
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Repair
26Figure from Brighton, et al, JBJS-A, 1991.
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Remodeling•
Woven bone is gradually converted to lamellar bone• Medullary cavity is reconstituted• Bone is restructured in response to stress and strain
(Wolff’s Law)
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Mechanisms for Bone Healing
•
Direct (primary) bone healing• Indirect (secondary) bone healing
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Direct Bone Healing
• Mechanism of bone healing seen when there is nomotion at the fracture site (i.e. rigid internalfixation)
• Does not involve formation of fracture callus• Osteoblasts originate from endothelial and
perivascular cells
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Direct Bone Healing
• A cutting cone is formed that crosses thefracture site
• Osteoblasts lay down lamellar bone behindthe osteoclasts forming a secondary osteon
• Gradually the fracture is healed by theformation of numerous secondary osteons
• A slow process – months to years
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Components of Direct BoneHealing
• Contact Healing – Direct contact between the fracture ends allows healing to be
with lamellar bone immediately• Gap Healing
– Gaps less than 200-500 microns are primarily filled withwoven bone that is subsequently remodeled into lamellar
bone – Larger gaps are healed by indirect bone healing (partially
filled with fibrous tissue that undergoes secondaryossification)
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Direct Bone Healing
32Figure from http://www.vetmed.ufl.edu/sacs/notes
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Indirect Bone Healing
• Mechanism for healing infractures that are not rigidlyfixed.
•
Bridging periosteal (soft)callus and medullary (hard)callus re-establish structuralcontinuity
• Callus subsequentlyundergoes endochondralossification
• Process fairly rapid - weeks
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Ligament
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Ligament Anatomy
• Type 1 collagen (70%)• Elastin• Extracellular matrix• Hierarchical structure• Fibrils > fibres >subfascicular unit >fasciculus•
Longitudinal fasciculi (MCL, LCL)• Helical fasciculi (ACL, PCL)
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Anatomic Features
• Bonding• Crimping• Random collagen alignment• Complex blood supply• Diffusion from synovium•
Proprioception and nociception
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Biomechanics
• Laxity• Stiffness• Strength• Viscoelastic behavior (creep, stress relaxation,
hysteresis)•
Dynamic properties
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Ligament Injury
Ligament - fibrous dense connective tissue -binds bones
injuries to these structures may be a precursor to osteoarthritis
has functional subunits that tighten or loosen depending on jointpositionis not densely innervated or densely vascularized
do contain some blood vessels and nerves in outer covering (epiligament)do contain proprioceptors
do transmits pain signals via type C fibers
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Ligament Injury
in bone-ligament-bone structures, ligament is the weakest linkweakest near ligament insertion (adolescent & osteoporotic exceptions)
ligaments are not readily weakened by inactivity (takes many weeks)ligaments show only a 10% - 20% u in tensile strength with exercise
It is currently not known whether any modalities aid in ligamenthealing
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surgical repair not done unless ends aresignificantly far apart
length of repair scar does not affect final functionalityor tensile strength
unless ends are far apart: r extra-long scar r d joint stability & u joint laxity
ACL tears most often result in ends unopposed r surgery required
surgical repair restores only about 80% - 90% of original tensile strength
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F ti l S b it f th L t l C ll t l Lig t L ft K
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Functional Sub-units of the Lateral Collateral Ligament - Left Knee
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Lig t S i
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Ligament Sprain
Ligament sprain classificationsgrade I - slight incomplete tear - no notable joint instabilitygrade II - moderate / severe incomplete tear - some joint
instabilityone ligament may be completely torngrade III - complete tearing of 1 or more ligaments - obviousinstability
surgery usually required
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In most cases, more than 1 ligament share loadsaround a joint
most sprains involve more than one ligament - example: ankle
most common sprain: ankle inversion accompanied by plantar flexionprimary ligaments: anterior talofibular and calcaneofibular ligaments
if sprain is severe, “backup” structures may sometimes be involved backup structures: posterior talofibular ligament & peroneal tendons
most common knee sprain: valgus force to knee r medial collateral tearbackup structure: anterior cruciate (cruciates blood supply inferior to collaterals)
joint instability in knee sprain likely to be evident only in injury positionrepeat injuries not only tear healed areas but backup structures as well
prevention of re-injury is of critical importance
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General Ligament Exam
• Difficult acutely• Early exam beneficial• Pt. relaxed• Displacement• Endpoint quality• Compare
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Ligament healing
• Immobilization – Loading dramatically affects recovery of normal
mechanical properties – Decrease strength – Insertion site vs. midsubstance
• Exercise – Favourable effect
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Ligament Healing
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Stage Pathology - Healing Treatment Implications
Inflammatory Intra-articular injury RICE (Protect & Immobilize <48 hrs)
(days 0 - 4) intra-articular pressure & hemarthrosis Immobilize ( r d osteoarthritis)
Extra-articular injury NSAID drugssubcutaneous hematoma light passive ROM exercise (>48 hrs)
Fibrin clot is formed in ligament tears in minutes exercises that “cross” the joint (straight leg raises for ACL injury)
Fibroplastic fibroblasts & angiogenic cells scar matrix progress to full active ROM exerciseProliferation macrophages remove damaged ligament debris resistance & weight bearing exercise
(day 4 - weeks) “decent” tensile strength within 3 weeks intensity of all types of exercisesbiomechanical evals began at 3 wks
Remodeling density of scar matrix progression of activityMaturation replacement of initial or inferior collagen tissues (intensity & duration)
(weeks to years) strength of molecular bonds of scar matrixnear maximum strength reach within 1 year** but not back to 100% of original
Ligament Healing
Healed Ligament never attain pre-injury tensile strength due to :d # of hydroxypyridinium cross linkages in collagenu quantity of type V (inferior) collagen r d collagen fibril diameter
u amount of fat cells, blood vessels, loose & disorganized collagen in the scar 46
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Capsule
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Definition
• A fibrous, membranous, or fatty sheath thatencloses an organ or part, such as the sacsurrounding the kidney or the fibrous tissues
that surround a joint.
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Anatomy
• Each capsule consists of two layers:• an outer layer ( stratum fibrosum )
composed of avascular white fibrous tissue• an inner layer ( stratum synoviale ) which is
a secreting layer, and is usually describedseparately as the synovial membrane
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Disease
• Apart from obvious involvement in injuriessuch as dislocations and fracture dislocations,abnormalities
• capsule itself may affect the functioning of the joint and predispose to other joint diseases.
• Laxity of the capsule is a common cause of dislocations
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Disease
• The mobility of a joint can be affected – adhesive capsulitis, which may occur after trauma – the capsule becomes thickened – adherent to adjacent structures, – Preventing normal motion
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'frozen shoulder'
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Treatment
• Laxity may have to be surgically treated bystapling folds of the capsule to adjacent bonystructures in order to restrict motion,
especially in the shoulder• Torn repair
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