fracture healing by dr rohit kumar
TRANSCRIPT
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GOOD MORNING
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DEPARTMENT OF ORTHOPAEDICS
MODERATORS: PRESENTED BY:
DR G C BASAVARAJA DR ROHIT KUMARPROFFESOR & UNIT HEAD PG IN ORTHOPAEDICS
DR SHAKEEL KHAN DATED:19.01.11ASSOCIATE PROFESSOR
J.J.M MEDICAL COLLEGE , DAVANGERE
SEMINAR ON
ANATOMY OF FRACTURE HEALING
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Fracture is defined as a break in the
continuity of bone. Fracture results in loss of its mechanical stability and also partial destruction of blood supply.
Healing means to make whole or sound again, to cure, leaving a scar behind. But following fracture a scar is not formed, instead a bone has formed a new at the original fracture site. So rather than bone healing the appropriate nomenclature would be BONE REGENERATION
INTRODUCTION
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History of fracture and its knowledge dates back
to Egyptian mummies of 2700 B.C
In 17th century Albrecht Haller, observed invading capillary buds in fracture callus and thought that blood vessels are responsible for callus formation.
John Hunter, a pupil of Haller, described the morphologic sequence of fracture healing.
HISTORY
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In 1873, Kolliker observed the role of
multinucleated giant cells, osteoclast to be responsible for bone resorption.
In1939, Gluksman suggested pressure and shearing stresses are possible stimuli for
fracture healing.
In 1961, Tonna and Cronkie demonstrated the role of local mesenchymal cells in fracture
repair.
Contd…..
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Bone is essentially a highly vascular, living,
constantly changing mineralized connective tissue which makes up body’s skeleton.
Other functions are:- Bone provides protection for the vital organs of the body( eg: heart and brain)- The hematopoietic bone marrow is protected by the surrounding bony tissue.- Storage of calcium and phosphate.
WHAT IS BONE ?
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Living bone is white, with either dense texture like ivory or honeycombed by large cavites .
Spongy bone (cancellous) : is composed of a lattice or network of branching bone spicules or trabeculae. The spaces between the bone spicules contain bone marrow.
Compact bone (cortical / outer): appears as a mass of bony tissue lacking spaces visible to the unaided eye.
MACROSCOPY
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Woven (Immature bone): Characterized by
random arrangement of cells and collagen ,associated with periods of rapid bone formation, such as in initial stage of fracture healing.
Lamellar bone (Mature bone) : Characterized by an orderly cellular distribution and properly oriented collagen fibres . This constitutes organised bone both cortical and cancellous
MICROSCOPY
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Comprises of
osteons (Haversian systems)
Osteons communicate with medullary cavity by Volkmann’s canals
CORTICAL BONE
.
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HAVERSIAN CANAL
Haversian canal
Cells, nerves &
vessels
Volkmann’s
canal
Connects osteons
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osteon
Haversian canal
osteocyte
Volkmann’s canal
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WOVEN BONE
Coarse with random
orientation
Weaker than lamellar
bone
Normally remodeled to
lamellar bone12
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Is a membrane that lines the outer surface of all bones except at the joints of long bones.
Is made up of : Outer FIBROUS layer : made up of white
connective and elastic tissue. Inner CAMBIUM layer : which has a looser
composition, is more vascular and contains cells with osteogenic potency.
PERIOSTEUM
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1. Anchors tendons and ligaments to bone.2. Acts as a limiting membrane.3. Participates in growth (appositional) and repair
through the activities of the osteoprogenitor cells .
4. Periosteum helps in fracture healing by forming periosteal callus.
5. It also lessen the displacement of the # and helps in reduction.
6. Allows passage of blood vessels, lymphatics and nerves into and out of the bone.
FUNCTIONS OF PERIOSTEUM:
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BLOOD SUPPLY OF BONE
Long bones have three
blood supplies
-Nutrient artery
(intramedullary) 80-85%
-Periosteal vessels
-Metaphyseal vessels
have hair pin
arrangement.
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In miniature long bones, the nutrient artery breaks up into a plexus immediately upon reaching the medullary cavity.
In contrast in cancellous bone the blood supply reaches its destinations more directly without significant branching . Therefore the healing where vascular re estabilishment is necessary happens rapidly.
The nerve supply to a bone comes along with the blood supply. Nerve supply includes sensory nerve supply, vasomotor nerve supply and sympathetic nerve supply.
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Accompanying the blood vessels there are
usually fine medullated /non medullated nerve fibres which extend into the haversian system and in large numbers to the periosteum.
These nerves are mainly concern with innervation of blood vessels, although periosteum and bone have been described in being sensitive to pain and vibration.
It is not clear whether bone has a direct neural input ..
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Fracture stimulates the release of growth
factors that promote angiogenesis and vasodilation.
Blood flow is increased substantially to the fracture site.
Peaks at two weeks after fracture
VASCULAR RESPONE IS FRACTURE REPAIR
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BONE COMPOSITION
CELLS 1. OSTEO PROGENITOR
CELLS2. OSTEOBLASTS3. OSTEOCLASTS4. OSTEOCYTES5. BONE LINING CELLS
EXTRACELLULAR MATRIX1. ORGANIC & WATER 35%
Type Ι Collagen 90% Osteocalcin,
Osteonectin, Proteoglycans, Glycosaminoglycans, Lipids (ground substance)
2. INORGANIC 65%Primarily hydroxyapatite
Ca10(PO4)6(OH)2
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1.OSTEO PROGENITOR CELLS
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Are basophilic, cuboidal to pyrimidal in shape ,
associated with bone formation, these cells are located where new bone is forming, eg: in the periosteum.
Osteoblasts often appear stratified as in an epithelium.
The nucleus is large with a single prominent nucleolus.
Osteoblasts contain the enzyme alkaline phosphatase used to calcify the osseous matrix.
2.OSTEOBLASTS
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The synthesis type 1 collagen, osteocalcin (bone Gla protein) and osteonectin
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Giant, multinuclear cells which vary greatly in
shape. They are found on the surfaces of osseous
tissue usually in shallow depressions called Howship’s lacunae.
The cytoplasm is slightly basophilic and contains lysosomal vacuoles.
Under E.M. the cell surface facing the osseous matrix shows numerous cytoplasmic projections and microvilli described as a ruffled border.
3.OSTEOCLASTS
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RUFFLED BORDER
MICROSCOPIC PICTURE ELECTRON MICROSCOPY
OSTEOCLASTS
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Basically, an osteoblast that has been enclosed within
the bony matrix in a space called the lacuna. The cytoplasm of the osteocyte is faintly basophilic
containing fat droplets and granules of glycogen with single dark stained nucleous.
In developing bone, the cytoplasmic processes from one osteocyte make contact with the processes (ie: cannaliculi) from adjoining osteocytes. In mature bone, the processes are withdrawn almost completely.
In mature bone the empty canaliculi remain as passage ways for the diffusion of nutrients and wastes between bone and blood.
4.OSTEOCYTES
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Are flattened epithelium in adult skeleton
found on resting surfaces. Plays active role in differentiation of progenitor
cells Controls osteoclasts, mineral hemostasis and
may secrete collagenase. Lines – endosteal surface of marrow cavity - periosteal surface
- vascular channels within osteons.
5.BONE LINING CELLS
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HEALING AFTER FRACTURE FIXATION
DIRECT/PRIMARY:
Mechanism of bone healing seen
when there is no motion at the
fracture site (i.e. rigid internal
fixation).
Does not involve formation of
fracture callus.
Osteoblasts originate from
endothelial and perivascular
cells.
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CONTD:
INDIRECT/SECONDARY:
Mechanism for healing in
fractures that are not rigidly
fixed.
Bridging periosteal (soft) callus
and medullary (hard) callus re-
establish structural continuity.
Callus subsequently undergoes
endochondral ossification.
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TYPES OF BONE HEALING
PRIMARY
1. CONTACT HEALING: When there is direct
contact between the cortical bone ends,
lamellar bone forms directly across the
fracture line , parallel to long axis of the
bone, by direct extension of osteons.
2. GAP HEALING: Osteoblasts differentiate
and start depositing osteoids on the
exposed surfaces of fragment ends, mostly
without a preceding osteoclastic resorption
which is later converted into the lamellar
bone .
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CONTD:
SECONDARY:
It is usual type consisting of
formation of callus either of
cartilaginous or fibrous. This
callus is later replaced by
lamellar bone. It is
comparable to healing of soft
tissue by filling of gaps with
vascular granulation tissue.
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OSTEOINDUCTION: This term mean that primitive,
undifferentiated and pleuripotent cells are somehow stimulated to develop into the bone forming cell lineage.one proposed definition is process by which osteogenesis is induced.
OSTEOCONDUCTION:A scaffold of collagenous network has developed, upon which the reparative cells produce callus and bone
OSTEOINDUCTION
CONDUCTIONINTEGRATION
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It facilitates bone deposition in an orderly fashion and helps the callus to bridge the gap between the fragments.
OSTEOINTEGRATION:The direct structural and functional connection between living bone and the surface of a load-bearing implant.
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1. Cutting Cones
2. Intramembranous Bone
Formation
3. Endochondral Bone Formation
MECHANISM OF BONE FORMATION
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Primarily a
mechanism to
remodel bone.
Osteoclasts at the
front of the cutting
cone remove bone.
Trailing osteoblasts
lay down new bone.
CUTTING CONES
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Mechanism by which a long bone grows in
width.
Osteoblasts differentiate directly from pre osteoblasts and lay down seams of osteoid.
Does NOT involve cartilage anlage.
INTRAMEMBRANOUS BONE FORMATION(PERIOSTEAL)
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INTRAMEMBRANOUS BONE FORMATION
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Mechanism by which a long bone grows in
length.
Osteoblasts line a cartilage precursor.
The chondrocytes hypertrophy, degenerate and calcify (area of low oxygen tension).
Vascular invasion of the cartilage occurs followed by ossification (increasing oxygen tension).
ENDOCHONDRAL BONE FORMATION
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There are 3 major phases with sub
divisions:
A. Reactive Phase: i. Fracture and inflammatory phase. ii. Stage of hematoma formation. iii. Granulation tissue formation.
B. Reparative Phase: iv. Cartilage Callus formation. v. Lamellar bone deposition.
C. Remodeling Phase: vi. Remodeling to original bone contour.
STAGES OF FRACTURE HEALING
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A.REACTIVE PHASE
I .Fracture & inflammatory
phase :
After fracture the first change seen by light and electron
microscopy is the presence of blood cells within the tissues
which are adjacent to the injury site. Soon after
fracture, the blood vessels constrict, stopping any
further bleeding.
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ii. Stage of Hematoma formation:
Within a few hours after fracture, the extravascular blood cells form a
blood clot, known as a hematoma. All of the cells within the blood clot
degenerate and die.
The fracture hematoma immobilizes
& splints the fracture.
The fracture haematoma provides a
fibrin scaffold that facilitates
migration of repair cells.
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iii. Granulation Tissue Formation:
Within this same area,
the fibroblasts survive and replicate.
They form a loose aggregate of cells,
interspersed with small blood vessels,
known as granulation tissue which
grows forward, outside and inside the
bone to bridge the fracture.
They are stimulated by vasoactive
mediators like serotonin and
histamine.
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B. REPARATIVE PHASE
iv. Cartilage Callus formation :
Days after the # the periosteal cells
proximal to the fracture gap and fibroblasts
develop into chondroblasts which
form hyaline cartilage.
The periosteal cells distal to the fracture
gap develop into osteoblasts which
form woven bone. These 2 tissues unite
with their counterparts and culminate into
new mass of heterogenous tissue called
Fracture Callus restoring some of its
original strength.
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v. Lamellar bone deposition:
Or consolidation ..where hyaline cartilage
and woven bone is replaced by lamellar
bone. This process is called
Endochondral ossification.
At this point, the mineralized matrix is
penetrated by channels, each containing
a microvessel and numerous osteoblasts.
This new lamellar bone is in the form
of trabecular bone which restores bone’s
original strength.
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C. REMODELLING PHASE
vi. Remodelling to original bone contour:
The remodeling process substitutes the
trabecular bone with compact bone. The
trabecular bone is first resorbed
by osteoclasts, creating a shallow
resorption pit known as a "Howship's
lacuna".
Then osteoblasts deposit compact bone
within the resorption pit.
Eventually, the fracture callus is
remodelled.
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STAGE 1- A healing bone subjected to torsion fails
through original # site with a low stiffness pattern. STAGE 2- The bone still fails through the # site ,
but the characteristic indicate high stiffness pattern(hard tissue pattern)
STAGE 3 – The bone fails partly through the original # site and partly through the previously intact bone with a high stiffness pattern .
STAGE 4 –Failure does not occur through the # site duplicates the mechanical properties of uninjured tissue.
STAGES BASED ON REACTION TO TORSIONAL TESTING
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# HEALING IN CANCELLOUS BONE
1.Cancellous bone heals by -
“CREEPING SUBSTITUTION”
New blood vessels can invade
the trabecular of cancellous
bone and bone opposition may
take place directly on to the
surface of trabeculum.
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2.Heals at the point of direct contact:
Cancellous bone certainly can unite
very rapidly, but it unites rapidly only
at the points of direct contact.
3.No bridging callus :
Cancellous bone unites only by
contact, not by throwing out callus
even when it is cut of due to dense
attachment of the periosteum.
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4.No death of osteocytes:
Takes place in the cut edges of divided trabeculae in cancellous bone. This must be because of the blood supply is good and large surface area of the trabecular spaces combined with relatively thin trabeculae, keep the osteocytes nourished.
5.Has tendency for late collapse :
This lack of callus production by cancellous bone explains the tendency to late collapse which have been distracted. Eg: after reduction of colle’s fracture a hallow cavity is left in the cancellous end of the radius.
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FRACTURE HEALING IN CHILDREN
Compared with the relatively static mature bone of adult, the changing structure and function both physiological and biomechanical of immature bones make them susceptible to different patterns of fracture.
Fracture in children are more common and are more likely to occur after seemingly insignificant trauma. Damage involving specific growth regions such as the physis or epiphyseal ossification center may lead to acute and chronic growth disturbances.
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Higher collagen to bone ratio- this lowers the
modulus of elasticity and tensile strength of bone.
Higher cellular and porus bone –reduces tendency of # to propagate explains why children dont have communited #’s.
Bone fails in both tension and compression- explains why buckle #’s happen in children.
Bone transitions- between metaphysis and dyphysis has discontinuity, leading to certain types of #’s…
PEDIATRIC BONE ??
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FEATURES OF PEDIATRIC BONE AND THEIR MANAGEMENT EFFECTS
FEATURE:
Thick cartilage Thick periosteum More collagen More cancellous
bone Growth plate
Stronger ligaments
MANAGEMENT EFFECT:
Not imaged by x rays. Healing rapid. Fractures easily. Simple # patterns. Remodels deformity.
Bone fails first.
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Growth plate:
The most obvious difference
The relative strength of plate with
the bone changes with age .eg:
physis in children is stronger than
adjacent bone so diaphyseal #’s are
more common.
HELPS # MANAGEMENT: by
remodeling..
INJURED GROWTH PLATE CAUSES
DEFORMITY due to asymmetry.
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PHYSIS/GROWTH PLATE : Physis or growth plates primary function is rapid integrated longitudinal and latitudinal growth. Ischemia of physis due to fracture can lead to growth disturbances.
zones within the physis :1. The resting cartilage zone 2. The proliferating cartilage zone 3. The zone of hypertrophy and 4. The zone of calcification.
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Accounts for ¼ of childhood fractures . Physeal injuries can occur from
infection,ischemia,tumors. They are more common in boys and in upper
limb. These are of great importance as they
determine growth and remodelling potential. Fractures generally occur in zone of
provisional calcification ,sparing the germinal zone.
Most sensitive to injury is proximal tibial epiphysis.
PHYSEAL INJURIES
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BUCKLE OR TORUS #
PLASTIC BOWING OF ULNA
GREENSTICK #AVULSION # OF TIBIAL SPINE … BONE FAILS BEFORE ACL
GENU RECURVATUM DUE TO PHYSEAL GROWTH ARREST
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FRACTURE REPAIR IN CHILDREN
Fracture healing in children follow same pattern of adults but with some peculiarities :
PERIOSTEUM:
In the contrast to adults the periosteum strips away easily from the underlying bone in children. Allowing fracture haematoma to dissect along the diaphysis
and metaphysis and this is evident in the subsequent amount of new bone formation along
the shaft. Dense attachment of the periosteum into the zone
of ranvier limit subperiosteal hematoma formation to the metaphysic and diaphysis.
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REMODELLING IN CHILDREN
The remodelling phase is the longest phase and in children may continue until skeletal maturation. Remodelling is better in children compared to adult, This is in response to constantly changing stress Patterns in children during skeletal growth and development.
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1. LOCAL FACTORS.
2. CHEMICAL FACTORS.3. VASCULAR FACTORS.4. SYSTEMIC FACTORS.
5. ELECTROMAGNETIC FACTORS.
6. TREATMENT FACTORS.
FACTORS INFLUENCING BONE HEALING
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A.Type of bone:
Calcellous (spongy) bone V/S cortical bone. B. Degree of Trauma:
Extensive soft tissue injury and comminuted #‘s V/S Mild contusions
C.Vascular Injury: Inadequate blood supply impairs healing. Especially
vulnerable areas are the femoral head, talus, and scaphoid bones.
D. Degree of Immobilization: Immobilized for vascular ingrowth and bone healing to occur.
1.LOCAL FACTORS
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Repeated disruptions of repair tissue, especially to areas
with marginal blood supply or heavy soft tissue damage, will impair healing.
E.Type of Fractures: Intraarticular fractures communicate with synovial fluid, which contains collagenases that retard
bone healing V/S Open fractures result in infections V/SSegmental fractures have disrupted blood supply.
F.Soft Tissue Interposition: G.others: Bone death caused by radiation, thermal or chemical burns or infection.
CONTD..
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1.MESSENGER 2.GROWTH 3.PERMEABILITYSUBSTANCES FACTORS FACTORS-Serotonin -Transforming GF -Proteases-Prostaglandins -Fibroblast GF -Polypeptides-Histamines -Platelet derived GF -Amines-Thromboxane -Insulin like GF -Bone morphogenic proteins(BMP)
2.CHEMICAL FACTORS
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1.MESSENGER SUBSTANCE:A.CYTOKINES- IL-1,4,6,11, macrophage and granulocyte/macrophage
(GM) (CSFs) & (TNF) stimulate bone resorption.IL-1 ,6 synthesis is decreased by estrogen
-May be mechanism for post-menopausal bone resorption & it regulates endochondral bone formation.
B. PROSTAGLANDINS of the E series--Stimulate osteoblastic bone formation and inhibit activity of isolated osteoclasts.
C.LEUKOTRINES-Stimulate osteoblastic bone formation and enhance the capacity of isolated osteoclasts to form resorption pits.
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2.GROWTH FACTORS: A.Transforming growth factor(TGF):
Superfamily of growth factors (~34 members) Act on serine/threonine kinase cell wall receptors
Promotes proliferation and differentiation of osteoblasts, osteoclasts and chondrocytes
Stimulates both endochondral and intramembranous bone formation and collagen type 2 synthesis.
B.Fibroblast growth factors(FGF):Both acidic (FGF-1) and basic (FGF-2) forms
Increase proliferation of chondrocytes and osteoblastsEnhance callus formation & stimulates angiogenesis.
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C.Platelet derived growth factor(PDGF):
A dimer, genes PDGF-A and PDGF-BStimulates bone cell growth
Increases type I collagen synthesis by increasing the number of osteoblasts.
PDGF-B stimulates bone resorption.
D.Insulin like growth factor(ILGF): Two types IGF1 &IGF2 out of which IGF1 is produced in liver and stimulated by growth
hormone.Stimulates bone collagen & matrix synthesis and replicates osteoblasts . It also inhibits collagen
degradation.
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E.Bone Morphogenic Proteins (BMP):
BMP was discovered by Marshall Urist in 1965. They are Osteoinductive proteins initially isolated from demineralized bone matrix.
FUNCTIONS: 1. Induce cell differentiation : BMP 3(osteogenin).
2. Promote endochondral ossification: BMP 2 & 7.
3. Regulate extracellular matrix production :BMP1.
4.Increase fusion rates in Spinal fusions (anterior lumbar interbody fusion): BMP 2
5.Non unions: BMP 7 as good as bone grafting .
These are included in the TGF-β family except BMP 1. Must be applied locally because of rapid systemic clearance .
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3.PERMEABILITY FACTORS:
-Protease – Plasmin , Kalikrein, Globulin permeability factor.-Polypeptides –leucotaxime, Bradykinin, Kallidin-Amines – Adrenalin, nor-adrenalin, Histamine.
These factors work in ways that : Increase capillary permeability Alteration in diffusion mechanism in intracellular
matrix Cellular migration Proliferation & differentiation New blood vessel formation Matrix synthesis Growth & development.
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3.VASCULAR FACTORS
A. Metalloproteinases:
Degrade cartilage and bones to
allow invasion of vessels
B. Angiogenic factors:
Vascular-endothelial growth factors
mediate neo-angiogenesis &
endothelial-cell specific mitogens.
C. Angiopoietin (І & ІІ)
Regulate formation of larger
vessels and branches.
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A.Age: Young patients heal rapidly and have a remarkable ability to remodel V/S old .
B.Nutrition: An adequate metabolic stage with sufficient carbohydrates and protein is necessary.
C.Systemic Diseases: and those causing an immunocompromised state will likely delay healing. Illnesses like Marfan’s syndrome and Ehlers-Danlos syndrome cause abnormal musculoskeletal healing.
4.SYSTEMIC FACTORS
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D.HORMONES: Estrogen
Stimulates fracture healing through receptor mediated mechanism.
Thyroid hormonesThyroxine and triiodothyronine stimulate osteoclastic
bone resorption. Glucocorticoids Inhibit calcium absorption from the gut causing increased
PTH and therefore increased osteoclastic bone resorption. Parathyroid Hormone Growth Hormone
Mediated through IGF-1 (Somatomedin-C)Increases callus formation and fracture strength
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In vitro bone deformation produces piezoelectric
currents and streaming potentials.Electromagnetic (EM) devices are based on
Wolff’s Law that bone responds to mechanical stress: Exogenous EM fields may simulate
mechanical loading and stimulate bone growth and repair
TYPES ARE : Ultrasound. Direct electrical current. Pulsed electromagnetic fields (PEMF).
5.ELECTROMAGNETIC FACTORS
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A.Ultrasound therapy:
Low-intensity ultrasound is approved
by the FDA for stimulating healing of
fresh fractures.
Modulates signal transduction,
increases gene expression (aggrecan ),
increases blood flow, enhances bone
remodeling and increases callus
torsional strength in animal models.
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B.Direct Electrical
current:
Electric stimulation of bone has
been taught to be an effective
and non invasive method for
fracture healing and treating
fracture non union. Studies
shows that electric field
generated helps in proliferation
of bone cells.
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A/K CAST WITH CATHODES ELECTEOMAGNETIC FIELD
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C.Pulsed electromagnetic fields (PEMF).
Approved by the FDA for
the treatment of non-unions
Efficacy of bone stimulation
appears to be frequency
dependant
are most effective (15 to
30 Hz range)
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APPOSITION OF FRACTURE FRAGMENTS.
LOADING AND MICROMOTION . FRACTURE STABILIZATION.
RIGID FIXATION.
BONE GRAFTING.
6.TREATMENT FACTORS
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OTHER RECENT ADVANCES:
GROWTH FACTOR THERAPY Due to their ability to stimulate proliferation and
differentiation of mesenchymal and osteoprogenitor cells they have shown great promise for their ability to promote fracture repair .
APPLICATION OF PLATELET RICH PLASMA Injecting platelet rich plasma at fracture site helps in
fracture healing .
TISSUE ENGINEERING, STEM CEELS AND GENE THERAPIES In past decade tissue culture and stem cells have
been implicated in enhancing fracture healing and articular cartilage regeneration.
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Fracture healing is influenced by many
variables including mechanical stability, electrical environment, biochemical factors
and blood flow etc…
Our ability to enhance fracture healing will increase as we better understand the interaction between these variables.
SUMMARY
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CAMPBELL TEXTBOOK OF ORTHOPAEDICS 11TH EDITION..
TUREK ORTHOPAEDICS 4TH EDITION.
WHEELES TEXT BOOK OF ORTHOPAEDICS.
INTERNET.
FUNDAMENTAL OF PEDIATRIC ORTHOPAEDICS By Lynn T. Stahel
BIBLIOGRAPHY
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