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Bone Changes During Orthodontic Treatment

Apr 04, 2018

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    BONE CHANGES DURING

    ORTHODONTIC TOOTHMOVEMENT

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    Bone is a specialized mineralized connective tissue made up

    of an organic matrix of collagen fibrils embedded in an

    amorphous substance with mineral crystals precipitated

    within the matrix.

    The main functions of bone are two fold.

    Function of Support

    Reservoir Function

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    Compact Bone or cortical bone - the

    dense outer shell of the skeleton.

    Cancellous Bone or trabecular bone -

    comprises of a system of plates, rods,

    arches and struts traversing the medullary

    cavity encased within the shell of compact

    bone.

    Intramembranous bone Eg.,

    Bones of cranial vault, maxilla,

    etc.

    Intracartilagenous bone Eg.,

    Vertebra, ribs, base of the skull,etc

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    : is subdivided into :

    Relatively weak ,disorganized and poorly

    mineralized. The first bone formed in response to orthodontic

    loading usually is the woven type.

    Bundle bone isa functional adaptation of lamellar structure

    to allow attachment ofSharpey's fibers

    Lamellar bonea strong, highly organized, well-mineralized

    tissue. Adult human bone is almost entirely of the remodeled

    variety: secondary osteons and spongiosa..

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    W Woven Bone L Lamellar Bone

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    Periosteum

    Compact Bone

    Circumferential lamellae

    Concentric lamellae

    Interstitial lamellae

    Bony trabeculae

    Bone Marrow

    HISTOLOGY OF BONE

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    CELLS OF THE BONE

    Any cell that forms bone.Differentiation of Osteoblasts

    Mesenchymal stem cells differentiate into osteoblasts when

    they are exposed to bone morphogenic proteins (BMP). Cbfa1 isnecessary for osteoblast differentiation.

    Osteoblast

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    Osteoblast

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    RECEPTOR ACTIVATION

    In the nucleus, different second messengers account for immediate early

    gene (IEG) expression.. The transcription of the IEGs (c-fos, c-jun, andegr-1) has been shown to increase when cells are exposed to

    cytokines, growth factors, or mechanical stimulation. Protein products

    from the c-fosand c-jungenes form activator protein-1 (AP-1) whichregulates osteoblast differentiation.

    Functions of osteoblasts

    production of the proteins of bone matrix type I and IV collagen and other

    non collagenous proteins

    Osteoblasts secrete the growth factors.

    Osteoblasts mineralize newly formed bone matrix.

    Osteoblast may be required for normal bone resorption to occur.

    Functional lifespan of osteoblasts may range from 3 4 months to 1-5 years

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    Lining Cells

    Lining Cells are remnants ofosteoblasts that previously laid down

    bone matrix, forming a bone

    membrane that controls ion fluxes

    into and out of bone.

    Osteocytes

    As osteoblasts secrete bone matrix,

    some of them become entrapped in

    lacunae and are then calledosteocytes.

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    Osteoclasts

    Osteoclasts are multi nucleated giant cells which resorb bone.

    They occupy shallow pits called Howships lacunae on flat bone surfaces.

    Positive staining for tartarate - resistant acid phosphatase.The part of an osteoclast that is directly responsible for carrying out bone

    resorption is a transitory and highly motile structure called its ruffled border

    Theirlifespan is uncertain, though it may be as long as 7 weeks.

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    Origin and Cell Lineage

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    Differentiation of Osteoclasts

    The molecule that inhibits osteoclastogenesis is OPG (osteopotegerin)

    and OCIF (osteoclastogenesis inhibiting factor).OPG is secreted by

    osteoblasts and blocks the formation of osteoclastsOsteoclast differentiation factor (ODF) or OPG-L was able to induce

    osteoclastogenesis.

    The ratio of OPG/OPG-L regulates the osteoclast' s lifecycle

    Cytokines TNF, interleukin-1 [IL-1 ], prostoglandin E2 [PGE2] and

    growth factors (TGF-B, BMP) are upstream signals which regulate

    the OPG/ OPG-L ratio.When the balance favors OPG, there are fewer active osteoclasts;

    when the balance favors OPG-L, there is an increased number of

    active osteoclasts.

    RECEPTOR ACTIVATION

    Osteoclasts also express integrin receptors including the vitronectinreceptor which leads to adhesion of osteoclasts to bone surface.

    Peptides containing the RGD motif have been shown to inhibit oste-

    oclast-mediated bone resorption

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    Structural composition of bone

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    Organic MatrixOrganic matrix consists of 90% of collagen and remaining 10% is

    composed of other non-collagenous molecules.

    Bone CollagenCollagen is defined as a molecule composed of three polypeptide chains

    termed chains which associate into a triple helical molecule.Bone consists predominantly of type I collagen with traces of type III, V &

    XI collagen.Non-collagenous proteinsProteoglycan & Glycoproteins

    Osteonectins

    RGD containing proteins (Arg Gly ASP) Fibronectin,

    Thrombospondin, Osteopontin, Bone Sialo Protein.Fibronectin

    Thrombospondin

    Osteopontin

    Bone sialo proteinBone acidic glycoprotein (B A G)

    Osteocalcin & Matrix Gla Protein

    Growth Factors

    Inorganic Component

    calcium hydroxy apatite - Ca10(PO4)6(OH)2

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    ORTHODONTIC TOOTH MOVEMENT

    PEIZOELECTRIC THEORY

    Bone responds to an applied strain. Strain represents a change in length.

    Application of small bending forces result in compression on one side and

    tension on the opposite side. This produces a flow of interstitial fluid,

    through the canalicular network, generating streaming potentials.

    Because of the negative charge of proteoglycans, there is an excess of

    positive mobile ions in the fluid.

    Charges are symmetrically arranged so that no net macroscopic electric fieldis present.

    Compression of bone produces streaming potentials by the displacement of

    mobile ions relative to charged proteoglycans entrapped by collagen.

    Fluid movement over the cell surface may directly stimulate bone cells

    because it generates shear stress.

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    ORTHODONTIC TOOTH MOVEMENT AS RELATED TO BONEDEFORMATION

    BIOELECTRICITY: First suggested by Farrar (1888)

    Piezoelectricity is a phenomenon observed in many crystalline materials inwhich deformations of the crystalline materials results in the flow of electric

    currents. Collagen itself is piezoelectric.

    A quick decay rate

    The production of an equivalentsignal, opposite in direction, when

    the force is released.

    Piezoelectricity signals have twounusual characteristics:

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    Zengo et al (1973-74) showed that bending of bone may create negativefields occurring in the concave aspects of the bone surface leading to bone

    deposition and positive fields occuring on the convex bone surface leading

    to bone resorption

    Baumrind and Buck et al suggested that the major physiologic andmechanical changes might occur not in the periodontal ligament but

    rather in the alveolar bone.

    A second type of endogenous electric signal, which is called the bioelectric

    potential can be observed in bone that is not being stressed.

    Electronegative charges are observed in areas of metabolically active bone

    or connective tissue where bone growth or remodeling is occurring.

    Inactive cells and areas are nearly electrically neutral.

    The purpose of this bioelectric potential is not yet known.

    Davidovitch showed that modifying the bioelectric potential, atooth moves faster than its control.

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    ORTHODONTIC TOOTH MOVEMENT

    The orthodontic response is divided into three elements of tooth

    displacement: initial strain, lag phase, and progressive tooth movement.

    Initial strain of 0.4 to 0.9 mm occurs in about 1 week because of PDLdisplacement (strain), bone strain, and extrusion .

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    CHANGES IN THE PERIODONTAL LIGAMENTProgressive displacement of the tooth relative to

    its osseous support stops in about 1 week, of

    PDL necrosis. This lag phase lasts 2 to 3 weeks

    but may be as long as 10 weeks. Afterundermining resorption restores vitality to the

    necrotic areas of the PDL, tooth movement

    enters the secondary, or progressive, tooth

    movement phase. The mechanism of sustained

    tooth movement is a coordinated array of bone

    resorption and formation events.

    PRESSURE TENSION THEORY

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    CHANGES IN THE ALVEOLAR BONE

    Modeling, a change in shape or size of anosseous structure, is achieved by

    differential bone formation and resorption

    along the periosteal and endosteal

    surfaces. Internal turnover of osseous

    tissue is termed remodeling

    The remodeling process has evolved a

    vascularized multicellular unit for removing

    and replacing cortical bone which is called

    a cutting/filling cone. Cutting cones

    create resorption cavities in the corticalbone thereby reducing the density of

    cortical bone

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    Remodeling of dense alveolar bone may enhance the rate of

    tooth movement and replace the less mature osseous tissue

    formed by rapid PDL osteogenesis. These intraosseous

    resorption cavities are the initial remodeling events that occurduring the first month of the remodeling cycle.

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    CELLULAR EVENTS

    The activation of osteoclast may occur because of the integrins on

    osteoclast cell membrane with proteins in bone matrix which contain R GD amino acid sequences such as Osteopontin.

    Has a dual function of allowing osteoclastic access to mineralized bone

    matrix and releasing factors from the matrix such as osteocalcin which are

    chemotactic for osteoclasts or their precursors.

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    How do osteoclasts work?The ruffled border area carries out the

    resorption process itself.. Osteoclasts contain largeamounts of carbonic anhydrase to facilitate the

    conversion of CO2 and H2O to H2CO3. The

    degradation of bone matrix is presumably the result of

    the activity of a number of lysosomal enzymes which

    can degrade bone at low pH.

    There is a correlation between activation of boneresorption and acid phosphatase release.

    A variety of cathepsins and other lytic enzymes which

    are produced by the osteoclast are able to degrade

    collagen at low pH.

    There is a evidence that oxygen-derived free radicals

    are produced by osteoclasts and may be localized inthe ruffled border area.

    Superoxide dismutase,, has been identified in

    osteoclasts.OCL - Osteoclast

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    Reversal

    The reversal phase lasts from 7 to 14 days

    The resorption bays are now devoid of osteoclasts and are occupied by

    Osteocytes, macrophage like mononuclear cells and preosteoblast..Osteoblasts are summoned into the reversal lacuna.by growth factors

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    Bone matrix formation

    Begins with the deposition by the osteoblasts of osteoid,. The second stage in bone

    formation is mineralization of the organic matrix,).

    The completed piece of new bone is termed either a basic structural unit or a bonestructural unit (BSU).

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    Bone mineralisation

    2 mechanisms.

    A) Matrix Vesicle :The matrix vesicle contains alkaline phosphatase, pyro-

    phosphates, Ca-ATPase, metallo proteinases, proteoglycan and anionic

    phospholipids which are able to bind to calcium and inorganic phosphate

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    B) Heterogeneous Nucleation : Non-collagenous proteins act as nucleators

    and others may act to control crystal growth. Dephosphorylation of the

    phosphoprotein provides the additional phosphate ions for nucleation

    and crystal growth.Additional crystallites may form by secondary nucleation from

    mineral phase particles

    Factors influencing mineralization

    Local FactorsCollagen Collagen has holes and pores in which nucleation, crystal

    growth, secondary nucleation and multiplication of the solid phase can

    occur.

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    Non Collagenous Molecules

    Name Composition Possible Function

    Osteopontin Phosphoprotein inhibits crystal growth

    Osteonectin Phosphoprotein inhibits crystal growth

    Bone Sialo Phosphorylated nucleator for mineralization

    Protein glycoprotein

    GLA Protein Protein & Regulator of crystal growth

    r-carboxy glutamic acid

    Biglycan & Chondroitan Sulfate Removed at mineralization front

    Decorin Proteo glycans to permit mineralization

    Phospholipids calcium binding at mineralization

    front.

    Pyrophosphate inhibitor of calcification

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    Growth Factors

    FGF : Increase osteo blastic precursor population and also

    increase collagen synthesis.

    IGF : Increase bone cell proliferation and total proteinsynthesis.

    TGF, PGDF : increase proliferation of osteo-progenitor and total

    protein synthesis.

    Interleukin 1 : At low doses, it stimulates collagen synthesis but is

    inhibitor in higher concentrations.

    Tumor necrosis factor: stimulate proliferation and collagen synthesis in pre-

    osteoblasts.

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    Systemic Factors

    PTH, 1,25 - Dihydroxy Vitamin D3, estrogen

    Role of alkaline phosphates

    hydrolyzes phosphate ions from organic radical at an

    alkaline pH

    Marker of osteoblast activity.

    Incremental lines

    Due to variations in the degree of mineralization at the

    boundaries between periods of activity and rest.

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    HISTOLOGICAL ASPECT

    Primary compacta is formed by

    woven bone which fills in with lamellar

    bone to form primary osteons.

    Within weeks, the new primary bone

    is remodeled to more mature

    secondary osteons by a progressive

    wave of cutting/filling cones .

    . Supporting bone continues to adapt

    to the new position of the tooth for up

    to a year after the end of active tooth

    movement.

    Cortical bone is formed along

    periosteal and PDL/bone surfaces bythe same mechanism.

    During the retention period the newly

    formed bone remodels and matures..

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    The osteogenic layer of the suture is called

    the cambium, and the inner leaf thecapsule. Between these two layers is aloose cellular and vascular tissue.

    Sutures experience, absorb, and transmit

    mechanical stresses generated from either

    functional activities such as mastication, or

    exogenous forces such as orthopedic

    loading.

    Mechanical stresses transmitted through

    the bone are experienced as tissue level

    bone strain, interstitial fluid flow that in turninduces cell level strain on the bone cells

    and subsequent anabolic or catabolic

    responses , resulting in regional

    acceleration of bone adaptive activity

    SUTURES

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    Rapid palatal expansion.- the adjacent expanded suture experiencedhemorrhage, necrosis, and a wound healing response. Chang et al

    demonstrated the angiogenic capillary-budding process associated with the

    propagation of perivascular osteogenic cells

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    Functional appliances exert the skeletal effect by inducing the actionof masticatory muscles expressed by multiple lines of stresses exerted

    by the masticatory muscle attachment .

    Sutural expansion within physiologic limits is a clinically viable means ofrepositioning the bones of the craniofacial complex to improve esthetics

    and function.

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    Factors Regulating Tooth movement

    Growth;

    Bone density

    Type of tooth movement

    Role of Periodontium

    Duration and force magnitude

    Circadian rhythm

    Effect of chemicals

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    Parathyroid hormone- effects on bone resorption

    - effects on bone formation- effects on Ca++ homeostasis

    Calcitonin- short term regulator of Ca++

    homeostasis

    - inhibits osteoclastic boneresorption

    1,25 - Dihydroxyvitamin D3- Calcium homeostasis

    - bone remodeling

    - bone resorption

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    Prostaglandins

    bidirectional effect on osteoclasts - an immediate transient effect

    to slow bone resorption and a sustained effect to Osteoclastic

    bone resorption.

    Interleukin - 1

    - powerful and potent stimulator of bone resorption

    Tumor necrosis factor

    - Osteoclastic bone resorption

    Osteoprotegrin

    - inhibitor of bone resorption

    Interleukin - 6

    Gamma interferon

    G th f t