Bone changes during ortho. tooth movement dr.anusha /certified fixed orthodontic courses by Indian dental academy

BONE CHANGES DURING BONE CHANGES DURING ORTHODONTIC TOOTH ORTHODONTIC TOOTH

MOVEMENTMOVEMENT

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Bone is a specialized mineralized connective tissue made up of an Bone is a specialized mineralized connective tissue made up of an organic matrix of collagen fibrils embedded in an amorphous organic matrix of collagen fibrils embedded in an amorphous substance with mineral crystals precipitated within the matrix.substance with mineral crystals precipitated within the matrix.

The main functions of bone are two fold.Function of Support Reservoir Function


Classification of bone

Based on Structure.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.

Based on development

Intramembranous bone – Eg., Bones of cranial vault, maxilla, etc.

Intracartilagenous bone – Eg., Vertebra, ribs, base of the skull, etc


Based on the arrangement of the collagenous matrix.

Immature Bone : is subdivided into :Woven Bone : Relatively weak ,disorganized and poorly

mineralized. The first bone formed in response to orthodontic loading usually is the woven type.

Bundle boneBundle bone is a functional adaptation of lamellar structure to allow attachment of Sharpey's fibers

Mature Bone or Lamellar boneLamellar bone a strong, highly organized, well-mineralized tissue. Adult human bone is almost entirely of the remodeled variety: secondary osteons and spongiosa..


W – Woven Bone L – Lamellar Bone


HISTOLOGY OF BONE


Periosteum

Compact Bone

Circumferential lamellae Concentric lamellae Interstitial lamellae

Bony trabeculae

Bone Marrow

HISTOLOGY OF BONE


CELLS OF THE BONE

Any cell that forms bone.

Differentiation of OsteoblastsMesenchymal stem cells differentiate into osteoblasts when

they are exposed to bone morphogenic proteins (BMP). Cbfa1 is necessary for osteoblast differ entiation.

Osteoblast


Osteoblast


RECEPTOR ACTIVATION

In the nucleus, different second messengers account for immediate early gene (IEG) expression.. The transcription of the IEGs (c-fos, c-jun, and egr-1) has been shown to increase when cells are exposed to cytokines, growth factors, or mechanical stimulation. Protein products from the c-fos and c-jun genes form activator protein-1 (AP-1) which regulates 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


Lining Cells

Lining Cells are remnants of osteoblasts 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 called osteocytes.


Osteoclasts

Osteoclasts are multi nucleated giant cells which resorb bone.They occupy shallow pits called ‘Howship’s 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

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


Origin and Cell Lineage


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 osteoclasts •Osteoclast 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 ACTIVATIONOsteoclasts also express integrin receptors including the vitronectin receptor which leads to adhesion of osteoclasts to bone surface. Peptides containing the RGD motif have been shown to inhibit oste-oclast-mediated bone resorption


Structural composition of bone


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.FibronectinThrombospondinOsteopontinBone sialo protein Bone acidic glycoprotein (B A G)Osteocalcin & Matrix Gla ProteinGrowth Factors

Inorganic Componentcalcium hydroxy apatite - Ca10(PO4)6(OH)2www.indiandentalacademy.comwww.indiandentalacademy.com

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 field is present. Compression of bone produces streaming potentials by the displacement of mobile ions relative to charged proteoglycans en trapped by collagen. Fluid movement over the cell surface may directly stimulate bone cells because it generates shear stress.


ORTHODONTIC TOOTH MOVEMENT AS RELATED TO BONE DEFORMATION

BIOELECTRICITY: First suggested by Farrar (1888)

Piezoelectricity is a phenomenon observed in many crystalline materials in which deformations of the crystalline materials results in the flow of electric currents. Collagen itself is piezoelectric.

A quick decay rateThe production of an equivalent signal, opposite in direction, when the force is released.

Piezoelectricity signals have two unusual characteristics:


Zengo et al (1973-74) showed that bending of bone may create negative fields 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 and mechanical 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, a tooth moves faster than its control.


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 PDL displacement (strain), bone strain, and extrusion .


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. After undermining resorption restores vitality to the necrotic areas of the PDL, tooth movement enters the secondary, or progres sive, tooth movement phase. The mechanism of sustained tooth movement is a coordinated array of bone resorption and formation events.

PRESSURE TENSION THEORY


CHANGES IN THE ALVEOLAR BONE

Modeling, a change in shape or size of an osseous 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 cortical bone thereby reducing the density of cortical bone


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 occur during the first month of the remodeling cycle.


CELLULAR EVENTS

The activation of osteoclast may occur because of the integrins on osteoclast cell membrane with proteins in bone matrix which contain R G D 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.


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

resorption process itself.. Osteoclasts contain large amounts 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 bone resorption 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 in the ruffled border area. Superoxide dismutase,, has been identified in osteoclasts. OCL - Osteoclast


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


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 bone structural unit (BSU).


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


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.


Non Collagenous Molecules

Name Composition Possible FunctionOsteopontin Phosphoprotein inhibits crystal growthOsteonectin Phosphoprotein inhibits crystal growthBone Sialo Phosphorylated nucleator for mineralizationProtein glycoproteinGLA Protein Protein & Regulator of crystal growth

r-carboxy glutamic acid

Biglycan & Chondroitan Sulfate Removed at mineralization frontDecorin Proteo glycans to permit mineralization

Phospholipids calcium binding at mineralizationfront.

Pyrophosphate inhibitor of calcification


Growth Factors

FGF : Increase osteo blastic precursor population and also increase collagen synthesis.

IGF : Increase bone cell proliferation and total protein synthesis.

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.


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.


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 by the same mechanism. During the retention period the newly formed bone remodels and matures..


The osteogenic layer of the suture is called the cambium, and the inner leaf the capsule. Between these two layers is a loose 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 turn induces cell level strain on the bone cells and subsequent anabolic or catabolic responses , resulting in regional acceleration of bone adaptive activity

SUTURES


Rapid palatal expansion.- the adjacent expanded suture experienced hemorrhage, necrosis, and a wound healing response. Chang et al demonstrated the angiogenic capillary-budding process associated with the propagation of perivascular osteogenic cells


Functional appliances exert the skeletal effect by inducing the action of masticatory muscles expressed by multiple lines of stresses exerted by the masticatory muscle attachment .

Sutural expansion within physiologic limits is a clinically viable means of repositioning the bones of the craniofacial complex to improve esthetics and function.


Factors Regulating Tooth movement

Growth;

Bone density

Type of tooth movement

Role of Periodontium

Duration and force magnitude

Circadian rhythm

Effect of chemicals


Parathyroid hormone - effects on bone resorption - effects on bone formation - effects on Ca++ homeostasis

Calcitonin - short term regulator of Ca++

homeostasis - inhibits osteoclastic bone resorption

1,25 - Dihydroxyvitamin D3 - Calcium homeostasis - bone remodeling - bone resorption


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

Growth factors www.indiandentalacademy.comwww.indiandentalacademy.com

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Bone changes during ortho. tooth movement dr.anusha /certified fixed orthodontic courses by Indian dental academy

Technology

lamellar bone lamellar

bone osteoblast

bundle bone bundle bone

bone changes

cortical bone

intracartilagenous bone

bone membrane

trabecular bone