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PRESENTER DR.PUNIT

(I YEAR PG)

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CONTENTS

Introduction

Synonyms

Shape of pdl

Development

Composition

PDL as specialized connective tissue

Blood supply

Nerve supply

Function

Clinical considerations

Conclusion

References

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INTRODUCTION

Periodontium/Attachment

apparatus/Supporting tissues of

teeth):

gingiva

attachment apparatus (alveolar bone,

periodontal ligament and cementum)

• Main function –It attaches the tooth to

the bone of jaws.

Maintains the integrity of the surface

of masticatory mucosa of the oral

cavity 4

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A ligament is defined as a band of fibrous tissue binding

together skeletal elements.

The root of tooth connected to the socket in alveolar bone by

dense fibrous connective tissue which can be regarded as a

ligament.

PDL is very unique from all other ligaments in the body

connects and restricts the hard tissues-tooth cementum and

alveolar bone.

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The periodontal ligament is a soft, fibrous specialized

connective tissue which is present in the periodontal space,

which is situated between the cementum of root of the tooth

and the bone forming the socket wall.

The periodontal ligament extends coronally up to the most

apical part of connective tissue of gingiva

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DEFINITIONS

Periodontal ligament is composed of soft complex vascular and

highly cellular connective tissue that surrounds the tooth root and

connects to the inner wall of the alveolar bone (Mc Culloch CA,

Lekic P, Mc Kee MD Periodontol 2000 24:56,2000)

ACCORDING TO BERKOVITZ:

“it is the dense fibrous connective tissue that occupies theperiodontal ligament space between the roots of teeth andalveolus. It is derived from the dental follicle above alveolarcrest and is continuous with connective tissue of gingiva andthe apical foramen which is further continuation with dentalpulp.

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It is a narrow and highly cellular CT that forms theinterface between alveolar bone and cementum.(Periodontol 2000,vol.3,1993)

Soft, richly vascular and cellular connective tissue whichsurrounds the roots of the teeth and joins the rootcementum with the socket wall. (Jan Lindhe 5th ed)

The periodontal ligament occupies the periodontal space,which is located between the cementum and theperiodontal surface of alveolar bone and extends coronallyto the most apical part of the lamina propria of the gingiva.(Orban’s)

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COMPOSITION 53 – 74 % of periodontal ligament volume consists of

collagen and oxytalan fibers.

1 – 2 % consist of vascular elements.

Remainder consists of cells and neural elements.

The connective tissue of periodontal ligament

comprises collagen

Proteoglycan, glycoprotein and small amount of

glycogen.

Major component is Type – I collagen with Type III

collagen accounting for 15 – 20 % of total collagen

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SHAPE OF PERIODONTAL LIGAMENT

HOUR GLASS SHAPE

Thinnest around the middle third of the root & widens both

apically and near the crest.

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It is neither a typical membrane nor typical ligament .

However , because it is a complex, soft connective tissue

providing continuity between two mineralized tissue

(cementum and bone).

Width variable = average 0.15 mm– 0.38mm.

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Age in years

Width

11-16 0.21mm

32-52 0.18mm

51-67 0.15mm

PERIODONTAL LIGAMENT DECREASES WITH AGE(TENCATE 6TH EDITION)

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SYNONYMS OF PERIODONTAL LIGAMENT

1. Desmondont

2. Pericementum

3. Dental Periosteum

4. Alveolodental ligament

5. Periodontal membrane

(PERIO 2000 volume 3)

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EVOLUTION Reptiles have ankylosed teeth.

During the period of transition following changestakes place :

a. Size of jaw decreased

b. Change in articulation of jaw

c. Change in size and shape of the teeth

(ORBANS TEXTBOOK 13TH EDITION)

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DEVELOPMENT

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DEVELOPMENT OF PERIODONTAL LIGAMENT

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Development of periodontal ligament begins with root

formation ,prior to the tooth eruption. Continuous proliferation

of internal and external epithelium forms cervical cusp of tooth

bud. Sheath of epithelial cells grows apically in form of

HERTWIG’S ROOT SHEATH.

(Jan Lindhe 5th edition and Berkovitz 2nd edition)

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Sheath forms a circumferential structure enclosing dental

papilla separating it from the dental follicle cells. Dental follicle

cells located between alveolar bone and epithelial root sheath

composed of two cells:

A. mesenchymal cells of dental follicle proper

B. proliferative mesenchyme

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Mesenchymal cells of perifollicular mesenchyme bounded bydental follicle proper & developing alveolar bone is stellateshaped. Cells are widely separated & contain euchromaticnucleus, very little cytoplasm, short cisternae of roughendoplasmic reticulum, mitochondria, free ribosomes.

As the root formation continues cells in perifollicular area gaintheir polarity and cellular volume & synthetic activity increases.These cells become elongated & contain increased amount ofROUGH ENDOPLASMIC RETICULUM, mitochondria &active Golgi complex. As a result actively synthesize collagenfibrils

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DEVELOPMENT OF PRINCIPAL FIBERS

Immediately before tooth eruption active fibroblasts adjacent to

cementum of coronal third of root aligned in oblique direction to

long axis of the tooth. Soon thereafter the First collagen fiber

bundles of ligament become discernible and these are the

precursor of alveolar crest fiber bundles.

Further apically organized fibers are not seen but examination of

root surface at higher magnification reveals fine brush like fibers

extending from cementum.

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Similar fibers are observed on the adjacent osseous surfaces of

the developing alveolar process . Both set of fibers cemental

and alveolar continue to elongate towards each other ultimately

to meet intertwine and fuse.

By the time first occlusal contact of the tooth with its

antagonist the principal fibers around the coronal third of root

the horizontal group are almost completely developed.

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Oblique fibers in the middle of the root still being formed as

eruption continues & definite occlusion is established there is

progressive apical migration of oblique fiber bundles. With the

formation of apical fiber group definite periodontal architecture

is established.

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Development….

Fig 2 Fig 1 Fig 3

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DEVELOPMENT OF CELLS

Prior to the root formation cells of follicle show very feworganelles. With onset of root formation organelles in cellsincrease, collagen & ground substance formation begins &fills in extracellular space.

Stem cells which give rise to cementoblasts, osteoblasts &fibroblasts in perivascular location. Osteoclasts appear atthe alveolar bone surface allowing remodeling of bone inassociation with tooth eruption.

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PERIODONTAL LIGAMENT

HOMEOSTASIS

Studies have indicated that population of the cells of

periodontal ligament both during development and

regeneration secrete molecules that can regulate the extent

of mineralization and prevent the fusion of the tooth root

with surrounding bone (ankylosis).

Various molecules have been proposed which play a role in

maintaining an unmineralized periodontal ligament.

MSX2 prevents osteogenic differentiation of periodontal

ligament fibroblasts by repressing RUNX2(RUNT RELATED

TRANSCRIPTION FACTOR 2)also known as cbfa1(core

binding factor alpha1)

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Balance between activities of bone sialoprotein and osteopontin

also contributes towards maintaining an unmineralized

periodontal ligament region.

MATRIX ‘GLA’ protein an inhibitor of mineralization is also

present in periodontal ligament. It plays a role preserving

periodontal ligament region.

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RGD-CEMENTUM ATTACHMENT PROTEIN a collagen

associated protein play a role in maintaining the unmineralized

state of periodontal ligament.

TGF-BETA isoforms synthesized by periodontal ligament cells

can induce mitogenic effects and also downregulate osteoblastic

differentiation of periodontal ligament cells.

Prostaglandins which are also produced by the periodontal

ligament cells can inhibit mineralized bone nodule formation and

prevent mineralization by periodontal ligament cells in vitro

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The periodontal ligament has the capacity to adapt to functional

changes, when functional changes increase width of periodontal

ligament increases as much as by 50% and fiber bundles also

increases its thickness.

A reduction in function leads to narrowing of the ligament and

decrease in number and thickness of fiber bundles.

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PERIODONTAL LIGAMENT:

EXTRACELLULAR

CELLULAR

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EXTRACELLULAR STRUCTURES

Collagen Proteoglycans

Elastic Glycoproteins

RETICULAR Glycosaminoglycan's

INDIFFERENT FIBER PLEXUS

OXYTALAN

FIBERS GROUND

SUBSTANCE

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PERIODONTAL FIBERS

Most important elements of periodontal ligament arethe principal fibers which are collagenous & arrangedin bundles & follow a wavy course when viewed inlongitudinal section.

Terminal portions of principal fibers are inserted intocementum called SHARPEY’S FIBERS. It forms acontinuous anastomosing network b/w tooth andbone.

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Sharpey’s fibers are abundant non collagenous proteins found in

bone and cementum among these are OSTEOPONTIN AND

SIALOPROTEIN(regulators of mineralization).

Collagen is protein of different amino acids most important are

GLYCINE,

PROLINE,HYDROXYPROLINE,HYDROXYLYSINE.

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1.Mesenchymal Cells & Their Derivatives

FIBROBLASTS ( major cells )

Chondrocytes

Osteoblasts

Odontoblasts

CEMENTOBLASTS

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COLLAGEN

It is a protein – most abundant protein in animalkingdom.

Derived from – Greek – kolla(glue) and gene.- French – glue producing constituents.

Rigid, rod-like structure-resists stretching and fibers madeof collagen have high tensile strength.

Also participates in biologic functions-cell shape,differentiation.

It is an important constituent of PDL where mechanicalforces must be transmitted without loss

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SEQUENCE OF EVENTS

A. Sequence of intracellular collagen biosynthesisAssembly pro-alfa chains (directed by specific mRNAs)

Proline hydroxylation

Lysine hydroxylation

Hydroxylysine glycosylation

Disulphide bond formation/incorporation of C Terminal Propeptides.Secretion

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several enzymes are involved in the destruction of matrix

components collage breakdown is mediated primarily by

the COLLAGENASES ( Type of MMP) These are

specialized enzymes that have evolved specifically to

hydrolyze collagens ,because their triple helical collagen

structure is resistant to most common proteinases.

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Fibroblasts are responsible for theproduction of the extracellular matrixcomponents.They reside in close proximity to thecollagen fibers.The nucleus appears as an elongated or disklike structure in H & E preparations. Thethin, pale staining, flattened processes thatform the bulk of the cytoplasm are usuallynot visible.

Myofibroblast is an elongate, spindle

connective tissue cell that displays typical

characteristics of the fibroblast along with

characteristics of smooth muscle cells

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Sequence of extracellular collagen biosynthesis

Amino terminal extension cleavage (procollagen aminopeptidase)

Carboxyl terminal extension cleavage ( procollagen carboxypeptidase)

formation of collagen fibrils and spontaneous arrangement of fibrils

cross link formation by the action of lysyl oxidase enzyme,deamination of lysyl

residues and maturation of cross-links. Growth and reorganization of fibers.

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CHARACTERISTIC FEATURES OF COLLAGEN1)Triple helical structure- alfa chains-left handed helices.The triple helix may be continuous/interrupted by non-collagenous segments.

2)Within triple helical domain, glycine –every 3rd

position in the amino acid sequence Gly-X-Y,where X , Y –amino acids other than glycine.(Proline)

3) Contains 2 unique amino acids- Hydroxyproline andHydroxylysine.

4)Collagen is stabilized through formation of Lysine-derivedintra- and intermolecular cross-links.

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COLLAGEN TYPES

So far 19 types of collagen have been discovered.

Collagen classes

a. Interstitial collagens ---- Type I,II,III

b. Basement membrane type ---- Type IV,VI,VII

c. Short chain collagens ---- Type IX,X

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Based on their ability to form fibrils, collagens are of 3 groups:

-FIBRIL-FORMING : triple helix has uninterrupted stretch of Gly-X-Y

residues. Includes types 1,2,3,5,11.

-FACIT : (Fibril Associated Collagens with Interrupted Triple helices)-collagenous domains interrupted by non-

collagenous sequences. Includes Types 9,12,14(contains GAG) and may be16

-NON-FIBRILLAR: Forms sheets/membranes enclosing tissues andorganisms.

Types 4,8,10- Network forming

Type 6-Beaded

Type 7-Anchoring fibrils

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Collagen is responsible for maintenance of frameworkand tone of tissue biosynthesis of collagen insidefibroblasts to form procollagen molecules. It has atransverse striations with characteristic periodicity of64nm. These striations are caused by overlappingarrangement of tropocollagen molecules.

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Collagen is gathered to form bundles approximately 5micrometers in diameter. These bundles are calledPRINCIPAL FIBERS. within each bundle subunits arepresent called COLLAGEN FIBRILS.

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Type I, III, V, XII – Periodontal Ligament

Type VI, II – cartilage

Type IV - Basement membrane

Type VI – Ligaments, skin, bone

Type VII - Anchoring fibrils of basement

membrane

Type IX - Cartilage

Type X, XI - Cartilage, Bone

Type XIII - Epidermis Cartilage

Collagen is synthesized by fibroblasts , chondroblasts ,osteoblasts, odontoblasts and other cells.

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Principal fibers composed of mainly TYPE I

RETICULAR FIBERS COMPOSED OF TYPE III

BASAL LAMINA COMPOSED OF TYPE IV

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TYPES OF COLLAGEN FIBERS TYPE I – SKIN,TENDON, VASCULAR

LIGATURE,ORGANS,BONE

TYPE II – CARTILAGE

TYPE III – RETICULAR

TYPE IV – FORMS BASAL LAMINA

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TYPE V – CELL SURFACES , HAIR AND PLACENTA

TYPE VI – SUBSTANCE FOR CELL ATTACHMENT & AS AN ANCHORING MESHWORK THAT CONNECTS COLLAGEN FIBERS , NERVES & BLOOD VESSELS TO SURROUNDING MATRIX.

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TYPE VII – ACTS AS AN ANCHORING FIBRILS.

TYPE XII – ASSOCIATED WITH TOOTHDEVELOPMENT,ALIGNMENT, ORGANIZATION OFPERIODONTAL FIBERS.

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NON-COLLAGENOUS PROTEINSFIBRONECTIN:-2 forms-soluble plasma form(pFN) & cross-linked fibrillar

form in most tissues (cellular/cFN) .

-Functions: -Within matrix, bridge between cells & collagen-(cell adhesion, migration)

-Has specific domains to bind to Heparin, fibrin,collagen hence role in matrix

assembly & stabilization-Reservoir for cytokines, growth factors.

-In wounds, it’s a chemotactic, helps to clear fibrinfrom inflamed sites.

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LAMININ In embryonic tissues-the first extracellular protein detected &

in mature tissues –universally found as the major noncollagen component in basement membranes.

-Involved in cell attachment, cell proliferation and cell differentiation .

-Has domains for the attachment of cells, heparin ,elastin,

type IV collagen , nidogen,entactin and galactoside-binding lectins.

- Associated with cell rests of Malassez of PDL.

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OSTEOCALCIN / BONE Gla ProteinOsteocalcin is a small protein –odontoblasts & osteoblasts .

-Osteocalcin is highly specific for calcified tissues.

-The post-translational vitamin K dependent carboxylation ofglutamic acid residues allows the osteocalcin molecule tobind calcium .

- The molecule undergoes a conformational shift

when associated with hydroxyapatite.

-Serum osteocalcin levels correlates with histomorphometricanalysis of new bone.

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BONE SIALOPROTEIN (BSP II)

Major structural protein of bone matrix, expressed byfully differentiated osteoblasts.

-15% of non-collagenous proteins.

-Found in reversal lines of rapidly remodeling bone

-Expressed by cementoblasts during cementogenesis &also during early formation of dentin

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OSTEOPONTIN

High content –serine,asparagine,glutamate.

-Found primarily in bone & several nonskeletal tissues (thecentral nervous system, kidney and placenta).

-In bone, the synthesis and release of Osteopontin by osteoblasts -endocrine (calcitriol, corticosteroids, and parathyroid hormone)and paracrine(TGF) control.

-Functions not clear-proposed that Osteopontin is involved inboth the attachment and movement of osteoblasts andosteoclasts in bone via integrin mediated cell binding.

- implicated in calcium regulation

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HOW OSTEOPONTIN HELPS IN

MINERALIZATION??

In native bone tissue 10-30% of the tissue mass is proteinaceous and the

remaining 70-90% is comprised of calcium phosphate mineral, which is

primarily hydroxyapatite (HA).

The protein component of bone has been shown to be ∼90% collagenous,

while the remaining 10% of the protein content is believed to play a role in

bone formation, growth, repair, and cellular adhesion to the matrix.

The primary group of non-collagenous proteins found in bone are the SIBLING (small integrin-binding ligand, N-linked glycoprotein) family of proteins and they are believed to play a key role in these processes.

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Continuation…….

The SIBLING family of proteins consists of five members: osteopontin (OPN),

matrix extracellular phosphoglycoprotein (MEPE), bone sialoprotein (BSP),

dentin matrix protein 1 (DMP1), and dentin sialophosphoprotein (DSPP).

The SIBLING proteins have a number of shared characteristics including a

collagen binding domain, a HA binding domain, and a cell binding arganine-

glycine-aspartic acid (RGD) sequence. Additionally, they are all located on the

same human chromosome (4q21)

all of the proteins are post-translationally phosphorylated and have been immunolocalized in mineralized tissues.Together, these characteristics suggest that the SIBLING family of proteins play an important role in bone development by facilitating cellular adhesion, mineral nucleation, and mineral maturation.

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MEPE has been shown to be a potent inhibitor of mineralization both in

vitro and in vivo and therefore is not expected to play a role in the induction of

biomineralization.

DMP1 is believed to regulate the mineralization process, possibly mediating

the transformation of amorphous calcium phosphate to crystalline HA.

OPN has been shown to either inhibit or induce mineralization based on its

phosphorylation state, but most likely regulates the mineralization process in

bone.

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SPARC / OSTEONECTIN

-SPARC: Secreted protein acidic and rich in cysteine.

-Found in greatest abundance in osseous tissue, tissuescharacterized by high turnover ,basement membranes .

-Osteonectin is expressed -chondrocytes,fibroblasts, platelets,endothelial cells, epithelial cells, Leydig cells, Sertoli cells,adrenal cortical cells and numerous neoplastic cell lines.

-Functions- mineralization of bone and cartilage-inhibiting mineralization.-modulation of cell proliferation.-anti adhesive, disrupts focal adhesion in fibroblasts.

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TENASCIN/CYTOTACTIN

-Star shaped structure with central knot.

-Binds to fibronectin, chondrointin sulphate.

-Mediates both adhesive & repulsive interactions.

-Detected in attachment zone of periodontal ligament atinterface between mineralized & non mineralized tissues.

-Role in wound healing, tumourogenesis and cell migration.

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NIDOGEN/ ENTACTIN

-Dumb bell shaped with 2 globular domains.

-Crucial role in basement membrane organization & stabilization.

-Interacts with both cell surface proteins & extra cellular matrix proteins.

-Binds to laminin & type 4 collagen

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PERIODONTAL LIGAMENT FIBERS

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ARRANGED IN 6 GROUPS TRANSSEPTAL

OBLIQUE

INTERRADICULAR

APICAL

ALVEOLAR CREST

HORIZONTAL

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TRANSSEPTAL FIBERS:

Extend interproximally over alveolar crest and are embedded in cementum of adjacent tissue.

Reconstructed even after destruction of alveolar bone resulting from periodontal disease.

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ALVEOLAR CREST GROUP:

Extend obliquely from cementum just beneath cementoenamel junctional epithelium to alveolar crest.

Fibers also run from cementum over the alveolar crest & to the fibrous layer of periosteum covering the alveolar bone.

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These fibers RESIST TILTING, INTRUSIVE, EXTRUSIVE, ROTATIONAL FORCES.

It is often confused with the dentoperiosteal groups of fibers.

Any collagenous fibers located apical to the line joining the height of the each interdental bony septum termed as periodontal and those coronal to the line is gingival.

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HORIZONTAL GROUP:

These fibers run at right angles to the long axis of the tooth from cementum to alveolar bone and parallel to the occlusal plane of the arch.

Found immediately apical to the alveolar crest group. These fibers pass from their cemental attachment directly across the periodontal ligament space to become inserted in alveolar process as sharpey’s fibers .

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Limited to the coronal one- fourth of periodontal ligament space.

These fibers RESIST HORIZONTAL AND TIPPING FORCES.

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OBLIQUE GROUP:

These are the most numerous and occupy nearly 2/3rd of the ligament.

Inserted into the alveolar bone at a position coronal to their attachment to cementum resulting in their oblique orientation within periodontal space. RESIST VERTICAL AND INTRUSIVE FORCES

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APICAL GROUP :

From cementum at the root tip , fibers of the apicalbundles radiate through the periodontal space tobecome anchored into the fundus of bony socket.

RESIST FORCES OF LUXATION, PREVENT TOOTHTIPPING & PROTECT DELICATE BLOOD AND LYMPHVESSELS AND NERVES TRAVERSING PERIODONTALLIGAMENT SPACE AT ROOT APEX.NOT SEEN ININCOMPLETE FORMED ROOTS.

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INTERRADICULAR GROUP:

Principal fibers of this group are inserted into thecementum from crest of interradicular septum inmultirooted tooth.

RESIST TOOTH TIPPING , TORQUING ANDLUXATION.

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These fibers are lost if age related gingival recession proceeds to the extent that the furcation area is exposed. Total loss of these fibers occur in chronic inflammatory periodontal disease.

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Some author consider GINGIVAL FIBER GROUP to be part of the principal fibers of the periodontal ligament.

The gingival fiber groups are found within the lamina propria of marginal gingiva. These gingival fibers are separate but adjacent fiber groups which support the marginal gingival tissues to maintain the relationship of the teeth.

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SHARPEYS’ FIBERS ;

Collagen fibers are embedded into the cementum on one side of the periodontal space & into the alveolar bone on the other.

The embedded fibers are called SHARPEY’S FIBERS.

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These are the most numerous but smaller at their attachment into cementum than alveolar bone. The mineralized parts of the sharpey’s fibers in alveolar bone proper appear as projecting stubs covered with mineral clusters.

The mineralization is at right angles to long axis of fibers, indicating that fibers are subjected to tensional forces.

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Sharpey’s fibers in primary acellular cementum aremineralized fully those in cellular cementum and boneare mineralized partially at their periphery.

Few Sharpey's fibers pass uninterruptedly through thebone of alveolar process termed (TRANSALVEOLARFIBERS)to continue as principal fibers of adjacentperiodontal ligament or mingle buccally or linguallywith fibers of periosteum that cover the outer plates ofalveolar process.

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These fibers pass through the alveolar process only when process consists entirely of compact bone and contains no haversian system.

Once embedded in either the wall of alveolus or the tooth Sharpey’s fibers calcify to certain degree & are associated with abundance of non collagenous proteins namely OSTEOPONTIN AND BONE SIALOPROTEIN.

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INTERMEDIATE PLEXUSES :

It was believed that principal fibers frequently followed a wavy course from cementum to alveolar bone and are joined in the mid region of periodontal space giving rise to a zone of distinct appearance called INTERMEDIATE PLEXUSES

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The plexuses was considered to be an area of high metabolic activity in which splicing and unsplicing of fibers might occur. Studies have indicated that once cemental fibers meet and fuse with the bone no such plexuses remains.

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ELASTIC FIBERS :

There are three types of elastic fibers which are histochemically and ultrastructurally different.

They are :

MATURE ELASTIC FIBERS

ELASTIN FIBERS

ELAUNIN FIBERS

OXYTALAN FIBERS

(BERKOVITZ 2ND edition)

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MATURE ELASTIC FIBERS:

Consist of microfibrillar component surrounding an amorphous core of elastin protein. Elastin protein contains high percentage of GLYCINE,PROLINE , HYDROPHOBIC RESIDUES with LITTLE HYDROXYPROLINE & NO HYDROXYLYSINE.

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Microfibrillar component is located around the periphery & scattered throughout the amorphous component.

These fibers are observed only in walls of different blood vessels where they constitute the elastic laminae of larger arterioles and arteries of greater caliber.

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ELAUNIN FIBERS :

These are seen as bundles of microfibrils embedded in a relatively small amount of amorphous elastin.

These fibers found within the fibers of gingival ligament. An elastic meshwork has been described in pdl as being composed of many elastin lamellae with peripheral oxytalan fibers and elaunin fibers .

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OXYTALAN FIBERS:

It is a type of immature elastic fibers, consist of microfibrillar component only.

It forms a three dimensional meshwork that extends from cementum to peripheral periodontal blood vessels. The meshwork is largely oriented in apico-occlusal plane & interconnected with fine lateral fibrils.

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Depending on site & species oxytalan fibers measures between 0.2 -1.5 micrometer in diameter in electron microscope and occupy 3% pdl in humans.

In contrast in light microscopy they measure 0.5 – 2.5 micrometer in diameter.

These fibers are not susceptible to acid hydrolysis .

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Orientation of oxytalan fibers is completely different when compared to the other collagen fibers.

Instead of running from bone to cementum they run in axial direction. One end being embedded in cementum or bone and other end in wall of blood vessel.

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In the cervical region they follow the course of gingival and trans septal fibers. Within the periodontal ligament proper, these fibers are longitudinally arranged, crossing the oblique fibers perpendicularly. In the vicinity of the apex they form a complex network.

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Function of oxytalan fibers is unknown but it has been suggested that they may a play a pivotal role in supporting the blood vessels of periodontal ligament.

They are thicker and more numerous in teeth subjected to high loads as in orthodontic tooth movement. Thus, these fibers play a role in tooth support.

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RETICULAR FIBERS:

These are fine immature collagen fibers with argyrophilic staining properties and are related to basement membrane of blood vessels and epithelial cells which lie within the periodontal ligament. These fibers are composed of TYPE III collagen.

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SECONDARY FIBERS:

These are located between and among the principal fibers.

These fibers are relatively non directional and randomly oriented.

Represent newly formed collagenous elements that have not yet incorporated into principal fiber bundles.

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These fibers traverse the periodontal ligament space corono-apically and are often associated with paths of vasculature and nervous elements.

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INDIFFERENT INTERMEDIATE PLEXUSES :

Small Collagen fibers in association with the larger principal collagen fiber

Run in all directions forming a plexus

Described by Shackleford, 1971

Once the tooth has erupted into clinical occlusion such an intermediate plexus is no longer demonstrable

Intermediate plexus has been reinterpreted by Sloan as representing merely an optical effect explained entirely by the arrangement of middle layer collagen into sheets rather than bundles.

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Small collagen fibers associated with large principal collagen fibers have been described.

These fibers run in all directions forming a plexus called INDIFFERENT FIBER PLEXUSES.

Some studies reported this plexuses seen in ground section examined under scanning electron microscope but not under transmission electron microscope. Hence, some authors consider it to be an artifact.

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continuation of indifferent fiber plexuses:

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CELLS OF PERIODONTAL LIGAMENT The principal cells of healthy, functioning periodontal

ligament are concerned with the synthesis andresorption of alveolar bone and fibrous connective ofthe ligament and cementum . The cells of the PDLmay be divided as -

Synthetic cells

Resorptive cells

Cells rests of malassez

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FIBROBLASTS:

The fibroblasts is the predominant cell in the pdl . Thesefibroblasts origin in part of from the ectomesenchyme ofinvesting layer of dental papilla and from the dental follicle .Pdl contains a fibroblasts cell populations with differentfunctional characteristics .

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These fibroblasts are regularly distributed throughout theligament and are oriented with their long axis parallel tothe direction of collagen fibrils .

Fibroblasts of pdl generate an organizational pattern asthey have ability to both synthesize and shape the proteinsof the extracellular matrix in which collagen fibrils formbundles that insert into tooth and bone as SHARPEY’Sfibers .

Once embedded in the wall of alveolus or tooth ,these fibers calcify to a certain degree and are associatedwith an abundance of non collagenous proteins found inthe bone i.e. osteopontin and bone sialoprotein .

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Difference b/w periodontal and gingival fibroblasts

Periodontal ligament fibroblasts are ectomesenchymalin origin whereas gingival fibroblasts are mesodermalin origin.

Expression of alkaline phosphatase & cyclic AMP ismore in periodontal ligament fibroblasts. Gingivalfibroblasts are less proliferative.

Periodontal ligament fibroblasts can generate force fortooth eruption as they are motile and contractile

Fibroblasts of pdl are capable of collagen degradation.

(Orban’s textbook of histology 13 th edition)

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OSTEOCLASTS • These cells covering the periodontal surface of the alveolar

bone constitute a modified endosteum and not a periosteum .

• A cellular layer but not an fibrous layer is present on the

periodontal surface of the alveolar bone . The surface of the

bone is covered largely by osteoblasts as well as by occasional

osteoclasts .

• These are the cells lining the tooth socket and are cuboidal in

shape with a prominent round nucleus at the basal end of the

cell .

• These cells appear basophilic due to the presence of abundant

rough endoplasmic reticulum . The cells contact one another

through desmosomes and tight junctions .

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CEMENTOBLASTS Its distribution is similar to that of osteoblasts on the

bone surface . These cells line the surface of cementum. They are cuboidal with a large vesicular nucleus ,with one ore more nucleoli and abundant cytoplasm.

All the organelles are required for protein synthesisand secretion are present . Cells actively depositingcellular cementum exhibit abundant basophiliccytoplasm and cytoplasmic processes

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RESORPTIVE CELLS

OSTEOCLASTS : - These resorb bone and tend tobe large and multinucleated but can also be small andmononuclear . Multinucleated osteoclasts are formedby fusion of precursor cells similar to circulatingmonocytes.

These when viewed in light microscope are cellsoccupy bays in bone or surround end of bone spicule .

The part of plasma membrane lying adjacent to bonethat is being resorbed is raised in characteristic foldsand is termed the ruffled or striated border.

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The ruffled border is separated from the rest of plasma membrane by a zone of specialized membrane that is closely applied to the bone the underlying cytoplasm of which tends to be devoid of organelles and has been called the clear zone .

The area of bone that is sealed off by virtue of active pumping of protons by the osteoclast into this environment .

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FIBROBLASTS: - These cells show rapid degradation of collagen by fibroblast phagocytosis and is the basis for fast turnover in periodontal ligament . Collagen degradation was an extracellular event involving the activity of the enzyme collagenase .

Intracellular collagen profiles are organelles present . These are associated with the degradation of collagen that has been ingested from extracellular environment . Some studies suggested that collagen degradation is intracellular .

The extracellular elements in degradation of collagenase involve Collagenase which cleaves the triple helical portion of molecules within the fibrils .

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INTRACELLULAR DEGRADATION - Fibroblasts arecapable of phagocytosing collagen fibrils from extracellularenvironment and degrading them inside phagolysomalbodies . Collagenase is not involved in the intracellularphase of degradation of collagen fibrils .

CEMENTOCLASTS: - These resemble osteoclasts andsometimes found in normally functioning periodontalligament . Cementum is not remodeled in the fashion ofalveolar bone and periodontal ligament . Its origin isunknown bit it is conceivable that they arise in the samemanner as osteoclasts .

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PROGENITOR CELLS : - All connective tissues includingperiodontal ligament contain progenitors for synthetic cells thathave the capacity to undergo mitotic division .

If they were not present there would be no cells available to replacedifferentiated cells lying at the end of their life span or as a result oftrauma.

These cell populations within the ligament appear to be in highestconcentrations in locations adjacent to blood vessel and exhibitsome of the classical cytological features .

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Epithelial rests of malassez

The ligament contains epithelial cells that are found closeto the cementum . At the time of cementum formation thecontinuous layer of epithelium that covers the surface ofnewly formed dentin breaks into lacelike stands . Theepithelial rests persist as a network stands islands ortubelike structures near and parallel to the surface of theroot .

Their function is not clear but they could be involved inperiodontal repair and generation .

These cells rests can be distinguished from fibroblasts inpdl by the close packing of their cuboidal cells and theirnucleus stains more deeply . They are more numerous inolder individuals and more numerous in children . Thesecells may proliferate to form cysts and tumors. These cellsmay undergo calcification to become CEMENTICLES.

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DEFENCE CELLS

MAST CELLS – These are relatively small round or oval cell having a diameter of about 12 to 15 um . Mast cells are often associated with blood vessels . These cells are characterized by numerous cytoplasmic granules which frequently obscure the small , round nucleus .

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Mast cells histamine plays a role in the inflammatoryreaction and have been shown to de granulate in response toantigen – antibody reaction on their surface .

The release of histamine into the extracellular environmentcauses proliferation of endothelial cells and mesenchymalcells .

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MACROPHAGES- These are found in the ligament and are predominantly located adjacent to blood vessels . The wandering type are derived from blood monocytes has a characteristic ultrastructure that permits it to be readily distinguished from fibroblasts .

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EOSINOPHILLS – These are seen in the periodontal ligament . They posses granules that consist of one or more crystalloid structures . These are capable of phagocytosis

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GROUND SUBSTANCE Ground substance composed of glycoproteins and

proteoglycans . Ground substance has been estimated to contain 70 % water and is thought to have a significant effect on the tooth ‘s ability to withstand stress loads .

Ground substance is a gel like matrix in which are embedded the cellular components such as collagen . Berkovitz et al estimated that ground substance accounted for 65 % of the volume in the pdl

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All anabolites reaching the cells from the microcirculation in the ligament and all catabolites passing in the opposite direction must pass through the ground substance . Its integrity is essential if the cells of ligament are to function properly

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The ground substance consists of mainly ofhyaluronate , glycosaminoglycans , proteoglycans andglycoproteins . All components are presumed to besecreted by fibroblasts .

Proteoglycans are compounds containing anionicpolysaccharides covalently attached to a protein .

Glycosaminoglycans are linear polymers ofdisaccharide repeat sequence which contains ahexosamine,,heparin sulfate and hexuronic acid .

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Substrate adhesion molecules such as tenascin ,osteonectin , laminin , undulin , and fibronectin have beenidentified in pdl .

INTERSTITIAL TISSUE

Some of blood vessels , lymphatics , and nerves of the pdlare surrounded by loose connective tissue and can be readilyrecognized in light microscope .

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STRUCTURES PRESENT IN CONNECTIVE TISSUE

The following discrete structures are present in connective tissue of pdl

Blood vessels

Lymphatics

Nerves

Cementicles

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The blood supply to the periodontal ligament are derived from three sources:

-Branches from apical vesselssupplying the dental pulp.

-Branches from intra-alveolar vessel, runs horizontally through nutrient canals.

-Branches from gingival vessels, enter the PDL from the coronal direction.

BLOOD SUPPLY OF PERIODONTAL LIGAMENT

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-Vessels form basket-like network.

-Runs parallel to long axis of tooth between the principle fibres.

-Main supply: SUPERIOR & INFERIOR ALVEOLAR artery- intraostealcourse – gives alveolar branches ascending within the bone.

-Branches then run horizontally, penetrating alveolar bone and then PDL. Hence called PERFORATING ARTERIES.

-Maximum in mandible & maximum in posterior teeth.

-Single rooted teeth-more in the gingival third followed by apical third.( Significant in wound healing).

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The interradicular arteries branch into vessels of lesser caliber to emerge from the cribiform plate as perforating arteries and supply the pdl along most of the coronoapicalextent including the bifurcation and trifurcation arteries .

The interdental artery also exit the bone to supply the middle three fifth of the pdl though most of the interdental arteries emerge from the crest of the alveolar process and supply the coronal aspect of pdl .

The pdl has some specialized features in the vasculature namely the presence of large number of fenestrations in the capillaries and a cervical plexus of capillary loops .

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124

Alignment of alpha chains by formation of disulphide bonds at C-terminal ends

Formation of collagen alpha chains

Hydroxylysine residues are glycosylated by addition of galactosein the presence of galactosyltransferase

Hydroxylation of proline and lysine residues by vitamin C-dependent enzyme prolylhydroxylase and lysylhydroxylase

Translocated into lumen of RER for post-translational modifications

Initial polypeptides formed (one and a half times longer than final collagen molecule as they have N- and C- terminal extensions)

m-RNA directs specific amino acids into polypeptide chains on ribosomes associated with RER

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VENOUS DRAINAGE- The venous channels accompanying their arterial counterparts . The channels are larger in diameter with mean average of 28 um . These channels receive blood from the capillary network and also specialized shunts called glomera in the pdl . These shunts provides an arteriovenous anastomosis .

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LYMPHATIC DRAINAGE - A network of lymphatic vessels following the path of the blood vessels , provides the lymph drainage of the pdl . The flow is from the ligament toward and into the adjacent alveolar bone .

It may course apically through the substance of pdl to arise and pass through the fundus of the socket or may through the cribiform plate . They finally enter into larger channels after pursuing intraosseous path .

The flow is via the alveolar lymph channels which are joined by the dental and interrradicular lymph channels

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NERVES – The pdl has functionally two types of nerve fibers sensory and autonomic . The sensory fibers are associated with nociception and of mechanoception , with touch , pressure , pain and proprioceptive sensations . The autonomic fibers are associated with pdl vessels .

All pdl innervations are mediated by the dental branches of alveolar nerves which enter through apical perforation of the tooth socket and perforating branches of interalveolar nerves traversing the bone .

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INNERVATION OF LIGAMENT

According to Tencate:

There are 3 patterns of nerve innervation

i)general anatomic configuration

ii)regional variation in termination of neural elements

iii)types of neural terminations.

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ANATOMIC CONFIGURATION

-Nerve fibres run from apical region towards gingival margin.

-They are joined by fibers entering laterally through the foramina of the socket wall.

-They divide into branches -one extending apically -the other gingivally .

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-Nerve bundles divide into single myelinated fibers-then lose their myelin sheaths and end in one of the

4 neural terminations:

Free endings-tree like configuration: pain sensation Ruffini-like mechanoreceptors: primarily in apical area coiled Meissner’s corpuscles: mechanoreceptors

found in mid-root region

Spindle-like pressure and vibration endings: surrounded by fibrous capsule, located

mainly in apex.

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REGIONAL VARIATION

Apical region –more nerve endings.

-Maxillary incisors-more innervated than molars.

-Dense distribution also seen in coronal half of labial PDL and also apically

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TYPES OF NEURAL TRANSMISSION

4 types- BYERS,1985

a)Tree –like pattern:

-most frequent type

-along root length

-free nerve endings in tree like pattern.

-originate mostly from unmyelinated nerve fibres

- they carry Schwann cell envelope & processes projecting into surrounding CT.

- Endings carry-mechanoreceptors & noci receptors

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RUFFINI CORPUSCLES Found at the root apex.

-Appears dendritic .

-Ends in terminal expansions among fiber bundles.

-Electron microscopic study -i) simple receptors – single neurite

ii) compound receptors- several terminations.

-Both have ensheathing schwann cells that are especially close to collagen fiber bundles

-Mechanoreceptors.

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COILED MEISSENER’S CORPUSCLES

• -Nerve terminal in coiled form

• -Found in the mid region of the PDL.

• -Function and the ultra structure- not yet determined.

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SPINDLE LIKE ENDINGS

Lowest frequency.

-Found associated with the root apex

-Consists of the spindle like endings surrounded by fibrous capsule.

-Said to sense pressure & vibration.

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Nerves which usually are associated with blood vessels pass

through foramina in the alveolar bone including the apical

foramen to enter the pdl . In the region of apex apex they run

toward the cervix whereas along the length of root they branch

and run both coronally and apically .

Nerve fibers are either of large diameter and myelinated or

small diameter in which case they may or not be myelinated .

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The pdl is abundantly supplied with sensory nerve fibers capable of transmitting tactile pressure and pain sensations by the trigeminal pathways . Nerve bundles pass into pdl from the periapical area and through channels from the alveolar bone that follow the course of the blood vessels .

The bundles divide into single myelinated fibers which ultimately loose their myelin sheath and end in one of four types of neural termination

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CEMENTICLES - Calcified bodies called cementicles , sometimes found in the pdl . These bodies are seen in older individuals and they may remain free in the connective tissue and may fuse into large calcified masses or they may be joined with the cementum . As the cementum thickens with advancing age it may envelop these bodies . When they are adherent to the cementum they form excementoses. The origin of these calcified bodies is not established . It is possible that degenerated epithelial cells form the nidus for their calcification .

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MECHANISM OF SHOCK ABSORPTION

TENSIONAL THEORY

Principal fibers of the PDL are the major factor in supporting the

tooth and transmitting forces to the bone.

When forces are applied to tooth, principal fibers unfold and

straighten and then transmit the forces to alveolar bone, causing

elastic deformation of socket.

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Force applied to crown

Principles fibres first unfold and straighten

Transmit forces to alveolar bone(causing elastic deformation of the bony socket)

Once alveolar bone reaches its limit , load is transmitted to basal bone

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A. Tooth in a resting state

B. The periodontal ligament fibers are

compressed in areas of pressure and

stretched in area of tension.

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VISCOELASTIC THEORY

• According to it, the fluid movement largely controls the

displacement of the tooth, with fibers playing a secondary role.

• When forces are transmitted to the tooth, the extracellular fluid

is pushed from periodontal ligament into marrow spaces

through the cribriform plate.

• After depletion of tissue fluids, the bundle fibers absorb the

shock and tighten.

• This leads to blood vessel stenosis arterial lack pressure

ballooning of vessels tissue replenishes with fluids.

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THIXOTROPIC GEL THEORY

PDL fluid acts as a gel.

-When pdl fibers are disturbed the gel which is present between pdl fibers becomes fluid

-Forces on tooth gel to fluid.

-Removal of forces fluid to gel.

-Helps in shock absorption.

(perio 2000 volume 13,1997)

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TRANSMISSION OF OCCLUSAL FORCES TO BONE

Arrangement of principle fibres is similar to a suspension bridge/hammock

Axial force when applied

Root displaces into the alveolus

Oblique fibres alter their wavy course, assume full length and sustain major part of the axial force.

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When horizontal forces are applied- 2 phases of movements occur.

i)within confines of ligament.

ii)displacement of facial & lingual bony plates.

-Force - tension & pressure areas.

-Tension side - fibres taut.

- Pressure side - fibres are compressed, tooth displaced, distortion of bone in direction of root movement.

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AXIS OF ROTATION

Single rooted teeth: Between the apical and middle third

-In multirooted teeth: Bone between roots

-Compression resorbs

-Tension deposition

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FUNCTIONS OF PERIODONTAL LIGAMENT

Periodontal ligament has following functions:

1.Supportive

2.Sensory

3.Nutritive

4.Homeostatic

5.Eruptive

6.Physical

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SUPPORTIVE

When a force is applied on tooth either by mastication or orthodontic tooth

movement there is compression of pdl and other areas widening of pdl.

The compressed pdl fibers will act as support for the loaded tooth, water

molecules and other molecules bound to collagen act as cushion for

displaced tooth. The pressure of blood vessels also provides a hydraulic

cushion for the support of the teeth.

Load is dissipated to alveolar bone through oblique fibers of pdl when

placed in tension and on release elastic recoil of tissue enables the tooth in

original position.

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SENSORY

Nerve supply of pdl provides most efficient proprioceptive mechanism and

allows to detect the application of the most delicate forces of teeth.

Mechanoprotection protects both supporting structures of the tooth and the

substances of the crown from excessive masticatory forces.

Cortin actin assembly regulates the activity of stretch activated calcium

permeable channels since forces desensitizes channels to force applications.

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continuation

ACTIN BINDING PROTEIN – 280 plays a pivotal role in

mechanoreception by :

a. Reinforcing the membrane cortex and preventing force induced membrane

disruption.

b. Increasing the strength of cytoskeletal links to extracellular matrix

c. Desensitizing stretch activated ion channel activity

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NUTRITIVE:

Ligament contains blood vessels provide anabolites required by the cells of

pdl.

Any extirpation of ligament results in necrosis of underlying cells.

Occlusion of blood vessels leads to necrosis of cells in affected parts of

ligament- when too heavy forces is applied to teeth in orthodontic therapy.

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HOMEOSTATIC:

The cells of pdl have the ability to resorb and synthesize the extracellular

substance of the connective tissue of the ligament , alveolar bone and

cementum .

Alveolar bone appears to be resorbed and replaced at a rate higher than

other tissue in jaws . Furthermore the collagen of pdl is turned over at a

rate that may be the fastest of all connective tissues in the body and the cells

in the bone half of ligament may be more active than those on the

cementum side

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ERUPTIVE

The cells of vascular elements and extracellular matrix proteins

of pdl function collectively enable the teeth to limited eruption

and adjust the position while remaining fibers attach the teeth

firmly to the alveolar bone.

It provides a space and acts as a medium for cellular

remodeling and hence continued eruption and approximal shift

occurs.

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PHYSICAL :

1. Provision of a soft tissue “casing” to protect the vessels &nerves from injury by mechanical forces.

2. Transmission of occlusal forces to the bone.

3. Attachment of the teeth to the bone.

4. Maintenance of the gingival tissues in their properrelationship to the teeth.

5. Resistance to the impact of occlusal forces (shockabsorption

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HOMEOSTATIC MECHANISM

• The resorption and synthesis are controlled procedures.

• If there is a long term damage of periodontal ligament, which is

not repaired, the bone is deposited in the periodontal space.

• This results in obliteration of space and ankylosis between

bone and the tooth.

• The quality of tissue changes if balance between synthesis and

resorption is disturbed.

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• If there is deprivation of Vit. C which are essential for

collagen synthesis, resorption of collagen will continue.

• So there is progressive destruction and loss of extra

cellular substance of ligament.

• This occurs more on bone side of ligament.

• Hence, loss of attachment between bone and tooth and at

last, loss of tooth.

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NORMAL CELL BIOLOGY

The production and destruction of tissue matix ( turnover ) in a

healthy state , involves interaction among a myriad of effector

molecules that are synthesized and secreted by resident cell of

periodontal ligament .

Cytokines are a series of multifunctional polypeptides and

glycoproteins that are secreted by one or several cell types and act

locally or systemically . These includes Interleukins , cytotoxic

factors , interferons , growth factors , colony stimulating factors.

Growth factors have been defined as substances capable of re –

initiating proliferation of cells that are in a quiescent state .

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In vivo cytokines play an important role in numerous biological events , including development , homeostasis , regeneration , repair , inflammation and neoplasia

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1 . Fibroblast growth factors (FGF) - Two of seven isoforms of

fibroblast growth factors have been described in particular one is

acidic and other basic .

Acidic fibroblast growth factors has effects on endothelial cell

replication and neovascularisation . It stimulates dna synthesis

and cell replication , in bone tissue cultures which results in

increased protein synthesis especially type 1 collagen .

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Basic fibroblast growth factors has angiogenicproperties has highly chemotactic and mitogenicfor a variety of cell types . It stimulates bone cellreplication and increases the number of cells ofosteoblastic lineage .

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2 . Platelet derived growth factor ( PGDF ) This factor ispotent growth factor for various connective tissuecells and is released from the a – granules in plateletsin conjunction with blood coagulation .

PGDF is a promoter of cell migration and a potentmitogen for cells bearing PGDF receptors . It actssynergistically with other growth factors as acompetence factor .

PGDF stimulated type v collagen formation and adrop in type III production in gingival fibroblasts .

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Transforming Growth factor ( TGF ) : - Thesefactors are polypeptides from normal andneoplastic tissues which are known to cause achange in normal cell growth . TGF is of 2 types αand b according to relationship to EGF .

TGF – α similar isolated biological effects actingthrough EGF receptor .

TGF – β was originally purified from humanplacenta , platelets and bovine kidney . Itstimulates the synthesis of connective tissue matrixcomponents such as collagen , fibronectinproteoglycan and glycosaminoglycans .

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. Interleukin- 1 ( IL – 1 ) : - Interleukin – 1 is apolypeptide with a great number of roles inimmunity , inflammation , tissue breakdown andtissue homeostasis . It is synthesized by various celltypes including macrophages , monocytes ,lymphocytes vascular cells brain cells skin cells andfibroblasts following cellular activation . 2 types ofIL are known interleukin – 1 α and 1β .

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Interferon – ɤ : - It posses importantimmunomodulatory effect and thus is alymphokine as much as an interferon . Itsproduction is modulated by other cytokines suchas interleukin – 1 . Many biological activities havebeen ascribed to interferon like action on B and Tlymphocytes , antibody production , natural killercells , macrophages and tumour cells .

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Matrix metalloproteinases and theirtissue inhibitors : - Connective tissue cellsparticipate in both the formation and breakdown ofconnective tissue matrix . Such cells are found tosynthesize and secrete a family of enzymes knownas MMP’s .

MMP gene family encodes a total 24homologous proteinases classified into collagenases, gelatinases , stromeolysins , membrane type MMPdepending on their susbstrate specificity andmolecular structures .

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COLLAGEN TURN OVER RATE

Sodek ,1977 found collagen synthesis in PDL of adult rat to be

- two fold greater than that of gingiva,

- four fold greater than that of skin, &

- six fold greater than that of bone.

Almost all the newly synthesized collagen in the ligament was converted to

mature cross linked collagen, whereas much less was converted in the

gingiva & skin.

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Continuation…. Half-life for collagen turnover: in ligament – 1 day,

in bone – 6 days

in gingiva - 5 days,

in skin - 15 days

According to Rippin: half life

in the apical areas 2.45 days,

in the crestal areas 6.42days,

fibers in mid-root region 5.7 days,

transseptal fibers 8.4 days

for dentogingival fibers 25 days.

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EXTERNAL FORCES & PDL

Within physiologic limits, the pdl can accommodate increased function with

an increase in width,

a thickening of its fiber bundles, and

an increase in diameter & number of

Sharpey’s fibers.

Forces that exceed the adaptive capacity of the periodontium produce injury called trauma from occlusion.

Slight excessive pressure: resorption of bone, widening of PDL space

Slight excessive tension: elongation of PDL fibers & apposition of bone

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Replantation & transplantation

To have any chance of success , it is essential to maintain the

viability of PDL .

Avoid dehydration of PDL.

Avoid loss of viability of its cell rests.

Transplantation

Best results when unerupted tooth with partially formed roots

as there is less damage to PDL.

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AGE CHANGES IN PERIODONTAL LIGAMENT -Rate of collagen synthesis decreases.

-Rate of maturation of the synthesized collagen changes.

-Decrease in the number of fibers.

-Collagen fibril diameter – decreases by 50%

-Degenerative vascular changes seen.

-Sharpey's fiber insertion – the alveolar bone surface jagged and uneven with irregular fiber insertions

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CLINICAL CONSIDERATIONS

• The primary role of periodontal ligament is to support the toothin the bony socket.

• The width of periodontal ligament varies from 0.15 to0.38mm. The average width is:

- 0.21mm at 11 to 16 years of age.- 0.18mm at 32 to 50 years of age.- 0.15mm at 51 to 67 years of age.

• So, the width of periodontal ligament decreases as age advances.

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WIDTH OF PERIODONTAL LIGAMENT

Conflicting results have been obtained

Klein & Tozat concluded – width increases with age

Tonna et al (1972) – width decreases with age

Why the width of periodontal ligament in hour glass shape??

Root convexity

Acts as fulcrum

Width of cementum is more at center

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With age

Less teeth present

Forces acting on remaining teeth increases

INCREASE WIDTH OF PDL SPACE WITH AGE

175

Masticatory forces decreases with age

DECREASE WIDTH OF PDL SPACE WITH AGE

Tonna et al (1972)

Klein & Tozat

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• In the periodontal ligament, aging results in more number ofelastic fibers and decrease in vascularity, mitotic activity, fibroplasiaand in the number of collagen fibers and mucopolysaccharides.

• If gingivitis is not cured and supporting structure become involved,the disease is termed as periodontitis.

• There are few coccal cells and more motile rods and spirochetes inthe diseased site than in the healthy site. The bacteria consists ofgram-positive facultative rods and cocci in healthy site while indiseased site, gram-negative rods and anaerobes are more innumber.

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• Resorption and formation of both bone and periodontal

ligament play an important role in orthodontic tooth

movement. If tooth movement takes place, the compression of

PDL is compensated by bone resorption whereas on tension

side, apposition takes place.

• Periapical area of the tooth is the main pathologic site.

Inflammation of the pulp reached to the apical periodontal

ligament and replaces its fiber bundles with granulation tissue

called as granuloma, which then progresses into apical cyst.

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• Chronic periodontal disease can lead to infusion of

microorganisms into the blood stream.

• The pressure receptors in ligament have a protective

role. Apical blood vessels are protected from excessive

compression by sensory apparatus of the teeth.

• The rate of mesial drift of tooth is related to health,

dietary factor and age. It varies from 0.05 to 0.7mm per

year.

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Effect of hyper & hypo glycaemia on PDL

Nishimura et al, 1998 - PDL cells - susceptible to hyper & hypoglycemia & effects - mediated via the integrin system.

Hyperglycemia – increased expression of fibronectin receptor → results in reduced cellular adhesion & motility → probable tissue impairment.

Hypoglycemia – decreased expression of fibronectin receptor → lowers the viability & ultimately results in cell death & hence tissue impairment

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PDL space Radiographic appearance

Thin radiolucent line interposed between the root & lamina dura.

Occlusal Trauma → widened PDL space or funneling of coronal aspect of PDL space.

It can also widened in case of vertical fractures & progressive systemic sclerosis (Scleroderma).

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EMD & PDL Gestrelium et al, 1997 studied effects of EMD on periodontal ligament cell

migration, attachment, proliferation, biosynthetic activity mineral noduleformation & ability to absorb a large range of polypeptide growth factors &cytokine.

In culture, EMD formed protein aggregates which appeared to provide idealconditions for cell-matrix interactions.

Under these conditions EMD enhanced the proliferation of PDL cells,increased protein & collagen production of PDL cells & promoted mineralnodule formation by these cells.

However, no effect on migration, attachment & spreading of these cells nordid they absorb any of the growth factor or cytokine that were tested.

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NEOPLASTIC INVOLVEMENT OF PDL

Mostly reactive rather than neoplastic.

Oxytalan fibers are found in peripheral odontogenicfibromas & Adenomatoid odontogenic tumors

Epithelial rests of malassez --- neoplastic change

Infiltration of PDL by 1º or 2° malignant tumors --- widening of PDL space--- mobility –malignant loosening of teeth.

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BLOOD & LYMPHO RETICULAR DISORDERS

Changes due to reduced host response to plaque.

Destruction of PDL follows neutrophil defeciencies or functional defects such as defeciency of leucocyte adhesion receptors

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PERIODONTAL CYSTS

Inflammatory ---- Radicular cyst

Developmental ---- Lateral periodontal cyst

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SOFT C.T.DISORDERS & PDL

a. PROGRESSIVE SYSTEMIC SCLEROSIS

Radiographically ---- PDL widening upto 3mm

thickening

Collagen ---- dense, mature & more hyalinised than

normal

Oxytalan fibers increased.

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. LATHYRISM

Condition caused by drugs that inhibit cross linking in collagen

& elastin (cystamine)

Fragile collagen fibers

Retard eruption

c. DISUSE ATROPHY

Narrowing of PDL & reduction in no. of principal fibers.

Fibers oriented parallel to the long. Axis of root & PDL shows

reduced rate of collagen turn over.

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NUTRITION & PDL

a. FOOD TEXTURE

Little correlation between the advent of soft, fiber deficient

diet & dental health.

Significant factor in chronic inflammatory periodontal

disease is loss of natural masticatory function, leading to

accumulation of dental plaque.

Influences pattern of mastication & hence the mode of

support offered by the PDL.

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CARBOHYDRATES

Refined carbohydrates in the diet influence the severity of PDL

disease in humans (Holloway et. Al 1963)

No direct evidence showing the direct effect of carbohydrates

per se on PDL , though in some circumstances there could be

an influence as a result of modifying the diet consistency.

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PROTEINS

Deficiency of protein might be expected to produce changes

within it.

Reduction in PDL transseptal fibers ( Stien & Ziskin 1949; Ten

Cate et..al.1976)

Reduction in cementoblasts, fibroblasts

Occlusal trauma exacerbates these effects (Chawla & Glickman

1951)

Healing is delayed in rats fed on protein deficient diet.

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PERIODONTITIS

CHRONIC PERIODONTITIS

AGGRESSIVE PERIODONTITIS

PERIODONTITIS AS A MANIFESTATIONS OF SYSTEMIC DISEASES

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CHRONIC PERIODONTITIS

The most prevalent form in adults

Amount of destruction consistentwith local factors

Associated with a variable microbial pattern

Subgingival calculus frequently found

Slow to moderate rate of progression

Possibly modified by or associatedwith the following:

- Systemic diseases- Local factors predisposing

factors- Environmental factors

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CLASSIFICATION OF CHRONIC

PERIODONTITIS

I. Localized form: <30% of sites

involved

Generalized form: >30% of sites

involved

II. Slight: 1-2 mm of clinical

attachment loss

Moderate: 3-4 mm of clinical

attachment loss

Severe: ≥5 mm of clinical

attachment loss

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AGGRESSIVE PERIODONTITIS

Primary Features1. Except for the presence of periodontitis, patients are

otherwise clinically healthy

2. Rapid attachment loss and bone destruction

3. Familial aggregation

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Secondary Features

1. Amounts of microbial deposits are inconsistent with the severity of periodontal tissue destruction

2. Elevated proportions of Aggregatebacter actinomycetemcomitans and, in some populations, Porphyromonas gingivalis may be elevated

3. Phagocyte abnormalities

4. Hyper-responsive macrophage phenotype, including elevated levels of PGE2 and IL-1β

5. Progression of attachment loss and bone loss may be self-arresting

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HEALING AFTER PERIODONTAL THERAPY

REGENERATION is the reproduction or reconstitution of a lost or injured part.

REPAIR is the healing of a wound by tissue that does not fully restore the architecture or the function of the part.

PERIODONTAL REGENERATION is defined histologically as regeneration of the tooth’s supporting tissues, including alveolar bone, periodontal ligament, and cementum over a previously diseased root surface.

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NEW ATTACHMENT is defined as the union of connective

tissue or epithelium with a root surface that has been deprived

of its original attachment apparatus. This new attachment may

be epithelial adhesion and/or connective tissue adaptation or

attachment and may include new cementum.

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TO SUMMARIZE:PERIODONTAL LIGAMENT

The PDL is the means of attaching the tooth to the bone for mastication. As a labile connective tissue, it:

Adapts to varying load

senses loads for proprioceptive feedback controlling muscle actions

helps to move the teeth for better occlusion

supplies & nourishes cementum & alveolar bone

defends against microbes

prevents damage to cementum

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REFERENCES

Carranza’s Clinical Periodontology, 10th Edition

Clinical Periodontology and Implantology by Jan Lindhe, 5th edition

Oral Histology and Embryology by Orban, 13th edition

Tencate oral histology, 5th edition

Textbook of biochemistry – HARPER’S 2nd edition

Xiong J, Gronthos S, Bartold PM. Role of the epithelial cell rests of

Malassez in the development, maintenance and regeneration of periodontal

ligament tissues. Periodontol 2000, Vol. 63, 2013, 217–233.

Bosshardt DD, Selvig KA.Dental cementum: the dynamic tissue covering of

the root. Periodontol 2000 1997;13:41-75

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Fundamentals of Periodontics, 2nd Edition, by Thomas G. Wilson, Kennath

S. Kornman

Textbook of oral pathology by Shafer, 5th edition.

The periodontal ligament in health and disease: 2nd edition, Barry K B

Berkovitz

Bartold PM, Walsh LJ, Sampath Narayan A. Molecular and cell biology of

gingiva. Periodontol 2000, Vol. 24, 2000, 28–55

Ertsenc W, Mcculloc HG , Sodek HJ. The periodontal ligament: a unique,

multifunctional connective tissue. Periodontol 2000. Vol. 13, 1997, 20-40.

Wright JM. Reactive, dysplastic and neoplastic conditions of periodontal

ligament origin. Periodontol 2000, Vol. 21, 1999, 7-15.

Cho MI, Garant PR. Development and general structure of the periodontium, Periodontol 2000, Vol. 24, 2000, 9–27

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