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CEMENTUM IN HEALTH CEMENTUM IN HEALTH AND DISEASE AND DISEASE
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CEMENTUM IN HEALTH CEMENTUM IN HEALTH

AND DISEASEAND DISEASE

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INTRODUCTION

The periodontium is defined as those tissues supporting and investing the tooth and

consists of the cementum, the periodontal ligament, the bone lining of the alveolus

and that part of the gingiva facing the tooth. The term cementum is derived from

the Latin term “Cemaentum”

The Cementum is a hard, avascular, clcified connective tissue that covers the root

dentin and gives insertion to the periodontal fibre bundle. It can be regarded as a

“bone of attachment”. It is pale yellow and softer than dentin. The thickness of

cementum varies considerably and the coronal third may be only 16-60 µm thick.

The apical third can be 200 µm or even thicker. The greatest thickness of the

cementum is formed at the apex or the furcation area. Cementum is formed

throughout life and is resistant to resorption.

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Cemento Enamel junction (CEJ)Three types of relationships

1. Exist at the CEJ

2. 60% - 65% cases, cementum

overlaps the enamel

3. 30% there is an edge to edge

butt joint and in 5% to 10% the cementum

and enamel fail to meet

Cementodentinal junction The dentinal surface upon which the

cementum is deposited is relatively smooth

Attachment between cementum and

dentin is quite firm.

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CHEMICAL COMPOSITION OF CEMENTUM

Dry weight basis

Permanent teeth contains about 45% in organic substance and 50-55% organic material

and water.

The inorganic portion consists mainly of calcium and phosphate in form of

hydroxyapatite.

The mineralized component consists of thin, needle-shaped crystals of hydroxyapatite.

Account for approximately 61% by weight (33% by volume) of radicular cementum. The

remaining fraction consists of organic matrix 27% by weight (31% by volume) and water

12% by weight (36% by volume). The degree of mineralization varies in different layers

of cementum.

The cemental mineralization of teeth less in older subjects.

The organic portion of the cementum consists primarily of type I collagen and protein

polysaccharides.

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CEMENTOGENESISPrimary Cementum Formation

Hertwigs’s epithelial root sheath initiates the differentiation of the root odontoblasts from the dental papilla. Before primary cementum can form, the root sheath must fragment to allow the follicular cells to reach the newly formed root surface. In this location, the follicular cells differentiate into cementoblasts. Once differentiated, they insert cytoplasmic processes into the unmineralized hyaline layer and begin to deposit collagen fibrils within it at right angles to the root surface.

Cementoblasts then migrate away from the hyaline layer but continue to deposit collagen so that the fine fiber bundles lengthen. Once this primary cementum and its fibrous fringe are established, it is thought that the cementoblasts that form it drifts away from the cementum surface. This condition continues until the forming periodontal ligament fiber bundles become stitched to the fibrous fringe. At this point the ligament fibroblasts are thought to be responsible for further deposition of mineral on the root surface around and within the collagen fiber bundles, which explaining the slow but continuous increase of cementum of the root surface.

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Secondary cementum formation

Cementoblasts initially lay down an organic matrix consisting of non collagenous

proteins and collagen fibrils aligned roughly parallel to the root surface. This

organic matrix becomes mineralized. At the same time, the cementoblasts

become trapped in the matrix they are forming to occupy lacunae. Once in this

situation, their secretory activity declines, and the cells become cementocytes.

When the periodontal ligament becomes organized, cellular cementum

continues to be deposited around the ligament fiber bundles, which become

incorporated into the cementum is confined to the apical third of the tooth and

interradicular regions of premolar and molar teeth.

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CELLS OF CEMENTUM

Cementoblasts: Cementoblasts originate form the ectomesenchymal cells in

the dental follicle surrounding the developing tooth. These cells have

numerous mitochondria, a well formed golgi apparatus and large amount of

endoplasmic reticulum. These cellsw line the cementoid tissue. Their

cytoplasmic volume and basophilia may increase during periods of active

cementogenesis.

Cementocytes: These are spider like cells incorporated into cellular

cementum. They lie in lacunae. A typical cementocyte has numerous cell

processes or canaliculi radiating from it’s cell body. These processes may

branch and they frequently anastomose with those of a neighboring cell.

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The cytoplasm of cementum in the deeper layers, contain few

organelles, the ER appears dilated and the mitochondria is scarse.

These characteristics indicate that the cementocytes are either

degenerating or marginally active cells.

Cementoclasts: Cementum is not remodeled but it can occur under

certain circumstances and in these instances mononuclear

cementoblasts or multinucleated giant cells, often located in

howship’s lacunae, are found on surface of cementum.

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PROTEINS ASSOCIATED WITH CEMENTUM

Osteonectin

Osteonectin is an acid phosphate containign glycoprotein rich in cysteine, which is

mainly secreted by osteoblasts (Gage et al; 1989) it is composed of a single

polypeptide chain and has a strong affinity for calcium ions (Sage and Borstein,

1991) important for mineralization process. It has been found in the periodontal

ligament, particularly strongly around the Sharypey’s fibers, at the attachment sites

between the ligament, alveolar bone and the cementum.

Osteocalcin

It is also called as bone gla protein as it ontains -carboxyglutamic acid (gla) residues.

It is mainly secreted by osteoblasts (Mariotti, 1993), role in the mineralization

process. The expression of osteocalcin by the cells lining the tooth root surface has

been shown during root development in mice (D’Errico et al, 1997)

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Bone sialoprotein protein

It also known as BSP II. It is a phosphoglycoprotein containing up to 20% of sialic acid

residues (Bilezikian et all 1996). Primarily found in the bone.

It is expressed by cells lining the root surface at early stage of cementogenesis during tooth

development. The cementoblasts appear to secrete this protein onto the root surface, which

then becomes covered by cementum. So they may serve as attachment factor since it has an

affinity for collagen fibers and enhances the attachment of osteoblasts and fibroblasts to

plastic surface.

Osteopontin

It is also termed as BSP I due to its high sialic acid content, and is a glycoprotein. It is found

primarily Mac-Neil et al, 1995 suggested that it functions as an inhibitor of mineralization

during periodontal ligament development. D’Errico reported that it was expressed by the

cells lining the tooth root surface.

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CLASSIFICATION OF CEMENTUM1. Based on location

a. Radicular cementum – it accounts for the bulk of cementum in humans

b. Coronal cementum – it is cementum over enamel in humans it is thin and poorly developed but it is better developed in herbivorous animals.

2. Based on time of formation

a. Primary cementum formed before tooth eruption

b. Secondary cementum formed after tooth eruption

3. Based on it’s cellularity

a. Acellular cementum – which lacks embedded cells.

b. Cellular cementum – in which cells are located with in the mineralized matrix.

4. Based on the presence or absence of collagenous fibrils

a. Afibrillar cementum – it lacks dense array of collagen fibrils although rare isolated fibrils will be presented

b. Fibrillar cementum – Contians well defined densely packed collagen fibrils in it’s matrix.

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5. Based on the origin of collagenous fibrils

a. Intrinsic fibers – which are formed due to cementoblasts activity.

b. Extrinsic fibers – incorporation of the periodontal ligament fibers.

Schroder in 1986 gave the classification of cementum as: -

1. Acellular afibrillar cementum

2. Acellular extrinsic fiber cementum

3. Cellular mixed fiber cementum

4. Cellular intrinsic fiber cementum

5. Intermediate cementum

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NORMAL FEATURES OF CEMENTAL SURFACES

Extensive variation in surface topography of cementum can

be observed with scanning electron microscope (SEM).

Resting cemental surfaces, where mineralization is more

or less complete, exhibit low rounded projections known

as cemental mounts. Cemental surfaces with actively

mineralizing fronts have numerous small openings.

Represent unmineralized cores of fibers.

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TYPES OF CEMENTUM

1. Acellular Afibrillar Cementum (Aac): Found deposited

on mature enamel surfaces. It may be deposited during

tooth formation, during tooth eruption or after it. Appears

as cemental spurs or cementum islands on the crown of

erupted teeth. This type of cementum is probably of little

significance as it is not involved in fiber insertion and

tooth anchorage. It represents an aberration of the

developmental process in which part of the reduced

enamel epithelium disaggregates and allows cells from

the dental follicle to interact with the exposed enamel

matrix, leading to cementum deposition.

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2. Acellular Extrinsic Fiber Cementum (Aefc): It contains

densely packed collagen fibres that project in a

perpendicular manner from the cementum matrix into the

periodontal ligament. This type of cementum forms on

the newly synthesized dentin surfaces after dissolution of

the Hertwigs epithelial root sheath and the subsequent

exposure of the root surface to the dental follicle cells.

Once the PDL fiber bundles are formed and connected to

the fibrous fringe bundles of the primary acellular

intrinsic fiber cementum, further deposition of mineral

about and within the bundles result in the formation of

acellular extrinsic fiber cementum, which becomes the

principal tissue of attachment. It extends from the

cervical margin of the tooth and covers at least two thirds

of the root.

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3. Cellular mixed fiber cementum (Cmfc): It contains

both collagen fibers and calcified matrix and appears to

be synthesized solely by the cementoblasts. A distinct

feature of this cementum is the presence of the intrinsic

collagen fibers produced by the cementoblasts that run

parallel to the root surface. In addition to theses, some

extrinsic sharpey’s fibers can be also seen. Thus, CMFC

consists of both acellular extrinsic fiber cementum and

cellular intrinsic fiber cementum that alternate and appear

to be deposited in irregular sequence upon one another.

With organization of the PDL, future deposition of

cellular cementum incorporates ligament fiber bundles of

the PDL, thereby creating CMFC. It consitutes the bulk

of secondary cementum.

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Cellular cementumCIFC

Acellular cementum

AEFC

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AEFC

CB

PDL

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4. Cellular intrinsic fiber cementum (Cifc): Component of

cellular mixed stratified cementum, CIFC is considered to

be a form of reparative cementum. This type of

cementum is commonly associated with the repair of

resorptive defects and healing of root fractures. The

principles cells involved in the synthesis of this type of

cementum.

5. Acellular intrinsic fiber cementum (Aifc): It is a

acellular variant of cellular intrinsic fiber cementum that

is also deposited during adaptive responses to external

forces. It forms without leaving cells behind. (Bosshardt

and Schroeder 1990)

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6. Intermediate cementum: It is a form of secondary

cellular intrinsic fiber cementum restricted to the apex of

the tooth. It is not involved in tooth attachment and has

no functional significance.

7. Mixed stratified cementum: It describes a layered

arrangement of apical cementum that consists of alternate

layers of acellular extrinsic and cellular fiber cementum.

This layered pattern may simply represent alternating

mineralization occurring upon successive waves of

cellular intrinsic fiber cementum deposited in response to

adaptive needs.

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CEMENTUM FROM NORMAL ROOT SURFACES

This procedure was first done by hanes and Polson in 1989. For the preparation of cementum specimens from normal root surfaces, the remnants of the periodontal ligament fibers were removed from the root surface with 12 strokes of Gracey curet. The remaining cementum on the root was not removed.

Following implantation into incisional wounds, epithelial migration was observed adjacent to non-acid treated cementum surfaces and was associated with extrusion and exfoliation of these control specimens. In contrast, the surface demineralization experimental specimens remained within the connective tissue and had a cell and fiber attachment system established within 10 days. Demineralized cementum had more fibers attached per unit area than did demineralized dentin surfaces.

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CHANGES IN DISEASED CEMENTUM

Actinomyces species may penetrate small distance into cementum

and bacterial products such as lipopolysaccharides may

contaminate it. However, the penetration of these products into

the cementum appears to be superficial (Moore et al, s1986).

Many Gram negative bacteria have the ability to attach to gram

positive bacteria in the cementum and the epithelial cells (Slots

and Genco, 1984). This ability is an important factor in their

colonization of the subgingival environment and also allows

them to colonize the surface cells of pocket epithelium

bacterial invasion of the cementum and radicular dentin was

thought by early investigators to be an important factor in the

pathogenesis of periodontal disease. Miller (1890) described

bacteria invading the radicular dentin of periodontally diseased

tooth.

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CEMENTUM FROM PERIODONTITIS AFFECTED TEETH

Cementum specimens were harvested from areas on the root

surfaces beneath deposits of calculus. Calculus was

removed carefully with an ultrasonic scaler, so that the

underlying root surface was not gouged. Unlike the

observations on root dentinal surface, a distinct zone of

demineralization of surface was not apparent on

periodontitis affected cementum surface following acid

treatment surface. In addition, epithelial down growth

and connective tissue cell and fiber attachment did not

differ between experimental and control surfaces at any

time. The findings of this study suggested that the

periodontitis affected root surface inhibited the

demineralization effects of citric acid.

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Citric acid treatment of cementum from normal root

surfaces produced a fibrillar surface morphology that was

consistent with the exposure of a fibrillar, collagen

substrate. Periodontitis affected cementum, however, was

not appreciably altered in appearance, having only a

faintly mat-like surface texture. These findings suggest

that calculus affected cementum undergoes changes that

reduce the effects of demineralizing agents.

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ROOT SURFACE WALL OF PERIODONTAL POCKET

In normal cementum the collagen fibers are embedded in the cementum. These fibers are destroyed in pathological pocket wall with the exposure of cementum. Collagen remnants of Sharpey’s fibers in cementum undergo degeneration creating a environment favorable for penetration of bacteria. Bacterial penetration into the cementum can be found as deep as the CDJ and may also enter the dentinal tubules penetration and growth of bacteria leads to fragmentation and breakdown of the cementum surface and result in areas of necrotic cementum separated form the tooth by masses of bacteria. These changes manifested clinically as softening of cementum surface which is usually asymptomatic but painful when probe penetrates the area.

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DECALCIFICATION AND REMINERALIZATION OF CEMENTUM

Areas of increased mineralization on exposure to oral cavity as a result of mineral and organic components at cemental saliva interface. The mineral content of exposed cementum increases. Microhardness remains unchanged. This hypermineralized surface increases the tooth resistance to decay. Areas of demineralization are commonly related to root caries. Exposure to oral fluorides and bacterial plaque results in proteolysis of embedded remnants of Sharpey’s fibers. The cementum may be softened and undergo fragmentation and condensation. Active lesion appears as well defined yellowish or light brown areas frequently covered by plaque and a softened and leathery consistency on probing. Inactive lesions are well defined darker lesions smooth surface and harder consistency on probing. A.Viscosus, A naslundii, S. mutans, S salivarius and S. Sanguis are the microorganisms usually involved in root caries.

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CEMENTUM IN LOCALIZED AGGRESSIVE PERIODONTITIS

Gottleib (1923) suggested defects in cementum to be the

central cause of disease. Ruben and Shapiro (1978) and

Lindslong and Blomlof carried out a comparative

histological study on teeth from patients with healthy

teeth and those with diseased roots in localized and

generalized aggressive periodontitis patients. They found

that generalized aggressive periodontitis patients had

extensive areas of defects which were defects in

cementum formation rather than pathology of pocket.

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Changes in cementum after instrumentation

Firm scaling strokes used to remove subgingival calculus

also remove a small amount of cemetnum resulting in

some notching of root surface.

Necrotic Cementum

Cementum exposed by apical migration of junctional

epithelium is altered by exposure to subgingival plaque

within the pocket. It may become hypermineralized,

demineralized (in case of root caries) or necrotic.

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AGE CHANGES IN CEMENTUM

Cementum deposition appears to be continuous throughout

life, a direct relationship has been shown between age

and cementum thickness. Cementum deposition is less

near CEJ and greater in apical areas.

Cemental deposition slows in old age. In addition, the

attachment of cementum to dentin may be weakened. The

frequent cemental tears seen in specimens of aging

humans may be related to age changes in the ground

substance of cementum or reduced vascular supply or to

thickened and less extensible ligament fibers embedded

in cementum. Suprring of cementum is sometimes the

result of fusion of calcospheroid bodies near cementum

or of calcification of epithelial rest aggregates.

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DEVELOPMENTAL AND ACQUIRED ANOMALIES ASSOCIATED WITH CEMENTOGENESIS

There are certain anomalies in cementogenesis that may have an impact on the susceptibility of teeth to periodontal diseases and treatment of affected teeth.

1. Enamel projection: Occur in localized areas, particularly in furcations of mandibular teeth. It is suggested that projections may predispose the teeth to periodontal defect involving the furcation

2. Enamel Pearls: This anomaly consists of globules of enamel on the root surface in the cervical region. They resemble small pearls upto several millimeters in diameter. They appear to form as a result of localized failure of Hertwig’s root sheath to separate from the dentin surface. They mimic calculus clinically and radigraphically, they cannot be sealed off and elimination can only be accomplished by grinding. Large pearls may contain pulp extensions.

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3. Cementicles: These are globular masses of acellular

cementum, generally less than 0.5 mm in diameter which

form within periodontal ligament. It has been postulated that

cementicles originate from foci of degenerating cell or

epithelial rests in periodontal ligament. Cementicles are not

not of clinical significance unless they become exposed to

oral environment where they may act as sites for plaque

retention.

4. Hypercementosis: Hypercementosis is a non neoplastic

deposition of excessive cementum that is continuous with the

normal radicular cementum. It occurs predominantly in

adulthood, and the frequency increases with age.

Hypercementosis can be classified as:

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LOCAL FACTORS Abnormal occlusal trauma,

Unopposed teeth (e.g. impacted, embedded, without antagonist)

Adjacent inflammation

SYSTEMIC FACTORS Acromegaly and pituitary gigantism

Arthritis

Calcinosis

Paget’s disease (Generalized hypercementosis)

Rheumatic fever

Thyroid goiter

Vitamin A deficiency

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Radiographically, affected teeth demonstrate a thickening or

blunting of root. The enlarged root is surrounded by

radiolucent ligament space and adjacent intact lamina dura

premolar teeth are most commonly affected.

5. Ankylosis: Eruption continues after the emergence of the teeth

to compensate for the masticatory wear and the growth of the

jaws. The cessation of eruption after emergence is termed as

ankylosis and occur from an anatomic fusion of the tooth

cemetnum or dentin with alveolar bone. Other terms for this

in the literature are infraocclusion, secondary retention,

submergence, reimpaction and reinclusion. Pathogenesis

disturbances from changes in local metabolism, traums,

injury, chemical or thermal irritation, local failure of bone

growth and abnormal pressure from tongue the periodontal

ligament might act as a barrier that prevents osteoblasts form

applying bone directly into the cementum.

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Ankylosis may occur at any age clinically they are most

obvious if the fusion develops during the first two decades of

life. The most commonly involved tooth is primary first

molar, the majority of cases occuring in the mandible. A

sharp, solid sound may be noted on percussion of the

involved teeth. Radiographically, absence of periodontal

ligament space may be noted; Ankylosed teeth lead to a

number of dental problems The adjacent teeth often incline

towards the affected tooth, with the development of

subsequent occlusal and periodontal problems. In addition the

opposing teeth often show supra eruption. Occasionally, the

ankylosed teeth lead to impaction of the underyling

permanent teeth.

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6. Hypophosphatasia: It is a rare familial disease, characterized by incomplete bone mineralization. This condition was first described by Rathbun 91984) and is characterized by low levels of serum kidney and bone alkaline phosphatase and elevated levels of phosphoethanolamine in serum and urine (Watanabe et al, 1993)

Radiographically, the teeth appear to have a characteristic “shell” appearance poorly formed and haphazardly arranged periodontal ligament (Listgarten and Houpt. 1969). The pathological alterations are due to insufficient levels of alkaline phosphatase. This enzyme is a key step in the production of a competent organic matrix in both bone and cementum. The decreased production and activity of this enzyme is likely to result in accumulation of inorganic phosphate, which inhibits mineralization. This leads to defective cementogenesis and formation of an incompetent attachment apparatus, making the teeth more prone to exfoliation and the root surfaces more susceptible to bacterial colonization (baab et al, 1986)

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CENTRAL LESIONS RELATED TO CEMENTUM

Based on clinical radiographic and histological features,

bony lesions of cementum were classified by Pinborg et

al in 1971 as:

1. Periapical cemetnal dysplasia

2. Benign cementoblastoma

3. Cementifyign fibroma

4. Gigantiform cementoma

5. Cemento – osseous dysplasia.

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The dental cementum and normal periodontal cells covering the root surface have been reported to contain a potent collegenase inhibitor, which forms a protective barrier against root resorption. Resorption of the mineralized tissues occur if clastic cells obtian access to the mineralized tissue by a break in this barier or when the precementum is mechanically damaged or scraped off. The mineralized or denuded root areas attract resorbing cells to colonize the damaged areas of root.

Cementum of erupted as well a unerupted teeth is a subject to resorptive changes that may be of microscopic proportion or insufficiently extensive to present a radiographically detectable alterations in root contour. Microscopic cementum resorption is very common. In one study conducted by Henry and Winmann, it occurred in 236 of the 261 teeth ie; about 90.4%.t he average number of resorption areas per tooth was 3.5 about 76.8% of these sites were located in the apical third of the root, 19.2% in the middle third and 4% in the gingival third. About 70% of all resorption areas were confined to the cementum involving the dentin. The various causes of cemental resorption are:-

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Local factors of cementum resorption:

1. Trauma from occlusion

2. Orthodontic movement

3. Pressure from malaligned teeth, cysts and tumors,

4. Teeth without functional antagonist

5. Embedded teeth

6. Replanted and transplanted teeth

7. Periapical disease

8. Periodontal disease

Systemic conditions predisposing to or inducing resorption are:

1. Calcium deficiency

2. Hypothyroidism

3. Hereditary fibrous osteodystrophy

4. Paget’s disease.

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cementum resorption appears microscopically as bay like

concavities in the root surface. Multinucleated giant cells and

large mononuclear macrophages are generally found adjacent

to the cementum undergoing active resorption. The resorptive

process may extend into the underling dentin. Cementum

resorption is not necessary continuous and may alternate with

periods of repair and deposition of new cementum. The newly

formed cementum is demarcated from the root by a deeply

stainign line termed as the reversal line. Which delineates the

border of the previous resorption. Embedded fibers of the

periodontal ligament reestablish a functional relationship with

the new cemenntum cementum repair requires the presence of

viable connective tissue. If the epithelium proliferates into the

area of resorption, repair will not take place. Cementum repair

can occur in devitalized as well as vital teeth.

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CEMENTAL REPAIR

After resorption has ceased, the damage is usually repaired, either

by formation of acellular or cellular cementum or by both.

CHEMICAL BIOMODIFICATION

Changes in the root surface wall of the periodotnla pocket

interfere with new attachment. Several substance have been

used in attempts to better condition the root surface for

attachment of new connective tissue fibers.

Although acid treatment was used in 19th century, register and

Burdick (1975) re credited with the revival of this technique.

Having tested several acids including citric acid and

hydrochloric acid, they concluded that citric acid was the

most effective and least toxic of all acids tested.

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In animals, they noted widening of the orifice of dentinal tubules

(creating a “blunderluss” effect) and on healing, the

cementum formed within these tubules. They referred to this

cementum as “cementum pins”. They further speculated that

citric acid may expose the collagen fibrils that may “splice”

with collagen fibrils in the flap or graft. Other researchers

have given credibility to the theory of “Collagen Splicing”

(Codelli 1991). Register and Burdick further noted an

accelerated healing and accelerated cementogenesis as well as

connective tissue attachment when citric acid was used. Citric

acid has been found to remove the smear layer normally

found after root planning. It citric acid may produces a root

more amendable to attachment.

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FORMATION OF NEW CEMENTUM

Regenerative cementogenesis on previously diseased root surface is most unpredictable. The most common outcome is the formation of new tissue that is the formation of new tissues that resembles cementum or bone, is cellular and contains collagen fibres which are not functionally attached to previously diseased root surfaces. In order for periodontal regeneration to occur, the conditions of cementogenesis present initial formation should be duplicated.

Evidence indicates that systemic and local factors are likely to participate in the regeneration process. The role of local factors is especially relevant in cementum which like other calcified strucutres, stores a variety of growth factors and adhesion molecules yet it does not regenerate readily (macNeiland, Somerman 1993). These molecules are likely to be the motivating force to recruit cells to the dentinal surface, select or induce the cementoblast phenotype, permit their attachment to the dentinal surface and encourage their proliferation.

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CEMENTUM FORMATION STIMULANTS

Enamel matrix derivative (EMDOGAIN). Enamel matrix proteins were first demonstrated on the root analogue surfaces of rabbit incisors by Schonfield and Slavkin in 1977. Their origin is based on the experiments that showed that the inner layer of the epithelial root sheath had a secretory stage and that enamel like material was formed in the root surface prior to cementum formation. It was also shown that the cellular cementum contains proteins that are immunologically related to proteins present in the enamel matrix. Further support to importance of enamel derived proteins in cementum development comes from the fact that coronal cementogenesis seems to be initiated by exposure of cells of dentla follicle to developing enamel.

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The ability of enamel matrix protein to induce cementum

formation and periodontal regeneration was firs

tinvestigated by Hammarstrom in a buccal dehiscence

monkey model in 1977. The ability of EDM to produce

periodontal regeneration in buccal dehiscence model

was also tested in human experimental defect by Heijl in

1997. Studies have shown that EMD will stimulate the

regeneration of firmly attached a cellular cemetum in

experimentally prepared root surfaces and will also

produce complete regeneration of periodontal ligament.

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CONCLUSION

Cementum is probably the least understood of all dental

tissues. But this does not lessen it’s role in the

periodontal attachment apparatus. With the development

of newer concepts of regenerative cementogenesis and

role of cementum in implants, the need for us to better

understand this basic tissue should be understood and

implemented.

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7. Selvig, K.A (1965). The fine structure of human cementum acta odontologica scandinavica 23, 423-441.

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