Cementum in Health and Disease

CONTENTS

INTRODUCTION DEFINITION SIMILARITIES WITH BONE CEMENTOGENESIS PROPERTIES CLASSIFICATION CEMENTOENAMEL JUNCTION CEMENTODENTINAL JUNCTION THICKNESS FUNCTION METABOLISM (TURNOVER) AT THE TISSUE AND

MOLECULAR LEVELS

AGE CHANGES RESORPTION AND REPAIR CEMENTUM IN DISEASE

DEVELOPMENTAL ANOMALIES REGRESSIVE ALTERATIONS OF TEETH ALTERATIONS RESULTING FROM PERIODONTAL

PATHOLOGY NEOPLASMS OF THE CEMENTUM SYSTEMIC DISEASES AND ITS INFLUENCE ON

CEMENTUM APPLICATION IN FORENSIC ODONTOLOGY CONCLUSION REFERENCES

Introduction

Periodontium consists of investing layer and supporting tissues of the tooth: gingiva, periodontal ligament, cementum and alveolar bone.

Divided into 2 parts: Gingiva : protects the underlying tissues Attachment apparatus : composed of PDL, cementum and

alveolar bone Cementum is considered a part of the periodontium because,

with the bone - supports fibres of PDL. It was demonstrated microscopically in 1835 by 2 pupils of

Purkinje (Bhaskar SN, 1991) Hard bone like tissue covering the anatomic roots of the teeth

(Newman et al, 2006) .

Word is derived from Latin word Caementum, “quarried stone”- chips of stone used in making mortar (Nanci A, 2003).

Its a specialized mineralized tissue covering root surfaces and occasionally small portions of crown of teeth

Has many features in common with bone tissue.

Definition Cementum is the calcified, avascular mesenchymal tissue that

forms the outer covering of the anatomic root (Newman et al, 2006).

Cementum is the thin, calcified tissue of ectomesenchymal origin covering the roots of the teeth (glossary of periodontology).

Similarities with bone (Saygin et al, 2000)

Diseases that affect the bone, often alter cementum’s properties as well. Eg. Paget’s disease results in hypercementosis, hypophosphatasia results in no cementum formation, etc..

Composition is similar to that of bone Differences are

Avascular Lack Haversian canals Not innervated Exhibits little or no remodeling Less readily resorbed – therefore permits orthodontic

movement

Differences in physicochemical or biological properties Properties of precementum Increased density of Sharpey’s fibers (particularly in

acellular cementum) Proximity of epithelial cell rests to the root surface

Cementogenesis (Bosshardt and Selvig, 1997) Formation of cementum can be subdivided into

Prefunctional developmental stage : formed during the root development - 3.5 and 7.5 years - prefunctional development is extremely long

Functional developmental stage : commences when the tooth is about to reach the occlusal level associated with attachment of root to bone continues throughout life - adaptive and reparative

processes are carried out by the biological responsiveness of cementum

influences the alterations in the distribution and appearance of the cementum varieties on the root surface with time.

Root formation

Cementoblast origin Precursors of cementoblasts and PDL fibroblasts - dental

follicle Factors within local environment regulate - cementoblasts of

cementum, fibroblasts of PDL or osteoblasts of bone tissue Infiltrating dental follicle cells receive reciprocal inductive

signal from the forming dentin and differentiate into cementoblasts

HERS cells may undergo epithelial-mesenchymal transformation into cementoblasts during development

Extracellular matrix proteins - noncollagenous proteins found in bone – bone sialoprotein - precementoblast chemoattraction, adhesion to root surface and cell differentiation.

Enamel proteins - to be involved in early cementogenesis.

Development of dentinocemental junction Precementoblasts differentiate along external surface of

predentin into cementoblasts Implant initial collagen fibrils (fibrous fringe) of cementum

matrix into predentin by extending numerous tiny cytoplasmic processes

Leads - intimate interdigitation of 2 different fibril populations - forming dentinocemental junction - gets mineralized later

Intermediate cementum - interfacial layer between dentin and cementum - observed particularly between acellular extrinsic fiber cementum and dentin in rodent teeth and not in humans

Development of Primary (acellular) cementum (Berkowitz et al,2002)

PDL fibers oriented more parallel to the root surface and not gained any attachment to fibrous fringe.

Subsequent development of acellular cementum involves Slow increase in thickness Establishment of continuity between collagen fibers of the

periodontal ligament with those of the fibrous fringe at the surface of root dentin

Continued slow mineralization of collagen Establishment of continuity with PDL occurs only after tooth

has erupted into the mouth, when 2/3 of root has formed and acellular cementum may be only about 10 µm thick

Cementum lining tooth before this time - acellular intrinsic fiber cementum

Once PDL fibers become attached, cementum - acellular extrinsic fiber cementum.

Increases slowly and evenly throughout life at a rate of about 2-2.5 µm per year

Mineralization of cementum Does not appear to be controlled by cementoblasts No matrix vesicles observed Likely that presence of hydroxyapatite crystals in the

adjacent dentin initiates mineralization Adjacent PDL fibroblasts, which are rich in alkaline

phosphatase, may also pay a role Proceeds very slowly in a linear fashion, therefore no

evidence of a layer of precementum

Calcospherites not observed As the initial formation of cementum is closely associated

with mineralization of predentin or hyaline layer, when mineralization of initial root dentine is interfered with by administration of drugs known as bisphosphonates, there is inhibition of cementogenesis.

Cementogenesis Occurs rhythmically – periods of activity alternating with

periods of quiescence Structural lines observed indicating the incremental

nature of formation Periods of decreased activity associated with incremental

lines called incremental lines of Salter

These lines contain higher content of ground substance and mineral and lower content of collagen.

As acellular cementum is formed slowly, the incremental lines are closer together than that of cellular cementum which is deposited more rapidly.

Development of acellular afibrillar cementum Deposited as a thin layer overlying enamel at the cervical

margin of the tooth Presumably, the protection of the reduced enamel epithelium

overlying this enamel in an unerupted tooth is damaged or lost

Adjacent connective tissue cells of the dental follicle then come into contact with the enamel surface and are induced to form cementoblasts

These secrete an afibrillar matrix that calcifies

Development of Secondary (cellular) cementum Secondary cementum appears in the apical region of the root at

time tooth erupts. Also in furcation area of multirooted teeth. Associated with increase in the rate of formation of the tissue Following loss of continuity of the HERS, large basophilic cells

are seen to differentiate from adjacent cells of the dental follicle against the surface of the root dentine – form a distinct layer of cementoblasts

These cementoblasts possess more cytoplasm and cytoplasmic processes than the cells associated with acellular cementum

Basophilia is due to roughened endoplasmic reticulum – their presence suggests that cementoblasts secrete the collagen (together with ground substance) that forms the intrinsic fibers of secondary, cellular cementum

These fibers are oriented parallel to root surface Due to increased rate of formation, thin unmineralized

precementum layer (about 5 µm thick) will be present on the surface of cellular cementum

Precementum is less mineralized than primary cementum Multipolar mode of matrix secretion by the cementoblasts

will result in cells becoming incorporated into the forming matrix – thus called cementocytes

Incremental lines are more widely spaced due to increased rate of formation

Properties Physical properties: (Berkowitz et al, 2002)

Pale yellow with a dull surface Softer than dentine Permeability

cellular variety more permeable as the canaliculi in some areas are contiguous with the dentinal tubuli

more permeable than dentine decreases with age

Soft and thin cervically – readily removed by abrasion when gingival recession exposes the root surface to the oral environment

Chemical properties: (Berkowitz et al, 2002) and Bosshardt and Selvig,1997)

On a wet weight basis: Inorganic – 65% Organic – 23% Water – 12%

By volume: Inorganic – 45% Organic -33% Water -22%

Inorganic Acellular cementum is more mineralized than cellular

cementum - presence of uncalcified lacunae and core of Sharpey’s fibers in cellular cementum and slow formation of acellular cementum which allows longer direct contact of tissue fluids

CDJ shows a zone of high mineral content and low organic content delineated by zones of low mineral content on the dentin and sometimes on cementum side

Principle inorganic component- hydroxyapatite (Ca10(PO4)6(OH)2) with small amounts of amorphous calcium phosphates present These crystals are thin and plate like and similar to those in

bone and arranged parallel to the long axis of collagen fibril

Avg- 55nm wide and 8nm thick Length varies Minute size of mineral crystals allows for greater

capacity for adsorption of fluoride and other elements and more readily decalcifies in the presence of acidic conditions

Concentration of fluoride tends to be higher at the external surface, conc. of 0.9% ash weight – increases with age and varies with the nutritional fluoride supply to the individual

Contains 0.5-0.9% Mg – occupies the place of an equal no. of Ca ions in hydroxyapatite crystal lattice Similar to that of bone but half of that of dentine Mg conc. appears to be lower at the surface than in deeper layers

of cementum Contains 0.1-0.3% sulfur as a constituent of the organic

matrix Trace elements – Cu, Zn and Na

Organic Collagen :

Primarily collagen type I and III, like in bone and PDL

90% of organic matrix – type I collagen and approximately 5% - type III

Wang et al suggested that type I fibrils are coated by type III collagen whereas some other authors suggest that both the collagens are co – localized in the same fibril

Non – collagenous proteins : Glycolipids, glycoproteins or proteoglycans Non-collagenous proteins are similar to that of bone - bone

sialoprotein and osteopontin – both are phosphorylated and sulfated glycoproteins

Bind tightly to collagenous matrices and hydroxyapatite

Participate in mineralization process Reveal cell attachment properties through tripeptide

sequence Arg-Gly-Asp that binds to integrins Acellular cementum contains much more of these

than cellular cementum

Osteonectin – another glycosylated protein Found in extracellular matrix of mineralized

tissue Close relation between osteonectin and

collagen seems to exist in mineralization process

Enzyme alkaline phosphatase believed to participate in cementum mineralization (Beertsen and Everts, 1990) Supersaturation of phosphate ions, released from

organic phosphate esters, would result in the precipitation of calcium phosphate salts

Although it exists in a plasma membrane bound form, part of the enzyme may also be bound to extracellular matrix

Enzyme activity adjacent to cellular intrinsic fiber cementum is higher than that to acellular extrinsic fiber cementum and thickness of the latter correlates positively with the enzyme activity (Groeneveld et al, 1995)

Glycoproteins – fibronectin and tenascin – more widely distributed High molecular weight and multifunctional proteins

of the extracellular matrix Fibronectin binds cells to components of

extracellular matrix During tooth development, both are present in the

basement membrane of HERS at the time of odontoblast differentiation

Later, they are also found at the attachment site of PDL to cementum but not in the cementum layer itself (Lukinmaa et al 1991)

Enamel related proteins – have been detected Proteoglycans – core protein to which sulfated

polysaccharides are covalently linked – chondroitin sulfate, dermatan sulfate and hyaluronic acid

Classification (Berkowitz et al, 2002)

Based on presence or absence of cells Cellular cementum:

Contains cells (cementocytes) Found in the apical and interradicular areas and

overlying the acellular cementum Formed after acellular - secondary cementum Fast rate of matrix formation – incremental lines farther Presence of precementum Spaces that the cementocytes occupy are called lacunae

and the channels that their processes extend along are the canaliculi

Adjacent canaliculi are often connected and the processes within them exhibit gap junctions

Cementocytes are more widely dispersed and more randomly arranged

Canaliculi preferentially oriented towards PDL - chief source of nutrition

Once embedded cementocytes become relatively inactive Their cytoplasmic/nuclear ratio is low Sparse organelles responsible for energy

production and for synthesis Some unmineralized matrix may be seen in the

perilacunar space Border with dentine clearly demarcated

Acellular cementum: Appears relatively structureless – no cells. First formed – primary cementum Covers the root adjacent to the dentine more in the

cervical 2/3 Slower rate of matrix formation Incremental line closer Precementum virtually absent

Border with dentin not clearly demarcated

Based on the nature and origin of the organic matrix Cementum derives its organic matrix from 2 sources

Extrinsic fibers: from the inserting Sharpey’s fibers of the periodontal ligament – perpendicular or oblique to root surface

Intrinsic fibers: from cementoblasts – run parallel to root surface and approximately at right angles to extrinsic fibers

Mixed fiber cementum: both the above fibers are present

Based on presence or absence of cells and the nature and origin of the organic matrix – Schroeder’s classification (Newman et al, 2006) Acellular afibrillar cementum (AAC):

Contains neither cells nor extrinsic or intrinsic collagen fibers

Only mineralized ground substance Product of cementoblasts Found as coronal cementum Thickness – 1-15µm

Acellular extrinsic fiber cementum (AEFC): Composed almost entirely of densely packed bundles of

Sharpey’s fibers Product of fibroblasts and cementoblasts Cervical third of roots but may extend farther apically Thickness – 30-230µm

Cellular mixed stratified cementum (CMSC): Composed of extrinsic (Sharpey’s) and intrinsic fibers May contain cells Co-product of fibroblasts and cementoblasts Primarily in the apical third, apices and in furcation areas Thickness – 100-1000µm

Cellular intrinsic fiber cementum (CIFC): Contains cells, but no extrinsic collagen fibers Formed by cementoblasts Fills resorption lacunae

Intermediate cementum: Poorly defined zone near cementodentinal junction of

certain teeth that appears to contain cellular remnants of Hertwig’s sheath embedded in calcified ground substance

Cementoenamel junction (Newman et al, 2006)

Cementum overlaps enamel – 60-65% Edge-to-edge butt joint – 30% Cementum and enamel fail to meet – 5-10%

In this case, gingival recession may result in accentuated sensitivity because of exposed dentin

Cementodentinal junction Terminal apical area of cementum where it joins the internal

root canal dentin Obturating material in RCT should be at the CDJ No increase or decrease of width of the CDJ with age –

remains relatively stable CDJ – 2-3 µm wide Here the fibrils intermingle between cementum and dentin

Thickness (Berkowitz et al, 2002)

Varies at different levels of the root Thickest at the root apex and interradicular areas of

multirooted teeth – 50-200µm (may exceed to 600µm) Thinnest cervically – 10-15µm Thickest in distal side than mesial due to mesial drift Between ages 11 and 70 – thickness increases 3 fold – 95µm

at 20yrs and 215µm at 60yrs (Zander and Hurzler, 1958) Impacted teeth have thin cementum

Function Its contiguous with the periodontal ligament on its outer

surface and is firmly adherent to dentine on its deep surface – gives attachment to collagen fibers of the periodontal ligament

Maintains the tooth in functional position in the mouth Maintains the integrity of the root

Metabolism (turnover) at the tissue and molecular levels (Bosshardt and Selvig, 1997)

Cementum is excluded from metabolic processes of the body Variety of noncollagenous proteins are stored in the mineralized

matrix of the cementum, among which those specific for cementum are Cementum derived attachment protein – mediates attachment

of connective tissue cells Cementum derived growth factor – during root resorption and

surgical instrumentation, proteins exposed to root surface could possibly influence the initiation of repair process by cell migration, division, attachment and differentiation

Fluoride accumulates in the surface layer which is exposed to the circulating tissue fluids in the periodontal ligament

Age changes (Bosshardt and Selvig, 1997)

Continuous deposition: Cementum formation continues throughout life unless

disturbed by periapical or periodontal pathology Deposited at a linear rate (Azaz et al, 1974) More cementum is formed apically than cervically Cementum thickness shows variations among tooth

groups and surfaces Thick layers may form in root surface grooves and

furcations of multirooted teeth Great variations in incremental lines indicate that rate of

cementum formation may vary

Changes in tooth position may exert temporal and spatial variations in pressure and tension on root and bone surfaces – biological responsiveness of cementoblasts to these stimuli may influence the rate as well as pattern of cementum deposition – maintaining the tooth in proper position and relation to adjacent teeth

Nonfunctioning, impacted teeth appear to have thicker cementum and structural architecture is different

Impacted teeth – Sharpey’s fibers may be nearly completely absent in the cementum and it is built up mainly by intrinsic fibers arranged parallel to root surface

Physiological activity of cementocytes: No. of cells that become incorporated into cementum matrix

while its formation is proportional to the rate of cementum deposition

Cementocytes close to cementum surface may resemble cementoblasts but the amount of cytoplasm is reduced and they contain less endoplasmic reticulum and fewer mitochondria

Most well developed cell processes point towards root surface – indicate that exchange of metabolites through cellular intrinsic fiber cementum is limited

In deeper layers of CIFC, more advanced nuclear and cytoplasmic changes may occur or lacunae may appear empty – could be due to starvation or consequence of age

Cementum reactions to physiological tooth movement and occlusal forces: Presence of cementum on impacted teeth indicates that

occlusal forces are not necessary to stimulate cementum deposition

In posterior teeth, cementum is markedly thicker on the distal than on the mesial root surface – indicating relationship to mesial drift

Cementum like bone is dynamically responsive and its growth may be stimulated by tensional forces

Cementum thicker in areas exposed to tensional forces

Resorption and repair (Bosshardt and Selvig, 1997)

Types of resorption: Physiological root resorption : normal phenomenon of

deciduous teeth during tooth shedding Causes for resorption of permanent teeth

pathological like infectious, systemic diseases like calcium deficiency, hypothyroidism, hereditary fibrous osteodystrophy and Paget’s disease or tumors

nonpathological like trauma (mechanical, chemical or thermal) or sustained overcompression of the PDL

idiopathic Root resorption classified according to location as

Internal External

According to degree of persistence Transient Progressive

Root surface more resistant to resorption than bone No. of teeth resorbed and severity of resorption are markedly

increased by orthodontic treatment Appears microscopically as bay like concavities in the root

surface Multinucleated giant cells and large mononuclear macrophages

are generally found adjacent to cementum May extend into underlying dentin Not necessarily continuous, may alternate with periods of repair

and deposition of new cementum, new cementum is demarcated from the root by a deeply staining irregular line - reversal line

Repair: Following detachment of odontoclasts from the root

surface, cementogenic cells repopulate the Howship’s lacunae and attach the initial repair matrix to a thin decalcified layer of residual and exposed collagen fibrils

Basophilic and electron dense reversal line forms at the fibrillar junction

Deposited repair matrix resembles cellular intrinsic fiber cementum

Cementum repair requirea viable connective tissue Can occur in devitalized and in vital teeth

CEMENTUM IN DISEASE

Developmental anomalies

Concrescence (Shafer et al, 2006) Form of fusion which occurs after root formation Teeth are united by cementum Thought to arise as a result of traumatic injury or

crowding of teeth with resorption of interdental bone, so that 2 roots are in approximate contact and become fused by deposition of cementum

May occur before or after tooth eruption Diagnosed radiographically Extraction of 1 may result in the extraction of the other

Ectopic enamel (Neville et al, 2002) Presence of enamel in unusual locations, mainly tooth rooth Enamel pearl :

Hemispheric structures consisting entirely of enamel or contain underlying dentin and pulp tissue

Project from surface of root, more in maxillary molars Thought to arise from localized bulging of odontoblastic

layer – bulge may provide prolonged contact between HERS and developing dentin, triggering induction of enamel formation

Majority occur in furcation area or CEJ Precludes normal periodontal attachment with connective

tissue and a hemidesmosomal junction probably exists – less resistant to breakdown, once separation exists – rapid loss of attachment

Conducive to plaque retention and inadequate cleansing

Cervical enamel projections : Represent dipping of enamel from CEJ toward the

bifurcation More in mandibular molars – buccal surface Correlated positively to localized loss of periodontal

attachment with furcation involvement Have been associated with development of inflammatory

cysts – histopathologically identical to periapical cysts – develop along buccal surface over the bifurcation – called buccal bifurcation cysts

Both cases meticulous oral hygiene to prevent localized loss of periodontal support

Sometimes removal of the enamel is advised to achieve a more durable periodontal attachment

Hypercementosis (Neville et al, 2002) Nonneoplastic deposition of excessive cementum that is

continuous with the normal radicular cementum Radiographically – thickening or blunting of the root, surrounded

by radiolucent PDL space and adjacent intact lamina dura Also appears in form of spike-like excrescences called cemental

spikes created by either coalescence of cementicles to the root or calcification of PDL fibers

May be isolated, may involve multiple teeth or may appear as a generalized process

Premolar teeth involved most frequently Occurs predominantly in adulthood and frequency increases with

age

Factors associated Local factors

Abnormal occlusal trauma Adjacent inflammation Unopposed teeth (eg. Impacted, embedded, without

antagonist) Systemic factors

Acromegaly and pituitary gigantism Arthritis Calcinosis Paget’s disease of bone Rheumatic fever Thyroid goiter

Histopathologically Periphery of root demonstrates deposition of an excessive

amount of cementum over the original layer of primary cementum

Excessive cementum may be hypocellular or exhibit areas of cellular cementum that resemble bone(osteocementum)

Often arranged in concentric layers May be applied over the entire root or be limited to the

apical portion Use of polarized light clearly separates dentin and cementum

Treatment – require no treatment, certain cases extraction has been difficult where sectioning of the tooth may be required

Ankylosis (Shafer et al, 2006) Cessation of continued eruption Anatomic fusion of tooth cementum or dentin with alveolar bone Other terms – infraocclusion, secondary retention, submergence,

reimpaction and reinclusion Pathogenesis is unknown and may be secondary to disturbances

from Changes in local metabolism Trauma Injury Chemical or thermal irritation Local failure of bone growth Abnormal pressure from the tongue

Periodontal ligament might act as a barrier that prevents osteoblasts from applying bone directly onto cementum, ankylosis could arise from a variety of factors that result in a deficiency of this barrier – could be due to trauma or genetically decreased periodontal ligament gap

Other theories point to a disturbance between normal root resorption and hard tissue repair

Several investigators believe genetic predisposition has a significant influence and point to monozygotic twins who demonstrate strikingly similar patterns of ankylosis

Clinical and radiographic features May occur at any age, mainly 7-18 years Most commonly involved tooth – mandibular primary 1st

molar

Occlusal plane is below that of adjacent dentition Sharp solid sound on percussion when more than 20% of

the root is fused to bone Radiographically – absence of periodontal ligament space,

but the area of fusion is often in the bifurcation and interradicular root surface making radiographic detection difficult

Ankylosed teeth that are allowed to remain in position – adjacent teeth incline towards it leading to occlusal and periodontal problems

Opposing tooth exhibits overeruption It also leads to impaction of the underlying permanent tooth

Treatment Fail to respond to orthodontic treatment When an underlying permanent successor is present, extraction

should not be performed until it is obvious that exfoliation is not proceeding normally or adverse occlusal changes are developing

In permanent teeth or primary teeth without underlying successors – prosthetic buildup can be placed to augment the occlusal height

Luxation of affected permanent teeth may be attempted with extraction forceps to break the ankylosis – subsequent inflammatory reaction may result in the formation of a new fibrous ligament in the area of previous fusion – reevaluation in 6 months is mandatory

Regressive alterations of teeth (Shafer et al, 2006)

Abrasion : Pathologic wearing away of tooth substance through some

abnormal mechanical process Usually occurs on exposed root surfaces Robinson stated that the most common cause of abrasion is the

use of an abrasive dentifrice Modern dentifrices are not sufficiently abrasive and can cause

remarkable wear of cementum and dentin if toothbrush carrying it is injudiciously used, particularly in horizontal direction

V-shaped or wedge shaped ditch on root side of CEJ in teeth with some gingival recession – angle formed in lesion - sharp and dentin appears highly polished

Improper use of dental floss and toothpicks may produce lesions on proximal exposed root surface

Cementicles : Small foci of calcified tissue, not necessarily true cementum,

which lie free in the PDL of lateral and apical root areas Exact cause is unknown Mostly represent areas of dystrophic calcification and thus are an

eg. of regressive or degenerative change Develop by

Calcification of epithelial cells – enlarge by further deposition of calcium salts in the adjacent surrounding connective tissue – continued peripheral calcification may result in eventual union or even inclusion of the cementicle in the root cementum or alveolar bone – pattern of calcification is of a circular lamellated structure. Only when embedded in the cementum, it may impart a roughened globular outline to the root surface

Focal calcification of connective tissue between Sharpey’s bundles with no apparent central nidus – occurs as small round or ovoid globules of calcium salts

Small spicules of cementum torn from the root surface – cemental tears – or fragments of bone detached from the alveolar plate, if lying free in the PDL may resemble cementicles, particularly after they have undergone some remodeling through resorption and repair

Calcification of thrombosed capillaries in PDL, as Mikola and Bauer pointed are analogous to phleboliths – too small to be seen on radiographs – 0.2-0.3mm in diameter

Clusters of cementum may form and the apices these have been regarded as a cementoma particularly as they unite through interstitial deposition of bone or cementum

No clinical significance

Root caries Defined by Hazen et al as soft progressive lesion that is found anywhere

on the root surface that has lost connective tissue attachment and is exposed to the oral environment

Dentitions of older age group with significant gingival recession and exposed root surfaces

Was earlier referred to as caries of cementum Initiates on mineralized cementum and dentin surfaces which have

greater organic component than enamel Frequently on buccal and lingual surfaces of roots Dental plaque and microbial invasion are an essential part of the cause

and progression of the lesion Organisms – filamentous Microorganisms appear to invade the cementum either along Sharpey’s

fibers or between bundles of fibers

Since cementum is formed in concentric layers and presents a lamellated appearance, microorganisms tend to spread laterally between various layers

After decalcification of cementum, softening and destruction of the remaining matrix takes place

Later invasion of microorganisms into dentinal tubules – matrix destruction – pulpal involvement

Westbrook et al – as there are less dentinal tubules per unit area in root than in crown, there is difference in rate of caries progression and amount of dentinal sclerosis present

According to Katz et al – most frequently affected teeth are mandibular molars, next the mandibular premolars and then the maxillary cuspids, interproximal areas were mostly affected in the maxillary arch and the buccal surface in mandibular arch

Attachment of calculus Zander in 1953 investigated calculus attachment and observed

four types of attachment (Shafer et al, 2006) Attachment to the secondary cuticle Attachment to microscopic irregularities in the surface of

cementum corresponding to previous location of Sharpeys fibers

Penetration of microorganisms of calculus matrix into cementum

Attachment into areas of cementum resorption Calculocementum: Calculus embedded deeply in cementum may

appear morphologically similar to cementum (Newman et al)

Alterations resulting from periodontal pathology (Bosshardt and Selvig, 1997)

Effect of gingival inflammation Subsurface alteration :

Alterations in structure and composition of its organic and inorganic components consequential to pathological changes

Longstanding presence of inflammatory process in gingival connective tissue results in net loss of collagen and in breakdown of dentogingival fibers - enzymatic breakdown of collagen fiber is obvious in the gingival soft tissue and extension of this process into the hard tissue of the root, with loss of collagen cross-banding and dissolution of mineral crystals has also been described – surface limited with diffuse transition to subjacent unaffected tissue

Cervical root resorption : Development of large root resorption defect in cervical region

is, most likely, triggered by inflammatory processes in adjacent connective tissue

Such resorption generally has an undermining character Tooth is resorbed after the alveolar bone – immunity to

resorption has been linked to presence of an uncalcified, vital layer of precementum on root surface Another explanation could be because cementum is

avascular Odontoclasts take their origin from bone marrow and

cannot attack the root surface as fast as the osteoclasts reach the bone surface

Exposure to oral environment Bacterial contamination:

Obvious alterations may occur following exposure of cementum to the environment of periodontal pocket or oral cavity

Root surface wall of periodontal pockets is significant as they may perpetuate periodontal infection, cause pain and complicate periodontal treatment

The root cementum suffers structural, chemical and cytotoxic changes.

Structural changes: (Carranza and Newman, 1996) Presence of Pathologic Granules:

First reported by Bass,1951 Represent areas of collagen degeneration or areas where

collagen fibrils have not been mineralized initially These granules extend 3-12 µm into the surface of

cementum from overlying plaque Granules appeared in 4 basic morphologic patterns:

Grape like structure Long chain aggregate Small isolated vacuoles Very long fissure like area (Garrett, 1975)

Areas of increased mineralization: Probably a result of an exchange, on exposure to oral cavity,

of minerals and organic components at cementum-saliva interface

Microhardness remains unchanged Development of highly mineralized superficial layer may

increase the tooth resistance to decay Hypermineralized zones are detectable by electron microscopy

and are associated with increased perfection of the crystal structure and organic changes suggestive of a subsurface cuticle – seen in microradiographic studies as a layer 10-20µm thick with areas as thick as 50µm

Lack of preferred crystal orientation

Crystals are more densely packed and appeared as distinct, tablet shaped, polygonal structures (Selvig, 1969)

No decrease in mineralization found in deeper areas, therefore indicating that increased mineralization does not come from adjacent areas

Increase in calcium, magnesium, phosphorus and fluoride (Wirthlin et al, 1979)

Loss of, or reduction in, the cross-banding of collagen near the cementum surface and subsurface condensation of organic material of exogenous origin have also been reported

Areas of demineralization Commonly related to root caries Exposure to oral fluid and bacterial plaque results in

proteolysis of the embedded remnants of Sharpey’s fibers Cementum may be softened and may undergo

fragmentation and cavitation Progress around teeth and appear as well defined yellowish

or light brown areas, covered by plaque and have a soft or leathery consistency on probing

Dominant microorganism - actinomycosis viscosus Root caries may be the cause of toothache in patients with

periodontal disease and no evidence of coronal decay

Areas of cellular resorption of cementum and dentin Common in roots unexposed by periodontal disease Symptom free As long as root is covered by PDL, they are likely to

undergo repair If root is exposed before repair occurs, these areas appear

as isolated cavitations that penetrate into dentin

Chemical changes: Mineral content is increased Following minerals are increased in diseased root surfaces

Calcium Magnesium Phosphate Fluoride

Exposed cementum may absorb calcium, phosphorus and fluoride from its local environment forming a highly calcified layer that is resistant to decay

This ability of cementum to absorb substances may be harmful if the absorbed materials are toxic

Cytotoxic Changes: Bacterial penetration into the cementum can be found as deep

as the cemento dentinal junction - facilitated by the occurrence of minifracture and cracks of cemetum or a common sequence to chronic periodontal disease

Bacterial lypopolysaccharide have been detected in the 40-70µm deep surface of periodontally diseased roots

Bacterial endotoxins have also been detected in the cemental wall of periodontal pockets, whether the toxin is actually absorbed to or trapped in the tissue has not been established

Reduced opacity, cavitation and partial decalcification extending as deep as 300µm without any loss of surface contour can exist

These imperfections can harbour endotoxin on a submicroscopic basis and serve as a substrate for inflammatory exudate.

Components of this exudate can include substance such as histamine, bradykinin, high molecular weight immunoglobulins IgG, IgA, IgM and complement

Endotoxin which has been found in the cementum also may act to produce direct labializations of the lysozomal enzyme found within the cells of the tissue which then spill out into the tissues to effect their resorptive activities

Cementum may act to perpetuate the destructive effects of periodontal disease by acting as a reservoir for potentially destructive material.

Aleo et al observed that endotoxin was found to be present in the cementum of untreated periodontally involved teeth having 30% or more loss of supporting bone. The biologic effects of this cementum - bound endotoxin, studied in vitro concentration as low as 0-30 mg/ml of culture medium, were effective in depressing cell proliferation and viability

When compared to endotoxin form E-coli the cementum – bound endotoxin was found to be more toxic. Either biologic activities of endotoxins studied are not present to an equal degree, or the cementum bound material contain heat resistant toxic substances (Aleo et al, 1974)

Surface changes (SEM descriptions) (Garrett, 1975) 3-D view of the ultrastructural level Landay et al 1971 showed numerous surface projections

above cemental plane in normal cementum Landay 1972 – areas exposed to periodontal disease

At base of pocket – most recently exposed cementum showed partial filling in spaces between projections

Cementum which has undergone longer exposure showed complete covering of normal projections with what appeared to be flat sheet of calculus

No holes or spaces where Sharpey’s fibers had been once

Surface morphology of the tooth wall of periodontal pockets: (Newman et al,2006)

The following zones can be found Cementum covered by calculus Attached plaque, which covers calculus and extends apically

from it to a variable degree, probably 100 to 500 µm Zone of unattached plaque that surrounds attached plaque &

extends apically to it Zone of attachment of junctional epithelium to tooth - The

extension of this zone, which in normal sulci is more than 500 µm, is usually reduced in periodontal pockets to less than 100 µm

Zone of semidestroyed connective tissue fibers – apical to junctional epithelium

Zones 3,4 & 5 compose - plaque free zones seen in extracted teeth.

The total width of the plaque free zone varies according to type of tooth (It is wider in molars than incisors) and the depth of the pocket (It is narrower in deeper pockets).

Term plaque-free zone refers only to attached plaque because unattached plaque contains a variety of gram-positive coli and various gram negative morphotypes including cocci, rods, filaments, fusiforms and spirochetes. Most apical zone contains predominantly gram-negative rods and cocci.

Neoplasms of the cementum (Shafer et al, 1997)

Benign cementoblastoma (True Cementoma): Probably a true neoplasm of functional cementoblasts

which form a large mass of cementum or cementum like tissue on the tooth root.

Clinical features: Frequently, under age of 25 years No significant sex predilections Mandibular first permanent molar - most frequently

affected tooth Other teeth involved - mandibular second and third

molars, bicuspids, maxillary bicuspids and first, second and third molars

Associated tooth is vital unless coincidentally involved Lesion is slow growing and may cause expansion of

cortical plates of bone, but is usually otherwise asymptomatic

Radiographic features: Tumor mass is attached to tooth root Appears as a well circumscribed dense radioopaque mass

often surrounded by a thin, uniform radiolucent line Outline of the affected root is generally obliterated

because of resorption of root and fusion of the mass to the tooth.

Histologic features: Main bulk of tumor mass is composed of sheets of

cementum – like tissue, sometimes resembling secondary cellular cementum, but, other times being deposited in a globular pattern resembling giant cementicles

Reversal lines scattered throughout this calcified tissue are quite prevalent

Variable soft-tissue component consisting of fibrillar, vascular & cellular elements

Many cemental trabeculae in areas of activity are bordered by layers of cementoblast

Away from these trabecular surfaces, cementoclasts may be evident

Frequently microscopically indistinguishable from the benign osteoblastoma or giant osteoid osteoma - discussed by Larsson et al

Some areas are so cellularly active that they bear strong resemblance to osteosarcoma

Periphery of tumour generally shows a soft tissue cellular layer resembling capsule - here cemental trabeculae are almost arranged at right angles

Treatment and prognosis : Because of tendency for expansion of the jaw, it is believed that

extraction of the tooth is justified despite the fact, that the pulp is vital – recurrence rare

Distinguish from severe hypercementosis or chronic focal sclerosing osteomyelitis (i.e., condensing osteitis) both of which may superficially resemble

Periapical cemental dysplasia Other names

Cementoma Periapical Osteofibroma Osteofibrosis Cementifying fibroma Localized fibro-osteoma Cementoblastoma Periapical fibrous Dysplasia.

Etiology Unknown Suggested to occur as a result of mild chronic trauma or

traumatogenic occlusion

Clinical feature : Age - 20 years – common More common in females and more often in mandible Lesion occurs in PDL around the apex of the tooth usually

mandibular incisor Almost asymptomatic, when localized near the mental

foramen appear to impinge mental nerve and produce pain, paresthesia and even anaesthesia

Histologic and radiographic features: The lesion progress through three distinct stages:

Osteolytic phase: Periapical bone is replaced by a fibrous connective tissue, there is fibroblastic proliferation that may contain small foci of osteoid formation – Radiographically a radiolucent area

Cementoblastic phase: Islands and spicules of cementum like matrix form within the connective tissue – Radiographically calcification in radiolucent area

Mature stage: The lesion is predominantly composed of irregular cementum like material, which is densely mineralized. Roentenogram has a well defined radioopacity that is usually bordered by a thin radiolucent line or band

Treatment and Prognosis : Periodic observation, since its harmless, under no

circumstances should one extract the tooth or institute endodontic procedures or otherwise disturb the tooth unless, for reasons not related to the condition

Central cementifying fibroma Neoplasm of the bone Close histogenetic relationship between central

cementifying fibroma and central ossifying fibroma Clinical features:

Common in young and middle aged adults, avg-35 yrs Females : males = 2:1 Marked predilection for mandible Generally asymptomatic until growth produces

noticeable swelling and mild deformity Displacement of teeth may be an early feature Relatively slow growing tumour, the cortical plates of

bone and overlying mucosa or skin are intact

Radiographic features: Variable depending upon stage of development Well circumscribed, demarcated from surrounding bone Early stages – appears radiolucent As tumor matures – increasing calcification – radiolucent

areas becomes flecked with opacities until it appears as an extremely radioopaque mass

Displacement of adjacent teeth is common Have a centrifugal growth pattern – grow by expansion in all

directions When it reaches the inferior border of mandible, produces an

expansion thats in continuity with outline of tumor mass

Histologic features: Composed of many delicate interlacing collagen fibers

interspersed by large numbers of active, proliferating fibroblasts or cementoblasts

Many small foci of basophilic masses of cementum-like tissue – irregularly round, ovoid or slightly elongated

As lesion matures, islands increase in no. enlarge and coalesce

Treatment and prognosis: Should be excised conservatively Recurrence is rare

Gigantiform cementum (Familial Multiple Cementoma) Very rare condition which may or may not prove to be

distinct entity Clinical features:

Onset at young age Develops slowly and involves all four jaw quadrants

Radiographic features: Diffuse radioopaque masses scattered throughout the

jaw, sometimes expanding the jaw Described as consisting of dense, highly calcified, almost

totally acellular cementum which is poorly vascularized and frequently becomes infected with ensuing suppuration and sequestration

Focal cementoosseous dysplasia Benign lesion, occupies a portion of the spectrum between

periapical and florid cemento osseous dysplasia Posterior mandible is predominant site Asymptomatic and detected only on radiographic examination Smaller than 1.5 cm in diameter May occur on dentulous and edentulous areas Histologic feature:

Tissue consists of fragments of cellular mesenchymal tissue composed of spindle shaped fibroblasts and collagen fibers with numerous small blood vessels

Trabeculae of woven bone and cementum like material are interspersed throughout the fibrous framework

Systemic diseases and its influence on cementum (Shafer et al,

2006)

Cleidocranial dysplasia

Characterized by abnormalities of the skull, teeth jaws and shoulder girdle and occasionally stunting of the long bones

Oral findings - prolonged retention of deciduous teeth and subsequently delay in eruption of the succedaneous teeth Roots of the teeth are often short and thinner than usual

and may be deformed Surprising and unexplained feature was the absence of

cellular cementum on the erupted teeth in both dentition, with no increased thickening of primary acellular cementum

Hypophasphatasia

Hereditary disease due to deficiency of enzyme alkaline phosphatase in serum or tissues and excretion of phosphoethanolamine in urine

Earliest manifestation - may be loosening and premature loss of deciduous teeth, chiefly incisors

Teeth present a unique appearance characterized by the absence of cementum, presumably, as a result of cementogenesis, so that there is no sound functional attachment of the tooth to bone by PDL – accounts for spontaneous exfoliation of deciduous teeth. Occasionally a foci of poorly formed cementum may be found on some teeth.

Hyperpituitarism

Increase in no. of granules in acidophilic cells or an adenoma of anterior lobe of the pituitary gland – gigantism or acromegaly

Enlargement of jaws- mainly mandible, macroglossia, anterior openbite

Root of posterior teeth enlarge as result of hypercementosis - may be the result of functional and structural demands on teeth, instead of a secondary hormonal effect

Supraeruption of the posterior teeth may occur in an attempt to compensate for the growth of the mandible

Hypothyroidism (Neville et al, 2002)

Cretinism in infants or myxedema in adults Decreased levels of thyroid hormone Clinical features – lethargy, dry coarse skin, swelling of face

and extremities, husky voice, constipation, weakness and fatigue, bradycardia, hypothermia

Oral findings – enlarged tongue, teeth my fail to erupt if developed during childhood, in adults external resorption of roots may occur

Hyperparathyroidism Excess production of PTH, usually occurs in response to low

levels of serum calcium Clinical features

Stones – renal calculi, metastatic calcifications involving other soft tissues

Bones – subperiosteal resorption of phalanges of index and middle fingers, loss of lamina dura around teeth and root resorption, brown tumor which is dark reddish brown color of tissue specimen because of abundant hemorrhage and hemosiderin deposition in th tumor – ground glass appearance radiographically

Abdominal groans – due to duodenal ulcers

Paget’s disease of bone (Neville, 2002)

Multicentric benign tumor of osteoclasts has been suggested Characteristic deformities of skull, jaw, back, pelvis and legs Facial appearance – leontiasis ossea Ground glass change in alveolar bones Loss of lamina dura and root resorption Generalized hypercementosis sometimes

Application in forensic odontology

Age estimation from incremental lines of cementum Kagerer and Grupe suggested the possibility of age

estimation from acellular cementum Used mineralized unstained cross sections of teeth, preferably

mandibular central incisors and third molars Authors claimed an accuracy of within 2 or 3 yrs of

chronologic age Pathologic state of periodontium may compromise the

precision of ageing Hypermineralized bands gave an indication of events such as

pregnancies, skeletal trauma, and renal disorders

CONCLUSION (Bosshardt and Selvig, 1997)

The periodontal tissues form a functional unit designed to maintain tooth support and protection. In particular, cementum by virtue of its structural and dynamic qualities, provides tooth attachment and maintenance of occlusal relationship. These multiple functions are fulfilled by the biological activity and reactivity of cementoblast, which deposit two collagen – containing varieties of cementum with

completely different properties.

The discovery of variety of non collagenous proteins in cementum has opened a new research area of great therapeutic potential, cementum specific matrix proteins - cementum derived growth and/or attachment factors may result in accelerated wound healing and in controlled neocementogenesis following periodontal regenerative surgery.

REFERENCES

Aleo J, DeRienzis FA, Farber PA and Varboncoeur A. The presence and biologic activity of cementum bound endotoxins. J Periodontol 1974,45:672

Bartold and Narayanan. Biology of the periodontal connective tissue, 1998

Bath-Balogh and Fehrenbach. Dental embryology, anatomy and histology,2nd ed

Berkowitz BKB, Holland GR and Moxham BJ. Oral anatomy, embryology and histology – 3rd ed, 2002

Bhaskar SN. Orban’s Oral histology and embryology – 11th ed,1991

Bosshardt DA and Selvig KA. Dental cementum : the dynamic tissue covering of the root. Perio 2000, Vol. 13, 1997, 41-75

Carranza and Newman. Clinical periodontology – 8th ed, 1996

Eley and Manson. Periodontics – 5th ed,2004 Emslie RD. Some considerations on the role of cementum in

periodontal disease. J Clin Perio 1997;5:1-12 Garant PR. Oral cells and tissues, 2003 Garrett JS. Cementum in periodontal disease. Perio Abstracts

1975,6-12 Grant, Stern and Listgarten. Periodontics – 6th ed, 1988 Lindhe J. Clinical periodontology and implant dentistry – 4th

ed,2003 Nanci A. Ten Cate’s Oral histology – 6th ed,2003

Nanci and Bosshardt. Structure of periodontal tissues. Perio 2000, 2006

Neville, Damn, Allen and Bouquot. Oral and maxillofacial pathology – 2nd ed, 2002

Newman, Takei, Klokkevold and Carranza. Carranza’s clinical periodontology – 10th ed, 2006

Polson. Periodontal regeneration, 1994 Rose, Mealey, Genco and Cohen. Periodontics medicine,

surgery and implants, 2004 Saygin, Giannobile and Somerman. Molecular and cell

biology of cementum. Perio 2000, vol. 24,2000,73-98 Selvig KA. Biological changes at the tooth-saliva interface in

periodontal disease. J Dent Res, Vol 48, 1969

Selvig KA and Hals E. Periodontally diseased cementum studied by correlated microradiography, electron probe analysis and electron microscopy. J Perio Res .12:419-429, 1977

Shafer, Hine and Levy. Shafer’s textbook of oral pathology. 4th and 5th ed, 1993 and 2006

Stahl SS. The nature of healthy and diseased root surfaces. J Periodontol 1975,46(3),156-181

Warren, Hansen, Swartz and Phillips. Effects of periodontal disease and of calculus solvents on microhardness of cementum. J Periodontol 1964

Wirthlin, Pederson, Hancock, Lamberts and Leonard. The hypermineralization of diseased root surfaces. J Periodontol 1979,50(3),125-127