INTRODUCTION

The primary cause of gingival inflammation is bacterial plaque, along with other predisposing factors. Calculus is one of the common predisposing factors. This calculus plays an important role in maintaining and accentuating periodontal disease by keeping plaque in close contact with the gingival tissue & creating areas where plaque removal is impossible. Calculus consists of mineralized bacterial plaque that forms on the surfaces of natural teeth and dental prosthesis.

HISTORICAL BACKGROUND
The first formal association between dental deposits and oral disease can be found in the writings of H !!"C#$T%& ' ()*+ ,--.C/ He noted the deleterious effects on the teeth and gums of !ituita 'Calculus/, which insinuated itself under the roots of the teeth. The middle ages: $lbucais '0,) +1*1,/ had a clear understanding of the ma2or etiologic role of calculus deposits and described the technique of scaling the teeth The renaissance: !aracelsus '1(0, 3 14(1/ developed an interesting and unusual theory of disease 5 doctrine of calculus. He understood that pathologic calcification occurred in a variety of organs and considered it the result of metabolic disturbances whereby the body takes nourishment from food and discards the refuse as 6 tartarus7, material that cannot be broken down and is the ultimate matter or 6 materia ultima8 !aracelsus recognized the e9tensive formation of the tartar on the teeth and related this to toothache. Toothache was thus comparable to the pain produced by calculus in other organs such as kidney $mbroise pare '14*0 3 140*/ understood the etiologic significance of calculus and used the set of scalers to remove the hard deposits on the teeth n 1):, ;an <eeuwenhoek described microorganisms in tartar. He called them 6animalcules7 Nineteenth centur =auchard, in 1->:, termed it tartar or slime! and referred to it as ?a substance which accumulates on the surface of the teeth and which becomes, when left there, a stony crust of more or less considerable volume. <eonard koecker '1-:4 +1:4*/ , in a paper in 1:>1 , described inflammatory changes in gingiva and calculus on teeth that led to their looseness and e9foliation.

D"#INITION
Calculus: $bnormal concretion composed of mineral salts, usually occurring within the hollow organs or their passages, also called stones, such as gallstones or kidney stones.

@ental calculus can be considered as an ectopic mineralized structure.

Calculus is defined as a deposit of inorganic salts composed primarily of calcium carbonate and phosphate mi9ed with food debris , bacteria and desquamated epithelial cells'Greene, 10)-/ Calculus can be defined as a hard concretion that forms on teeth or dental prosthesis through calcification of bacterial plaque. '$eri%d%ntal Literature Re&ie'/ Calculus is calcified plaque. '(ans%n ) "le / Calculus is essential mineralized plaque covered on its e9ternal surface by vital tightly adherent, non mineralized plaque. 'Genc%/ Calculus consists of mineralized bacterial plaque that forms on the surface of the teeth and dental prosthesis. '*ames " Hinrichs/ Calculus is a calcified mass which forms on and adheres to the surface of the teeth and other solid ob2ects in the mouth e. g. restoration and denture. Ahen dental plaque calcifies the resulting deposit is called dental calculus. These calcified deposits occur as hard, firmly adhering masses on the clinical crowns of the tooth. 'Grant/ Calculus consists of mineralized bacterial plaque that forms on the surfaces of natural teeth and dental prosthesis. BCarran+a C $ hard deposit that forms by mineralization of dental plaque and is generally covered by a layer of unmineralized plaque. $ hard deposit attached to the teeth usually consisting of mineralized bacterial plaque BAA$ ,--.C. Dineralized dental plaque phosphates'Schr%eder!,-/-/ that is permeated with crystals of various calcium

Calculus is also known as %d%nt%lithiasis %r tartar0 t is also called 1%ssili+ed 2la3ue0

CLASSI#ICATION
@ental calculus is classified by its location on a tooth surface as related to the ad2acent free gingival margin5 SU$RAGINGI4AL CALCULUS 5 o L%cati%n 3 "n the clinical crown coronal to the margin of the gingiva and visible in the oral cavity. Distri6uti%n 3

o o o o o

Dost frequent sites are on the lingual surfaces of the mandibular anterior teeth opposite Aharton7s and the .artholin7s duct and on the buccal surfaces of the ma9illary molars opposite &tenson7s duct. Crowns of teeth out of occlusionE non+functionalE or teeth that are neglected during daily plaque removal. &urfaces of dentures and dental prostheses. n e9treme cases calculus may form a bridge+like structure along ad2acent teeth or cover the occlusal surface of teeth without functional antagonist. &and'10(0/+ found nearly 1**F in mandibular anterior teeth, decreasing posteriorly to >*F of the third molars.in ma9illa, 1*F of the anterior teeth and )*F of first molars had supragingival calculus.s

o o o o

Other names 1%r su2ragingi&al calculus 7 &upramarginal %9tragingival Coronal, indicating that the calculus is on the anatomic crown. &alivary, a term that indicates that the source of the minerals is the saliva. SUBGINGI4AL CALCULUS 5

o o

L%cati%n7 "n the clinical crown apical to the margin of the gingiva, usually in periodontal pockets, not visible upon oral e9amination. %9tents to bottom of the pocket and follows contour of soft tissue attachment.

o o

Distri6uti%n 5 Day be generalized or localized on single teeth or a group of teeth. !ro9imal surfaces have heaviest deposits, lighest deposits on facial surfaces.'<ovdal et al.104:/

o o

Other names 1%r su6gingi&al calculus7 &ubmarginal. &erumal, term indicates that the source of the mineral is the blood serum.

Ahen the gingival tissue receede, subgingival calculus become e9posed and is therefore reclassified as supragingival. Thus, supragingival calculus can be composed of both supragingival calculus and previous subgingival calculus. The location and e9tent of subgingival calculus may be evaluated by careful tactile perception with a delicate dental instrument such as an e9plorer. Clerehugh et al, used a AH" G)>1 to detect and score subgingival calculus. &upra gingival calculus and subgingival calculus generally occur together, but one may be present without the other. Dicroscopic studies demonstrate that deposits of subgingival calculus usually e9tend to the base of periodontal pockets in chronic periodontitis but do not reach the 2unctional epithelium.

CLINICAL CHARACT"RSTICS
CHARACT"RISITC COLOR SU$RAGINGI4AL CALCULUS Ahite or whitish yellow. nfluenced by tobacco and food pigments SUBGINGI4AL CALCULUS @ark brown or greenish black.
color derived from blood pigments from diseased pocket

SHA$"

$morphous, bulky =orm interpro9imal bridge between ad2acent teeth. %9tend over the margin of gingiva &hape of calculus is determined by5 $natomy of teeth Contour of gingival margin !ressure of tongue and cheeks

=lattened to conform to pressure "f !ocket wall. Combination of following forms Day occur5 crusty, spiny, or nodular <edge or ring like forms thin, smooth veneers finger and fern+like forms ndividual calculus islands

CONSIST"NC8 AND T"9TUR"

Doderately hard Clay like consistency

.rittle, flint+like. Harder and more dense than supra gingival calculus.

SI:" AND

Huantity has direct relationship to5

#elated to pocket depth ncreased amount with age

;UANTIT8

1. !ersonal oral care procedure and plaque control measures. >. !hysical character of diet. ,. ndividual tendencies. (. =unction and use 4. ncreased amount in tobacco smokers

because of accumulation Huantity is related to personal care, diet, and individual tendency as it is with supragingival. &ubgingival is primarily related to the development and progression of periodontal disease.

$R"4AL"NC"
Aneurd A! L%e H and B% sen H5 observed the periodontal status of a group of &ri <ankan tea labourers and a group of Iorwegian academicians for a 14 year period. The Iorwegian population had ready access to preventive dental care throughout their lives, whereas the &ri <ankan tea labourers did not. n &ri <ankan individuals+ o =ormation of supragingival calculus was observed early in life, probably shortly after the teeth erupted. o The first areas to e9hibit calculus deposits were the facial aspects of ma9illary molars and the lingual surfaces of mandibular incisors. o @eposition of supragingival calculus continued as individuals aged, reaching a ma9imal calculus score around >4 to ,* years of age. o $t this time most of the teeth were covered by calculus, although facial surfaces had less calculus than lingual or palatal surfaces. o Calculus accumulation appeared to be symmetric and by age (4 only a few teeth, typically the premolars were without calculus. o &ubgingival calculus appeared first either independently or on the interpro9imal aspects of areas where supragingival calculus already e9isted. o .y age,*, all surfaces of all teeth had subgingival calculus without any pattern of predilection. n Iorwegian academicians+ o %9hibited a marked reduction in the accumulation of calculus as compared with &ri <ankan group.

o However, despite the fact that :*Fof teenagers formed supragingival calculus on the facial surfaces of the upper molars and the lingual surfaces of lower incisors, no additional calculus formation occurred on other teeth, nor did it increase with age. Dore recently, the Third Nati%nal Health and Nutriti%n "<aminati%n Sur&e =NHAN"S> evaluated 0):0 adults in the Jnited &tates between 10:: and 100(. This survey revealed that 91.8% of the subjects had detected calculus and 55.1% had subgingival calculus.

COMPOSITION: Supragingival calculus consists of inorganic (7 to 9 per cent! and

organic components (" to # %! INORGANIC CONTENT$ %s b& 'luc( and )urra&. norganic portion consist of5 -4.0F calcium phosphate, Ca'!"(/> ,.1F calcium carbonate, CaC",. Traces of magnesium phosphate,Dg,'!"(/> Traces of other metals.' Donetite & calcite/

$rinci2al c%m2%nents+ calcium + ,0F phosphorus + 10F carbon dio9ide 3 1.0F magnesium 3 *.:F

Trace elements 5 sodium zinc strontium bromine copper manganese tungsten gold aluminium silicon iron fluorine

#LOURID" IN CALCULUS+

 Concentration+ of fluoride in calculus varies and is influenced by the amount of fluoride, received from fluoride in the drinking water, topical application, dentifrices, or any form that is received by contact with the e9ternal surface of calculus. =luoride concentrations were highest in or near the outermost regions of the calculus. The concentration decreased markedly toward the interior, rising again as the tooth surface was approached.'"kumura et al/. &upragingival calculus tended to show a smoother distribution for fluoride than did subgingival calculus. &ite 3 specific differences 3 fluoride concentrations tended to be relatively high at the cervical margin both in supra+ and subgingival calculus. However, in subgingival calculus, fluoride concentration decreased markedly toward the apical region, whereas in supragingival calculus it did not change toward the incisal or occlusal region. =luoride concentrations appeared to be higher in high mineral contents 'phosphorus and calcium concentrations/. &ite differences and profiles of fluoride concentrations reflect their possible mechanisms of formation of calculus and the influence of oral andKor crevicular environments. CR8STALS+ at least two thirds of the inorganic component is crystalline in structure. %lectron microscopy & 9+ray diffraction studies,( distinct phosphate crystals 5 Hydro9yapatite Ca1*'"H/>'!"(/) 3 appro9imately 4:F Dagnesium whitlockite Ca0'!"(/)L!"( + >1F "ctacalcium phosphate Ca(H'!"(/,.>H>" + 1>F .rushite CaH!"(.>H>" + 0F

Menerally, two or more crystal forms are typically found in a sample of calculus.

Hydro9yapatite and octacalcium phosphate are detected most frequently' in 0-+1**F of all supragingival calculus/ and constitute the bulk of the specimen. .rusite is more common in the mandibular anterior region. Dagnesium whitlockite is common in the posterior areas and sublingually. The incidence of the four crystals forms varies with the age of the deposit. %arly calculus 3 brusite

<ater 3 octacalcium phosphate'Nani et al.10:,,&undberg & =riskopp 10:4/ Dature calculus 3 hydro9yapatite and whitelockite.'Iewesely 10):/

@ifferent layers of same calculus have different compositions. %9terior layers have "C! and inner layers have hydro9yapatite. &upragingival calculus 3 clearly built up in layers & yields a great heterogeneity from one layer to another with regard to mineral content. .rushite has CaK!.1.>0 $patite has CaK!5>.1)

CALCULUS CO($AR"D ?ITH T""TH AND BON"7

@ental enamel+ 0)sF inorganic salts @entine + )4F Cementum and bone 3 (4 to 4*F Dature calculus 3 -* to 0*F

$ comparison of calculus with the tooth parts provides insight into the effects of instrumentation, the difficulty of distinguishing calculus from cementum or dentine when scaling subgingivally, and the modes of attachment of calculus to the tooth surface. @ental calculus, salivary duct calculus, and calcified dental tissues are similar in inorganic composition. ORGANIC CONT"NT Consist of mi9ture of protein+ polysaccharide comple9es, desquamated epithelial cells, leukocytes, and various types of microorganisms. Carbohydrat 3 1.0F and 0.1F of organic component, consist of 5 Malactose Mlucose #hamnose Dannose Mlucuronic acid Malactosamine sometimes5 arabinose galacturonic acid glucosamine

Salivary prot ins 3 4.0F to :.>F of organic component, include most amino acids. !ipids" *.>F of organic component, in the form of5 Ieutral fats =ree fatty acids Cholesterol Cholesterol esters !hospholipids Subgingival calculus+ has composition similar to supragingival calculus, with some differences.

&ub gingival calculus, somewhat more homogenous with equally high density of minerals. &ubgingival calculus has the same hydro9yapatite content, more magnesium whitelockite 'Oensen & #owles 104-/, and less brusite and octacalcium phosphate than supragingival calculus. The ratio of calcium to phosphate is higher subgingivally. The sodium content increases with the depth of periodontal pockets. &alivary protein found in supragingival calculus is not found subgingivally.

@ental calculus, salivary duct calculus and calcified dental tissues are similar in inorganic composition.

ATTACH("NT O# CALCULUS TO TOOTH SUR#AC"

@ifferences in the manner in which calculus is attached to the tooth surface affect the relative ease or difficulty encountered in its removal. &everal modes of attachment has been observed by conventional histological techniques and by electron microscopy. "n any one tooth and in any one area, more than one mode of attachment may be found. Pander 74( described four methods of attachmentE Doskow 7)0 suggested the 4th method. ,0 Attachment 6 means %1 an %rganic 2ellicle %n enamel7 Calculus attachment is superficial because no interlocking or penetration occurs.

 !ellicle attachment occur most frequently on enamel and newly scaled and planned root surfaces Calculus can be readily removed because of smooth attachment. >. (echanical l%c@ing int% sur1ace irregularities. %namel irregularities include cracks, lamellae, and carious defects Cemental irregularities include resorption lacunae , cemental tears. @ifficult to be certain all calculus is removed when it is attached by this method.

,. Cl%se ada2tati%n %1 calculus undersur1ace de2ressi%ns t% the gentle sl%2ing m%ulds %1 the unaltered cementum sur1ace. (. !enetration of the calculus bacteria into cementum.

4. $ttachment of organic matri9 of calculus into minute irregularities that were previously insertion locations of sharpey7s fibres.

(OD"S O# ATTACH("NT

D"@%& "= $TT$CHD%IT @%M#%% "= $TT$CHD%IT $cquired pellicle or cuticle &uperficialE no interlocking or penetration e9ists, easily removed

CH$#$CT%# &T C& !ellicle is postioned between the calculus and tooth surface. "ccurs on enamel and recently &caled Kroot planedKdebrided &urface

Dechanical locking into Dinute irregularities

Challenging to remove because of Cemental irregularities The <ocking into the tooth surface include locations of previous shrapey7s fibers, resorption lacunae, instrumentation grooves, cemental fragmentation. tears or

@irect contact between

Hard to distinguish between

norganic crystals of the tooth

10

calcified intercellular matri9 and surface

calculus and cementum

interlock with bacterial plaque.

the

mineralized

Calculus embedded deeply in cementum may appear morphologically similar to cementum and thus has been termed calculocementum.'by &elvig. O/ > modes of mineralization centers+ Type $ and Type . have been distinguished ultrastructurally. Type $ are formed only in the presence of and in association with micro organisms. Type . are apparently not related to micro organisms but have atleast one common border with the type $ centre and included micro organisms. The crystals associated with type $+ Hydro9yapatite by L+ ray diffraction. The crystals associated with type .+ "C!, . or A.

#OR(ATION O# CALCULUS
Calculus is dental plaque which has undergone mineralization. Calculus formation occurs in three basic steps5 1. P llicl #or$ation+ $ll surfaces of the oral cavity are coated with a pellicle. =ollowing tooth eruption or a dental prophyla9is, a thin, saliva+ derived layer, called the acquired pellicle, covers the tooth surface.The pellicle consist of numerous components, including glycoproteins, proline+ rich proteins, phosphoproteins, histidine 3 rich proteins, enzymes, and other molecules that can function as adhersion sites for bacteria. %& Initial adh sion and attach$ nt o# bact ria " Transport to the surface 3 involves the initial transport of the bacterium to the tooth surface. nitial adhesion 3 reversible adhesion of the bacterium, initiated by the interaction between the bacterium and the surface , through long+range and short+range forces $ttachment 3 a firm anchorage between bacterium and surface will be established by specific interactions. ,. C%l%ni+ati%n and $la3ue (aturati%n 5 when the firmly attached microorganisms start growing and the newly formed bacterial clusters remain attached, microcolonies or a biofilm can develop. Mram+ positive coccoidal organisms are the first settlers to adhere to the formed enamel pellicle, and subsequently, filamentous bacteria gradually dominate the maturing plaque biofilm '&cheie, 100(/. '& Min rali(ation ) The soft plaque is hardened by the precipitation of mineral salts, which usually starts between the first and fourteenth days of plaque formation. Calcification can occur as soon as ( to : hours.

11

Calcifying plaque may become 4*F mineralized in > days and )*F to 0*F mineralized in 1> days. %arly plaque contains a small amount of inorganic material, which increases as the plaque develops into calculus. &eparate foci of calcification increase in size and coalesce to form solid masses of calculus. $ll plaque doesnot necessarily undergo calcification. !laque that doesnot develop into calculus reaches a plateau of ma9imal mineral content within > days. Dicro organisms are not always essential in calculus formation because calculus occurs readily in germ free rodents.

S%urces %1 minerals+ o &upragingival calculus 3 the source of elements for supragingival calculus is saliva. o &ubgingival calculus 3 the gingival sulcus fluid and inflammatory e9udate supply the minerals for the subgingival deposits. because the amount of sulcus fluid and e9udate increases in inflammation, more minerals are available for mineralization of subgingival plaque. !laque has the ability to concentrate calcium at > to >* times its level in saliva. Calcium and phosphate are two salivary ions which are ?raw materials8 for dental calculus formation. Theoretically, supersaturation of saliva, especially plaque fluid, with respect to calcium phosphate salts is the driving force for dental plaque mineralization. n heavy calculus formers, early plaque contains more calcium, three times more phosphorus, and less potassium than non 3 calculus formers. !hosphorus is more critical than calcium in plaque mineralization. Calcification entails the binding of calcium ions to the carbohydrate+ protein comple9es of the organic matri9 and the precipitation of crystalline calcium phosphate salts. Crystals form initially in the intercellular matri9 and on the bacterial surfaces and finally within the bacteria. Calculus formation begins with the deposition of kinetically favoured precursor phases of calcium phosphate, "C! and .rusite, which are gradually hydrolysed and transformed into less soluble H$! and AHT mineral phases '#owles, 10)(/. Calcification begins along the inner surface of the plaque ad2acent to the tooth in separate foci of cocci which increases in size and coalesce to form solid masses of calculus. Calcification may be accompanied by alteration in the bacterial content and staining qualities of the plaque. $s calcification progresses, o Iumber of filamentous bacteria increases o =oci of calcification changes from basophilic to eosinophilic o There is reduction in the staining intensity of groups e9hibiting a positive periodic acid+ &chiff reaction, sulfhydryl and amino groups also are reduced and instead stain with toluidine blue, which initially orthochromatic but becomes metachromatic and disappears.

12

!$& Q toluidine blue'orthochromatic/ Q metachromatic Q disappear. Calculus is formed in layers, which are often separated by a thin cuticle that becomes embedded in the calculus as calcification progresses.

D"SCRI$TION O# CALCULUS SI:"

LIGHT (OD"RAT" H"A48 =ine granules,grainy or spicule $ bump with thickness readily <edge encircling thick and <ocated along line angles, marginal discernible. dense. areas and or under contacts <ocated along a marginal ring =ills or interpro9imal interpro9imal.8click8 space or is a marginal ledge. &light vibration or roughness @etected with e9plorer. @efinite vibration felt with @efinite vibration. %9plorer. &ometimes vibration binds $ 2ump also detected with curet, e9plorer, also detected with nterpro9imal deposit sometimes curet, interpro9imal deposit detected from lingual and buccal @etected from lingual and buccal.

Calculus usuall 1%rms in a h%ri+%ntal 1ashi%n %n r%%t circum1erence! that is 'h initial e<2l%rat%r str%@es sh%uld 6e &ertical and %6li3ue and n%t h%ri+%ntal0

RAT" O# #OR(ATION AND ACCU(LATION

;aries from person to person and in different teeth and at different times in the same person. .ased on these differences, individuals may be classified as hea& ! m%derate or slight calculus formers or as a nonformers. The average daily increment in calculus formers is from *.1*F to *.14F of dry weight. The calculus on the lingual surface of the mandibular anterior teeth is a reliable indication of the amount of entire dentition. Ninet 2er cent %1 all the calculus %ccurs %n the mandi6ular anteri%r Calculus formation continues until it reaches a ma9imum from which it may be reduced in amount. The time required to reach the ma9imum level has been reported as ten weeks, and si9 months. The decline from ma9imum accumulation 're&ersal 2hen%men%n/ may be e9plained by the vulnerability of bulky calculus to mechanical wear from food and the cheeks, lips and tongue.

TH"ORI"S ON (IN"RALI:ATION O# CALCULUS

n 1:-:, Dagitat was of the opinion that tartar consisted mainly of mineral matter formed by the precipitation of earthy carbohydrates and phosphates from the saliva. These mineral salts were united with organic matter, epithelial cells, fatty globules, leukocytes, filiform algae. He felt that an alkaline saliva was essential for the precipitation of the mineral salts. Theories regarding the mechanism whereby plaque is mineralized to form calculus fit into two principal concepts5

13

.""&T%# C"IC%!T+ according to this concept mineral precipitation results from a local rise in the degree of saturation of calcium and phosphate ions which may be brought about in several ways5 1. Sali&ar 2H the%r 3 Hodge & <eung 104* $ rise in the pH of saliva causes precipitation of calcium phosphate salts by lowering the precipitation constant. The pH may be elevated by the loss of carbon dio9ide, by the formation of ammonia by dental plaque and bacteria, or by protein degradation during stagnation. .urchard postulated that precipitation of calcium salts from supersaturated saliva was the result of an increased pH caused by the loss of C"> from the saliva. The presence of carbonic anhydrase was demonstrated in the saliva by #app. This enzyme supposedly caused an increased uptake as well as an increased liberation of C"> from the saliva. >. C%ll%idal 2r%teins in saliva bind calcium and phosphate ions and maintain a supersaturated solution with respect to calcium phosphate salts. Aith stagnation of saliva colloids settle out, the supersaturated state is no longer maintained, leading to precipitation of calcium phosphate salts. '!rinz,10>1/. $h%s2hatase 'enzyme theory/liberated from dental plaque, desquamated epithelial cells or bacteria is believed to play a role in the precipitation of calcium phosphate by hydrolysing organic phosphatase in saliva and thus increasing the concentration of free phosphate ions. $nother enzyme esterase, present in the cocci, filamentous organisms, leukocytes, macrophages and desquamated epithelial cells of dental plaque, may initiate calcification by hydrolysing fatty esters into free fatty acids. The fatty acids from soaps with calcium and magnesium that are converted later into the less soluble calcium phosphate salts. nterest in phosphatase and its possible role in calculus formation was probably stimulated by #obinson7s investigations concerning the enzyme7s possible role in bone mineralization. His theory was that the enzyme phosphatase could hydrolyse phosphate esters of the blood to produce the local increase of phosphate ions until a precipitate of calcium phosphate would result. "$ITACTIC CONC"$T A S""DING TH"OR8AH"T"ROG"NOUS NUCL"ATION: 'Dandel 104-/ $ccording to this concept, seeding agents induce small foci of calcification, which enlarge and coalesce to form a calcified mass. The seeding agent in calculus formation are not known, but it is suspected that the intercellular matri9 of plaque plays an active role The carbohydrate protein comple9es may initiate calcification by removing calcium from the saliva 'chelation/ and binding with it to form nuclei that induce subsequent deposition of minerals. !laque bacteria have also been implicated as possible seeding agents. The carbohydrate protein comple9es may initiate calcification by removing calcium from saliva 'chelation/ and binding with it to form nuclei that induce subsequent deposition of minerals. INHIBITION TH"OR8:

,.

14

Calcification occurring only at specific sites because of the e9istence of an inhibiting mechanism at non+calcifying sites. "ne of the inhibiting substances is thought to the pyrophosphate and the controlling mechanisms is thought to be an enzyme alkaline pyrophosphate which can hydrolyse pyrophosphate to phosphate *Russ ll and +l isch, -./01& The pyrophosphate inhibits calcification by preventing the initial nucleus from growing possibly by poisoning the growth centres of the crystal.

ROL" O# (ICROORGANIS(S CALCULUS

IN

TH"

(IN"RALI:ATION

O#

$lthough calculus can be induced in germ+free animals 'Theilade et al., 10)(/, human calculus development invariably involves plaque bacterial calcification. Dineralization of plaque starts e9tracellularly around both gram 3 positive and gram 3 negative organisms, but may start intracellularly in some gram 3 positive bacteria. =ilamentous microorganisms , diphtheroids, and .acterionema and ;eillonella species have the ability to form intracellular apatite crystals. Calculus formation spreads until the matri9 and bacteria are calcified. &ome feel that plaque bacteria actively participate in the mineralization of calculus, by forming phosphatases, by decomposing the proteins & changing the plaque pH or inducing mineralization 'Iaeslund 10>4/ , but the prevalent opinion is that they are only passively involved and are simply calcified along with other plaque components. However, other e9periments suggest that transmissible factors are involved in calculus formation. t was also said that penicillin in the diets of some of these animals reduces calculus formation. Ion viable bacteria calcify more readily than viable organisms, and it has been suggested that nonviable organisms are essential to the mineralization process, but bacterial metabolic activity is not. =ilamentous organisms promote calcification by providing an intermicrobial environment suitable for calcification. *+ris2opp and 3a$$arstro$1 The fast growth of supragingival calculus, compared with the slower growth rate of subgingival calculus, with fewer filamentous organisms. The lack of nucleic acids in calculus indicates that the oral micro+organisms undergo e9tensive degradation, leaving only the cell walls for calculus formation.'little et al 10))/ Ion+calculus sites are associated with a significantly higher level of %ctinobacillus actinom&cetemcomitans '%a/ and a lower level of black+pigmented anaerobic rods than sites presenting with calculus. %a has, therefore, been proposed to e9ert an inhibitory effect on the colonization of plaque+producing and calcifiable bacteria *!istgart n, -.4/1

15

"TIOLOGIC SIGNI#ICANC"
t is difficult to distinguish between the effects of plaque and calculus on the gingiva. Calculus is always covered by a layer of unmineralized plaque. n young persons, periodontal conditions are more closely related to plaque accumulation than to calculus. Aith increasing age the above situation is reversed. The occurrence of calculus, gingivitis and periodontitis increases with age. The non mineralized plaque on the calculus surface is the principal irritant, but the underlying calcified portion may be a significant contributing factor. t does not irritate the gingiva directly but provides a fi9ed nidus for the continued accumulation of plaque and retains it close to the gingiva.

3EA!T35 TISS6ES 7 CA!C6!6S 8ISEASE

IN+!AMMATOR5 PERIO8ONTA!

However, it has clearly been established that surface roughness alone does not initiate gingivitis *9a rhaug -.:;1& @ental calculus is not in itself harmful and that the ma2or reason for preventing its formation or removing it once it has formed is because it is always covered by a layer of unmineralized, viable and metabolically active bacteria'Iewman 100(/ The non mineralized plaque on the calculus surface is the principal irritant, but underlying calcified portion may be a significant c%ntri6uting 1act%r0 !rovides fi9ed nidus for continued accumulation of plaque and retain it close to gingiva. Creates an area where plaque removal is impossible. nterfere with local self cleansing mechanism

&ubgingival calculus may be the 2r%duct rather than the cause %1 2eri%d%ntal 2%c@ets. !laque initiates gingival inflammation, which starts pocket formation, and the pocket in turn provides a sheltered area for plaque and bacterial accumulation. The increased flow of gingival fluid associated with gingival inflammation provides the minerals that convert the continually accumulating plaque into subgingival calculus.

16

 &upragingival calculus, by nature of its porosity '=riskopp &Hammarstrom 10:*, =riskopp 10:,/ may act as a reservoir for irritating substances such as endoto9ins, which can affect the chronicity and progression of periodontal disease 'Dandel & Maffar 10:)/. &upragingival calculus may 'Mreene 10)*, #amf2ord 10)1/ or may not always '<oe et al 10-)/ be associated with gingivitis or periodontitis, where as subgingival calculus invariably is associated with loss of periodontal attachment and pocket formation 'Aaerhaug 104>, <ovdal et al 104:/. &everity and type of periodontal disease+ there is an increase in the deposition of calculus with an increase in severity of disease. $nd it is accepted that in adult periodontitis, there is a greater accumulation of calculus than in early onset periodontitis 'Carranza 10:(a/. %lthough the bacterial plaque that coats the teeth is the main etiologic factor in the development of periodontal disease* the removal of subgingival plaque and calculus constitutes the cornerstone of periodontal therap&. Calculus plays an important role in maintaining and accentuating periodontal diseases.

#ACTORS A##"CTING TH" RAT" O# CALCULUS #OR(ATION :

Diet and nutriti%n 5the significance of diet in calculus formation depends more upon its consistency than upon its content. o Calculus deposition is retarded by coarse detergent foods. $nd hastened by soft and finely ground diets. o ncreased calculus formation has been associated with deficiencies of vitamin $, niacin, or pyrido9ine, and with an increase in dietary calcium, phosphorus, bicarbonate, protein and carbohydrate. Age 3 there is an increase calculus deposition with an increasing age.'&chroeder et al,10)0/. This increase, is not only for the increase in the number of surfaces, but also the size of calculus deposits increases with age. This may be due to change in quantity and quality of saliva with age, favouring the mineralization properties. Ha6its 5 o n populations that practice regular oral hygiene and with access to regular professional care have low tendency for calculus formation. o Sm%@ing7 is associated with an elevated risk for supragingival calculus deposition. &moking may e9ert its influence systemically 'elevated levels of salivary calcium and phosphorus/ or locally via a conditioning of tooth surfaces. o Tobacco +.etel chewing is also associated with an elevated risk of calculus formation.the quantity of tobacco consumed is directly related to the percentage of deposits. Sali&ar 2H7 increase pH increases the calculus formation. Ca1*'!"(/) R '"H/>1*Ca>SS)!"( ,+S>"H+.

17

o Ahen the calcium phosphate crystals in solution are in kinetic equilibrium, the rate of precipitation is equal to that of dissolution. f pH in solution drops 'the concentration of hydrogen ions increases/, "H+ and !"( ,+ tend to be removed by HS by forming water and more acidic forms of phosphate, respectively. o $s a result, the equilibrium is broken and is pulled to the rightE that is, the rate of dissolution e9ceeds that of precipitation, and the net result is the dissolution of H$! crystals and a decrease in the H$! saturation degree. o f pH in solution rises, the opposite event will occur5 "H+ forces the equilibrium in the equation to the left, thus resulting in an increased degree of H$! saturation in solution 'Cotton and Ailkinson, 10))/. Sali&ar 1l%' rate 3 increased salivary flow rate decreases the calculus formation. &alivary flow rate affects calcium phosphate saturation. Sali&ar calcium c%ncentrati%n+ %levated salivary calcium concentration, increases the rate of calculus formation. Higher total sali&ar li2id le&els 5 is associated with increased calculus formation

"m%ti%nal status+ increased calculus formation has been associated with disturbed emotional status. Nucleati%n inhi6it%rs 7 Dg blocks apatite crystallization and stabilizes calcium phosphate as amorphous mineral '%nnever and ;ogel, 10:1/. @iphosphonate7s, such as ethane+1+hydro9y+1, 1+@iphosphonate '%H@!/, inhibit both apatite nucleation '=leisch et al., 10-*/ and crystal growth '=rancis, 10)0/. mportantly, nucleation inhibitors should not be used clinically, because they have been found to interfere with normal mineralization of hard tissues '&chenk et al., 10-,/. Cr stal gr%'th inhi6it%rs7 o &ome salivary proteins containing negatively charged sequences may adsorb at active sites on the crystallite surfaces and thereby inhibit the growth and dissolution of calcium phosphate crystals. o "f these negatively charged salivary proteins, statherin and !#! are two representatives of salivary inhibitors of crystal growth. o n addition to these salivary proteins, pyrophosphate and zinc ions act as crystal growth inhibitors o mmunoglobulins present in dental plaque and calculus may also have an inhibitory effect on plaque mineralization. The gM and g$ detected in dental calculus are mainly distributed along the incremental lines, which contain fewer minerals. Organic acid and calculus 1%rmati%n 5 "ne could assume that the un+ionized, high pNa organic acids diffuse into dental calculus, dissolve the calcium phosphate crystals, and counteract the calculus calcification.

18

 Sali&ar "n+ mes 5 $n inverse relationship has been reported between the amount of calculus and pyrophosphate content of parotid saliva. Calci1icati%n 2r%m%ters 5

,0 Urea is a product from the metabolism of nitrogen+containing substances. Jrea can be secreted in normal saliva at concentrations of between 4 and 1* mmolK< but can be as high as ,* mmolK< in patients with renal disease o Mingival crevicular fluid contains up to )*mmolK< urea 'Molub et al., 10-1/. o Jrease is responsible for bacterial urea hydrolysis. $t a neutral pH, urea is hydrolyzed by urease to IH(S and bicarbonate o +he effect of urea metabolism on plaque p, " $mmonia produced from ureolysis of urea contributes to an increased plaque pH that is an essential factor in natural calculus formation. o .acteria suspected of having a role in ureolysis include -. salivarius, coagulase+ negative staphylococci 'CI&/ '&issons et al., 10::a,b/, %ctinom&ces viscosus.naeslundii 'Mallagher et al., 10:(/, transient /nterobacteriaceae, unknown anaerobes '=rostell, 10)*/, and ,aemophilus sp. '&alako and Nleinberg, 10:0/. o $mong these ureolytic bacteria, -. salivarius has attracted the most attention, ma2or contributor to ureolysis in natural saliva. .0 #lu%ride and calculus 1%rmati%n7 The caries+inhibiting ability of fluoride is well+known. o =luoride not only counteracts demineralization of hard tissue through the formation of lower+solubility fluorapatite by fluoride substitution for hydro9yl ions and adsorption onto apatite surfaces 'Aong et al., 10:-/, but also contributes to remineralization by precipitation of a fluoride+enriched apatite or calcium fluoride 'Ielsons et al., 10:(/. o =luoride also affect the morphology of the apatite crystals as it converts them from thin plates to short and slender needles *Ean s and M y r, -./41& o n addition, acid production by plaque bacteria can be inhibited by the presence of fluoride *<rin r and +rancis, -.;%1& o Therefore, fluoride may have the potential to increase the plaque pH, which may be another mechanism by which fluoride inhibits demineralization and promotes remineralization of hard tissue. o &odium fluoride may be able to inhibit the bacterial phosphatases and pyrophosphatases, the enzymes that are well+known to promote calculus formation *!ob n and =olp , -.4/1&

19

,. Silic%n 7 &ilicic acid has been reported as a strong promoter of both spontaneous precipitation of calcium phosphates and the growth of seeded crystals *8a$ n and t n Cat , -.4.1& "n the other hand, it is noteworthy that ,.*+ ,*.* mmolK< silicic acid and 1* mgKm< silica inhibit the rates of both amorphous calcium phosphate formation and H$! transformation. o The inhibitory effects on calcium phosphate precipitation of silicic acid and silica at relatively high concentration may be due to their increased chelating effects. C$<CJ<J& ="#D$T "I I !$T %IT& JI@%#M" IM H"D%"@T<$& &5 ncreased tendency for calculus deposition. =low rate is lower in dialysis patients, 9erostomia dry mouth common complaint of renal pts. @ialysis patients are heavy calculus formers. Day b due to elevated levels of !H"&!H"#J&, J#%$ "# !#"T% I&.

"9A(INATION
&J!#$M IM ;$< %L$D I$T "I5 @irect %9amination 3 supragingival calculus can be seen directly or indirectly, using a mouth mirror. Aith a combination of retraction, light and drying with air, small deposits can be seen. &J.M IM ;$< %L$D I$T "I5 ;isual %9amination 3 dark edge of calculus may be seen at or 2ust beneath the gingival margin.gentle air blast can deflect the margin from the tooth for observation into the pocket. Mingival tissue colour change 3 dark calculus may reflect through a thin margin and suggest its presence. Tactile e9amination+ Cl r hugh 100) used AH" U )>1 probe. $nd a fine subgingival e9plorer is also used. #adiographs3 although not always reliable

%ndoscopy %lectronic calculus detection Dagnification with eye loupes

!iezoelectric ultrasonic handpiece with a conventional scaler insert. The impulse response of the mechanical oscillation system is analyzed by a fuzzy logic+based computerized algorithm, which classifies various surfaces. )eissner ' et al >**) =luorescence &pectroscopy.

ASS"SS("NT O# CALCI#I"D D"$OSITS:

20

&implified calculus inde9 'Mreen & ;ermillion 7)( / Calculus component of periodontal disease inde9 '#amf2ord 740/ Calculus surface inde9 '%nnever O,, &turzenberger & #adike 7)1/ Calculus surface severity inde9 '%nnever O et al 7)1/ Darginal line calculus inde9 'Duhleman & ;illa 7)-/ ;olpe+ Danhold inde9 ';olpe $ # & Danhold O H 7)>/

IN 4ITRO $RODUCTION O# CALCULUS

&everal methods have been attempted to produce artificial calculus outside the mouth. &ome of these methods used stimulated saliva from human sub2ects, others used a calcifying solution and still others used e9tracts from salivary glands of animals. Chemically, in vitro calculus closely resembled natural calculus, but there was more organic material and less mineralization in the artificial deposit. The CaK! ratio and the L ray diffraction pattern 'hydro9yapatite/ were found to be similar to natural calculus. t is noted that artificial calculus had a regular uniform layering, in contrast to the characteristic irregular layering seen in natural calculus.

IN 4I4O $RODUCTION O# CALCULUS

n early 10th century, .lack observed the process of calculus formation by inserting glass plate in his own denture. The deposit was allowed to collect for varying periods of time and observed that calculus entered the mouth as a finely divided 6calculo+globulin7 that was deposited on the glass plateEthe early deposit had a greasy feel to the fingersE and if this material remained on the plate, it calcified. n 10(-, wasawa studied early calculus formation in his own mouth by attaching pieces of teeth on his own denture. Calculus was allowed to collect on these pieces of teeth for known time intervals. The pieces of teeth were then removed and processed for histological evaluation. He observed that calculus formation occurred in > stagesEthe formation of an organic matri9 and the infiltration and deposition of calcium salts. The organic matri9 was composed of bacterial plaque, salivary colloids and e9udates.

21

Dandel et al used thin celluloid strips wired to the lingual and pro9imal surfaces of lower anterior teeth to collect deposits. @eposits were allowed to collect on strips from >+>0 days, removed and studied in several ways. Their findings were as follows5 L ray diffraction revealed the crystalline structure to be mostly apatite with some whitlockite. Mrenz ray e9amination of the strips revealed granular mineralization by the seventh day and definite mineralization by the 1(th day. .acteriological cultures showed the presence of a variety of organisms, cocci and various types of filaments. Pander et al used electron microscopy in addition to light microscopy to study early calculus formation from 1 day to ( weeks. They stated that the process of calcification of calculus is the same as in calcified biologic tissues. The micro organisms and intermicrobial material are the matri9 that becomes calcified. Calcification follows a pattern in which crystals are laid down between bacteria and their surfaces and later inside them.

ANAL8SIS O# CALCULUS
@ental calculus as a mineralized structure, is readily available and thus has been the sub2ect of analysis by numerous investigators using various methodologies. CH%D C$< $I$<T& & Chemical analysis has been made by several investigators. Mlock and Durray analysed samples of calculus and found them to contain the following5 :>.0F inorganic salts -4F calcium phosphate ,F calcium carbonate (Fmagnesium phosphate

Traces of other minerals "rganic portion5 :F protein ,Ffat Aater

S$"CTROANAL8SIS

22

t is the process of analyzing light by breaking it into a spectrum measuring the amount of each wavelength to measure minute amounts of elements. t has revealed the presence of many minerals in dental calculus. The basic elements were found to be calcium !hosphorus Dagnesium "thers5 &odium !otassium <ead

t was noted that calculus formed on metal fillings or prosthetic appliances contained small traces of their ingredients. 9 RA8 DI##RACTION t finds the geometry or shape of molecules using L rays based on the elastic scattering of L rays from structure that have long range order, to know complete structure of crystalline material ranging from simple inorganic solid to comple9 protein. The most sensitive techniques have found the following crystalline structures5 Hydro9yapatite "ctacalcium phosphate Triphosphate trihydrate Dagnesium whitlockite .rushite Donelite Calcite'in small amounts/

.rushite is present in the early stages of mineralization and octacalcium phosphate in the later stages @iffraction studies revealed that the composition of dental calculus varies in people from different geographical locations and from the same area. t was also found that different layers of the same calculus specimen might have different compositions.

23

$R"4"NTION AND R"(O4AL O# CALCULUS

1. $r%1essi%nal rem%&al %1 calculus 3 scaling and root planning is done to provide a smooth tooth surface, which is easier for the patient to maintain and conducive to gingival healing. >. $ers%nal 6acterial 2la3ue c%ntr%l 3 tooth brushing, flossing and supplementary methods is a ma2or factor in the control of dental calculus reformation. ,. Anti7 calculus agents used in Commercial @entifrices + Chemotherapeutic agents have been used to supplement the mechanical removal of dental plaque '$leece and =orscher,104(E Mrossman, 104(E Pacherl et al., 10:4E ;olpe et al., 100>/. =ormation may be prevented or controlled by5 1. @ecreasing the amount of plaque available for mineralization using antimicrobial agents and enzymes >. Dodifying the attachment of plaque by antiadhesive agents ,. nhibiting the process of mineralization by crystal growth inhibitors.' it currently dominates/ (. @issolve or soften the mature deposit by removing the inorganic portion. 4. $ffect the calculus matri9 i.e to change the 6skeleton7 around which calculus is deposited. CLASSI#ICATION O# ANTI7 CALCULUS AG"NTS7 ,st G"N"RATION ,> DISSOLUTION o o o Chelating Agents %thylene diamine tetra acetic acid &odium He9a Detaphosphate Acids 5Ar%matic sul2huric acid >*F Trichloroacetic $cid S2ring Salts S%dium Ricin%late Al@alies

.> ALT"RING CALCULUS ATTACH("NTS o &ilicon o on e9change resins B>0$LA;U" INHIBITION $ntibiotics %9ample 5 Triclosan '*., F/ !olyvinylmethyl ether & maleic acid '>F/

24

$ntiseptics

%9ample 5 Chloramines

C> 0(ATRI9 DISRU$TION o %nzymes %9ample 5 Ducinase o Trypsin, chymotrypsin o Carbo9ypeptidase, lipase, amylase .nd G"N"RATION Inhi6iti%n %1 cr stal gr%'th ;itamin C '.y crystal poisoning mechanism / !yrophosphate !yrophosphate S &odium fluoride Pinc salts .isphosphonates !olymers & Co !olymers To date the most successful approach to the chemical inhibition of supragingival calculus has been with the use of crystal growth inhibitors. Dineralization inhibitors include chemicals5 !yrophospahtes @iphosphonates Pinc salts These adsorb on the surface of crystals, thereby decreasing the rate of crystal growth and phase transformation of calcium phosphate salts. n addition to coating the surface of crystals at the time of application, it is important that the inhibitors be retained within the plaque fluid to provide a reservoir that sustains activity between applications. #eadily formulated accepted products for consumer use are5 Denti1rices c%ntaining :n salts + *.4F+>F Pn Citrate, >F Pn Chloride. nhibit the growth of H$ crystal in+vitro & possesses the additional benefit of inhibiting plaque formation. Jnlike other, it is cationic & is consequently retained with in oral cavity Denti1rices c%ntaining 2 r%2h%s2hate salts 3 pyrophosphate inhibiting or delaying the transformation of the amorphous, precrystalline phase to H$!. @entifrice containing 4F pyrophosphate had greater uptake and retention than from a formulation containing ,.,F ncorporation of a copolymer of polyvinyl methyl ether and maleic acid also enhances the efficacy of pyrophosphate by inhibition of alkaline phosphatase and pyrophosphatase activator. This has enabled a lower concentration of pyrophosphate '1.,F/ to be used and yet maintain an effective level of calculus inhibition. !yrophosphate e9erts its effect by inhibition or delaying the transformation of amorphous, precrystalline phase to hydro9yapatite.

25

 Denti1rices c%ntaining tricl%san + Triclosan '*., F/. is a broad+spectrum antibacterial agent active on both Mram+positive and +negative micro+organisms. The target is the cytoplasmic membrane. Denti1rices c%ntaining di2h%s2h%nate c%m2%und + Di2h%s2h%nate: $zacytcloheptane+>, >+ diphosphonic acid '1.14F/. nhibit both apatite nucleation *+l isch t al& -./01 and crystal growth *+rancis, -.;.1& CALCULUS SO#T"NING G"L $ calculus softening gel is currently available that may enhance periodontal instrumentation effectiveness. The active ingredient is disodium ethylene diamine tetra acetic acid'%@T$/, which is a calcium+chelating agent. AG"NTS #OR SO#T"NING TH" (ATUR" CALCULUS A0 ACIDS "ne of the earliest techniques utilized a wooden stick which was moistened with ar%matic sul2huric acid before being introduced into periodontal pocket to dissolve calculus and to act on the soft tissues as an astringent. $fter > weeks, the tooth become firm and cured'.arker 1:->/. <ater on Iiles'1::1/ suggested to use nitro muriatic acid because of its superior dissolving action on dental calculus. "ther acids included5 >*Ftricholoacetic acid .ifluoride of mercury 1*Fsulphuric acid

The use of acids created some problems such as5 They are caustic to soft tissues @ecalcify tooth structures

&tones'10,0/ and Mrossman'104(/ noted that the ability of acid to dissolve tooth structure was greater than its ability to dissolve calculus which lead to discontinued use of acid as anti calculus agent. B0 ALKALI"S .adanes'10>0/ noted the beneficial effect of natural mineral water on the removal of calculus. He said that it was the action of mild alkalies contained in water that dissolved the , organic constituents of salivary calculus, globulin, mucin and calcium o9alate. C0 CH"LATING AG"NTS

26

Chelating agents are used to dissolve crystallized calcium salts and are capable of combining with calcium to form stable compounds. &odium he9ametaphosphate was found to remove supragingival calculus from e9tracted teeth in 1*+14 days.'Nerr and =ield 10((/ &ubsequent studies by Daynar et al'100(/, &mith et al'100(/, Harding et al'100)/ and Iagy et al'100:/ have failed to confirm that the use of chelating gel prior to scaling decreases the time taken for scaling.

"N:8("S
The mode of action of enzyme formation is to break down plaque matri9 or to affect the binding of the calculus to the tooth. The first enzyme to be tested was mucinase '&tewart 104>/, a preparation with proteolytic and amylolytic activity. $ 1.4F;iokase preparation was also incorporated into a chewing stick and sub2ects were instructed to chew one stick of gum for 4 minutes, five times per day. t produced a >>+ >)F reduction in calculus formation respectively compared to control groups. Harrison et al '10),/ investigated the effects of various fungal enzymes in tooth pastes on calculus deposition. The fungal enzymes retarded calculus deposition especially proteolytic enzymes are better tha amylolytic enzymes. 1. ; "N$&% t contains dehydrated pancreas preparation as antiplaque agent and retarding the stain on teeth'stable powder contain trypsin, chymotrypsin, amylase, lipase and nucleases/. These proteolytic enzymes are able to digest the to9ic protein material that constitiutes a favourable subsrate for bacterial growth. @isadvantage on chewing gum study by $llen and Courtney in 10-> &oft tissue retraction .urning sensation on tongue

>. $nother proteolytic enzyme, produced from a mutant strain of .acillus subtilis also had a favourable effect on reducing stainable, soft deposits. ,. Ducinase (. @e9tranase

UR"A
The idea of using urea as a potential anticalculus agent stems from its attributed solvent action on protein'Holder and Dackay 10,-, Duldavin and Holtzman,10,:, Holder and Dackay 10,0/

27

The anticalculus effect of urea was attributed to its ability to dissolve the muco proteinaceous material within which the calcium salts are deposited and Kor by increasing the solubility of calcium salts in saliva '.elting and Mordon 10))/

(ISC"LLAN"OUS CH"(ICAL AG"NTS

Hoffman et al '10),/ attempted to prevent calculus formation using an ion e9change resin applied to teeth as a thin film. The resin was sulphonated polystyrene membrane containing negatively charged ions. n theory, the negatively charged ions would repel the positively charged calcium ions and reduce the degree of mineralization of calculus. &chaffer et al '10)(/ found that teeth coated with an ammoniated polystyrene film significantly reduced the amount of calculus deposit. &chroeder et al '10)1/ tested 0 organic compounds administered as mouthwashes as their ability to inhibit plaque and calculus formation. Hidaka et al0100,/ demonstrated that a combination of herbs used in Chinese Nampo medicines has effectiveness in inhibiting calcium phosphate precipitation.

ANTI(ICROBIALS
1. Cetylpyridinium Chloride'C!C/ t is a cationic quaternary ammonium compound. t was tested for anticalculus activity as a mouth rinse for - days but there were no differences in calculus level in C!C and controlled rinses. @isadvantages of C!C .urning sensation of oral mucosa .rownish discoloration of teeth Tellow discoloration of tongue $ recurrent, apthous type of ulceration of oral mucosa

CHLORH"9IDIN" t is second generation anti plaque agent. t is a cationic bis+ biguanide which acts by being adsorbed onto the bacterial cell wall, leading to damage of the permeability barrier. &everal studies have confirmed that chlorhe9idine is an e9cellent anti plaque agent 'loe and &chitt 10-*, Hamp et al 10-,, Tepe et al10:,/.

28

Tates et al'100,/ tested the effect of 1F chlorhe9idine dentifrice on plaque, gingivitis, calculus and tooth staining. They found that there were increased calculus levels in the active dentifrice group. Therefore chlorhe9idine is a potent antiplaque agent , it has the disadvantage of actually increasing calculus levels. TRICLOSAN Triclosan is named scientifically as >,(,(+trichloro+> hydro9yphenyl ether, a non ionic antibacterial agent with a wide spectrum of activity against bacteria, fungi and yeasts. t when delivered from a dentifrice, seems to bind to oral mucous membranes and tooth surfaces and is particularly well retained in plaque'Mulbert et al 10:-, Milbert and Ailliams 10:-/ .ecause of its proven anti plaque effects , a dentifrice containing *.>F Triclosan and *.4F Pinc citrate are used as an anticalculus agent. t is a biocide. t can be made from the partial o9idation of benzene or benzoic acid by #aschig process and found as a product of coal o9idation. t is found in soaps'*.14+*.,*F/, toothpastes, deodorants, shaving cream moth washes. ANTIBIOTICS ,0 $"NICILLIN

Constant use of pastes containing penicillin appear to enhance the development of penicillin resistant streptococci in mouth. .0 4ANCO(8CIN

t is a bactericidal antibiotic, daily use of which reduced the quantity of already formed plaque in mentally retarded, institutionalized patients. B0 "R8THRO(8CIN

&uspension of this antibiotic applied ( times a day for - days reduced the quantity of plaque in adult volunteers by ,4F C0 KANA(8CIN

&ince mid 10-*s, interest in the use of antibiotic preparations to inhibit plaque growth and control gingivitis has waned considerably. The potential problems of bacterial resistance and hypersensitivity reactions are graeter than the potential benefits of using antibiotics in long term.

29

4ITA(IN C t is a surface active organophosphorus compound that has been shown to be effective in inhibiting the in vitro crystallization of calcium phosphate onto smears of supra gingival calculus. t has a characteristic taste which might have promoted saliva flow, thus reducing calculus levels. $ study was undertaken to compare the effect of quinine sulphate and vitamin C on calculus formation. n this study each sub2ect topically applied the test chloromethyl analogue of vitamin C and a *.>)F solution of quinine sulphate+ followed by a rest period of between 1 week and , months and then used the second solution. Calculus was carefully removed by scaling and then weighted. ;itamin C analogue reduced calculus weight by -*.0F. t was concluded that taste was not a significant factor in calculus formation by vitamin C analogue.

30

31