INTRODUCTION

Definition

Calculus is an adherent calcified or calcifying mass that forms on the surface of natural teeth or dental prosthesis. Calculus is essentially mineralized plaque covered on its external surface by vital tightly adherent non mineralized plaque.

CLASSIFICATION
According to location

supragingival calculus subgingival calculus

According to source of mineralization

salivary calculus serumal calculus (Jenkins, te!art "#$$%

According to surface

exogeneous endogeneous (&elz "#'(%

Supragingival calculus
Location )*he tightly adherent calcified deposites that form on the clinical cro!ns of the teeth above the free gingival margin. (visible in oral cavity% Color )usually !hite)yello! in colour but can darken !ith age and exposure to tobacco Texture an consistenc! +hard clay like consistency. ,asily detachable from tooth surface alivary secretions are the main source of mineral salts.

Composition
Inorganic" Calcium 0hosphorous #$% of r! &eig't -. + -#/ "$ + "1/

Carbonate - + 2/ odium ".' + -.'/ &agnesium (.$ + (.1/ 3luoride (.((2 +.(4/ *races of 5a,6n, t,Cu.7r,&g,3e,Al, i,*g,8old. (9ittle et al "#$2 9undberg et al "#$$ chroeder "#$#%

Organic"

total matrix ()*+$%

amount

contains '4.#/ protein and "(.-/ lipid. $".1/ are neutral lipids, including a high content of free fatty acids and a smaller of triglycerides.
-1/ 8lycolipids

(composed of "..-/ simple glycosphingolipids, mainly lactosyl) and glucosylceramine ,1-.1/ neutral and sulfated glyceroglucolipids.%
"(.-/0hospholipids

(24.-/ phosphatidylethanolamine, -'.'/ diphosphatidylglycerol, -.2/ phosphatidylinositol, and "../ phosphatidylserine %

Cr!stals
octacalcium phosphate :Ca1(0;4%4(<0;4%-'<;= (;C0%, hydroxyapatite :Ca"((0;4%$(;<%-= (<A0%,

-tricalcium phosphate or whitlockite :Ca"((<0;4%(0;4%$= (><*% form the inorganic part of both supragingival and subgingival calculus.

Brushite :Ca<0;4)-<-;? dicalcium phosphate dihydrate=

(@C0@% is present only in the early)stage supragingival calculus (Ao!les, "#$4%..

Lig't microscop!
*he interface !ith the tooth surface !as fairly

smooth and slightly curved follo!ing the shape of the tooth !hereas the external mineralised surface !as generally irregular and covered by a non)mineralised plaque layer of variable thickness.
containing many non)mineralised lacunae and, in

some sections, the lacunae formed a continuous connection !ith the external bacterial plaque, and extended to the calculusBtooth interface

scanning electron microscop!

upragingival calculus al!ays appeared in one piece !ith a relatively smooth surface.

Cnder lo! magnification the upragingival calculus !as thin at

the incisalBocclusal part and thickened apically.

Cnder high magnification the upragingival calculus is covered

!ith dense layer of filament .*hese filaments !ere "micron thick !ith an estimated length of -' to "(( microns.

3racture surface of upragingival calculus generally had a

smooth, crystalline appearance.

x*ra! ,eam iffraction anal!sis

@istribution of calcium phosphate compounds ;C0 !as detected in the areas of supragingival calculus near the superficial layer al!ays in contact !ith saliva
Dn the middle layer of the calculus <A !as the main

component .

upragingival calculus adEacent to the gingival and subgingival calculus contain >9.

7ru in calculus is very rare and is found only in the

supragingival calculus adEacent to the gingiva.

Distri,ution
-esti,ular surfaces. *ooth 4" had significantly more

supragingival calculus on its vestibular surface than had other teeth, !ith the exception of tooth -$. *he mandibular central and lateral incisors had significantly more supragingival calculus on their vestibular surfaces than had maxillary central and lateral incisors. Dn contrast, maxillary first molars had a significantly higher mean grade for supragingival calculus on their vestibular surfaces than did mandibular first molars.

 Lingual surfaces. *he lingual surfaces of the mandibular

anterior teeth (22)42% had significantly higher grades of supragingival calculus than the lingual surfaces of other teeth. ;f these lo!er anterior teeth, the lingual surfaces of the central incisors had higher mean calculus grades than those of the lateral incisors and both the central and lateral incisors had significantly greater amounts of supragingival calculus than did the canines.

Su,gingival calculus
Location)belo! the crest of marginal gingival (not visible on routine examination% Color)dark bro!n or greenish black Texture an consistenc!)hard and dense crusty, spiny or nodular deposites 3irmly attached to tooth surface. Crevicular fluid and inflammatory exudates are the main source of mineral salts. 3ound on any root surfaces !ith a periodontal pocket.

Inorganic. organic
Composition is similar to supragingival calculus except that it contains higher concentration of calcium,magnesium and fluoride then supragingival calculus,reflecting higher concentration of ions in 8C3 then in saliva. ;rganically its devoid of salivary proteins,more form 8C3 and inflammatory exudate .

Cr!stals
octacalcium phosphate :Ca1(0;4%4(<0;4%-'<;= (;C0%, hydroxyapatite :Ca"((0;4%$(;<%-= (<A0%, and F)tricalcium phosphate or !hitlockite :Ca"((<0;4%

(0;4%$= (><*% the ><*)to)<A0 (Jensen and @anG, "#'4% and calcium)to)phosphorus ratios (9ittle and <azen, "#$4% in supragingival calculus are lo!er than those in subgingival calculus

Lig't microscop!
Cnlike supragingival calculus, lacunae of stained

organic material !ere not seen !ithin the body of subgingival calculus. *he calculus surface previously in contact !ith the tooth !as usually flat and mineralised !hilst the externalBoral surface !as fairly regular and covered by a non)mineralised plaque layer of variable thickness

Distri,ution
5o significant differences !ere found for subgingival calculus

bet!een right and left sides of the mouth for a given site and a given tooth. 3or all teeth except -$, -., and 4", the amount of subgingival calculus !as higher on the lingual surface than on the vestibular surface

ignificant differences in the amounts of subgingival calculus among different teeth !ere detected. *he results of the @uncan tests sho!ed that for the vestibular surfaces of the -1 teeth, the mandibular anterior teeth and maxillary molar teeth had the greatest amount of subgingival calculus.

(Mandel I,1969)

/R0-AL0NC0
In mandible 100% mandibular anterior teeth had calculus decreasing posteriorly to 20% in mandibular third molar. In maxilla 10% of anterior teeth 60% of first molars. (Sand 19 9! "a#a$o Indians had more calculus then %aucasians . (&arfitt 19'9!

 Subgingi#al calculus is found in interproximal

surface and least on buccal surfaces. (he first teeth to sho) calculus deposit )ere maxillary first molar and mandibular incisor. *axillary incisors and bicuspids )ere least in#ol#ed. Supragingi#al calculus starts forming )ith 6 years of erruption age )hile Subgingi#al at + yrs of age,Subgingi#al is least before 20 yrs of age.

 (he formation of supragingi#al calculus )as

obser#ed early in life in the Sri lan-an indi#iduals, probably shortly after the teeth erupt. .eposition of supragingi#al calculus reaches maximal scores around 2' to /0 yrs of age.%alculus accumation appeared to be symmetric,and by age ' only a fe) teeth ,typically the premolars )here )ithout calculus. 0y age /0,all surfaces of all teeth had subgingi#al calculus )ithout any pattern of predilection.

 *he 5or!egian academicians had good oral

hygiene,resulting in reduced accumulation of calculus.ho!ever,supragingival calculus still formed on facial surfaces of upper molars and lingual surfaces of mandibular incisors in 1(/ of individual,it did not increase !ith age and did not involved other teeth.(Anerud etal "##"%

3actors affecting the amount of calculus in a population oral hygiene habits. access to professional care @iet (&acnill"#'$% Age ethnic origin <abits eg tobacco,bettel nut (0indborg"#4.% systemic disease use of prescription medications tress (0arodneck"#2.%

RAT0 OF FOR1ATION

oft plaque is hardened by mineralization bet!een "st and "4th days of plaque formation. Calcification is reported to occur in as little as 4)1 hrs. Calcifying plaque may become '(/ mineralized in - days and $(/ to #(/mineralization in "- days. All plaque does not necessarily undergo calcification. 0laque that does not develop into calculus reaches a plateau of maximal mineral content !ithin - days. Calculus is formed in layers !hich are often separated by a thin cuticle that becomes embedded in calculus as calcification progresses 0laque has the ability to concentrate calcium at - to -( times its level in saliva.

 *he initiation of calcification and the rate of calculus

accumulation vary from person to person for different teeth and at different times of same person
According to this they are classified as 'eav!2 mo erate or

slig't calculus former.(&uhlar and ,nnever "#$-%

slight

moderate

heavy

 ,arly plaque of heavy calculus former contains more calcium,

three times more phosphorous and less potassium than that of non)calculus former
*otal protein and total lipid levels are elevated in <eavy

calculus formers.
9ight calculus formers have higher levels of parotid

pyrophosphate.
Calcification of plague is delayed in children.(*uresky "#$"%

 *he average daily increment in calculus former is from (."(/

to (."'/ of dry !eight.(9obene etal "#$$%

Calculus formation continues until it reaches a maximum, after

!hich it may be reduced in amount. *he time required to reach the maximal level has been reported as "( !eeks and $ months. *he decline for maximal calculus accumulation, referred to as reversal phenonmenon may be explained by the vulnerability of bulky calculus to mechanical !ear from food and from the cheeks, lips and tongue.

 Dn the "()"' age group, 42/ of normal children and #()"((/

of children !ith cyctic fibrosis and asthma have calculus.*his clinical observation may reflect elevation in salivary calcium and phosphorus in children !ith these disease.(>otman etal "#.2%

T30ORI0S OF 1IN0RALISATION
4ooster 1ec'anism

According to this theory, calcification !ill occur in a particular locus !hen the local p< and calcium and phosphorous concentrations are high enough to allo! for precipitation of a calcium phosphate salt. 3actors such as loss of C;- and production of ammonia could account for an elevation in p<H acid or alkaline phosphatase activity could result in a higher phosphate concentrationH liberation of bound or complexed calcium from the salivary proteins !ould produce higher calcium levels.

 0pitaxic concept

;ne of the most !idely held theories has been the epitaxic concept, !hich recognizes that the concentration of calcium and phosphate ions is not high enough in tissue fluids and saliva to precipitate spontaneously, but is sufficient to support gro!th of a hydroxyaptite crystal once an initial seed or nucleus is formed. *issue fluids and saliva are thus called metastable solutions. *he formation of the initial crystal or nucleus is called nucleation and is thought to occur !hen a proper organic matrix is available on !hich the nucleus can crystallize in exact structural configuraton. (7oskey"#1"%

 In'i,ition t'eor!

Another approach considers calcification as occurring only at specific sites because of the existence of an inhibiting mechanism at noncalcifying sites. ;ne possible inhibiting substance is thought to be pyrophosphate (and possibly other polyphosphates% and among the controlling mechanisms is the enzyme alkaline phosphatase, !hich can hydrolyze the pyrophosphate to phosphate (Ausssel and 3leisch "#.(%. *he pyrophosphate inhibits calcification by preventing the initial nucleus from gro!ing, possibly by poisoning the gro!th centers of the crystal .

 Transformation

A most attractive hypothesis is the idea that hydroxypatite need not arise exclusively via epitaxy and nucleation. Amorphous noncrystalline deposits and brushite can be transformed to octocalcium phosphate and then to hydroxypatite (,anes et al. "#.(%. Dt has been suggested that the controlling mechanism in the transformation process may be pyrophosphate (3leich et al "#$1%

 4acteriological T'eor!

;ral microorganisms are the primary cause of calculus,and that they are invovled in its attachment to the tooth surface. 9eptotrichia and Actinomyces have been considered most often as the causative microorganism.(8alippe.I."11$%

 0nz!matic t'eor!

Calculus formation is the resultant of the action of phosphatases derived from either oral tissues or oral microorganism on some salivary phosphate containing complex,most probably phospheric esters of the hexophosphoric group.(Adamson.J* "#-#%

1ec'anism of /la5ue an 1icro,ial 1ineralization

3ollo!ing tooth eruption or a dental prophylaxis, salivary

proteins rapidly and selectively adsorb onto the enamel surface to form an acquired enamel pellicle. Dt is follo!ed by the adherence of various oral micro)organisms. 8ram) 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, "##4%.

0laque absorbs calcium and phosphate from saliva for

the formation of supragingival calculus and from crevicular fluid for the formation of subgingival calculus

6A7 a sorption of salivar! proteins

*hree types of time)dependent adsorption of salivary proteins have been observed (9amkin et al., "##$% alivary proteins, such as proline)rich protein+2 (0A0)2%, 0A0)4, and statherin, adsorb very fast onto <A0 !hereas the binding rate of )amylase, glycosylated proline)rich protein (0A8%, and cystatins is slo!. *he third type of protein adsorption can be seen in the case of 0A0)", 0A0)-, and histatins

647 micro,ial a 'erence

As Ian 9oosdrecht et al.("##(% and 7ollen et al. ("##$% have described, the microbial adhesion to solid surfaces (such as tooth surfaces and various implant surfaces% may proceed as a four)stage sequence initial approach of bacteria to a surface !here random contact, such as 7ro!nian motions and liquid flo!, or active movement of micro)organisms may occur *he attractive van der >aalsK forces and repulsive electrostatic forces are responsible for the second stage of microbial adhesion, !hich is a reversible process

 *he firm attachment of micro) organisms, Lthe third

stageK, is irreversible *he fourth stage of adhesion, i.e., bacterial colonization.

6(7 Surface proteins an ,acterial a 'erence

Appendages, such as fimbriae or pili 3lagellum, another microbial surface protein Collectively, flagella, fimbriae (pili% Streptococcus mutans surface proteins have been

most !idely investigated. 0", a "".)kd and a "-.)kd protein, and t!o glucosyltransferases (8*3ase%

6+7 1icro,ial co*aggregation an coa 'esion

1ral bacteria tend to associate )ith one another. In suspension, the association bet)een different oral bacteria is termed 2co3aggregation2, )hile it is referred to as co3adhesion if one partner of the pair is attached to a surface.

4ectin3sugar interaction cation3dependent non3cation3dependent (interfacial free energies ! extracellular #esicles cell3surface lipoproteins

87 1icro,ial a 'erence to implant surfaces

Since (i pellicle differs from enamel pellicle )ith regard

to protein composition, it is understandable that the microbial adherence and the subse5uent microbial coloni6ation on a (i surface may be different from that on an enamel surface (7dgerton et al., 1996!
(here is e#idence that (i implants harbour less mature

pla5ue, )hich is composed of more coccoid cells and fe)er motile rods, as compared )ith natural teeth (8uirynen and 4istgarten, 1990! 9
:igher le#els of microbial adherence ha#e been found

on rough (i surfaces than on smooth and polished surfaces in in vivo studies ("a-a6ato et al., 19+9 !


6C7 riving force for pla5ue mineralization
materialsL for dental calculus formation.
Dn a recent study (0off et al., "##.%, ho!ever, it !as reported Calcium and phosphate are t!o salivary ions !hich are Lra!

that no significant correlation existed bet!een calcium phosphate supersaturation in saliva and the rate of calculus formation for both unstimulated and stimulated saliva.
<o!ever, calculus formation is influenced by a variety of

factors, such as salivary flo! rate, and inhibitors and promoters of calculus formation, other than salivary supersaturation !ith calcium phosphate salts.

6D7 involvement of ,acteria in calculus formation

Although calculus can be induced in germ)free animals

(*heilade et al., "#$4%,

&icrobial mineralization occurs even !ithin LacidogenicL and

cariogenic bacteria (&oorer et al., "##2%.

*he filamentous micro)organisms (diphtheroids and Ieillonella

sp%are predominant in supragingival calculus and calculus) associated plaque, !hereas micro)organisms of various morphologies are found in the plaque adEacent to subgingival calculus (3riskopp and <ammarstrMm, "#1(%. Dn addition to dead micro)organisms, live and degenerated ones can also calcify in synthetic calcifying media ( ida!ay, "#1(%.

ubgingival calculus deposits appeared to have a significantly greater percentage of coccoid forms and fe!er motile rods (C& 7ro!n et al., "##"%.

0laque bacteria actively participate by forming

phosphatases,changing the plaque p< or inducing minerialization

5on)calculus sites are associated !ith a significantly higher

level of Actinobacillus actinomycetemcomitans (Aa% and a lo!er level of black)pigmented anaerobic rods than sites presenting !ith calculus. Aa has, therefore, been proposed to exert an inhibitory effect on the colonization of plaque)producing and calcifiable bacteria (9istgarten, "#1.%.

607 micro,ial mineralization

Dnitial deposition of apatite in calcifying bacteria is associated

!ith membrane or acidic membrane)associated components (7oyan and 7oskey, "#14%.

*he functions of acidic phospholipids in calcification depend upon their ability to bind calcium by their negatively charged groups.

 Calcium is bound to adEacent phospholipid molecules in the

membrane through a t!o)point electrostatic attachment to form a stern layer !hich facilitates the interaction of calcium !ith inorganic phosphate ions in solution (<auster et al., "#$#%. *he bound calcium ions can cause loss in !ater by dehydration due to the neutralization of electrostatic charge of membrane (<auster et al., "#.'%.
Dnorganic phosphate associates !ith the bound calcium to form a Ca)

phospholipid)phosphate complex (C09N%. ;nce C09N has formed, apatite deposition follo!s !hen sufficient calcium and phosphate ions are present and the concentration of inhibitors is lo!. *he availability of C09N exhibits bacterium)specificityH C09N is al!ays present in Corynebacterium matruchotii.

6F7 nucleation in'i,itors

Dt has been demonstrated that magnesium (&g% prevents

apatite nucleation by C. matruchotii.

@iphosphonates, such as ethane)")hydroxy)", ")

@iphosphonate (,<@0%, inhibit both apatite nucleation (3leisch et al., "#.(% and crystal gro!th (3rancis, "#$#%.
Dmportantly, nucleation inhibitors should not be used clinically,

because they have been found to interfere !ith normal mineralization of hard tissues ( chenk et al., "#.2%.

697 cr!stal gro&t' in'i,itors

5egatively charged salivary proteins, statherin and 0A0 are t!o

representatives of salivary inhibitors of crystal gro!th.

Cystatins in saliva, such as the acidic cystatin and the neutral

cystatin
Dmmunoglobulins present in dental plaque and calculus may

also have an inhibitory effect on plaque mineralization.

Dt !as found that albumin could bind to <A0 surfaces and

inhibit crystal gro!th.

Dn addition to these salivary proteins, pyrophosphate and zinc

ions act as crystal gro!th inhibitors

637 organic aci an calculus formation

@espite that fact, our kno!ledge of dental caries can lead one

to assume the potential role of organic acids in calculus formation, since both the enamel and supragingival calculus contain apatites and have similar oral environments !ell)kno!n

*he importance of lactic acid in demineralization of enamel is

As the un)ionized organic acids diffuse, they continually

dissociate partially into hydrogen ions and acid anions. *he released hydrogen ions attack the enamel crystals. Collectively, the process of demineralization is composed of the follo!ing three steps? diffusion of the un) ionized acids into enamel, partial dissolution of acids, and diffusion of calcium and phosphate out of enamel (3eatherstone and Aodgers, "#1"%.

6I7 enz!mes egra ing calcification in'i,itors

According to a study by >atanabe et al.("#1-%, calculus level

!as positively correlated !ith protease activity in human saliva. protease in saliva and plaque can degrade calcification inhibitors such as statherin and 0A0. &oreover, proteases may increase dental plaque p< through the production of ammonia, one of the proteolytic end) products of proteins (3rostell and Mder, "#.(%.
Acid and alkaline phosphatases may promote crystal gro!th by

degrading pyrophosphate, !hich is an inhibitor of crystal gro!th.

6:7 calcification promoters

Urea
Crea is a product from the metabolism of nitrogen)containing substances. Crea can be secreted in normal saliva at concentrations of bet!een ' and "( mmolB9 (&acpherson and @a!es, "##"%, T'e effect of urea meta,olism on pla5ue p3 Ammonia produced from ureolysis of urea contributes to an increased plaque p< that is an essential factor in natural calculus formation. *he ureolytic p< response (an increase in plaque p< by the production of ammonia from urea% promotes calculus formation by increasing the saturation degree of calcium phosphate in plaque fluid.

 T'e effect of salivar! flo& rate on urea* epen ent p3

response in pla5ue Dn the oral cavity, urea available to supragingival plaque bacteria comes from both saliva and extra)oral factors such as urea)containing che!ing gum and toothpastes. *he effects of salivary flo! rate on the p< responses induced by urea from these t!o sources are different. Dn the absence of exogenous urea, increased salivary flo! rate promotes the urea)dependent p< response in plaque. *hus, the sites !ith higher salivary film velocity have an increased urea)dependent p< response in plaque ( hannon and 0rigmore, "#$(%. *hat can partially explain the site)specificity of calculus distribution in the dentition.

 Fluori e

*he caries)inhibiting ability of fluoride is !ell)kno!n. 3luoride not only counteracts demineralization of hard tissue through the formation of lo!er)solubility fluorapatite by fluoride substitution for hydroxyl ions and adsorption onto apatite surfaces (>ong et al., "#1.%, but also contributes to remineralization by precipitation of a fluoride)enriched apatite or calcium fluoride.

fluoride may promote the maturation of spontaneous

precipitated calcium phosphate at physiological p< by reducing the stability of ;C0 (,anes and &eyer, "#.1% 3luoride has also been demonstrated to affect the morphology of the apatite crystals as it converts them from thin plates to short and slender needles (,anes and &eyer, "#.1%.

 Silicon
O

ilicic acid has been reported as a strong promoter of both spontaneous precipitation of calcium phosphates and the gro!th of seeded crystals (@amen and ten Cate, "#1#%. ilicic acid !as also found to stimulate the transformation from amorphous calcium phosphate to <A0 (<idaka et al., "##2%. ilica at a concentration of ()- mgBm9 !as reported to exert stimulating effects on calcium phosphate precipitation (@amen and ten Cate, "#1#%. ilica !as also reported to increase the rate of calculus formation 2' days after its incorporation into food.

 *here is also epidemiological evidence for the effect of

silicon on calculus formation. Dt has been reported that the rate of calculus formation is higher in the Dndonesian than in the 5or!egian population (8aare et al., "#1#%. *he difference in the silicon content of the food may partially explain the phenomenon. Dndonesian people consume larger amounts of rice, !hich is enriched in silicon. *he rice)based diet of Dndonesian people contributes to the greater calculus formation in this population

 ;n the other hand, it is note!orthy that 2.()2(.( mmolB9

silicic acid and "( mgBm9 silica inhibit the rates of both amorphous calcium phosphate formation and <A0 transformation. *he inhibitory effects on calcium phosphate precipitation of silicic acid and silica at relatively high concentration may be due to their increased chelating effects

CALCULUS ATTAC310NT
3irst study on modes of Calculus attachment 6ander in "#'2 A secondary cuticle interface bet!een calculus and tooth surface Attachment of calculus matrix to irregularities of cementum surface corresponding to previous insertion locations of harpeyKs fibers 0enetration of microbial organisms of calculus in cementum Attachment into areas of cementum resorption via mechanical locking into undercuts.

 Inorganic intercrystalline forces may represent

a significant factor for attachment.(Sel#ig 19;0! <ttachment to pure titanium is less intimate than to root surfaces structure. Smooth machined implants ha#e less microporosities for retension. (this )ould mean that calculus may be chipped off from implants )ithout affecting it!*atarraso etal 1996

CLINICAL SI9NIFICANC0
Cntil "#$( the prevailing vie! !as that calculus !as the maEor etiological factor in periodontal disease
Supragingival calculus

*he process is enhanced by supragingival calculus !hich provides further retention and thus promotes ne! plaque accumulations it is still not clear !hether calculus plus plaque provokes a greater reaction than plaque alone, though there is some suggestive evidence of the former. ( ch!artz et al "#."%
O bring the bacterial overlay closer to the supporting tissue O interfere !ith local self cleansing mechanism O make plaque removal more difficult for the patient.

 Su,gingival calculus
Clinical studies attest the importance of frequent and

thorough removal of root deposits by scaling and root planning to prevent attachment loss (0ihlstrom et al "#12%.

&orphologic studies sho! that calcified deposits are porous

and act as a reservoir for irritating substances.

,xperimental studies have established the permeability of

subgingival calculus to endotoxin (7aumhammers and Aohrbaugh "#.(% and the presence in the deposits of high level of toxic stimulators of bone resorption and antigens from Bacteroides gingivalis) (0atters et al "#1-% !hen coupled !ith the increasing buildup of plaque on the surface of calculus the combination has the potential for increasing the rate of displacement of the adEacent Eunctional epithelium and extending the radius of destruction of bone beyond that of plaque alone (&andel and 8affar "#1$%

 @efinite correlation bet!een subgingival calculus and bone

loss in adolescent !as established (&atsson "##(%

Allen and Jerr in "#$' have sho!n, calculus after

autoclaving to remove surface plaque, calculus still exerts a toxic effect on tissue cells.
Jing in "#'. sho!ed that retained calculus forms a nidus for

calculus reformation proceeding more rapidly than that !hich forms on a smooth surface.

Aeferences
%<==<">< ?%4I"I%<4 &7=I1.1"(141@A B<" 4I".:7 ? %4I"I%<4 &7=I1.1"(141@A

<". I*&4<"(141@A .ental %alculus %omposition. 2. Subgingi#al %alculusC <sh, %alcium, &hosphorus, and Sodium *<=@D7=I(7 E. 4I((47 and S(<"47A &. :<>7". 196/
A preliminary investigation into the

ultrastructure of dental calculus and associated bacteria Tan B, Gillam DG, Mordan NJ, Galgut PN A preliminary investigation into the ultrastructure of dental calculus and associated bacteria J !lin Periodontol "##$% &'( &)$*&)+
:istochemistry of %alculus Eormation by Ir)in ..

 @.:. "ancollas and *.<.S. Bohnsson. %alculus

Eormation and Inhibition. ADR 199 +C /0;

I. *andel. %alculus updateC pre#alence,

pathogenicity and pre#ention. B <m .ent <ssoc 199'G126G';/3'+0.

Ae Bin and :a-3Hong Aip. Supragingi#al

%alculusC Eormation and %ontrol. %=10* 2002 1/C 26. 9