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 HIPPOCRATES ( 460- 377BC)

He noted the deleterious effects on the teeth and gums of Pituita (Calculus), which insinuated itself under the roots of the teeth.

The middle ages: Albucais (936 -1013) had a clear understanding of the major etiologic role of calculus deposits and described the technique of scaling the teeth

The renaissance: Paracelsus (1493 – 1541) developed an interesting and unusual theory of disease : 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 ‘ tartarus’, material that cannot be broken down and is the ultimate matter or ‘ materia ultima”

Paracelsus recognized the extensive 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

Ambroise pare (1509 – 1590) understood the etiologic significance of calculus and used the set of scalers to remove the hard deposits on the teeth

In 1683 Van Leeuwenhoek described microorganisms in tartar. He called them ‘animalcules’

Nineteenth century

Fauchard, in 1728, 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.

Leonard koecker (1785 -1850) , in a paper in 1821 , described inflammatory changes in gingiva and calculus on teeth that led to their looseness and exfoliation.

DEFINITION

Calculus: Abnormal concretion composed of mineral salts, usually occurring within the hollow organs or their passages, also called stones, such as gallstones or kidney stones.

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Dental 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 mixed with food debris , bacteria and desquamated epithelial cells(Greene, 1967)

Calculus can be defined as a hard concretion that forms on teeth or dental prosthesis through calcification of bacterial plaque. (Periodontal Literature Review)

Calculus is calcified plaque. (Manson & Eley)

Calculus is essential mineralized plaque covered on its external surface by vital tightly adherent, non mineralized plaque. (Genco)

Calculus consists of mineralized bacterial plaque that forms on the surface of the teeth and dental prosthesis. (James E Hinrichs)

Calculus is a calcified mass which forms on and adheres to the surface of the teeth and other solid objects in the mouth e. g. restoration and denture.

When 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. [Carranza ]

A hard deposit that forms by mineralization of dental plaque and is generally covered by a layer of unmineralized plaque.

A hard deposit attached to the teeth usually consisting of mineralized bacterial plaque [AAP 1992].

Mineralized dental plaque that is permeated with crystals of various calcium phosphates(Schroeder,1969)

Calculus is also known as odontolithiasis or tartar. It is also called fossilized plaque.

CLASSIFICATION

Dental calculus is classified by its location on a tooth surface as related to the adjacent free gingival margin:

SUPRAGINGIVAL CALCULUS –

Location – o On the clinical crown coronal to the margin of the gingiva and visible in the oral cavity.

Distribution – o Most frequent sites are on the lingual surfaces of the mandibular anterior teeth opposite Wharton’s

and the Bartholin’s duct and on the buccal surfaces of the maxillary molars opposite Stenson’s duct.

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o Crowns of teeth out of occlusion; non-functional; or teeth that are neglected during daily plaque

removal.o Surfaces of dentures and dental prostheses.

o In extreme cases calculus may form a bridge-like structure along adjacent teeth or cover the

occlusal surface of teeth without functional antagonist.o Sand(1949)- found nearly 100% in mandibular anterior teeth, decreasing posteriorly to 20% of the

third molars.in maxilla, 10% of the anterior teeth and 60% of first molars had supragingival calculus.s

Other names for supragingival calculus - o Supramarginal

o Extragingival

o Coronal, indicating that the calculus is on the anatomic crown.

o Salivary, a term that indicates that the source of the minerals is the saliva.

SUBGINGIVAL CALCULUS –

Location-o On the clinical crown apical to the margin of the gingiva, usually in periodontal pockets, not

visible upon oral examination.o Extents to bottom of the pocket and follows contour of soft tissue attachment.

Distribution – o May be generalized or localized on single teeth or a group of teeth.

o Proximal surfaces have heaviest deposits, lighest deposits on facial surfaces.(Lovdal et al.1958)

Other names for subgingival calculus-o Submarginal.

o Serumal, term indicates that the source of the mineral is the blood serum.

When the gingival tissue receede, subgingival calculus become exposed and is therefore reclassified as supragingival. Thus, supragingival calculus can be composed of both supragingival calculus and previous subgingival calculus.

The location and extent of subgingival calculus may be evaluated by careful tactile perception with a delicate dental instrument such as an explorer. Clerehugh et al, used a WHO ≠621 to detect and score subgingival calculus.

Supra gingival calculus and subgingival calculus generally occur together, but one may be present without the other.

Microscopic studies demonstrate that deposits of subgingival calculus usually extend to the base of periodontal pockets in chronic periodontitis but do not reach the junctional epithelium.

CLINICAL CHARACTERSTICS

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CHARACTERISITC SUPRAGINGIVAL CALCULUS SUBGINGIVAL CALCULUS

COLOR White or whitish yellow.

Influenced by tobacco and food

pigments

Dark brown or greenish black.

color derived from blood pigments

from diseased pocket

SHAPE Amorphous, bulky

Form interproximal bridge between

adjacent teeth.

Extend over the margin of gingiva

Shape of calculus is determined by:

Anatomy of teeth

Contour of gingival margin

Pressure of tongue and cheeks

Flattened to conform to pressure

Of Pocket wall.

Combination of following forms

May occur:

crusty, spiny, or nodularLedge or ring like formsthin, smooth veneersfinger and fern-like formsIndividual calculus islands

CONSISTENCY AND

TEXTURE

Moderately hard

Clay like consistency

Brittle, flint-like.

Harder and more dense than

supra gingival calculus.

SIZE AND

QUANTITY

Quantity has direct relationship to:

1. Personal oral care procedureand plaque control measures.

2. Physical character of diet.3. Individual tendencies.4. Function and use5. Increased amount in

tobacco smokers

Related to pocket depthIncreased amount with age

because of accumulationQuantity is related to personal care,

diet, and individual tendency as it is with supragingival.Subgingival is primarily related to the development and progression of periodontal disease.

PREVALENCE

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Aneurd A, Loe H and Boysen H: observed the periodontal status of a group of Sri Lankan tea labourers and a group of Norwegian academicians for a 15 year period. The Norwegian population had ready access to preventive dental care throughout their lives, whereas the Sri Lankan tea labourers did not.

In Sri Lankan individuals-

o Formation of supragingival calculus was observed early in life, probably shortly after

the teeth erupted.o The first areas to exhibit calculus deposits were the facial aspects of maxillary molars

and the lingual surfaces of mandibular incisors.o Deposition of supragingival calculus continued as individuals aged, reaching a

maximal calculus score around 25 to 30 years of age.o At 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 45 only a few teeth,

typically the premolars were without calculus.o Subgingival calculus appeared first either independently or on the interproximal

aspects of areas where supragingival calculus already existed. o By age30, all surfaces of all teeth had subgingival calculus without any pattern of

predilection.

In Norwegian academicians-

o Exhibited a marked reduction in the accumulation of calculus as compared with Sri

Lankan group.o However, despite the fact that 80%of 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.

More recently, the Third National Health and Nutrition Examination Survey (NHANES) evaluated 9689 adults in the United States between 1988 and 1994. This survey revealed that 91.8% of the subjects had detected calculus and 55.1% had subgingival calculus.

COMPOSITION: Supragingival calculus consists of inorganic (70 to 90 per cent) and organic components (20 to 30%)

INORGANIC CONTENT- As by Gluck and Murray.

Inorganic portion consist of:

75.9% calcium phosphate, Ca(PO4)2 3.1% calcium carbonate, CaCO3. Traces of magnesium phosphate,Mg3(PO4)2 Traces of other metals.( Monetite & calcite)

Principal components-

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calcium - 39% phosphorus - 19% carbon dioxide – 1.9% magnesium – 0.8%

Trace elements –

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

FLOURIDE 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 external surface of calculus. Fluoride 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.(Okumura et al). Supragingival calculus tended to show a smoother distribution for fluoride than did subgingival calculus. Site – specific differences – 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. Fluoride concentrations appeared to be higher in high mineral contents (phosphorus and calcium concentrations). Site differences and profiles of fluoride concentrations reflect their possible mechanisms of formation of calculus and the influence of oral and/or crevicular environments.CRYSTALS- at least two thirds of the inorganic component is crystalline in structure. Electron microscopy & x-ray diffraction studies,4 distinct phosphate crystals : Hydroxyapatite Ca10(OH)2(PO4)6 – approximately 58% Magnesium whitlockite Ca9(PO4)6XPO4 - 21% Octacalcium phosphate Ca4H(PO4)3.2H2O - 12% Brushite CaHPO4.2H2O - 9%

Generally, two or more crystal forms are typically found in a sample of calculus. Hydroxyapatite and octacalcium phosphate are detected most frequently( in 97-100% of all supragingival calculus) and constitute the bulk of the specimen.

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Brusite is more common in the mandibular anterior region. Magnesium whitlockite is common in the posterior areas and sublingually. The incidence of the four crystals forms varies with the age of the deposit. Early calculus – brusite Later – octacalcium phosphate(Kani et al.1983,Sundberg & Friskopp 1985) Mature calculus – hydroxyapatite and whitelockite.(Newesely 1968) Different layers of same calculus have different compositions. Exterior layers have OCP and inner layers have hydroxyapatite. Supragingival calculus – clearly built up in layers & yields a great heterogeneity from one layer to another with regard to mineral content. Brushite has Ca/P.1.29 Apatite has Ca/P:2.16

CALCULUS COMPARED WITH TEETH AND BONE-

Dental enamel- 96s% inorganic salts Dentine - 65% Cementum and bone – 45 to 50% Mature calculus – 70 to 90%

A 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.

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

ORGANIC CONTENT

Consist of mixture of protein- polysaccharide complexes, desquamated epithelial cells, leukocytes, and various types of microorganisms.

Carbohydrate – 1.9% and 9.1% of organic component, consist of : Galactose sometimes: arabinose Glucose galacturonic acid Rhamnose glucosamine Mannose Glucuronic acid Galactosamine

Salivary proteins – 5.9% to 8.2% of organic component, include most amino acids. Lipids- 0.2% of organic component, in the form of:

Neutral fats Free fatty acids Cholesterol Cholesterol esters Phospholipids

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Subgingival calculus- has composition similar to supragingival calculus, with some differences.

Sub gingival calculus, somewhat more homogenous with equally high density of minerals. Subgingival calculus has the same hydroxyapatite content, more magnesium whitelockite

(Jensen & Rowles 1957), 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. Salivary protein found in supragingival calculus is not found subgingivally.

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

ATTACHMENT OF CALCULUS TO TOOTH SURFACE

Differences in the manner in which calculus is attached to the tooth surface affect the relative ease or difficulty encountered in its removal.Several modes of attachment has been observed by conventional histological techniques and by electron microscopy.

On any one tooth and in any one area, more than one mode of attachment may be found.

Zander ’54 described four methods of attachment; Moskow ’69 suggested the 5th method.

1. Attachment by means of an organic pellicle on enamel-

Calculus attachment is superficial because no interlocking or penetration occurs. Pellicle attachment occur most frequently on enamel and newly scaled and planned root

surfaces Calculus can be readily removed because of smooth attachment.

2. Mechanical locking into surface irregularities. Enamel irregularities include cracks, lamellae, and carious defects Cemental irregularities include resorption lacunae , cemental tears. Difficult to be certain all calculus is removed when it is attached by this method.

3. Close adaptation of calculus undersurface depressions to the gentle sloping moulds of the unaltered cementum surface.

4. Penetration of the calculus bacteria into cementum.

5. Attachment of organic matrix of calculus into minute irregularities that were previously insertion locations of sharpey’s fibres.

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MODES OF ATTACHMENT

MODES OF ATTACHMENT DEGREE OF ATTACHMENT CHARACTERISTICS

Acquired pellicle or cuticle Superficial; no interlocking or

penetration exists,

easily removed

Pellicle is postioned between

the calculus and tooth surface.

Occurs on enamel and recently

Scaled /root planed/debrided

Surface

Mechanical locking into

Minute irregularities

Challenging to remove because of

The Locking into the tooth surface

Cemental irregularities

include locations of

previous shrapey’s fibers,

resorption lacunae, instrumentation

grooves, cemental tears or fragmentation.

Direct contact between

calcified intercellular matrix

and surface

Hard to distinguish between

calculus and cementum

Inorganic crystals of the tooth

interlock with the mineralized bacterial plaque.

Calculus embedded deeply in cementum may appear morphologically similar to cementum and thus has been termed calculocementum.(by Selvig. J)

2 modes of mineralization centers- Type A and Type B have been distinguished ultrastructurally.

Type A are formed only in the presence of and in association with micro organisms.

Type B are apparently not related to micro organisms but have atleast one common border with the type A centre and included micro organisms.

The crystals associated with type A- Hydroxyapatite by X- ray diffraction.

The crystals associated with type B- OCP, B or W.

FORMATION OF CALCULUS

Calculus is dental plaque which has undergone mineralization. Calculus formation occurs in three basic steps:

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1. Pellicle formation- All surfaces of the oral cavity are coated with a pellicle. Following tooth eruption or a dental prophylaxis, 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 – rich proteins, enzymes, and other molecules that can function as adhersion sites for bacteria.

2. Initial adhesion and attachment of bacteria - Transport to the surface – involves the initial transport of the bacterium to the tooth

surface.Initial adhesion – reversible adhesion of the bacterium, initiated by the interaction

between the bacterium and the surface , through long-range and short-range forcesAttachment – a firm anchorage between bacterium and surface will be established by

specific interactions.3. Colonization and Plaque Maturation – when the firmly attached microorganisms start growing and the newly formed bacterial clusters remain attached, microcolonies or a biofilm can develop.

Gram- positive coccoidal organisms are the first settlers to adhere to the formed enamel pellicle, and subsequently, filamentous bacteria gradually dominate the maturing plaque biofilm (Scheie, 1994).

4. Mineralization – 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 4 to 8 hours. Calcifying plaque may become 50% mineralized in 2 days and 60% to 90%

mineralized in 12 days.Early plaque contains a small amount of inorganic material, which increases as the plaque develops into calculus. Separate foci of calcification increase in size and coalesce to form solid masses of calculus.All plaque doesnot necessarily undergo calcification. Plaque that doesnot develop into calculus reaches a plateau of maximal mineral content within 2 days.Micro organisms are not always essential in calculus formation because calculus occurs readily in germ free rodents.

Sources of minerals-o Supragingival calculus – the source of elements for supragingival calculus is saliva.

o Subgingival calculus – the gingival sulcus fluid and inflammatory exudate supply the

minerals for the subgingival deposits. because the amount of sulcus fluid and exudate increases in inflammation, more minerals are available for mineralization of subgingival plaque.Plaque has the ability to concentrate calcium at 2 to 20 times its level in saliva.Calcium and phosphate are two salivary ions which are “raw materials” for dental calculus formation.

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Theoretically, supersaturation of saliva, especially plaque fluid, with respect to calcium phosphate salts is the driving force for dental plaque mineralization.

In heavy calculus formers, early plaque contains more calcium, three times more phosphorus, and less potassium than non – calculus formers.Phosphorus is more critical than calcium in plaque mineralization.Calcification entails the binding of calcium ions to the carbohydrate- protein complexes of the organic matrix and the precipitation of crystalline calcium phosphate salts.Crystals form initially in the intercellular matrix and on the bacterial surfaces and finally within the bacteria.Calculus formation begins with the deposition of kinetically favoured precursor phases of calcium phosphate, OCP and Brusite, which are gradually hydrolysed and transformed into less soluble HAP and WHT mineral phases (Rowles, 1964).Calcification begins along the inner surface of the plaque adjacent 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.As calcification progresses,

o Number of filamentous bacteria increases

o Foci of calcification changes from basophilic to eosinophilic

o There is reduction in the staining intensity of groups exhibiting a positive periodic acid-

Schiff reaction, sulfhydryl and amino groups also are reduced and instead stain with toluidine blue, which initially orthochromatic but becomes metachromatic and disappears.

PAS » toluidine blue(orthochromatic) » metachromatic » disappear.Calculus is formed in layers, which are often separated by a thin cuticle that becomes embedded in the calculus as calcification progresses.

DESCRIPTION OF CALCULUS SIZELIGHT MODERATE HEAVY

Fine granules,grainy or spiculeLocated along line angles, marginal areas and or under contacts

A bump with thickness readily discernible.Located along a marginal ring or interproximal.”click”

Ledge encircling thick and dense.Fills interproximal space or is a marginal ledge.

Slight vibration or roughness Detected with explorer.

Definite vibration felt with Explorer.A jump also detected with curet, Interproximal deposit sometimes detected from lingual and buccal

Definite vibration.Sometimes vibration binds explorer, also detected with curet, interproximal deposit Detected from lingual and buccal.

Calculus usually forms in a horizontal fashion on root circumference, that is why initial exploratory strokes should be vertical and oblique and not horizontal.

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RATE OF FORMATION AND ACCUMLATION

Varies from person to person and in different teeth and at different times in the same person. Based on these differences, individuals may be classified as heavy, moderate or slight calculus

formers or as a nonformers. The average daily increment in calculus formers is from 0.10% to 0.15% of dry weight. The calculus on the lingual surface of the mandibular anterior teeth is a reliable indication of the

amount of entire dentition. Ninety per cent of all the calculus occurs on the mandibular anterior Calculus formation continues until it reaches a maximum from which it may be reduced in amount. The time required to reach the maximum level has been reported as ten weeks, and six months. The decline from maximum accumulation (reversal phenomenon) may be explained by the

vulnerability of bulky calculus to mechanical wear from food and the cheeks, lips and tongue.

THEORIES ON MINERALIZATION OF CALCULUS

In 1878, Magitat 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 concepts:

BOOSTER CONCEPT- 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 ways:1. Salivary pH theory – Hodge & Leung 1950

A 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 dioxide, by the formation of ammonia by dental plaque and bacteria, or by protein degradation during stagnation.

Burchard postulated that precipitation of calcium salts from supersaturated saliva was the result of an increased pH caused by the loss of CO2 from the saliva.

The presence of carbonic anhydrase was demonstrated in the saliva by Rapp. This enzyme supposedly caused an increased uptake as well as an increased liberation of CO2 from the saliva.

2. Colloidal proteins in saliva bind calcium and phosphate ions and maintain a supersaturated solution with respect to calcium phosphate salts. With stagnation of saliva colloids settle out, the supersaturated state is no longer maintained, leading to precipitation of calcium phosphate salts. (Prinz,1921).

3. Phosphatase (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.

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Another 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. Interest in phosphatase and its possible role in calculus formation was probably stimulated by Robinson’s investigations concerning the enzyme’s 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.

EPITACTIC CONCEPT / SEEDING THEORY/HETEROGENOUS NUCLEATION: (Mandel 1957)

According 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 matrix of plaque plays an active role

The carbohydrate protein complexes may initiate calcification by removing calcium from the saliva (chelation) and binding with it to form nuclei that induce subsequent deposition of minerals.

Plaque bacteria have also been implicated as possible seeding agents. The carbohydrate protein complexes may initiate calcification by removing calcium from saliva

(chelation) and binding with it to form nuclei that induce subsequent deposition of minerals.

INHIBITION THEORY: Calcification occurring only at specific sites because of the existence of an inhibiting mechanism

at non-calcifying sites. One 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 (Russell and Fleisch, 1970).

The pyrophosphate inhibits calcification by preventing the initial nucleus from growing possibly by poisoning the growth centres of the crystal.

ROLE OF MICROORGANISMS IN THE MINERALIZATION OF CALCULUS

Although calculus can be induced in germ-free animals (Theilade et al., 1964), human calculus development invariably involves plaque bacterial calcification. Mineralization of plaque starts extracellularly around both gram – positive and gram – negative organisms, but may start intracellularly in some gram – positive bacteria. Filamentous microorganisms , diphtheroids, and Bacterionema and Veillonella species have the ability to form intracellular apatite crystals. Calculus formation spreads until the matrix and bacteria are calcified. Some 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 (Naeslund 1925) , but the prevalent opinion is that they are only passively involved and are simply calcified along with other plaque components.

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However, other experiments suggest that transmissible factors are involved in calculus formation. It was also said that penicillin in the diets of some of these animals reduces calculus formation. Non 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. Filamentous organisms promote calcification by providing an intermicrobial environment suitable for calcification. (Friskopp and Hammarstrom) 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 extensive degradation, leaving only the cell walls for calculus formation.(little et al 1966) Non-calculus sites are associated with a significantly higher level of Actinobacillus actinomycetemcomitans (Aa) and a lower level of black-pigmented anaerobic rods than sites presenting with calculus. Aa has, therefore, been proposed to exert an inhibitory effect on the colonization of plaque-producing and calcifiable bacteria (Listgarten, 1987)

ETIOLOGIC SIGNIFICANCEIt is difficult to distinguish between the effects of plaque and calculus on the gingiva.Calculus is always covered by a layer of unmineralized plaque.In young persons, periodontal conditions are more closely related to plaque accumulation than to calculus.With 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.It does not irritate the gingiva directly but provides a fixed nidus for the continued accumulation of plaque and retains it close to the gingiva.

HEALTHY TISSUES + CALCULUS INFLAMMATORY PERIODONTAL DISEASE

However, it has clearly been established that surface roughness alone does not initiate gingivitis (Waerhaug 1956).

Dental calculus is not in itself harmful and that the major 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(Newman 1994)

The non mineralized plaque on the calculus surface is the principal irritant, but underlying calcified portion may be a significant contributing factor.

Provides fixed nidus for continued accumulation of plaque and retain it close to gingiva.

Creates an area where plaque removal is impossible.Interfere with local self cleansing mechanism

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Subgingival calculus may be the product rather than the cause of periodontal pockets.

Plaque 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.

Supragingival calculus, by nature of its porosity (Friskopp &Hammarstrom 1980, Friskopp 1983) may act as a reservoir for irritating substances such as endotoxins, which can affect the chronicity and progression of periodontal disease (Mandel & Gaffar 1986).

Supragingival calculus may (Greene 1960, Ramfjord 1961) or may not always (Loe et al 1976) be associated with gingivitis or periodontitis, where as subgingival calculus invariably is associated with loss of periodontal attachment and pocket formation (Waerhaug 1952, Lovdal et al 1958).

Severity and type of periodontal disease- there is an increase in the deposition of calculus with an increase in severity of disease. And it is accepted that in adult periodontitis, there is a greater accumulation of calculus than in early onset periodontitis (Carranza 1984a).Although 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 therapy. Calculus plays an important role in maintaining and accentuating periodontal diseases.

FACTORS AFFECTING THE RATE OF CALCULUS FORMATION:

Diet and nutrition –the significance of diet in calculus formation depends more upon its consistency than upon its content.o Calculus deposition is retarded by coarse detergent foods. And hastened by soft and

finely ground diets.o Increased calculus formation has been associated with deficiencies of vitamin A,

niacin, or pyridoxine, and with an increase in dietary calcium, phosphorus, bicarbonate, protein and carbohydrate.

Age – there is an increase calculus deposition with an increasing age.(Schroeder et al,1969). 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.

Habits – o In populations that practice regular oral hygiene and with access to regular

professional care have low tendency for calculus formation.o Smoking- is associated with an elevated risk for supragingival calculus deposition.

Smoking may exert its influence systemically (elevated levels of salivary calcium and phosphorus) or locally via a conditioning of tooth surfaces.o Tobacco -Betel chewing is also associated with an elevated risk of calculus

formation.the quantity of tobacco consumed is directly related to the percentage of deposits.

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Salivary pH- increase pH increases the calculus formation.Ca10(PO4)6 ↔ (OH)210Ca2++6PO4 3-+2OH-.

o When the calcium phosphate crystals in solution are in kinetic equilibrium, the rate of

precipitation is equal to that of dissolution. If pH in solution drops (the concentration of hydrogen ions increases), OH- and PO4 3- tend to be removed by H+ by forming water and more acidic forms of phosphate, respectively. o As a result, the equilibrium is broken and is pulled to the right; that is, the rate of

dissolution exceeds that of precipitation, and the net result is the dissolution of HAP crystals and a decrease in the HAP saturation degree.o If pH in solution rises, the opposite event will occur: OH- forces the equilibrium in

the equation to the left, thus resulting in an increased degree of HAP saturation in solution (Cotton and Wilkinson, 1966). Salivary flow rate – increased salivary flow rate decreases the calculus formation. Salivary flow rate affects calcium phosphate saturation.

Salivary calcium concentration- Elevated salivary calcium concentration, increases the rate of calculus formation.

Higher total salivary lipid levels – is associated with increased calculus formation

Emotional status- increased calculus formation has been associated with disturbed emotional status.

Nucleation inhibitors - Mg blocks apatite crystallization and stabilizes calcium phosphate as amorphous mineral (Ennever and Vogel, 1981). Diphosphonate’s, such as ethane-1-hydroxy-1, 1-Diphosphonate (EHDP), inhibit both apatite nucleation (Fleisch et al., 1970) and crystal growth (Francis, 1969). Importantly, nucleation inhibitors should not be used clinically, because they have been found to interfere with normal mineralization of hard tissues (Schenk et al., 1973).

Crystal growth inhibitors- o Some 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 Of these negatively charged salivary proteins, statherin and PRP are two

representatives of salivary inhibitors of crystal growth.o In addition to these salivary proteins, pyrophosphate and zinc ions act as crystal

growth inhibitorso Immunoglobulins present in dental plaque and calculus may also have an inhibitory

effect on plaque mineralization. The IgG and IgA detected in dental calculus are mainly distributed along the incremental lines, which contain fewer minerals.

Organic acid and calculus formation –

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One could assume that the un-ionized, high pKa organic acids diffuse into dental calculus, dissolve the calcium phosphate crystals, and counteract the calculus calcification.

Salivary Enzymes – An inverse relationship has been reported between the amount of calculus and pyrophosphate content of parotid saliva.

Calcification promoters –

1. Urea is a product from the metabolism of nitrogen-containing substances. Urea can be secreted in normal saliva at concentrations of between 5 and 10 mmol/L but can be as high as 30 mmol/L in patients with renal diseaseo Gingival crevicular fluid contains up to 60mmol/L urea (Golub et al ., 1971 ).

o Urease is responsible for bacterial urea hydrolysis. At a neutral pH, urea is

hydrolyzed by urease to NH4+ and bicarbonate

o The effect of urea metabolism on plaque pH - Ammonia produced from ureolysis of

urea contributes to an increased plaque pH that is an essential factor in natural calculus formation. o Bacteria suspected of having a role in ureolysis include S. salivarius, coagulase-

negative staphylococci (CNS) (Sissons et al., 1988a,b), Actinomyces viscosus/naeslundii (Gallagher et al., 1984), transient Enterobacteriaceae, unknown anaerobes (Frostell, 1960), and Haemophilus sp. (Salako and Kleinberg, 1989).o Among these ureolytic bacteria, S. salivarius has attracted the most attention, major

contributor to ureolysis in natural saliva.

2. Fluoride and calculus formation- The caries-inhibiting ability of fluoride is well-known.

o Fluoride not only counteracts demineralization of hard tissue through the formation of

lower-solubility fluorapatite by fluoride substitution for hydroxyl ions and adsorption onto apatite surfaces (Wong et al., 1987), but also contributes to remineralization by precipitation of a fluoride-enriched apatite or calcium fluoride (Nelsons et al., 1984).o Fluoride also affect the morphology of the apatite crystals as it converts them from

thin plates to short and slender needles (Eanes and Meyer, 1978). o In addition, acid production by plaque bacteria can be inhibited by the presence of

fluoride (Briner and Francis, 1962). 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 Sodium fluoride may be able to inhibit the bacterial phosphatases and

pyrophosphatases, the enzymes that are well-known to promote calculus formation (Lobene and Volpe, 1987).

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3. Silicon - Silicic acid has been reported as a strong promoter of both spontaneous precipitation of calcium phosphates and the growth of seeded crystals (Damen and ten Cate, 1989).

On the other hand, it is noteworthy that 3.0- 30.0 mmol/L silicic acid and 10 mg/mL silica inhibit the rates of both amorphous calcium phosphate formation and HAP 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.

CALCULUS FORMATION IN PATIENTS UNDERGOING HOMEODYLASIS:Increased tendency for calculus deposition.Flow rate is lower in dialysis patients, xerostomia dry mouth common complaint of

renal pts.Dialysis patients are heavy calculus formers. May b due to elevated levels of

PHOSPHORUS, UREA OR PROTEINS.

EXAMINATION

SUPRAGINGIVAL EXAMINATION: Direct Examination – supragingival calculus can be seen directly or indirectly, using a mouth

mirror. With a combination of retraction, light and drying with air, small deposits can be seen.

SUBGINGIVAL EXAMINATION: Visual Examination – dark edge of calculus may be seen at or just beneath the gingival

margin.gentle air blast can deflect the margin from the tooth for observation into the pocket. Gingival tissue colour change – dark calculus may reflect through a thin margin and suggest

its presence. Tactile examination- Clerehugh 1996 used WHO # 621 probe. And a fine subgingival

explorer is also used. Radiographs– although not always reliable Endoscopy

Electronic calculus detection Magnification with eye loupes Piezoelectric 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. Meissner G et al 2006 Fluorescence Spectroscopy.

ASSESSMENT OF CALCIFIED DEPOSITS:

Simplified calculus index (Green & Vermillion ’64 )

Calculus component of periodontal disease index (Ramfjord ’59)

Calculus surface index (Ennever J,, Sturzenberger & Radike ’61)

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Calculus surface severity index (Ennever J et al ’61)

Marginal line calculus index (Muhleman & Villa ’67)

Volpe- Manhold index (Volpe A R & Manhold J H ’62)

IN VITRO PRODUCTION OF CALCULUS

Several methods have been attempted to produce artificial calculus outside the mouth. Some of these methods used stimulated saliva from human subjects, others used a calcifying solution and still others used extracts 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 Ca/P ratio and the X ray diffraction pattern (hydroxyapatite) were found to be similar to natural calculus.

It is noted that artificial calculus had a regular uniform layering, in contrast to the characteristic irregular layering seen in natural calculus.

IN VIVO PRODUCTION OF CALCULUS

In early 19th century, Black 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 ‘calculo-globulin’ that was deposited on the glass plate;the early deposit had a greasy feel to the fingers; and if this material remained on the plate, it calcified.

In 1947, Iwasawa 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 2 stages;the formation of an organic matrix and the infiltration and deposition of calcium salts. The organic matrix was composed of bacterial plaque, salivary colloids and exudates.

Mandel et al used thin celluloid strips wired to the lingual and proximal surfaces of lower anterior teeth to collect deposits. Deposits were allowed to collect on strips from 2-29 days, removed and studied in several ways.

Their findings were as follows:

X ray diffraction revealed the crystalline structure to be mostly apatite with some whitlockite.

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Grenz ray examination of the strips revealed granular mineralization by the seventh day and definite mineralization by the 14th day.

Bacteriological cultures showed the presence of a variety of organisms, cocci and various types of filaments.

Zander et al used electron microscopy in addition to light microscopy to study early calculus formation from 1 day to 4 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 matrix that becomes calcified. Calcification follows a pattern in which crystals are laid down between bacteria and their surfaces and later inside them.

ANALYSIS OF CALCULUS

Dental calculus as a mineralized structure, is readily available and thus has been the subject of analysis by numerous investigators using various methodologies.

CHEMICAL ANALYSIS

Chemical analysis has been made by several investigators. Glock and Murray analysed samples of calculus and found them to contain the following:

82.9% inorganic salts

75% calcium phosphate

3% calcium carbonate

4%magnesium phosphate

Traces of other minerals

Organic portion:

8% protein

3%fat

Water

SPECTROANALYSIS

It is the process of analyzing light by breaking it into a spectrum measuring the amount of each wavelength to measure minute amounts of elements.

It has revealed the presence of many minerals in dental calculus.

The basic elements were found to be calcium

Phosphorus

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Magnesium

Others:

Sodium

Potassium

Lead

It was noted that calculus formed on metal fillings or prosthetic appliances contained small traces of their ingredients.

X RAY DIFFRACTION

It finds the geometry or shape of molecules using X rays based on the elastic scattering of X rays from structure that have long range order, to know complete structure of crystalline material ranging from simple inorganic solid to complex protein.

The most sensitive techniques have found the following crystalline structures:

Hydroxyapatite

Octacalcium phosphate

Triphosphate trihydrate

Magnesium whitlockite

Brushite

Monelite

Calcite(in small amounts)

Brushite is present in the early stages of mineralization and octacalcium phosphate in the later stages

Diffraction studies revealed that the composition of dental calculus varies in people from different geographical locations and from the same area.

It was also found that different layers of the same calculus specimen might have different compositions.

PREVENTION AND REMOVAL OF CALCULUS

1. Professional removal of calculus – 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.

2. Personal bacterial plaque control – tooth brushing, flossing and supplementary methods is a major factor in the control of dental calculus reformation.

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3. Anti- calculus agents used in Commercial Dentifrices - Chemotherapeutic agents have been used to supplement the mechanical removal of dental plaque (Aleece and Forscher,1954; Grossman, 1954; Zacherl et al., 1985; Volpe et al., 1992).

Formation may be prevented or controlled by:1. Decreasing the amount of plaque available for mineralization using antimicrobial agents and

enzymes2. Modifying the attachment of plaque by antiadhesive agents3. Inhibiting the process of mineralization by crystal growth inhibitors.( it currently dominates)4. Dissolve or soften the mature deposit by removing the inorganic portion.5. Affect the calculus matrix i.e to change the ‘skeleton’ around which calculus is deposited.CLASSIFICATION OF ANTI- CALCULUS AGENTS- 1st GENERATION

1) DISSOLUTIONChelating Agents

o Ethylene diamine tetra acetic acid

o Sodium Hexa Metaphosphate

Acids –Aromatic sulphuric acido 20% Trichloroacetic Acid

Spring SaltsSodium Ricinolate Alkalies

2) ALTERING CALCULUS ATTACHMENTS SiliconIon exchange resins

3).PLAQUE INHIBITION Antibiotics Example : Triclosan (0.3 %)

Polyvinylmethyl ether & maleic acid (2%)

Antiseptics Example : Chloramines

4) .MATRIX DISRUPTION Enzymes Example : Mucinase Trypsin, chymotrypsin Carboxypeptidase, lipase, amylase

2 nd GENERATION Inhibition of crystal growth

Vitamin C (By crystal poisoning mechanism ) Pyrophosphate Pyrophosphate + Sodium fluoride

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Zinc salts Bisphosphonates Polymers & Co Polymers

To date the most successful approach to the chemical inhibition of supragingival calculus has been with the use of crystal growth inhibitors.

Mineralization inhibitors include chemicals:PyrophospahtesDiphosphonatesZinc salts

These adsorb on the surface of crystals, thereby decreasing the rate of crystal growth and phase transformation of calcium phosphate salts.In 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.Readily formulated accepted products for consumer use are: Dentifrices containing Zn salts - 0.5%-2% Zn Citrate, 2% Zn Chloride. Inhibit the growth of

HA crystal in-vitro & possesses the additional benefit of inhibiting plaque formation. Unlike other, it is cationic & is consequently retained with in oral cavity

Dentifrices containing pyrophosphate salts – pyrophosphate inhibiting or delaying the transformation of the amorphous, precrystalline phase to HAP.

Dentifrice containing 5% pyrophosphate had greater uptake and retention than from a formulation containing 3.3%

Incorporation 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 (1.3%) to be used and yet maintain an effective level of calculus inhibition.

Pyrophosphate exerts its effect by inhibition or delaying the transformation of amorphous, precrystalline phase to hydroxyapatite.

Dentifrices containing triclosan - Triclosan (0.3 %). is a broad-spectrum antibacterial agent active on both Gram-positive and -negative micro-organisms. The target is the cytoplasmic membrane.

Dentifrices containing diphosphonate compound - Diphosphonate: Azacytcloheptane-2, 2-diphosphonic acid (1.15%). Inhibit both apatite nucleation (Fleisch et al. 1970) and crystal growth (Francis, 1969).

CALCULUS SOFTENING GEL A calculus softening gel is currently available that may enhance periodontal

instrumentation effectiveness. The active ingredient is disodium ethylene diamine tetra acetic acid(EDTA), which is a

calcium-chelating agent.

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AGENTS FOR SOFTENING THE MATURE CALCULUS

A. ACIDS

One of the earliest techniques utilized a wooden stick which was moistened with aromatic sulphuric acid before being introduced into periodontal pocket to dissolve calculus and to act on the soft tissues as an astringent.

After 2 weeks, the tooth become firm and cured(Barker 1872). Later on Niles(1881) suggested to use nitro muriatic acid because of its superior dissolving action on dental calculus.

Other acids included:

20%tricholoacetic acid

Bifluoride of mercury

10%sulphuric acid

The use of acids created some problems such as:

They are caustic to soft tissues

Decalcify tooth structures

Stones(1939) and Grossman(1954) 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.

B. ALKALIES

Badanes(1929) 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 3 organic constituents of salivary calculus, globulin, mucin and calcium oxalate.

C. CHELATING AGENTS

Chelating agents are used to dissolve crystallized calcium salts and are capable of combining with calcium to form stable compounds.

Sodium hexametaphosphate was found to remove supragingival calculus from extracted teeth in 10-15 days.(Kerr and Field 1944)

Subsequent studies by Maynar et al(1994), Smith et al(1994), Harding et al(1996) and Nagy et al(1998) have failed to confirm that the use of chelating gel prior to scaling decreases the time taken for scaling.

ENZYMES

The mode of action of enzyme formation is to break down plaque matrix or to affect the binding of the calculus to the tooth.

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The first enzyme to be tested was mucinase (Stewart 1952), a preparation with proteolytic and amylolytic activity.

A 1.5%Viokase preparation was also incorporated into a chewing stick and subjects were instructed to chew one stick of gum for 5 minutes, five times per day. It produced a 22- 26% reduction in calculus formation respectively compared to control groups.

Harrison et al (1963) 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. VIOKASE

It 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 toxic protein material that constitiutes a favourable subsrate for bacterial growth.

Disadvantage on chewing gum study by Allen and Courtney in 1972

Soft tissue retraction

Burning sensation on tongue

2. Another proteolytic enzyme, produced from a mutant strain of Bacillus subtilis also had a favourable effect on reducing stainable, soft deposits.

3. Mucinase

4. Dextranase

UREA

The idea of using urea as a potential anticalculus agent stems from its attributed solvent action on protein(Holder and Mackay 1937, Muldavin and Holtzman,1938, Holder and Mackay 1939)

The anticalculus effect of urea was attributed to its ability to dissolve the muco proteinaceous material within which the calcium salts are deposited and /or by increasing the solubility of calcium salts in saliva (Belting and Gordon 1966)

MISCELLANEOUS CHEMICAL AGENTS

Hoffman et al (1963) attempted to prevent calculus formation using an ion exchange resin applied to teeth as a thin film.

The resin was sulphonated polystyrene membrane containing negatively charged ions.

In theory, the negatively charged ions would repel the positively charged calcium ions and reduce the degree of mineralization of calculus.

Schaffer et al (1964) found that teeth coated with an ammoniated polystyrene film significantly reduced the amount of calculus deposit.

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Schroeder et al (1961) tested 9 organic compounds administered as mouthwashes as their ability to inhibit plaque and calculus formation.

Hidaka et al91993) demonstrated that a combination of herbs used in Chinese Kampo medicines has effectiveness in inhibiting calcium phosphate precipitation.

ANTIMICROBIALS

1. Cetylpyridinium Chloride(CPC)

It is a cationic quaternary ammonium compound. It was tested for anticalculus activity as a mouth rinse for 7 days but there were no differences in calculus level in CPC and controlled rinses.

Disadvantages of CPC

Burning sensation of oral mucosa

Brownish discoloration of teeth

Yellow discoloration of tongue

A recurrent, apthous type of ulceration of oral mucosa

CHLORHEXIDINE

It is second generation anti plaque agent.

It is a cationic bis- biguanide which acts by being adsorbed onto the bacterial cell wall, leading to damage of the permeability barrier.

Several studies have confirmed that chlorhexidine is an excellent anti plaque agent (loe and Schitt 1970, Hamp et al 1973, Tepe et al1983).

Yates et al(1993) tested the effect of 1% chlorhexidine dentifrice on plaque, gingivitis, calculus and tooth staining.

They found that there were increased calculus levels in the active dentifrice group.

Therefore chlorhexidine is a potent antiplaque agent , it has the disadvantage of actually increasing calculus levels.

TRICLOSAN

Triclosan is named scientifically as 2,4,4-trichloro-2 hydroxyphenyl ether, a non ionic antibacterial agent with a wide spectrum of activity against bacteria, fungi and yeasts.

It when delivered from a dentifrice, seems to bind to oral mucous membranes and tooth surfaces and is particularly well retained in plaque(Gulbert et al 1987, Gilbert and Williams 1987)

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Because of its proven anti plaque effects , a dentifrice containing 0.2% Triclosan and 0.5% Zinc citrate are used as an anticalculus agent.

It is a biocide.

It can be made from the partial oxidation of benzene or benzoic acid by Raschig process and found as a product of coal oxidation.

It is found in soaps(0.15-0.30%), toothpastes, deodorants, shaving cream moth washes.

ANTIBIOTICS

1. PENICILLINConstant use of pastes containing penicillin appear to enhance the development of penicillin resistant streptococci in mouth.2. VANCOMYCINIt is a bactericidal antibiotic, daily use of which reduced the quantity of already formed plaque in mentally retarded, institutionalized patients.3. ERYTHROMYCINSuspension of this antibiotic applied 4 times a day for 7 days reduced the quantity of plaque in adult volunteers by 35%4. KANAMYCIN

Since mid 1970s, 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.

VITAMIN CIt 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.It has a characteristic taste which might have promoted saliva flow, thus reducing calculus levels.A study was undertaken to compare the effect of quinine sulphate and vitamin C on calculus formation.In this study each subject topically applied the test chloromethyl analogue of vitamin C and a 0.26% solution of quinine sulphate- followed by a rest period of between 1 week and 3 months and then used the second solution.Calculus was carefully removed by scaling and then weighted.Vitamin C analogue reduced calculus weight by 70.9%.It was concluded that taste was not a significant factor in calculus formation by vitamin C analogue.

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