ANTI-PLAQUE

&
ANTI-CALCULUS
AGENTS
BY DR. TEJASHVI SETH
 INTRODUCTION
• Dental plaque is defined clinically as a structured, resilient, yellow-grayish
substance that adheres tenaciously to the intraoral hard surfaces, including
removable and fixed restorations. (Bowen W.H. ,1976)

• Dental plaque is an organized mass, consisting mainly of microorganisms, that

adheres to teeth, prostheses, and oral surfaces and is found in the gingival
crevice and periodontal pockets. Other components include an organic,
polysaccharide-protein matrix consisting of bacterial by-products such as
enzymes, food debris, desquamated cells, and inorganic components such as
calcium and phosphate. (glossary of periodontal terms, 2001)
 CLASSIFICATION
DENTAL PLAQUE

SUPRAGINGIVAL PLAQUE SUBGINGIVAL PLAQUE

• Found below the gingival

• Found at or above the margin, between the tooth and
gingival margin the gingival pocket
epithelium.
 Composition

PLAQUE

Micro-organisms Intercellular Matrix

70% 20%-30%

Bacterial Non-
bacterial Organic Inorganic
material materials
 PLAQUE FORMATION PROCESS

Pellicle Initial
formation on the Colonization/plaque
adhesion/attachment
tooth surface, maturation.
of bacteria,
 Pellicle Formation
• The thin layer of glycoproteins that are adsorbed to tooth surfaces is called the
acquired pellicle.
• Acquired pellicle -a homogenous, membranous, acellular film that covers the
tooth surface and frequently form the interface between the tooth ,the dental
plaque and calculus. (Schluger)

• The pellicle on tooth surfaces consists of

- peptides, proteins, and glycoproteins,
- including keratins, mucins,
- proline-rich proteins, phosphoproteins, histidine-rich proteins
 Attachment of bacteria

Phase I: Transport to the surface.

Phase II: Initial adhesion.

Phase III: Strong attachment.

 PHASE I
TRANSPORT TO THE SURFACE
 Random contact occurs through
• Active bacterial movement (chemotactic activity)
• Brownian motion ( avg. displacement 40 µm/hour)
• Liquid flow (several orders of magnitude faster than diffusion)
• Sedimentation of organisms
 Phase II: Initial adhesion.
• Reversible adhesion of the bacterium and the surface.
• Initiated by interactions b/w bacterium and surface through long range and short
range forces, including
- Van der Waals attractive forces
- Electrostatic repulsive forces
 DLVO theory of colloidal stability
• Derjaguin, Landau, Verwey & Overbeek (DLVO) have postulated that above a
separation distance of 1nm, the total interaction energy is the sum of attractive
forces and the electrostatic repulsive forces.
• the summation of previous two forces describes total range interaction also called
as Total Gibbs Energy (GTOT).
 Phase III: Strong attachment

• A firm anchorage between bacterium and surface will be

established by specific interactions ( ionic, covalent, or
hydrogen bonding)

• The bonding between bacteria and pellicle is mediated by

specific extracellular proteinaceous components (adhesions) of
the organism and complementary receptors (proteins,
glycoproteins, polysaccharides) on the surface (pellicle) and is
species specific.
 Colonization/plaque maturation
• Colonization of bacterial plaque mainly occurs by 2 mechanism: co-
aggregation and co-adhesion.
• The primary colonizing bacteria adhered to the tooth surface provide new
receptor of attachment by other bacteria in a process known as co-adhesion,
leads to the development of micro-colonies and eventually into a mature
biofilm.
• Coaggregation is Cell to cell recognition of a genetically distinct partner cell
type.
• Occurs primarily through
1. Highly specific interaction of proteins and carbohydrate molecules located on
the bacterial cell surfaces.
2. Less specific interaction resulting from hydrophobic electrostatic & van der
waals forces.
 PLAQUE CONTROL
• Regular removal of dental plaque & prevention of its accumulation on the
teeth & adjacent gingival surfaces. It also deals with prevention of calculus
formation.

• Bacterial plaque is the principle etiological agent in gingival and periodontal

diseases, both prevention and treatment of these conditions must be based to
a large measure on its control.

• Primary level of prevention of dental caries.

 HISTORY
• An Egyptian medical manual, the Ebers Papyrus, written about 1500 B.C.E.
and compiled from works dating to 4000 B.C.E., contains a recipe for
compounding tooth-cleaning preparations.

• Hippocrates (460-377 B.C.E.) is generally considered the first to recommend

the use of a dentifrice.

• Alcohol-based mouthrinses - were popular with the Romans and included

white wine & beer.
• Biggest change to toothpastes came with the chemo-parasitic theory of
tooth decay of W.D. Miller in 1890.

• The theory that organic acids were produced by oral bacteria acting on
fermentable carbohydrates in contact with enamel led to both the
introduction of agents in toothpaste to influence this process, & the
production of alkaline products.

• The first half of the 20th century - claims toothpastes for oral health
benefits, including tooth decay and periodontal disease.
METHODS OF PLAQUE CONTROL
MECHANICAL PLAQUE CHEMICAL PLAQUE
CONTROL CONTROL

Toothbrushes Antiadhesive agents

Interdental cleaning
Antimicrobial agents
aids

Oral irrigation Plaque removal

devices agents

Foam brushes,swabs Antipathogenic

and tooth towlettes agents
• Based on antimicrobial activity & substantivity
(Kornman,1986)

CHEMICAL PLAQUE CONTROL AGENTS

FIRST GENERATION eg. antibiotics, phenol,

quaternary ammonium compounds & sanguinarine

SECOND GENERATION: Eg: Bisbiguanides,

(chlorhexidine), amine fluoride and stannous
fluoride mouthrinse,

THIRD GENERATION : Eg: aminoalcohols

(octapinol, decapinol, delmopinol)
 According to Mandel (1988)

• antiseptic agents aimed at killing or preventing the proliferation of all the plaque
organisms.

• antibiotics capable of inhibiting or killing a specific group of bacteria.

• non-enzymatic, dispersing, denaturing, or modifying agents that can alter the

structure of the plaque or the metabolic activity of the plaque bacteria.

• single enzymes or combinations of enzymes that can break up or disperse the gel-like
matrix which holds the plaque together, or modify plaque activity.

• agents that can interfere with the attachment of all or some of the oral bacteria to the
pellicle surface.
 IDEAL REQUISITES OF ANTI-PLAQUE AGENT
• Eliminate pathogenic bacteria only.
• Prevent development of resistant bacteria.
• Exhibit substantivity.
• Safe to the oral tissues at the recommended conc. and dosage .
• Reduce plaque and gingivitis.
• Inhibit calcification of plaque.
• Do not stain teeth or alter taste.
• No adverse effects.
• Easy to use.
• Inexpensive.
(Bral M and Brownstein C N,1988)
 Terminology employed for agents in chemical
supragingival plaque control
 According to the European Workshop of Periodontology 1996

• Antimicrobial agents: chemicals that have a bacteriostatic or bactericidal

effect in vitro that alone cannot be extrapolated to a proven efficacy in vivo
against plaque.

• Plaque reducing/inhibitory agents: chemicals that have only been shown to

reduce the quantity and/or affect the quality of plaque, which may or may not
be sufficient to influence gingivitis and/or caries.
• Antiplaque agents: chemicals that have an effect on plaque
sufficient to benefit gingivitis and/or caries (Addy et al. 1983).

• Antigingivitis agents: chemicals which reduce gingival

inflammation without necessarily influencing bacterial plaque
(includes anti-inflammatory agents).
 Vehicles for delivery of agents
• Tooth Paste
• Mouth rinses
• Spray
• Irrigators
• Chewing gum
• Varnishes
• Gel
• Lozenges
 ANTIBIOTICS
• Mechanism of Action : Antimicrobial
• Eg; Penicillins,
Tetracycline
Vancomycin
Kenamycin
Erythromycin
Niddamycin
Spiromycin
Metronidazole
• Should not be used either topically or systemically as preventive
agents against these diseases.

• The risk-to-benefit ratio is high and even antibiotic use in the

treatment of adult periodontitis is open to debate (Addy &
Martin 2003)
 Disadvantages
• The development of bacterial resistance within human
populations, for example methicillin-resistant Staphylococcus
aureus (MRSA), which causes serious and life-threatening
wound infections, particularly within hospitalized patients.

• Hypersensitivity.
 ENZYMES
GROUP 1 GROUP 2

• Potential to disrupt the early • Aim to catalyse the conversion of

plaque matrix, endogenous and exogenous
• poor substantivity. thiocyanate to hypothiocyanite via
• unpleasant local side effects, the salivary lactoperoxydase
mucosal erosion. system.
• Eg. dextranase, mutanase, • Enhance the host defense
proteases mechanism
• Eg. Glucose oxidase and
amyloglucosidase
 splitting starch remnants in the oral cavity
Amyloglucosidase
Glucose
glucose oxidase
hydrolyzed to gluconic acid and hydrogen peroxide

Peroxide reacts with thiocyanate ions in the oral cavity in a reaction that is
catalysed by the naturally occurring salivary peroxidase

hypothiocyanite.
ion is a powerful oxidizing agent and can oxidize the thiol groups in the bacterial
enzymes responsible for acid production and inhibitory effect on oral bacteria.
 PHENOLS AND ESSESNTIAL OILS
• W.D. Miller in1884 suggested using an antimicrobial mouth rinse containing
phenolic compounds to combat gingival inflammation.
• Eg : thymol, menthol, eucalyptol, methyl salicylate.

• Listerine antiseptic, a combination of the phenol-related essential oils,

thymol and eucalyptol, mixed with menthol and methyl salicylate in a
26.9% hydroalcoholic vehicle.

• On direct comparision with chlorhexidine, one 6-month study has

demonstrated equivalent effects on plaque and gingivitis but without the
inherent side effects of chlorhexidine (Charles et al. 2004)
 Mechanism of action
• Anti-inflammatory action possibly due to an anti-oxidative activity (Firalti et
al.1994).

• Act as scavengers of oxygen-free-radicals. (Kuehl et al. 1977)

• Anti-inflammatory and Prostaglandin synthetase inhibitor activity at

concentration lower than that for antibacterial activity. (Goodson,1985)

• Have an effect on leucocyte activity by marked suppression of superoxide

anion generation in neutrophils as well as a comparable reduction in
neutrophil chemotaxis for a series of phenolic agents. (Azuma et al. 1986)
 Disadvantages
• The pH of the product is low (pH 4.3) and has been shown in vitro and in
situ to cause erosion of dentine and enamel respectively

 The non-ionic antimicrobial triclosan, a trichlora-2-hydroxy phenyl

ether, is usually considered to belong to the phenol group, acts by Triclosan
inhibition of cyclo-oxygenase and lipo-oxygenase pathway.

 In simple solutions, at relatively high concentrations (0.2%) and dose (20

mg twice per day), triclosan has moderate plaque-inhibitory action and
antimicrobial substantivity of around 5 hours (Jenkins et al. 1991)
• Three strategies have been developed to enhance the clinical effectiveness of
oral triclosan products:

1) Combine it with zinc citrate to enhance retention of triclosan whereas zinc

is thought to increase antimicrobial activity.

2) Incorporate triclosan in a copolymer Gantrez (methoxyethylene and maleic

acid) to enhance its retention time.

3) Combine it with pyrophoshates to enhance its calculus reducing properties.

• Long-term studies have suggested that triclosan-containing
toothpaste can reduce the progress of periodontitis, although
the effects have been considered small (Rosling et al. 1997;
Ellwood et al. 1998).

• Mouth rinses containing triclosan and the co-polymer are

available, with some evidence of adjunctive benefits to oral
hygiene and gingival health when used alongside normal tooth
cleaning (Worthington et al. 1993).
 QUATERNARY AMMONIUM COMPOUNDS
• They are cationic, antiseptics & surface active agents.
• Eg. Cetylpyridinium chloride,
Acetyl pyridinium,
Benzalconium chloride,
Benzathonuim chloride,
Doiniphen bromide

• Bactericidal to both gram-positive and negative bacteria,

 • Mechanism Of Action:
Molecules have net positive charge interact with negatively charged cell
membrane phosphates

rupture of cell wall structure

increase its permeability

subsequent loss of cell content.

 Cetylpyridinium chloride
• Antiseptic mouthrinse products usually at a conc. of 0.05%

• At oral pH they are monocationic and adsorb readily and quantitatively, to a

greater extent, than chlorhexidine to oral surfaces (Bonesvoll & Gjermo 1978)

• Substantivity appears to be only 3-5 hours due to rapid desorption (Roberts &
Addy 1981)
• The plaque inhibitory property of cetylpyridinium chloride are reduced by
toothpaste before or after the rinse. Thus may offer no adjunctive benefit to
mechanical plaque control (Sheen et al. 2001, 2003)

• In a 6 month study report (Lobene et al. 1977) there was a 14% reduction in
plaque and a 24 % reduction in gingivitis.

• A number of adverse effects have been reported such as tooth staining,

burning sensation and soft tissue irritation.

• At higher concentrations, such as 0.2% benzethonium chloride, oral

desquamative lesions have been reported (Gjermo et al. 1970).
 NATURAL PRODUCTS/ HERBAL EXTRACTS
Sanguanarine
• Sanguinarine, currently being employed as an antiplaque, anti-gingivitis agent
in both a mouth rinse and toothpaste.
• Contain alkaloid benzophenanthridine extract from the root plant
Sanguinaria canadensis.

Mechanism of action:
• Inhibiting the growth of gram negative bacteria
• Increases likelihood of oral precancerous lesion after cessation of mouth
rinse use
 METAL SALTS
• Zinc Salts
• Tin Salts (Stannous fluoride)
• Sodium fluoride
• Copper salts
• Silver nitrate
• Bichloride of mercury

• Mechanism of action
Plaque inhibitory capacity as they reduce glycolytic activity in micro-
organisms & delayed bacterial growth.
• Stannous fluoride use is difficult in oral hygiene products because of stability
problems, with hydrolysis occurring in the presence of water. Stable
anhydrous toothpaste & gels are available with evidence of efficacy against
plaque and gingivitis (Beiswanger et al. 1995; Perlich et al. 1995).

• 0.5% zinc citrate or zinc chloride can have an impact by binding to the
surface of oral bacteria and affecting adherence and altering metabolic
activity and reducing growth rate.

• Zinc, at low concentration, has no side effects and is used in a number of

toothpastes and mouth rinses; however, alone it has little effect on plaque
(Addy et al. 1980) except at higher concentrations.
 BISBIGUANIDES

• Eg. Chlorhexidine gluconate – 0.2 %, Alexidine, Octenidine

 Chlorhexidine

• Developed in 1940s by Imperial Chemical Industries, England, and marketed in 1954 as an

antiseptic for skin wounds.

• More widely used in medicine and surgery including obstetrics, gynaecology, urology and
pre-surgical skin preparations for both patient and surgeon.

• Suggested for oral use by Schroder in 1969.

• Plaque inhibition by chlorhexidine was first investigated in 1969 by Shroeder, but the
definitive study was performed by the Loe and Schiott in 1970 to study inhibition of
experimental caries by plaque prevention using chlorhexidine mouthrinse.
 CHEMICAL STRUCTURE

• A bisbiguanide antiseptic, being a symmetrical molecule consisting of 4

chlorophenyl rings and 2 biguanide groups connected by a central
hexamethylene bridge.

• Strong base and dicationic at pH levels above 3.5, with 2 positive charges one
on either side of the hexamethylene bridge (Albert & Sargeant, 1962)
• Dicationic nature of chlorhexidine, that makes it extremely interactive with
anions, which is relevant to its efficacy, safety, local side effects and
difficulties with formulation in products

• 3 forms- digluconate, acetate (water soluble)

hydrochloride salts (sparingly soluble).
• Spectrum – wide range of gram positive & gram negative bacteria, some
fungi, yeasts, dermatophytes and some lipophilic viruses including HIV
and Hepatitis B virus (Wade & Addy, 1989)
• Its antimicrobial activity is of the membrane-active type, used to describe
an anti-microbial agent that damages the inner (cytoplasmic) membrane
 ANTIBACTERIAL ACTIVITY
Cationic Chlorhexidine molecule is attached towards (-ve) charged bacterial cell
surface

adsorbed by phosphate containing compounds

chlorhexidine is attracted towards the inner cell membrane

alters the integrity of the bacterial cell membrane

Chlorhexidine binds to phospholipids in the inner membrane

leakage of low-molecular-weight components, such as K+ ions

• At low concentrations the agent is bacteriostatic

• At this bacteriostatic (sublethal) stage, the effects of

chlorhexidine are reversible

• removal of excess chlorhexidine by neutralizers allows the

bacterial cell to recover ( Denton GW, 1991)
 Increased conc. of chlorhexidine

Leakage of low molecular weight cytoplasmic contents falls

Coagulation + precipitation of the cytoplasm by the formation of phosphated

complexes, adenosine triphosphate & nucleic acid

coagulation of cytoplasmic proteins

Vital cell activity ceases, Bactericidal activity (irreversible)

 PLAQUE INHIBHITON MECHANISM
 Rolla & Melsen in 1975 postulated 3 mechanism of plaque inhibhition

• By blocking acidic groups on salivary glycoproteins thus reducing

glycoprotein adsorption on to the tooth surface and prevents pellicle
formation

• By binding to the bacteria to prevents adsorption of bacterial cell wall onto

the tooth surface

• By precipitating agglutination factors in the saliva and displacing calcium from

the plaque matrix which helps to prevent binding of mature plaque
 CHLORHEXIDINE AS GOLD STANDARD
• Addy (1986) and Kornman (1986) ascribed chlorhexidine’s superior
antiplaque activity to its property of substantivity and persistent bacteriostatic
activity.

• This property of chlorhexidine was associated with its ability to maintain

effective concentrations for prolonged periods of time and this prolongation of
its action made it especially suitable for the inhibition of plaque formation

• PIN CUSHION EFFECT - as one charged end of the chlorhexidine molecule

binding to the tooth surface and the other remaining available to initiate the
interaction with the bacterial membrane as the microorganism approaches the
tooth surface
 Roberts WR (1981) and Rolla G, Loe H, Schiott CR (1971)
• For a single rinse with CHX, the saliva itself exhibits antibacterial activity
for up to 5 hours, while persistence at the oral surfaces has been shown to
suppress salivary bacterial counts for over 12 hours
• 10ml of 0.2% aqueous solution of chlorhexidine for 1 minute, 30% of the drug
is retained in the mouth

 Hjelijord et al, 1973, hypothesized that CHX-protein interaction involves a

slight denaturation of the protein adsorbed to the teeth, & the slow reversibility
of this reaction explains the retention & slow release of CHX in the oral cavity
 DEACTIVATION
• Chlorhexidine is deactivated by forming insoluble salts with anionic
compounds, including the anionic surfactants commonly used as detergents in
toothpastes and mouthwashes, anionic thickeners such as carbomer, and anionic
emulsifiers such as acrylates/C10-30 alkyl acrylate cross-polymer, among many
others.

• For this reason, chlorhexidine mouth rinses should be used at least 30 minutes
after other dental products.

• For best effectiveness, food, drink, smoking, and mouth rinses should be
avoided for at least one hour after use
 VEHICLES FOR CLINICAL
APPLICATION
• Chlorhexidine has been formulated in number of products but mouth rinse is
most commonly documented in the literature.( Lang LP, et al. 1986).
• Chlorhexidine mouth rinse is available in aqueous and alcohol based
solution.
• Manufactured as 20% v/v conc. and marketed as 0.2% Chlorhexidine.
• In U.S, 0.12% conc. was manufactured but to maintain the optimum dose of
20mg dose derived from 10 ml of 0.2% of rinse the product was
recommended as 15ml rinse (18mg dose).
• The antimicrobial effects at 0.12% conc. is similar to 0.2% conc.
solution when used at appropriate similar dose. (Segreto et al., 1986)
• Various other formulations of chlorhexidine includes gels, usually
delivered in the form toothbrush and trays, sprays, varnishes, chewing
gums.
• Also available as a local drug delivery agent.
• Incorporated into periodontal dressing to decrease the bacterial load
during post surgical phase
 CLINICAL INDICATIONS
• Post-oral surgery including periodontal surgery or root planning -
reducing the bacterial load in the oral cavity and preventing plaque
formation at a time when mechanical cleaning is difficult because of
discomfort
• For patients with jaw fixation
• By the mentally and physically handicapped
• Medically compromised individuals predisposed to oral infections
especially Candidiasis
• High-risk caries patients (CHX+ fluoride rinse combinations)
• Recurrent oral ulceration
• Removable and fixed orthodontic appliance wearers
• Denture stomatitis
• In long-term hospital patients, elderly patients and terminally ill
patients
• Immediate preoperative chlorhexidine rinsing and irrigation
• Subgingival irrigation
• As an adjunct to mechanical oral hygiene, particularly in the oral
hygiene phase of periodontal treatment.
 TOXICOLOGY AND SIDE EFFFECTS
(1) Brownish discoloration of the teeth and some restorative materials and the
dorsum of the tongue (Eriksen et al. 1985, Addy & Moran 1995, Watts &
Addy 2001)

(a) Degradation of the chlorhexidine molecule to release parachloraniline

(Addy & Roberts, 1981)
(b) a non-enzymatic browning reaction (Maillard reaction) - Carbohydrates
& amino acid containing compound in the acquired pellicle are catalysed
at high pH to produce brown pigmented substances called melanoids.
c) Formation of metal sulfide by denaturation of proteins in the
pellicle by splitting sulphide bridges free sulphydryl groups,
which reacts iron or tin ions brown and yellow pigmented
products (Ellingsen et al., 1982). Again, the theory does not take
into account staining by other antiseptics and metal ions.

d) Precipitation of dietary chromogens by cationic antiseptics

like CHX & polyvalent metal ions – phenomenon of staining is
well supported (Addy & Moran 1995)
• (2) CHX-induced precipitation of the mucin layer of the oral
mucosa thus reducing its lubricating effect causing
desquamation, soreness and erosion of oral mucosa. (Flotra et
al., 1971)

• (3) Over-vigorous mouth rinsing, which creates a negative

pressure in the duct and aspiration of the solution into the
gland causing unilateral or bilateral parotid swelling but it
subsides spontaneously within a few days after discontinuing its
use (Flotra et al., 1971)
• Transient impairment of taste sensation where salty taste appears
to be preferentially affected.

• Hypersensitivity reactions is rarely reported.

• Precipitation of salivary proteins on to the tooth surface, thus

increasing pellicle thickness &/or precipitation of inorganic salts
on to or into the pellicle layer thereby enhancing supragingival
calculus formation.
 ANTI-DISCOLORATION SYSTEM (ADS)
• CHX with anti-discoloration system (ADS) was launched recently in Europe
• Different systems have been introduced in order to reduce the brown pigmentations by
adding to CHX different products such as:
- Peroxiborate
- Polyvinyl pyrrolidone
- Sodium metabisulphite
- Ascorbic acid
• Plaque regrowth study showed significantly reduced plaque inhibition for the ADS rinse
(Arweiler et al. 2006).

(Gründemann et al. 2000, Claydon et al. 2001, Bernardi et al. 2004, Addy et al. 2005,
Arweiler et al. 2006).
 AMINE ALCHOLOS
Delomopinol
• Inhibits plaque growth – reduce gingivitis
• It interferes with plaque matrix formation & also reduces bacterial adherence,
primary plaque-forming successional bacteria
• It is indicated as pre- brushing mouth rinse as it weakens binding of plaque to
the tooth surface.
• 0.1 & 0.2% in mouthrinses as a plaque inhibitor and anti gingivitis agent
(Addy M, 2006)
• Side effects include tooth discoloration, transient numbness of the tongue,
and burning sensations in the mouth (Claydon et al. 1996; Hase et al.1998;
Lang et al. 1998)
 OXYGENATED COMPOUNDS
• Hydrogen peroxide (1.5%) and peroxyborate mouth rinse
• Mechanism Action :
- Ability to alter membrane permeability.
- Hydrogen peroxide breaks down to form oxygen and hydrogen.
When applied to tissue, protective enzyme such as peroxidase
and catalase causing rapid decomposition with resulting
effervescence.
• Inhibits obligative anaerobes
• Products containing peroxyborate and peroxycarbonate were, until recently,
available in Britain and Europe with evidence of antimicrobial and plaque-
inhibitory activity (Moran et al. 1995).

• Branemark and Ekhol studied the effect of 3% hydrogen peroxide and

reported that the agent increased the degree of the injury to damage tissue,
thus delayed wound healing.

• Treatment of the acute phase of the ANUG (Wade et. al 1966).

 FLUORIDE
• Caries preventive, but the fluoride ion has no effect against the development of
plaque and gingivitis.

• Amine fluoride and stannous fluoride provide some plaque-inhibitory activity,

particularly when combined; however, the effects appear to be derived from the
non-fluoride portion of the molecules.

• A mouth rinse product containing amine fluoride and stannous fluoride is

available and there is some evidence from home use studies of efficacy against
plaque and gingivitis (Brecx et al. 1990, 1992), but less so than chlorhexidine.
 SALIFLUOR
• Salifluor, a salicylanide with both antibacterial and anti-
inflammatory properties, has been studied for its effects of
plaque inhibition and retardation of onset of gingivitis (Furuichi
et al. 1996).

• To improve oral retention and to maximize adsorption, Gantrez

(PVM/MA) has been incorporated in salifluor toothpaste and
mouth rinse formulations.
• An initial 4-day plaque regrowth studies and 14-day gingivitis studies have
suggested equivalent efficacy to a 0.12% chlorhexidine mouth rinse
(Furuichi et al. 1996).

• the mechanism behind the anti-microbial and anti-inflammatory properties

of salifluor are not yet properly understood.

• In spite of this evidence to suggest the potential value of the chemical as an

antiplaque agent, further long-term studies have yet to be carried out.
 DETERGENTS
• Sodium lauryl sulfate, common ingredient in toothpaste and mouth
rinse products
• Have antimicrobial activity (Jenkins et al. 1991)
• Provide most of modest plaque inhibitory action of toothpaste (Addy
et al. 1983)
• Alone -moderate substantivity, measured at between 5 and 7 hours,
and plaque-inhibitory action similar to triclosan (Jenkins et al. 1991)
• Detergent-only formulations are not available
 OTHER ANTISEPTICS
• Most have been found to have little or no effect in vivo; a few have been
formulated in mouthrinse products including povidone iodine and hexetidine.

• Povidone iodine at 1% has a substantivity of only 60 minutes (Addy & Wright

1978) and lacks appreciable plaque inhibitory activity(Addy et al. 1977)

• Hexetidine, a saturated pyrimidine, at 0.1% - limited plaque inhibitory action

(Bergenholtz & Hanstrom 1974)
 CALCULUS
• Calculus is a hard concretion that forms on teeth or dental
prosthesis through calcification of bacterial plaque.(Glossary of
periodontal terms, 2001)

• Calculus is a hard deposit that is formed by mineralization of

dental plaque on the surfaces of natural teeth and dental
prosthesis, generally covered by a layer of unmineralized
plaque. (Carranza's clinical periodontology,13th ed.)
 CLASSIFICATION
 According to location
• Supragingival calculus
• Subgingival calculus
 According to source of mineralization(Jenkins, Stewart 1966)
• Salivary calculus
• Serumal calculus
 According to surface (Melz1950)
• Exogenous
• Endogenous
 COMPOSITION
• Calcium and phosphorous constitute the major element and Ca/P ratio
ranges from 1.6 to more than 2.

INORGANIC
70%-80%

PHOSPHATE
CALCIUM CALCIUM
MAGNESIUM
PHOSPHATE 75.9% CARBONATE 3.1%
TRACES
ORGANIC MATRIX 20%- 30%

Proteins 5.9- Carbohydrates

Lipids 0.2%
8.2% 1.9-9.1%
• Salivary • Neutral fats • Galactose
proteins • Free fatty • Glucose
acids • Rhamnose
• Cholesterol • Galactosamine
• Phospholipids • Glucosamine
• Gluconate
 CRYSTALS
Hydroxyapatite 58%

Magnesium Whitolockite 21%

Octacalcium Phosphate 1.2%

Brushite 9%
• Hydroxyapatite and Octacalcium phosphate are detected most
frequently in supragingival calculus. (97-100%)

• Brushite - mandibular anterior region; present only in the early-

stage supragingival calculus (Rowles, 1964).

• Magnesium whitlockite - in the posterior areas

 MINERALIZATION OF CALCULUS
• The mechanisms by which plaque becomes mineralized can be stratified
into two categories.

1. Mineral precipitation results from local rise in the degree of saturation

of Ca and P ions
- may be due to rise in salivary pH causing precipitation of calcium and
phosphate ions.
- Maintenance of supersaturated solution by binding to calcium and
phosphate ions by colloidal proteins in saliva.
- Phosphatase liberated from dental plaque, desquamated
epithelial cells causing increased concentration of phosphate
ions

2. Seeding agents induces small foci of calcification that enlarge

and coalesce to form a calcified mass. This concept is referred to
as epitactic concept.
 ANTI-CALCULUS AGENTS
• First GENERATION:
1) DISSOLUTION
• Chelating Agents
• Ethylene diamine tetra acetate
• Sodium Hexa Metaphosphate
• Acids –Aromatic sulphuric acid
• Nitro-muriatic Acid
• 20% TrichloroaceticAcid
• Spring Salts
• Sodium Ricinolate
2)ALTERING PLAQUE ATTACHMENTS
• Silicones
• Ion exchange resins.
3)PLAQUE INHIBITION
• Antibiotics Example : Niddamycin
• Antiseptics Example : Chloramines
4)MATRIX DISRUPTION
• Enzymes Example : Mucinase
• Trypsin, chymotrypsin
• Carboxypeptidase, lipase, amylase
• 30% UREA( solvent action on protein)
 2nd GENERATION

1) Inhibition of crystal growth

• Vitcamine C
• Pyrophosphatase
• Pyrophosphatase + Sodium fluoride
• Zinc salts
• Biphosphonates
• Polymers & Co Polymers
 ACIDS
• Niles (1881) - the nitro muriatic acid.
• Other acids included - 20% trichloroacetic acid, bifluoride of
mercury and 10% sulphuric acid.
• Disadvantages:
• Grossman (1954) reported that the ability of an acid to dissolve
tooth material was greater than its ability to dissolve calculus.
The use of acids as anticalculus agents was thus discontinued.
 ALKALIS
• Badanes (1929) argued that it was the action of the mild alkalis
contained in the waters that dissolved the principal organic
constituents of salivary calculus.
• Globulin, mucin and calcium oxalate.
• These findings agreed with those of Prinz (1921), but the idea
failed to find support.
 PYROPHOSPHATE
• Eg. tetrasodium, tetrapotassium or disodium dihydrogen
pyrophosphate, Bisphosphonates
• Usually incorporated in toothpastes.

Pyrophosphate could prevent calcification by

1. Interrupting the conversion of amorphous calcium phosphate to
hydroxyapatite (Fleisch & Bisaz 1962)
2. Inhibiting crystal growth.
3. Reduce acquired pellicle formation.
• Pyrophosphate - binds to two sites on the HAP surface
• For crystal growth to occur and out of the two sites, one site needs to be
bound by phosphate ion. If this site is bound by pyrophosphate, phosphate
ion cannot adsorb onto crystal, and thus crystal growth is inhibited.

• Pyrophosphate undergo rapid hydrolysis in the oral cavity by bacterial and

host phosphatases (Gaffar et al 1986).

• The addition of co polymer PVM/MA is believed to prevent this

hydrolysis.
 CHELATING AGENTS

• These chemicals remove calcium from solution.

• Sodium hexametaphosphate was found to remove supragingival

calculus from extracted teeth in 10 to 15 days (Kerr & Field 1944).
• Warren et al. (1964) exposed extracted teeth to a saturated solution of
sodium hexametaphosphate for 24 h and found a large reduction in
the hardness of the cementum and the decalcification of the calculus
was less than that of cementum.
 EDTA
• Jabro et al. (1992) found that application of EDTA gel (Sofscale
TM ) resulted in ease of calculus removal.
• Smith et al. (1994) noted that sufficient time has to be allowed
for the gel to penetrate the bulk of the calculus deposit and this
may negate the reason for using it.
• Because of this nonspecific demineralization effect, the use of
chelating agents in anti-calculus dentifrices ceased.
 ENZYMES
• Mode of action – 1.To break down plaque matrix
2. To affect the binding of the calculus to the tooth.

• The first enzyme to be tested- mucinase .Calculus formation reduced &

calculus formed was softer and more easily removed (Stewart 1952).
• Aleece & Forscher (1954) - introduced mylase.

• Enzyme with high proteolytic and low amylase activity- most effective
inhibitor of calculus formation. Draus et al. (1963)
• Proteolytic enzyme activity - reduce calculus formation by 60% (Jensen
1959).
• Dehydrated pancreatin (Viokase) contains trypsin, chymotrypsin,
carboxypeptidase, amylase, lipase and nucleases.
• Viokase was introduced into chewing gum (Ennever & Sturzenberger 1961,
Packman et al. 1963).
• 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. The gum stick produced a 22% to 26% reduction in calculus
formation respectively compared to the control groups.
 UREA
• The anticalculus effect - ability to dissolve the mucoproteinaceous
material within which the calcium salts are deposited and/or by
increasing the solubility of calcium salts in saliva. (Belting & Gordon
1966).

• It was found that increasing the concentration of urea resulted in

progressive inhibition of calcium deposition.

• A maximum inhibition of 70% was reached at a concentration of 30%

urea.
• Urea concentrations greater than 30% led to a progressive decrease in
inhibition.
• Ethanehydroxydiphosphonate (EHDP) or acetohydroxamic acid (AHA)
were tested for their anti calculus potential.
• Results demonstrated a significant reduction in calculus formation in both
the EHDP and AHA group, but such changes were not significant in humans.
( Son &Muhlemann 1971)
• This finding together with the observation that AHA had been shown to
increase caries (Regolati & Muhlemann 1971) led to a decline in interest in
AHA as an anticalculus agent.
 MISCELLANEOUS CHEMICAL
AGENTS
• Attempts have been made to prevent calculus deposition by coating the teeth
with adhesive to alter the binding of the calculus to the tooth.
• Dimethylpolysiloxane and cyanoacrylate monomer adhesive,- no effect
• Silicones- no effect
• Lactone- effective but caused de-mineralisation of teeth.
• Sulphonated polystyrene membrane – effective but temporary
• Sodium ricinoleate - interferes with the attachment of
microorganisms to teeth. (Dossenbach & Muhlemann (1961)
• The results showed almost total absence of microorganisms, and
calculus formation was almost totally inhibited.
• Unfortunately, sodium ricinoleate had a particularly
unacceptable taste and needed to be applied at high
concentrations.
• Watt et al. (1993) postulated - changing the electrostatic nature of the
tooth surface in calculus prevention
• The magnetic water was thought to bring Ca2 and PO4 ions closer
together, consequently reducing attachment.
• The group using a magnetic water irrigator had 44% greater
reduction in calculus volume and a 42% greater reduction in
calculus area when compared with the group using an irrigator with
no magnetic water.
 CALCIUM LACTATE
• Schaeken et al. (1990) investigated a 5% calcium lactate solution on calcium
and phosphate levels in saliva, increased salivary calcium and phosphate
levels but unexpectedly showed a decrease in calculus levels in the test group.

• The group using the dentifrices with calcium lactate had a 44% reduction in
calculus and those using the calcium lactate with sodium lauryl sulphate had a
47% reduction in calculus with respect to the control group.

• The authors concluded that calcium lactate probably did not act as an inhibitor
of crystal growth but may offset secretion and activity of salivary
phosphoproteins.
 VICTAMINE C
• Victamine C is a surface active organophosphorus compound that has been
shown to be effective in inhibiting the in vitro crystallization of calcium
phosphate on to smears of supragingival calculus (Turesky et al. 1965).
 Mechanism:
• Victamine C has a characteristic taste which might have promoted saliva flow,
thus reducing calculus levels.(but Gilmore compared effect of quinine sulphate
and vitcamine C and found quinine sulphate having similar taste did not inhibit
calculus formation)
• Turesky et al.(1967) tested the efficacy of a chloromethyl analogue of victamine
C - victamine C solution reduced calculus deposition by 46.8% compared to
water controls.
 Antimicrobials
NIDDAMYCIN
 Strong activity toward a variety of gram positive organisms; streptococci,
enterococci, corynebacteria, bacilli and certain protozoas.

 No known medical uses; not significantly absorbed orally or systemically,

and no in vivo bacterial resistance had been reported(Stallard et al.1969).

 Research into the use of Niddamycin as an anticalculus agent was

discontinued - concern over the development of bacterial cross resistance to
other antimicrobials .
 METALS
• Use of heavy metals - suggested by Hanke (1940) - in solution, these metals
suffered from having a disagreeable metallic taste, or caused an unsightly
discoloration of the teeth.

• Mechanisms by which they can affect calculus formation:

i. Firstly, they inhibit plaque growth by the uptake of the metal salt by bacteria,
with a consequent disruption of intracellular metabolic processes (Aickien &
Dean 1976),
ii. Secondly, metal salts are potent inhibitors of mineralization. (Bachra & van
Harskamp 1970, Thomas 1982).
• Metal ions can bind to hydroxyapatite although this binding is reversible.
• Metal ion adsorbs to the surface of the growing crystal, and
prevents the attachment of lattice ions. Consequently, crystal
growth is slowed or inhibited.

• Zn at a conc of 0.1mmol/L inhibits the formation of DCPD,OCP

and amorphous Ca P but at a higher conc of 0.5-2 mmol/L
promotes the formation of amorphous CaP.
 PVM/ MA copolymer
• PVM/MA Copolymer is a copolymer of methyl vinyl ether and maleic anhydride
and is used as a binder.

• Promotes uptake of triclosan by enamel and buccal epithelial cells (Nabi et al.,
1989).

• Composed of two groups: an attachment group and a solubilizing group.

• The solubilizing group retains triclosan in surfactant micelles so that the

attachment group can have enough time to react with tooth surfaces via calcium in
the liquid adherent layer.
 CONCLUSION
• While 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 constitute the cornerstone of periodontal therapy.
• Chemical plaque control has been used only as an adjunct to mechanical
plaque control, not a substitute.
• Chlorhexidine is the most effective anti-plaque agent to date.
• Combinations of agents sometimes provide additive or synergistic action.
 REFERENCES
• Newman MG, Takei HH, Klokkevold PR, Carranza FA. 13th edition.
Carranza’s Clinical Periodontology.
• Clinical periodontology and Implant dentistry, 5thedition, Jan Lindhe.
• Strategies and agents in supragingival I chemical plaque control Michel
Brecx. Periodontology 2000, Vol. 15, 1997, 100-108
• Chetrus V, Ion IR. Dental Plaque-Classification, Formation, and
Identification. International Journal of Medical Dentistry. 2013 Apr
1;3(2):139.
• Chemical plaque control- prevention for the masses John M. Moran.
Periodontology 2000, Vol. 15, 1997, 109-117
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Munksgaard, 2000.
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Chlorhexidine-delivering toothbrush Jcp 2008;35,584-590
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G. A. Stain, plaque and gingivitis reduction by combining chlorhexidine and peroxyborate.
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