CURRENT TRENDS IN

CARIES PREVENTION
CONTENTS
TRADITIONAL AGENTS NOVEL AGENTS
1. Fluorides 1. Plant Extracts
2. Essential Oils
2. Measures beyond fluoride:
3. Trace Elements
• Chlorhexidine 4. CPP-ACP
• Triclosan 5. Synthetic antimicrobial Peptides
• Povidone Iodine 6. Arginine
• Mechanical Measures 7. Sucrose Replacement
• Dietry Measures 8. CO₂ LASERs
9. Probiotics
• Prophylactic Odontomy and
10. Gene Engineering and DNA
Fissure Eradication
Recombination Technology
• Pit and Fissure Sealants 11. Novamin
12. Caries Vaccine
13. Quorum Sensing Inhibitors
INTRODUCTION
DENTAL CARIES is an infectious microbiologic disease of the teeth that results in
localized dissolution and destruction of the calcified tissues.

Dental decay is mainly due to demineralization which is caused by acids produced

by bacteria, particularly mutans Streptococci and possibly lactobacilli that
ferment dietary carbohydrates. This occurs within a bacteria-laden gelatinous
material called dental plaque that adheres to tooth surfaces and becomes
colonized by bacteria. Thus, caries results from the interplay of three main factors
over time
• dietary carbohydrates,
•cariogenic bacteria within dental plaque, and
•susceptible hard tooth surfaces
Dental caries is one of the most common preventable childhood disease and
people are susceptible to this ailment throughout the lifetime.
The preventive care providers have the intention for prevention beyond the scope
of providing hygiene therapy and oral hygiene instructions.
The use of fluoridated toothpastes , other topically applied fluorides, fluoridated
municipal water and pit and fissure sealants along with dietary improvement
remain mainstays of caries management.
Since 1970‘s researches started to search for non-fluoride agents for the
prevention of dental caries. Non-fluoride agents may serve as adjunctive
therapeutics for preventing, arresting or even reversing dental caries.
 FLUORIDES

Fluoride has three principle topical mechanisms of action:

1. Decreasing demineralization when fluoride is present in the biofilm during an

acid challenge;
2. Enhancing remineralization and thereby forming a low solubility veneer
similar to the acid-resistant mineral fluorapatite, on the remineralized
crystals.
3. Inhibiting bacterial metabolism after diffusing into the bacteria as the
hydrogen fluoride, or HF, molecule when the plaque is acidified;
Fluoride is clinically effective in preventing the caries process and reducing the
formation of cavities, because it acts directly on the tooth mineral to prevent
mineral loss. During use of a fluoride toothpaste or mouthrinse, low levels of
fluoride are delivered to the oral cavity where they are retained in reservoirs on the
tooth surface and the soft tissues for sustained time periods after application. These
low, sustained levels of fluoride are able to modify the critical pH value below which
calcium and phosphate ions are solubilized from the tooth structure and, thus, are
able to reduce demineralization. These low, sustained levels of fluoride are likewise
able to enhance remineralization of demineralized tooth enamel and dentin. This is
believed to occur via formation of calcium fluoride on the tooth surface which acts
as a reservoir during periods of homeostasis, and is triggered by significant pH drops
to drive calcium ions into calcium-deficient hydroxyapatite sites in the caries lesion.
1. DECREASE DEMINERALISATION

Enamel is dissolved by the lowering of pH in dental plaque due to acid production

every time sugar is ingested. However, if F is present in the biofilm fluid, and the pH is not
lower than 4.5, hydroxyapatite (HA) is dissolved at the same time that fluorapatite (FA) is
formed. The net result is a decrease in enamel dissolution, since a certain amount of Ca
and Pi, which was lost as HA, is recovered by enamel as FA. This mineral gain as FA during
the pH drop has not been considered as remineralization but rather as a decrease in
demineralization because the mineral redeposited is different from that lost.
Furthermore, FA is deposited on the surface layer of enamel while HA is dissolved from
the subsurface.
 A goal of modern dentistry is to manage non-
2. ENHANCE REMINERALIZATION
cavitated caries lesions non-invasively through
REMINERALIZATION in an attempt to
prevent disease progression and improve
aesthetics, strength, and function

Thus understanding the process of

demineralisation & especially remineralisation

helps to salvage a tooth from being ravaged by

carious process.

After the exposure to sugars has ceased, acids

Remineralisation in biofilm
allows a moreare cleared by saliva and converted to
effective
salts. As a result, the pH increases and, at 5.5 or higher, the biofilm fluid is supersaturated with
respect to HA and FA. Thus, Ca and P, approach
conservative lost by enamel can be more efficiently recovered if F is
to demineralisation
still present in the biofilm.

process.
3. INHIBIT BACTERIAL METABOLISM
Fluoride has antimicrobial activity.
• In low concentrations, fluoride ion inhibits the enzymatic production of
glucosyltransferase and therefore prevents glucose from forming
extracellular polysaccharides, and this reduces bacterial adhesion and slows
ecologic succession. Intracellular polysaccharide formation also is inhibited,
preventing storage of carbohydrates by limiting microbial metabolism
between the host's meals. Thus, the duration of caries attack is limited to
periods during and immediately after eating.
• In high concentrations (12,000 ppm) used in topical fluoride treatments,
fluoride ion is directly toxic to some oral microorganisms, including MS.
•Suppression of growth of MS following a single topical fluoride treatment
may last several weeks . It is possible to greatly lengthen this suppression by
a change in dietary habits (especially eliminating sucrose) and by the
patient's conscientious application of a good oral hygiene program.
The mechanism by which fluoride works depends on the conditions of its use.
 At high concentrations(12000-22600ppm), used for topical therapy, there is
atleast a temporary effect on bacterial metabolism, inhibiting glycolysis and
suppressing S.mutans.
 At lower concentrations, such as systemic fluoride provided by water
fluoridation or supplements of topical fluoride from dentifrices and mouth
rinses, there is uptake of fluoride by hydroxyapatite, rendering it less soluble and
improving its crystallinity.
 FLUORIDE DELIVERY METHODS

1. TOPICAL FLUORIDES:
• PROFESSIONALLY APPLIED-
i. Aqueous solutions and gels: 2% NaF, 8% SnF₂, 1.23%APF
ii. Fluoridated prophylactic pastes.
iii. Foam based APF agents
iv. Fluoride varnish: Duraphat (NaF varnish containing 2.26%

fluoride in organic lacquer)

Fluorprotector (Silane Fluoride with 0.7% F in a
polyurethane based lacquer)
Carex (Lower Fluoride concentration than
duraphat- 1.8%)
• SELF APPLIED-
i. Dentifrices: Sodium fluoride
Stannous Fluoride
Monofluorophosphate
Amine fluoride
ii. Fluoride mouthrinses: Sodium fluoride( 0.2% for weekly and
0.05% for daily use)
Stannous Fluoride
Amine Fluoride
Ammonium Fluoride
iii. Fluoride Gels: NaF and APF (5000 ppm)
SnF₂ (1000 ppm)
2. SYSTEMIC FLUORIDES
i. Community water fluoridation: defined as “ the upward adjustment of the
concentration of fluoride ion in a public water supply in such a way that the
concentration of fluoride ion in the water may be consistently maintained at
1ppm by weight to prevent dental caries with minimum possibility of causing
dental fluorosis”.

ii. Salt fluoridation: controlled addition of fluoride, usually sodium or potassium

fluoride, during the manufacture of salt.
Recent investigations suggest that the level of fluoride can be kept at 200-350
mg of Fluoride per kg salt.
iii. Milk Fluoridation: Addition of measured quantity of fluoride to

bottled or packaged milk to be drunk by children.

Fluoridated milk is produced with different concentrations of
aqueous sodium fluoride, but a typical value may be 5ppm
fluoride.

iv. Fluodide Tablets/Drops/ Lozenges: Sodium Fluoride is most

commonly used.
Correct dosage depends on the concentration of fluoride in
drinking water, age of child and other available fluorides.
Not more than 1mg of F should be ingested each day from all
available systemic sources.
Chlorhexidine
• Chlorhexidine is a cationic bisbiguanide with broad spectrum antimicrobial
activity against Gram-positive and Gram-negative bacteria as well as yeasts at
high concentrations.
•Antiplaque and antibacterial activity.
• The superior antiplaque activity of CHX is due to its proprety of substantivity.
•Bacteriostatic at low concentration and bacteriocidal at high concentration.
Chlorhexidine inhibits plaque by:
1. Preventing pellicle formation by blocking acidic groups on salivary glycoproteins,
thereby reducing glycoprotein adsorption on to the tooth surface.
2. Preventing adsorption of bacterial cell wall onto the tooth surface by binding to
the bacteria.
3. Preventing binding of mature plaque by precipitating agglutination factors in the
saliva and displacing calcium from the plaque matrix.
CHX is available as rinsing solutions, gels, or dental varnishes at various
concentrations.
1. The traditional indication for CHX treatment is caries control in caries active
individuals, and the best mode of professional treatment seems to be
intensive treatments with gel in custom-made soft trays, 3 × 5 minutes for 2
consecutive days.
For homecare use, a 5minute application once a day for 14 days may be
preferred.
2. Varnishes exert a slow release of CHX but must be reapplied at regular
intervals (every 3 to 4 months).
Have moderate caries inhibiting effect, but the beneficial effect was
questionable in low caries populations.
3. CHX rinses have variable effects on mutans streptococci suppression and
caries control.
•Chlorhexidine is prescribed for home use at bedtime as a 30-second rinse. Used at
this time, when the salivary flow rate is decreased. It is used for approximately 2
weeks, and results in a reduction of MS counts to below caries potential levels. This
decrease is sustained for 12 to 26 weeks.
•CHX should not be used before/ immediately after using a toothpaste as interaction
with anionic surfactants found within formulations, will reduce effective delivery of
CHX in an active form. Toothpaste should be used prior to using chlorhexidine and
excess toothpaste rinsed away with water.
TRICLOSAN

• Triclosan is a synthetic broad-spectrum antimicrobial agent with antiviral

and antifungal properties.

• It acts by blocking the active site of an essential enzyme in the cell

membrane synthesis.
• Triclosan is also used to increase the ability of mouthwashes to bind to the
oral mucosa, and thus be available for long period of time.

Vered Y, Zini A, Mann J, et al. J Clin Dent

2009;20(2):62–5.
Povidone-Iodine
Iodine is highly efficient microbicide for bacterial, fungal, and viral infections.
Intraorally, short durations of PI contact with various periodontopathic bacteria
are effective in in vitro killing and exhibit marked anticytomegaloviral activity.
Small-scale studies of PI utility in young children, some with established active
early childhood caries, demonstrate promising data. But there is no firm
conclusion on the efficacy of PI in preventing caries can be drawn, and restrictive
use is further justified because PI may cause skin irritation and severe allergic
reactions.
Contraindications are patients with iodine hypersensitivity and thyroid pathosis,
as well as pregnant and nursing women.
Mechanical measures
The control of caries by mechanical measures refers to procedures specifically
designed for and aimed at removal of plaque from tooth surfaces. There are
numerous means of cleansing the tooth mechanically, and these were
reviewed and classified by Hine in a discussion of caries control measures as:
•Prophylaxis by the dentist.
•Tooth brushing.
•Use of dental floss or toothpicks.
•Incorporation of detergent foods in the diet.
DIET

Dietary sucrose has two important detrimental effects on plaque.

First, frequent ingestion of foods containing sucrose provides a stronger potential for
colonization by MS, enhancing the caries potential of the plaque.
Second, mature plaque exposed frequently to sucrose rapidly metabolizes it into
organic acids, resulting in a profound and prolonged drop in plaque pH.
•Despite this knowledge, dietary modification for the purpose of caries control has
failed as a public health measure. However, for an individual patient, dietary
modification can be effective if the patient is properly motivated and supervised.
• Minor dietary changes such as substitution of sugar-free foods for snacks are more
likely to be accepted than more dramatic changes.
 Physical nature of diet: The diet of the primitive man consisted generally of raw
unrefined foods containing a lot of roughage which cleanses the teeth of adherent
debris during mastication. In the modern diet, soft refined foods tend to cling to the
tooth and are not removed because of the general lack of roughage.
 Frequency of sugar intake:
Most people eat four to six times daily. Exceeding this with frequent nibbling and
sipping of sugary/starchy, highly processed foods and beverages for prolonged
periods (>30 minutes) increases caries .
Frequent consumption of cooked starches, simple sugars, or processed sugar-starch
combinations will sustain an oral environment that promotes demineralization in
preference to remineralization. With increased eating frequency, there is expected
increased total fermentable carbohydrate intake. Thus, the two are highly
associated.
• Amount of intake:Caries activity is most strongly stimulated by the frequency, rather
than the quantity of sucrose ingested.
 Type of carbohydrate:
• Acidogenicity and potential cariogenicity of sucrose, glucose, fructose, and
maltose are similar; however, lactose is less cariogenic.
• Grains, fruits, and vegetables that occur naturally are sources of intrinsic sugars
encapsulated in foods that include other protein, non digestible fiber, and
fatty acid constituents. There is lack of evidence to suggest these intrinsic
sugars support the caries process.
Starches cannot directly serve as substrate for oral bacterial fermentation .
Grains and vegetables such as potatoes, wheat, and beans contain starch granules
that are damaged when subjected to heat and mechanical forces, leading to the
formation of gelatinized starch. Through further hydrolysis by salivary and
bacterial amylases, maltose and maltotriose become available as substrate for
plaque bacteria and acid production. The bioavailability and cariogenicity of food
starches in the mouth vary with the basic genetic character and different cooking
and food processing methods (frying, boiling, and so forth) . Starchy foods such as
untreated whole grains and raw vegetables have lower caries promoting
potential than heat processed foods such as white breads, crackers, chips, and dry
cereal snacks.
Dairy products
i. Although milk is associated with early childhood caries in infants because
of its lactose (5% sugar) content and linked infant feeding practices that
allow for prolonged contact with tooth surfaces, milk has beneficial
implications for caries management.
Calcium and phosphorous bound to casein protein in milk are believed to
be responsible for a protective effect on tooth enamel.

2. Likewise, cheese is considered to be an excellent anticariogenic food.

When consumed after a sugary food, it is a strong stimulate of salivary
flow, resulting in both a buffering effect and neutralization of plaque
acids. Like milk, cheese contains casein phosphopeptides that appear to
reduce demineralization and enhance remineralization.
A cube of cheese eaten after sugary meals or snacks reduces the
demineralization process.
Sugar Substitutes And Alternative Sweeteners:
Sorbitol (glucitol) is fermented so slowly by whole plaque that the acid produced may
diffuse away and be neutralized by salivary buffers.

Xylitol is not fermented by cariogenic plaque bacteria and thus does not lower the pH
of the plaque.
It reduces the accumulation of plaque on the surface of the tooth.
It accumulates intracellular in MS and inhibits the bacterial growth by altering their
metabolic pathways.
•Chewing a xylitol gum such as Xylimax three times daily for a minimum of five
minutes each time for three months may give a 10 fold reduction in salivary levels of
MS, bringing in the important advantages of increased salivary clearance, buffering
and remineralization; a strategy which would be useful in high caries risk patients, as
an adjunct to other suppressive approaches such as chlorhexidine therapy.
One important advantage of this approach is that it is suitable for maintaining long-
term suppression of pathogens without concerns of safety with prolonged use.

Aspartame, maltol, monellin, thaumatin and miraculin are some of other sugar
substitutes.
Plant foods:
Plant foods such as grains and vegetables have natural protective factors that act
as anticariogenic agents. These are prevalent in unrefined foods and include
organic phosphates, inorganic phosphates, polyphenols, phytate, and other
nondigestible fibers.
Fibrous foods stimulate salivary flow and, as part of a healthy diet, contribute to
oral health.
Other foods:
Green, oolong, and black teas contain fluoride and polyphenols or flavonoids
that suppress oral bacterial growth in vitro and reduce the acidogenic potential
of sucrose.
Oleic and lenolic fatty acids in cocoa bean husk have shown bactericidal activity
against Streptococcus mutans in laboratory studies. These results indicate that
chocolate possesses some anticariogenic potential, but its anticaries activity is
not strong enough to suppress significantly the cariogenic activity of the sucrose
in chocolate foods.
Licorice candies made of glycyrrhizinic acid have been shown to increase plaque
buffering capacity and inhibit bacterial metabolism but can cause enamel
staining.
Peanuts high in monounsaturates promote mechanical stimulation and salivary
flow and are characterized as having a low caries potential.
Phosphated diets:
2% dibasic calcium phosphate and 0.2-1% calcium sucrose phosphate are added
to carbohydrate component of diet.
It is hypothesised that these penetrate the surface crystalline layers of enamel,
tightening the attachment between crystals. This reinforcing action protect
enamel from disintegration by acids.
But, the results of clinical tests of dietary phosphate additions for the sole
purpose of controlling dental caries are yet inconclusive.
DIETRY MEASURES
Factors to be considered Measures to reduce caries risk and/or to stop ongoing caries activity
Frequency of meals Number of meals and snacks should be kept on a low level.
Amount and concentration of
Low sugar consumption is desirable from a cariological point of view.
sucrose in meals
Sugars should be eliminated as fast as possible from the oral cavity.
Elimination of sugars and
Foods needing active chewing lead to an increased salivation which is
consistency of food
desirable.

Polysaccharides, disaccharides and monosaccharides contribute to acid

Fermentable carbohydrates formation in the oral cavity, but the capacity differs between different

products.

Sugar substitutes Use of sugar substitutes results in lower acid formation.

1.
Fluorides in food or drinking water have a pronounced caries-inhibiting
Protective and favorable effect.
elements in diet 2. Phosphates, calcium, fat, proteins, cheese etc. have been tested and
found to have a certain caries inhibiting effect in animals.
 Prophylactic Odontotomy and Fissure
Eradication
• This conservative approach was advocated by Bodecker in 1929.

• Initially, he advocated cleansing the fissure with an explorer and flowing a thin
mix of oxyphosphate cement into the fissure in order to seal it.
• Later, he advocated prophylactic odontotomy, which involved mechanical
eradication of fissures into cleansable ones. He suggested widening the
fissures mechanically so that they would be less retentive to food particles
(fissurotomy).
Pit and fissure sealants

Bunocore (1955) advocated the filling of pit and fissures with bonded resin based
sealants.
Sealants have three important preventive effects:
•Sealants mechanically fill pits and fissures with an acid resistant resin.
•They deny streptococci mutans and other micro-organisms their preferred
habitat.
•They render pit and fissures, easier to clean by tooth-brushing and mastication.

Obturation of occlusal pits, fissures and grooves by occlusal sealants greatly

reduces number of cariogenic bacteria in the mouth, without whole-sale
disruption of remainder of the oral flora and also prevents retention of cariogenic
substrate.
• Dental sealants can be effective in preventing the progression of early non-
cavitated carious lesions, even when sealing over existing bacteria. They are
shown to be more effective saving if placed in patients with a high rather than
low caries risk.
• Cavitated carious fissures cannot be sealed as adequately as sound fissures due
to presence of biofilms left in the deeper parts, which are difficult to assess.
• Also older high-risk patients with suspect fissures will benefit from sealants.
• A high-risk patients, those with appliances, also will benefit greatly from sealing
tooth areas with a high potential of future caries activity (e g, around
orthodontic brackets and removable partial denture clasps).
• Sealant protection is in particular indicated during periods of tooth eruption

(ages 5 to 6 years and 10 to 12 years).

• When moisture control is a problem, glass ionomer sealants may be indicated
for erupting first molars.
• SEM studies show that sealants are superior in comparison to latest
remineralizing agents as they occlude the fissures without any gap and with
least probability of microleakage. They are also superior to fluoride varnishes
for the prevention of occlusal caries
Various types of pit and fissures are available in the market depending upon
the type of polymerization, type of light cure used, color, filler particles etc.
Considering the material factor, resin bonded sealants proved to be more
efficient due to their higher retention rate than their counterpart glass
ionomer sealants.
Pit and fissure sealant with ACP- Light cure material that contains ‘smart
material’- amorphous calcium phosphate which is more flexible, resilient,
creating a stronger and long lasting sealant.
Sealants should be placed as part of an overall prevention strategy based on
assessment of caries risk, ideally used in combination with patient education,
effective personal oral hygiene, nutritional counselling, fluorides and regular
dental visits.
Altering Saliva Production
Saliva is a major protective factor in the oral cavity, and a reduction in saliva output
can occur from numerous systemic diseases and pharmaceutical interventions.
Loss of antimicrobial capacity, pH buffering, and remineralization properties of saliva
may lead to rapid and severe caries formation, and may also leave the mouth
susceptible to infections, mucosal pain, and difficulties chewing and swallowing.
By increasing salivary function and its natural protective factors, these oral
complications can be avoided and,
when combined with other caries prevention techniques, can provide a synergistic
approach in prevention of caries formation.
Clinical attempts at increasing secretory output first start at a local level within
the mouth, and typically begin by increasing oral activity.
•Salivation physiologically increases in response to chewing or taste, particularly
sour and bitter tastes. The use of sugar-free gums and lozenges will increase
salivary output for a patient, and still remains the mainstay therapy for patients
suffering from xerostomia (dry mouth).
•Other topical therapies include artificial saliva that attempt to mimic the
composition and abilities of natural saliva in the forms of oral rinses, gels, and
flavored mouthwashes.
These topical treatments are limited however by their transient nature, and
stimulating saliva output over a prolonged period of time would be more
desirable.
Several systemic agents that can stimulate saliva production can have a more
profound and consistent effect.
Pilocarpine is the drug with the most extensive background of clinical evidence,
as it has been a treatment for dry mouth for over 100 years.
Pilocarpine was initially utilized in Sjogren’s syndrome and postradiation therapy
to stimulate saliva production. Pilocarpine is a parasympathomimetic agent with
a mild β-adrenergic stimulating property that can be utilized without serious
adverse side effects, although treatment for patients with cardiovascular disease
is not advised.
Typically an orally ingested form of pilocarpine HCL is delivered 3 times a day,
and common side effects include excess sweating and urination.

Cevimeline is a drug that has recently gained clinical backing in increasing

salivary output.
The pharmacological profile is very similar to Pilocarpine, and the important
properties of the drug are the later onset time and longer
duration of the action.
A therapy using a combination of both Pilocarpine and Cevimeline is
under review, that could potentially deliver a longer lasting, consistent increase
in saliva production.
Therapeutic Dentifrices

Tooth-pastes are the valuable adjuncts to oral hygiene as they make brushing
more pleasant and more effective. Many attempts have been made at various
times to add-therapeutical agents with the objective of interfering with oral flora,
limiting plaque formation and making teeth more resistant to caries.

Chlorophyll: Chlorophyll was one of the earliest agents added to

the paste and is still present in some tooth-pastes. Although in vitro
tests showed that chlorophyll- containing tooth pastes limits bacterial
growth, but clinical trials have not shown any anti- caries effects .
Ammoniated tooth-paste: This usually contains urea, and developed in an attempt
to control the acid production in plaque. A numbers of clinical trials were carried
out, but all gave very little positive or inconclusive results.
Ammoniated pastes have been superseded by more effective agents, Anti-biotic
toothpastes containing penicillin, triclosan or topical anti-biotic such as tyrothricin
have also been tried. It was based on the assumption that if acidogenic bacteria are
destroyed, caries will be controlled.

Anti-enzyme paste: These toothpastes were introduced on the basis that they
interfere with enzyme systems of the bacteria and thus with their growth and
function. Still their effectiveness has not been evaluated by clinical trials .
Various other dentrifices containing herbal products like neem, tulsi, clove oil, propolis
are available which show beneficiary effect in preventing dental caries.
Plant extracts
A number of phytochemicals, including antibacterial agents have been derived from
edible plants and demonstrate antibacterial properties against Streptococcus mutans.
•Neem, Azadirachta indica: inhibitory effects upon bacterial aggregation, growth and
adhesion to hydroxyapatite and production of insoluble glucan.
•Tulsi, Ocimum sanctum: The antimicrobial activity of tulsi is attributed to its
constituents namely ursolic acid and carvacrol. Agarwal et al. Demonstrated maximum
antimicrobial potential at 4% concentration level.
•Prunus mume: a common fruit in Asia, is considered to be the potential candidate for
developing an oral antimicrobial agent to control or prevent dental diseases associated
with oral pathogenic bacteria like Streptococcus mutans, S. sobrinus, S. mitis, S.
Sanguinis, Lactobacillus acidophilus, P. gingivalis, Aggregatibacter actinomycetem
comitans.
Green and black tea (Camellia sinensi): Various component in green and black
tea notably simple catechins, have anticariogenic activity. These include: a
direct bactericidal effect against S mutans and S sobrinus; prevention of
bacterial adherence to teeth; inhibition of glucosyl transferase, thus limiting the
biosynthesis of sticky glucan; inhibition of human and bacterial amylases.
Hop plant (Humulus lupulus): antimicrobial activity against S. Mutants and
other oral streptococci.
Oleic acid, Linoleic acid, epicatechin polymer (Cacao bean husk): These shows
antimicrobial activity against planktonic cells of mutans Streptococci. It has an
inhibitory effect on water-insoluble substances, polymer glucan synthesis,
adherence, acid production by mutans streptococci.
Meswak chewing sticks (Twigs of Salvadora persica): sticks embedded in
agar or suspended above the agar plate had strong antibacterial effects
against all tested bacteria.
Propolis: a natural beehive product, when used as a mouthwash exhibits an
in vivo antimicrobial activity against S. mutans and might be used as an
alternative measure to prevent dental caries.
Chinese Licorice Root: A new cavity fighting herbal lollipop that contains a
special herbal formula extracted from the Chinese licorice root can help to
immobilize major organisms responsible for tooth decay.
Proanthocyanidins, phenolic acids, flavonols (Cranberry): These shows antimicrobial
activity against streptococci. It causes disruption of acidogenic/aciduric properties of
planktonic and biofilm cells of S. mutans. It has inhibitory effects on Gtf activity and
adherence by mutans Streptococci and causes reduction of formation of S. mutans
biofilms and EPS content.
Apigenin and tt Farnesol: two naturally occurring agents that affect the development
of cariogenic biofilms. Apigenin inhibits the activity of glucosyltransferases . tt-
Farnesol showed modest antibacterial activity.
It also enhances the cariostatic effectiveness of fluoride.
The combination of these novel agents with fluoride may represent a potentially
useful and an alternative approach to the current chemotherapeutic strategies by
reducing the expression of virulence of S. mutans without necessarily suppressing the
resident oral flora .
Essential oils:
Essential oils have also been extensively studied for antimicrobial activity against
caries-related bacteria.
Essential oils derived from plants are typically a complex mixture of
approximately 20-60 compounds that are in solution at various concentrations.
Overall, the main chemical group is primarily composed of terpenoids,
followed by aromatic and aliphatic constituents. Thymol and eugenol inhibit the
growth of a wide range of oral microorganisms including mutans streptococci
Trace elements
Different trace elements has been investigated were zinc, tin, aluminium, copper,
iron, strontium, barium, manganese and molybdenum, gold, lead etc.
Aluminum, copper, and iron have the most commonly used as cariostatic agent,
although each would probably have organo-leptic problems if used in oral care
products as simple salts. Moreover, the toxicity of many metals like aluminum,
copper, barium molybdenum, would restrict the concentration at which they could
be safely used.
 CPP-ACP
Recent developments in the area of remineralization include casein phosphopeptide-
amorphous calcium phosphate (CPP-ACP).
The casein phosphopeptides (CPP) are derived from casein present in dairy products
by tryptic digestion.
All CPPs contain the sequence motif -Pse-Pse-Pse-Glu-Glu-, where Pse is a
phosphoseryl residue. Through these multiple phosphoseryl residues, CPPs have a
marked ability to stabilize calcium phosphate ions in solution and to form an
amorphous calcium phosphate (ACP) complex, referred to as CPP-ACP . The CPP-ACP
is taken up by dental biofilms and localizes to the enamel surface as nanoparticles.
Calcium, phosphate and fluoride from CPP-ACP, which are released During Acidogenic
challenge, help to maintain the supersaturated state of these ions in the biofilm and
so promote remineralization over demineralization.
•CPP may also affect adhesion of MS and modulate fermentation by dental plaque
bacteria.
• Their metabolism in plaque (with a half life of 2.8 hours) also results in a pH
elevating effect because of their substantial arginine content.
•Cai et al. demonstrated the effect of CPP-ACP incorporated into a sugar free
lozenges on enamel remineralization in a human in situ model.
ACP-CPP may be a Supplement in
– Chewing gums

– Mouth wash

– Toothpaste

– Topical application

– GIC cement

• When CPP-ACP is integrated into glass ionomer restoration materials, significant

reductions in secondary caries adjacent to these restorations have been seen in
laboratory investigations.
Bonlac Foods Limited (an Australian company) has exclusive manufacturing and

marketing rights for CPP-ACP and is the owner of the trademark , Recaldent.

Recaldent is an active ingredient derived from caesin. It works safely; strengthen

teeth by delivering calcium and phosphate in a unique soluble form to
remineralize enamel.

Recaldent will not affect people with lactose intolerance.

Products containing recaldent are marketed in the United States( GC America)
as:
MI Paste - CPP-ACP
MI Paste Plus – CPP-ACP and 900 parts per million fluoride.

Outside the United States (GC Europe), the products are marketed as:
GC Tooth Mousse and
Tooth Mousse Plus

Trident Advantage gum introduced with Recaldent.

According to the manufacturer (GC America)

1. CPP-ACP is a useful cariostatic agent for the control of dental caries

2. It can be used as an adjunct preventive therapy to reduce caries in high-risk

patients

3. To reduce dental erosion in patients with gastric reflux or other disorders

4. To reduce decalcification in orthodontic patients

5. To repair enamel in cases involving white-spot lesions, orthodontic

decalcification, fluorosis or before and after tooth whitening

6. To desensitize teeth (for example, reducing hypersensitivity resulting from

whitening procedures, treating sensitive dentin in patients with dental
erosion and reducing sensitivity resulting from exposed root surfaces after
professional tooth cleaning).
 Synthetic Antimicrobial Peptides
An important issue with chemotherapies and antimicrobial therapies today is
the
proliferation of antibiotic-resistant organisms that lessen the efficacy of
conventionally
utilized antibiotics.
Just recently antimicrobial peptides (AMPs) have come forward as agents that
exhibit a wide spectrum antimicrobial activity against bacteria, including drug
resistant strains. Antimicrobial peptides vary in their peptide sequence and
posttranslational modifications.
The action of AMPs typically involves binding to the negatively charged
functional groups of microbial membranes (eg. lipopolysaccharides) and creating
a disruption by insertion into the membranes.
A pheromone produced by S. Mutans, was used to deliver lethal nanomolar
concentrations of synthetic AMP directly to the S. Mutans bacteria and did not
affect other streptococci that were present.
(Eckert) Researchers linked an AMP peptide sequence to the S. Mutans
pheromone peptide sequence using a chain of amino acids, termed the linker
region.
The functionality of both the pheromone and the AMP remained consistent,
and the resulting peptide showed specific lethality to the S. Mutans bacteria.
This pheromone-guided ‘smart’ antimicrobial peptide potentially achieves a
level of clinical specificity that avoids the clearance of all bacteria within the
domain, protecting the host from opportunistic pathogens. Specifically targeted
antimicrobial peptides (STAMP’s) could be delivered in current oral care
products such as mouthwash, toothpaste, or dental floss and could help with
the suppression of cariogenic bacteria.
 ARGININE
The production of acid by dental plaque is the direct cause of dental caries; it is
noteworthy that increases in the proportions of aciduric organisms appear to occur
at the expense of species that are less aciduric and generally associated with dental
health; including Streptococcus sanguinis and Streptococcus gordonii.
Some of the less aciduric organisms associated with dental health derive protection
from plaque acidification by hydrolysing urea or arginine to ammonia, either by
expressing a urease enzyme or by the arginine deiminase system (ADS), respectively.
• Production of ammonia by oral bacteria can positively influence the balance
between remineralization and demineralization of the tooth and may help to
prevent the emergence of a cariogenic microflora. Therefore, the capacity of oral
biofilms to generate alkali appears to be a major caries-inhibiting factor.
• Urea and arginine can be rapidly metabolized by oral bacteria to elicit a rise in
environmental pH.
Supplying substrate for these two enzyme pathways is the basis for poly-arginine
(arginine bicarbonate/calcium carbonate, CaviStat) and V-6 chewing gum.
Carbon dioxide laser
• This laser uses a mixture of CO2, N2 and He, with CO2 being the active
laser medium (molecules that will collide with nitrogen molecules and will
give out energy).
• Wavelengths ranging from 9 to 11 µm.
• Irradiation of dental enamel by specific wavelengths and energy densities
of CO2 laser alters the hydroxyapatite crystals reducing the acid reactivity
of the mineral;
• CO2 laser irradiation in combination with fluoride treatment is more
effective in inhibiting caries like lesions than CO2 laser irradiation or
fluoride alone;
• When a CO2 laser and fluoride are combined, it is possible to reduce laser
energy density and fluoride levels;
• If this CO2 laser technology becomes available at a reasonable cost and the
results can be applied in clinical practice, there is a promising future for
this laser in caries prevention.
• Laser treatments for caries inhibition are still considered experimental and
cannot be recommended.
Journal of Dentistry (2004) 32, 531–540
Probiotics
Probiotics are defined as live micro-organisms, principally bacteria, that are safe for
human consumption and when ingested in sufficient quantities, have beneficial
effect on human health, beyond basic nutrition .
First probiotic species to be introduced in research was Lactobacillus acidophilus by
Hull et al. in 1984; followed by Bifidobacterium bifidum by Caglar et al.
In oral cavity, probiotics can create a biofilm, acting as a protective lining for oral
tissues against oral diseases.
Such a biofilm keeps bacterial pathogens off oral tissues by filling a space pathogens
would invade in the absence of the biofilm; and competing with cariogenic bacteria
and periodontal pathogens growth. Comelli et al. studied 23 dairy bacterial strains for
the prevention of dental caries and reported that only two strains namely
Streptococcus thermophilus and Lactcoccus lactis were able to adhere to saliva-coated
hydroxyapatite and were further successfully incorporated into a biofilm similar to the
Gene engineering and DNA recombination technology
This method is the so-called replacement therapy. Replacement therapy involves
the use of a natural or genetically modified effector strain that is used to
intentionally colonize the sites in susceptible host tissues that are normally
colonized by a pathogen.
If the effector strain is better adapted than the pathogen, colonization or
outgrowth of the pathogen will be prevented by blocking the attachment sites, by
competing for essential nutrients, or via other mechanisms.
S. mutans strain BCS3-L1 is a genetically modified effector strain designed for use in
replacement therapy to prevent dental caries. To be an effective effector strain,
BCS3-L1 must satisfy four prerequisites:
• It must have a significantly reduced pathogenic potential to promote caries.
• It must persistently colonize the S. mutans sites, thereby preventing colonization
by disease causing strains whenever the host comes into contact with them.
• It must aggressively displace indigenous strains of S. mutans and allow previously
infected subjects to be treated with replacement therapy.
•It must be safe and not make the host susceptible to other disease conditions.

From a standpoint of replacement therapy for caries prevention, implantation of an

effector strain would best be achieved in children immediately after tooth eruption
and before the acquisition of a caries-inducing strain.
NovaMin
The brand name of a particulate bioactive glass that is used in dental care
products for remineralisation of teeth. The active ingredient is calcium sodium
phosphosilicate (CaNaO6PSi).
NovaMin particles bind to the tooth surface and, when the particle comes in
contact with saliva and water, reacts with the water to release calcium and
phosphate ions.
A calcium phosphate layer then forms and crystallizes as hydroxyapatite.
Also the physical occlusion of dentinal tubules results from both the
hydroxyapatite layer and the residual NovaMin particles.
Immunizations
Recent work has focused on using S. mutans antigens to initiate an antibody
secretion, and subsequently eliminate S. mutans colonization in the body.
Immune defense from dental caries is mediated mainly by secretory IgA (sIgA)
antibodies produced in the oral mucosa. Mucosal immunization with antigens at the
local lymphoid tissues, including the gut-associated and nasopharynx-associated
lymphoid tissue, results in the migration of IgA-producing B cells to the salivary
glands.
sIgA is able to inhibit the adhesion of S. mutans to hydroxyapatite and their
subsequent colonization on the tooth surface.
Vaccines focused on the glucosyltransferase enzymes and glucan-binding proteins of
the bacteria have also been tested. Both of these methods have been shown to
mediate an exaggerated immune response, inhibiting the aggregation of S. mutans in
animal models to some degree.
QUORUM SENSING INHIBITORS
Biofilm properties may also be manipulated by affecting the pathways of biofilm
communication or of cell to cell signaling within the biofilm. Blocking this
“quorum sensing” would reduce the ability of the biofilm to tolerate stresses
such as reductions in nutrients or assault by external chemical agents (such as
biocides). Slowing the biofilm accumulation rate may be possible using agents
such as furanone, which affect quorum sensing. These compounds act by
accelerating degradation of the transcriptional regulator that binds to the signal.