CLINICAL
CLINICAL
CARIES AND THE ORAL ENVIRONMENT:
MANAGING CARIES IN THE 21ST CENTURY
JULIETTE REEVES
Abstract
Dental caries is a major oral and public health concern in the 21st
Century. Despite a global decline in caries, the disease still remains
persistent, particularly among poor and disadvantaged groups in
developed and developing countries.1 According to the World Oral
Health Report 2003, dental caries remains a major public health
problem in most industrialised countries, affecting 60–90% of
schoolchildren and the vast majority of adults.2
THE CARIES BALANCE
PATHOLOGiCAL FACTORS
 Acid producing bacteria
 Frequent eating/drinking of
fermentable carbohydrates
 Subnormal saliva flow and function
The global burden of oral conditions is shifting from severe tooth loss
toward severe periodontitis and untreated caries, increasing the burden
on health care resources. Oral conditions affected 3.9 billion people, and
untreated caries in permanent teeth was the most prevalent condition
evaluated for the entire Global Burden of Disease 2010 Study with a
global prevalence of 35% for all ages combined.3
Our understanding of the aetiology of dental caries has evolved over
the last 100 years with recent research highlighting the need to adopt a
minimally invasive approach to the treatment and prevention of dental
caries. This includes a focus beyond fluoride and diet, incorporating risk
management techniques such as chairside evaluation of saliva buffering
capacity, modulation of plaque ecology and the use of sugar free gum.
This article presents management and prevention strategies for dental
caries in the 21st Century.
Current concepts in the aetiology of dental caries
Our understanding of the aetiology of dental caries has evolved over
the last 100 years from that of the non-specific plaque hypothesis
(Miller 1890) through the specific plaque hypothesis (Loesche 1979)
to our present day understanding of the ecological plaque hypothesis
(Marsh 1991). The ecological plaque hypothesis proposes that carious
disease can be attributed to changes in the oral environment that
disrupt homeostasis between the plaque microflora and the host and is
considered a modified hypothesis of Loesche and Miller.4
This hypothesis states that bacteria of the non-mutans species are crucial
for maintaining stability and balance of the oral microflora. In the
presence of fermentable carbohydrates these bacteria within plaque,
rapidly metabolise sugars, producing acids at the tooth surface. When
formed in sufficient amounts and for adequate periods of time, this
creates conditions that favour dissolution of calcium and phosphates
from the tooth surface effecting demineralisation of enamel.5
When plaque pH is lowered, the concentration of calcium and
phosphate ions needed for salivary saturation increases, reaching
“critical pH” at 5.5 to 5.7 when the hard tissues will start to dissolve
to maintain salivary saturation levels.6 The extent of dissolution/
demineralisation depends on the oral environment, specifically, the
extent and duration of pH drop, the presence of fluoride, the presence
and composition of saliva (buffering capacity), the frequency of sugar
challenges and the presence of anti bacterials. The prevention of caries
therefore can be seen as maintaining a balance between pathological
factors and protective factors.7 (Fig 1)
Volume 53 No 5 of 6 September 2014
CARIES
PROTECTIVE FACTORS
 Saliva flow and components
 Fluoride-remineralisation
with calcium and phosphate
 Antibacterials: chlorhexidine, xylitol
NO CARIES
Figure 1
The protective capacity of saliva in mineralisationremineralisation
Saliva plays an important role in buffering plaque acids and provides the
medium for remineralisation. Saliva contains calcium and phosphate
concentrations that supersaturate saliva with respect to hydroxyapatite,
thereby neutralising acids.
Demineralisation occurs at below pH 5.5 when the oral environment
is undersaturated with mineral ions, relative to the mineral content of
enamel. Calcium and phosphate ions from hydroxyapatite are liberated,
resulting in net loss of minerals. 5, 6
Remineralisation occurs when dietary carbohydrate is removed and
calcium and phosphate ions in saliva are re-incorporated in the enamel
matrix. Once the pH of the biofilm is raised to approximately pH 7.0
demineralisation is arrested. An early carious lesion therefore may be
arrested and prevented from reaching cavitation by altering the oral
environment in favour of remineralisation.8
The buffering capacity of saliva plays a critical role in helping restore
a neutral pH at the tooth surface, modulating the Stephan Curve,
providing mouth clearance and dilution of plaque acids and restoring
the oral environment to a neutral pH. Kleinberg et al were able to
demonstrate the effect of saliva in bringing plaque pH back to neutral
more rapidly than in saliva deficient subjects. 6
Caries can therefore be considered a dynamic equilibrium between
demineralisation and remineralisation mediated by saliva composition
and dietary factors.
Bacterial adaptation in the aetiology of dental caries
Dental caries can be observed in the absence of pathogenic bacteria
(i.e. S. mutans and Lactobacilli) as the acidic environment may select other
acid thriving (aciduric) bacteria that are also capable of significant acid
production, albeit at a slower rate. 9
29
CLINICAL
The ability for cariogenic bacteria to adapt to an acid environment has
also been observed. Pathogenic bacteria are normally unable to survive
acid conditions, however, mutans streptococci ( S. mutans) for example
have adapted to enable them to be acid tolerant and thus survive and
flourish in dental plaque.10 This has enabled S. mutans to dominate other
non pathogenic bacteria that do not posses this mechanism. The ability
of S. mutans to survive at low pH is an important virulence factor in the
pathogenesis of dental caries. 11
The role of arginine in modulating the composition of plaque
Other bacteria such as S. sanguinis have developed a mechanism known
as the arginine deiminase pathway to break down arginine present in
saliva into its (basic) alkali components, ammonia and carbon dioxide.
The elevated pH induced by urea and arginine catabolism is thought
to be important in inhibiting the development of tooth decay and in
modulating the composition of plaque ecology.12
A correlation between higher concentrations of arginine in saliva and
a lower incidence of dental caries has been demonstrated13 further
strengthening the idea that base production is one of the key factors
in oral health and oral biofilm pH homeostasis. These base substances
directly neutralise acids in plaque.
The use of genetically engineered, ammonia-producing oral
streptococci as potential agents for the control of dental caries has been
demonstrated. This may provide the foundation for the potential use of
arginine to moderate plaque acidification and to control the emergence
of a cariogenic biofilm. 14
A new technology based on arginine and insoluble calcium in a
fluoride toothpaste was released offering superior caries prevention and
modification of plaque biofilm composition.15,16
21st Century management and prevention strategies
The acid tolerance of bacteria in the carious lesion is much higher than
that of healthy commensal (ie non-cariogenic) bacteria. The resting
plaque pH in the healthy mouth is therefore higher than that with active
carious lesions.
The long term eradication of oral biofilms is not possible as this would
adversely affect the oral ecology. Beneficial and commensal bacteria
compete with pathogens for colonisation.
The key to maintaining caries balance is to focus on rebuilding and
maintaining a healthy biofilm and influencing the oral environment.
Healthy biofilm acts as a storage reservoir for fluoride (and other ions
such as calcium and phosphate) causing enhanced fluoride retention and
exchange between these ions and tooth enamel, increasing the length of
remineralisation time to combat caries.17
The essential aspects of prevention and management of caries involve
assessing the underlying caries risk factors, which cannot be detected
during a routine examination. The main risk factors implicated in the
oral environment include:
Diet: the frequency of sugar and acid hits. The most common method
is via dietary analysis with the patient. It is important that the dental
team update their knowledge on the nutrition facts and the cariogenic
potential of various foods.
Bacteria: the composition of the individual’s plaque e.g.: Streptococcus
mutans count and an evaluation of bacterial activity as measured by
lactic acid production. Chair-side assessment methods are commercially
available that are based on a species-specific monoclonal antibody
30
response, where the results are obtained within 30 minutes. An increased
Mutans streptococci level is usually evident in the presence of more
incipient lesions. Lactobacilli require retentive areas to proliferate and
hence, a high count is usually associated with the presence of frank
cavitations.18
Fluoride: past and current exposure. Fluoride inhibits
demineralisation, by penetrating and coating the enamel crystals to
prevent dissolution, and by enhancing remineralisation, resulting in
enamel with a higher F content and lower acid solubility.19
When fluoride is present, the critical pH for demineralisation is lowered,
meaning a lower plaque pH can be tolerated before demineralisation
occurs.20 The formation of calcium fluoride on the tooth surface acts as
a reservoir and is driven into hydroxyapatite in response to significant
drops in pH.21 Whilst fluoride is efficient in providing protective factors
that reduce the susceptibility of the tooth surface to demineralisation
and cavitation, it does not reduce pathological factors by inhibiting
plaque formation or by altering the microbiology of plaque biofilms in
favour of non-pathogenic organisms.
Saliva composition: Salivary flow rate is the most important clinical
parameter affecting dental caries susceptibility. With a reduced quantity
of saliva, the oral clearance of microorganisms and food remnants is
impaired.22 In addition, the pH and buffering capacity is reduced and a
more acidic environment results in the growth of the aciduric cariogenic
organisms.18 The calcium and phosphate content is also lower with
reduced saliva, and thus the remineralisation capacity is compromised.
A low salivary flow rate accentuates the pH decrease in dental plaque.23
The buffering capacity of the saliva and its ability to reduce the acidity
can be measured by chair-side saliva testing.
The role of sugarfree gum in caries management
Saliva stimulation from chewing gum helps in the management of caries
by neutralising plaque acids and remineralising tooth enamel. The
chewing of sugarfree gum stimulates saliva production which can last
up to 2 hour with increases in both flow rate and pH being observed
following chewing for 20 minutes. 24,25 Stimulated saliva also contains
increased levels of salivary electrolyte and protein concentrations, in
particular bicarbonate and calcium ions. This allows recovery of plaque
pH above 5.5 within 20 minutes compared to two hours without gum.26
In terms of caries prevention, a randomised clinical study from
Beiswanger et al27 demonstrated an 11% drop in DMF scores in children
using sugarfree gum after meals. A further study has also shown a 38%
reduction in DMF scores over a two year period.28
The modern approach to caries prevention
Minimal intervention and management of the oral environment is
a modern approach to caries prevention. The public is also aware
that restorative dentistry is not enough to ensure good oral health. It
is important for the profession to now consider how new treatment
and prevention modalities can be incorporated into everyday clinical
practice.
Acknowledgement: FDI Annual World Dental Congress, Istanbul 2013
Over this four day congress, modern concepts in the aetiology, diagnosis,
prevention and management of caries were explored, along with evidence-based
strategies and contemporary therapeutic approaches for the prevention and
management of this global health issue: caries.
This report contains information from the following presentations:
Hien Ngo: Managing caries in clinical practice; the oral environment.
DENTAL HEALTH
CLINICAL
N Pitts, R Burne, R Ellwood Colgate Symposium: Can we change what we do
about caries? Evidence based approaches for the prevention and control of early
caries.
M Dodds: Saliva and oral health; the science behind the chewing gum claims.
14. Clancy KA, Pearson S, Bowen WH et al: Characterization of
recombinant, ureolytic Streptococcus mutans demonstrates an
inverse relationship between dental plaque ureolytic capacity and
cariogenicity. Infect Immun 2000;68(5):2621-29.
15. Wolff M, Corby P, Klaczany G et al. In Vivo effects of a new
About the author: Juliette Reeves is a dental hygienist and trained
nutritionist with over thirty years’ experience. She is an international
speaker and author and is an editorial advisor to a number of dental
journals. Juliette is an advisor to the Wrigley Oral Healthcare Program,
clinical director of Perio-Nutrition, an elected ADI Committee Member
and Secretary to the BSDHT Eastern Regional Group.”
Address for correspondence: Juliette Reeves gjr50@talktalk.net
References
1.
Patel R: The State of Oral Health in Europe. Report
Commissioned by the Platform for Better Oral Health in Europe.
Available at: http://www.oralhealthplatform.eu/state-oral-healtheurope Accessed 26th September 2013.
dentifrice containing 1.5% Arginine and 1450ppm fluoride on
plaque metabolism. J Clin Dent 2013;24 (Special Iss A):A45-54.
16. Cantore R, Petrou I, Lavender S et al. In situ clinical effects of new
dentifrices containing 1.5% agrinine and fluoride on enamel deand remineralisation and plaque metabolism. J Clin Dent 2013;24(
Spec Iss A): A32-44.
17. Stoodley P, Nguyen D, Longwell M, et al.
Effect of the Sonicare
Flexcare power toothbrush on fluoride delivery through Streptococcus
mutans biofilms. Compendium 2007; 28 No 9 (Suppl 1): 15-22.
18. Carounanidy U and Sathyanarayanan R. Dental caries: A complete
changeover (Part II)-Changeover in the diagnosis and prognosis. J
Conserv Dent. 2009;12(3): 87–100.
19. Buzalaf MA, Pessan JP, Honorio HM et al. Mechanisms of action
for fluoride for caries control. Monogr Oral Sci 2011;22:97-114.
20. Lynch RJ, Navada R, Walia R. Low levels of fluoride in plaque and
2.
Pederson PE. World Oral Health Report 2003. Geneva,
Switzerland: World Oral Health Organisation 2003.
3.
Marcenes W, Kassebaum NJ, Bernabé E et al. Global burden of
oral conditions in 1990-2010: a systematic analysis. J Dent Res.
2013;92(7):592-7.
21. Rolla G, Ogaard B, Cruz Rede A. Topical application of fluorides
4.
Marsh PD. Microbial ecology of dental plaque and its significance
in health and disease. Adv Dent Res 1994;8(2):263-71.
22. Lingstrom P, Birkhed D. Plaque pH and oral retention after
5.
Featherstone JD.The caries balance: contributing factors and early
detection. J Calif Dent Assoc 2003;31(2):129-33.
6.
Kleinberg I. The other side of confectionary use and dental caries.
J Can Dent Assoc 1989;55(10):837-8.
7.
Featherstone JD. Caries prevention and reversal based on the caries
balance. Pediatr Dent 2006;28(2):128-32.
8.
Kidd EA, Fejerskov O. What constitutes dental caries?
Histopathology of carious enamel and dentin related to the action
of cariogenic biofilms. J Dent Res 2004;83 Spec No C:C35-8.
25. Dawes C, Dong C. The flow rate and electrolyte composition of
Samaranayake L. Essential microbiology for dentistry. 3rd ed.
Edinburgh: Elsevier Ltd; 2006.
26. Manning RH, Edgar WM. pH changes in plaque after eating
9.
10. Belli WA, Marquis RE . Adaptation of Streptococcus mutans and
Enterococcus hirae to acid stress in continuous culture. Appl Environ
Microbiol. 1991; 57(4):1134–38.
11. Li YH, Hanna MN, Svensäter G et al: Cell density modulates
acid adaptation in Streptococcus mutans: Implications for survival in
biofilms. J Bacteriol. 2001 December;183(23):6875–84.
12. Burne, RA., Marquis RE. Alkali production by oral bacteria and
saliva and their effects on demineralisation and remineralisation
of enamel: role of fluoride toothpastes. Int Dent J 2004;54(5 Suppl
1):304-9.
on teeth. New concepts of mechanisms of interaction. J Clin Perio
1993;20(2):105-8.
consumption of starchy snack products at normal and low salivary
secretion rate. Atca Odonto. Scand. 1993 51(6);379-388.
23. Dawes C, Kubieniec K. The effects of prolonged gum chewing on
salivary flow rate and composition. Arch Oral Biol 2004;49(8):665-9.
24. Pollard KE, Higgins F, Orchardson R. Salivary flow rate and
pH during prolonged gum chewing in humans. J Oral Rehabil.
2003;30(9):861-5.
whole saliva elicited by the use of sucrose containing and sugar free
chewing gums. Arch Oral Biol. 1995;40(8):699-705.
snacks and meals and their modification by chewing sugared- or
sugar-free gum. Br Dent J. 1993; 174(7):241-4.
27. Beiswanger BB, Boneta AE, Mau MS et al. The effect of chewing
sugar-free gum after meals on clinical caries incidence. J Am Dent
Assoc. 1998;129(11):1623-6.
28. Szóke J, Proskin HM, Bánóczy J [Effect of chewing sugar-free gum
on dental caries].Fogorv Sz. 2002;95(1):21-5. [Article in Hungarian]
protection against dental caries. FEMS Microbiol Lett. 2000;193(1):1-6.
13. Van Wuyckhuyse BC, Perinpanayagam HE, Bevacqua D, et al
Association of free arginine and lysine concentrations in human
parotid saliva with caries experience. J Dent Res 1995;74(2):686-90.
[PubMed]
Volume 53 No 5 of 6 September 2014
31