View
3
Download
0
Category
Preview:
Citation preview
'"LLI
BY JOHN O.B. FEATHERSTONE, MSC, PHO
D::~ With an in-depth understanding of the caries process, dental hygienists can lead the fight
IIIIIiIIIIIIIII to reduce or eliminate caries.
UT
he dental hygienist should be at the forefront ofcaries prevention and intervention in the dentaloffice and in the community. Understanding the
caries process is essential to perform this role. Dentalhygienists should be major players in driving a cross dis-
ciplinary approach to caries risk assessment and cariesmanagement with the goal of significantly reducing theprevelance of dental decay in our population.Comprehensive knowledge and the application of this
knowledge to practice are necessary for this result.Caries is a transmissible bacterial infection. Caries
progress or reversal is determined by the balance betweenpathological and protective factors. Pathological factorsinclude acid-producing bacteria, fermentable carbohy-drates, and reduced salivary function. Protective factorsinclude salivary components, fluoride together with calci-um and phosphate to remineralize the lesion, and anti-bacterial therapy. The hygienist can provide education,
participate in caries risk assessment, and provide therapyand follow-up for successful control of caries.
Dental caries is a transmissible bacterial infection, yetwe do not deal with the infection in our management of
dental decay. Co~ventional oral hygiene is simply notenough iR many instances. Remineralization is our naturalrepair mechanism for carious lesions, provided they are
not cavitated. Fluoride therapy enhances this repairprocess. However, if the bacterial challenge is too high,our efforts at repair are overcome and caries progresses to
a cavity. This simple concept is the caries balance.During the 1960s and 1970s, the fluoridation of water
supplies in the United States reduced dental caries preva-lence considerably.' In the 1970S .and 1980s, the almostuniversal use of fluoride-containing dentifrices brought
14 Dimensions OF DENTAL HYGIENE wIMN.dimensionsofdentalhygiene:com
further reductions in decay.> During this same period,the acceptance of fluoride and remineralization in the
dental office, together with fluoride topicals and sealantapplications, made a major impact. However, we all knowthat millions of hours are spent annually in the UnitedStates placing restorations to "fix" caries.
, Many people continue to get caries and some childrenand adults have a continual caries problem in spite ofour preventive efforts.3.4 In these high risk individuals,
we need to deal with the bacterial infection if the pre-ventive measures are to be effective. We need a para-
digm shift in our approach.
BACTERIAL INFECTIONThe primary requirement for dental decay is the presenceof acid-producing (acidogenic) bacteria. The bacteria needa substrate of fermentable carbohydrates to feed on to pro-duce the acids that dissolve our tooth mineral.5,6 Certainspecies of bacteria have gone in and out of favor as the cul-
prit over recent decades. It is now well established thatmultiple species are involved. We have all heard ofSteptococcus mutans and, during the 1980s, this was pro-
posed as the only causative agent by several sources.6Efforts were considerable in studying this species and itsmany strains, in finding a vaccine, genetically altering thespecies, and trying to find ways to eliminate it}
The key point, however, is that multiple species areinvolved, especially the mutans streptococci group and the
lactobacillus species.5os The mutans streptococci groupincludes several species of which S. mutans and S. sobrinusare the two most common that appear in human plaque. S.sobrinus does not occur as commonly as S. mutans butwhen it does, it is associated with high caries individuals.
FEBRUARY 2004
Several lactobacillus species are associ-ated with dental caries-both coronal and
root caries. It was previously thought thatlactobacilli colonized when cavities had
already formed but several clinical studieshave shown that lactobacilli are strongly
associated with caries progression beforethe observation of cavities.s.B Further, in
patients with cavities, the lactobacilli arepresent in the remainder of the mouthafter restorations are completed and con-tinue to thrive and produce acids to cause
future caries. These acidogenic bacteria
only occupy about 1% or less of the totalflora in the plaque. That such a small frac-
tion of the bacteria present can cause such
major problems is amazing.The bottom line is that multiple species
of acidogenic bacteria cause dental cariesand the predominant groups identified sofar are the mutans streptococci and the lac-tobacilli. Actinomyces species and some
yeasts have also recently been suggested.From a practical therapeutic perspective,this means we need to use a broad spectrum
antibacterial to reduce or eliminate theseacidogenic bacteria in order to control cariesin patients with a high bacterial loading.
Studies in the 1970S showed that specificstrains of S. mutans are transmitted frommother to child.7.1O.1l This conclusion wasconfirmed in the 1980s by DNA technolo-
gyp> It has taken 20 years for us to accept
FEBRUARY 2004
THE CARIES BALANCE
this conclusion and to start thinking aboutthe source of the pathogenic (cariogenic, ie,
caries-causing) bacteria that colonize themouth. Studies have now established that
early colonization, even before the teetherupt, can occur in infants by transmissionfrom the mother or caregiver. Transmissionfrom child-to-child and adult-to-adult has
also been reported for S. mutans.
Presumably the same is also the case for lac-tobacilli. Children who are colonized earlyhave more decay later.'3'14 From a preven-
tive perspective, we should target mothersand caregivers with high caries risk and con-trol their bacteria, and, in the case of preg-nant mothers, even before a child is born.
rather than total amount of carbohydrate
ingested. Every time we ingest one or moreof these carbohydrates, the acidogenic bac-teria produce acids, such as lactic, acetic,formic, or propionic acids, that within min-utes lower the pH in the plaque and dis-
solve some tooth mineral. So snacking
throughout the day and night producesmultiple acid attacks. Substitution of the
fermentable carbohydrates by noncario-genic sweeteners, such as aspartame, sor-bitol, or xylitol, can playa big part in reduc-
ing the acid challenge to the teeth.
Chewing gum enhances salivary function,helps neutralize any acids present, and pro-motes remineralization.
FERMENTABLECARBOHYDRATES
SALIVARY DYSFUNCTIONThe saliva is a very complex fluid that con-
tains calcium and phosphate necessary for
remineralization, proteins that keep calci-um in solution, proteins and lipids that form
the protective pellicle on the tooth surface,
antibacterial pro;teins and immunoglobu-lins, and components that buffer and neu-
tralize the acids produced by the bacteria.'sWhen salivary function is reduced or elimi-nated by disease or radiation therapy, all of
these protective functions are reduced orlost and rampant caries can result.'6
In some patients, the reduction in sali-
vary function is the primary determinantof caries progression for them. The protec-
The acidogenic bacteria described abovecan metabolize carbohydrates consumed byhumans. They derive energy from them,
just as we do, but the byproduct of theirmetabolism is organic acid. Common fer-mentable carbohydrates are glucose,
sucrose, fructose, and cooked starch.Sucrose is particularly bad because themutans streptococci can produce extracel-lular polysaccharides from sucrose that
sticks the plaque together and also providesa food source for the bacteria between the
times when eating provides that source.
Frequency of ingestion is the key factor
www.dimensionsofdentalhygiene.com Dimensions OF DENTAL HYGIENE 15
THE CARIES PROCESS1 proposed the caries balance concept as asimple way to look at the caries process and
see whether it was progressing or revers-ing.S"9 The most important components areillustrated in Figure 2 (see page 18). The
pathological factors are: 1) acidogenicbacteria, 2) frequency of ingestion of fer-
mentable carbohydrates, and 3) salivary dys-function. The three most important protec-tive factors are: 1) salivary components and
flow, 2) fluoride, calcium, phosphate, andremineralization, and 3) antibacterial thera-
py. Additional therapies, such as sealants, canbe added to the protective factors.
So what are the practical implicationsof this concept? The balance can be usedto assess the risk of an individual develop-ing caries in the future, to determine whythe individual has caries now, or to drive a
preventive or interventive program forthe individual or even community.'8,20 Thebalance between demineralization and
remineralization is the key to progressionor reversal of caries at any time. We canintervene to tip the balance.
Additional fluoride therapy will usuallyenhance remineralization, whereas in thecase of high bacterial challenge, we need
to apply aggressive antibacterial therapy toreduce the acidogenic bacterial loading inthe mouth. Placing a restoration does not
reduce the overall bacterial loading in themouth.2l It certainly removes the bacteriafrom that specific cavity, but does little tohelp reduce the future bacterial challenge.
Chlorhexidine mouthrinse can be used
to help with this. In the United States, wehave 0.12% chlorhexidine gluconate.22Studies suggest that daily mouthrinsing for
2 weeks substantially reduces the loadingof mutans streptococci but they recolonize
within a few weeks. Therefore, repeatedtreatments are necessary to control the bac-terial infection. A useful regiment is torinse daily for 1 week every month. This
regimen enhances compliance and reducesthe bacterial loading over several months.
CONCLUSIONDental caries progression or reversal is
18 Dimensions OF DENTAL HYGIENE WWVi
determined by the balance betweenpathological and protective factors.Fluoride inhibits demineralization and
enhances remineralization. Saliva is veryimportant as a protective factor and sali-
vary dysfunction is a common pathologi-cal factor. If the bacterial challenge ishigh, then protective factors may not besufficient to overco"me the demineraliza-tion process. Antibacterial therapy andintervention in the transmission of bacte-
ria must become part of the standard ofcare in caries control and part of the tool
chest of the dental hygienist. The dental
hygienist should be responsible for edu-cating patients, for delivering caries risk
assessment, for providing preventivecare, and being the front line person inthe paradigm shift to reduce or eliminatedental caries. .
john D.B. Featherstone, MSc, PhD, is pro-
fessor and chair of the Department ofPreventive and Restorative Dental
Sdences at the University of California,San Frandsco.
al. Caries risk assessment in a longitudinal dis-
crimination study. J Dent Res. 1993;72:538-543.
9. Krasse B. Biological factors as indicators of
future caries. fnt Dent J. 1988;38:219-225.
10. Berkowitz RJ, Jordan HV, White G. The early
establishment of Streptococcus mutans in the
mouths of infants. Arch Oral BioI.
1975;20:171-174.
11. Berkowitz RJ, Jordan HV. (1975) Similarity of
bacteriocins of Streptococcus mutans from moth-
er and infant. Archs Oral Bioi. 1975;20:725-730.
12. Caufield PW, Childers NK, Allen ON, Hansen
JB. Distinct bacteriocin groups correlate with dif-
ferent groups of Streptococcus mutans plas-
mids./nfect Immun.1985;48:51-56.
13. Alaluusua S, Kleemola-Kujala E, Nystrom M,
Evalahti M, Gronroos L. Caries in the primary
teeth and salivary Streptococcus mutans and
lactobacillus levels as indicators of caries in per-
manent teeth. Pediatr Dent. 1987;9:126-130.
14. Alaluusua S, Renkonen OV. Streptococcus
mutans establishment and dental caries experi-
ence in children from 2 to 4 years. Scand J Dent
Res. 1983;91:453-457.
15. Lamkin MS, Oppenheim FG: Structural fea-
tures of salivary function. Crit Rev Oral Bioi Med.
1993;4:251-259.
16. Mandel 10. The role of saliva in maintaining
oral homeostasis. J Am Dent Assoc.
1989;119:298-304.
17. Ten Cate JM, Featherstone JOB. Mechanistic
aspects of the interactions between fluoride and
dental enamel. Crit Rev Oral Biology Med.
1991;2:283-296.
18. Featherstone JOB. The caries balance: con-
tributing factors and early detection. J Calif
Denta Assoc. 2003;31:129-133.
19. Featherstone JOB. Prevention and reversal of
dental caries: role of low level fluoride.
Community Dent Oral Epidemiol. 1999;27:31-40.
20. Featherstone JOB, Adair SM, Anderson MH,
et al. Caries management by risk assessment:
consensus statement, April 2002. J Calif Denta
Assoc. 2003;31:257-269.
21. Featherstone JOB, Gansky SA, Hoover 0, Li L,
Weintraub JA, White JM. Cariogenic bacteria trends
in a randomized caries management clinical trial. J
Dent Res. 2002;81:A-467. Abstract 3813.
22. Anderson MH. A review of the efficacy of
chlorhexidine on dental caries and the caries
infection. J Calif Denta Assoc. 2003;31:211-214.
REFERENCES1. Newbrun E. Effectiveness of water fluorida-
tion. ) Public Health Dent. 1989;49:279-289.
2. Jenkins GN. Recent changes in dental caries. Br
Med ).1985;291:1297-1298.
3. Winn DM, Brunelle JA, Selwitz RH, et al.
Coronal and root caries in the dentition of adults
in the United States, 1988-1991. ) Dent Res.
1986;75:642-651.
4. Kaste LM, Selwitz RH, Oldakowski RJ, Brunelle
JA, Winn DM, Brown U. Coronal caries in the pri-
mary and permanent dentition of children and
adolescents 1-17 years of age: United States,
1988-1991.) Dent Res. 1996;75:631-641.
5. Featherstone JOB. The science and practice of
caries prevention. ) Am Dent Assoc.
2000;131:887-899.
6. Loesche WJ. Role of Streptococcus mutans in
human dental decay. Microbiol Rev.
1986;50:353-380.
7. Berkowitz RJ. Acquisition and transmission of
mutans streptococci. ) Calif Dent Assoc.
2003;3:135-137.
8. Leverett DH, Proskin HM, Featherstone JDB, et
FEBRUARY 2004www.dimensionsofdentalhygiene.com
Recommended