Journal of the California Dental Association Feb 2003

7/29/2019 Journal of the California Dental Association Feb 2003

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e b r u a r y 2 0 0 3

d e p a r t m e n t sThe Associate Editor/Side by Side

Impressions/Study Supports Removal of Third Molars

Dr. Bob/Dont Make Me Take off My Belt

eatures

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An introduction to the issue.

J D.B. F, MS, PD, J R. R, CAE

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New strategies are needed to reduce the risk of dental disease in California children and to expand access to effective

services.

J J. C, DDS, SD

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Dental health is a balance between factors that demineralize and remineralize teeth.

J D.B. F, MS, PD

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Studies indicate that mutans streptococci can colonize the mouths of predentate infants and that horizontal, as well as

vertical, transmission occurs.

R J. Bkwz, DDS

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Early childhood caries can affect children from all socioeconomic classes but is most often found in children of new

immigrants or those with lower socioeconomic status, and treatment is expensive.

P DB, DDS, R Bkwz, DDS

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The training of pediatric dental residents in caries risk assessment and prevention must be strengthened.

S M. A, DDS, MS

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Community-based systems to improve oral health for people with special needs have not been as successful as they might

be because of lack of effective preventive protocols specifically designed for people with special needs.

P G, DDS, MA, MBA, C M, RDH, MSH, MA

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h e a dAssociate Editor

ebruary is widely known

throughout the dental proes-

sion as National Childrens

Dental Health Month. Tis

year, proessional and public

awareness o this designation is evenhigher thanks to the ADA-driven Give

Kids a Smile program. Tis campaign

will no doubt receive an ample amounto well-deserved coverage in both dental

and nondental publications. Tereore, I

would like to acknowledge the other des-

ignation given to the month o February,Black History Month.

When I was a second-year dental

student, I had the privilege o attending

the ADA Annual Session or the rst time.I remember walking through the maze

o exhibitors and seeing a booth or theNational Dental Association. I surmised

that this was an association o AricanAmerican dentists. I wondered to mysel

why black dentists had an organization

o their own and what the relationship

o this organization is to the ADA. Ittook nearly 10 years, but I was nally

enlightened to the answers. Black dentists

ormed their own proessional organi-

zation because, at one time, they weredenied membership in the ADA and its

component societies. And as or the rela-tionship o the NDA to the ADA, it is ever

evolving and steeped in a rich history.Te history o Arican American

dentistry and the National Dental As-

sociation has been orged by the eorts

o many individuals spanning more than150 years to the present day. Space will

not allow mentioning all o these men

and women here. For a most detailed and

eruditely written chronicle o the entireNDA story, I recommend the book NDA

II, Te Story o Americas Second National

Dental Association by Dr. Cliton O. Dum-

mett and Lois Doyle Dummett (reviewed

in the March 2001 CDA Journal, Vol. 29,

Page 3). I have relied shamelessly on it or

the ollowing accounts.Consider the courage and persever-

ance o Dr. Robert anner Freeman. Ater

being denied admission to several dentalschools on account o his race, he was

accepted at Harvard Universitys School o

Dental Medicine, and in 1869 became the

rst Arican American to receive a dentaldoctorate degree rom a U.S. university.

Ten there was the vision and leadership

o Dr. Robert Fulton Boyd, who in 1895

became the rst president o the NationalMedical Association, at that time en-

compassing the proessions o medicine,dentistry, and pharmacy. Boyd was well-

prepared or this role, having receivedboth an MD degree and a DDS degree;

and he admirably served his proession

and community in many capacities during

his career.At the onset o the turbulent 1960s,

the daring and uncompromising actions

o Drs. Roy C. Bell and Eugene . Reed,

both staunch civil rights advocates,underscored the act that progress toward

racial equality is not always gained withpatience, civility, and deliberate negotia-

tion. In March o 1961, Bell, a Georgiadentist, led a contingent o eight black

dentists in a picket line outside o the

Tomas P. Hinman meeting in Atlanta. In

spite o their prior peaceul and legitimateattempts at proessional racial integra-

tion, the Hinman meeting remained

closed to Arican American dentists.

Meanwhile Reed, a New York dentist,was staging his own protest against overt

F

b Seven A. Gold, DDS


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h e a dImpressions

M

Te next time you see a patient who isexperiencing no problems with his or her

third molars, what should you do?A recent study sponsored by the

American Association o Oral and Maxil-

loacial Surgeons and the Oral and Maxil-

loacial Surgery Foundation and publishedin the November 2002 Journal o Oral and

Maxilloacial Surgery strongly suggests the

removal o third-year molars beore age

25. Te results o the study are challenging

two long-held belies: that third molars that

have broken through the tissue and eruptedinto the mouth in a normal, upright posi-

tion have minimal problems, and that the

absence o symptoms rom retained thirdmolars indicates that the teeth are ree rom

problems.

Investigators led by Raymond P. White,

Jr., DDS, PhD, and Richard H. Haug, DDS,conducted the 30-month institutional

review board-approved longitudinal clini-

cal trial. Tey examined the health o the

tissues supporting teeth throughout themouth, including the third molars o more

than 300 healthy patients between the ageso 14 and 45, who had our symptom-ree

third molars with adjacent second molars.Tey used standard methods o evaluating

the tissues that surround and support the

teeth, including probing depth analysis,

calculation o a gingival index, and X-rayexamination. Tey also took dental plaque

samples and determined the presence and

levels o bacteria in these samples. I the

probing depth analysis measured a deptho 5 mm or greater, which is an accepted

determining sign o periodontitis, theyobserved that:n 25 percent o all study-enrolledpatients, and 34 percent o Arican

American patients, had at least one

probing depth equal to or greater than 5

mm behind a second molar and arounda third molar.n A higher proportion o patients 25 years

old or older (33 percent) had a probing

depth equal to or greater than 5 mm

behind a second molar and around athird molar compared with patients

younger than 25 (17 percent).n Complexes o bacteria previously

shown in scientically designedclinical studies to be associated with

periodontitis, were detected at higher

levels in plaque samples o patients

who had at least one probing depthequal to or greater than 5 mm behind a

second molar and around a third molar.

Te results o this large, ongoing study

only serve to reinorce what many o us

have suspected and seen over the years,

said John S. Bond, DMD, president o theCaliornia Association o Oral and Maxil-

loacial Surgeons. Frequently, even when

third molar teeth are erupted in the mouth,they oten result in problems with the adja-

cent second molar teeth over the years.

Te results o these investigations ur-

ther indicate that patients who do not havetheir third molars removed prior to age 25

may be at greater risk or the development

o disease aecting the tissues surrounding

the second and third molars and that earlystages o periodontitis may present rst in

the third molar regions in young adults.Te investigators note that disease be-

hind second molars or around third molarsmay be attributable in part to the patients

inability to keep the area clean. Tis would,

in turn, allow inectious bacteria to grow

and begin the disease process, which couldworsen over time. Additionally, third molars

that have broken through the tissue and

erupted into the mouth in a normal, up-

right position are as likely to exhibit diseaseas those third molars that remain impacted

or buried.Having a patients third molars evalu-

ated and removed by an oral and maxillo-acial surgeon where indicated prior to the

patient reaching the age o 25 results in a ar

easier postsurgical course or the patient,

Bond said. Importantly, it also preventsor eliminates the problems that all too

requently arise as the patient ages i they

are ignored or orgotten until pocketing or

other disease processes present.

Use o Nitrous Oxide Can

Afect Vision o Some EyeSurgery Patients

Patients may lose their sight ithey receive nitrous oxide anes-

thesia within one month ater

having retinal surgery, a new study

reported by Reuters suggests.Researchers rom New Zealand

described the cases o three patients

who received intraocular gas, which

is used to hold the retina in placeduring surgery to repair retinal

detachment.Within one month, the patients

had other types o surgery unrelat-ed to their eye operation. All three

patients, who received nitrous oxide

gas as anesthesia or their second

surgery, suered severe vision lossimmediately ater they received the

anesthetic. Vision loss was perma-

nent in two o the patients.

Dr. David R. Worsley, the studyslead author, explained that nitrous

oxide can cause an intraocular gasbubble to expand, increasing the

pressure within the eye and inhibit-ing circulation to the optic nerve

and retina.

Without a blood supply, these

tissues are soon irretrievably dam-aged, resulting in vision loss that is

requently severe, Worsley said.

For urther inormation on the study,contact the American Association o

Oral and Maxilloacial Surgeons at (847)678-6200 or visit their Web site at www.

aaoms.org.


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h e a d

z K F

A team o scientists rom the Forsyth

Institute and the National Institute o

Dental and Cranioacial Research havediscovered that an enzyme known as matrix

metalloproteinase-20 is essential or proper

ormation and development o dental

enamel in mice.Since the enzyme is expressed in human

teeth, the nding, in studies o mice, maybe relevant to sciences understanding o

a human disease known as amelogenesisimperecta, which causes one in approxi-

mately 7,000 children to be born with

deective dental enamel, according to John

Bartlett, PhD, associate member o the staat the Forsyth Institute, and the principal

investigator.

In the United States, the teeth o such

children are ordinarily capped. Let un-treated, the disease results in pain and even-

F F Cf-

Te Food and Drug Administration hasannounced its nal rule that changes the

classication o intraoral devices or thetreatment o snoring and obstructive sleep

apnea to Class II (special controls). Tis rule

became eective Dec. 12, 2002.

Formerly, these appliances remainedunclassied as medical devices by the FDA.

According to Dr. Susan Runner o the Cen-

ter or Devices and Radiological Health, the

regulation will help increase the legitimacy

o oral appliance therapy or the treatment

o sleep-disordered breathing. Tis may alsoadd to the recognition o oral appliances

by insurance providers, thus increasing the

possibility or reimbursement to practitio-ners perorming these procedures.

Class II reers to medical devices requir-

ing special controls to ensure public health

and saety, such as intraoral soreness, MD,obstruction o oral breathing, loosening or

aring o lower teeth, general tooth move-

ment, and others dened by an FDA guid-

ance document. Mandating these consider-ations will add medical validity to the use o

these appliances.Dr. Harold A. Smith, president o the

Academy o Dental Sleep Medicine, said,Te FDA classication o oral devices is a

orward step in the uture o oral appliance

therapy, but more importantly, will ensure

the eective treatment and overall health opatients.

For more inormation regarding the

FDA regulation on medical devices, a copy

o the FDA guidance document, or a list odevices currently cleared by the FDA, please

visit the Academy o Dental Sleep Medi-cines Web site at www.dentalsleepmed.org.

i m p r e s s i o n s

UCSF Receives $1.2 Million Grant to Prevent Oral Cancer

In a nationwide project to ght oral cancer through prevention and early detection,

the National Cancer Institute has awarded $1.2 million to researchers at the Universityo Caliornia at San Francisco School o Dentistry to create a program o oral cancer

prevention in collaboration with the American Dental Association.

Oral cancer strikes more than 30,000 Americans and accounts or more than 9,000

deaths each year in the United States. Despite advances in oral cancer treatment, onlyabout one-hal o all people diagnosed with the disease survive more than ve years.

Early detection is the most important approach in decreasing the morbidity and

mortality o oral cancer, said Sol Silverman, Jr., DDS, UCSF proessor o oral medicine

and principal investigator o the ve-year project. Silverman is a consultant to the

ADA Council on Access, Prevention, and Interproessional Relations and a pioneer and

expert in oral cancer education, patient care, and research.Te UCSF researchers will develop and implement a continuing education program

ocusing on oral cancer prevention education or practicing dentists in the United

States. Key components will include risk assessment and risk reduction or tobaccoand alcohol use, chemoprevention, early detection, and diagnosis.

Data indicate that the majority o at-risk Americans do not benet rom oral cancer

screening rom their primary care proessionals, and survival rates have not signicant-

ly changed in the past 20 years, according to Silverman. Te plan is to increase dentistsskills in early detection o oral cancer because, thus ar, this is the most important

approach in decreasing morbidity and mortality o oral cancer.

tual loss o teeth. Because o similaritiesbetween the mouse and human genomes,

it is possible that loss o this enzyme in

humans would cause this disease, Bartlett

said.Te article, Enamelysin (MMP-20)

decient mice display an amelogenesis

imperecta phenotype was published in

the Dec. 20, 2002, issue o the Journal oBiological Chemistry. It is available at www.

jbc.org.

John C. Greene, DMD, MPH, has been

honored with the 2002 uttle Award, given

annually by the National Spit obacco

Education Program or national leadershipin spit tobacco education and prevention.

Dr. Greene is dean emeritus at the Univer-

sity o Caliornia at San Francisco School o

Dentistry.


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Mussels and Barnacles May Some Day Yield New DentalAdhesives

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c d a j o u r n a l , v o l 3 1 , n 2

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h e a di n t r o d u c t i o n

ince the early 1960s, when the healthcare model began emphasizing preven-

tion, the dental proession has struggled

with the balance between expending

resources on preventive health measuresand on surgical treatment or oral diseases.

We are all amiliar with the success o wateruoridation in reducing the prevalence o dental

caries in the 1960s and 1970s. Te introduction ouoride dentirice and other uoride products led to

another major reduction in dental caries in the late

1970s and 1980s. Te gold standard or preven-

tion became dentists convincing their patients toengage in a routine regimen o brushing with a

uoride dentirice and engaging in regular ossing.

Still today, dentists and their sta spend count-

less hours educating patients on the importance othis daily exercise; and yet, dental caries continues

to be a major problem in children and adults.Tis preventive model, as well as a ocus on

community water uoridation nationwide, reducedthe prevalence o dental caries in the United States.

However, as the demography o Caliornia and the

rest o the nation shits at a rapid rate, we nd our-

selves in a contradictory circumstance with dentalcaries dramatically increasing in some segments

o the population. Dental caries is now the single

most common chronic disease in children. Tere

are ve times more children in the United Stateswith untreated dental disease than with childhood

asthma, and the maniestation results in morethan 50 million missed school hours every year.

With so much disease, it is easy to get caught up

in an endless treatment cycle to x the problem

using traditional surgical restorative approaches.However, we need also to keep ocused on the

wonderul partial success o prevention that tookus to new levels o health in the 1970s and 80s.

Fluoride therapy has taken us to a point, but aloneit is not enough; and we must continue exploring

additional new procedures or reducing dental car-

ies that will advance prevention to the next level.

Dental caries is a bacterial inection that is transmis-sible. We have to deal with the bacteria as well as to

enhance remineralization and repair o early lesions.

In this two-part series, we hope to provide an

update not only on the biological research and back-ground o cariology, but also on the application o

innovative methods to manage dental caries basedupon risk assessment, intervention, and preven-

tion o this transmissible inection. Tis two-partseries is the outgrowth o a conerence hosted by the

Caliornia Dental Association Foundation in April

2002, where experts came together to review and

update the science and practice o caries prevention.In Part I o this series, we asked some o the

leading researchers in dental caries to help us

set the stage with inormation on the biologi-

cal mechanisms o caries, the current problems,especially in Caliornia, and to begin to suggest

C w: M F PJohn D.B. Feahersone, MSc, PhD, and Jon R. Roh, CAE

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John .B. Featherstone,

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Resoraive Denal

Sciences a heUniversiy o Caliornia

a San Francisco. He is

he Leland and Gladys

Barber disinuished

proessor o denisry

a UCSF.


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i n t r o d u c t i o n

residents in caries risk assessment and

prevention, including the suggestion

that pediatric dental training programs

become dental homes or theirpatients.n n Paul Glassman, DDS, MA, MBA,

will share his extensive experience

in providing services to people with

special needs. He reviews strategies or

overcoming inormational, physical,and behavioral barriers to oral health

care or people with special needs and

presents a summary o the results oa conerence, held early in 2002, on

Practical Preventive Protocols or

Prevention o Dental Disease in People

with Special Needs in CommunitySettings.

Next month, we will share hands-on

clinical applications, based on these and

additional reviews, as new interventionsto advance caries prevention. We will also

provide a risk assessment orm or you touse in your practice that incorporates this

research and represents the consensus othose at the April 2002 conerence in Sac-

ramento. Ultimately, we hope to provide

you with tools to elevate the preventive

gold standard in your own practice.Also included in this issue is a ree

DVD, sponsored by the CDA Founda-

tion, which provides you with six patient

education videos (three English, threeSpanish) using the concepts derived rom

the research presented in Part I and Part IIo this series. We believe you will nd this

valuable educational series, titled EasySteps to Oral Health, an important com-

munication linkage between the research

discussed in these papers and your daily

practice and interaction with patients.

ways to deal with the situation in the

home, in dental practices, and in com-

munity settings. Teir work will share

revealing inormation regarding thescope o dental caries as a health con-

cern as well as the clinical identication

and transmission o dental caries.n n James C. Crall, DDS, ScD, shares his

expertise in the prevalence o caries.

His paper will serve as a baseline orunderstanding the magnitude o the

problem o dental caries, particularly

among Caliornias children.n n John D.B. Featherstone, MSc, PhD,

will illustrate the caries balance

as the basis or understanding and

dealing with caries. Te article willpresent a brie overview o the dental

caries process -- in particular, the

management o dental caries -- with

the role o early detection methods inthe clinical management o caries.

n n Robert J. Berkowitz, DDS, willcontinue the epidemiological discussion

with a paper on dental caries as aninectious and transmissible disease.

His review will illustrate new ndings

demonstrating that predentate inants

acquire mutans streptococci rom theircaregivers and that horizontal as well as

vertical transmission occurs.n n Pamela K. DenBesten, DDS, MS,

shares inormation pertaining to theetiology and maniestations o early

childhood caries, a major issue inCaliornia.n n Steven M. Adair, DDS, MS, willillustrate how advanced specialty

education programs in pediatric

dentistry are oten overwhelmed with

patients who need restorative andsurgical care, oten on an emergency

basis. His paper contains several

recommendations or strengthening

the training o pediatric dental


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C l F

aliornia is considered by many

to be the nations trendsetter

in health consciousness and

health promotion. But beneaththis popular image o healthy

Caliornians are troubling trends andreports about the oral health o substan-

tial and growing numbers o Caliorniachildren and their inability to access basic

services that can help promote, restore,

and preserve their oral health. Marked

increases in the number o childrenliving in poverty in Caliornia, dental

disease rates that ar exceed national

averages, and ewer than one in three

Medicaid-eligible children having accessto dental services paint a picture that

stands in sharp contrast to commonly

held perceptions o health in this vast

and diverse geosocial entity that is home

to one in eight American children.1-4Tis paper highlights undamental

elements o the challenge o securingoral health or Caliornias children, now

and in the uture, and underscores theneed or new strategies to reduce the risk

o dental disease and expand access to

eective services. Developing eective

strategies to gain optimal oral health orCaliornia children, especially those that

are most vulnerable to dental disease and

its consequences, requires an appreciation

o key dynamic actors that dene thischallenge and the degree to which these

C C : CJames J. Crall, DDS, ScD

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author

James J. Cra, ,

c, is direcor o he

Maernal Child and

Healh Bureau Naional

Oral Healh PolicyCener a Columbia

Universiy, Ne Yor, NY.

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amilies in poverty.

l : Pbn Prevalence rates two times national

averages.n Even higher disease rates in rapidly

emerging groups within the population.

Collecting state-level data on dental

disease in children has not been a priorityin Caliornia. In act, a 1993-94 statewide

oral health needs assessment o Caliornia

children4 was reported to be the rst suchsurvey in Caliornia history, and it has

not been repeated. Tus it represents the

most recent comprehensive source o data

or characterizing the dental status oCaliornia children.

Key ndings rom the 1993-94 Cali-

ornia Oral Health Needs Assessment o

Children4 include:n More than 50 percent o all Caliornia

school-age children were ound to haveuntreated decayed teeth.

In 1993-94, the percentage o 6- to8-year-old Caliornia children with

untreated decay (55 percent) was

more than twice the U.S. aver-

age or this age group in 1986-87.Comparisons with data rom the

Tird National Health and Nutrition

Examination Survey conducted rom

1998 to 19945 indicate that Caliorniachildren also were more than twice as

likely to have untreated decay com-pared to national averages.

More than hal (54 percent) oCaliornia 10th-graders were ound

to have untreated decayed teeth, and

nearly 40 percent o 10th-graders in

need o treatment had urgent dentalcare needs or extensive decay, pain,

or inection.

Asian, black, and Latino children

were ound to have signicantly high-er rates o untreated decay compared

growing majority o the poor children in

Caliornia. Hispanic children now account

or 61 percent o all poor children in Cali-

ornia (up rom 41 percent two decadesago), while the proportion o poor chil-

dren who are white has decreased rom

30 percent to 21 percent. Te share o

poor children who are Arican American

has allen rom 16 percent to 7 percent.3

Tirty-our percent o Caliornias His-panic children live in poverty, a 14 percent

increase rom two decades ago. Poverty

rates or Arican-American children de-clined rom 32 to 24 percent during that

same time rame, while the rate or white

children remained nearly at at about

11 percent. Te poverty rate or Asian-American children was 19 percent during

1996-2000.b

Immigration has had a major inu-

ence on the changing demographic proleo Caliornias low-income amilies. Te

National Center or Children in Povertyreport3 notes that some 46 percent o all

children in Caliornia are immigrants, andnearly 60 percent o the poor children in

Caliornia are immigrants. At 29 percent,

the poverty rate or immigrant children

is signicantly higher than the 17 percentrate or nonimmigrant children. Tese

children present a challenge not only rom

the standpoint o their sheer numbers,

but also by virtue o diverse cultures andlinguistics.

Te National Center or Children inPoverty analyses o U.S. Census Bureau

data also point out that Caliornia chil-dren are much more likely to live in work-

ing and two-parent amilies than they

were two decades ago.3 More than two-

thirds o poor children in Caliornia nowlive in amilies with at least one employed

parent; and 48 percent o poor children

in Caliornia are in two-parent amilies.

Immigrants in poverty are more likely tobe in working amilies than native-born

actors are modiable in the near and long

term. Particular attention is directed to-

ward three principal elements: population

demographics, levels o dental disease inCaliornia children, and actors aecting

access to services or vulnerable groups o

children. Te concluding section addresses

the need or strategic action.

: Mj Fn Increases in childhood poverty.n Challenges o dealing with diversecultures.n Te demographic prole o Caliornias

children has undergone dramatic

changes during the past two decades. Arecently released report by the National

Center or Children in Poverty3

identied the ollowing trends:n Te number o low-income childrenin Caliornia has increased by almost

1.6 million since the early 1980s,rom 2.77 million to 4.36 million.

Te number o Caliornia children inpoverty has increased by 850,000,

rom 1.27 to 2.12 million.an One in six poor children in the

United States currently lives inCaliornia compared to about one in

10 two decades ago.n Caliornia alone has accounted or

all o the net national increase o800,000 in the number o children in

poverty since the late 1970s.n Te child poverty rate in Caliornia

increased rom less than 20 percentduring the period rom 1979 to 1983

to 22 percent during the period

rom 1996 to 2000. During the same

averaged time period, the nationalchild poverty rate decreased rom 19

percent to 18 percent.

Te National Center or Children

in Poverty report3 also points out thatHispanics have become a large and rapidly


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C l F

urban, containing 3.06 million people

(8.9 percent o the states population);

andn O the 32 study areas that had nodentists, 31 were rural.n Related data also indicate that o the

487 study areas in Caliornia, 108 had

no active Medicaid dentists and that

hal o the study areas in Caliornia

had less than one Medicaid dentist per1,000 Medicaid beneciaries.11Public sector infrastructure Al-

though the public oral health saety netinrastructure can include a broad array o

entities and activities, attention is limited

herein to care delivered in public com-

munity clinics. A recent report publishedby the University o Caliornia at San

Francisco11 noted that approximately 204

(30 percent) o the licensed community

clinics in Caliornia oer some level ooral health care. Although the mission o

most community health centers and othercommunity clinics is to provide ree or

low-cost primary care to low-income anduninsured people, these centers gener-

ally ace ongoing challenges o recruiting

and retaining dental proessionals and

maintaining adequate nancing. Withouta mixture o ederal, state, county, and

private grants and reimbursement/pay-

ment, most clinics would not be sustain-

able.11

P Improving childrens oral health andultimately the oral health o the popu-lation requires attention to two broad

strategies:n Reducing the burden o oral diseases

in the population through provenpreventive measures andn Providing disease management and

treatment services to individuals who

demonstrate clinical maniestations ooral diseases and their sequellae.

lation ratio o all 50 states in 1998, but

ranked 26th in dental hygienist-to-popu-

lation ratio and eight in dental assistant-

to-population ratio. During the periodrom 1991 to 1998, Caliornias dentist-to-

population ratio declined by 8 percent.

Te number o dental hygiene graduates

per 100,000 population declined by 4

percent rom 1985-86 to 1995-96, while

the number o dental assistant graduatesper 100,000 population declined by 38

percent during that same period.Dentist participation in Medicaid

Data rom the National Conerence

o State Legislatures7 indicate that 66

percent o practicing Caliornia dentists

received at least one payment romMedicaid (Denti-Cal) in 2000 and that the

percentage o dentists receiving at least

one payment increased by 35 percent over

the gure reported or 1998. Te coner-ence report also indicates that 29 percent

o Caliornia dentists received paymentso at least $10,000 rom Medicaid in 2000.

In 1998, Medi-Cal payment rates variedrom 17 percent to 68 percent o average

regional dental ees, depending on proce-

dure.8 Low ees are the main reason cited

by dentis ts or not participating in theMedi-Cal program.9

Dental workforce distribution In

spite o relatively high dentist Medicaid

participation rates in Caliornia, a recentreport on the geographic distribution o

Caliornia dentists10 ound that:n O the 487 Medical Service Study Areas

in Caliornia, 97 (20 percent) were at orbelow the ederal Health Proessional

Shortage Area ratio o primary care

dentists-to-population o 1:5000 in

1998;n Sixty-six o the 97 shortage study areas

(68 percent) were rural and contained

1.06 million people (3.1 percent o

Caliornias population), while 31 o theshortage study areas (32 percent) were

to their white counterparts. Dispari-

ties were particularly pronounced

or young (preschool and elementary

school) children regardless o race orethnicity and or Hispanic adoles-

cents.n Nearly one-third o Caliornia

preschoolers, 69 percent o Caliornia

children in grades K-3, and 78 percent

o Caliornia 10th-graders hadexperienced tooth decay.

Te striking levels o untreated tooth

decay in large proportions o Calior-nia children -- more than 40 percent o

nonwhite preschoolers, 40 percent to 68

percent o all elementary school children,

and 38 percent to 75 percent o all highschool-age youths -- highlight two distinct

dimensions o the challenge o provid-

ing oral health or Caliornia children: (1)

nding eective ways to extend knowneective preventive interventions to all

Caliornia children and (2) ensuring accessto quality dental care or the millions o

Caliornia children in need o treatmentas well as preventive services.

: KC n rends in numbers o dental service

providers.n Extent o provider participation in

public programs.n Workorce distribution issues.n

Public sector inrastructure.Space limitations do not allow or

extensive discussion o the complexactors aecting access to services that

could improve the oral health o Calior-

nia children or related trends. However,

observations and trends regarding severalkey areas are highlighted below.

State dental workforce According

to data published by the Health Resources

and Services Administration,6 Caliorniahad the 10th-highest dentist-to-popu-


13/39

12 8 e b r u a r y 2 0 0 3

c d a j o u r n a l , v o l 3 1 , n 2

C l F

T q , : J

J. C, DDS, SD, C U S D

O Sg, 6 W. 68 S., 7 F, Nw Yk, NY -

7 @..

e erences. U.S. C B: S C QkF, D

P E, C

P Hg, 99 C P

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B Pt, 997 E C, M-

W-Ow B, Bg P, C

F F R, 997 C G A

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46: A EPSDT : C FY .

U.S. D H H S C

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: g , 997. A I

t://www..g//

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5. Vg C, C J, S D, Sg

: NHANES III, 988-994.

J Am Dent Assoc 9:9-8, 998.

6. H R S A, B

H P, HRSA S H Wk P:

C, D . A I ://

..g//wk/CA., O , .

7. G S, Hk P, S J, Ig

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9. Mz E, M-Bk C, , Ig

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. Mz E, G K, , Gg

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C S F C C Wk

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.g.

Te actors underlying attainment othese goals are complex and require stra-

tegic planning and action that emphasize

outreach, education, prevention, early

intervention, access to quality care, andprogram evaluation and management

based on sound data.c

Considerable inormation and recom-

mendations related to these issues have

been compiled by various groups through-

out Caliornia o late; however, absent asustained, adequately supported, unied

public-private eort and strong leader-

ship, advances are unlikely. Additionalpapers in this issue and the next provide a

oundation or developing new approach-

es or major oral health challenges acing

Caliornia. Developing strategic initiativesand programs to eectively translate this

inormation within the emerging contex-

tual environment will be the key to uture

oral health in Caliornia.

Notesa. Te National Center or Children in

Poverty report denes a low-incomechild or amily as living in a household

with annual income less than 200

percent o the ofcial poverty line

($35,048 in 2000 or a amily o our).In looking at the larger population o

low-income amilies, it also includes

demographic analyses o poor children

and amilies using the poverty line($17,524 in 2000 or a amily o our).

b. Te Census Bureau did not collectinormation to determine the child

poverty rate among Asian-Americansduring the 19791983 period.

c. Additional background material on

related oral health policy issues12 and

an example o using state-specicinormation to generate strategic

planning and actions13 can be ound at

www.cthealth.org.


14/39

c d a j o u r n a l , v o l 3 1 , n 2

e b r u a r y 2 0 0 3 1 2

c a r i e s

ental caries is simply toothdecay. Tere is a small number

o key contributing actors.1

First, specic bacteria are

involved that can metabolizeermentable carbohydrates and generate

acids as waste products o their metabo-

lism. Te two principal groups o bacteria

that have been implicated in dental cariesare the mutans streptococci and the Lacto-

bacilli species. Te principal species in themutans streptococci group are S. mutans

and S. sobrinus. Tese bacteria are all calledacidogenic because they produce acids

rom carbohydrates. When the acids are

produced by the bacteria, they diuse into

the tooth enamel or dentin and dissolve orpartially dissolve the mineral rom crystals

down inside the tooth. Te tooth enamel

and dentin are tissues made up o millions

o tiny crystals. Te mineral involved is

termed a carbonated hydroxyapatite.2 Tisis a calcium phosphate with numerous

impurity inclusions, the most important

o which is the carbonate ion, which makes

the mineral more acid-soluble than purehydroxyapatite. I the dissolving o the

mineral is not halted or reversed, the early

subsurace lesion becomes a cavity. Last,

dental caries is a transmissible bacterialinection.3-6

Dental caries occurs in deciduous teeth andpermanent teeth, regardless o the age o

the individual. Lesions vary rom the veryearly lesion o enamel, which is maniested

as a white spot, to rank open cavities.

Early childhood caries is a similar process

to later childhood and adult dental caries oenamel.7 Root caries is dental decay o the

tooth root, which occurs in adults ater the

gingiva recede.8

C B: CbF John D.B. Feahersone, MSc, PhD

author

John .B. Featherstone,

Mc, Ph, is

proessor and chair

o he Deparmen

o Prevenive and

Resoraive Denal

Sciences a he

Universiy o Caliornia

a San Francisco.

astract T w ,

, g

g .


15/39

1 e b r u a r y 2 0 0 3

c d a j o u r n a l , v o l 3 1 , n 2

In most individuals, there are numer-

ous acid challenges daily as ermentable

carbohydrates are ingested and the strugglebetween the pathological actors and the

protective actors takes place. First, as the

acid is produced by the bacteria, mineral

dissolves; and subsequently, as the salivaneutralizes the acid, mineral is replaced.

Fluoride enhances this remineralizationprocess when it comes rom topical sources

such as drinking water, ood and beverages,toothpastes/dentirices in general, mouth

rinses, ofce-applied uoride preparations,

or rom higher-concentration products

including uoride varnish (Figure 1).Te next question that we must ask is i

uoride is so eective why do millions o

people still require treatment annually in

the United States or dental decay. Simply, ithe bacterial challenge is too high, the ben-

ecial eects o uoride can be overcomeby the acid attack. In the case o high-

caries-risk individuals, although uoridehelps to reduce the amount and severity

o the decay, it cannot overcome the high

bacterial challenge. Figure 2 illustrates the

mean decayed, missing, and lled suracesin three national surveys in the United

States. A dramatic reduction in decay levels

was observed between 1970 and 1990. Prior

to 1970, dramatic reductions in decay werealso observed due to the uoridation o

the surace o the tooth. Tese aspects

were thoroughly reviewed and agreement

reached at an international consensus con-erence in 1989 and have been summarized

extensively in other review papers.13-15 In

summary:n Fluoride inhibits demineralization;n Fluoride enhances remineralization;

andn Fluoride can inhibit plaque bacteria.

Te Caries BalanceBased upon the above summary o our

in-depth knowledge o the car ies process,

it is very useul and constructive clinicallyto consider caries in its progression or

reversal as an ongoing and oten changing

balance between pathological actors and

protective actors.1,16 As illustrated in Fig-ure 1, i the pathological actors outweigh

the protective actors, then caries pro-gresses. In the reverse situation, caries is

arrested or even reversed. Te pathologicalactors include the acidogenic bacteria, re-

duced salivary unction, and the requency

o ingestion o ermentable carbohydrates.

Te protective actors include saliva andits numerous caries-protective compo-

nents: the saliva ow; antibacterials, both

intrinsic rom saliva and extrinsic rom

other sources; and other actors that canenhance remineralization.

w w K b CTe process o dental caries is well-under-

stood.1 We know how demineralization(loss o mineral) and remineralization

(regaining o mineral) occur, and we havea very good understanding o how uoride

works to inhibit or reverse dental caries.

Much is known about the multiple roles o

saliva and salivary components.9 We knowthat acidogenic bacteria (described above)

cause demineralization and, thereore, car-

ies. Tese bacteria are also termed cario-

genic. Te one major remaining area where

much is still to be learned is in the complex

microbiology that occurs in the dentalplaque or so-called biolm on the surace o

the tooth. Te role o ermentable carbohy-

drates in oods and beverages is well-under-stood; and it is known that sucrose, glucose,

ructose, and cooked starch all contribute

to the caries process.1

Demineralization, i.e., loss o mineral romthe tooth, is initiated by the cariogenic

(acidogenic) bacteria that produce organic

acids during their metabolism. Tese acids

include lactic, acetic, propionic, and ormic.All o these acids can readily diuse into

the tooth and dissolve the susceptiblemineral. Te dental mineral dissolves to

produce calcium and phosphate into theaqueous solution between the crystals; and

these ions diuse out o the tooth leading

to the ormation o an initial carious lesion,

which eventually can become a cavity i theprocess continues without reversal.10 Te

reversal o the process is remineralization

(replacement o mineral), which occurs

when the acid in the plaque is buered bysaliva allowing calcium and phosphate,

primarily rom the saliva, to ow back intothe tooth and orm new mineral on the

partially dissolved subsurace crystal rem-nants.11 Te new veneer on the surace o

the crystal is much more resistant to subse-

quent acid attack, especially i it is ormed

in the presence o sufcient uoride.1,12

Fluoride Mechanism of ActionIt is now known that the primary mecha-

nisms o action o uoride are topical, i.e.they work by uoride being available at

c a r i e s

F i u re . Schemaic illusraion o he caries balance. Adaped romFeahersone.1,1


16/39

c d a j o u r n a l , v o l 3 1 , n 2

e b r u a r y 2 0 0 3 1 1

to the current standard o care. Te levelso mutans streptococci and lactobacilli were

measured at the beginning o the study andater restorations were completed, with the

net result that mutans streptococci levelswere not statistically signicantly dierent

ater the completion o restorations unless

antibacterial therapy by chlorhexidine

was used. Tis means that or high-riskindividuals with high levels o cariogenic

bacteria, we must take steps to reduce the

bacterial loading along with restorative

work. Tere are several guiding principals

that can be ollowed:n

Fluoride is eective only up to a point;n A high bacterial challenge cannot be

completely overcome by even high-

concentration uoride therapy;n Placing restorations and conducting

restorative work does not reduce the

overall cariogenic bacterial loading in

the mouth; andn We need to break the chain o inection

i caries is to be controlled in these

individuals.

As described briey above, caries involvesmultiple acidogenic species o bacteria,

which means that a vaccine or one particu-lar species will not necessarily have a bene-

cial eect on the overall caries status o theindividual. We need to utilize antibacterial

therapy to reduce the bacterial challenge and

allow the protective actors in the above-de-

scribed caries balance to take over. We needto nd ways to break the chain o inection,

or example, rom mother to child. It is now

well-established that mutans streptococci

can be readily transerred rom mother tochild or caregiver to child or indeed rom

child to child or adult to adult.4 Antibacterialtherapy with chlorhexidine is one immediate

alternative, but this is eective or mutansstreptococci and not or lactobacilli.25 New

antibacterial therapy is needed. As reviewed

by Den Besten and Berkowitz, it is possible

that iodine therapy may be more eectivethan chlorhexidine.7 Recent studies have

shown that xylitol has properties that inhibit

the establishment o cariogenic bacteria, and

this appears to be an excellent method obreaking the chain o inection.26

caries, the decay is rampant and requiresaggressive and multiple intervention strate-

gies to control it.

Caries Is a ransmissible BacterialInfectionIt has been known or many years that car-

ies is a bacterial inection.22 Studies during

the past 25 years clearly indicate that thebacteria involved are transmissible, and

the transmission, especially o S. mutans,

is reviewed thoroughly by Berkowitz.4 In

practical dentistry in the United States, we

pay little attention to this basic act about

caries. We treat the maniestations o thedisease rather than treating the disease

itsel. It is obvious that the next steps that

must be taken to control, i not eradicate,dental caries must ocus on the bacteria.

One startling act, which is not considered

in practical dentistry, is that placing resto-

rations to ll the cavities has no measurableeect on the cariogenic bacterial loading in

the remainder o the mouth.23 Tese earlier

ndings have been borne out by an ongoing

study24 in which a group o adult subjectswith initial rank cavitation has been re-

ceiving conventional dental care according

public water supplies. From 1970 onward,several actors were involved including the

almost universal utilization o uoridedentirices.20

Unortunately, since 1990 there has beena plateau in the reduction o caries. Tis

means that to urther reduce the preva-

lence o dental caries and to address those

who continue to have high levels o dentalcaries, we must use other measures. A

recently published survey on the dental

health o Caliornias children rom data

that was accumulated in 1993 and 199421

illustrated that:n

27 percent o preschoolers haveuntreated decay;n 53 percent o 6- through 8-year-olds

have untreated tooth decay;n 50 percent to 75 percent o minority

high school students need dental care;n Caliornias children on average have

twice the national average o untreatedtooth decay.

In Caliornia, early childhood caries is a

major issue.7 Essentially the process and

etiology are the same as caries in olderchildren and adults and involves the same

bacteria. In the case o early childhood

c a r i e s

F i u re . M g (DMFS) U.S. (g g w) .7-9


17/39

1 2 e b r u a r y 2 0 0 3

c d a j o u r n a l , v o l 3 1 , n 2

Caries Risk AssessmentPractical caries risk assessment and the

consequent clinical actions were the basisor the conerence that generated this is-

sue o the Journal. Te importance to the

pediatric dentist is that such procedureswill change the way care is delivered.33

Similarly, in a public health setting, it will

change the way interventions are done and

how money is spent on programs to helplower-income/high-risk populations. Te

basis o caries risk assessment as we are

currently introducing it into the predoctor-

al dental teaching clinics at the Universityo Caliornia at San Francisco is the caries

balance described above (Figure 1). Eacho the pathological and protective actors

must be assessed in coming to a judg-ment as to whether the patient is at risk o

progression or initiation o dental caries.

We have developed a orm or the clinician

with instructions on the back to guide inrisk assessment. When the risk assessment

is complete, this inuences the treatment

plan. I the patient is required to conduct

home care, a second orm with appropri-ate instructions highlighted is given to the

patient with a prescription, i needed. Tereverse side o this orm has a lay-person

one-page description o dental decay.Te guiding principle (risk actor) ques-

tions or this risk assessment tool were as

ollows:n Is there existing or has there beennew untreated cavities in the past two

years?n Has there been orthodontic appliances

or removable partial dentures?n Is there reduced salivary unction as

very dierent. In this case, there is a large

amount o surrounding sound enamel that

absorbs the X-rays; and only an advancedlesion can be detected in this ashion with

conventional bitewing radiographs. Tis

is illustrated in Figure 3, where the lesionunder the occlusal surace was a hidden

lesion extending histologically to the pulp.

It showed only as a aint line at the DEJ in

the radiograph. We need methods that candetect occlusal lesions while they are still in

the enamel and can be reversed or arrested

by uoride therapy and remineralization.

Recently, the FDA approved a device calledthe Diagnodent, (KaVo, Ill.) which shines

a red laser into the tooth via a speciallydesigned handpiece and tip. Te tip is

applied to the occlusal pits and ssuresindividually. Te red light readily penetrates

the tooth; and i it interacts with a subsur-

ace lesion that contains certain bacterial

byproducts, uorescence is produced. Teuorescent light comes back rom the le-

sion into the handpiece, interacts with the

detector, and is read out as a number and

an audible signal i there is a lesion. Tisinstrument is a good rst step in providing

the practitioner with a tool that can indi-cate whether there is a hidden lesion under

the occlusal surace. Even better devices areexpected to become available to detect early

enamel lesions in occlusal suraces.

Te uture will see improvements in these

and other techniques, and the tools orearly detection will be available. Te bottom

line is that we must use early detection or

the purposes o intervention, not to justiy

more drilling and lling.32

Conservative Caries ManagementConservative caries management has the

idealized outcome that more tooth struc-ture is preserved and ewer teeth become

aected by dental decay. Tere are a ewguiding principles:n n Detect caries lesions early enough

(see below) so that the early,

noncavitated lesion can be reversedor at least arrested rom progressing

by chemical means rather than by

restoration (placing llings);n n Assess the individual risk o caries

progression (see below);n

n Use uoride to enhanceremineralization and/or reduce the

bacterial challenge by the use o

antibacterial therapy;1,25,27-29 andn n Use minimally invasive restorative

procedures to conserve tooth

structure.28,30n Te longevity o the tooth is muchgreater in the scenario o conservative

caries management; many more teeth

are preserved as caries ree, and those

that do require restorative work havemuch smaller restorations leading to

much less racture in the long term.

Early Caries DetectionUntil recently, caries detection methods

have been visual, tactile (with an explorer),

and radiographic. Visual inspection can

be quite eective when done by an experi-enced dentist, and new classications are

in use in Europe that could well be useul

in the United States.31 However, this is

obviously limited where the surace o thetooth is obscured and in occlusal suraces,

where hidden lesions may be missed.Radiographs as done with bitewings have

long been useul or detecting interproxi-mal lesions. Te current standard o care

is that i an enamel lesion, as detected by

the radiograph, is not past the dentino-

enamel junction, then it can be arrestedor reversed by remineralization, whereas

an opacity into the dentin requires clinical

physical intervention (drilling and ll-

ing). Tis method is quite reliable or theselesions. However occlusal suraces are

c a r i e s

Fiure 3. he et paneshos a conentionaitein radioraph ith an

interproima esion on theet and a shado at the Junder the occusa surace(arros). he riht paneshos a hemi-section o thesame tooth iustratin thehidden esion etendin tothe pup under the occusasurace (courtes o..youn).


18/39

c d a j o u r n a l , v o l 3 1 , n 2

e b r u a r y 2 0 0 3 1

c a r i e s

O E :8-4, 99.

4. F JDB, Gk SA, , Cg

z g . J Dent

R , .5. A MH, Cx: Hw tg

g ? J C D A I

, .

6. L H, Mg P, X : A w

. J C D A I , .

7. A MH, B DJ, O K-A, M g

: tg g . J Am

Dent Assoc 4:7-44, 99.

8. Hk J, G-G F, , F-g

. J C D A

I , .

9. D K, F . J C D A I ,

.

. A SM, T

g. J C D A I , .

. Ek KR, Rkt DNJ, , D, gg,

g g

: A x w

g . C R :47-54, 998.

. F JDB, C

: Nw g . I, Sk

GH, Bwg B, , I C: E D

D C. I U, 996, 85-9.

. Sw RE, T g :

A . J C D A I ,

.

T q , : J

D.B. F, MS, PD, D P

R D S, U C, S

F, 77 P A., Bx 758, S F, CA

944 @...

nia is thanked or support o pilot studiesrelevant to this work.

e erences. F JDB, T

.J Am Dent Assoc :887-99, .

. LG RZ, C ,

. I, M HM, , C P O Bg

M, . 5. Kg, B, 99, 8-9.

. C PW, C GR, Dk AP, I q

:

ww . J Dent R 7:7-45, 99.

4. Bkwz RJ, Aq

. J C D A ():XX-XX, .

5. L WJ, R S

. Mg Rw 5:5-8, 986.

6. L WJ, Sg ML, P HR, I

S x. J Dent R

58:765-7, 979.7. D B PK, Bkwz RJ, E : A

w w x C. J C

D A ():XX-XX, .

8. W JS, Ck BH, H JR, N :

g g . J O P

4:65-, 985.

9. Lk MS, O FG, S

. C Rw O Bg M 4:5-9, 99.

. S LM, T , g

. O S R :-6, 97.

. T C JM, D PPE, Ag

. C R

6:-, 98.

. F JDB, C /z

. I, F JDB, , C A D/

z T, . 9. A D R

9, 995, -4.. F JDB, G R, , D

z z

f . J Dent R 69:6-5, 99.

4. T C JM, F JDB, M

w f . CRC C

Rw O B :8-96, 99.

5. H IR, Bw GHW, F

. I, Fk O, Ek J, B BA, , F

D. Mkg, Cg, 996, -5.

6. F JDB, P :

w f. C D O E

7:-4, 999.

7. NIDR, T U S

: T N D C P S:

979-8. NIH P N. 8-45. N I

H, 98.

8. NIDR, O H S N I D R. Dg . NIH

P # 9-87, B, MD, 99.

9. NCHS, N C H S. G

Pg O, Wg DC, 974.

. Jk GN, R g . B M J

9:97-8, 985.

. Pk HF, R C O H N

A C, 99-994. T D H

F, Ok, CA, 999.

. L WJ, Hkt RN, S SA, T

f q

z . A O B 7:-5, 97.

. Wg JT, Ct GR, , E

. C D

measured by stimulated saliva ow lessthan 0.7 ml/minute?n Is there use o hyposalivatorymedications?n Is there requent ingestion oermentable carbohydrates (by

questioning the patient)?n Is current use o uoride products

inadequate? andn Is there high caries bacterial challenge

as measured by testing mutans

streptococci and lactobacilli?

Te number o yes answers to the above

questions places the patient into one o

three risk categories. I the answers to therst ve questions are mostly no, then bac-

terial testing is not needed. I bacterial test-

ing is needed, the Ivoclar (Amherst, NY)caries resistance test is used; and results

are known in 48 hours. Tis orms the basis

or uture monitoring o the eectiveness

o antibacterial therapy. I the person is athigh risk, this initiates:n Bacterial testing;n Fluoride therapy (uoride ofce topical

ollowed by higher concentration homeuse uoride is used);

n Chlorhexidine therapy (0.12 percentchlorhexidine gluconate or two weeks

daily every three months); andn Regular recall to monitor lesion

progress or arrestment and

antibacterial therapy success.

In the uture, we anticipate that improvedchairside bacterial testing and improved an-

tibacterials will be available. For example, it

is theoretically possible to design antibac-

terials to target receptors on the cell wall othe cariogenic bacteria involved. With new

advances, these will enhance the success othe principles proposed in this presentation

toward the eradication o dental caries.Acknowledgments

Te contributions o many individuals

to the work and ideas reviewed here are

acknowledged with thanks. Tey are toonumerous to mention specically. Te

support o NIH grant RO1-DE 12455 or

the ongoing study titled caries manage-

ment by risk assessment is acknowl-edged. Te Delta Dental Plan o Calior-


19/39

c d a j o u r n a l , v o l 3 1 , n 2

e b r u a r y 2 0 0 3 1

m u t a n s s t r e p t o c o c c i

he mouth o a normal preden-tate inant contains only muco-

sal suraces exposed to salivary

uid ow. Mutans streptococci

could persist in such an envi-ronment by orming adherent colonies

on mucosal suraces or by living ree

in saliva and multiplying at a rate that

exceeds the washout rate caused by sali-vary ow. Because the oral ora averages

only two to our divisions per day1 andswallowing occurs every ew minutes,

it is reasonable to assume that bacteriacannot maintain themselves ree in

saliva solely by prolieration, but instead

must become attached to an oral surace.

Previous studies, reviewed by Gibbonsand van Houte (1975),2 have demonstrat-

ed that mutans streptococci have a eeble

capacity to become attached to epithelial

suraces. Tereore, it seemed unlikelythat these organisms could colonize the

mouth o a normal inant beore theeruption o teeth. Earlier clinical stud-

ies reported that mutans streptococci

could not be detected in the mouths o

normal predentate inants3-8 but couldater the insertion o acrylic clet-palate

obturators or eruption o primary teeth.

A longitudinal investigation by Carls-

son3 and coworkers reported that mutansstreptococci were detected in ve o 25

(20 percent) inants age 12 months to 16months. In addition, these organisms

were not detected in any o the 25 subjectsduring their rst year o lie. Although

Carlsson and colleagues did not report

the stage o dental development, the age

range o 12 to 16 months is compatiblewith an inant having six to 10 primary

teeth. Berkowitz and coworkers4 reported

that mutans streptococci were detected in

9 o 20 (22 percent) inants who had onlyprimary incisor teeth. In a subsequent

M Rober J. Beroi, DDS

author

oert J. Berkoit,

, is a proessor

o denisry a he

Universiy o Rocheser

Easman Denal Cener

in Rocheser, N.Y.

astract D . T L w g g g

w . E q

. M

z

z, w , . T g w k

g g,

g .


20/39

1 6 e b r u a r y 2 0 0 3

c d a j o u r n a l , v o l 3 1 , n 2

be related to several actors which, in part,include magnitude o the inoculum,26

requency o small dose inoculations,27and a minimum inective dose.28 A study

carried out by Berkowitz and cowork-ers26 reported that the requency o

inant inection (58 percent) was approxi-

mately nine times greater when maternal

salivary levels o the organism exceeded105 colony-orming units per ml relative

to the requency o inant inection (6

percent) observed when maternal salivary

reservoirs were less than or equal to

103 cu per ml. Suppression o maternal

reservoirs o mutans streptococci clearlyshowed that inection o the baby could

be prevented or delayed;29 only three o

28 (11 percent) babies whose mothers hadtheir mutans streptococci reservoirs sup-

pressed by dental treatment and topical

antimicrobial therapy were inected by

age 23 months. In contrast, 17 out o 38(45 percent) babies in the control group

whose mothers levels o mutans strepto-

cocci were not suppressed were inected.

In both groups, the percentage o inectedbabies increased with age; nevertheless

at age 4 ewer babies were inected in thetest group than in the control group.

z wo recent reports indicate that verti-

cal transmission is not the only vector by

which mutans streptococci are perpetu-ated in human populations. Mattos-Gra-

ner and colleagues30 isolated mutans

streptococci rom groups o nursery

school children (age 12 to 30 months) andgenotyped the isolates utilizing primed

polymerase chain reaction and restrictionragment-length poylmorphism analy-

sis. Tey reported that many childrencontained identical genotypes o mutans

streptococci strains, which indicates

that horizontal transmission may be

another vector or acquisition o theseorganisms. In addition, van Loveren and

coworkers,31 utilizing bacteriocin typing,

demonstrated that when a child acquires

mutans streptococci ater age 5, there maybe similarity between mutans strepto-

is required or their oral colonization.

M C

Early colonization by mutans strepto-cocci is a major risk actor or uture caries

experience. Children were longitudinally

assessed rom age 2 to 4 by Alaluusua

and Renkonen13 or mutans streptococcicolonization and dental caries; those chil-

dren who harbored mutans streptococci

in their plaque at age 2 were the most

caries active by age 4. Teir mean dms

score was 10.6 as compared with children

who were colonized later who had a meandms score o 3.4 by age 4 (p < 0.005).

Similar observations were made by Kohler

and coworkers:14 Tey observed that 89percent o children colonized by mutans

streptococci by age 2 had experienced

caries lesions by age 4 and had a mean

ds score o 5.0. In contrast, 25 percento children who were not inected with

mutans streptococci prior to age 2 had

experienced dental caries by age 4 and

had a mean ds score o 0.3. An additionallongitudinal investigation15 evaluated

786 children at age 1 or caries risk actors(mutans streptococci inection, uoride

exposure, dietary habits, oral hygiene)and re-examined them at 3.5 years o

age or the presence o dental caries. Te

presence o mutans streptococci at age 1

was the most eective predictor or cariesat age 3 1/2. Tese observations and other

published results16,17 clearly illustrate

that early inection with mutans strepto-

cocci is a signicant risk actor or uturedevelopment o dental caries lesions.

Vertical ransmissionTe major reservoir rom which in-

ants acquire mutans streptococci is theirmothers. Te evidence or this concept

comes rom several clinical studies that

demonstrate that mutans streptococci

strains isolated rom mothers and theirbabies exhibit similar or identical bacte-

riocin proles18-20 and identical plasmid

or chromosomal DNA patterns.21-25 Suc-

cessul inant colonization o maternallytransmitted mutans streptococci cells may

study,5 Berkowitz and colleagues reportedthat these organisms were detected in 3

o 43 (7 percent) inants (mean age = 8.9months) with one to ve primary incisor

teeth and 12 o 42 (29 percent) inants(mean age 13.8 months) with six to eight

primary incisors. Likewise, Stiles and

coworkers6 detected these organisms in

12 o 56 (22 percent) o inants (medianage = approximately 14 months) with

six to eight primary incisors and one o

38 (2.6 percent) o inants (median age

= approximately 9 months) with two

to our primary incisors. Catalanotto

and colleagues7 were unable to isolatethese organisms rom 10 inants who

had only primary incisor teeth; mutans

streptococci were detected only aterthe eruption o primary rst molars.

A more recent study by Caueld and

coworkers8 reported that 25 percent o

their inant population (n = 46) acquiredmutans streptococci by 19 months o age.

Extrapolation o Caueld and colleagues

data rom a gure depicting the cumula-

tive probability o mutans streptococciacquisition as a unction o age indicated

that approximately 5 percent o theirstudy population acquired these organ-

isms by approximately 9 months o ageand approximately 15 percent o the

subjects were colonized by approximately

12 months o age. Accordingly, the con-

cept that mutans streptococci required anonshedding oral surace or its persis-

tent oral colonization became a basic

tenet o oral microbial ecology. However,

more recent clinical studies9-11 havedemonstrated that mutans streptococci

can colonize the mouths o predentateinants. Te urrows o the tongue ap-

pear to be an important ecological niche.anner and coworkers,12 utilizing DNA

probe technology, reported that mutans

streptococci were ound to be present

in 55 percent o plaque samples and70 percent o tongue scraping samples

o 57 children age 6 to 18 months liv-

ing in Saipan. Tese recent studies on

acquisition o mutans streptococci raisedoubts that a nonshedding oral surace



21/39

c d a j o u r n a l , v o l 3 1 , n 2

e b r u a r y 2 0 0 3 1 7

g. O M I :4-7, 988.

5. G M, , Sw

.5 g. C R :56-66, 995.

6. Fw T , C - J. C D

O E 9:5-4, 99.

7. R RJM, , L, ,

: g

g 5 . C R 9:7-9, 995.

8. Bkwz RJ, J H, S

S . A O B

:75-, 975.

9. D AL, Rg AH, M

S -

. A O B 9:45-6, 984.

. Bkwz RJ J P, M--

S w

. A O B :77-9, 985.

. C PW, W Y, H J, F g

S

. I I 8:785-7, 98.. C PW, C NK, , P S

; g k

w . I, H S, Mk S, ,

, Pg ,

S .

E S P, Bg, A, 7-, 985.

. C PW, C NK, , D

w g S

. I I 48:5-6 985.

4. C PW, Rk K, , P-g

S w

; . I

I 56:6-, 988.

5. Kk GV, C KH, S HJ, A g

.J Dent

R 68:55-6,989.

6. Bkwz RJ, T J, G P, M

S .

A O B 6:47-9, 98.

7. L W, R S

. M R 5:5-8, 986.

8. V H J G DB, R w

z

. I I 9:64-, 974.

9. K B, , P f

S .

A O B 8:5-, 98.

. Mt-G R, L Y, , G

Bz gg z

. J C M 9(6):-8, .

. L C, B JF, C JM, S

w w q g 5.

C R 4:48-5, .

T q , :

R J. Bkwz, DDS, U R, E

D C, 65 Ew A., R, NY 46,

R_Bkwz@...

colonize the mouth o predentate inantsand are acquired by vertical and horizon-

tal transmission rom human reservoirs.Tis inormation should acilitate the

development o clinical strategies thatprevent or delay inant inection, thereby

reducing the prevalence o dental caries.

Cn Primary oral inection by mutans

streptococci may occur in predentate

inants.n Inants may acquire mutans

streptococci via vertical and horizontal

transmission.n Improvements in the prevention o

dental caries may likely be realized

through intervention strategies thatocus on the natural history o this

inectious disease.

e erences. G RJ, Bg . J Dent R

4:-8, 964.

. G RJ, H H, D . B

g. A R M 9:9-44, 975.

. C J, G J, J G, L

. C R 9:-9, 975.

4. Bkwz RJ, J HV, W G, T

S . A OB :7-4,975.

5. Bkwz RJ, T J, G P, P

w S . A O B 5--4,

98.

6. S HM, M R, , O S

S g

g . I, S HM, L WJ, OB

TC, , M A D C. V . I

R, L, 976, 87-99.

7. Ct FA, Sk IL, K HJ, P

z S . J

Am Dent Assoc 9:66-9, 975.

8. C PW, Ct GR, Dk AP, I q

:

ww . J Dent R 7:7-45,99.

9. W AKL, Sw K, , A S

- . J Dent R 8():945-8, .

. W AKL, Sw K, , O z S

x . J Dent R

8():6-5, .

. R-Gz FJ, , B,

w .

J C Pediatr Dent 6:65-7, .

. T ACR, , T g

g . J Dent R, 8():5-7, .

. A S Rk OV, S

x

4 . S J Dent R 9:45-7, 98.

4. K B, , T z

, g 4

cocci strains in mother, ather, and child,indicating that horizontal transmission

can also occur between amily members.

C fKnowledge regarding the natural his-

tory o an inectious disease acilitates a

more comprehensive approach or preven-

tion (e.g., yellow ever; acquired immuno-deciency syndrome). Studies by Kohler

and colleagues14,29(discussed previously)

utilized this concept to prevent and/or

reduce dental caries in young preschool

Swedish children by reducing the risk

or vertical transmission via suppres-sion o mutans streptococci reservoirs in

their mothers. Recent inormation30,31

indicates that horizontal transmission isanother vector or acquisition o these

bacteria. Tis nding is o importance

given the socioeconomic changes in

U.S. culture during the past two to threedecades (or example, the utilization o

day care acilities or preschool children

o amilies where both parents are em-

ployed). In addition, recent studies9-12have reported that mutans streptococci

may colonize the mouths o predentateinants. Tis nding implies that the

timing o intervention strategies toprevent or delay transmission should take

into consideration that a nonshedding

oral surace (primary teeth) is probably

not a requisite or oral colonization bythese organisms. Collectively, this review

indicates that urther clinical trials are

needed to translate knowledge regard-

ing the acquisition and transmission omutans streptococci into clinical interven-

tions that will likely prevent dental caries.

Dental caries is an inectious and

transmissible disease. Detailed knowledge

regarding the acquisition and transmis-

sion o inectious agents acilitates a morecomprehensive approach toward preven-

tion. Mutans streptococci are important

organisms in the initiation and patho-

genesis o dental caries. Recent evidencedemonstrates that these bacteria can



22/39

c d a j o u r n a l , v o l 3 1 , n 2

e b r u a r y 2 0 0 3 1

o e r i e

C C: w CPamela DenBesen, DDS, and Rober Beroi, DDS

authors

Pamea enBesten, ,

is chair o the iision

o Pediaric Denisry

a he Universiy o

Caliornia a San

Francisco.

oert Berkoit, ,

is he chie o Division

o Pediaric Denisry

a he Universiy o

Rocheser, Rocheser,

N.Y.

astract D g q x

, w q g kg t

w fw. T - g

. ECC

w g w w

. T ECC , q.

P ECC gw . Sg

g q x , w g

gw . T w

ECC g .

aries in children requentlymaniests in a pattern o pro-

gression related to the eeding

requirements o young chil-

dren who suck rom a bottle orbreast. Early initiation o caries in inants

and toddlers has been termed early child-hood caries. In young children, caries can

begin as soon the teeth erupt and canrapidly progress to extensive decay o all

primary teeth (Figure 1). Te pattern o

decay in early childhood caries is re-

lated to salivary ow patterns within aninants mouth. Te mandibular incisors

are protected by the tongue and bathed

in saliva and thus show decay only with

extremely severe caries challenge. Milkor other liquids sucked rom a bottle

pool in areas o the mouth that are lessexposed to sal ivary ow, particularly the

acial suraces o the maxillary primary

incisors, where early chi ldhood caries is

rst detected. As caries becomes moresevere, the decay appears on the occlu-

sal suraces o the maxillary primarymolars and then spreads throughout the

mouth, which can result in an over-whelming inection with destruction o

primary teeth throughout the mouth.

CStudies o the cariogenicity (caries-

causing potential) o inant oods show

that milk has minimal car iogenicity

relative to that o inant ormulas andruit juices.1-3 However, by the time

C


23/39

1 e b r u a r y 2 0 0 3

c d a j o u r n a l , v o l 3 1 , n 2

the mandibular and maxillary primary

incisors erupt, bottle or breast eeding issupplemented by a variety o solid oods.

Tese oods include starches and othersucrose-containing oods with cariogenic

potential, which provide an improvedsubstrate to promote the prolieration o

cariogenic bacteria. In addition, adding

a sweetener in bottles ed to inants is

a major risk actor or early caries.4,5Young inants may eed rom a bottle

or breast six or more times per day. As

the inant grows older, the number o

eedings does not dramatically change,but the variety and amount o ood that

a child ingests increases. Te requencyo eeding o inants and toddlers makes

them particularly susceptible to caries.I the requent eedings are accompanied

by prolonged exposure o the teeth to

liquids, as occurs when liquid is ingested

rom a bottle, susceptibility increaseseven more.4-8 Te relative requency

with which young children eed is likely

to aect the so-called caries balance

between actors that promote demin-eralization and those that promote

o e r i e

remineralization.9 Te requent andprolonged introduction o cariogenic

ood substrates (as occurs in bottle eed-ing with sweetened liquids), with the

subsequent lowering o plaque pH andtooth demineralization, can push the

balance toward tooth demineralization.

By ar the most caries-promoting ood

substrate is sucrose;2,3,10 but other car-bohydrates -- including glucose, ructose,

and cooked starch -- also contribute.

P bTis childhood dental disease is a public

health problem that aects babies,toddlers, and preschool children world-

wide. Te epidemiology o early child-

hood caries shows that disadvantagedchildren -- regardless o race, ethnicity,

or culture -- are most vulnerable.11,12

Early caries in inants and toddlers also

results in a higher risk or continuedtooth decay as the children grow older.

High-risk North American populations

include children o new immigrants

and children rom lower socioeconomicpopulations. In Caliornia, the relative

size o the new immigrant population ishigh compared with other states. Early

childhood caries is particularly prevalentin this population.13 Mexican-Ameri-

cans, who were shown in the NHANES

III data to be a vulnerable population or

caries in children,14,15 make up a largepercentage o the immigrant popula-

tion in Caliornia. In 1993, Serwint and

co-workers ound that 20 percent o the

110 Mexican-American children (18 to36 months o age) who were patients o a

hospital-based pediatric practice in LosAngeles, had early childhood caries.16

More recently, Ramos and coworkersound that in a predominantly Mexican-

American population in San Francisco,

43 percent o the children younger than

5 had caries in their primary teeth.17Native American children are at high risk

or caries, with prevalence rates o early

childhood caries reported rom 40 per-

cent to 72 percent.18,19 In 1996, Georgeand coworkers examined 4-year-old

Apache children to determine how carieslevels and patterns were dierent rom 15

years beore. Neither the caries preva-lence (95 percent) nor the prevalence

o caries patterns diered between the1978-79 and 1993 cohorts. However, the

level o treatment received in 1993 was

greater than that in 1978-79. Studies such

as this one suggest that our current eortat caries prevention, which are largely

conned to caries treatment or high-risk

populations, has had minimal eect in

reducing the prevalence o this disease.

Te act that caries is a transmissibledisease involving the cariogenic bac-

teria mutans streptococci has beenwell-established.20-25 Te major reser-

voir rom which babies acquire mutans

streptococci is their mothers or primary

caregivers, though cariogenic bacteriacan be transmitted rom other caregivers

or children in close contact.26 Suppres-

sion or alteration o maternal reservoirs

o mutans streptococci has shown thatinection o a baby can be prevented or

delayed.27,28 However, a single treat-ment o mothers with an oral antibac-

terial may not be sufcient to preventmutans streptococci transmission and

subsequent caries in children.29 Like-

wise, antibacterial treatment o children

may not be sufcient to reduce inec-tion i maternal levels remain high.

C w CTe current standard o care or treat-

ment o severe early childhood cariesusually necessitates general anesthesia

with all o its potential complications,because the level o cooperative behavior

o babies and preschool children is less

than ideal. Te cost o treating a child

with ECC exceeds $2,000.30 More recentdata show that costs have escalated. For

example, the estimated cost or acili-

ties and general anesthesia, excluding

dental services, or the treatment oa child with ECC at the University o

Fiure a. I g w x .

Fiure . Ex g x . T w

g -.


24/39

c d a j o u r n a l , v o l 3 1 , n 2

e b r u a r y 2 0 0 3 1 1

Iodine as an Oral Bactericidal AgentIodine is among the most potent o

bactericidal agents. Its eect is nottime-dependent; once bacterial contact

is made, its action is immediately lethal.Iodine has excellent penetrability into

dental plaques.37,38 Tese characteristics

make it an excellent agent or oral use.

Earlier studies by Gibbons and cowork-ers showed that a single two-minute

application o a 2 percent iodine/potas-

sium iodine ( I2-KI ) solution eliminated

mutans streptococci rom accessible hu-

man tooth sites or up to 13 weeks.39 In

1977, Caueld and Gibbons showed thata dental prophylaxis ollowed by three

applications o a 2 percent I2-KI solution

signicantly reduced mutans streptococcilevels in ssure and proximal-surace

plaques and saliva. Reductions persisted

or 20 to 24 weeks in proximal plaque

and saliva; ssure plaques were sig-nicantly suppressed or our weeks but

gradually returned to baseline levels in

the absence o dietary restrictions.40

Recently, the inuence o bimonthlytopical application o 10 percent povi-

done iodine was assessed in a placebo-controlled double-blind clinical trial in

preventing the development o white spotlesions on the maxillary primary incisors

o Puerto Rican babies at high risk or

developing early childhood caries.41 Te

study population consisted o 83 subjects(age 12 to 19 months, 40 emale and 43

male). Te healthy caries-ree children

were included in the study i they had

our maxillary primary incisors with novisible deects, used a nursing bottle at

naptime and/or bedtime that containeda cariogenic substrate, and had two

consecutive mutans streptococci positivecultures rom pooled maxillary primary

incisor plaque. Te subjects were random-

ized into two groups that were evalu-

ated every two months during the studyperiod. At each evaluation, the subjects

had 10 percent povidone iodine (experi-

mental group) or placebo (control group)

applied to their dentition. Te resultso this study showed that the children

children to ermentable carbohydrates,in particular sucrose, and developing sae

and eective antibacterial approachesto reducing the number o acidogenic

(acid-producing) oral bacteria in children.A variety o topical antimicrobial agents

has been tested to suppress oral popu-

lations o mutans streptococci. Tese

agents, in part, include antibiotics(vancomycin and kanamycin), stannous

uoride, the bisguanidines (alexidine and

chlorhexidine), iodine, and combinations

o these agents. Selection o an agent to

suppress oral mutans streptococci and

lactobacilli reservoirs must consider anumber o actors; saety is o particular

concern in babies and preschool chil-

dren. Utilization o stannous uorideis contraindicated in children younger

than 4 because o the potential risk o

uorosis (Clinical Guidelines, American

Academy o Pediatric Dentistry, 2000).Te bisguanidines are not recommended

or use in young children because o

lack o inormation regarding saety,

alcohol content, staining o teeth, andthe potential or disruption o taste. Te

antibiotics -- vancomycin34 and kanamy-cin35 -- have very short-term suppressive

eects on oral populations o mutansstreptococci and have not been shown

to be eective in reducing caries. One

promising approach is the u

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Journal of the California Dental Association Feb 2003

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