Comprehensive Notes on Dental Caries Management CH25
History of Dental Caries Management
Early 20th century approaches: placing restorations, removing diseased teeth, and providing prosthetic replacements.
1945 onward: reductions in caries incidence of 40% to 60% in the United States for communities with water fluoridation. 40\% \text{ to } 60\%
Later part of the 20th century: decline generally linked to widespread home fluoride dentifrices, mouthrinses, and professional topical applications (solutions, gels, varnishes).
Early 21st century: prevalence remained the same or increased in some US populations due to lack of access to care.
Evidence shows untreated caries in preschoolers decreased in 2011–2014, but the proportion of children/adolescents with no caries in permanent teeth has remained unchanged.
Dental caries remains a major public health problem across ages.
The Dental Caries Process
Caries is a biofilm-mediated, diet-modulated, multifactorial, noncommunicable, dynamic disease resulting in a net mineral loss of hard tissues. \text{Caries} = \Delta\text{mineral content (net)} < 0
Affects a majority of the world’s population across the life span.
Cariogenic bacteria are not present at birth and are usually transmitted from mother to child via vertical transmission.
When caries lesion occurs, strategies exist to control, reverse in early stages, and prevent progression.
Dental hygienists have current evidence-based resources to educate patients about the caries process and prevention.
The extended ecological plaque hypothesis: caries results from a shift in dental plaque toward a more cariogenic flora.
Basic caries process: acidogenic and aciduric bacteria metabolize fermentable carbohydrates, producing acids that demineralize enamel, cementum, and/or dentin, leading to mineral loss and cavity formation.
On the tooth surface, demineralization and remineralization occur in a continuous, life-long cycle.
Protocols exist to address caries prevention and management at various lesion stages; goal is to halt and control the disease process.
Interrelationship among microorganisms, tooth, salivary factors, and cariogenic foods is discussed in Chapter 33.
I. Acidogenic and Aciduric Bacteria
Acidogenic and aciduric bacteria produce acid by metabolizing fermentable carbohydrates.
When these bacteria predominate, caries risk increases.
Predominant groups include:
Mutans streptococci: Streptococcus mutans and Streptococcus sobrinus
Lactobacillus and Actinomyces and non-Actinomyces species
Bifidobacteria are associated with early childhood caries.
Mutans streptococci are infectious and colonize teeth, creating a sticky biofilm environment.
Transmission of these organisms is typically from close family members, especially the mother.
Candida albicans is sometimes detected with S. mutans in plaque samples from children with early childhood caries.
II. Role of Fermentable Carbohydrates
Common fermentable carbohydrates: sugars (sucrose, glucose, fructose) and processed starches.
Metabolism produces acids: \, ext{acetic}, lactic, formic, propionic.
Frequency and form of carbohydrate intake increase biofilm and acid production, leading to more demineralization.
III. Acid Production
Acid diffuses into diffusion channels between enamel rods or into exposed root surfaces.
Acids dissolve enamel crystals into calcium and phosphate ions.
Subsurface initial carious lesion forms and clinically appears as a white spot lesion.
IV. Demineralization
Demineralization and remineralization are natural, ongoing processes in the oral cavity.
Demineralization is mineral loss from tooth structure due to acids produced by bacteria metabolizing fermentable carbohydrates.
Repeated acid exposure can outpace remineralization, leading to cavitated lesions.
Smooth surface and pit-and-fissure caries occur when cariogenic nutrients are available.
V. Remineralization
Remineralization is the natural repair process that moves minerals back into subsurface enamel.
Saliva provides protective factors that promote remineralization.
A. Saliva: protective roles include buffering acids and clearing debris, supplying minerals (Ca and PO4) for remineralization, and maintaining a neutral/basic pH.
Low saliva flow (hyposalivation/xerostomia) reduces buffering and aids demineralization.
A neutral pH (approximately pH 7) maximizes remineralization.
After carbohydrate exposure, the pH can drop to the critical level where demineralization occurs.
Critical pH: pH_{critical} = 5.5
Topical fluoride exposure can raise salivary fluoride levels; saliva serves as a fluoride reservoir aiding remineralization.
Saliva accumulates fluoride from multiple sources: water, dentifrice, mouthrinse, and professionally applied therapies.
B. Fluoride Mechanisms of Action
Inhibits demineralization: Fluoride in biofilm and saliva can flow into enamel diffusion channels and root surfaces, forming hydrogen fluoride (HF) as the environment seeks equilibrium.
Enhances remineralization: Adequate saliva supports remineralization; fluoride shifts equilibrium to drive calcium, phosphate, and fluoride ions into the tooth surface, forming a stronger surface.
The fluorapatite bond is stronger and less acid-soluble than hydroxyapatite, improving resistance to future acid attacks:
Fluorapatite: \text{Ca}5(\text{PO}4)_3\text{F}
Hydroxyapatite: \text{Ca}{10}(\text{PO}4)6(\text{OH})2
Inhibits bacterial growth: Fluoride ions diffuse into bacterial cells and interfere with essential enzymes in the cell wall, reducing acid production.
Dental Caries Classifications
Caries classifications span noncavitated to cavitated lesions using either ADA Caries Classification System (CCS) or International Caries Classification and Management System (ICCMS).
Early diagnosis/detection of subsurface, incipient, or noncavitated lesions allows education, risk-reduction strategies, and preventive treatments to reverse lesions.
Clinically and radiographically, detection is reviewed in Chapter 16.
I. Reversible Stages of Dental Carious Lesion
ICCMS Initial Stage Caries or CCS Initial Caries Lesion: no cavitation (see Figure 25-1).
Reversible when addressed early with preventive care and remineralization strategies.
Stages Irreversible
ICCMS Moderate Stage Caries or CCS Moderate Caries Lesion: cavitation of the enamel.
ICCMS Extensive Stage Caries or CCS Advanced Caries Lesion: lesion extends into the dentin.
Caries Risk Assessment Systems
CRA is used to assess risk factors to develop individualized prevention/management plans.
CRA defines the probability of developing new caries or changes to existing lesions over a time period.
The most powerful single predictor of caries risk across ages is previous caries experience.
Ideal CRA characteristics: evidence-based, inexpensive, and easy to use in patient care.
Validation of CRA tools for long-term prevention and lesion progression is ongoing.
Risk factors are categorized as Modifiable vs Nonmodifiable.
I. ADA Caries Risk Assessment (ADA CRA)
Based on expert opinion and available evidence.
Age-based forms: 0–6 years and >6 years.
Factors:
Contributing conditions: fluoride exposure, intake of sugary foods/drinks, eligibility for government programs, dental home, family caries experience (0–6).
General health conditions: special healthcare needs, eating disorders, medication-induced xerostomia, substance abuse, chemo/radiation therapy.
Clinical conditions: radiographic caries, missing teeth due to caries, noncavitated lesions, visible plaque biofilm, interproximal restorations, exposed root surfaces, prosthetic/orthodontic appliances, salivary flow.
Risk levels: Low, Moderate, High.
II. American Academy of Pediatric Dentistry (AAPD) Caries-Risk Assessment Tool (CAT)
For infants, children, and adolescents.
Age application:
0–3 years: nondental providers
0–5 years: dental providers
Older than 6 years: dental providers
Factors:
Biologic: sugar-containing snacks/beverages, special healthcare needs, recent immigrant status, low socioeconomic status, active caries in the primary caregiver.
Protective: fluoride exposure, daily brushing, professional topical fluoride, regular dental care.
Clinical findings: decayed/missing/filled surfaces, white spots, elevated streptococci, plaque.
Risk levels: Low/High for nondental providers; Low/Moderate/High for dental providers.
III. Cariogram
A visual model showing interaction of etiologic factors to predict future risk.
History: developed in 1976; online since 1997 after validation.
Factors:
Bacteria: plaque amount and mutans streptococci count.
Diet: fermentable carbohydrates and frequency.
Susceptibility: fluoride exposure, saliva secretion, buffering capacity.
Circumstances: past caries experience and related diseases.
Output: a pie chart showing the chance to avoid new caries and the contribution of each factor to risk.
IV. Caries Management by Risk Assessment (CAMBRA)
Initiated after two consensus conferences beginning in 2003 in California; pilots in 2007 and updated in 2021.
Forms for age 0–5 years and age 6 years through adult.
For ages 6+:
Disease indicators: visible/radiographic caries, white spot lesions, new noncavitated lesions, caries restorations in last 3 years.
Biological risk factors: heavy plaque, deep pits/fissures, reduced saliva flow, exposed roots, orthodontic appliances.
Biological/environmental risk factors: frequent snacking, meds causing xerostomia, recreational drug use.
Protective factors: normal salivary flow, fluoridated water, fluoride toothpaste, fluoride varnish 2x/year, 0.05% sodium fluoride mouthrinse, prescription fluoride toothpaste, chlorhexidine use 7 days/month.
Risk levels: Low, Moderate, High, or Extreme.
V. International Caries Classification and Management System (ICCMS)
Developed by an international expert panel after evidence review.
Factors considered: medical history (drugs causing hyposalivation, head and neck radiation), sugary foods/beverages, low fluoride exposure, primary caregiver caries experience, oral hygiene, socioeconomic status, active lesions, exposed root surfaces, oral appliances, etc.
Risk levels: Low, Medium, or High.
Implementation of CRA in the Process of Care
Step 1: Identify which CRA system to implement in the clinic.
Step 2: Review medical, dental, and psychosocial history to identify caries risk factors (e.g., xerostomia from meds or health conditions; see Chapter 11).
Step 3: Complete the portion related to history, including diet assessment.
Step 4: Use radiographic and clinical examinations to assess risk factors (see Chapters 13, 15–17, 20).
Step 5: Some CRA systems require assessment of saliva and bacteria; implement as part of care.
Step 6: After assessment, use clinical judgment to identify risk level and modifiable risk factors to target in the care plan.
Planning Care for the Patient’s Caries Risk Level
The dental hygienist selects a caries management strategy tailored to the individual.
The care plan must address existing nonreversible lesions and create a framework to modify patient behaviors to prevent new lesions.
Caries lesions harbor many acidogenic/aciduric bacteria, especially mutans streptococci and lactobacilli.
Restorative materials containing fluoride are recommended where possible.
Family involvement is important since close family members can harbor cariogenic microorganisms; addressing lesions in family members reduces exposure.
Care plans are individualized based on disease risk level, patient abilities, and patient/parent goals.
Essential step: partner with the patient to set goals and plan care (refer to Chapter 24 for more detail).
General recommendations for management by risk level are summarized below; see Table 25-1 for details.
The Patient with Low Caries Risk
Primary prevention remains the top priority; address habits that might increase risk.
Provide positive feedback and education to maintain oral, periodontal, and dental health.
Review habits associated with low caries risk: good daily biofilm removal, healthy snacking, normal salivary flow, and consistent use of fluoridated toothpaste/water.
Recommend routine continuing care appointments.
The Patient with Moderate Caries Risk
Moderate risk factors: present factors that increase caries risk.
Provide positive feedback and support for protective factors (fluoride use, healthy snacking, sugar-free gum).
Use motivational interviewing to engage patient in behavior changes to reduce risk.
Collaborate to plan strategies to reduce risk factors (acidic beverages, frequent snacks, suboptimal biofilm removal).
Increase protective factors: prescription fluoride toothpaste, fluoride varnish, sealants.
Discuss caries-preventive foods (e.g., nuts, sugar-free yogurt, cheese).
Increase protective factors through hygienist-driven actions (varnish application, sealants).
Recommend an appropriate continuing care schedule.
The Patient with High and Extreme Caries Risk
High risk: active carious lesions, recent restorations for caries, or systemic factors causing severe dry mouth (extreme risk when dry mouth is present).
Interventions: improve biofilm removal; dietary counseling to reduce fermentable carbohydrate intake.
Fluoride: initial 1–3 varnish applications, then repeat every 3 months; consider diamine fluoride for early lesions to prevent progression.
Continuing Care
Continuing care appointments include:
Biofilm control assessment: use a disclosing agent and record the biofilm score; address self-care issues.
Reassess caries risk.
Clinically detect demineralization areas, assess need for sealants, evaluate margins of restorations.
Radiographs prescribed as indicated by risk level and clinical findings.
Assess patient compliance with caries management recommendations.
Determine any changes needed in the caries management protocol.