6 Dental Caries and Periodontal Conditions
Chronic infectious diseases of the oral cavity include dental caries and periodontal diseases. Dental caries causes destruction of the teeth, while periodontal disease is a group of inflammatory conditions that affect the supporting structures of the dentition. The role of the microbial challenge in the initiation and progression of these oral diseases is well established, ultimately leading to the destruction of teeth and/or periodontal structures. This chapter will discuss factors contributing to the diagnosis of dental caries and periodontal diseases.
6.1 Dental caries
Dental caries is a chronic, microbial disease caused by shifts from protective factors favoring tooth remineralization, such as good oral hygiene and fluoride exposure, to destructive factors leading to demineralization, such as plaque formation, frequent ingestion of foods with high carbohydrate contents, and salivary hypofunction. Carious lesions are in a dynamic state of demineralization and remineralization, with fluoride playing an important role in enhancing the remineralization process. Caries results from complex interactions among the tooth structure, the dental biofilm, and dietary, salivary, and genetic influences. Streptococcus mutans has been implicated in the etiology of dental caries to cause disease when extracellular polymer formation promotes bacterial attachment and the pH decreases to create a caries-promoting environment. Although S. mutans is one of the most researched cariogenic microorganisms, it is only one of more than 500 species found in dental plaque, supporting the hypothesis that S. mutans is one of many endogenous microorganisms involved in the complex biofilm that leads to caries activity.
The overall prevalence of dental caries has been declining in the past 40 years, primarily because of increased use of fluoride and more emphasis on oral hygiene, as well as disease prevention and control. Nevertheless, dental caries continues to be a major public health problem, particularly among certain segments of the U.S. population. People of lower socioeconomic status, in particular those who are minorities, homeless, migrants, and children with disabilities, have the highest prevalence and severity of dental caries.
|Caries disease indicators|
|Clinical||Cavitations into dentin on clinical or radiographic examination|
|White spots on smooth enamel surfaces|
|Restorations placed in the last 3 years due to caries activity|
|Radiographic||Radiographic enamel interproximal lesions|
|Caries Risk Factors|
|Clinical||Deep pits and fissures|
|Behavioral||Visible heavy plaque on teeth|
|Frequent (>3× daily) snacking between meals|
|Diet high in fermentable carbohydrates|
|Recreational drug use|
|Salivary†||Salivary hypofunction (< 1 mg/mL unstimulated)|
|Saliva-reducing factors (medications/radiation/systemic)|
|Microbiological||Medium or high Mutans streptococci and Lactobacillus species bacteria counts by culture|
|Caries Protective Factors|
|Sealants||Sealants present on permanent molar teeth|
|Fluoride||Lives/works/school in a fluoridated community|
|Fluoride toothpaste at least once daily|
|Topical supplements||Fluoride mouth rinse (0.05% NaF) daily|
|5,000 ppm F fluoride toothpaste daily|
|Fluoride varnish in last 6–12 months‡|
|Office fluoride topical in last 6–12 months‡|
|Calcium and phosphate supplement paste daily during the last 6–12 months‡|
|Antimicrobial agents||Chlorhexidine prescribed/used daily for 1 week in the last 6–12 months‡|
|Xylitol gum/lozenges 4 times daily in the last 6–12 months‡|
|Salivary||Adequate saliva flow (≥ 1 mL/min unstimulated)|
*Modified from Dental Clinics of North America, 54(3), Young DA and Featherstone JDB, Implementing caries risk assessment and clinical interventions, pgs. 495–505, 2010 with permission from Elsevier.
†See chapter 8.
‡Based on routine annual or semi-annual dental visits.
6.1.1 Caries risk assessment
Caries risk assessment (CRA) determines an individual’s probability of developing new carious lesions during a specific period of time and the probability of a change in the size or activity of existing lesions over time. This assessment is useful in evaluating the effectiveness of attempts to control caries (e.g., sealants), whether additional diagnostic (e.g., salivary flow rate, diet analysis) and/or caries-control measures (e.g., plaque control, diet control, increased fluoride exposure, antimicrobial agents) are warranted, suitability of treatment plans, and frequency of dental recall appointments.
By assessing patient information, a clinician may be able to predict the risk of future demineralization by weighing all the disease indicators and risk factors against existing protective factors (Table 6.1). Caries disease indicators are clinical observations that indicate current caries disease or a history of caries disease. A positive disease indicator automatically places the patient at caries risk. Caries risk factors are biologic and behavioral factors thatcontribute to the level of risk for the patient of having new caries lesions in the future or having existing lesions progress. Caries protective factors are biologic and therapeutic factors that may collectively offset the pathologic challenge presented by caries risk factors. With more extensive and severe caries risk factors, the intensity of protective factors must be increased at an appropriate level to minimize the caries process. While there are numerous CRAs available in the literature that similarly measure etiologic and protective factors involved in the disease process, taken together they indicate that past caries experience is the strongest predictor of future caries disease. Examples of CRA tools have been developed and are available through the American Dental Association and American Academy of Pediatric Dentistry.
188.8.131.52 Caries risk groups
Implementation of a CRA in clinical practice can be accomplished in a single visit by assessing the CRA components and categorizing a patient as “low,” “moderate,” or “high” caries risk based upon the prediction of new caries development in the next 1–2 years. Low-risk patients have no active caries, have been caries-free for at least 5 years and have negligible risk factors indicating a very low risk of future dental caries disease. Patients at high risk for caries have active caries status (development of at least one new carious lesion or progression of an existing lesion in the previous 1–2 years), exhibit high-risk behaviors such as frequent ingestion of foods with high carbohydrate contents and poor oral hygiene, and may have additional risk factors such as low to no fluoride exposure and/or salivary hypofunction. Moderate-risk patients have a moderate likelihood of new caries development due to a recent history of caries activity and the presence of risk behaviors and additional risk factors.
Caries management by risk assessment (CAMBRA) is a clinically based approach to preventing, reversing, and, when necessary, repairing early damage to teeth. Clinical intervention protocols vary based upon the caries risk and should be individualized based upon a patient’s risk factors and behaviors. Interventions may involve the frequency of bitewing radiographs, frequency of caries recall examinations, choice of restorative materials, and use of salivary tests (flow rate and bacterial culture), antimicrobials (xylitol, a naturally occurring sugar alcohol that maintains the oral pH at 7.0 and inhibits S. mutans attachment in the oral environment), fluoride, pH control agents (acid-neutralizing rinses, baking soda gum), calcium phosphate topical supplements, and dental sealants.
184.108.40.206 Plaque biofilms
The plaque biofilm is one contributor to the complex caries process, and only biofilm-covered tooth surfaces have the potential to develop carious lesions. Within moments of erupting or being cleaned, tooth surfaces become coated with a protective barrier of molecules (proteins and glycoproteins) derived mainly from saliva, termed the acquired pellicle. Bacterial colonizers bind to the acquired pellicle via adhesins and multiply, and as the plaque biofilm develops, the attached bacteria produce extracellular polymers (the plaque matrix) that further consolidate attachment of the biofilm. The microbial composition of the biofilm varies at distinct sites on a tooth and reflects the inherent differences in the anatomy of the tooth and biology of the biofilm. Once established, the composition of the microflora remains stable over time unless there are marked changes to the oral environment. Importantly, the dental plaque bacteria interact and display increased tolerance to both host defenses as well as antimicrobial agents.
Dental caries has a strong association with the frequency of fermentable carbohydrate intake. Sticky complex carbohydrates that can remain in the grooves of teeth and simple sugars, particularly sucrose, are very cariogenic. These fermentable carbohydrates are freely diffusible in dental plaque and readily metabolized by oral bacteria, leading to the production of organic acids (e.g., lactic acid) in sufficient concentration to lower the pH of dental plaque enough to allow enamel demineralization to occur. Further, sucrose is involved in the bacterial synthesis of extracellular polysaccharides that can favor the further accumulation of S. mutans and other cariogenic bacteria in the dental biofilm. Therefore, reducing the amount and frequency of fermentable carbohydrate consumption is important for people at a high risk of experiencing caries.
220.127.116.11 Salivary function and buffering capacity
It is well established that saliva contains numerous protective factors that play a role in maintaining the health of the hard and soft tissues of the oral cavity. Higher salivary flow allows for increased availability of organic and inorganic constituents of saliva, including antimicrobial enzymes and secretory IgA as well as calcium and phosphate ions that maintain the integrity of teeth by regulating the demineralization/remineralization processes. Further, salivary buffering capacity plays a major role in maintaining the oral cavity at a neutral pH, which is optimal for maintaining oral health.
An objective finding of salivary hypofunction (see chapter 8) is a strong indicator of increased caries risk and is an important factor in caries risk assessment, while decreased buffering capacity has a weak but positive association with caries activity. Salivary buffering capacity can be evaluated with chairside commercial kits that assess the bicarbonate buffer system. Dentobuff Strip (Orion Diagnostica, Espoo, Finland) and Saliva-Check Buffer (GC America, Alsip, IL) utilize a few drops of saliva on a test strip and categorize saliva as having poor, intermediate, or normal buffer capacity (see chapter 8). Guidelines regarding the evaluation of salivary buffering capacity in caries risk assessment have not been developed, and the utility of this test remains unclear.
18.104.22.168 Microbial tests
Quantification of S. mutans and lactobacilli in saliva may be utilized to assess caries risk. The theoretical principle behind this test is that high levels of S. mutans indicate a cariogenic environment and are associated with an increased caries risk, while high lactobacilli counts suggest a high content and frequency of intake of carbohydrates in the diet.
Commercial kits for mutans streptococci and lactobacilli quantification (CRT bacteria, Ivoclar Vivadent, Amherst, NY; Dentocult SM Strip Mutans and Dentocult LB, Orion Diagnostica, Espoo, Finland; Saliva-Check Mutans, GC America, Alsip, IL) can be performed chairside utilizing saliva or plaque samples (dependent upon the specific kit instructions) on test strips that undergo selective adherence and growth of bacteria. The density of colony growth is evaluated and scored in categories from no detectable growth to high counts (greater than 5–10 × 106 colony-forming units). Guidelines regarding microbial quantification in caries risk assessment have not been developed, and the utility of this test remains unclear.
6.1.2 Diagnosis of dental caries
Historically, caries was thought to be a progressive disease that eventually destroyed the tooth unless surgical intervention was performed. However, the understanding of the caries process has undergone a paradigm shift. In 2001, a National Institutes of Health Consensus Statement recommended improved diagnosis of non-cavitated, incipient lesions and non-surgical treatment for prevention and arrest of such lesions. Based on this approach, diagnosis of caries involves establishing the presence or absence of cavitation (caries lesion detection) as well as assessing whether or not a lesion is active (lesion activity assessment). An active carious lesion progresses over time and requires management (remineralization or restoration), while an inactive lesion may be visible either clinically or radiologically but does not progress or change over time. The combination of lesion detection plus activity assessment is necessary to arrive at the disease diagnosis and the appropriate clinical treatment decisions.
Reprinted from Dental Clinics of North America, 54(3), Braga MM, Mendes FM, and Ekstrand KR, Detection activity assessment and diagnosis of dental caries lesions, pgs. 479–493, 2010 with permission from Elsevier.
|0||No or slight change in enamel translucency after prolonged air drying (5 seconds)|
|1||First visual change in enamel (seen only after prolonged air drying or restricted to within the confines of a pit or fissure)|
|2||Distinct visual change in enamel|
|3||Localized enamel breakdown in opaque or discolored enamel (without visual signs of dentin involvement)|
|4||Underlying dark shadow from dentin|
|5||Distinct cavity with visible dentin|
|6||Extensive distinct cavity with visible dentin (involving more than half of the surface)|
*Original table created from data in Ismail AI, Sohn W, Tellez M, Amaya A, Sen A, Hasson H, et al. The International Caries Detection and Assessment System (ICDAS): />