Why Do I Get Cavities and How to Prevent Them
Edited: Oct 9, 2018 - Dr. C
‘‘It is somewhat disturbing to the biologically orientated clinical teacher to witness the overly focused attention of some dentists upon the operative and restorative phases of dentistry, the ‘drilling and filling’ of teeth, to the neglect of the disease process which caused the lesion (cariology) and the preoperative treatment of the wounded tooth–bone.’’
- Dr. Maury Massler, 1967
When you visit the dentist for a check-up, you’re likely to have a discussion about cavities (aka dental caries). You’re likely familiar with getting fillings placed in your mouth. You brush and floss diligently, but on your next checkup, you are told that you have more cavities and need another filling. You think: “How could that be?! Is it something I’m doing wrong? Is the dentist pulling a quick one on me? This article is for the individual who wants to verify the claim that he/she has cavities, and further understand what could be done to prevent them.
Just how common are cavities?
The WHO (World Health Organization) reports that dental caries (cavities) are still a major health problem in most industrialized countries, in which 60–90% of children and the vast majority of adults are affected. Untreated caries in permanent teeth was the most prevalent condition evaluated across all medical conditions, with a global prevalence of 35% for all ages combined, with 2.4 billion people affected - see Global burden of oral conditions in 1990-2010: a systematic analysis.
Problems with the old paradigm
Traditional management of caries was primarily focused on operative treatment. This often started an irreversible, restorative cycle, leading to several replacements over time with increasing restoration size, and every so often iatrogenic damage. Placing restorations has no statistically significant effect on mean bacterial levels in the whole mouth, either initially or over a 2-year follow-up period after the restorative work was complete.
Over time, there has been a shift in treatment protocols regarding dental caries, led by increasing insight about the process of caries development and its causal and continual factors. Prevention is more important than operative intervention for the successful long-term management of dental caries.
What causes caries?
It’s worth emphasizing that dental caries is a microbial disease. The mouth, like other surfaces of the body, is colonized from birth by a diverse array of microorganisms. The resident oral microorganisms benefit from a warm and nutritious habitat. In return, the microoganisms act to repel invading microorganisms and contribute to the host’s defences. The oral microbiota which grows on teeth is termed “dental plaque.” Dental plaque is an example of a biofilm.
The normally synergistic relationship between the resident microbiota and the host is dynamic and can be perturbed by changes in lifestyle or alterations to the biology of the mouth - these changes can predispose sites to disease. The regular exposure of plaque to fermentable dietary sugars results in repeated conditions of low pH in the biofilms that favour the growth and metabolism of acid-tolerating bacteria while inhibiting beneficial organisms that preferentially grow at neutral pH. Dental caries is a consequence of net low-pH metabolic activity of the biofilm.
Thus, dental caries is not an example of a classic infectious disease, but is a consequence of an ecological shift in the balance of the normally beneficial oral microbiota, driven by a change in lifestyle and in the oral environment. Perhaps dental caries can be described best as a biofilm-mediated disease that can be mostly ascribed to behaviours involving frequent ingestion of fermentable carbohydrate (sugars such as glucose, fructose, sucrose and maltose) and poor oral hygiene in combination with inadequate fluoride exposure.
Cyclical periods of hurting and healing
I mentioned that the metabolic activity of dental plaque is a dynamic and always-changing. As the mouth is exposed to low and high pH levels, teeth subsequently undergo many cycles of demineralisation and remineralisation. The core strategy for stopping cavities is to have longer cycles of remineralisation than demineralisation. The approximate pH level at which demineralisation will occur in enamel is pH < 5.5 (pH < 6.2 - 6.7 for cementum and dentin).
Demineralisation (low pH): occurs under acidic conditions by the loss of calcium, phosphate and hydroxyl ions that react with the hydrogen ions being produced by the metabolic activity of the covering biofilms in the presence of fermentable carbohydrates. Minerals are released from multiple sources: saliva, bacteria, calculus, calcium-fluoride formations, and the tooth surface itself.
Remineralisation (high pH): When enough minerals (mainly calcium, phosphate, and hydroxyl ions) are available, minerals can remineralise partially demineralised enamel crystals. Although pH is the strongest determinant leading to demineralisation or remineralisation, it is not the only important factor because remineralisation is significantly affected by other factors such as the available concentration of calcium and phosphate ions.
Different foods have different levels of cariogenicity
An example of intraoral pH cycles throughout the day
The crucial role of fluoride
Dental enamel is composed mostly of mineral in the form of hydroxyapatite (HAp), chemically represented by Ca10(PO4)2(OH)2. There are mineral composition differences which determine the stability of the crystals forming the structure of enamel, subsequently affecting its solubility. In theory, if one could decrease the acid solubility of enamel, this would decrease the caries susceptibility of a tooth. The more stable the crystals, the less soluble they will be. Fluorapatite (substitution of OH– by F– ions) is a highly stable crystalline form, even more than hydroxyapatite.
Now that we know the basics of cariology, we can now develop strategies to prevent the formation of dental caries.
To prevent cavities (encourage remineralisation):
Reduce FREQUENCY of fermentable carbohydrate intake (glucose, fructose, galactose, sucrose, lactose, maltose)
from an etiology basis, diet still remains the main driver of the caries process
Complex carbohydrates (starches) are considered less cariogenic (potential to cause caries) because starches are not readily soluble in oral fluids and have a low diffusion rate in biofilm
Simple sugars (sucrose, glucose, fructose) are more cariogenic, with sucrose being possibly the most; therefore, it has been implicated as an important determinant of dental caries disease
Cheese and peanuts can reduce the acid production after a previous intake of sucrose-containing foods
Soda, coffee with sugar, and energy drinks are extremely cariogenic
Use a Risk Assessment Form to evaluate your sugar intake
Use a fluoridated toothpaste
The caries-preventive effect of regular use is typically 20% to 40% over 2 to 3 years
If you’re in a high risk group, consider NOT rinsing out excess toothpaste after brushing.
How much fluoride to use?
High caries risk individuals aged 10+ years may use toothpaste containing 2800 ppm F
High caries risk individuals aged 16+ years may use toothpaste containing 5000 ppm F
Another therapeutic use of toothpaste is to apply the paste locally (with finger or brush) directly onto the cleaned active caries lesion before going to bed (taking advantage of the decreased salivary secretion at night)
Frequently disrupt the plaque (good oral hygiene)
Brush twice daily
Brush just before going to bed, and one other time during the day after mealtime (preferably breakfast or lunch)
Brushing twice a day provides a further 14% caries reduction compared with once a day
Floss daily
Lack of definitive evidence to support flossing, but removing plaque that accumulates between teeth is uncontroversial
Increase salivary flow
Saliva plays a major role in protecting the teeth
Chew 2 pieces of sugar-free gum for >5 min, 3 times a day (after each meal preferred) to stimulate salivary production
Clinical trials of xylitol in chewing gum have been conducted, Turku chewing-gum study, the Ylivieska study, the Montreal study, and the Belize study. All these studies have shown that the use of xylitol helps in the prevention of dental caries
Use a fluoridated mouthrinse
Fluoride rinses reduce caries in the permanent dentition by 26%
May be indicated particularly for orthodontic patients and special needs patients with poor dexterity
Should be used daily and at a different time from brushing in order to maintain the concentration of fluoride in plaque throughout the day
Rinses are produced in two formulations; 0.05% for daily application and 0.2% for weekly application
Professional fluoride applications
Low-risk individuals may not receive additional benefits from professionally applied topical fluoride application
Chemical Therapy
Daily antimicrobial therapy of 0.12% w/v chlorhexidine gluconate (CHX) mouth rinse can be used to reduce the bacterial challenge and modify the biofilm
has been shown to reduce the caries increment by about 20% to 38% in high-caries-risk adult patients
Used in conjunction with high-concentration fluoride products
However, it is recommended to separate the application of an anionic product such as fluoride and a cationic product like CHX by at least a few hours to avoid binding of the active ingredients
The Case for Sealants
Sealants protect the underlying tooth surface by blocking renewed and continuous attacks by plaque acids, and prevent plaque accumulation and dissolution of minerals from the tooth tissues
When caries risk is moderate to high, teeth with caries-susceptible pits and fissures will greatly benefit from sealing
Sealed noncavitated lesions consistently had better outcomes than unsealed lesions, while the percentage of sealed carious surfaces that progressed was low
Sealing of cavitated lesions significantly reduced bacteria levels (50% to 99% of mean bacteria counts), and this effect increased with time
Controversial methods of preventing caries:
Fluoride tablets and drops
Consequently, their use in many countries is not recommended, although they still have a place in preventive care for high caries risk and medically compromised individuals
Calcium-Based Strategies
Supplementing calcium and phosphates is likely to have a positive effect, in particular when effective fluoride levels are available at the same time
Inhibition of enamel and dentin demineralization, promotion of remineralization, and a slow-down of the caries process as well as regression of subsurface lesions have been reported for casein phosphopeptide– amorphous calcium phosphate (CCP-ACP)
Although a remineralizing effect is reported for chewing gum and mints with CPP-ACP, solid evidence to support clinical efficacy for specific delivery modes remains lacking
Although persuasive scientific evidence from randomized clinical trials (RCTs) is not yet available,48 the off-label use of CPP-ACP technology may hold potential as an adjunct to fluoride treatment in the noninvasive management of early caries lesions
Calcium sodium phosphosilicate bioactive glass is another new agent that reacts with an aqueous environment and releases calcium and phosphate ions
Used as a desensitizer and approved as hypersensitivity agent
Off-label use as remineralizing agent is promoted, but simultaneous delivery of the right amounts of calcium, phosphate, and fluoride ions at the same time and location might be problematic and cause undesired adverse effects (eg, rapid precipitation).
More research is needed to provide scientific evidence supporting claims of caries prevention and remineralization
Second-generation ACPs and multimodal approaches are being developed to prevent caries
These include new compounds with antimicrobial and remineralization potential
These strategies, however, are only recently available, too recent to be supported by solid evidence of their anticaries efficacy
The level of evidence for calcium-based strategies reported in the literature remains incomplete and insufficient to substantiate claims by manufacturers or researchers
Laser ablation technology
Lasers have been used to coalesce enamel fissures and to provide greater caries resistance to the outer enamel surface
No evidence of anticaries efficacy in controlled clinical studies has been reported so far. Laser treatments for caries inhibition are still considered experimental and cannot be recommended
How to assess your level of caries risk
The strategy you use to prevent cavities should be custom-tailored for you, recognising that individuals have different risk profiles. A low-risk individual will have a different regimen compared to a high-risk individual.
A system such Caries Management by Risk Assessment (CAMBRA®) has been developed in California with the aforementioned goal in mind. The process should resemble the following:
1. Take your complete dental and medical history
2. Conduct comprehensive clinical examination
3. Detect caries lesions early enough to reverse or prevent progression.
4. Assess the caries risk as low, high, moderate, or extreme using data from 1, 2, and 3 and a short questionnaire
5. Produce a treatment plan that includes chemical therapy appropriate to the caries risk level
6. Use chemical therapy that includes fluoride and/or antibacterial agents based on risk level
7. Use minimally invasive restorative procedures to conserve tooth structure and function
8. Recall and review at intervals appropriate to the caries risk status
9. Reassess caries risk level at recall and modify the treatment plan as necessary
If you’re coming back to me with increased caries, I’m not doing my job well as the dental professional in charge of your oral health. - Dr. Richard Cheung