Why Do I Get Cavities and How to Prevent Them

Edited: Oct 9, 2018 - Dr. Richard Cheung

‘‘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.

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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.

Biofilm.png

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

Different foods have different levels of cariogenicity

 An example of intraoral pH cycles throughout the day

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):










Controversial methods of preventing caries:


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