Healing tooth decay; what a novel idea! Aren’t oral health care providers already doing this? Isn’t the placement of a restoration healing dental caries? Not really. Restoring the effects of tooth decay by restoring a tooth is not really “healing” the tooth. It is treating the after effects of the disease. Healing is defined as curing, helping to heal or growing back sound tissue. One could argue that dental restorations do restore tissue but are we really healing dental caries or could we possibly heal caries by actually re-crystallizing or remineralizing the damaged enamel surface? The answer is yes, we are already doing this but there are new techniques and approaches that can help us.
The key is to find the right system to monitor tooth decay or dental caries and then the right combination of preventive or remineralization products to actually stabilize or re-crystalize early areas of tooth decay.
The Canary System is the only system on market that can monitor changes in the tooth crystal structure. It can become the anchor in a dental preventive program to monitor therapeutic outcomes.
Lots more information to share in the next few blogs.
Dental caries or tooth decay is a disease that results in the destruction of tooth structure. It arises from an overgrowth of specific bacteria that can metabolize fermentable carbohydrates and generate acids as waste products of their metabolism. Streptococci mutans and Lactobacillus are the two principal species of bacteria involved in dental caries and are found in the plaque biofilm on the tooth surface [i] [ii] [iii]. When these bacteria produce acids, the acids diffuse into tooth enamel, cementum or dentin and dissolve or partially dissolve the mineral from crystals below the surface of the tooth. If the mineral dissolution is not halted or reversed, the early subsurface lesion becomes a “cavity”.
The tooth surface undergoes demineralization (breakdown) and remineralization continuously, with some reversibility. When exposed to acids, the hydroxyapatite crystals dissolve to release calcium and phosphate into the solution between the crystals. These ions diffuse out of the tooth leading to the formation of the initial carious lesion. The reversal of this process is remineralization. Remineralization will occur if the acid in the plaque is buffered by saliva, allowing calcium and phosphate present primarily in saliva to flow back into the tooth and form new mineral on the partially dissolved subsurface crystal remnants[iv]. The new “veneer” on the surface of the crystal is much more resistant to subsequent acid attack, especially if it is formed in the presence of sufficient fluoride. The balance between demineralization and remineralization is determined by a number of factors. Featherstone describes this as the “Caries Balance”, or the balance between protective and pathological factors [v].
These early lesions (both enamel and root surface) typically have an intact hard outer surface with subsurface demineralization. The tooth surface remains intact because remineralization occurs preferentially at the surface due to increased levels of calcium and phosphate ions. The clinical characteristics of these early carious lesions include:
- Loss of normal translucency of the enamel resulting in a chalky white appearance particularly when dehydrated,
- Fragile surface layer susceptible to damage from probing, particularly in the pits and fissures,
- Increased porosity, particularly of the subsurface, with increased potential for uptake of stain,
- Reduced density of the subsurface, which may be detectable radiographically (depending upon mineral loss and location) or with transillumination (depending upon location and loss of mineral),
- Potential for remineralization with increased resistance to further acid challenge particularly with the use of enhanced remineralization treatments[viii].
In summary, bacteria consume sugars and produce acids which then breakdown the tooth surface. In the early stages of this disease, the lesions may be remineralized or re-crystalized depending upon the conditions on the tooth surface and in the mouth. These early lesions may appear as chalky white spots. They may be fragile and crystal structure may be disrupted or destroyed if they are picked or probed. This dynamic disease process can be reversed or stabilized if detected early.
More to follow.
[i] Van Houte, J., “Bacterial specificity in the etiology of dental caries”, Int. Dent. J., 1980; 30: 305 – 326
[ii] Van Houte, J., “Role of Microorganism in the caries etiology”, J. Dent. Res., 1994; 73: 672- 681
[iii] Featherstone, J. D. B., “The Caries Balance: Contributing Factors and Early Detection”, CDA Journal, 2003; 13 (2): 129 – 133
[iv] Melberg, J. R., “Remineralization: A status report for the American Journal of Dentistry, Part 1, Am J. Dent., 1988; 1 (1): 39 – 43
[v] Featherstone, J. D. B., “The Science and Practice of Caries Prevention”, JADA, 2000; 131: 887 – 899
[viii] Mount, G. J., “Defining, Classifying, and Placing Incipient Caries Lesions in Perspective”, Dent Clin N. Am, 2005, Volume 49, pages 701 – 723
Dental caries or tooth decay, according to the United States Surgeon General report on Oral Health in America, is one of the most common chronic diseases among five to seventeen year olds[i]. In their study, it was more common than asthma, hay fever or chronic bronchitis. Although we do not have this type of data available in Canada, one can assume that dental caries is extremely prevalent in the population. A great deal of a general dental practitioner’s time is spent treating dental caries. The dental profession’s understanding of caries and treatment approach has been evolving as new diagnostic devices and preventive techniques are introduced to our practices. In 2001, the National Institute of Health’s (NIH) Consensus Conference on the Diagnosis and Management of Dental Caries throughout Life concluded:
“Dental caries is an infectious, communicable disease resulting in destruction of tooth structure by acid-forming bacteria found in dental plaque, an intraoral biofilm, in the presence of sugar. The infection results in the loss of tooth minerals that begins with the outer surface of the tooth and can progress through the dentin to the pulp, ultimately compromising the vitality of the tooth.”[ii]
This statement combines a number of new components from the traditional approach taught over the last twenty years in dental schools. Our patients assume that tooth decay is caused by eating sugary foods, not that dental caries is an infectious communicable disease caused by acid forming bacteria. One can place a number of restorations in a mouth, without treating the underlying disease. The bacteria remain in the plaque biofilm on the remainder of the teeth capable of creating new areas of decalcification and cavitation. Patients are beginning to expect that we can treat this disease or at least provide them with a reason as to why they or their children continue to develop carious lesions.
Over the next few blogs, I hope to provide you with some information on tooth decay, methods for detection and things patients and dentists can do to prevent decay or minimize the destruction of the tooth.
[i] Department of Health and Human Services, “Oral Health in America: A Report of the Surgeon General”, National Institute of Dental and Craniofacial Research, 2000, page 63
[ii] “NIH Consensus Development Conference on Diagnosis and Management of Dental Caries Throughout Life March 26 – 28 2001”, Journal of Dental Education, Volume 65, # 10, 2001, page 1162
Welcome to The Canary System blog. This blog is designed to provide the reader with some pertinent information on tooth decay or dental caries and how both you and your oral health care provider can treat this very common disease. Yes, tooth decay is a disease and it can be treated in a number of ways ranging from the placement of a filling when the hole or lesion is large to actually trying to stabilize or remineralize a small early lesion. All this depends upon detecting the tooth decay and developing a treatment approach tailored to the size of the lesion, the existing oral environment and the patient’s diet. Lets explore together.