Demineralization and Remineralization
While the underlying pathophysiologic process in caries
disease is infection, the outward manifestation of the disease is a defect in
enamel. This defect is an end result of a process of gradual dissolution of the
calcium and phosphate of the tooth by acid leading to softening of the enamel. The
oral cavity is a balanced ecosystem where teeth are continuously exposed to
acidic challenges from foods and the acid produced by fermenting bacteria. Acid
dissolves calcium and phosphate ions from the enamel in the process of
demineralization, allowing defects to form in the enamel. Homeostasis is
sustained when there is a balance between protective factors and pathological
factors. This balance is achieved when the net mineral loss (demineralization)
and net mineral gain (remineralization) remain in equilibrium. Protective
factors consist of exposure to fluoride, the presence of phosphate and calcium
ions in saliva, and adequate salivary flow, while pathological factors include
the presence of acidogenic bacteria, frequent ingestion of fermentable carbohydrates
and acidic foods, and decreased saliva.1
Caries is a dynamic disease that results from an imbalance between
demineralization and remineralization due to altered pH levels in the oral
cavity. As the pH in the oral cavity falls below 5.5, the protective factors
are overwhelmed by the pathological factors. This decrease in pH results in a
favorable environment for acidogenic and acid-tolerant cariogenic bacteria. (See
Figure 1 and Figure 2.)
The oral cavity is home to a wide variety of aerobic and
anaerobic bacteria, many of which produce acid as a result of their metabolism.
Saliva provides a buffering effect to neutralize the acid. Such controlled
changes in the oral environment do not necessarily combat the oral microbes
directly but instead reduce the impact of these bacteria.
When food is digested, acidogenic bacteria ferment the
carbohydrates to produce lactic acid which decreases the pH in the mouth and
results in demineralization of dental enamel. Streptococcus
mutans and Lactobacillus are both acidogenic bacteria that contribute to
dental caries. S. mutans is the major microbiological cause of decay because it
can metabolize carbohydrates at a low pH and adhere to hard dental surfaces and
plaque. Lactobacillus is not as able to colonize into biofilm, making it less virulent
than S. mutans. S. mutans and other pathogens may be passed from mother to
When patients consume a diet high in acid or simple sugars,
fermentable carbohydrates become readily available to acidogenic bacteria. 3
Individuals with poor saliva production (xerostomia) also are at increased risk
of caries because they lack the buffering effect of saliva. Xerostomia is often
seen in cancer therapy, autoimmune systemic diseases such as Sjögren's
syndrome, lupus, and scleroderma, systemic diseases including diabetes, Crohn's
disease, and HIV/AIDS, and the use of certain medications such as
antihistamines, antidepressants, and some antihypertensives. With decreased
flow of saliva, the acid produced by fermenting bacteria is allowed to remain
in contact with the enamel, leaching the calcium and phosphate ions and
softening the enamel.
Healthy salivary flow provides cleansing and buffering, effectively
diluting and neutralizing the acids produced by bacteria. Saliva forms a
protective layer on the tooth in the form of an enamel pellicle, replenishes
the demineralized tooth surface with calcium and phosphate ions, provides a
hostile environment for bacteria, and buffers acids. Continuous salivary flow
clears unattached microorganisms and limits pathogenic bacteria from attaching
to the tooth surface. Higher volumes of saliva lead to more frequent
swallowing, reducing the length of time of acid exposure. Saliva also provides
additional antimicrobial proteins such as lysozyme, lactoperoxidase,
lactoferrin, and antimicrobial peptides.
Saliva is essential to remineralizing demineralized tooth
surfaces. The formation of the enamel pellicle retards the loss of minerals
from the tooth surface and acts as a protective layer against the tooth surface
while also serving as a reservoir for calcium and phosphate. The availability
of calcium and phosphate ions is an important component in promoting
remineralization and protecting teeth against demineralization.
Remineralization of the enamel occurs when calcium and phosphate ions from
saliva are reintegrated with the hydroxyapatite of the enamel.
Remineralization can be accomplished in several ways,
including targeting the pathogenic factor (acidogenic bacteria) and modifying
key environmental factors, such as diet, salivary flow, and mineral ion
availability. Comprehensive caries prevention strategies involve not only
removal of damaged enamel but also treatment of infection and restoration of
healthy saliva.1 In order to
achieve this, antimicrobial treatments may be required in addition to other remineralization
Fluoride controls the rate at which caries develop. When
fluoride ions are present in plaque fluid along with dissolved hydroxyapatite,
and the pH is higher than 4.5, a fluorapatite-like remineralized veneer is
formed over the remaining surface of the enamel. This veneer is much more
acid-resistant than the original hydroxyapatite, and is formed more quickly
than ordinary remineralized enamel would be. Topical application is the most
common delivery method, and the 2014 American Dental Association guidelines
recommend applying topical fluoride, consuming fluoridated water, and using
over-the-counter fluoride toothpastes for all individuals, regardless of their
caries risk. 4-7
Chlorhexidine is effective in reducing the number of S.
mutans and other acidogenic and cariogenic bacteria in the mouth, but the
number of pathogenic bacteria often returns to pretreatment levels within
months of discontinuing chlorhexidine use. Also, reducing the number of S.
mutans does not always reduce caries risk because there are many other
contributing factors, such as xerostomia, diet, and poor oral self-care.
Chlorhexidine varnish may exert a longer effect on acidogenic bacteria, but
this product is not currently available in the United States. For some patients,
chlorhexidine mouth rinse is an effective adjunct to other anticaries
The amount of acid produced by bacteria in the oral cavity
can be greatly reduced by replacing sugar with sweeteners such as xylitol,
reducing consumption of acidic foods, and drinking more water. Xylitol is a
natural sweetener that is safe and noncariogenic because it is unable to be
fermented by bacteria.
Strategies that provide symptomatic relief of xerostomia, as
well as therapies to stimulate salivary flow, should be recommended for
patients with reduced saliva flow. Artificial saliva products, oral lubricants,
and xylitol gum may provide relief from symptoms. Secretagogues, including
pilocarpine and cevimeline, stimulate salivary flow and may be helpful for
individuals with dry mouth. To encourage remineralization, calcium
phosphate-based systems such as amorphous calcium phosphate (ACP), casein
phosphopeptide-ACP (Recaldent®), calcium sodium phosphosilicate (NovaMin®), and
tricalcium phosphate can be implemented to incorporate the ions into the enamel
These systems can be effective when a patient's saliva does not contain enough
calcium and phosphate to provide adequate levels of the ions for calcium
hydroxyapatite to form in the demineralized enamel.
From a public health standpoint, much work has been done in
developing outreach programs for delivery of fluoride toothpastes, dentifrices,
and varnishes to preschool and school-age children, the elderly, and
Mobile dental clinics have been able to reach inner city impoverished
populations and rural communities with poor access to care.11 Through these
efforts, dental hygienists have been able to identify early caries disease and
treat evidence of demineralization.
Advocates of minimal intervention dentistry have
investigated simply sealing early and incipient caries lesions with epoxy
rather than removing damaged enamel. The effect is to protect the vulnerable
softened enamel from oral acids and bacterial invasion. While
sealed, the enamel remineralizes. Results have been positive, with very few
failures in carefully selected patients. 12-15
Studies have evaluated the use of silver diamine fluoride
for preventing and arresting early caries lesions, finding significantly higher
levels of fluoride in biofilm without significant changes in caries rate
relative to fluoride pastes.16 Another product, 45S5
bioglass paste, was studied in comparison with fluoride treatment and produced
significantly greater improvements in microhardness of enamel.17
Topical application of antimicrobials helps control bacterial invasion of
vulnerable tooth surfaces and may allow remineralization to occur.18,19
The delicate balance
of the oral ecosystem is constantly challenged by internal and external
factors. Even in a healthy oral cavity, demineralization occurs due to tooth
enamel's porous structure and its susceptibility in a low pH environment.
Clinicians with an understanding of the demineralization process and available
approaches to encourage remineralization will be better prepared to treat
lesions before the cavitation of tooth structure progresses. Accurately
assessing an individual's caries risk and implementing preventive measures comprise
a conservative approach to caries prevention.References
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