Parting the “Acid Curtain”

Dental blog article written April 12, 2012

New (and old) evidence indicates the body is much more active in fighting and preventing caries from within the tooth than previously believed possible.

Recent research findings indicate that the tooth is more than just a passive entity during the decay process. The “acid attack” explanation of caries has held currency for decades, with good reason …. attacks by acid do result in cavitation. But there is clearly more to the story than acid acting on a tiny spot of the tooth surface. Any excessive presence of acid(s) in the oral cavity leads to poor oral health of varying degrees. Nearly every day there is another finding that links poor oral health to body-wide systemic disease processes.

Many of the tooth’s dentinal defense mechanisms were uncovered and characterized quite some time ago by researchers at Loma Linda dental school, Ralph Steinman (DDS, MS) and John Leonora (PhD, Endocrinology), as early as the 1960s.¹ For years, their findings met with strong resistance by many wedded to the uncomplicated “Acid Curtain” theory of caries.

Today, there is renewed interest in dentinal physiology, as dental researchers are beginning to look at carious disease from the pulpal (dentinal fluid) side, instead of attributing decay to simple acidic destruction of the tooth’s surface. Another reason for renewed interest in the inner workings of dentin is the growing understanding of dentinal fluid transport. This knowledge is essential in the development of new restorative materials. The time is right to explore the architecture of dentinal tissue and its regulation.

The dominant acid-destruction paradigm that has prevailed since the 1940s for explaining enamel decay also applies to dentinal decay. This is because enamel and dentin share the same hydroxyapatite crystal hard tissue constituents (albeit in different percentages of composition with enamel having a higher crystal content than dentin). Advanced enamel destruction almost inevitably leaves the underlying dentin openly exposed to the hostile environment of the oral cavity.
Hyroxyapatite crystalline structure is composed of tightly packed molecules of calcium, phosphate, and hydroxyl ions of the formula Ca10(PO4)6(OH)2. This same structure is also found in bone.

The effect of acids on enamel’s hydroxyapatite crystalline structure is well understood, and it is characterized as demineralization at the tooth’s surface. In other words, enamel destruction is treated as a chemical event confined to the oral cavity and limited in scope to the local site of acid attack. Acid’s high proton concentration in solution reacts with the crystalline molecule’s hydroxyl and unprotonated phosphate groups and dissolves the crystalline structure.

Numerous events and stages are required in order to successfully form two sets of human teeth. Specialized cells lay down collagen matrix-like scaffolding during amelogenesis and dentinogenesis (starting at week 13 in human embryogenesis). Cells dedicated to laying down these scaffolds, known as ameloblasts and odontoblasts, respectively, form each tooth under a fascinating, elaborately orchestrated series of genetically regulated steps.

Ameloblasts lay down a collagen matrix that will shortly be mineralized to form enamel rods. Odontoblasts elaborate slightly different patterns of collagen matrices that will be mineralized as dentinal tubules. Vesicles of calcium phosphate ions are delivered to these matrices and the mineralization process is set in motion – largely as a passive chemical event driven by local differences in ion concentration and precipitation – once localized nucleating centers have been created.

Hydroxyapatite crystal can be strengthened when a native hydroxyl group is replaced with fluoride. This “improved” crystal (referred to as fluorapatite) is then less vulnerable to acid attack because it has a higher energy requirement for its dissociation. Fluoride is approximately the same size as the hydroxyl group and does not appreciably distort the crystal’s packed structure. Unlike the hydroxyl group it replaced, the fluoride atom will remain intact and the molecule undisturbed when exposed to moderate acid exposure in the mouth.

During tooth formation, while rods and tubules are being mineralized, fluoride can be incorporated into the developing tooth structure, if it is made available. For adults, incorporation of fluoride is only possible topically upon the tooth’s outer surface, since the tooth’s deepest structures were completed long ago. There is no way for an adult to gain access to deeper layers of tissue via fluoridation.

Acids of any source may demineralize the hydroxyapatite crystal of enamel and dentin, provided the pH is low enough. To be clear, we can distinguish between carious cavitation caused as a result of bacterial metabolism acid products and noncarious cavitation caused by the presence of acids not of bacterial origination. Common acids of this category include dietary sources such as soda drinks, fruit juices, and milk. An important nondietary source can be the body’s own digestive acids. When introduced into the oral cavity, stomach acid from bulimia and GERD demineralize enamel, leaving behind a characteristic pattern of cavitation and destruction in their wake.

Acids produced by bacterial metabolism are special, however, because the bacteria themselves elicit an immune response from the host. Bacteria is often in continual and intimate contact with the tooth at the lesion if plaque has been allowed to form. It is now obvious why two important dental treatment modalities involve both the physical removal of plaque as well as the introduction of fluoride treatment in order to “harden” the tooth’s remaining surface.

While having a lower hydroxyapatite content than enamel, the dentinal layer of the tooth is living tissue. Its soft tissue component within hard tissue dentinal tubules includes odontoblasts, dentinal fluid, and innervation with nonmylinated nerve fibers (as anyone who has ever had a toothache will vividly recall)!

Mechanoreceptors on these nerve endings are exquisitely sensitive to changes in dentinal fluid movements registered within the affected dentinal tubules. For example, a change in osmolarity in the oral cavity (such as the introduction of sugar) immediately induces dentinal fluid movement, activating the mechanoreceptors’ ion channels. This results in pain that is characteristic to the nature of the insult, especially in the case of heat or cold. This characteristic pain response provides important diagnostic symptoms that give the clinician insight to the severity of damage to the pulp. Or, in the case of a chronic lesion, there may be no response to either temperature extreme, usually indicating pulpal necrosis or a chronic lesion.

Through dentinal tubules, the body brings host defenses to bear on what happens to be a very small piece of real estate in the case of decay. Today it is recognized that caries are not merely a surface phenomenon of an acid attack on a passive rock in the mouth. Thanks to countless advances in molecular biology and immunology, cariology is being revisited with the body’s full host defenses and dentinal behavior in mind.

[1] Early on, Ralph Steinman (DDS, MS) and John Leonora (PhD, Endocrinology) investigated dentinal fluid transport and its physiological mechanisms at Loma Linda University School of Dentistry. During decades of collaboration, they established DFT regulation by a parotid-hypothalamic axis.

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