Biological Factors

Oral Biofilm (acquired salivary pellicle): Acquired salivary Pellicle is a layer of structureless, homogeneous biofilm formed post-eruptively, on the surface of mineralized tooth surfaces, by the selective adsorption of hydroxyapatite-reactive salivary glycoprotein.²⁷ This layer forms within minutes on the surface of a tooth surface after its removal by toothbrushing, chemical dissolution, or prophylaxis.^28-30 This biofilm has been shown to protect the tooth surface against ETW by serving as a barrier that prevents the direct contact of an acid and the tooth’s surface through its diffusion-limiting properties (semi-permeability) as well as serving as a reservoir of remineralizing electrolytes.¹⁹ Figure 3 shows a scanning electron microscopy images of 2-hour formed acquired salivary pellicle before and after 10-minute exposure to orange juice where it was able to reduce ETW by the juice.¹⁹ This ability to protect against ETW depends on its thickness and enzymatic composition.^28-30 The enzymatic composition of the pellicle also plays an important role: The presence of the enzyme carbonic anhydrase VI in the pellicle may protect against tooth erosion because it speeds the neutralization of demineralizing hydrogen ions on the tooth’s surface.³⁰

Figure 3.(A) Transmission electron microscopy image of the 2-h in situ formed pellicle on enamel surface. (B) The 2-h pellicle after 10 min of erosive challenge in situ by orange juice.

Figure 3.(A) Transmission electron microscopy image of the 2-h in situ formed pellicle on enamel surface. (B) The 2-h pellicle after 10 min of erosive challenge in situ by orange juice.

Adapted from: Lussi A. From diagnosis to therapy. Basil, Switzerland: Karger; 2006. Monographs in Oral Science Series. Vol 20.

Physiological movement of oral soft tissues: It has been demonstrated that enamel surface softened by an erosive agent may be worn by abrasion from the surrounding oral soft tissues, such as the keratinized surface of the tongue, before it can be remineralized by saliva, with consequent loss of mineralized tooth substance and manifestation of ETW.^31-33 The most severe erosive lesions are typically found in the palatal surfaces of the upper teeth (Figure 4), because of the abrasive effect of the tongue. It has been shown that the tongue is able to remove already softened enamel and dentin.^31-33

Figure 4. Example of ETW on the palatal surface of upper teeth.

Figure 4. Example of ETW on the palatal surface of upper teeth.

Tooth Position: The position of teeth determines their susceptibility to ETW because different sites in the mouth are affected by variations in salivary flow and composition. As such, facial surfaces of upper incisors have higher susceptibility to erosion because the exposure to saliva is lower (figure 5), while lingual surfaces of lower teeth have lower erosion susceptibility because the exposure to protective saliva is higher.³⁴

Figure 5. ETW on facial surface of upper incisors.

Figure 5. ETW on facial surface of upper incisors.

Tooth Structure and Composition: Differences in the structure and chemical composition between various type of enamel (human permanent and deciduous) has been shown to play role in the development and progression of ETW.³⁵ Erosive lesion progressed 1·5 more rapidly in human deciduous than in human permanent enamel.³⁵ The fluoride and the calcium phosphate concentrations in deciduous enamel are lower than in permanent enamel formed under the same condition, with a slightly higher proportion of organic matter in deciduous enamel than in permanent enamel, indicating a lower degree of mineralization in deciduous than in permanent enamel.^36-38 Furthermore, variation in chemical composition of different areas of the enamel of deciduous and permanent teeth has long been established.³⁷ These variations may determine the variation in severity of ETW among individuals, different teeth within same individual, and different areas of the same tooth.

Saliva and its properties: Saliva is the most important biological factor in the prevention of ETW.^39-42 It starts acting even before the acid attack with an increase in salivary flow in response to visual or olfactory stimuli or to chewing, increasing the buffering system and diluting and clearing acids on tooth surfaces during the erosive challenge.³⁹ The chemical composition, pH, flow Rate, buffering capacity as well as the remineralization potential of saliva varies among individuals, and determine their susceptibility to ETW.^39-42 A low salivary flow rate due to xerostomia, dehydration, use of certain medications, salivary gland pathology, or when there are no stimuli to trigger a protective salivary response (such as when a patient is suffering with GERD) means that teeth are less protected during an acid attack. A high salivary flow rate, on the other hand, has a protective effect against acid, particularly because it has the ability to clear acids from teeth surfaces.^39,42 Effect of saliva flow rate with respect to ETW is more devastating in GERD patients because of the low saliva flow rate during sleeping and in Xerostomic patients. A higher hydrogen bicarbonate content increases the capacity of saliva in neutralizing and buffering acids to protect from ETW, while a low buffering capacity is strongly associated with increased erosion. Furthermore, saliva that is supersaturated with calcium and phosphate ions is more effective at maintaining the integrity of teeth by remineralizing the hydroxyapatite in enamel, while saliva that is undersaturated with calcium and phosphate cannot replenish enamel’s mineral content.^34,39 The degree of supersaturation of hydroxyapatite, fluorapatite and calcium fluoride also increases as saliva flow is stimulated and increases. It is also important to note that sites poorly bathed by saliva or mainly bathed with mucous saliva (which typically contains fewer mineralizing ions) are more likely to show ETW when compared to sites protected by saliva that is serous in nature.^34,43