Etiology and Prevention of Acid Erosion

David Bartlett, BDS, PhD, MRD, FDS, RCS

The definitions of the components of tooth wear are recognized internationally.¹ Erosion is the loss of enamel and dentin caused by the action of acids unrelated to bacterial action; attrition is the loss of tooth structure caused by tooth-to-tooth contact; and abrasion is the loss of tooth structure caused by physical wear other than teeth. However, interpretations differ regarding how important each component is when analyzing a patient’s pattern of wear.² Traditionally in Europe, the impact of acid erosion has been recognized as probably being the most important component.³ However, the impact of abrasion, particularly toothbrushing, often is emphasized in North America. Recently, the role of acids in tooth wear has become more acknowledged partly because of research and mounting clinical evidence.

It is challenging, based solely on the appearance of teeth, to separate the various components of tooth wear. In some instances, the flattened incisal edges of incisors strongly suggest that attrition is a dominant factor. However, when there is cupping associated with the flattened surfaces, other factors will also be active, most notably erosion (Figure 1). The hollowed-out appearance of these types of lesions, in theory, also could be attributed to abrasion, but the force needed to cause this degree of wear is unlikely to occur on the occlusal surfaces. Therefore, many professionals consider acid erosion the predominant reason for cup-shaped lesions.

The knowledge that acid was responsible for erosion was first recognized in patients who had the eating disorders anorexia nervosa or bulimia nervosa.⁴ The appearance of periomylosis on the palatal surfaces of upper incisors has been acknowledged widely to be caused by acid regurgitation or vomiting (Figure 2). Periomylosis is the historical term used to describe the pattern of erosive tooth wear seen on the palatal surfaces of the upper incisor teeth. It was first recognized in patients with eating disorders and believed to be caused by vomiting and regurgitated gastric acids in the mouth.⁵ Eventually, clinical and laboratory evidence suggested the pattern similar to a palatal veneer preparation was caused by the low-pH gastric acid being either vomited or regurgitated.⁴ Some laboratory evidence indicates that the shape of the lesion is modified in some way by the abrasive action of the tongue.⁶ Therefore, a hollowed-out or scooped-out appearance strongly suggests active acid erosion.

Appearance

Probably the most easily recognizable component of tooth wear is attrition. The action of bruxing opposing tooth surfaces causes the flattening of occlusal or incisal surfaces. The physical force of the massester and temporalis muscles has been predicted to approach 911 N.⁷ Theoretically, applying this level of force to restorations increases the risk of fracture or chipping, particularly in those with porcelain bonded to metal. The site of attrition, by definition, will be along the incisal or occluding surfaces, whereas smooth surface lesions, in theory, can be caused by abrasion or erosion.

The etiology of cervical wear lesions has caused more debate than any other aspect of tooth wear. Early literature proposed excessive force applied by toothbrushing was a cause of cervical wear.⁸ However, clinical and laboratory investigative work performed simulanteously contradicted this clinical opinion and indicated that brushing of enamel caused insignificant wear. Despite this research, many clinicians continue to believe that toothbrushing is a major cause of cervical lesions. It is possible that excessive force applied while toothbrushing can cause cervical wear, but this role has not been fully investigated. More recent research suggests that the cause of cervical wear is probably a combination of erosion and abrasion.^8,9 It has been known for some time that mechanical wear—in this case tooth brushing—when combined with acid disolution is synergistic.¹⁰ Recent laboratory and clinical evidence indicates that brushing within 10 to 20 minutes following a dietary acid increases wear to a signifantly greater extent than pure brushing.¹¹

Dentin sensitivity, which often is present in association with cervical wear, has been suggested to be a direct clinical outcome of erosion.¹² These researchers suggested that sensitivity is a clinical sign of acid erosion because it does not occur in patients with poor oral hygiene. Acid erosion, by definition, is caused by the action of dietary or gastric acids dissolving tooth surfaces and is quite unlike dental caries, which is a subsurface effect related to the metabolism of plaque microorganisms. This clinical evidence suggests that dentine sensitivity is a feature of clean tooth surfaces. The action of acids removes the smear layer, which opens dentinal tubules to the oral environment and increases the risk of developing sensitivity.

It is probably safe to conclude that the impact of normal toothbrushing in the absence of acid is unlikely to cause tooth wear.⁸ However, excessive pressure or brushing soon after acid consumption may increase the risk of wear significantly.¹¹ Smooth surface lesions are seen on the facial surfaces of teeth and often noted adjacent to cervical wear lesions. On occlusal surfaces, erosive lesions appear to be hollowed-out, strongly suggesting the involvement of acids in the formation (Figure 3).³

Etiology

The evidence that dietary or gastric acids cause erosion has been extensively investigated, and its role has been subject to a number of reviews.^3,13,14 The role of dietary acids is considered by many researchers probably to be the most common cause of acid erosion and may account for the finding that as much as 70% of patients have at least one tooth with wear.^15,16 Although gastric acids also cause acid erosion, the prevelance of regurgitation, eating disorders, and alcoholism is insufficient to account for the prevalence data on erosion.¹⁷ A common misconception is that all acidic foods and drinks carry a high risk of acid erosion. Laboratory-based research strongly implicates that dietary acids have the potential to cause acid erosion.^14,16,18 However, the pH and titrability of an acid (the volume of alkali needed for neutralization) are both important indicators of erosion risk.¹⁹ Common dietary acids and their erosion risk are shown in Table 1.²⁰ The erosion risk from a strong acid, such as grapefruit, is higher than that of a cola drink. Although the pH is similar in both, the amount of alkali needed to neutralize the fruit means it is a stronger acid. The titrability of an acid is believed to give a stonger indication of the risk of acid erosion whereas pH—a measure of the amount of hydrogen ions in a solution—is imprecise. For example, carbonated water has a relatively low pH, approximately 4 to 5. Its erosive potential is low whereas a cola drink with the same pH would have a much greater erosive potential because of the much higher concentration of hydrogen ions.²¹ Therefore, in the risk assessment of someone with acid erosion, the type of acidic beverage or fruit is important to identify.

The other major risk factor with dietary acids is the frequency of consumption. Clinical evidence has suggested that the pattern of acid neutralization is unlike the pattern observed in dental caries.²² The typical drop and slow recovery seen with acid production in dental plaque is not replicated in acid erosion. Dietary acids cause an immediate drop in oral pH, commensurate with the pH of the food or drink. Then, after saliva has neutralized it, the pH returns to physiologic pH 7 within a couple of minutes. These findings, along with clinical evidence, suggest that it is the frequency of acid consumption that is important. Any dietary habit, such as holding or swilling acids before swallowng, holding fruit against the incisors, or continual snacking is indicative of an increased risk of developing erosion.^22,23

The concept of abfraction has been suggested by some clinicians as a possible cause of cervical wear. The laboratory support for this hypothetical cause is varied, with some laboratory investigations supporting the view²⁴ and others not.²⁵ Evidence from finite-element analysis also supports this view, but the studies are computer models, which may not provide sufficient complexity to model teeth.²⁶ Also, no clinical studies support this hypothesis.²⁷ Despite the temptation that abfraction is a real phenomena, the evidence does not support it.²⁸

Prevention

The epidemiologic evidence suggests that tooth wear and acid erosion are common in adults,²⁹ children,³⁰ and adolescents.³¹ Because of its widespread impact, prevention¹⁶ of tooth wear is important. The role of fluoride delivered in a toothpaste has been investigated and observed to have a beneficial effect.^11,32 Most evidence on fluoride’s protective effect has been based on laboratory investigations.^32-34 The fluoride ions appear to increase the microhardness of enamel and so improving its resistance to acid dissolution.³⁵ There are some in situ studies that support the laboratory evidence concluding fluoride is protective, but no clinical interventional research to date.^35,36 Also, some clinical and laboratory evidence suggests toothbrushing immediately after consuming acids increases the risk of erosion and abrasion.³⁶ Conjunctive application of a topical mouthrinse containing fluoride also may be beneficial. Although there is no research available to support frequent application of flouride, findings from caries studies suggest that mouthrinsing at times other than during normal brushing improves the availability of fluoride and hardens tooth surfaces. In high-risk patients, there may be some justification also to consider brushing teeth at least 15 to 20 minutes after consuming an acidic beverage or fruit.³⁶ The synergistic action of the acid and brushing increases the potential for developing erosive wear lesions.

Dietary modification is probably important in prevention. Clinical studies suggest that frequent consumption of acidic foods increases the risk of developing erosive tooth wear.^23,37,38 However, the strength of this evidence continues to be based on association rather than causation. It remains challenging to properly investigate the role of dietary acids in interventional studies because of ethical issues. Therefore, in a similar way to understanding the role of refined carbohydrates in dental caries, the evidence must be based on assimilating clinical knowledge, case reports, and laboratory investigations.³⁹ By amassing this data, the current consensus is that frequent consumption of carbohydrates causes caries. The strength of the evidence for a similar statement in acid erosion is unavailable; however, increasing clinical knowledge strongly indicates that behavior modification can be effective in preventing erosive tooth wear.²¹

Early laboratory evidence implies that calcium-based products have the potential to prevent erosive tooth wear.⁴⁰ The mode of action is not fully understood, but these products containing casein and calcium products might be protective. The casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) complex is believed to maintain a sufficiently high concentration of calcium and phosphate ions to promote enamel remineralization. Further, laboratory studies indicate CPP-ACP may be absorbed into the salivary pellicle⁴¹ and plaque⁴² and so provide a rich calcium reservoir, improving the potential for remineralization.

Another method to improve the resistance of teeth to acid erosion is application of dentin-bonding agents or fissure sealants to worn and eroded teeth. Clinical evidence implies that 3- to 6-month protection is afforded by a single application of a dentin-bonding agent.⁴³ There also may be some benefit to the application of fissure sealants to teeth to provide a barrier to erosive wear, which is more resilient than a dentin-bonding agent.

Summary

The role of acids in tooth wear is recognized as an important reason why teeth wear. Increasingly, dietary habits rather than the quantity of acidic food and drinks is being recognized as the most important factor in increasing the risk. Fluoride and dentin-bonding agents appear to have the potential to increase the teeth’s ability to resist acidic attack, but behavioral changes are likely to be as effective in prevention.

References

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About the Author

David Bartlett, BDS, PhD, MRD, FDS, RCS
Professor
Department of Prosthodontics
Kings College London Dental Institute
London Bridge
London, United Kingdom