AGD - Academy of General Dentistry

Dental erosion is a demineralization process that affects hard dental tissues (such as enamel and dentin), independent of any microbial action. This study evaluated certain common beverages and their abilities to initiate cervical erosion lesions. The progression of these lesions was monitored in an accelerated test condition over the duration of 20 weeks. Morphotopographic and radiographic profile assessments of the disassociated human teeth in vitro illustrated the differences of each tested fluid’s potential to cause erosion. The outcome of the erosion process was found to be acidic fluid-specific.

Unlike caries, which progresses in a triangulated fashion, the erosion lesions in enamel and dentin both appeared to progress in a pattern characterized by incremental decalcification in a parallel plane. The disparity between the changes of the radiographic and photographic images of the involved tissues (enamel and dentin) reflected the differences in terms of the inorganic and organic contents of each one. Close examination of the dynamic changes in the cervical region of the disassociated human teeth revealed the mechanism of cervical erosion lesion formation that was a coincidental finding of this study’s results.

Root exposure is a common occurrence that results from a physiological process. Once an actively erupting tooth reaches the occluding position with the opposing arch, the passive eruption phase begins and continues at a fairly slow pace throughout the life of the individual tooth.^1,2 This phase explains the frequent occurrence of root exposure among mature adults and the elderly. The passive eruption phase often is accelerated by conditions that may affect the dentition or the peridontium, such as mechanical trauma (for example, incorrect toothbrushing techniques, traumatic occlusion, orthodontic mobilization, accelerated attrition, and postsurgical intervention) and/or pathological etiologies. Pathological etiologies associated with inflammatory conditions of the peridontium could lead to breakdown of the periodontal attachment, gingival recession, and exposure of the root.³

Root exposure at any stage of human development may have clinically significant implications, the foremost being accelerated wear of the protective cementum layer and increased potential for the development of dentin hypersensitivity. Second, continued aggressive wear also may cause abrasion lesions to form in susceptible locations in the dentition. These abrasion lesions could progress and eventually strangle the pulp/root canal complex. Third, the softer, less calcified, denuded dentin relative to enamel is prone to root caries in susceptible individuals. Finally, the significantly low hydroxyapatite content of dentin, compared with enamel, renders this tissue vulnerable to erosion by acid challenge in the oral cavity from certain foods and beverages that are consumed on a frequent basis.^4-6 Several of these foods and beverages contain organic and inorganic acids that may be present naturally or added during the manufacturing process.⁵ Citric, malic, succinic, tartaric, ascorbic, acetic, and phosphoric acids are among the most common acids in the daily diet.⁷ The presence and concentration of each acid differs among various beverages and within each type of beverage (for example, among citrus fruit juices).

For dental professionals, prevention is an integral modality in a patient’s dental management. Various aspects of preventive approaches are incorporated to control disease processes and avoid recurrence. The primary goal of preventing dental diseases is avoiding the formation and maturation of bacterial plaque. The secondary goal is to provide the patient with sound nutritional advice that emphasizes the virtues of a low-sugar diet.⁴ The tertiary goal is to decrease the risk of erosion by reducing the volume, frequency, and duration of acidic food and beverage intake and by avoiding other etiological factors.

Three steps must be followed before dentitions affected by erosion can be rehabilitated: Identifying the culprit source of erosion, determining and understanding how this source affects the dentition, and stopping or reducing consumption of the suspected food or beverage. A series of studies have sought a clear understanding of some commonly consumed beverages and their part in the development of dental erosion.^8-10

This study was conducted specifically to investigate how cervical erosions developed on exposed human permanent teeth that were subjected to challenges from selected acidic beverages. The study also sought to determine how these fluids influenced the cervical root segment of the human dentition, how long-term exposure to the acidic challenges from these beverages affected the segments, and the characteristics of erosive patterns caused by the test beverages on the cervical root segment.

This study focused on assessing topographic and morphologic changes in the cervical region of human teeth following exposure to selected acidic beverages. Seven popular non-alcoholic beverages were used as test fluids, while vinegar and water were employed as active and passive controls. The test fluids included two acidulated carbonated beverages (one caramelized soda and one non-caramelized soda), three commercially available fruit juices, and two popular types of tea.

The caramelized soda (Pepsi-Cola) had a pH level of 2.7 and contained carbonated water, high fructose corn syrup and/or sugar, caramel color, phosphoric acid, caffeine, citric acid, and natural flavors. The acidulated non-caramelized carbonated beverage (Sprite) had a pH level of 2.8 and contained carbonated water, high fructose corn syrup and/or sugar, citric acid, natural flavors, potassium benzoate, potassium citrate, ascorbic acid, and calcium di-sodium ethylene diamene tetra-acetic acid.

The three commercially available citrus fruit juices were orange juice (pH 4.0), grapefruit juice (pH 3.0), and lemon juice (pH 2.0). All were rich in ascorbic acid and contained other organic acids (including citric, malic, and succinic acids) in various concentrations. The orange juice averaged 0.64% citric acid, 0.13% malic acid, and 0.54% succinic acid, while the grapefruit juice contained 0.86% citric acid, 0.13% malic acid, and 0.46% succinic acid. The lemon juice contained the highest amount of citric acid (4.19%) and an average level of malic acid (0.17%) but no succinic acid.⁷

For this study, cups of green or black tea were prepared by infusing 2.5 g of tea leaves in 200 mL of boiling water for three minutes.¹¹ The green and black teas contained similar amounts of proteins; amino acids; carbohydrates; lipids; minerals; pigments; caffeine; vitamins A, C, and E; fibers; and tannic acid. They differed in terms of the percentage of phenolic compounds (flavonoids) that are considered antioxidants: green tea contained approximately 30% non-oxidized phenolic compounds compared with the 5% found in black tea. The balance of the flavonoid content in the black tea (25%) constituted the oxidized phenolic compounds.¹2 The pH levels of the black and green teas ranged from 4.9–6.5.¹³

The two control fluids were vinegar (acetic acid 5.0%) with a pH of 2.4, which served as an active control, and tap water (pH ~6.8), which was used as a passive control.⁸

To evaluate the erosive effects of the aforementioned fluids on the cervical segment of the human dentition, this in vitro study was designed to be independent of all extraneous influencing factors. Under controlled accelerated in vitro conditions, the erosive effects of the nine selected fluids on the cervical segments of disassociated human teeth were monitored. The methodology adopted in this study had been employed in previous investigations with proven efficacy.^8-10

Fifty-six recently extracted, sound human premolars and canines were selected randomly from among discarded teeth that had been stored in Cidex (Advanced Sterilization Products, Irvine, CA; 800.595.0200) for one week. To ensure privacy, these teeth were neither identifiable nor traceable to the source. The teeth were cleaned of any hard and soft deposits and polished with slurry. A No. 6 round dental bur was used to bore a tunnel through the apical third of the root of each specimen in a mesiodistal direction. The apical two-thirds of the roots, including the bored tunnels, were coated with red nail varnish to protect them from the test fluids. The cervical third of the roots and the entire coronal segments were left exposed for test purposes.

The initial baseline observation and subsequent follow-ups were documented by employing standardized techniques. Changes in color, translucency, and texture of root surfaces and the presence of enamel were assessed; these assessments were complemented by sequential photographs. Radiographic images of the specimens’ buccolingual and mesiodistal profiles were made via the paralleling technique, using a 12 in. round position-indicating device and a radiographic unit (GX-770, Gendex Corporation, Lake Zurich, IL; 888.275.5286) at 70 kVp, 7 mA, and 10 impulses. After exposure, all radiographs were processed using the same automatic dental film processor (A/T 2000, Air Techniques, Hicksville, NY; 800.595.7871) and converted to digital images using a film scanner at 600 dpi.

During the 20 weeks of the test, the crown and cervical root portions of the specimens were incubated in the corresponding static fluids at room temperature. The specimens were monitored weekly for topographic changes, while photographic and radiographic recordings were repeated every four weeks. The sequential analog radiographs were digitized and printed on graph paper using a standard magnification. The upper border of the bored root tunnels were used as a stationary reference point for geometrical grade scale analysis of the digitized serial radiographs. Four parameters were used for assessing the digitized images: the height of the exposed root, the buccolingual widths of the root trunk at the cemento-enamel junction (CEJ), the buccolingual width of the root trunk at the deepest point of the exposed root, and the height of the unsupported cervical enamel.

The baseline topographic observation of the cervical crown/root trunk segments of all specimens displayed normal enamel and dentin color, translucency, surface texture, consistency, and morphologic landmarks. Initial radiographic profiles demonstrated intact delineation of specimen contours with sharply defined outlines.

All specimens demonstrated various degrees of altered topography and/or morphology except for the tap water, which showed no changes. The alterations that affected enamel manifested as one or more of the following conditions: translucency, color, texture, morphology, and loss of cervical enamel margin. Alterations that affected dentin included exposure of coronal dentin, changes in root dentin color, and changes in dentin texture.

During the first two weeks of the study, the vinegar specimens revealed a loss of enamel translucency. Meanwhile, the root dentin of these specimens appeared to change to grades of yellowish discoloration, which intensified over time.

By the four-week assessment, the cervical enamel had become opaque white with a rough surface that lacked morphological landmarks. At the same assessment, the CEJ had lost its smooth continuity due to disintegration and chipping of the knife-edged cervical enamel.

By the eighth week, the entire enamel cap of several vinegar specimens had eroded completely and the remaining specimens showed a few scattered remnants of enamel islands. In addition, the color of the exposed root dentin had turned a darker yellow and then a light brown. The exposed coronal and root dentin showed differences in the intensity of discoloration and yielded under exploration; by week 12, they had become leathery. All active control specimens lost their entire enamel cap between the 12- and 16-week assessments, leaving a light brown, leathery underlying dentin that turned darker over time. The coronal core and root trunk dentin did not show visible signs of morphological or volumetric changes.

By the second week, white enamel spots had formed on the Pepsi-Cola specimens. These spots were followed by a loss of translucency on the entire enamel surface by the fourth week; the surfaces became opaque white by the eighth week. At the eight-week evaluation, it was noted that segments of the knife-edged cervical enamel had crumbled, showing irregularity in the continuity of the CEJ. A gradual but slight enamel loss at the CEJ continued for the remainder of the study. Enamel color continued to change from opaque white to yellow to dark yellow to light brown at the 12th week, turning dark brown at the 20-week evaluation. The dentin surface of the root trunk of this group became a turbid yellow color by the third week and showed brownish tints at the four-week evaluation. This discoloration of root dentin continued to intensify, becoming dark brown at the 12th week and turning black by the 20-week assessment. Detectable changes in dentin surface texture were noted at the eight-week assessment as the surface yielded by exploration and became softer by the 12-week assessment.

Specimens exposed to Sprite showed a similar (albeit delayed) response to that of the Pepsi-Cola specimens. While Pepsi-Cola specimens demonstrated a change in enamel texture at eight weeks, the Sprite specimens showed a similar change at the 12-week evaluation. Visible enamel loss at the CEJ was evident on the Pepsi-Cola specimens at eight weeks and on the Sprite specimens by weeks 10–11. The cervical enamel of Pepsi-Cola specimens showed distinct height loss by 12 weeks, while the Sprite specimens showed similar loss at 16 weeks. The root trunk dentin of the Sprite specimens showed a faint change in color by the third week that became yellowish by the fourth week. This discoloration continued to intensify, becoming light brown and dark brown by the eight-week evaluation. A change in root surface texture was noted at the 12-week assessment and softening of the surface became evident by 16–20 weeks. The color of the exposed coronal dentin was a darker brown than the root trunk dentin. Throughout the study, no notable change in root morphology was detected for either the Pepsi-Cola or Sprite specimens.

Among all tested specimens, lemon juice demonstrated the highest erosive damage to enamel topography and morphology within the first four weeks. Grapefruit juice specimens ranked second in terms of severe enamel loss, followed by orange juice.

During the first two weeks, lemon juice specimens demonstrated progressively increasing roughness of the enamel surface and severe irregularity of the CEJ continuity; meanwhile, the enamel color had changed rather quickly from normal color and translucency to opaque white to yellow and finally to dark yellow by the end of the third week. The chalky color and consistency of the enamel surface that developed during the first few weeks tended to yield upon exploration and could be scratched easily. Excessive loss of cervical enamel for the entire coronal circumference was noted before the four-week evaluation. Among lemon juice specimens, the majority of enamel caps were lost by the four-week assessment. By week eight, the exposed coronal dentin core and root trunk displayed a leathery consistency that flaked easily upon exploration, although no volume change of dentin was noticeable.

Signs of changes in enamel and root dentin color began to appear at the first week for the grapefruit juice specimens. These changes started with a loss of enamel translucency, followed by increased opacity and the development of white discoloration. The white discoloration progressed to maximum intensity at the four-week evaluation; in addition, the enamel surface consistency remained hard upon exploration with increased surface roughness. Subsequent weekly monitoring revealed a breakdown of the continuum of the enamel surface and the CEJ. Some specimens had lost their coronal enamel by the eight-week evaluation, exposing their underlying dentin cores. The cervical enamel yielded upon exploration and crumbled under slight pressure. Prolonging the incubation time for grapefruit juice specimens beyond the 12th week caused more enamel caps to break down until they were lost completely by the 16-week evaluation.

Root discoloration started one week after inserting the specimens in the grapefruit juice, as specimens turned dark yellow, brown, and then dark brown. An intense dark brown discoloration was noted at the four-week assessment. During these phases, both the texture and consistency of the root dentin were degraded. The dark brown discoloration turned bluish-black and continued incubation in grapefruit juice caused further degradation of the coronal and root trunk tissues. The deteriorating dentin consistency that was noted in the grapefruit juice specimens at the 20-week assessment closely matched that of the lemon juice specimens at the four-week assessment, although no change in the root trunk morphology was noted by the end of the study.

The enamel topography of the orange juice specimens changed at a much slower rate and with less intensity than the lemon and grapefruit juice specimens. These changes were manifested by loss of enamel translucency, indicated by a gradual increase in the opaque white color that continued through the first eight weeks, became a dull yellow-brown by the 12th week, and darkened further thereafter. Increased enamel surface roughness and disintegration of the CEJ were noted at the eighth week. These particular changes were accompanied by a superficial loss of topographic and anatomic features. The root dentin color became light brown at four weeks and dark brown by the eight-week assessment. This dentin color continued to intensify to become an ashy black discoloration by the 12-week assessment; at that time, it was noted that the consistency of the exposed dentin had softened, while the cervical enamel became severely decalcified and chalky white and crumbled easily. No volumetric change in cervical dentin was noted.

Topographic observations of this group of specimens revealed a gradual browning of the root trunk color after one week of exposure to black tea and three weeks of exposure to green tea. This superficial discoloration started as varying shades of yellow, all of which turned to shades of brown by the fourth week. The discoloration of the enamel in both the black and green tea specimens was lighter than the dentin, becoming a slightly opaque white with scattered brown patches at the 16-week assessment. There was no visible loss of the CEJ, coronal morphology, or root trunk volume, nor was there any visible loss of enamel caps or exposure of coronal dentin by the 20-week evaluation. The surface consistencies of enamel and dentin maintained the normality of the pre-test condition for 16 weeks. Slight changes in dentin surface texture of the black and green tea specimens began after the 16-week evaluation. By the 20-week assessment, the dentin surface became rough and could be scratched by exploration.

The quantitative assessments of the studied parameters on the digitized radiographic images are presented in Tables 1–3 and Charts 1–4.

Table 1 lists the average increase in root length (in µm) for both the buccal and lingual profiles of the tested specimens at 4, 8, 12, 16, and 20 weeks. The values for each fluid represent the elongation of the root length that resulted from the loss of cervical enamel height. The changes in these values from the baseline evaluation are listed for each of the five assessments. For ease of comparison, the total gain in root length at the end of the study was calculated in terms of weekly and daily gains (see Table 1). The combined average gains in root length of the buccal and lingual profiles for the tested fluids are presented in Chart 1.

Based on the total gain in root length at the end of the study, the tested fluids were categorized into three groups. The first group consisted of fluids (vinegar, lemon juice, and grapefruit juice) that caused maximum erosion to cervical enamel, which led to maximum increase in root length. The second group consisted of fluids (orange juice, Pepsi-Cola, and Sprite) whose specimens showed one-third to one-half of the cervical enamel loss caused by the first group of fluids. The third group included the black and green teas, which caused negligible changes in root length; these changes were close to that of tap water, which had no erosive effect.

Tables 2 and 3 and Charts 2 and 3 present the average loss of tissues in an axial direction from both the root trunk at the CEJ level and the deepest point of the root defect. Unlike the morphologic observations that revealed no detectable changes in root geometry, grade scale analysis of the digitized serial radiographs revealed various degrees of tissue loss for all of the fluids tested except for tap water. Accordingly, three groups were identified based on the degree of dentin loss due to decalcification of the root trunk. The first group included the citrus fruit juices and vinegar, the second group included Pepsi-Cola and Sprite, and the third group included black and green tea. Tap water produced no changes.

The changes in height for the undermined cervical enamel margins of the specimens disclosed an interesting dynamic pattern. The average values were similar for the buccal and lingual profiles of each group of specimens; the representative averages were plotted against time and are presented in Chart 4. The linear tracings that represent orange juice, Sprite, and Pepsi-Cola showed an exponential increase in the height of the unsupported cervical enamel; by the 16th week, these increases average 100 µ, 120 µ, and 200 µ, respectively. The Pepsi-Cola and Sprite specimens then showed a slight decrease of the unsupported cervical enamel height at the 20-week evaluation. The black tea specimens exhibited a minor increase in unsupported cervical enamel height that began at 16 weeks and measured approximately 35 µ by the end of the 20-week study. There was no detectable change in the height of the unsupported cervical enamel for the green tea and tap water specimens; however, both the vinegar and grapefruit juice specimens demonstrated erratic changes until most of their enamel caps disappeared. The specimens incubated in lemon juice lost their entire enamel cap by the four-week assessment.

Determining the etiology of cervical lesions can be a difficult task, as reflected in a 1998 survey that Lyttle et al conducted among general practitioners in Nova Scotia to explore the perceived causes of non-carious cervical lesions.¹⁴ Of the 216 dentists who completed the survey, 203 (94%) identified abrasion as the causative etiology of cervical lesions; among this group, 134 (66%) rated toothbrushing as the most likely cause of abrasion.¹⁴

Because of the synchronous, sequential, and interdependent relationship between erosion, abrasion, and abfraction lesions, accurate identification is subject to speculation. This clinical judgment frequently stems from the biases of individual views and personal experience with destructive lesions on human dentition. To diagnose such lesions accurately, it is necessary to investigate each of the etiologies thoroughly. Erosion as a principal etiological factor for the formation of cervical lesions was the main focus of the present study.

The development of dental erosion lesions is subject to the nature of the acid or acidic fluids, the neutralizing capacity of salivary constituents that are governed by the influencing factors of salivary flow rate, the anatomic location in the dental arch, and the level of mineralization of the affected tissues. The presence and nature of the mechanical stresses in the oral environment contribute to the wear of the decalcified softened tissues. All of these factors are interdependent and synchronous, making it difficult to assess a single factor accurately, particularly in vivo.

To identify the potential for erosion of commonly consumed beverages on the cervical region of the human dentition, the present in vitro investigation rendered all other influencing variables constant. This study used visual examinations of the topographic and morphologic changes combined with the tactile perception of suspected lesions, since these are the most commonly used examination methods. Meanwhile, because the erosion process involves decalcification of hard dental tissues, resulting in dissolution of the inorganic contents, radiographs were analyzed to assess potential changes in enamel and dentin; these means of assessment have been employed successfully in previous studies.^8-10

The erosion process for enamel and dentin is a chemical reaction that involves an acid and the calcium hydroxyapatite components. In the present study, there was a difference between the measurements taken from the radiographic images and the corresponding morphotopographic findings (Fig. 1). Signs of enamel erosion appeared as altered translucency and increased optical opacity that rendered the surface opaque white. The chalky, textured surface of the enamel became rough with scattered pitting, which facilitates the attraction of extrinsic stains and contributed to the color of the enamel changing to yellow and eventually to brown. Changes in color of the dentin surface were noted by increased intensity as the samples turned yellow, followed by shades of brown discoloration, and finally almost blue-black for some specimens. The consistency of the dentin surface changed, becoming tacky and yielding under exploration before becoming leathery and finally soft.

The deeper discolorations in enamel and dentin were intrinsic in nature; these discolorations resulted from the acid in the beverage reacting with the glycoprotein compounds. These compounds are present in abundant quantities in dentin (compared with the limited amount found in enamel), which explains the intense deep discoloration of the dentin. The carbohydrate constituents of dentin are hexosamine (in the odontoblastic processes) and sulfated acid mucopolysaccharides (in the pre-tubular regions); chondroitin sulfuric acid similar to that found in cartilage also has been isolated.¹⁵

The organic matrix of enamel contains several hexoses, including galactose, glucose, and mannose, in addition to traces of pentose sugars.¹⁵ Even though enamel has relatively minute amounts of these sugars as compared to dentin, their presence explains the change in color following exposure to acid. This reaction is known as browning, non-enzymatic glycosylation, or Maillard reaction.^16,17 As demonstrated by the topographic changes of the test specimens, prolonging the exposure time to acid or increasing the concentration of polysaccharide or sugar contents in the medium increases the intensity of these discolorations.

Additional topographic and morphologic changes of enamel were demonstrated by loss of surface details and a reduction in volume from the baseline evaluation. Despite the altered color of the root surface, no volumetric change of dentin was noted visually in the present study; however, radiographic images of both enamel and dentin showed distinct incremental losses in their profiles.

The disparity between the morphotopographic and radiographic changes of enamel and dentin can be explained by the differences in their basic constituents. Tooth enamel is the hardest tissue in the human body, consisting mainly (95%) of inorganic substance (calcium hydroxyapatite), with 1% organic matrix and 4% water. Meanwhile, dentin contains 18–23% organic matter (essentially collagen fiber), 12% water, and 65–70% calcium hydroxyapatite.¹⁸

Enamel loses approximately 95% of its total volume when the calcified inorganic core is dissolved. The few remnants of the organic matrix cannot maintain the morphologic shape and disintegrate readily, even in a static solution (Fig. 1).

By contrast, the hydrated dentin matrix holds the shape of its structure once the inorganic salts dissolve in the acidic fluid medium. The remaining organic matrix, with its complex web of collagen fibers, maintains the morphology of the affected tissues (Fig. 1). In the oral environment, the thin layer (50–100 µ) of the cementum next to the cervical line is revealed upon exposing the root.¹⁸ Once subjected to minimal mechanical wear forces (induced by toothbrushing and mastication), the speedy removal of this cementum layer by these abrasion processes enhances the disclosure of the vulnerable dentin to chemical and mechanical stresses. Subjecting the exposed root dentin to acids from either intrinsic or extrinsic sources leads to dissolution of the calcium hydroxyapatite contents. The challenging acidic fluid decalcifies exposed dentin, producing a densely compacted collagen fibrous structure. This massive organic lattice of collagen fibers maintains the integrity of the volume and shape configuration of the dentin tissue as long as it is hydrated by saliva.

The absence of volumetric changes in the erosion morphology of root lesions could render detection difficult and accurate diagnosis unsuccessful unless tactile testing and radiographic investigation are used. The softened dentin surface is vulnerable to abrasion processes that lead to eventual loss; this loss facilitates the visual detection of lesions. Dehydration of this tissue may occur in patients with xerostomia and also may cause the collagen fibrous structure of dentin to collapse, thus altering the morphologic configuration of the root lesion to make it clinically detectable.

The findings from the present study agree with those obtained in a 2001 study by White et al, who used polarized light microscopy and found that the process of root dentin erosion was quite different from that of enamel erosion.¹⁹ Their observation and the findings of the present study explain the difficulty in diagnosing cervical erosion lesions that involve root dentin. Studying the various influencing factors of erosion in the oral environment and evaluating the clinical and radiographic features of the lesion in question before outlining a definitive diagnosis could establish a basic foundation for sound therapeutic measures.

The changes in the profiles of the specimens’ cervical root segments were explored by making a geometrical grade scale analysis of the digitized serial radiographs. The pattern and extent of cervical tissue loss noted on the radiographs were assessed by measuring the length of exposed root consequent to the loss of cervical enamel, the reduction of the buccolingual width of the root trunk at the level of the CEJ, the reduction of the buccolingual width of the root trunk at the deepest point of the root defect, and changes in the unsupported cervical enamel heights. Using these measurements made it possible to disclose precisely the presence and extent of erosive activities in the cervical segment of the roots (Charts 1–4 and Fig. 1).

The baseline value for the root length was measured from the CEJ to the crest of the tunnel located at the apical third of the root. The data listed in Table 1 represent the average changes in the heights of the buccal and lingual profiles of the root due to the loss of cervical enamel (Fig. 2). Loss of cervical enamel height at the buccal and lingual profiles was similar for the soda and tea speciments. Lemon juice, vinegar, grapefruit juice, and orange juice all presented variations in terms of the differences in cervical enamel loss on the two profiles. All fluids tested showed higher enamel loss from the buccal profile than the lingual profile.

Chart 1 shows the combined average increase in root length for the specimens; these specimens were ranked in ascending order, based on the gain in root length. Tap water imposed no change and thus holds the lowest rank. Black and green teas showed very little change. The two sodas were in the mid-range, between the tea specimens and the orange juice specimens. In descending order, grapefruit juice, vinegar, and lemon juice demonstrated the highest potential for erosion, since their specimens demonstrated the greatest root length increase among the tested fluids.

The erosive effects of tea, soda, and orange juice showed a gradual increase in root length that progressed slowly to the end of the study. However, at no time did the tea, soda, or orange juice specimens achieve the maximum increase in root length, since these specimens retained their enamel caps to the end of the study.

By comparison, the grapefruit juice, vinegar, and lemon juice specimens demonstrated high increases in root length after only four weeks. These sudden increases escalated until the majority of the enamel caps were lost for these specimens. Maximum root length was recorded at eight weeks for the lemon juice specimens, 12 weeks for the grapefruit juice specimens, and 16 weeks for the vinegar specimens.

Subsequent evaluations revealed that the root lengths decreased slightly and gradually, which reflected the continued decalcification process of the exposed surface layer of the coronal dentin core. The amount and rate of tissue loss recognized in this study are specific to the tested fluids under in vitro test conditions. The numeric values obtained for these particular acidic fluids could be altered in the oral environment, based on the interplay of the chemical and mechanical factors encountered.

The extent and rate of cervical root tissue loss were assessed on the digitized radiographic images at the level of the CEJ and at the deepest point of the root defect. For the majority of fluids, the average values of dentin loss at the CEJ level and the deepest point of the root defects were comparable (see Tables 2 and 3). These data suggest that the decalcification of dentin due to erosion progressed incrementally with equidistant penetration at these two levels in a plane parallel to the outer surface of the root (Fig. 3).

The numerical values representing the loss of dentin tissues varied dramatically among the tested fluids. The tap water specimens recorded no changes, while specimens placed in tea showed the smallest change. The citrus fruit juices (orange, grapefruit, and lemon) and vinegar exerted the most tissue damage. The two sodas caused relatively less damage (<50%) than the acidic fluids but significantly more damage than the teas. The effect of orange juice on enamel was similar to that of Pepsi-Cola and Sprite but was much less than that of the grapefruit and lemon juices. The erosive effect of orange juice on dentin was similar to that of the other citrus fruit juices.

The degree of damage caused by orange juice to enamel and dentin could be related to the level of mineralization of these tissues. Dentin has significantly less calcium hydroxyapatite than enamel and may have offered less resistance to the erosive effect of the orange juice. As a result, the erosive potential of orange juice on dentin was elevated to the level of other citrus fruit juices, which supports the principle that the calcification level of the substrate is as important a factor in the erosion mechanism as the challenging acidic fluid’s potential for erosion. It also suggests that the erosive effect of orange juice on enamel may be similar to that of soda for individuals without exposed roots, while its erosive effect on the exposed roots of the human dentition can be similar to that of grapefruit and lemon juices.

The erosion process at the cervical segments of the dentition appears to be a surface phenomenon (Fig. 2). This decalcification process begins when acidic fluid contacts the enamel or exposed dentin surfaces. Although the erosion process may affect these two tissues with different degrees of intensity, both experience surface damage due to the loss of calcium hydroxyapatite. The collagen-rich matrix either disintegrates (as with enamel) or wears away (as with dentin). The erosion defects that may be observed clinically on the cervical crown/root segment are saucer-shaped with beveled margins. The advanced stage of these defects can be seen on radiographic images as well-defined semicircular radiolucent areas located at the cervical segments of the affected dentition.

In the present study, the undermined cervical enamel profile demonstrated erratic changes; for some fluids, these changes were represented by an increase in height, followed by an abrupt decrease (Chart 4). These erratic patterns indicated a continuum of dynamic changes that differed in intensity and frequency among the tested fluids, although the erosion process was the same. In the wake of this incidental observation, the radiographic images of the cervical segments and surrounding structures were reviewed to disclose the sequence of events that caused this dynamic process. The detailed inspection revealed a scenario that departed from the conventional erosion mechanism for the cervical segment of human dentition.

It was noted that the cervical segments began to show signs of decalcification after exposure to acid challenge, which manifested as decreased radiopacity in enamel and root dentin. This radiolucency began to penetrate in an axial direction into the subsurface dentin layer of the root and soon enveloped the knife-edged cervical enamel margin.

The different levels of calcification for dentin and enamel allow a tunneling defect to form at the interface (Fig. 1 and 3). The decalcification process progressed into the softened dentin structure of the tunnel, which allowed additional erosive acidic fluids to penetrate behind the knife-edged cervical enamel margin. These fluids in turn caused erosive action on the inner surface of the cervical enamel edge and the opposing supporting dentin, enlarging the interfacial tunnel and increasing the height of the unsupported cervical enamel margin. Simultaneously, the outer surface of the cervical enamel was subjected to the erosive action of the acidic fluid. The combined erosive effect of the acidic fluid on the outer and inner surfaces of cervical enamel weakened its unsupported, inherently brittle structure. The weakest terminal edge of this cervical enamel segment eventually crumbled, which led to a shortening of root height, even in a static solution. A dynamic environment could accelerate the loss of this unsupported, weakened cervical enamel.

Disintegration and shortening of the unsupported enamel exposed more root surface (Fig. 2) and allowed more erosive fluid to exert additional damage. Eventually, the entire enamel cap could be dissolved, either partially or completely, as seen in the lemon juice, grapefruit juice, and vinegar specimens in the present study. The description of the aforementioned dynamic process suggests that a cervical erosion lesion develops due to multiple action processes acting simultaneously on the surface and subsurface of the cervical enamel ledge. Given this erosion phenomenon, one might question the mechanism that causes repeated failure of cervically bonded restorations, particularly among those who avidly consume acidic beverages. The cause of these restoration failures may go beyond the weakened adhesive bond strength. The chemico-bio-mechanical process described in the present study could be an integral part of the etiology of these cervical restoration failures. This hypothesis should be subjected to additional investigations to support its validity.

The results of this study clearly illustrate the short- and concomitant long-term erosive effects of exposure to acidic challenge from certain common beverages. The erosive effect was found to be fluid-specific. Although profiles of radiographic images demonstrated tissue damage, the lack of volumetric changes in root trunk dentin demonstrated a difference between enamel and dentin erosion patterns. Unlike dentin, the radiographic evidence of enamel erosion complemented the morphologic changes. This investigative process disclosed and explained the mechanism of how cervical erosion lesions form. Collectively, these findings could be important to the diagnostic process and could be applied to nutritional counseling.

The author extends his appreciation to Drs. Jie Yang and Shuntaro Kuroda for their technical assistance.

Dr. Bassiouny is a professor, Department of Restorative Dentistry, Temple University, School of Dentistry in Philadelphia, Pennsylvania.

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