Dental erosion and acid reflux disease: An overview
By David A. Lazarchik, DMD
Kevin B. Frazier, DMD
Featured in General Dentistry, March/April 2009
Pg. 151-156
Posted on Friday, March 06, 2009
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Dental erosion can be difficult to detect, especially in the early stages when lesions are subtle and can be easily overlooked. Patients often are not aware of erosion until the dentition has sustained severe damage that requires extensive and expensive dental rehabilitation. The pH of stomach acid is much lower than the critical pH of enamel dissolution; therefore, reflux of stomach contents into the oral cavity over an extended period of time can cause severe loss of tooth structure. Dental treatment for reflux-induced erosion should focus not only on appropriate restoration but also on all available preventive measures, such as neutralization of acid and remineralization or strengthening of enamel against acid attack. Dentists must maintain a high degree of suspicion for reflux-induced erosion whenever a patient displays symptoms of acid reflux disease or a pattern of erosion that suggests an intrinsic source of acid exposure.
Received: March 4, 2008
Accepted: May 9, 2008
Over the last 15 years, awareness that acid reflux is a significant cause of dental erosion has increased dramatically. This increased awareness was revealed in an Ovid MEDLINE search that combined the keywords “tooth erosion” and “gastroesophageal reflux” and found 17 articles published from 1950–1992 and 112 articles published from 1993–2007.
Acid reflux-induced erosion is especially relevant to the practicing general dentist for four reasons: The subtle appearance of early erosion lesions makes them difficult to diagnose and therefore easy to overlook; the causes of erosion are difficult to define without a detailed history; acid reflux-related erosion is common in the general population; and undiagnosed erosion, combined with other forms of tooth substance loss such as attrition, can cause devastating damage to the dentition over time. Patients often are not aware of the damage that reflux-induced erosion causes to their dentition until it has reached an advanced stage of destruction. It is incumbent upon all clinicians to be educated about this topic, to remain vigilant in detecting the initial stages of erosion, and to utilize all preventive techniques to minimize the impact of acid reflux on the oral cavity.
Dental erosion is defined as the “loss of tooth structure due to nonbacterial chemical causes.”1 It was first reported more than 200 years ago in early reports that documented severe dental lesions without identifying their etiology. One of the first detailed reports was a 1968 study that documented dental erosion in industrial workers.2 Study subjects worked in industries such as metal plating, acid-engraving, crystal glasswork, and the manufacture of munitions or lead acid batteries; approximately one-third of the subjects demonstrated signs of dental erosion. The author theorized that the erosion was caused by exposure to acidic aerosols associated with these industrial processes.2
Eccles and Jenkins were the first to use a numerical scale to classify the severity of erosion by appearance and to note patterns of erosion distribution by tooth surface.3 They linked erosion in their patients to dietary acids in fruit juice, carbonated beverages, and lemonade and noted that the labial surfaces of anterior teeth were affected most commonly, with decreasing incidence in the posterior teeth. The lingual surfaces were relatively unaffected, which was empirically consistent with an external source of acid such as dietary substances. The erosion scale they developed (see the table) still is used in research studies, but its simplicity also allows dentists to use it in clinical practice for establishing a baseline measure of erosion and monitoring its progress over time.
In the Eccles and Jenkins scoring system, each of the three exposed surfaces (buccal, lingual, and occlusal or incisal) for all teeth is assigned a number from 0 (no erosion) to 3 (severe erosion), corresponding to the severity of erosion. Each tooth will have three scores; by adding the erosion scores for all teeth to give a single sum (known as a cumulative erosion score), dentists can get an overall picture of the severity of erosion in a particular dentition.3
Dental erosion among the adult population has a reported prevalence of 4–82%, with differences among studies related to differences in the age, diet, and acid exposure of the population sample, the tooth surfaces studied, and erosion scoring systems used.4
The clinical appearance of early erosion lesions can be quite subtle and difficult to diagnose. The first signs of beginning erosion (Grade 1—confined to enamel) include a loss of surface detail, giving the enamel a smooth, glazed, or frosted appearance (Fig. 1). As the enamel thins, the underlying dentin begins to show through and the teeth develop a yellowish hue. Posterior teeth in this condition viewed from an occlusal direction may show a “ring” or circular feature that surrounds the occlusal surface. This ring is the dentino-enamel junction (DEJ) of the tooth’s four axial surfaces (mesial, buccal, distal, and lingual), which has become visible through the eroded occlusal enamel (Fig. 2).
With moderate erosion (Grade 2; less than one-third of the surface affected), broad cervical concavities become apparent on facial surfaces and dentin becomes exposed. Acid-weakened enamel can chip away at occlusal or incisal surfaces, producing a “cupped” appearance at the points of occlusal contact. In addition, amalgam restorations can extend beyond adjacent eroded enamel and dentin, a condition sometimes described as standing proud (Fig. 3).5
Severe erosion (Grade 3; one-third or more of the surface affected) manifests as a dramatic loss of enamel with significant dentin exposure. Often, all of the enamel overlying a surface is lost and pulp horns may become visible. When the forces of attrition work on eroded surfaces, severe destruction can result in deeply cupped occlusal and incisal surfaces and tall shells of enamel without dentin support (Fig. 4 and 5).
Dental enamel begins to dissolve at a pH of 5.5.6 Because stomach acid has an extremely low pH (< 2.0), it has the potential to cause significant chemical erosion.7 Many medical conditions (including gastritis, hepatitis, pregnancy, motion sickness, alcohol intoxication, and bulimia) are associated with chronic vomiting, which repeatedly exposes the dentition to the stomach’s contents. Although gastric acid reflux is much less dramatic than chronic vomiting, it is very common in the general population; approximately 10% of
Acid reflux is defined as the abnormal propulsion of stomach contents into the esophagus. Reflux occurs when the lower esophageal sphincter (LES), a muscular valve controlling the flow of food and fluids between the stomach and esophagus, malfunctions. This malfunction causes an inappropriate relaxation of the sphincter at times other than when food and fluids are being transported from the esophagus into the stomach or when gas is expelled from the stomach into the esophagus (in the form of belching). Ongoing reflux episodes can result in acid reflux disease, also known as gastroesophageal reflux disease (GERD).
Heartburn (a restrosternal burning sensation) is the hallmark symptom of GERD; it usually occurs within 30–60 minutes of eating and is associated with large meals or lying down within one to two hours after eating. Other esophageal symptoms include regurgitation, belching, globus (a feeling of fullness or a lump in the throat), and dysphagia. Symptoms also can manifest outside of the esophagus; these include chronic cough, hoarseness, laryngitis, asthma, sleep apnea, and non-cardiac chest pain (severe heartburn occasionally can mimic angina pectoris).9
One oral symptom of GERD is water brash, the sudden production of copious salty saliva in response to heartburn. Water brash is thought to be a compensatory antacid mechanism to neutralize stomach acid in the esophagus.10 Although symptoms of GERD may seem more of an inconvenience to some patients than a significant medical condition, chronic or severe GERD can result in Barrett’s esophagus, in which the stomach lining attempts to heal acid-induced ulcerations by growing into the esophagus. Compared to the general population, patients with Barrett’s esophagus have a significantly increased risk of developing esophageal adenocarcinoma.11
Acid reflux can be caused by a hormonal imbalance (as occurs in pregnancy) or by anticholinergics, antihistamines, theophylline, meperidine, and calcium channel blockers (CCBs) used to treat hypertension. More commonly, reflux is associated with acidic foods, including tomatoes, tomato-based sauces, citrus fruits and juices; spicy foods such as onions, garlic, and peppers; fried foods; fatty meats and dairy products; chocolate; caffeine; and alcohol. Certain habits such as smoking, eating to excess, and lying down soon after meals also have been associated with reflux.
Acid reflux disease usually is easy to diagnose, as the primary symptom is heartburn in association with the foods and habits described above. In cases where a diagnosis cannot be made based solely on symptoms, improvement after a trial of prescription medication (or after using antacids or other OTC anti-reflux medications) may confirm the condition. pH monitoring is the only medical test for detecting acid reflux directly.12 Ambulatory 24-hour esophageal pH monitoring documents the actual presence of acid in the esophagus by using a pH probe that runs through the nasal cavity into the esophagus and measures the pH at the upper border of the LES over a 24-hour period.
An alternative to this test uses a wireless capsule that is attached temporarily to the esophageal mucosa and transmits pH data to a receiver worn by the patient. The wireless method of testing may be more accurate than the standard nasal catheter test, since it does not require the patient to wear a potentially uncomfortable nasal catheter that could alter normal diet and physical activity.13 Another form of analysis, upper gastrointestinal endoscopy, does not detect the presence of refluxed acid but documents the damage it causes (that is, erosions and ulcerations) and/or the body’s attempt to compensate (Barrett’s esophagus).14
Once a definitive diagnosis is established, medical therapeutic goals include eliminating symptoms, healing esophageal damage, and preventing complications. Lifestyle modification is the key to successful treatment of reflux, although it often can present a major behavioral challenge, similar to that encountered by dentists who try to motivate their patients toward good dietary and oral hygiene practices. The most important step is avoiding the foods and habits that are associated with reflux. The National Heartburn Alliance has published a useful chart of foods that GERD patients may consume safely, as well as those that should be eaten in moderation or avoided completely.15 GERD patients also should maintain normal body weight and avoid lying down for two to three hours after eating. Those patients with severe reflux should consider elevating the head of the bed on 6 in. wooden blocks, allowing gravity to relieve pressure on the esophageal sphincter and inhibit refluxed acid from moving up the esophagus.
Because they are inexpensive and readily available, OTC antacids are an important part of acid reflux treatment; approximately one-third of patients with heartburn-related symptoms use antacids at least twice weekly.16 Antacids provide rapid but short-term relief (typically one to two hours) by neutralizing stomach acid in the esophagus. Oral H2 receptor antagonists, such as cimetidine (Tagamet HB200, GlaxoSmithKline, Research Triangle Park, NC; 888.825.5249), famotidine (Pepcid AC, Johnson & Johnson, New Brunswick, NJ; 800.526.3967), nizatidine (Axid AR, Wyeth Pharmaceuticals, Madison, NJ; 800.395.9938), and ranitidine (Zantac, GlaxoSmithKline) prevent histamines from binding to receptors that activate the gastric acid pump in the parietal cells in the lining of the stomach, thus reducing the amount of acid produced. They offer relief in approximately 60% of patients for 6–12 hours and are available OTC for short-term use of a few weeks or by prescription for longer term use under the supervision of a physician.17
When H2 receptor blockers are not completely effective for controlling reflux, proton pump inhibitors (PPIs) can be prescribed; according to the literature, these provide relief for 80–90% of patients.18 PPIs available commercially include rabeprazole (Aciphex, Eisai Inc., Woodcliff Lake, NJ; 888.274.2378), esomeprazole (Nexium, AstraZeneca LP, Westborough, MA; 800.236.9933), lansoprazole (Prevacid, Takeda Pharmaceutical Co., Lake Forest, IL; 877.226.4589), omeprazole (Prilosec, AstraZeneca LP), and pantoprazole (Protonix, Wyeth Pharmaceuticals). These drugs work by blocking the production of stomach acid at the source—the gastric proton pump—and provide 24-hour relief, offering convenient once-daily dosing. All PPIs require a prescription, except for the OTC version of Prilosec.
In rare cases where drug therapy is not effective, surgery may be indicated. The Nissen fundoplication (often performed laparoscopically) involves wrapping a portion of the stomach around the lower esophagus to strengthen the LES and prevent stomach contents from backflowing into the esophagus. The less-invasive Stretta procedure involves placing a radiosurgical probe at the level of the LES to heat and scar the tissue and thus strengthen the valve.19
It is well-documented that patients with GERD have acidic stomach contents that can reach the pharyngeal level and cause atypical (extraesophageal) symptoms such as chronic cough, hoarseness, wheezing, laryngitis, and even asthma.20 An early attempt to document a connection between GERD and dental erosion showed that patients who display gastric symptoms (heartburn, acid taste, sour stomach, gastric pain on waking) on a weekly basis have a 10 times greater chance of having dental erosion than those who do not. Patients who experienced these symptoms for 10 years or longer were at a much higher risk for severe Grade 3 erosion.21
A more definitive study used ambulatory 24-hour esophageal pH testing at the LES level and near the pharyngeal level of the esophagus in two groups of patients. One group (dental group) consisted of patients with idiopathic erosion identified by dental examination; these patients then were referred for pH testing. For the second group of patients (gastroenterology group), GERD was confirmed by esophageal pH testing and the patients were referred for dental examination. In the dental group, 24-hour esophageal pH monitoring diagnosed GERD in 83% of patients. Among patients in the gastroenterology group, 40% had dental erosion, including 70% of those with reflux that reached the pharyngeal level. When all patients with erosion were analyzed, the cumulative erosion score (that is, the summation of erosion scores) correlated with pharyngeal level reflux; only 10% of those with no documented reflux had dental erosion. The authors suggested that dental erosion should be considered an extraesophageal manifestation of GERD.22
It should be noted that erosion resulting from exposure to stomach acid generally is found on the
Patients suspected of reflux-associated erosion should undergo thorough questioning and provide a history of gastric symptoms and past use of antacids or other medications that treat or even cause reflux as a side effect. A patient with undiagnosed reflux who responds positively to these questions should be referred to a gastroenterologist for evaluation. Unfortunately, because GERD can be clinically silent for a significant percentage of patients, some patients without obvious symptoms will resist referral and require thorough education about their problem.24
All patients should record their dietary history over a four-day period to rule out dietary contributions to erosion; high consumption of carbonated beverages, sports drinks, fruit juices (especially those involving citrus fruit), yogurt, vinegar products, or other acidic foods may contribute to erosion.25 A comprehensive dental examination should include photos and diagnostic models and should document erosion distribution and severity by using a numerical scale such as the Eccles and Jenkins scale.3
Jarvinen et al estimated that patients with low unstimulated salivary flow rates (0.1mL/min or less) are five times more likely to have dental erosion than those with normal flow rates.26 With that in mind, a dental examination should include checking the patient’s salivary function, including flow rate, pH, and buffering capacity. Salivary parameters can be tested easily by using the Saliva Check kit (GC America Inc.,
Once GERD-related erosion has been diagnosed, the clinician should take advantage of all available preventive measures to reduce the rate of erosion and protect the remaining tooth structure. The patient should be counseled to avoid foods that can cause gastric reflux and acidic foods (such as soft drinks, citrus fruits and juices, and vinegar products) that have been demonstrated to cause erosion. Patients should avoid brushing for 60 minutes after reflux episodes to avoid damaging acid-softened enamel.27 In the period between reflux and brushing, acid in the oral cavity can be cleared away by rinsing with water or a baking soda solution (1 teaspoon per 8 ounces of water) or by allowing a sugar-free antacid to dissolve slowly in the mouth. To stimulate salivary flow and neutralize acidic challenges, patients can chew xylitol gum or other sugarless gums, lozenges, or candies.28
Enamel remineralization strategies include the use of products such as Trident White or Trident Xtra Care chewing gum (Cadbury Adams, Parsippany, NJ) or MI Paste (GC America Inc.), all of which contain a casein phosphopeptide-amorphous calcium phosphate complex, which can remineralize enamel subsurface lesions with mineral that is resistant to acid challenges from sources such as cariogenic bacteria or stomach acid.29 To increase enamel’s resistance to acid dissolution, a 1.1% neutral sodium fluoride gel such as Prevident (Colgate Oral Pharmaceuticals, New York, NY) can be placed via fluoride gel carriers fabricated from soft mouthguard or bleaching tray material.30 Trays should be lined with neutral sodium fluoride gel and worn for a minimum of 10 minutes daily, preferably just before bedtime. Trays without fluoride gel can be worn overnight to act as a protective device during sleep by shielding teeth from nighttime reflux. As with toothbrushing, patients should delay using a fluoride tray for 60 minutes after a reflux episode to prevent physical damage on softened enamel.
Rehabilitation of teeth should be conservative and may range from using desensitizing and remineralizing agents to full-mouth restoration, depending on the extent of erosion. Early-to-moderate lesions may be restored with resin-modified glass ionomer (RMGI) or resin-based composite restorations, while severe lesions may require veneers or crowns as part of a complex full-mouth rehabilitation, in conjunction with restoring lost vertical dimension of occlusion.31
Summary
When erosion is detected on
After diagnosis, the progress of acid reflux-induced erosion can be managed by appropriate medical referral and use of all available preventive measures. Potentially severe destruction of the dentition can be avoided through diagnosis, prevention, and treatment of GERD-induced erosion.
Disclaimer
The authors have no financial relationship with any of the manufacturers listed in this article.
Author information
Dr. Lazarchik is an associate professor, Department of General Dentistry, Medical College of Georgia School of Dentistry in
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General Dentistry, March/April 2009 , Volume 57 , Issue 2
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