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The Effect of Chewing Sugar-free Gum on Gastro-esophageal RefluxDepartment of Prosthodontics, Floor 26, Guy’s Tower, St. Thomas’ Street, London Bridge, London SE1 9RT, UK; Correspondence: * corresponding author, Rebecca.moazzez{at}kcl.ac.uk
Regurgitated acid entering the mouth in gastro-esophageal reflux disease can cause dental erosion. Chewing gum could induce increased swallowing frequency, thus improving the clearance rate of reflux within the esophagus. The null hypothesis of this study was that chewing gum does not have any effect on the clearance of reflux from the distal esophagus. Thirty-one subjects presenting with symptoms of reflux were given a refluxogenic meal twice and were randomly selected to chew gum for half an hour after eating the meal. Esophageal pH was measured, and pH data were analyzed and compared during the postprandial periods for 2 hrs on the 2 occasions. The median (IQ range) values for the % time pH < 4 during the postprandial period without chewing gum were 5.7 (1.7–13.5) and, with chewing gum, 3.6 (0.3–7.3), respectively (p = 0.001). Chewing sugar-free gum for half an hour after a meal can reduce acidic postprandial esophageal reflux.
Key Words: chewing gum • reflux • esophageal • pH.
Gastro-esophageal reflux disease is common and occurs in 60% of the population. Approximately 10% of the population seeks medical advice for symptoms such as heartburn, epigastric pain, retrosternal discomfort, and regurgitation (Jones and Lydeard, 1989). The prevalence of gastro-esophageal reflux disease has resulted in Proton Pump Inhibitors (PPIs) being the most commonly prescribed drug on the UK National Health Service (NHS) pharmacy list, costing over £400M per annum. In many cases, PPIs are prescribed as a first line of treatment where there is doubt or on an empirical basis. However, there are some concerns regarding long-term PPI therapy, including possible intragastric bacterial overgrowth and increased susceptibility to gastro-intestinal infections (Pereira et al., 1998). Lifestyle changes—such as avoiding eating fatty meals, especially late at night, losing weight, and raising the head of the bed—are useful, but medication is the most common method of gastro-esophageal reflux disease management (Richter, 1986). Medication, although effective in most patients, can result in side-effects, such as hypertrophy of the parietal cells in the stomach, resulting in exaggerated symptoms on withdrawal (Gillen and McColl, 2001). It would therefore be helpful to consider simpler methods to control acid reflux. Over the last 20 years, 24-hour pH measurement has been accepted as the gold standard for objective assessment of the level of refluxed gastric juice within the esophagus (Johnson and DeMeester, 1974). The results are used as part of the decision-making process for medication to control the gastro-esophageal reflux. It is generally accepted that 24-hour ambulatory pH monitoring is objective and reproducible, as well as the most sensitive and specific method for the investigation of gastro-esophageal reflux disease (Wiener et al., 1988). The role of gastro-esophageal reflux disease in dental erosion has been widely reported. Regurgitated acid entering the mouth causes dental erosion. The pattern of erosion is similar to that in other conditions involving stomach juice, such as eating disorders, rumination, and chronic alcoholism. Bartlett et al.(1996), in a controlled study, investigated 36 patients with palatal dental erosion assessed according to the Smith and Knight tooth wear index (TWI) (1984). The results were compared with those from ten subjects with neither tooth wear nor symptoms of gastro-esophageal reflux disease. Oral pH was also measured simultaneously. Twenty-three (64%) patients were found to have gastro-esophageal reflux disease, according to the Johnsson and DeMeester criteria (1974). Interestingly, 16 patients were found to have gastro-esophageal reflux symptoms; the remaining seven did not complain of any symptoms. The term "silent refluxers" was used to describe these latter patients. A statistically significant relationship was observed between the pH in the distal esophagus and the pH in the mouth. When gastro-esophageal reflux occurs, refluxate volume and acid clearance from the esophagus depend on two major mechanisms. Peristalsis initiates esophageal clearance, and swallowed saliva neutralizes the residual acid (Helm, 1989). Helm et al. recognized that salivary flow rate and buffering capacity are important in the protection of the esophagus against gastro-esophageal reflux (Helm et al., 1987). Furthermore, Sarosiek et al. observed increased bicarbonate levels in patients, diagnosed with reflux esophagitis, at endoscopy, and suggested that the increase may have a therapeutic value in the control of reflux (Sarosiek et al., 1996). A common dietary stimulant of saliva is chewing gum. Chewing gum increases salivary flow rate (Edgar and O’Mullane, 1996) and bicarbonate levels within the saliva, and thus increases the buffering capacity. This could, in theory, induce increased swallowing frequency, thus improving the clearance rate of reflux within the esophagus. Schonfeld et al.(1997) investigated esophageal acid clearance times in ten healthy volunteers chewing a piece of gum after infusion with 0.1 M HCl, and observed that their esophageal clearance times were significantly shorter with gum chewing. Smoak and Koufman investigated the effects of chewing gum in a study of 40 consecutive patients with larynogopharyngeal reflux (Smoak and Koufman, 2001). Twenty subjects received regular chewing gum, and 20 chewed a gum containing bicarbonate. The subjects recorded the chewing episodes during the test period. The authors observed that chewing gum increased esophageal and pharyngeal pH, and suggested that chewing gum might be an effective adjunct to anti-reflux therapy. In another study, Avidan et al. also investigated the effect of chewing gum after meals, in 12 subjects with reflux disease, and compared the results with those from a group of 24 healthy controls (Avidan et al., 2001). Over 3 separate days, pH was measured for a four-hour period, but on the third day, following the meal, gum was chewed. The authors observed that chewing gum reduced reflux after provocation by food. The null hypothesis of this study was that chewing gum does not have any effect on the clearance of reflux from the distal esophagus. The aim of this study was to assess the role of chewing gum, with a reflux-provoking meal, on distal esophageal pH in patients presenting with symptoms of gastro-esophageal reflux.
Patients presenting with symptoms of gastro-esophageal reflux, referred to the Esophageal Laboratory at St. Thomas’ Hospital, London, for 24-hour ambulatory pH testing, were recruited into the study. Each patient’s symptoms were recorded prior to the pH study and all patients were requested to stop PPI for 7 days and H2-blocker or pro-kinectic agents for 48 hrs prior to the tests. Each subject had standard manometry followed by a 24-hour ambulatory pH study, according to conventional guidelines, when pH was measured continuously for the entire period (Richter et al., 1992). Ethical approval was obtained prior to the study from the Guy’s and St. Thomas’ Ethics Committee. Patients consumed a standardized refluxogenic meal containing 60% fat (2 bars of full-fat cheddar cheese, green salad with 2 tablespoons of mayonnaise, 15 large chips, half a pint of full-fat milk) on the first and second days for lunch after a four-hour fast. They were randomly selected to chew a standard piece of gum (Orbit Chewing gum, Wrigley’s, Plymouth, UK) for half an hour after eating the meal. The random selection was carried out to ensure that patients chewed gum on either the first or the second day, to avoid the insertion of catheters on the first day to have any effect on the results. Esophageal pH was recorded over 24 hrs by means of antimony electrodes (Synectics, Stockholm, Sweden) positioned at 5 cm above the lower esophageal sphincter, the position determined by manometry. The antimony electrodes were calibrated according to the manufacturer’s recommendations, and the pH data were recorded onto a digital data-logger (Digitrapper, Synectics, Stockholm, Sweden). Subjects recorded times of their symptoms and meal and supine periods during the study onto the recorder. At the end of the study, the catheters were removed and the data analyzed.
Analysis of Data
Thirty-one patients with gastro-esophageal reflux symptoms (mean age, 49 yr) (Standard Deviation [SD], 11.2; 19 males, 12 females) successfully took part in this study over a 24-hour period. Subjects had gastro-esophageal reflux symptoms for a median time of 8 yrs (Inter-quartile Range, 4–15 yrs) (Table 1  ). Patients suffered from symptoms of gastro-esophageal reflux disease—in particular, heartburn—whether they suffered from pathological levels of reflux or not. There were variations in the reported symptoms between the pathological gastro-esophageal reflux and the non-pathological group—for example, the gastro-esophageal reflux group complaining of regurgitation more than the non-gastro-esophageal reflux group (p = 0.06). The non-gastro-esophageal reflux group, however, complained of chest pain more often than the gastro-esophageal reflux group, whereas the gastro-esophageal reflux group complained of asthma more than the non-gastro-esophageal reflux group, and these differences were statistically significant (p = 0.05). All subjects had a median 8.1% (IQR 1.3–15.5) of the time pH < 4 in the distal esophagus. The median time for the longest episode of reflux was 21 min (IQR, 4–35 min).
When the groups were divided into those with pathological and those with non-pathological gastro-esophageal reflux, 19 patients (nine males, ten females) (mean age, 50 yrs) (SD 10.8) had pathological gastro-esophageal reflux, and 12 patients (ten males, two females) (mean age, 47 yrs) (SD 12.1) had non-pathological gastro-esophageal reflux (Table 2 ). Those with pathological gastro-esophageal reflux had a median duration of symptoms for 10 yrs (IQR, 7–20), and those with non-pathological gastro-esophageal reflux, 3.5 yrs (IQR, 2–9). Subjects with pathological gastro-esophageal reflux had a median 14% (IQR 8.8–17.6) of the time pH < 4 in the distal esophagus, and those with non-pathological gastro-esophageal reflux had 1.2% (IQR, 0.4–1.4).
The percentage time was less after the patient had chewed gum for half an hour, compared with the postprandial period when no gum was chewed (median of 5.7, going down to 3.6), and this difference reached statistical significance (p < 0.001) (Table 3 ). There were statistically significant differences for the longest episode and the number of reflux episodes for all patients and those diagnosed with pathological gastro-esophageal reflux (p < 0.001), but not for those patients with non-pathological levels of reflux (longest episode, p = 0.096; number of reflux episodes, p = 0.24) (Table 4). There were no statistically significant differences for the number of reflux episodes greater than 5 min in any group.
The symptom index is the percentage of reflux episodes related to symptoms. Nine patients complained of heartburn, and the symptom index was calculated during the postprandial periods. Chewing gum seemed to improve heartburn in six of these patients, made no difference in one patient, and made heartburn worse in two. The other 22 patients recorded no symptoms during the 2 two-hour postprandial periods. The mean (SD) of the symptom index for heartburn for the postprandial periods with no gum and with gum were 10.2% (21.7%) and 2.6% (7.1%), respectively, but the difference was not statistically significant.
Chewing gum for 30 min after the meal reduced acid reflux in both groups. The concept of using chewing gum to reduce reflux was first investigated by von Schonfeld et al. (von Schonfeld et al., 1997) on ten healthy volunteers, but these investigators used 0.1 M HCl to provoke acid reflux, while this study used a fatty meal. Previous work has shown that the flow rate and buffering capacity of saliva are increased by chewing (Edgar, 1990). Saliva buffers the acid within the distal esophagus, and swallowing increases the rate of peristalsis; both are recognized as major factors in esophageal acid clearance. Chewing gum, therefore, has the potential to be used as a cheap and convenient method for controlling reflux. The patient group as a whole had levels of reflux approaching pathological values in the distal esophagus. The inclusion criteria specifically targeted patients presenting with symptoms of reflux, so this result is not surprising. The finding that some patients had percentage levels of reflux below pathological values is also not surprising, considering the periodic nature of the disease process and the problem of associating symptoms with the presence of disease. Within the confines and design of this study, postprandial reflux could be measured only for 2 hrs after the meal. Avidan et al. asked their subjects to chew gum for 1 hr, and reported statistically significant differences (Avidan et al., 2001). In the present study, the effect of chewing gum for half an hour was considered more convenient for the patients, since some might find chewing for 1 hr difficult. Control subjects were considered to be unnecessary, since the patients acted as their own controls, and the postprandial period without chewing gum was the control part of the study. The number of pathological reflux episodes was also reduced, after chewing gum, in those with symptoms and in the gastro-esophageal reflux disease group, but not in the group with non-pathological levels of gastro-esophageal reflux. The same was true for the longest episode of reflux. These results suggest that, although chewing gum is effective in clearing acid from the esophagus in patients with gastro-esophageal reflux as well as those without, it may have a slightly different effect in the two groups. Those subjects with symptoms during the postprandial period experienced less severe symptoms after chewing gum; however, in a few subjects, although acid reflux was cleared, symptoms persisted, despite the reduction in the pH recording. The presence of symptoms is well-recognized to be a poor diagnostic indicator of disease (Bartlett et al., 1996). Despite this, the potential to use chewing gum to control acid reflux and symptoms of gastro-esophageal reflux needs further evaluation. The most common symptom of gastro-esophageal reflux is heartburn (Anggiansah et al., 1993), and all patients in this study suffered from this symptom. The use of chewing gum with other conservative measures could provide a comparatively safe and effective method of controlling acid reflux and symptoms. It may be effective in esophageal symptoms of reflux, but further studies are necessary to assess its use in patients presenting with extra-esophageal symptoms.
This study was supported by the Department of Conservative Dentistry at GKT and by the Oesophageal Department at St Thomas’ hospital. Received for publication May 4, 2004. Revision received July 1, 2005. Accepted for publication July 14, 2005.
Journal of Dental Research, Vol. 84, No. 11,
1062-1065 (2005)
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ABSTRACT
INTRODUCTION