Content uploaded by Rebecca Moazzez
Author content
All content in this area was uploaded by Rebecca Moazzez on Feb 04, 2014
Content may be subject to copyright.
http://jdr.sagepub.com/
Journal of Dental Research
http://jdr.sagepub.com/content/84/11/1062
The online version of this article can be found at:
DOI: 10.1177/154405910508401118
2005 84: 1062J DENT RES
R. Moazzez, D. Bartlett and A. Anggiansah
The Effect of Chewing Sugar-free Gum on Gastro-esophageal Reflux
Published by:
http://www.sagepublications.com
On behalf of:
International and American Associations for Dental Research
can be found at:Journal of Dental ResearchAdditional services and information for
http://jdr.sagepub.com/cgi/alertsEmail Alerts:
http://jdr.sagepub.com/subscriptionsSubscriptions:
http://www.sagepub.com/journalsReprints.navReprints:
http://www.sagepub.com/journalsPermissions.navPermissions:
What is This?
- Nov 1, 2005Version of Record >>
at Kings College London - ISS on February 4, 2014 For personal use only. No other uses without permission.jdr.sagepub.comDownloaded from
International and American Associations for Dental Research
at Kings College London - ISS on February 4, 2014 For personal use only. No other uses without permission.jdr.sagepub.comDownloaded from
International and American Associations for Dental Research
INTRODUCTION
G
astro-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
ABSTRACT
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.
Received May 4, 2004; Last revision July 1, 2005;
Accepted July 14, 2005
The Effect of Chewing
Sugar-free Gum
on Gastro-esophageal Reflux
R. Moazzez*, D. Bartlett,
and A. Anggiansah
Department of Prosthodontics, Floor 26, Guy's Tower, St.
Thomas' Street, London Bridge, London SE1 9RT, UK;
*corresponding author, Rebecca.moazzez@kcl.ac.uk
J Dent Res
84(11):1062-1065, 2005
RESEARCH REPORTS
Clinical
1062
at Kings College London - ISS on February 4, 2014 For personal use only. No other uses without permission.jdr.sagepub.comDownloaded from
International and American Associations for Dental Research
J Dent Res 84(11) 2005 Chewing Gum and Reflux Activity 1063
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 larynogo-
pharyngeal 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.
MATERIALS & METHODS
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 H
2
-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
The pH data were analyzed for the entire 24-hour study period for
each subject, according to internationally recognized assessments
(Johnson and DeMeester, 1974; Richter et al., 1992). Reflux times
for healthy subjects, as generally recognized in the literature
(DeMeester and Richter), were as follows: total 5.78%, upright
8.15%, and supine 3.45%. These are internationally recognized
normal values for the percentage time below pH 4 in the esophagus
over the 24-hour period. These criteria were used to subdivide the
patient group into those with pathological levels of reflux and others
within normal parameters. The DeMeester score uses 6 parameters
(supine reflux, upright reflux, total reflux, number of episodes,
number of episodes longer than 5 min, and the longest episode) to
calculate a score that indicates the severity of reflux. It is calculated
from the equation (patients value-mean)/standard deviation +1 for
each parameter, the final score being the sum of the scores for the 6
different parameters. Data were also analyzed for the postprandial
periods for 2 hrs on the 2 occasions, one where the standard
refluxogenic meal was eaten and the patients spent the following 2
hrs resting, and the other, when the refluxogenic meal was eaten
followed by patients chewing a piece of gum for half an hour. The %
time esophageal pH was below 4 was analyzed between the 2
postprandial periods, and the results were compared by the
Wilcoxon signed-rank test. The number of episodes and the longest
episode were also compared by the same test. We calculated the
symptom index by correlating the percentage of reflux episodes that
occurred at the same time the patient was experiencing normal
symptoms. It was calculated according to the formula (Number of
symptoms with pH < 4 /total number of symptoms x 100).
RESULTS
Thirty-one patients with gastro-esophageal reflux symptoms
(mean age, 49 yr) (Standard Deviation [SD], 11.2; 19 males,
Table 1. The Distribution of Symptoms in the Patient Group and
Grouped into Those Diagnosed with Pathological and Non-pathological
Levels of Reflux
Patients with Patients
without
gastro-esophageal gastro-esophageal
reflux (n = 19) reflux (n = 12) p value
% Heartburn 100 100 N/A
% Belching 79 50 0.10
% Regurgitation 63 41 0.06
% Chest pain 58 83
0.05
% Vomiting 21 8 0.23
% Sore throat 42 42 0.53
% Asthma 42 8
0.05
% Globus 26 16 0.44
% Hoarseness 21 16 0.57
at Kings College London - ISS on February 4, 2014 For personal use only. No other uses without permission.jdr.sagepub.comDownloaded from
International and American Associations for Dental Research
1064 Moazzez
et al. J Dent Res
84(11) 2005
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.
DISCUSSION
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
Table 2. Median and Interquartile Range (IQR) for Patients with Pathological gastro-
esophageal reflux and Non-pathological gastro-esophageal reflux for Total, Upright, and
Supine Percentage Times (min) when pH Fell below 4 during the 24-hour pH Recording,
Together with the DeMeester Score (DeMeester
et al.
, 1976)
Total Reflux Upright Reflux Supine Reflux DeMeester Score
Pathological gastro-esophageal reflux
Median (IQR) 14 (8.8-17.6) 10.4 (7.4-17.3) 11.2 (5.5-23.4) 53.2 (34.2-75.7)
Non-pathological gastro-esophageal reflux
Median (IQR) 1.2 (0.4-1.4) 1.8 (0.45-2.0) 0.1 (0.05-0.55) 6.05 (2.6-6.9)
Table 3. Median and Interquartile Range (IQR) for % Time pH was Below 4 for the Two
Postprandial Periods for All Patients, Patients with gastro-esophageal reflux, and Patients
without gastro-esophageal reflux (p values are shown for the difference between the periods
with and without gum.)
Patients with Patients without
All Patients gastro-esophageal reflux gastro-esophageal reflux
(n = 31) (n = 19) (n = 12)
No gum Median (IQR) 5.7 (1.7-13.5) 10.5 (4.6-23.4) 1.7 (0.3- 4.4)
Gum Median (IQR) 3.6 (0.3- 7.3) 5.8 (2.5-10.7) 0.2 (0.05-2.0)
p value 0.001 0.017 0.013
Table 4. Median and Interquartile Range (IQR) for Number of Reflux
Episodes and the Longest Episode of Reflux pH was below 4 for the Two
Postprandial Periods for All Patients (p values are shown for the
difference between the periods with and without gum.)
No. of Reflux Episodes Longest Reflux Episode
All Patients (n = 31) All Patients (n = 31)
No gum Median 2 8
IQR 1-4 4-16
Gum Median 1 6
IQR 0-2 0-11
p value 0.001 < 0.001
at Kings College London - ISS on February 4, 2014 For personal use only. No other uses without permission.jdr.sagepub.comDownloaded from
International and American Associations for Dental Research
J Dent Res 84(11) 2005 Chewing Gum and Reflux Activity 1065
(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.
ACKNOWLEDGMENTS
This study was supported by the Department of Conservative
Dentistry at GKT and by the Oesophageal Department at St
Thomas' hospital.
REFERENCES
Anggiansah A, Owen WA, Owen WJ (1993). The investigation and
management of gastro-oesophageal reflux disease. Br J Clin Pract
47:256-261.
Avidan B, Sonnenberg A, Schnell TG, Sontag SJ (2001). Walking and
chewing reduce postprandial acid reflux. Aliment Pharmacol Ther
15:151-155.
Bartlett DW, Evans DF, Anggiansah A, Smith BGN (1996). A study of
the association between gastro-oesophageal reflux and palatal
dental erosion. Br Dent J 181:125-132.
DeMeester TR, Johnson LF, Joseph GJ, Toscano MS, Hall AW,
Skinner DB (1976). Patterns of gastroesophageal reflux in health
and disease. Ann Surg 184:459-469.
Edgar WM (1990). Saliva and dental health. Clinical implications of
saliva: report of a consensus meeting. Br Dent J 169:96-98.
Edgar WM, O'Mullane DM, editors (1996). Saliva and oral health. 2nd
ed. London: British Dental Journal.
Gillen D, McColl KE (2001). Problems associated with the clinical use
of proton pump inhibitors. Pharmacol Toxicol 89:281-286.
Helm JF (1989). Role of saliva in esophageal function and disease.
Dysphagia 4:76-84.
Helm JF, Dodds WJ, Hogan WJ (1987). Salivary response to
esophageal acid in normal subjects and patients with reflux
esophagitis. Gastroenterology 93:1393-1397.
Johnson LF, DeMeester TR (1974). Twenty four hour pH monitoring
of the distal esophagus. Am J Gastroenterol 62:325-332.
Jones R, Lydeard S (1989). Prevalence of symptoms of dyspepsia in
the community. Br Med J 298:30-32.
Pereira SP, Gainsborough N, Dowling RH (1998). Drug induced
hypochlohydria causes high bacterial counts in the elderly.
Aliment Pharmacol Ther 12:99-106.
Richter JE (1986). A critical review of current medical therapy for
gastroesophageal reflux disease. J Clin Gastroenterol 8(Suppl
1):72-80.
Richter JE, Bradley LA, DeMeester TR, Wu WC (1992). Normal 24-hr
ambulatory esophageal pH values; influence of study centre, pH
electrode, age and gender. Dig Dis Sci 37:849-856.
Sarosiek J, Scheurich CJ, Marcinkiewicz M, McCallum RW (1996).
Enhancement of salivary esophagoprotection: rationale for a
physiological approach to gastroesophageal reflux disase.
Gastroenterology 110:675-681.
Smith BG, Knight JK (1984). An index for measuring the wear of
teeth. Br Dent J 156:435-438.
Smoak BR, Koufman JA (2001). Effects of gum chewing on
pharyngeal and esophageal pH. Ann Otol Rhinol Laryngol
110:1117-1119.
von Schonfeld JV, Hector MP, Evans DF, Wingate D (1997).
Oesophageal acid and salivary secretion: is chewing gum a
treatment option for gastro-oesophageal reflux? Digestion 58:111-
114.
Wiener GJ, Morgan TM, Copper JB, Castell DO, Sinclair JW, Richter
JE (1988). Ambulatory 24-hour esophageal pH monitoring. Dig
Dis Sci 33:1127-1133.
at Kings College London - ISS on February 4, 2014 For personal use only. No other uses without permission.jdr.sagepub.comDownloaded from
International and American Associations for Dental Research