Oral manifestations of gastroesophageal reflux disease

REVIEW jgh_6945 21..27

Oral manifestations of gastroesophageal reflux diseaseSarbin Ranjitkar, Roger J. Smales and John A. Kaidonis

School of Dentistry, The University of Adelaide, Adelaide, South Australia, Australia

AbstractNumerous case-control and other studies involving confirmation of gastroesophageal refluxdisease (GERD) by esophageal pH-metry and the assessment of dental erosions haveshown significant associations between the two conditions in both adults and children. Bycontrast, when asked to vote on whether GERD may cause dental erosions, only 42% ofphysicians strongly agreed that such an association existed in adults, and just 12.5%strongly agreed for children, respectively in two global consensus reports. Part of thisdivergence between the perceptions of physicians and the findings of research publicationsmay reflect a general lack of oral health education during medical training, and cursory oralexaminations being made under less-than-ideal conditions. Adequate salivary secretionsare essential for the protection of the teeth and the oropharyngeal and esophageal mucosa.The quantity and quality of the saliva require monitoring as many drugs, including severalof the proton pump inhibitors (PPIs), can cause hyposalivation. In addition, PPIs do notalways result in adequate acid suppression. Therefore, collaboration between physiciansand dentists is strongly advocated to prevent or ameliorate possible adverse oral effectsfrom both endogenous and exogenous acids, and to promote adequate saliva production inpatients with GERD.

Key words

collaborative management, dental erosion,gastroesophageal reflux disease, prevention.

Accepted for publication 18 September 2011.

Correspondence

Dr Sarbin Ranjitkar, School of Dentistry, TheUniversity of Adelaide, North Terrace,Adelaide, SA 5005, Australia. Email:[email protected]

Conflict of interest: None.

IntroductionThere is relatively little information in general medical and gas-troenterology literature regarding tooth erosion that may be asso-ciated with gastroesophageal reflux disease (GERD). Thisassociation is commonly observed by dentists, but is given verycursory mention or omitted entirely when describing extra-esophageal (supra-esophageal) manifestations of GERD.1–7

When 44 medical experts and family physicians from 18 coun-tries voted in the World Congress of Gastroenterology presentationin Montreal on the statement that “The prevalence of dental ero-sions, especially on the lingual and palatal tooth surfaces, isincreased in patients with GERD” (Extra-esophageal Syndromes:Established Associations, Statement #48), the result was a high-grade consensus agreement of 96%.8 However, only 42% of theconsensus votes “agreed strongly” with the above statement, 35%“agreed with minor reservations,” and 19% “agreed with majorreservations.” Just three selected clinical studies were quoted tosupport the statement.9–11

Subsequently, when eight pediatric gastroenterologists using arevision of the original Montreal presentation protocol voted onthe statement that “GERD may cause dental erosions in pediatricpatients” (Extraesophgeal Syndromes: Definite Associations,Statement #53), the result was a low-grade consensus agreement of100%.12 But, only 12.5% of the votes “agreed strongly,” 37.5%“agreed moderately,” and 50% “just agreed.” One systematic

review article13 and four other selected clinical articles14–17 werequoted to support the above statement. Dental erosion was onlyone of two extra-esophageal conditions considered to be definitelyassociated with GERD in pediatric patients, the other being San-difer’s syndrome (torticollis).12

In the two previous global consensus reports,8,12 the relativelylow percentages of physicians’ votes agreeing strongly that GERDmay cause tooth erosion in both adults and children is possibly areflection of a lack of oral health training. One random surveyinvolving 611 graduating pediatric residents found that mostreceived either no training or less than 3 h of oral health training,with only 14% spending clinical observation time with a dentist.18

A national survey of pediatricians also found that only 54% exam-ined the teeth of more than half of their 0–3-year-old patients.Fewer than 25% of these pediatricians had received any oral healtheducation at all during their career.19 In both surveys, most of thepediatricians stated that they should be trained to undertake basicoral health screenings. Compounding this problem, another ques-tionnaire survey found that only three of 104 pediatricians wereaware of tooth erosion caused by acidic pediatric medications.20 Arecent review article concluded that, “the primary care physicianand the gastroenterologist need to pay more attention to the oftenneglected oral examination.”13

Tooth erosion is usually a slow process occurring over manyyears, and its subtle appearance is often not adequately observedduring a cursory examination under less-than-ideal conditions. It is

doi:10.1111/j.1440-1746.2011.06945.x

21Journal of Gastroenterology and Hepatology 27 (2012) 21–27

© 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd

not surprising that advanced erosive tooth wear is usually detectedonly after significant damage has occurred to the dentition and themasticatory system.21 Therefore, the diagnosis and preventivemanagement of early stages of erosive tooth wear should be a keystep to avoiding a lifetime of debilitating dentition and complexrestorative therapy.22 It should also be realized that expensive andextensive treatment for advanced erosive tooth wear can fail cata-strophically and may need long-term maintenance.

Tooth wear is a multifactorial condition caused by tooth grind-ing, abrasion from coarse food or objects, exogenous erosion (e.g.dietary acids and acidic medications) and endogenous erosion (e.g.gastric regurgitation and vomiting). It is beyond the scope of thisarticle to conduct a detailed review of all these wear processes.Therefore, we have focused on issues relating to endogenouserosion associated with GERD (gastric regurgitation). Specifically,these issues include the oral manifestations of GERD, the occur-rence of gastric regurgitation with tooth grinding, the oral defensesystem including salivary protection, and the collaborative medicaland dental management.

Oral manifestations attributed to GERDThe principal difficulty with investigating the links betweenGERD and its possible oral manifestations in humans has been theneed to subject them to unacceptable invasive investigative proce-dures and to withhold any required treatments during long-termprospective studies. Therefore, the principal evidence for suchlinks has been from studies of patients with confirmed GERD whoare then found to have tooth erosion, and vice versa.

The most commonly described oral manifestation attributed toGERD (and other causes of stomach contents reaching the mouth),is tooth erosion, which has been widely investigated and reportedin dental literature9–11,13–17,23–30 These mainly case-control studiesreported that GERD was associated with at least 20–30% ofpatients with tooth erosion. The majority of clinical studies oftooth erosion with confirmed evidence of GERD (using esoph-ageal endoscopy and pH-metry), have also found similar signifi-cant associations between tooth erosion and GERD.9,11,15,17,23–25,30,31

Using optical coherence tomography, a 3-week randomized,double-blind and prospective clinical trial of 29 patients withconfirmed GERD reported significantly less enamel erosion in theesomeprazole-treated group than in a placebo group.29 However,several clinical studies have not found significant associa-tions,16,28,32 although one of these studies reported a strong asso-ciation with other oral manifestations of GERD in the form ofburning mucosal sensation, halitosis and mucosal erythema.28 Inanother study, up to 25% of individuals with tooth erosions andconfirmed GERD had silent regurgitation.23 It should be appreci-ated that a loss of tooth substance is usually only readily observedafter a long period of endogenous acid contact and, therefore, earlysigns of erosion may be easily overlooked.

Because of the large number of persons with undiagnosedGERD are “silent refluxers,”33,34 dentists may be the first to suspectthe presence of this potentially serious condition from their obser-vations of otherwise unexplained dental erosion.23 Apart fromtooth erosion, the surfaces of glass-ionomer and ceramic dentalrestorative materials that contain a matrix of glass particles alsomay be damaged by acids to varying extents. In addition, personswith GERD may complain of a sour or acidic taste, impaired taste

(dysgeusia), an oral burning sensation and water brash (flooding ofthe mouth with saliva in response to an esophageal reflux stimu-lus). However, oral mucosal changes that may be associated withGERD are described far less frequently.28,35

Tooth erosion (corrosion)

Dental erosion or, more correctly, dental corrosion is described astooth surface loss produced by chemical or electrolytic processesof non-bacterial origin, which usually involves acids.36 The acidsare of endogenous (intrinsic) origin from regurgitated gastricjuices and of exogenous (extrinsic) origin from usually dietary,medicinal, occupational and recreational sources. Tooth erosion ishighly unlikely to be caused by alkaline bile juices from duode-nogastroesophageal regurgitation (DGER).37 The majority ofextraesophageal symptoms are more likely to be associated withacid regurgitation than DGER. Acid regurgitation has been impli-cated as the major factor, even in patients suffering from refractoryGERD to proton pump inhibitor (PPI) therapy,38 contrary to pre-vious beliefs about the role of DGER.39

The potential for tooth erosion from gastric contents is modi-fied by many secondary factors. Gastric acid has a pH of approxi-mately 1.2, but the regurgitated gastric contents may also containvarying amounts of partly digested foodstuffs and pepsin, as wellas bile acids and the pancreatic enzyme trypsin when there is anaccompanying duodenal regurgitation.27 Antacid medicationsreduce the acidity of the gastric contents, and proton pump inhibi-tor (PPI) medications decrease the acid output. Therefore, thepotential for tooth erosion will vary, and will be modified byfactors such as the composition and pH of the refluxate, the fre-quency and the form it reaches the mouth (regurgitation or belch-ing of acidic vapors), the flow rate and buffering (bicarbonate ion)capacity of stimulated saliva and the duration for clearance fromthe mouth, and whether patients brush the softened tooth surfacesimmediately after regurgitation episodes. The “critical pH” fordemineralization of enamel is approximately 5.5 (and even higherfor dentin), which may readily be exceeded by the regurgitatedgastric contents.

The detection of the early stages of tooth erosion requiresadequate isolation of dried tooth surfaces and retraction of oral softtissues, good lighting and a small mouth mirror. The affectedenamel appears smoothly glazed or “silky” with rounded surfaces,which may appear very clean because of the removal of stains,dental plaque and acquired dental pellicle by the gastric juices(Fig. 1). Other characteristic features of erosion lesions includeenamel thinning leading to an increased incisal and proximaltranslucency (Fig. 2a), and a yellowish appearance of the teethfrom “shine-through” of the underlying dentin (Fig. 2b). Subse-quent erosion of the less-mineralized dentin results in more rapidocclusal “cupping” of posterior cusp tips and anterior incisaledges. The thin unsupported enamel breaks off to leave jaggededges. During active erosion the exposed dentin may become verysensitive to temperature changes (e.g. hot and cold stimuli) andtouch (e.g. tooth brushing). The rate of tooth erosion may beexacerbated by superimposed mechanical wear processes (referredto as “erosive tooth wear”) and by exogenous acid sources.40

Mechanical tooth wear can occur from both tooth grinding andmastication occlusally, and from toothbrush abrasion cervically,whereas exogenous acids produce a more generalized pattern of

Dental erosion and GERD S Ranjitkar et al.

22 Journal of Gastroenterology and Hepatology 27 (2012) 21–27


tooth substance loss.40 Each of these wear processes has a specificwear pattern that can be generally identified at both macroscopicand microscopic levels.

Classically, tooth erosion from acid regurgitation involves theloss of enamel and dentin from initially the palatal surfaces of themaxillary teeth, taking several years to become clinically obvious(Fig. 2c). In long-standing instances, erosion can also affect theocclusal and other surfaces of maxillary teeth as well as mandibu-lar teeth (Fig. 2d). Existing non-eroded restorations appear raisedabove the adjacent eroded tooth surfaces. The pattern of erosion isaffected by the presence and distribution of oral biofilm (dentalplaque), the quantity and quality of saliva (which is protective ofthe mandibular anterior teeth in particular), the number and posi-tion of the teeth, and other conditions (such as mouth breathingassociated with incompetent lips, facial paralysis and major sali-vary gland pathology).

Oral mucosal lesions

Oral mucosal lesions may result from GERD by direct acid oracidic vapor contact in the oral cavity. However, there is a paucityof information on the effect of GERD on oral mucosal changes.One large case-controlled study observed a significant association

of GERD with erythema of the palatal mucosa and uvula.28 And, ahistologic examination of palatal mucosa found a greater preva-lence of epithelial atrophy, deepening of epithelial crests in con-nective tissue and a higher prevalence of fibroblasts in 31 GERDpatients compared with 14 control subjects.35 But, these changeswere not visible to the naked eye, unlike the mucosal changes thatmay be more readily observed in esophagitis and laryngitis wherethe pH of the gastric refluxate at these sites is lower than in themouth.23,25 Other studies have not found any abnormal appearancesof the oral mucosa or associated oral symptoms in patients withconfirmed GERD.41,42 However, acid regurgitation may exacerbateoral mucosal changes associated with co-existing hyposalivation,which can arise from systemic conditions, local salivary glandconditions and intake of drugs including PPIs.

Sleep bruxism and GERDBruxism (tooth grinding or clenching) is defined as contact of teethfor reasons other than eating and is a common cause of tooth wearin humans.43 It can occur both during the awake state as toothclenching, and during sleep as tooth grinding or clenching.44 Sleepbruxism sounds or noises are often reported by partners or parents,

Figure 1 (a) Early erosion lesion has a cleanand smoothly glazed appearance, with loss ofsurface morphology (i.e. grooves and pits) as aresult of acid dissolution. (b) Non-eroded teethshowing the presence of pronounced occlusalfissures towards the centre of the teeth.

Figure 2 (a) Broad shallow erosion with thin-ning of the enamel has resulted in anincreased translucency of the incisal region ofthe anterior maxillary central incisors, associ-ated with increased grayness (Courtesy Dr A.Dickson). (b) The thinner enamel in the cervicalregions (around the neck) of the teeth hasbeen eroded to varying degrees, accentuatingthe yellow appearance of the underlyingdentin. (c) Erosion has resulted in the loss ofpalatal and incisal enamel of the maxillary inci-sors. (d) Long-standing erosion has causedsevere loss of occlusal enamel and dentin oflower molar teeth, resulting in cupping ofthese teeth. For example there is a severecupping of the occlusal surface of the man-dibular first molar tooth adjacent to the resincomposite restoration (black arrow).

S Ranjitkar et al. Dental erosion and GERD



although bruxism may also occur in silence.45 Some researchershave described bruxism as a sleep-related stereotyped movementdisorder,46 and a “devastating” parafunctional habit, because of itsassociation with undesirable dental restorative treatment failures47

and, possibly, temporomandibular pain and dysfunction.48

However, leading experts now describe sleep bruxism as an asymp-tomatic occurrence in the majority of healthy individuals rather thana pathological condition, raising doubt over its generic classifica-tion as a sleep disorder.45

Previous sleep studies support the notion that sleep bruxism isan exaggerated form of oromotor activity associated with sleepmicroarousal49 and the swallowing of stimulated saliva produc-tion.50 Oromotor movements and the significance of saliva duringsleep have been reviewed previously.51 Though the etiology ofsleep bruxism is poorly understood, it is believed to involve thecentral and autonomic nervous systems rather than peripheralsensory mechanisms from the orofacial region.44,52 There is a largevariation in the occurrence of bruxism episodes during differentstages of sleep, with some reports showing its occurrence pre-dominantly during the rapid eye movement (REM) stage whileothers describing its occurrence during both REM and non-REMstages.53,54 By comparison, gastric regurgitation episodes in indi-viduals suffering from reflux esophagitis have been noted to occurmore frequently during non-REM sleep.55

Given the physiology of both sleep bruxism and GERD, it ispossible that these conditions may occur concurrently in someindividuals. Randomized clinical trials have established a highlysignificant relationship between sleep bruxism and experimentalintraesophageal acidification,56 and between sleep bruxism andphysiologic gastroesophageal reflux episodes.57 However, we areunaware of any sleep studies that have investigated associationsbetween sleep bruxism and GERD. The current understanding ofthis relationship has been extrapolated from the findings of a fewcase reports and observational epidemiological studies reportingthe association between GERD and tooth wear.27 Clinically, it isnot unusual for patients with a history of both sleep bruxism andGERD to present with advanced tooth wear, which requires exten-sive treatment.58 Experimental findings support these observationsand indicate that tooth wear under simulated bruxism and gastricacid conditions can occur at an alarming rate.59 While these find-ings point to the need for early preventive strategies, furtherresearch is also required to gain an insight into the relationshipsbetween GERD, various oromotor movements, and salivary glandsecretions during the different stages of sleep.

The essential roles of salivaEarlier studies of persons with and without GERD reported anabsence of significant differences in stimulated salivary flowrates,35,60,61 buffering capacities and pH values.35,60 However, morerecent studies have found a significant association betweenGERD, hyposalivation and the subjective sensation of “drymouth” (xerostomia), which is frequently associated with an oralburning sensation.28,62

Though mixed saliva secretions consist of more than 99% water,numerous other variable and complex interacting components alsoare responsible for the normal functioning and protection of theoropharynx and esophagus. Saliva coats all of the relevant internalanatomical surfaces with mucin-rich secretions, providing a pro-

tective diffusion barrier or pellicle against mechanical, thermal,chemical and microbial damage. Saliva also lubricates these sur-faces to allow efficient mastication, swallowing and speech. Inresponse to various stimuli, a rapid increase in parotid gland seroussecretions containing a high concentration of bicarbonate ions inparticular dilutes, neutralizes and clears harmful oral material andacidic esophageal contents by either spitting, or swallowing toinduce esophageal peristalsis.

Varying degrees of hyposalivation may result in complaints ofxerostomia and an oral burning sensation,62 as well as othercommon symptoms and signs such as impaired mastication, swal-lowing and speech, a painful mouth and throat, tooth sensitivity,difficulties in wearing dentures, cracked lips and angular cheilitis,and the frequent need to sip water and chew gum or candies.Furthermore, hyposalivation reduces the potential for saliva tobuffer (neutralize) esophageal acid from GERD, resulting inesophageal mucosal damage (reflux esophagitis).63

A subjective assessment of the quantity and quality of the sali-vary secretions in the mouth should be determined. Scantyunstimulated (resting) saliva may appear foamy and bubbly or, lessoften, viscous and stringy. After gently blotting the surface of theeverted lower lip, seromucous globules of unstimulated salivafrom the minor labial glands will take longer than one minute toappear.64

Because acidic and proteolytic stomach contents may readilyoverwhelm the protective functions of the saliva, resulting in theremoval of dental plaque and acquired pellicle from tooth surfaces,the teeth are then very susceptible to demineralization and abra-sion. Saliva is readily displaced by acids,65 with the dissolutionproducts of the hydroxyapatite crystals being lost permanentlyfrom the exposed tooth surface (Fig. 3).

Collaborative medical anddental managementThe prevention by physicians of chronic acid regurgitation isrequired to halt its potential for tooth erosion. A recent Cochranereview found that both PPIs and H2RAs were effective in short-term heartburn remissions (over a period of 2–8 weeks) in adultGERD patients, but PPIs were the most effective.66 However, PPIswere not effective in relieving GERD symptoms in infants, andcontrolled trials in older children were lacking.67 Another reviewarticle found that the effectiveness of PPIs in relieving regurgita-tion symptoms in adults was modest and lower than that for heart-burn, pointing to the need for a more effective treatment.68 Thisfinding is supported by another Cochrane review confirming themore effective relief of symptoms (heartburn, reflux and bloating)by surgical intervention (laparoscopic fundoplication) comparedwith pharmacologic management, although surgical interventioncarries the risk of rare but serious complications.69 With the recentdevelopment of novel techniques for the diagnosis and manage-ment of GERD, researchers are now realizing the true complexityof the GERD diagnosis, and the much lower effectiveness of PPIsin adults than was originally believed.70 Thus, the complete cessa-tion of nocturnal acid regurgitation in particular may be difficult toachieve by pharmacologic treatment.

Salivary flow rates are usually reduced considerably whileasleep,71 and several of the drugs commonly prescribed for GERD




and other extra-esophageal conditions may lead to a further reduc-tion in the quantity and quality of stimulated salivary secre-tions.62,73 Physicians should be aware of any drugs or medicinesconsumed by patients that may cause or exacerbate hyposalivationand lead to xerostomia. In some instances, saliva substitutes maybe prescribed or recommended.

Patients often consume many exogenous dietary acids, whichwill exacerbate any tooth erosion associated with acid regurgita-tion. Patients with xerostomia may eat acidic fruits, chew or suckacidic sour-tasting candies and gums, use citric acid candy sprays,and rinse their mouths with acidic cola-type beverages to stimulatesaliva production and to remove the remnants and taste of regur-gitated stomach contents. Patients should be advised to avoid suchacidic foods and beverages and instead rinse their mouths eitherwith water, milk, sodium bicarbonate solutions or sodium fluoridemouth rinses. Tooth brushing and chewing hard foods and sugar-free gums should be avoided for approximately 2 h after a regur-gitation episode to allow for the re-establishment of salivarypellicle and subsequent tooth surface remineralization. Recurrentacid regurgitation and partial remineralization of exposed rootsurfaces of maxillary posterior teeth, particularly in older persons,may result in dark, softened, sensitive dentin that is susceptible toabrasion. Tooth brushing should be done carefully, using a softmultitufted tooth brush and a low-abrasive high sodium fluoride-containing dentifrice.

Patients with GERD should be referred for dental consultationsfor the collaborative management of any associated oral manifes-tations. Erosive tooth wear may be accelerated by parafunctionalhabits and abrasive diets, and wear rates should be monitoredperiodically to evaluate tooth wear progression. Prevention offurther tooth wear is a priority involving local preventive, restor-ative and maintenance phases.74 Preventive measures may involvethe stimulation or substitution of salivary secretions (after assess-ing their quantity and quality), neutralizing the effects of endog-

enous and exogenous acids, reducing tooth sensitivity, providingdietary advice (regarding dental erosion, dental caries and oralmucosal sensitivity), enhancing tooth surface integrity (usingacidulated phosphate fluoride, metallic ions), and placing adhesivephysical barriers on susceptible tooth surfaces.58 Oral discomfortand malodor caused by xerostomia should be alleviated both byhome and professional dental care. The importance of adequatefluid intake should be reinforced in GERD sufferers, especially inthe elderly living in hot and dry conditions. As saliva flowdecreases during sleep, a humidifier may be required to relievesymptoms of sleep-related xerostomia.58

ConclusionsAccording to many research publications, the association of tootherosion and GERD is stronger than generally perceived by physi-cians. Tooth erosion usually progresses slowly, and its signs areoften subtle and not readily observed during a cursory oral exami-nation under less-than-ideal conditions. Failure to diagnose earlysigns of erosive tooth wear can result in significant damage to thedentition and the masticatory system before treatment is sought.Therefore, early diagnosis and preventive management is impor-tant to prevent a lifetime of debilitating dentition and the need forcomplex restorative therapy. Preventive management shouldinvolve restoration of the host defense, including salivary param-eters. The quality and quantity of saliva should also be monitoredby physicians during treatment of GERD with PPIs. Collaborationbetween physicians and dentists during the management ofpatients with GERD is also strongly advocated.

AcknowledgmentWe gratefully acknowledge financial assistance from the Austra-lian Dental Research Foundation and Dentsply Australia Pty Ltd insupport of our research projects on dental erosion.

Figure 3 When dental pellicle is removedby sustained endogenous acid attacks, dem-ineralized tooth products are lost into the oralenvironment. HA, hydroxyapatite. (AmendedFigure 2.5, pp. 15, from Smales et al.72 Withcopyright permission from Jaypee MedicalPublishers 2011.)




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Oral manifestations of gastroesophageal reflux disease