Gastroesophageal Refluks Disease   (GERD)

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Gastroesophageal Reflux Disease (GERD), merupakan gerakan membaliknya isi lambung (mengandung asam dan pepsin) menuju esophagus. GERD juga mengacu pada berbagai kondisi gejala klinik atau perubahan histology yang terjadi akibat refluks gastroesofagus. Ketika esophagus berulangkali kontak dengan material refluk untuk waktu yang lama, dapat terjadi inflamasi esofagus (esofagitis refluks) dan dalam beberapa kasus berkembang menjadi erosi esofagus (esofagitis erosi).

ETIOLOGI DAN FAKTOR RESIKO

Umur dapat mempengaruhi terjadinya GERD, karena seiring dengan pertambahan umur maka produksi saliva, yang dapat membantu penetralan pH pada esofagus, berkurang sehingga tingkat keparahan GERD dapat meningkat. Jenis kelamin dan genetik tidak berpengaruh signifikan terhadap GERD.

Faktor resiko GERD adalah kondisi fisiologis/penyakit tertentu, seperti tukak lambung, hiatal hernia, obesitas, kanker, asma, alergi terhadap makanan tertentu, dan luka pada dada (chest trauma). Sebagai contoh, pada pasien tukak lambung terjadi peningkatan jumlah asam lambung maka semakin besar kemungkinan asam lambung untuk mengiritasi mukosa esofagus dan LES.

PATOFISIOLOGI

Faktor kunci pada perkembangan GERD adalah aliran balik asam atau substansi berbahaya lainnya dari perut ke esofagus. Pada beberapa kasus, refluks gastroesofageal dikaitkan dengan cacat tekanan atau fungsi dari sfinkter esofageal bawah (lower esophageal sphincter/LES). Sfinkter secara normal berada pada kondisi tonik (berkontraksi) untuk mencegah refluks materi lambung dari perut, dan berelaksasi saat menelan untuk membuka jalan makanan ke dalam perut. Penurunan tekanan LES dapat disebabkan oleh (a) relaksasi sementara LES secara spontan, (b) peningkatan sementara tekanan intraabdominal, atau (c) LES atonik.

Masalah dengan mekanisme pertahanan mukosa normal lainnya, seperti faktor anatomik, klirens esofageal (waktu kontak asam dengan mukosa esofageal yang terlalu lama), resistensi mukosa, pengosongan lambung, epidermal growth factor, dan pendaparan saliva, juga dapat berkontribusi pada perkembangan GERD.

Faktor agresif yang dapat mendukung kerusakan esofageal saat refluks ke esofagus termasuk asam lambung, pepsin, asam empedu, dan enzim pankreas. Dengan demikian komposisi, pH dan

volume refluksat serta durasi pemaparan adalah faktor yang paling penting pada penentuan konsekuensi refluks gastroesofageal.

TANDA DAN GEJALA

Gejala klinis GERD digolongkan menjadi 3 macam, yaitu gejala tipikal, gejala atipikal, dan gejala alarm.

1.  Gejala tipikal (typical symptom)

Adalah gejala yang umum diderita oleh pasien GERD, yaitu: heart burn, belching (sendawa), dan regurgitasi (muntah)2. Gejala atipikal (atypical symptom)

Adalah gejala yang terjadi di luar esophagus dan cenderung mirip dengan gejala penyakit lain. Contohnya separuh dari kelompok pasien yang sakit dada dengan elektrokardiogram normal ternyata mengidap GERD, dan  separuh dari penderita asma ternyata mengidap GERD. Kadang hanya gejala ini yang muncul sehingga sulit untuk mendeteksi GERD dari gejala ini. Contoh gejala atipikal: asma nonalergi, batuk kronis, faringitis, sakit dada, dan erosi gigi.

3.  Gejala alarm (alarm symptom)

Adalah gejala yang menunjukkan GERD yang berkepanjangan dan kemungkinan sudah mengalami komplikasi. Pasien yang tidak ditangani dengan baik dapat mengalami komplikasi. Hal ini disebabkan oleh refluks berulang yang berkepanjangan. Contoh gejala alarm: sakit berkelanjutan, disfagia (kehilangan nafsu makan), penurunan berat badan yang tidak dapat dijelaskan, tersedak.

Penting untuk diperhatikan bahwa keparahan gejala tidak selalu berkaitan dengan keparahan esofagitis, tetapi berkaitan dengan durasi reflux. Pasien dengan penyakit yang nonerosif dapat menunjukkan gejala yang sama dengan pasien yang secara endoskopi menunjukkan adanya erosi esophagus.

DIAGNOSIS

Cara yang paling baik dalam diagnosa adalah dengan melihat sejarah klinis, termasuk gejala yang sedang terjadi dan faktor resiko yang berhubungan. Endoskopi tidak perlu dilakukan pada pasien yang mengalami gejala tipikal, terutama jika pasien merespon baik terhadap pengobatan GERD. Endoskopi dilakukan pada pasien yang tidak merespon terapi, pasien yang mengalami gejala alarm, atau pasien yang mengalami gejala GERD terus menerus. Selain endoskopi, tes yang sering digunakan untuk diagnosa adalah pengamatan refluksat ambulatori, dan manometri.

1. Endoskopi dilakukan untuk melihat lapisan mukosa pada esophagus, sehingga dapat diketahui tingkat keparahan penyakit (erosif atau nonerosif) dan kemungkinan komplikasi yang telah terjadi, karena memungkinkan visualisasi dan biopsi mukosa esofagus.

2. Pengamatan refluksat ambulatori meliputi pengamatan pH refluksat. Pengamatan ini berguna untuk mengetahui paparan asam yang berlebih pada mukosa esofagus dan menentukan hubungan gejala yang dialami dengan paparan asam tersebut. Pasien diminta untuk mencatat gejala-gejala yang dialami selama pengamatan pH sehingga dapat diketahui hubungan gejala dengan pH dan efektivitas pengobatannya.

3. Manometri esophageal digunakan untuk penempatan probe yang tepat dalam pengukuran pH dan untuk mengevaluasi peristaltik serta pergerakan esofagus sebelum operasi antirefluks. Metode ini mengukur tekanan pada lambung, LES, esofagus, dan faring.

TERAPI

Terapi GERD ditujukan untuk mengurangi atau menghilangkan gejala-gejala pasien, mengurangi frekuensi atau kekambuhan dan durasi refluks esofageal, mempercepat penyembuhan mukosa yang terluka, dan  mencegah berkembangnya komplikasi.

Terapi diarahkan pada peningkatan mekanisme pertahanan yang mencegah refluks dan / atau mengurangi faktor-faktor yang memperburuk agresifitas refluks atau kerusakan mukosa. Secara spesifik, yaitu:

1. Mengurangi keasaman dari refluksat.2. Menurunkan volume lambung yang tersedia untuk direfluks.3. Meningkatkan pengosongan lambung.4. Meningkatkan tekanan LES.5. Meningkatkan bersihan asam esofagus.6. Melindungi mukosa esophagus.

Terapi GERD dikategorikan dalam beberapa fase, yaitu:

Fase I: mengubah gaya hidup dan dianjurkan terapi dengan menggunakan antasida dan/atau OTC antagonis reseptor H2 (H2RA) atau penghambat pompa proton (PPI).

Fase II: intervensi farmakologi terutama dengan obat penekan dosis tinggi.

Fase III: terpai intervensional (pembedahan antirefluks atau terapi endoluminal).

TERAPI NON FARMAKOLOGI

1.  Modifikasi Gaya Hidup

Mengangkat kepala saat tidur (meningkatkan bersihan esofageal). Gunakan penyangga 6-10 inchi di bawah kepala. Tidur pada kasur busa.

Menghindari makanan yang dapat menurunkan tekanan LES (lemak, coklat, kopi, kola, teh bawang putih, bawang merah, cabe, alkohol, karminativ (pepermint, dan spearmint))

Menghindari makanan yang secara langsung mengiritasi mukosa esofagus (makanan pedas, jus jeruk, jus tomat dan kopi)

Makan makanan yang tinggi protein (meningkatkan tekanan LES)

Makan sedikit dan menghindari tidur segera setelah makan (jika mungkin 3 jam) (menurunkan volume lambung)

Penurunan berat badan (mengurangi gejala) Berhenti merokok (menurunkan relaksasi spontan sfingter esofagus). Menghindari minum alkohol (meningkatkan amplitudo sfinter esofagus, gelombang

peristaltik dan frekuensi kontraksi). Menghindari pakai pakaian yang ketat. Menghentikan, jika mungkin, penggunaan obat-obat yang dapat menurunkan tekanan

LES (Antikolinergik, barbiturat, benzodiazepin (misalnya diazepam), kafein, penghambat kanal kalsium dihidropiridin, dopamin, estrogen, etanol, isoproterenol, narkotik (meperidin, morfin), nikotin (merokok) nitrat, fentolamin, progesteron dan teofilin).

Menghentikan, jika mungkin, penggunaan obat-obat yang dapat mengiritasi secara langsung mukosa esofagus (tetrasiklin, quinidin, KCl, garam besi, aspirin, AINS dan alendronat).

2.  Pendekatan Intervensi

Pembedahan Antirefluks

Intervensi bedah adalah alternatif pilihan bagi pasien GERD yang terdokumentasi dengan baik. Tujuan pembedahan antirefluks adalah untuk menegakkan kembali penghalang antirefluks, yaitu penempatan ulang LES, dan untuk menutup semua kerusakan hiatus terkait. Operasi ini harus dipertimbangkan pada pasien yang

gagal untuk merespon pengobatan farmakologi; memilih untuk operasi  walaupun pengobatan sukses karena pertimbangan gaya hidup,

termasuk usia, waktu, atau biaya obat-obatan; memiliki komplikasi GERD (Barret’s Esophagus/BE, strictures, atau esofagitis kelas 3

atau 4); atau mempunyai gejala tidak khas dan terdokumentasikan mengalami refluks pada monitoring

pH 24-jam.

Terapi Endoluminal

Beberapa pendekatan endoluminal baru untuk pengelolaan GERD baru saja dikembangkan. Teknik-teknik ini meliputi endoscopic gastroplastic plication, aplikasi endoluminal radiofrequency heat energy (prosedur Stretta), dan injeksi endoskopik biopolimer yang dikenal sebagai Enteryx pada penghubung gastroesofageal.

TERAPI FARMAKOLOGI

1.  Antasida dan Produk Antasida-Asam Alginat

Digunakan untuk perawatan ringan GERD. Antasida efektif mengurangi gejala-gejala dalam waktu singkat, dan antasida sering digunakan bersamaan dengan terapi penekan asam lainnya. Pemeliharaan pH intragastrik di atas 4 dapat menurunkan aktivasi pepsinogen menjadi pepsin,

sebuah enzim proteolitik. Netralisasi cairan lambung juga dapat mengarah pada peningkatan tekanan LES.

Produk antasid yang dikombinasikan dengan asam alginiat adalah agen penetral yang tidak ampuh dan tidak meningkatkan tekanan LES, namun membentuk larutan yang sangat kental yang mengapung di atas permukaan isi lambung. Larutan kental ini diperkirakan sebagai pelindung penghalang bagi kerongkongan terhadap refluks isi lambung dan  mengurangi frekuensi refluks.

2.  Penekanan Asam dengan Antagonis Reseptor H2 (simetidin, famotidin, nizatidin, dan ranitidin)

Terapi penekanan asam adalah pengobatan utama GERD. Antagonis reseptor H2 dalam dosis terbagi efektif dalam mengobati pasien GERD ringan hingga sedang.

Kemanjuran antagonis reseptor H2 dalam perawatan GERD sangat bervariasi dan sering lebih rendah dari yang diinginkan. Respons terhadap antagonis reseptor H2 tampaknya tergantung pada (a) keparahan penyakit, (b) regimen dosis yang digunakan, dan (c) durasi terapi.

3.  Proton Pump Inhibitor (PPI) (esomeprazol, lansoprazol, omeprazol, pantoprazol, dan rabeprazol)

PPI lebih unggul daripada antagonis reseptor H2 dalam mengobati pasien GERD sedang sampai parah. Ini tidak hanya pada pasien erosif esofagtis atau gejala komplikasi (BE atau striktur), tetapi juga pasien dengan GERD nonerosif yang mempunyai gejala sedang sampai parah. Kekambuhan umumnya terjadi dan terapi pemeliharaan jangka panjang umumnya diindikasikan.

PPI memblok sekresi asam lambung dengan menghambat H+/K+-triphosphatase adenosin lambung dalam sel parietal lambung. Ini menghasilkan efek antisekretori yang mendalam dan tahan lama yang mampu mempertahankan pH lambung di atas 4, bahkan selama lonjakan asam setelah makan.

PPI terdegradasi dalam lingkungan asam sehingga diformulasi dalam tablet atau kapsul pelepasan tertunda. Pasien harus diinstruksikan untuk meminum obat pada pagi hari, 15 sampai 30 menit sebelum sarapan untuk memaksimalkan efektivitas, karena obat ini hanya menghambat secara aktif sekresi pompa proton. Jika dosisnya dua kali sehari, dosis kedua harus diberikan sekitar 10 hingga 12 jam setelah dosis pagi hari dan sebelum makan atau makan makanan ringan.

4.  Agen Promotilitas

Khasiat dari agen prokinetik cisaprid, metoklopramid, dan bethanechol telah dievaluasi dalam pengobatan GERD. Cisapride memiliki khasiat yang sebanding dengan antagonis reseptor H2

dalam mengobati pasien esofagitis ringan, tetapi cisaprid tidak lagi tersedia untuk penggunaan rutin karena efek aritmia yang mengancam jiwa bila dikombinasikan dengan obat-obatan tertentu dan penyakit lainnya.

Metoklopramid, antagonis dopamin, meningkatkan tekanan LES, dan mempercepat pengosongan lambung pada pasien GERD. Tidak seperti cisapride, metoklopramid tidak memperbaiki bersihan esofagus. Metoklopramid dapat meredakan gejala GERD tetapi belum ada data substantial yang menyatakan bahwa obat ini dapat memperbaiki kerusakan esofagus.

Agen prokinetik juga telah digunakan untuk terapi kombinasi dengan antagonis H2-reseptor. Kombinasi dilakukan pada pasien GERD yang telah diketahui atau diduga adanya gangguan motilitas, atau pada pasien yang gagal pada pengobatan dengan penghambat pompa proton dosis tinggi.

5.  Protektan Mukosa

Sucralfat, garam aluminium dari sukrosa oktasulfat yang tidak terserap, mempunyai manfaat terbatas pada terapi GERD. Obat ini mempunyai laju pengobatan yang sama seperti antagonis reseptor H2 pada pasien esofagitis ringan tapi kurang efektif dari pada antagonis reseptor H2

dosis tinggi pada pasien dengan esofagitis refrakter. Berdasarkan data yang ada, sukralfat tidak direkomendasikan untuk terapi.

ALGORITMA TERAPI

Journal of Dental Researchhttp://jdr.sagepub.com/content/88/5/422The online version of this article can be found at:DOI: 10.1177/0022034509336530J DENT RES 2009 88: 422W.P. Holbrook, J. Furuholm, K. Gudmundsson, A. Theodórs and J.H. MeurmanGastric Reflux is a Significant Causative Factor of Tooth ErosionPublished by:http://www.sagepublications.comOn behalf of:International and American Associations for Dental ResearchAdditional services and information for Journal of Dental Research can be found at:Email Alerts: http://jdr.sagepub.com/cgi/alertsSubscriptions: http://jdr.sagepub.com/subscriptionsReprints: http://www.sagepub.com/journalsReprints.navPermissions: http://www.sagepub.com/journalsPermissions.navWhat is This?>> Version of Record - Jun 3, 2009Downloaded from jdr.sagepub.com by guest on November 10, 2011 For personal use only. No other uses without permission.© 2009 International & American Associations for Dental Research

422

RESEARCH REPORTSClinicalDOI: 10.1177/0022034509336530Received November 29, 2007; Last revision October 19,2008; Accepted January 21, 2009

W.P. Holbrook1*, J. Furuholm2,K. Gudmundsson3, A. Theodórs3,and J.H. Meurman2

1University of Iceland, Vatnsmyrarvegi 16, IS 101 Reykjavik,Iceland; 2Institute of Dentistry, University of Helsinki, andDepartment of Oral and Maxillofacial Diseases, HelsinkiUniversity Central Hospital, Finland; and 3University Hospital,Reykjavik, Iceland, and Department of Gastroenterology,St. Joseph’s Hospital, Hafnafjordur, Iceland; *correspondingauthor, phol@hi.isJ Dent Res 88(5):422-426, 2009

AbstractDental erosion is caused by dietary or gastric acid.This study aimed to examine the location and severityof tooth erosion with respect to causative factors,and to determine whether the clinical pattern oferosion reflected the dominant etiological factor.The study involved 249 Icelandic individuals andincluded: a detailed medical history; clinical oralexamination; salivary sampling, and analysis for flowrate, pH, and buffering capacity. Reflux was assessedin 91 individuals by gastroscopy, esophageal manometry,and 24-hour esophageal-pH monitoring. Refluxsymptoms were reported by 36.5% individuals.Manometry results were abnormal in 8% of studyparticipants, abnormal esophageal pH in 17.7%, anda pathological 24-hour pH recording in 21.3%. 3.6%were positive for Helicobacter pylori. Normal salivaryflow was found in 92%, but low salivary buffering(10.4%) was associated with erosion into dentin(P < 0.05). Significant associations were found

between erosion and diagnosed reflux disease (OR2.772; P < 0.005) and daily consumption of acidicdrinks (OR 2.232; P < 0.005).Key words: Dental erosion, location, risk factors,saliva, gastro-esophageal reflux.

Gastric Reflux is a SignificantCausative Factor of Tooth ErosionINTRODUCTION

Erosion is an increasingly common type of tooth wear, defined as the loss

of tooth substance by a chemical process not involving bacteria (Pindborg,1970). It is caused by acid that may be extrinsic, usually in the form of softdrinks, or intrinsic, in the form of refluxed gastric acid (Jarvinen et al., 1988;Meurman et al., 1994). The etiology is complex, with an interplay of extrinsicand intrinsic factors together with other types of tooth wear, such as attritionor abrasion. Epidemiological studies of erosion suggest that either theprevalence of erosion is rising (Nunn et al., 2003), or there is an increasingawareness of the disease, for example, in young adults and adolescents (Lussiet al., 1991; Jaeggi and Lussi, 2006) and young children (Downer, 1995). Milddegrees of dental erosion have been reported as affecting over 20% of teenageand young-adult population groups, with severe erosion extending wellinto dentin in several teeth being seen in about 5% (Arnadottir et al., 2003).Erosion is usually linked to a high consumption of soft drinks in Europeanstudies, but the problem has received less attention in the American literature(Bartlett et al., 1999).An initial study (Holbrook, unpublished observations) of 150 consecutiveIcelandic individuals was used for the assessment of erosion and the planningof further investigations. Persons with erosion were predominantly male.Some had only incisor erosion, while others showed involvement of molarsand incisors. Severity of erosion varied from being limited to enamel throughto severe dentinal erosion of several adjacent teeth, typically 4-6 maxillaryanterior teeth. Concern about the possible role that gastro-esophageal refluxmight play in causing tooth erosion in Iceland had been raised in 2001 by oneof the authors (Theodors, unpublished observations), who found the prevalenceof reflux symptoms occurring once a month to be 26%. This supportedthe possibility that intrinsic acid attack might play a role in causing erosion.In situ pH electrodes had previously failed to demonstrate acid reflux into themouth in persons with a history of reflux disease (Gudmundsson et al., 1995).While erosion was clearly caused by acid attack from either intrinsic andextrinsic sources, or both, there is no evidence in the literature that the clinicalmanifestations of observed erosion might differ depending on the causativefactor. Wide variation in the prevalence of tooth erosion has been reportedamong persons with reflux, even from the same research group (Jarvinenet al., 1988; Meurman et al., 1994). Thus, the purpose of the present studywas to investigate a larger group of referred individuals in a standardizedmanner to determine the interplay of possible causative and reparative factorsin tooth erosion. Furthermore, the aim was to record erosion with respect tolocation and severity, to determine if the clinical picture might give a clue tothe dominant etiological factor of the erosion.Downloaded from jdr.sagepub.com by guest on November 10, 2011 For personal use only. No other uses without permission.© 2009 International & American Associations for Dental Research

J Dent Res 88(5) 2009 Gastric Reflux and Tooth Erosion 423MATERIALS & METHODSStudy participants (N = 249) were referred from dentists and theState Health Insurance scheme in Iceland to one clinician (WPH)for examination, diagnosis, and further investigation. They were

informed of the investigations at each stage and consented to theprocedure in question, whether history-taking and examination,saliva sampling, esophageal pH measurement, or gastroscopy.Permission for the investigation was given by the relevant Icelandicauthorities for data protection (Personuvernd no. 2006030131) andethics (Vísindasidanefnd no. VSNb2006030008/03-1).Clinical ExaminationThis was standardized to allow for comparisons and to facilitateanalysis. All participants were examined by the same clinician(WPH), who was experienced in examining and recording erosionfor clinical and research purposes within this population. Erosionwas recorded separately for the anterior teeth and molars, and thescore for the most affected tooth surface was noted for subsequentdata analysis. Severity of erosion was recorded as being: inenamel only (score 1); into dentin (score 2); or severely affectingthe tooth or series of teeth—for example, as seen frequently inerosion of the palatal surfaces of 4 maxillary incisor teeth (score3). Criteria for scoring erosion were modified from the Index ofLussi (1996) (Table 1) as used in previous studies in Iceland(Jensdottir et al., 2004). Instances of xerostomia were followed upand recorded. Because the participants were referred specificallyfor diagnosis and investigation, it did not prove possible to recalla proportion to measure consistency of the erosion scores.Reliability was dependent on the previous experience of the singleexaminer, and on standardized criteria. There is an acknowledgedproblem in the accurate diagnosis of erosion just into dentin(Holbrook and Ganss, 2008), but the clinician had gained experienceand calibration from participation as a clinical examiner in asurvey, concurrent with the beginning of the present study, of erosionin individuals with and without reflux disease conducted bytwo observers blinded to the underlying cause of the observederosion (Jensdottir et al., 2004).History-takingDetailed dental and medical histories were taken. These includedsymptoms of gastric reflux, any history of vomiting, and previousinvestigations for gastro-intestinal complaints. Medicationwas recorded, including: drugs for reflux disease; drugs causingdry mouth; and regular use of asthma sprays, inhalers, or othermedications with a low pH taken orally and on a regular basis.Dietary FactorsParticipants recorded their consumption of soft drinks and particularpreferences for acidic foods, including acid-preservedfoods, using a modification of a dietary questionnaire extensivelyused in Iceland for studies of caries and erosion (Arnadottir et al.,2003). Attempts were made to quantify the amount of acidicdrink consumed per day, and consumption of >0.5 L/cola drinkor fruit juice per day was recorded as a risk factor. Personsattending the clinical examination were informed of the potentialerosive effect of consuming excessive amounts of acidic drinksand were advised to drink non-acidic drinks or carbonated water,as suggested by the findings of Jensdottir et al. (2005).Salivary ParametersParticipants provided a sample of stimulated saliva by chewingon a piece of paraffin wax for 1 min, swallowing the saliva thathad collected, and then spitting out fresh saliva for a period of 1min while continuing to chew the wax. Using pH paper strips(Whatman http://www.whatman.com), we used the samplesimmediately to determine salivary pH. We determined buffer

capacity by placing one drop of saliva on a Dentobuff test strip(Orion Diagnostica, Espoo, Finland) and reading the result after3 min, using the manufacturer’s color chart for comparisonwhen recording the buffer capacity (low, pH 4; medium, pH 5;high, pH 6). Stimulated salivary flow rates under 0.7 mL permin were considered lowered.Gastro-intestinal ExaminationPersons with molar erosion and those reporting symptoms ofgastric reflux (N = 91) were referred to a gastroenterologist(AT) for further investigation and, if necessary, medication.Investigations included gastroscopy to determine the presenceof mucosal inflammation, hiatal hernia, and sampling for thepossible presence of Helicobacter sp. from the gastric mucosa.Esophageal manometry was performed together with 24-hourmonitoring of esophageal pH, the recognized measure of pathologicalreflux. This was carried out by a single examiner (KG)using standard methods (Johnsson et al., 1987). Esophageal pHTable 1. Criteria Used for Assessment of Dental Erosion (Lussi, 1996)Score Criteria for Anterior Teeth Criteria for Posterior Teeth0 No evidence of erosion No evidence of erosion1 Loss of surface enamel, dentin not involved Enamel erosion of fissure system or cusps that cannot be attributed to attrition;amalgam restorations stand above the enamel surface2 Erosion extending into dentin in at least one tooth Erosion into dentin that cannot be attributed to attrition, noting especially palatalaspects of maxillary molar cusps and buccal aspects of mandibular molar cusps3 Erosion into in at least four anterior teeth and/ Dentin exposed and clear loss of tooth morphology and/or erosion extendingor pulp chamber visible in at least one tooth close to the pulpDownloaded from jdr.sagepub.com by guest on November 10, 2011 For personal use only. No other uses without permission.© 2009 International & American Associations for Dental Research

424 Holbrook et al. J Dent Res 88(5) 2009values < 4 recorded for > 3.4% of the 24-hour time period wereregarded as indicative of pathological reflux.Statistical AnalysisData were collated from the various investigations and enteredonto an Excel™ chart. Data were made anonymous before beingtransferred to the statistician (JF) for analyses. SPSS forWindows version 12 was used for statistics, i.e., χ2, correlation,and logistic regression analyses.RESULTSOf the 249 referred individuals in this study, 168 were males(P = 0.013; mean age, 26.7 } 12.4 yrs; age range, 6-65 yrs).�Spearman’s coefficient for correlation between age and theseverity of erosion was 0.166 (P < 0.05). A pattern of severe erosion,clearly into dentin and with marked loss of normal toothcontour recorded in adjacent teeth, was seen in 84 persons(33.7%). Of these, 60 (24.1%) had predominantly incisal erosion,but 24 (9.6%) persons had severe erosion in adjacent molars,with loss of normal tooth contour, in addition to some incisalerosion. Less severe erosion involving enamel with no, or onlyminimal, dentin involvement was seen in the remaining 165 persons(66.3%), most commonly on the palatal surfaces of upperincisor teeth. Molar erosion was often seen on occlusal and buccalsurfaces of lower molar teeth, and the palatal surfaces ofupper molars. Labial erosion of upper incisor teeth was rarelyseen, and erosion of the lower anterior teeth was not observed.Distribution of erosion is further described in Table 2.A daily consumption of >0.5 L of acidic soft drinks, usuallycola-type, was reported by 133 persons (53.4%). Remainingparticipants reported no significant exposure to dietary acid.

Analysis of salivary parameters (Table 3) showed that 10.4% ofparticipants had a low buffering capacity, while 36% of personsreported symptoms of reflux, as confirmed in 21.3% of the sampleaccording to the 24-hour intra-esophageal measurement (Table 3).Step-wise logistic regression analyses (Table 4) showed thatthe highest odds ratios were found between erosion and dietaryfactors, low salivary buffering, and reflux disease. Only 20 participantshad low salivary flow, and this negative associationbetween low salivary flow and erosion, although statisticallysignificant (Table 3), may not be clinically relevant.Reflux parameters (odds ratio 1.33; P < 0.005) and dailyconsumption of >0.5 L of acidic drinks (odds ratio 3.17; P <0.001) were significantly associated with palatal erosion ofthe maxillary incisor teeth. Low salivary buffer capacity wasassociated only with severe erosion into dentin in several adjacentteeth (χ2 6.57; P < 0.05).Erosion of molar teeth into dentin was associated with atleast one parameter of reflux disease being positive (odds ratio1.58; P < 0.001). There was little consistency in which refluxparameter was positive, but hiatal hernia and pathologicalreflux, as measured by 24-hour esophageal pH monitoring, weremost commonly found (Table 3). No significant association wasseen between dietary or salivary parameters and erosion inmolars. Combining the factors measured to explain variations inobserved erosion (R2) gave a value of only 15.1%.DISCUSSIONThe results confirmed our study hypothesis by showing a significantassociation between the severity and location of dentalerosion and specific risk factors. The nature of the sample makesit likely that the degree of erosion was greater than that for thegeneral population in Iceland, where erosion is common.Accurate diagnosis of the cause of observed tooth wear is oftendifficult (Holbrook et al., 2003), as is assessment of the extentof tooth wear through enamel into dentin (Holbrook et al., 2003;Holbrook and Ganss, 2008). Thus, the reproducibility of the erosionscores may be problematic, but, for most analyses, scores 1and 2 were combined, and score 3 was used for erosion intodentin with loss of tooth contour as described earlier. The use ofa single, experienced examiner was expected to have increasedthe reliability of the scores recorded.It was not feasible to include a control group in this study,since participants had been specifically referred. However, acase-control study of erosion in Icelandic teenagers conductedat the same time (Arnadottir et al., 2003) may be considered asTable 2. Distribution of Erosion Recorded in the Teeth of the 249 StudyParticipants and Scored According to Severity and Location in theMolar/Premolar Teeth or the Incisor/Canine Teeth in Both Maxillaryand Mandibular ArchesIncisor Teeth Molar TeethErosion Maxillary Mandibular Maxillary MandibularScore (%) (%) (%) (%)0 8 (3.2) 202 (81.1) 41 (16.5) 32 (12.8)1-2 181 (72.7) 45 (18.1) 184 (73.9) 193 (77.5)3 60 (24.1) 2 (0.8) 24 (9.6) 24 (9.6)Table 3. Investigation of Stimulated Saliva and Gastro-intestinalParameters in 249 Persons with Tooth ErosionNo. of Cases %SALIVANormal salivary flow 229 92.0Salivary pH > 7.5 232 93.2Buffer capacity high 183 73.5

Buffer capacity moderate 40 16.1Buffer capacity low 26 10.4GASTRO-INTESTINALReported symptoms of reflux 91 36.5Abnormal manometry (lower esophageal 20 8.0sphincter pressure)Low esophageal pH 44 17.7Pathological reflux diagnosed (24-hour pH) 53 21.3Hiatal hernia diagnosed 46 18.5Helicobacter present 9 3.6Downloaded from jdr.sagepub.com by guest on November 10, 2011 For personal use only. No other uses without permission.© 2009 International & American Associations for Dental Research

J Dent Res 88(5) 2009 Gastric Reflux and Tooth Erosion 425Table 4. Results of the Stepwise Logistic Regression (odds ratios with 95% confidence intervals and P-values of the final step)Independent Variable OR (95% CI) P-valueMale gender 0.420 (0.212 – 0.831) 0.013Age 1.032 (1.006 – 1.058) 0.014Dietary risk (> 0.5 L of acidic drink/day) 2.632 (1.397 – 4.958) 0.003Low salivary flow 0.189 (0.049 – 0.726) 0.015Low buffer capacity (< pH 4 using DentoBufftest kit) 2.490 (1.562 – 3.968) 0.000Diagnosed reflux disease 2.772 (1.403 – 5.475) 0.003a meaningful comparison group; with a prevalence of erosion of21.6% in 15-year-olds, 68.3% of whom were male.Recent attention paid to erosion relates to the assumed associationwith consumption of acidic drinks and the pattern of thisconsumption (Johansson et al., 2002; Jensdottir et al., 2006).One Icelandic study (The Iceland Nutritional Council, 2002) hasshown that teenagers and young adults, especially males, consume1 L of cola-type drinks per day, whereas females consume0.5 L/day. Strong dietary evidence supports the association ofcarbonated-drink consumption with the age and gender of participantsin this study, while the association of drink consumptionwith incisor erosion is probably explained by the pattern ofdrinking (Johansson et al., 2002). Although no link was seen inthe present study between molar erosion and high consumptionof acidic drinks, one Icelandic study (Jensdottir et al., 2004)found a significant association between consumption of >1 Lof acidic drink per day and severe erosion of the molar teeth.A low salivary buffer capacity may be an additional risk factor,since neutralization of dietary acid and consequent apatiteremineralization will be less. Conflicting data exist on the associationbetween low buffer capacity and tooth erosion (Woltgenset al., 1985; Bevenius and L’Estrange, 1990). The present findingthat a low buffer capacity becomes significantly associatedwith only more severe grades of erosion may explain the earlieranomalous findings.There appear to be strong links between indicators of gastricreflux and the presence of tooth erosion, especially in the molar teeth,suggesting that careful history-taking is important if this problem isto be diagnosed. Unfortunately, no clear single factor could be measuredthat allowed a diagnosis of reflux-disease-associated erosion tobe made. Both gastroscopy and 24-hour monitoring of esophagealpH appear to be necessary for a diagnosis, and this is clearly timeconsuming,expensive, and invasive. A problem remains with personsseen to have severe molar erosion, but in whom no pathologicalreflux can be found. Criteria for pathological reflux (esophageal pH< 4 for > 3.4% of the 24-hour time period) may need to be reconsideredwith particular respect to teeth. From the clinical appearance ofthe dentition in many persons in this study, there is a strong suggestionthat gastric acid passes over the dorsum of the posterior third ofthe tongue to erode the palatal surfaces of the upper molar teeth, and

then passes over the buccal aspect of the lower molars. The ventralsurface of the tongue presumably protects the lingual aspect of lowermolars. Acid also passes over the dorsum of the tongue to erode thepalatal surfaces of the maxillary anterior teeth.Erosion appears to be the result of an interaction of intrinsicand extrinsic acidic risk factors with the protective factors ofenamel integrity, acquired pellicle, salivary flow, and buffercapacity. Conflicting evidence has been reported on the protectiveand preventive effects of fluoride in dental erosion. Salivaryglycoprotein pellicle has a protective role against erosive actions,as shown by several clinical and in vitro studies (Meurman andFrank, 1991; Westergaard et al., 2001; Johansson et al., 2002,2004). Erosion is thus usually seen in the areas where salivarypellicle has been lost following acid attack.Clearly, the interplay of causative and protective factors withrespect to erosion is complex (Meurman and Sorvari, 2000;Johansson et al., 2004), but the low explanatory value of all thefactors measured in this study was surprising. It was assumed,initially, that tooth erosion was a simpler disease to understandthan dental caries, although similar in also having a multi-factorialetiology. Etiological and protective factors are routinelyfound to explain approximately 25-50% of variability in cariesscores (R2) (Granath et al., 1991; Holbrook et al., 1993).Therefore, it was surprising that factors measured in this investigationof tooth erosion were not able to explain differences inerosion severity more than 15.1%. Perhaps there remain importantetiological or pathogenic factors of tooth erosion to beinvestigated. Future studies might also separate the severe andless severe forms of erosion, instead of categorically analyzingcases as being with or without erosion.Persons with gastric reflux are at risk of developing erosion,a form of irreversible tooth damage that is technically difficultto restore. Consequently, attention should be focused on earlydiagnosis and on individuals at particular risk.ACKNOWLEDGMENTSThe author JHM was supported by grant TYH 3245 of theHelsinki University Central Hospital, Finland. WPH was supportedby the University of Iceland Research Fund.