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Gastroesophageal Refluks Disease (GERD)

By Neng Leave a Comment Categories: Catatan Kuliah and Farmakoterapi Tags: Gastroesofageal refluks disease, refluks esofageal
April 2010

http://storiku.wordpress.com/ 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. 2. 3. 4. 5. 6. Mengurangi keasaman dari refluksat. Menurunkan volume lambung yang tersedia untuk direfluks. Meningkatkan pengosongan lambung. Meningkatkan tekanan LES. Meningkatkan bersihan asam esofagus. 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 610 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 (Barrets 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 Research


http://jdr.sagepub.com/content/88/5/422 The online version of this article can be found at: DOI: 10.1177/0022034509336530 J DENT RES 2009 88: 422 W.P. Holbrook, J. Furuholm, K. Gudmundsson, A. Theodrs and J.H. Meurman

Gastric Reflux is a Significant Causative Factor of Tooth Erosion


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422

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

W.P. Holbrook1*, J. Furuholm2, K. Gudmundsson3, A. Theodrs3, and J.H. Meurman2


1University

of Iceland, Vatnsmyrarvegi 16, IS 101 Reykjavik, Iceland; 2Institute of Dentistry, University of Helsinki, and Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Finland; and 3University Hospital, Reykjavik, Iceland, and Department of Gastroenterology, St. Josephs Hospital, Hafnafjordur, Iceland; *corresponding author, phol@hi.is J Dent Res 88(5):422-426, 2009

Abstract
Dental erosion is caused by dietary or gastric acid. This study aimed to examine the location and severity of tooth erosion with respect to causative factors, and to determine whether the clinical pattern of erosion reflected the dominant etiological factor. The study involved 249 Icelandic individuals and included: a detailed medical history; clinical oral examination; salivary sampling, and analysis for flow rate, pH, and buffering capacity. Reflux was assessed in 91 individuals by gastroscopy, esophageal manometry, and 24-hour esophageal-pH monitoring. Reflux symptoms were reported by 36.5% individuals. Manometry results were abnormal in 8% of study participants, abnormal esophageal pH in 17.7%, and a pathological 24-hour pH recording in 21.3%. 3.6% were positive for Helicobacter pylori. Normal salivary

flow 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 (OR 2.772; P < 0.005) and daily consumption of acidic drinks (OR 2.232; P < 0.005). Key words: Dental erosion, location, risk factors, saliva, gastro-esophageal reflux.

Gastric Reflux is a Significant Causative Factor of Tooth Erosion


INTRODUCTION

rosion 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 soft drinks, 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 extrinsic and intrinsic factors together with other types of tooth wear, such as attrition or abrasion. Epidemiological studies of erosion suggest that either the prevalence of erosion is rising (Nunn et al., 2003), or there is an increasing awareness of the disease, for example, in young adults and adolescents (Lussi et al., 1991; Jaeggi and Lussi, 2006) and young children (Downer, 1995). Mild degrees of dental erosion have been reported as affecting over 20% of teenage and young-adult population groups, with severe erosion extending well into 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 European studies, but the problem has received less attention in the American literature (Bartlett et al., 1999). An initial study (Holbrook, unpublished observations) of 150 consecutive Icelandic individuals was used for the assessment of erosion and the planning of further investigations. Persons with erosion were predominantly male. Some had only incisor erosion, while others showed involvement of molars and incisors. Severity of erosion varied from being limited to enamel through to severe dentinal erosion of several adjacent teeth, typically 4-6 maxillary anterior teeth. Concern about the possible role that gastro-esophageal reflux might play in causing tooth erosion in Iceland had been raised in 2001 by one of the authors (Theodors, unpublished observations), who found the prevalence of reflux symptoms occurring once a month to be 26%. This supported the possibility that intrinsic acid attack might play a role in causing erosion. In situ pH electrodes had previously failed to demonstrate acid reflux into the mouth in persons with a history of reflux disease (Gudmundsson et al., 1995). While erosion was clearly caused by acid attack from either intrinsic and extrinsic sources, or both, there is no evidence in the literature that the clinical manifestations of observed erosion might differ depending on the causative factor. Wide variation in the prevalence of tooth erosion has been reported among persons with reflux, even from the same research group (Jarvinen et al., 1988; Meurman et al., 1994). Thus, the purpose of the present study was to investigate a larger group of referred individuals in a standardized manner to determine the interplay of possible causative and reparative factors in tooth erosion. Furthermore, the aim was to record erosion with respect to

location and severity, to determine if the clinical picture might give a clue to the dominant etiological factor of the erosion.
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J Dent Res 88(5) 2009 Gastric Reflux and Tooth Erosion 423

MATERIALS & METHODS


Study participants (N = 249) were referred from dentists and the State 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 the procedure in question, whether history-taking and examination, saliva sampling, esophageal pH measurement, or gastroscopy. Permission for the investigation was given by the relevant Icelandic authorities for data protection (Personuvernd no. 2006030131) and ethics (Vsindasidanefnd no. VSNb2006030008/03-1).

Clinical Examination This was standardized to allow for comparisons and to facilitate analysis. All participants were examined by the same clinician (WPH), who was experienced in examining and recording erosion for clinical and research purposes within this population. Erosion was recorded separately for the anterior teeth and molars, and the score for the most affected tooth surface was noted for subsequent data analysis. Severity of erosion was recorded as being: in enamel only (score 1); into dentin (score 2); or severely affecting the tooth or series of teethfor example, as seen frequently in erosion of the palatal surfaces of 4 maxillary incisor teeth (score 3). Criteria for scoring erosion were modified from the Index of Lussi (1996) (Table 1) as used in previous studies in Iceland (Jensdottir et al., 2004). Instances of xerostomia were followed up and recorded. Because the participants were referred specifically for diagnosis and investigation, it did not prove possible to recall a proportion to measure consistency of the erosion scores. Reliability was dependent on the previous experience of the single examiner, and on standardized criteria. There is an acknowledged problem in the accurate diagnosis of erosion just into dentin (Holbrook and Ganss, 2008), but the clinician had gained experience and calibration from participation as a clinical examiner in a survey, concurrent with the beginning of the present study, of erosion in individuals with and without reflux disease conducted by two observers blinded to the underlying cause of the observed erosion (Jensdottir et al., 2004). History-taking Detailed dental and medical histories were taken. These included symptoms of gastric reflux, any history of vomiting, and previous investigations for gastro-intestinal complaints. Medication was recorded, including: drugs for reflux disease; drugs causing dry mouth; and regular use of asthma sprays, inhalers, or other medications with a low pH taken orally and on a regular basis. Dietary Factors Participants recorded their consumption of soft drinks and particular preferences for acidic foods, including acid-preserved foods, using a modification of a dietary questionnaire extensively used in Iceland for studies of caries and erosion (Arnadottir et al.,

2003). Attempts were made to quantify the amount of acidic drink consumed per day, and consumption of >0.5 L/cola drink or fruit juice per day was recorded as a risk factor. Persons attending the clinical examination were informed of the potential erosive effect of consuming excessive amounts of acidic drinks and were advised to drink non-acidic drinks or carbonated water, as suggested by the findings of Jensdottir et al. (2005).

Salivary Parameters Participants provided a sample of stimulated saliva by chewing on a piece of paraffin wax for 1 min, swallowing the saliva that had collected, and then spitting out fresh saliva for a period of 1 min while continuing to chew the wax. Using pH paper strips (Whatman http://www.whatman.com), we used the samples immediately 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 after 3 min, using the manufacturers color chart for comparison when recording the buffer capacity (low, pH 4; medium, pH 5; high, pH 6). Stimulated salivary flow rates under 0.7 mL per min were considered lowered. Gastro-intestinal Examination Persons with molar erosion and those reporting symptoms of gastric reflux (N = 91) were referred to a gastroenterologist (AT) for further investigation and, if necessary, medication. Investigations included gastroscopy to determine the presence of mucosal inflammation, hiatal hernia, and sampling for the possible presence of Helicobacter sp. from the gastric mucosa. Esophageal manometry was performed together with 24-hour monitoring of esophageal pH, the recognized measure of pathological reflux. This was carried out by a single examiner (KG) using standard methods (Johnsson et al., 1987). Esophageal pH
Table 1. Criteria Used for Assessment of Dental Erosion (Lussi, 1996) Score Criteria for Anterior Teeth Criteria for Posterior Teeth 0 No evidence of erosion No evidence of erosion 1 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 surface 2 Erosion extending into dentin in at least one tooth Erosion into dentin that cannot be attributed to attrition, noting especially palatal aspects of maxillary molar cusps and buccal aspects of mandibular molar cusps 3 Erosion into in at least four anterior teeth and/ Dentin exposed and clear loss of tooth morphology and/or erosion extending or pulp chamber visible in at least one tooth close to the pulp
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424 Holbrook et al. J Dent Res 88(5) 2009 values < 4 recorded for > 3.4% of the 24-hour time period were regarded as indicative of pathological reflux. Statistical Analysis Data were collated from the various investigations and entered onto an Excel chart. Data were made anonymous before being transferred to the statistician (JF) for analyses. SPSS for Windows version 12 was used for statistics, i.e., 2, correlation, and logistic regression analyses.

RESULTS
Of 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). Spearmans coefficient for correlation between age and the severity of erosion was 0.166 (P < 0.05). A pattern of severe erosion,

clearly into dentin and with marked loss of normal tooth contour 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 incisal erosion. Less severe erosion involving enamel with no, or only minimal, dentin involvement was seen in the remaining 165 persons (66.3%), most commonly on the palatal surfaces of upper incisor teeth. Molar erosion was often seen on occlusal and buccal surfaces of lower molar teeth, and the palatal surfaces of upper molars. Labial erosion of upper incisor teeth was rarely seen, 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, usually cola-type, was reported by 133 persons (53.4%). Remaining participants reported no significant exposure to dietary acid. Analysis of salivary parameters (Table 3) showed that 10.4% of participants had a low buffering capacity, while 36% of persons reported symptoms of reflux, as confirmed in 21.3% of the sample according to the 24-hour intra-esophageal measurement (Table 3). Step-wise logistic regression analyses (Table 4) showed that the highest odds ratios were found between erosion and dietary factors, low salivary buffering, and reflux disease. Only 20 participants had low salivary flow, and this negative association between low salivary flow and erosion, although statistically significant (Table 3), may not be clinically relevant. Reflux parameters (odds ratio 1.33; P < 0.005) and daily consumption of >0.5 L of acidic drinks (odds ratio 3.17; P < 0.001) were significantly associated with palatal erosion of the maxillary incisor teeth. Low salivary buffer capacity was associated only with severe erosion into dentin in several adjacent teeth (2 6.57; P < 0.05). Erosion of molar teeth into dentin was associated with at least one parameter of reflux disease being positive (odds ratio 1.58; P < 0.001). There was little consistency in which reflux parameter was positive, but hiatal hernia and pathological reflux, as measured by 24-hour esophageal pH monitoring, were most commonly found (Table 3). No significant association was seen between dietary or salivary parameters and erosion in molars. Combining the factors measured to explain variations in observed erosion (R2) gave a value of only 15.1%.

DISCUSSION
The results confirmed our study hypothesis by showing a significant association between the severity and location of dental erosion and specific risk factors. The nature of the sample makes it likely that the degree of erosion was greater than that for the general population in Iceland, where erosion is common. Accurate diagnosis of the cause of observed tooth wear is often difficult (Holbrook et al., 2003), as is assessment of the extent of tooth wear through enamel into dentin (Holbrook et al., 2003; Holbrook and Ganss, 2008). Thus, the reproducibility of the erosion scores may be problematic, but, for most analyses, scores 1

and 2 were combined, and score 3 was used for erosion into dentin with loss of tooth contour as described earlier. The use of a single, experienced examiner was expected to have increased the reliability of the scores recorded. It was not feasible to include a control group in this study, since participants had been specifically referred. However, a case-control study of erosion in Icelandic teenagers conducted at the same time (Arnadottir et al., 2003) may be considered as
Table 2. Distribution of Erosion Recorded in the Teeth of the 249 Study Participants and Scored According to Severity and Location in the Molar/Premolar Teeth or the Incisor/Canine Teeth in Both Maxillary and Mandibular Arches Incisor Teeth Molar Teeth Erosion Maxillary Mandibular Maxillary Mandibular Score (%) (%) (%) (%) 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-intestinal Parameters in 249 Persons with Tooth Erosion No. of Cases % SALIVA Normal salivary flow 229 92.0 Salivary pH > 7.5 232 93.2 Buffer capacity high 183 73.5 Buffer capacity moderate 40 16.1 Buffer capacity low 26 10.4 GASTRO-INTESTINAL Reported symptoms of reflux 91 36.5 Abnormal manometry (lower esophageal 20 8.0 sphincter pressure) Low esophageal pH 44 17.7 Pathological reflux diagnosed (24-hour pH) 53 21.3 Hiatal hernia diagnosed 46 18.5 Helicobacter present 9 3.6
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J Dent Res 88(5) 2009 Gastric Reflux and Tooth Erosion 425
Table 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-value Male gender 0.420 (0.212 0.831) 0.013 Age 1.032 (1.006 1.058) 0.014 Dietary risk (> 0.5 L of acidic drink/day) 2.632 (1.397 4.958) 0.003 Low salivary flow 0.189 (0.049 0.726) 0.015 Low buffer capacity (< pH 4 using DentoBufftest kit) 2.490 (1.562 3.968) 0.000 Diagnosed reflux disease 2.772 (1.403 5.475) 0.003

a meaningful comparison group; with a prevalence of erosion of 21.6% in 15-year-olds, 68.3% of whom were male. Recent attention paid to erosion relates to the assumed association with consumption of acidic drinks and the pattern of this consumption (Johansson et al., 2002; Jensdottir et al., 2006). One Icelandic study (The Iceland Nutritional Council, 2002) has shown that teenagers and young adults, especially males, consume 1 L of cola-type drinks per day, whereas females consume 0.5 L/day. Strong dietary evidence supports the association of carbonated-drink consumption with the age and gender of participants in this study, while the association of drink consumption with incisor erosion is probably explained by the pattern of drinking (Johansson et al., 2002). Although no link was seen in the present study between molar erosion and high consumption of acidic drinks, one Icelandic study (Jensdottir et al., 2004) found a significant association between consumption of >1 L

of 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 apatite remineralization will be less. Conflicting data exist on the association between low buffer capacity and tooth erosion (Woltgens et al., 1985; Bevenius and LEstrange, 1990). The present finding that a low buffer capacity becomes significantly associated with only more severe grades of erosion may explain the earlier anomalous findings. There appear to be strong links between indicators of gastric reflux and the presence of tooth erosion, especially in the molar teeth, suggesting that careful history-taking is important if this problem is to be diagnosed. Unfortunately, no clear single factor could be measured that allowed a diagnosis of reflux-disease-associated erosion to be made. Both gastroscopy and 24-hour monitoring of esophageal pH appear to be necessary for a diagnosis, and this is clearly timeconsuming, expensive, and invasive. A problem remains with persons seen to have severe molar erosion, but in whom no pathological reflux can be found. Criteria for pathological reflux (esophageal pH < 4 for > 3.4% of the 24-hour time period) may need to be reconsidered with particular respect to teeth. From the clinical appearance of the dentition in many persons in this study, there is a strong suggestion that gastric acid passes over the dorsum of the posterior third of the tongue to erode the palatal surfaces of the upper molar teeth, and then passes over the buccal aspect of the lower molars. The ventral surface of the tongue presumably protects the lingual aspect of lower molars. Acid also passes over the dorsum of the tongue to erode the palatal surfaces of the maxillary anterior teeth. Erosion appears to be the result of an interaction of intrinsic and extrinsic acidic risk factors with the protective factors of enamel integrity, acquired pellicle, salivary flow, and buffer capacity. Conflicting evidence has been reported on the protective and preventive effects of fluoride in dental erosion. Salivary glycoprotein pellicle has a protective role against erosive actions, as shown by several clinical and in vitro studies (Meurman and Frank, 1991; Westergaard et al., 2001; Johansson et al., 2002, 2004). Erosion is thus usually seen in the areas where salivary pellicle has been lost following acid attack. Clearly, the interplay of causative and protective factors with respect to erosion is complex (Meurman and Sorvari, 2000; Johansson et al., 2004), but the low explanatory value of all the factors measured in this study was surprising. It was assumed, initially, that tooth erosion was a simpler disease to understand than dental caries, although similar in also having a multi-factorial etiology. Etiological and protective factors are routinely found to explain approximately 25-50% of variability in caries scores (R2) (Granath et al., 1991; Holbrook et al., 1993). Therefore, it was surprising that factors measured in this investigation of tooth erosion were not able to explain differences in erosion severity more than 15.1%. Perhaps there remain important etiological or pathogenic factors of tooth erosion to be investigated. Future studies might also separate the severe and

less severe forms of erosion, instead of categorically analyzing cases 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 difficult to restore. Consequently, attention should be focused on early diagnosis and on individuals at particular risk.

ACKNOWLEDGMENTS
The author JHM was supported by grant TYH 3245 of the Helsinki University Central Hospital, Finland. WPH was supported by the University of Iceland Research Fund.