Dental Erosion in
Ga s t roesophageal Re flux Di s e a s e
Ro b e rt P. Ba r ro n , DMD, BSc, FADSA •
Ro b e rt P. Ca rm i c h a e l , BSc, DMD, MSc, FRCD(C) •
Ma r g a ret A. Ma rc o n , MD, FRCPC •
George K.B. Sàndor, MD, DDS, FRCD(C), FRCS(C), FACS •
Dentists are often the first health care professionals to diagnose dental erosion in patients with gastroesophagealreflux disease (GERD). Gastroesophageal reflux (GER) is the passage of gastric contents into the esophagus, andGERD is defined as symptoms or complications of GER. Twenty-four-hour monitoring of esophageal pH is helpfulin diagnosing GERD. Treatment of dental erosion resulting from GERD involves a multidisciplinary approach amongfamily physician, dentist, prosthodontist, orthodontist and gastroenterologist. When possible, dental erosion shouldbe treated with minimal intervention, and such treatment should include control of microflora, remineralization,adhesive restorations and use of biomimetic materials. MeSH Key Words: dental enamel/pathology; gastroesophageal reflux/complications; tooth erosion/etiology
J Can Dent Assoc 2003; 69(2):84–9 This article has been peer reviewed. Dentists are often the first health care professionals 16 years of age, 12% had at least one permanent tooth with to diagnose a systemic disease through observation grade 1 erosion, and up to 0.2% of patients had at least one of its oral manifestations. One such condition is permanent tooth with grade 2 erosion.5 Other studies have gastroesophageal reflux disease (GERD), which may be reported a similar prevalence of erosion in adults (between evidenced by dental erosion. Dental erosion is defined as 5% and 16%).6,7 It has been our observation, working in the progressive loss of hard dental tissues caused by a chem- the dental department of a tertiary care facility with a catch- ical process not involving bacterial action.1 It has been asso- ment area of 10 million people, that many causes of dental ciated with ingestion of acidic foods,2 bulimia,3 rumination erosion go unnoticed or undiagnosed in adolescence, and and GERD.4 In addition to causing dental erosion, undi- the problems are not identified until early adulthood, when agnosed and untreated GERD may also result in esophagi- the damage is much more severe and much more difficult tis, Barrett's epithelium, esophageal adenocarcinoma and aspiration pneumonitis of various degrees. It is thereforeimportant that dentists recognize GERD so that timely preventive and treatment measures can be instituted. This Erosion begins as superficial demineralization of the paper discusses the relationship between dental erosion and enamel, which can cause dissolution of the subsurface layers GERD, the prevalence and causes of these conditions, diag- and eventual loss of tooth structure. Any acid with a pH nostic approaches and treatments.
below the critical pH of dental enamel (5.5) can dissolvethe hydroxyapatite crystals in enamel. Gastric refluxate has a pH of less than 2.0 and thus has the potential to cause dental erosion.8 In vitro experimental erosion has been In a 5-year longitudinal study,5 71% of children had shown to occur at an oral pH of less than 3.7.
erosive lesions of at least grade 1 affecting their primary Causes of dental erosion are classified as extrinsic or dentition, and 26% had grade 2 erosions (Table 1). By
intrinsic. Extrinsic causes include carbonated or acidic February 2003, Vol. 69, No. 2 Journal of the Canadian Dental Association Dental Erosion in Gastroesophageal Reflux Disease Figure 1: Dental erosion, facial view of lips
Figure 2: Dental erosion, facial view.
Figure 3: Dental erosion, palatal view.
and teeth. beverages, acidic foods,2 citric lozenges, various medica- reduction of overjet toward or beyond an edge-to-edge tions, oral hygiene swab sticks, saliva substitutes,10 recre- incisal relationship. These sequelae can be exacerbated if ational exposure to water in gas-chlorinated swimming attrition from bruxism is superimposed upon erosion, or if pools10 and occupational exposure to corrosive agents such either the acidic oral environment or pre-existing or contin- as battery acid fumes and industry aerosols.8,10 uing erosion increases susceptibility to caries.
Intrinsic causes of dental erosion include bulimia, rumi- nation or voluntary reflux phenomenon, subclinical regur- The immediate goal in the treatment of dental erosion gitation due to chronic gastritis associated with alcoholism, resulting from GERD is formulation of the correct differ- xerostomia, malabsorption syndrome, chronic vomiting ential diagnosis and prompt referral to a gastroenterologist.
during pregnancy and GERD.10–12 Meurman and others13 It is not unusual, particularly in medically underserv i c e d examined 117 patients with GERD, of whom 28 (24%) regions of the country, to encounter waits of up to 6 months also had dental erosion. Schroeder and others4 identified or more to see a medical specialist. In the meantime, it is dental erosion in 11 (55%) of 20 patients with GERD.
important to provide symptomatic relief and to discourage further progression of the erosion.
The mandibular molars in both the primary and perma- It has been known for many years that demineralized nent dentitions are the teeth most commonly subject to lesions can be remineralized and repaired.14 It is likely that erosion.5 Patients exposed to extrinsic acids suffer more the same factors controlling remineralization of carious damage to the labial or occlusal surfaces of the upper ante- lesions also control remineralization of areas of erosion.
rior teeth,8 with severity decreasing posteriorly, whereas Table 1 Erosion grading scale of Ganss and
intrinsic acid causes more damage to the lingual surfaces of the teeth. The pattern of erosion caused by intrinsic acidmay be modulated by the protective influence of the tongue, which forces regurgitated acid over the tongue, No visible erosion along the palate and into the buccal vestibule.8 Thinning of Small pits and slightly rounded cusps, flattened the enamel imparts an unesthetic yellowish hue to the teeth fissures, moderate cupping, preservation of occlusal (Figs. 1 and 2). Eroded teeth have the appearance of having
surface morphology been lightly prepared for full-coverage restorations with a Depression of cusps with severe cupping and chamfer margin (Fig. 3) and are more prone to wear. Once
grooving, restoration margins raised above level of dentin is exposed, the loss of dentin progresses faster than surrounding tooth, flattening of occlusal surfacemorphology the loss of enamel, such that "cupping" of lesions on theocclusal surfaces occurs.8 Amalgam restorations in erodedteeth appear highly polished and seem to "stand above" the Table 2 Erosion grading scale of Eccles and
tooth surface (Table 2).
Exposure of the dentinal tubules results in hypersensi- tivity to hot, cold, sweet and tactile stimuli. The pulp maye ventually be exposed, with the attendant need for endodontic therapy.8 – 1 0 Additional sequelae of dental Loss of surface detail; change confined to enamel erosion include compensatory eruption of eroded teeth, Exposure of dentin affecting less than one-third tipping and drifting of teeth, formation of diastemae, loss of vertical dimension, overclosure and bite collapse, all Exposure of dentin affecting one-third or more of which result in autorotation of the mandible and Journal of the Canadian Dental Association February 2003, Vol. 69, No. 2 Barron, Carmichael, Marcon, Sàndor Saliva is already supersaturated with calcium and phosphate to inadequate clinical crown length, namely elective ions, so if the ambient pH rises above pH 5.5, erosive endodontic treatment, post and core fabrication or surgical lesions will begin to remineralize. Successful remineraliza- crown lengthening.20 In cases of advanced breakdown, tion requires control of cariogenic microflora through these traditional approaches will in fact be necessary, and diligent home care and reduction of intake of refined carbo- cemented ceramo-metal or ceramic crowns may be the hydrates. Daily rinsing with 0.12% chlorhexidine15 is help- treatment of choice.
ful in reducing accumulation of bacterial plaque, especially Because many patients treated for dental erosion caused during the early phase of patient education and motivation.
by GERD are young or middle-aged adults, most dental To prevent the acidity on the surface of the teeth from restorations will require replacement over the patient's life- falling below pH 5.5, at which point demineralization time. The speed of deterioration of restorations is deter- occurs, the consumption of carbonated and acidic beverages mined by many factors, not least the presence of residual must be curtailed. Saliva can reduce the potential for reflux, which may contribute to demineralization of the demineralization, and therefore any deficiency in flow rate hard dental tissues, particularly in the area of the restoration or buffering capacity of the saliva should be noted.16 margins. In the absence of adequate control of GERD, the If necessary, saliva substitutes can be re c o m m e n d e d .
restoration margins are at risk for development of caries.
Chewing antacid tablets or rinsing with a solution of The most serious consequence is that the restoration will be sodium bicarbonate can neutralize the demineralizing effect so deeply undermined that it cannot be replaced (which of acid on the dentition.8 necessitates removal of the tooth), or it cannot be replaced Fluoride facilitates remineralization and, because the without further adjunctive periodontal or endodontic critical pH of fluoroapatite is 4.5, confers greater resistance p ro c e d u res. Rigorous medical follow-up for re c u r re n t to demineralization.17 Furthermore, fluoride is bacteriosta- GERD is imperative to avoid this scenario.
tic18 and buffers the pH on the surface of the tooth.19To maximize the potential for remineralization and mini- mize the potential for demineralization, daily use of both a neutral 0.05% fluoride mouth rinse and 1.1% fluoridetoothpaste is recommended. In addition to the value of GERD is an important cause of dental ero s i o n .
mouthguards as a physical barrier to protect the teeth from Gastroesophageal reflux (GER) is defined as the passage of exposure to acid during periods of reflux, they are also gastric contents into the esophagus, whereas GERD is useful carriers for fluoride gel.
defined as symptoms or complications of GER.29 The most Once the diagnosis of GERD has been established and widely accepted criterion for diagnosis of GERD is the the condition brought under control, some orthodontic o c c u r rence of heartburn 2 or more times per we e k .
treatment is usually necessary, unless wholesale crowning of However, although heartburn is specific for GERD, it is not one or both arches with an attendant increase in vertical very sensitive in this diagnosis. Thus, given the limitations dimension of occlusion is indicated. The dentition may of currently available diagnostic tests, the epidemiology of have to be realigned to compensate for overeruptions, GERD has been difficult to ascertain.30 drifting and loss of arch length.
In view of the potential application of biomimetic mate- Estimates of the prevalence of GERD range from 6% to rials and techniques20 in the restoration of eroded teeth, and 10%,31,32 although up to 59% of the population reports in keeping with a modern, minimally invasive approach to heartburn monthly,32,33 up to 20% report weekly symp- dentistry,21 the natural tooth structure should be preserved toms,33 and 18% use prescription drugs to manage their whenever possible. Cupped lesions on cuspal tips and minor contour defects can be re s t o red with adhesiveresins.22 Bonded porcelain restorations can be used to Table 3 Nonmedicinal treatment alternatives
restore extensive loss of tooth structure in the anterior (lifestyle measures) for gastroesoph-
teeth.23,24 There is some early evidence that the biomimeticprinciples used to restore anterior teeth can also be applied ageal reflux disease (Andreoli and
to the restoration of posterior teeth.25–27 Many posterior teeth can be treated ultraconservatively Elevate head of bed with directly applied composite resins, especially if the Avoid food and liquids 2–3 hours before bedtime marginal ridges remain intact. When full coverage of eroded Avoid fatty and spicy foodsAbstain from smoking cigarettes and drinking alcohol vital posterior teeth is indicated, indirect ceramic overlays may be considere d2 8 both to pre s e rve natural tooth P r o p hylactic use of liquid antacid (aluminum hy d r o x i d e -magne- structure and to avoid traditional prosthodontic approaches sium hydroxide), 30 mL 30 minutes after meals and at b e d t i m e February 2003, Vol. 69, No. 2 Journal of the Canadian Dental Association Dental Erosion in Gastroesophageal Reflux Disease Table 4 Medical therapy for gastroesophageal reflux disease (Andreoli and others,41 Rubin,42)
Acid-neutralizing agents Sodium bicarbonate (NaHCO3) (baking soda) 1 suppository PR 325–650 mg PO Magnesium hydroxide (milk of magnesia) Aluminates (Maalox, Pepto-Bismol) 15–45 mL q3–6h Histamine-2 blockers Cimetidine (Tagamet) 800 mg PO hs 400 mg bid Ranitidine (Zantac) 300 mg PO hs 150 mg bid Famotidine (Pepcid) Nizatidine (Axid) Metoclopramide (Reglan) 10–20 mg PO, IM or IV(IV given over 1–2 min) Prokinetic agents Cisapride (Propulsid) 10–20 mg PO qid Proton pump inhibitors Omeprazole (Prilosec) 20–40 mg qd every morning Lansoprazole (Prevacid) 15–30 mg qd every morning Nissen fundoplication PR = per re c t u m , PO = per os, qd = eve ry day, q3–6h = eve ry 3–6 hours, hs = at bedtime, bid = 2 times daily, IM = intramuscular, IV = intrave n o u s , qid = 4 times daily Causes and Pathophysiology
include gastric juice in the mouth, chronic laryngitis, laryn- In healthy individuals, most gastric refluxate is returned geal granuloma and ulcers, laryngeal carcinoma, chronic to the stomach by peristalsis stimulated by swallowing. The sore throat, subglottic stenosis, vocal cord polyps, night- remaining refluxate is cleared by secondary peristalsis stim- time cough and globus pharyngeus.
ulated by direct contact of the juice with the esophageal Reflux affects individuals differently at different times of mucosa.34 In contrast, patients with GERD have delayed the day. Some patients report continuous reflux throughout acid clearance. Bartlett and others35 found that patients the day, whereas others experience it primarily nocturnally with dental erosion were less able to clear refluxate from the or intermittently during the daytime.39 esophagus, and this problem appeared to be correlated with poor esophageal motility. Gastroparesis, increased abdomi- There is as yet no single test that can consistently detect nal distension and myopathy affecting gastro i n t e s t i n a l GERD,30 although, depending on the clinical situation, motility are all etiologic agents in GERD.
reflux can be demonstrated with several diagnostic tests, GERD has been classified into 2 types: physiologic and pathologic. The physiologic form occurs postprandially and such as barium esophagography, endoscopic examination, is associated with eructation or belching. It is usually esophageal acid perfusion, measurement of lowe r temporary and does not require medication. Physiologic esophageal sphincter pressure, mucosal biopsy, standard GERD is common in infants, in whom it usually resolves acid reflux test and radionuclide scintography.40 spontaneously by 1 year. In some adults, however, pain and The most useful diagnostic tool currently available to other symptoms may accompany belching. If clearance diagnose GERD is 24-hour monitoring of esophageal pH40 mechanisms cannot return the refluxate back to the stom- by means of a catheter passed through the nares to a point ach and the condition becomes chronic, it is known as 5 cm above the lower esophageal sphincter. If the pH pathologic GERD.11,35 The demarcation between physio- in the distal esophagus remains below 4.0 for more than logic and pathologic GERD remains ill-defined because of 4% of the time, the condition is considered pathologic.11,29 a lack of consensus.30 Hiatus hernia can cause both physiologic and pathologic The goals of treatment for patients with GERD are GERD. It may be associated with an incompetent reflux multifocal. From the medical perspective, accurate diagno- barrier but is not a prerequisite for GERD.11 Some drugs sis is imperative. Treatment may combine nonmedicinal (specifically nitrates and calcium-channel blockers) and therapy such as elevating the head of the bed and avoiding cigarette smoking have also been implicated in GERD.
fatty and spicy foods (Table 3), as well as drug therapy
(Table 4).
Extra-esophageal manifestations of GERD are common Medicinally, histamine-2 (H2) blockers and drugs that and invo l ve both soft and hard tissues.3 6 He a rt b u r n , enhance gastric motility have been the mainstay of treat- noncardiac chest pain, chronic cough, chronic hoarseness, ment. Proton pump inhibitors are efficacious in controlling asthma37 and idiopathic pulmonary fibrosis have all been GERD refractory to therapy with H2 blockers (Table 4 ).42
associated with GERD.3 8 Additional signs of GERD Successful control of GERD by medicinal therapy is Journal of the Canadian Dental Association February 2003, Vol. 69, No. 2 Barron, Carmichael, Marcon, Sàndor confirmed through repeat monitoring of esophageal pH.
It is our hope that future collaboration between the disci- When medicinal therapy is ineffective, surgical intervention plines of dentistry and gastro e n t e rology will further elucidate (Nissen fundoplication) has been useful.38 the causal relationship between GERD and dental ero s i o n .
The complications of untreated GERD include Fu rt h e r m o re, in restoring dental erosion, a minimally inva- esophageal stricture, esophageal ulcer, Barrett's esophagus, s i ve approach that takes advantage of all the modern adva n c e s increased risk of transformation to esophageal adenocarci- in fluoride use, adhesive dentistry and biomimetic materials noma, pulmonary aspiration and upper gastrointestinal should be employed whenever possible. C Dr. Barron is a former senior exchange resident in oral and maxillo
facial surgery at the University of Toronto, visiting from the Hebrew Treatment of dental erosion resulting from GERD University Hadassah School of Dental Medicine in Israel. He is involves a multidisciplinary approach among family physi- currently in private practice in Toronto, Ontario. cian, dentist, prosthodontist, orthodontist and gastroen- Dr. Carmichael is assistant professor
, department of prosthodontics,
University of Toronto, and coordinator of prosthodontics, Hospital for terologist. Most patients with dental erosion who undergo Sick Children and Bloorview MacMillan Children's Centre, Toronto, treatment have been referred, not by physicians, but rather by the family dentist. This pattern reflects our belief that Dr. Marcon is associate professor, department of pediatrics, division of
gastroenterology and nutrition, University of Toronto and Hospital

dentists are usually the first health care providers to recog- for Sick Children, Toronto, Ontario. nize GERD because of its oral manifestations.
D r. S à n d o r is associate professor, Toronto General Hospital,
For many patients with dental erosion, there is sufficient director, graduate training program in oral and maxillofacial surgery evidence of pathological reflux, both clinically and on department of oral and maxillofacial surgery, University of Toronto,and coordinator of OMFS, Hospital for Sick Children and Bloorview monitoring of esophageal pH, to warrant medical interven- MacMillan Children's Centre, Toronto, Ontario. tion. When medical treatment is indicated, a careful assess- Correspondence to: D r. Robert P. Carmichael, Coordinator of
ment of the risk-benefit ratio is required, because the conse- Prosthodontics, Hospital for Sick Children and Bloorview MacMillanChildren's Centre, 350 Rumsey Rd., Toronto, ON M4G 1R8. quences of long-term medication are unknown. Generally, medical treatment leads to amelioration of GERD and The authors have no declared financial interests. paves the way for dental treatment. Medical follow-up isnecessary to monitor for recurrence of GERD, which would not only put healthy, unrestored tooth surfaces at 1. Pindborg JJ. Pathology of dental hard tissues. Copenhagen: risk of erosion, but would also risk undermining the usually Munksgaard; 1970. p. 312–25.
extensive oral reconstruction.
2. Asher C, Read MJ. Early enamel erosion in children associated with the Paradoxically, in some patients with dental erosion, in excessive consumption of citric acid. Br Dent J 1987; 162(10):384–7.
whom neither an extrinsic cause nor any intrinsic cause 3. Jones RR, Cleaton-Jones P. Depth and area of dental erosions anddental caries in bulimic women. J Dent Res 1989; 68(8):1275–8.
other than GERD can be identified, there is insufficient 4. Schroeder PL, Filler SJ, Ramirez B, Lazarchik DA, Vaezi MF, Richter evidence of pathological reflux to justify medical treatment.
JE. Dental erosion and acid reflux disease. Ann Intern Med 1995; This situation creates a dilemma. Withholding restorative treatment because a cause has not been identified could lead 5. Ganss C, Klimek J, Giese K. Dental erosion in children and adolescents– a cross-sectional and longitudinal investigation using study models.
to further deterioration of the dentition, and the patient Community Dent Oral Epidemiol 2001; 29(4):264–71.
and his or her family may feel that the dentist lacks 6. Jarvinen VK, Rytomaa II, Heinonen OP. Risk factors in dental erosion.
diagnostic acumen or has denied the patient necessary treat- J Dent Res 1991; 70(6):942–7.
ment. Howe ve r, the provision of defin i t i ve re s t o r a t i ve 7. Lussi A, Schaffner M, Hotz P, Suter P. Dental erosion in a populationof Swiss adults. Community Dent Oral Epidemiol 1991; 19(5):286–90.
procedures in the continuing presence of an oral acid 8. Lazarchik DA, Filler SJ. Dental erosion: predominant oral lesion challenge will lead to premature failure of treatment and in gastroesophageal reflux disease. Am J Ga s t ro e n t e ro l 2000; will likely leave the patient in worse condition than before treatment. Nevertheless, even when the cause of dental 9. Eccles JD, Jenkins WG. Dental erosion and diet. J Dent 1974;2(4):153–9.
erosion cannot be ascertained, some form of reconstruction 10. Habsha E. The etiology and pathogenesis of tooth wear: Part I. Oral may be necessary. Therefore, when initiating restorative Health 1999; 83–92.
treatment in the absence of a definitive diagnosis of GERD, 11. Bartlett D, Smith B. Clinical investigations of gastro-oesophageal it behooves dental professionals to also prescribe strategies reflux: Part 1. Dent Update 1996; 23(5):205–8.
12. Ibbetson R, Eder A. Tooth surface loss: editors' introduction. Br De n t J such as plaque control and reduction of intake of refined carbohydrates and carbonated beverages to maximize the 13. Meurman JH, Toskala J, Nuutinen P, Klemetti E. Oral and dental potential for remineralization and optimize the pH- manifestations in gastroesophageal reflux disease. Oral Surg Oral Med buffering capacity of the oral environment. Si m i l a r l y, Oral Pathol 1994; 78(5):583–9.
14. Kid EA, Jayston-Bechal S. Essentials of dental caries: The disease and patient behaviour that might reduce putative GERD its management. Dental practitioners handbook 1. Bristol, England: should be encouraged.
Wright; 1987.
February 2003, Vol. 69, No. 2 Journal of the Canadian Dental Association Dental Erosion in Gastroesophageal Reflux Disease 15. Katz S. The use of fluoride and chlorhexidine for the prevention of 40. Sontag SJ, O'Connell S, Khandelwal S, Miller T, Nemchausky B, radiation caries. J Am Dent Assoc 1982; 104(2):164–70.
Schnell TG, and other. Most asthmatics have gastroesophageal reflux with 16. Edgar WM. Saliva and dental health, clinical implications of saliva: or without bronchodilator therapy. Gastroenterology 1990; 99(3):613–20.
report of a consensus meeting. Br Dent J 1990; 169(3–4):96–8.
41. Diseases of the esophagus. In: Andreoli TE, Bennett JC, Carpenter 17. Silverstone LM. The effect of fluoride in the remineralization of CJ, Plum F, editors. Cecil essentials of medicine. W.B. Sa u n d e r s enamel caries and caries-like lesions in vitro. J Public Health Dent 1982; Company; 1997. 34:282–4.
42. Rubin DC. Gastroenterologic diseases. In: The Washington manual.
18. Loesche WJ, Straffon LH. Longitudinal investigation of the role of Manual of medical therapeutics. Little, Brown and Company, USA.
S. mutans in human fissure decay. Infect Immun 1979; 26(2):498–507.
1993; 15:293–4.
19. Nicholson JW, Czarnecka B, Limanowska-Shaw H. Effect of glass- 43. Friedman LS, Peterson WL. Peptic ulcer and related disorders. In: ionomer and related dental cements on the pH of lactic acid storage Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper solutions. Biomaterials 1999; 20(2):155–8.
DL, and others. Harrison's principles of internal medicine. 14th ed.
McGraw Hill, USA; 1998. 2:284; 1592.
20. Magne P, Belser U. Bonded porcelain restorations in the anteriordentition; a biomimetic approach. Chicago: Quintessence Publishing Co,Inc.; 2002.
21. Mount GJ, Ngo H. Minimal intervention: a new concept for opera-tive dentistry. Quintessence Int 2000; 31(8):527–33.
22. Peumans M, Van Meerbeek B, Lambrechts P, Vanherle G. The 5-yearclinical performance of direct composite additions to correct tooth formand position. I. Esthetic qualities. Clin Oral Investig 1997; 1(1):12–8.
23. Walls AW. The use of adhesively retained all-porcelain veneers duringthe management of fractured and worn anterior teeth: Part 2. Clinicalresults after 5 years of follow-up. Br Dent J 1995; 178(9):337–40.
24. Magne P, Douglas WH. Additive contour of porcelain veneers: a keyelement in enamel preservation, adhesion and esthetic for the agingdentition. J Adhes Dent 1999; 1(1):81–92.
25. Morin D, DeLong R, Douglas WH. Cusp reinforcement by the acidetch technique. J Dent Res 1984; 63(8):1075–8.
26. McCullock AJ, Smith BG. In vitro studies of cusp reinforcement withadhesive restorative material. Br Dent J 1986; 161(12):450–2.
27. McPherson LC, Smith BG. Reinforcement of weakened cusps bya d h e s i ve re s t o r a t i ve materials: an in-vitro study. Br De n t J 1 9 9 5 ;178(9):341–4.
28. Magne P, Dietschi D, Holtz J. Esthetic restorations for posteriorteeth: practical and clinical considerations. Int J Periodontics RestorativeDent 1996; 16(2):104–19.
29. Pediatric GE. Reflux clinical practice guidelines. J Pe d i a t rGastroenterol Nutr 2001; 32(2 Suppl):S1–31.
30. Eisen G. The epidemiology of gastroesophageal reflux disease: whatwe know and what we need to know. Am J Ga s t ro e n t e rol 2001; 96(8 Suppl):S16–8.
31. Bloom BS, Glise H. What do we know about gastroesophageal refluxdisease? Am J Gastroenterol 2001; 96(8 Suppl):S1–6.
32. Talley NJ, Zinsmeister AR, Schleck CD, Melton LJ 3rd. The naturalhistory of gastroesophageal reflux. Gastroenterol 1992, 102:A28.
33. Locke GR 3rd, Talley NJ, Fett SJ, Zinsmeister AR, Melton LJ 3rd.
Prevalence and clinical spectrum of gastroesophageal reflux: a population-based study in Olmsted County, Minnesota. Gastroenterology 1997;112(5):1448–56.
34. Kruse-Anderson S, Wallin L, Madsen T. Acid gastro-oesophagealreflux and oesophageal pressure activity during postprandial and noctur-nal periods. A study in subjects with and without pathologic acid gastro-oesophageal reflux. Scand J Gastroenterol 1987; 22(8):926–30.
35. Bartlett DW, Evans DF, Anggiansah A, Smith BG. The role of theesophagus in dental erosion. Oral Surg Oral Med Oral Pathol Oral RadiolEndod 2000; 89(3):312–5.
36. Paterson WG. Extraesophageal complications of gastroesophagealreflux disease. Can J Gastroenterol 1997; 11(Suppl B):45B–50B.
37. Ekstrom T, Tibbling L. Influence of theophylline on gastroesophagealreflux and asthma. Eur J Clin Pharmacol 1988; 35(4):353–6.
38. DeVault KR. Overview of therapy for the extraesophageal manifesta-tions of gastroesophageal reflux disease. Am J Ga s t ro e n t e ro l 2000; 95(8 Suppl):S39–S44.
39. Demeester TR, Johnson LF, Joseph GJ, Toscano MS, Hall AW,Skinner DB. Patterns of gastroesophageal reflux in health and disease.
Ann Surg 1976; 184(4):459–69.
Journal of the Canadian Dental Association February 2003, Vol. 69, No. 2

Source: http://mineralmed.com.pt/documentos/pdf/ced72af4-19e9-4064-8819-b52abb787d6a.pdf


A Patient This guide aims to outline why antidepressants(or other treatments) may be recommended by yourdoctor and also provides information about how theyshould be used. What is depression?Feeling unhappy and depressed is part of the range of normal andunderstandable human emotions, often as a result of difficultcircumstances and happenings in our lives. Everyone knows how it feelsto feel sad and low. Some people find that their low mood becomes sosevere that it affects their usual ability to function, for example look afterthemselves, in their home or at work. Normally pleasurable activities feeldifficult and are not enjoyed. Sleep may be disturbed and appetite oftenreduced. Similarly the ability to concentrate on simple tasks like readingor watching the television can be difficult. Everyday thoughts are oftenbleak and thoughts of hopelessness and even suicide may be present.If such symptoms last for over a couple of weeks it is quite likely thatthe person is suffering from depression.


Recent Developments in Greece – the milk, oil and pharmaceuticals Cases Despina D SamaraCalavros & Partners The year 2006-2007 saw three industry sectors coming under the public consultation procedure, announced concrete structural meas-scrutiny of the Hellenic Competition Commission, namely, milk, oil ures and behavioural recommendations that it considered absolutely and pharmaceuticals. Following either ex-officio investigations or necessary to establish and enforce effective competition in the oil complaints filed by other market participants the national authority market. These measures relate mainly to observance of the principles was dealing with all three sectors by late 2006. Of particular note, in of transparency, non-discriminatory treatment, accounting separa-the pharmaceuticals sector, after almost seven years of proceedings, tion and cost-orientation in setting prices. A more specific look at the Competition Commission reached a much-anticipated decision the measures follows.in the Syfait case.