Dental erosion was defined as dissolution of tooth by a solution that is low in pH either after the consumption of extrinsic acidic fluids or when gastric fluids come into the oral cavity. Gastro esophageal reflux (GERD) is a condition defined as an involuntary passage of gastric juice against the normal flow of digestive tract. It can be abnormal phenomena on in newborns and usually disappears with age; however, in some individuals, its maintenance can be considered a pathological condition. (1)
The association between acid reflux and dental erosion was first described by Howden in 1971 and was confirmed in other studies later, both in the adult population and in children. (2, 9, 23)
This association is commonly observed by dentists, but is given very cursory mention or omitted entirely when describing extra esophageal (supra-esophageal) manifestations of GERD. (3)
A recent systematic review found a median prevalence of 24% for tooth erosion in patients with gastro esophageal reflux disease (GERD) and a median prevalence of 32.5% for GERD in adult patients who had tooth erosion Therefore, from their observations of tooth erosion, dentists may be the first persons to diagnose the possibility of GERD, particularly in the case of “silent refluxes.” This diagnosis is important, as GERD has increased in prevalence in many countries, and may have severe health effects if not adequately treated. Consequently, dentists should before aware of the various manifestations of GERD. (4)
The aims of the study were to investigate dental erosion prevalence, location and severity and also to determine the effect of oral hygiene level, dietary behavior, dental behavior and GERD related medication and chronic illness in erosion.
Patients and methods
This study was conducted at the Departments of Oral Medicine and Gastroenterology of Sahloul Hospital, Sousse Tunisia.
The study group consisted of 100 patients with GERD.
All patients with GERD for 6 months with typical symptoms (heartburn and / or acid regurgitation, minimum weekly lasting for six months or more), atypical symptoms (epigastria pain, nausea, belching, halitosis, pseudo-angina pain) or with erosive GERD discovered during endoscopic examination (reflux esophagitis) or at the stage of GERD complications (peptic stenosis of the esophagus, Barrett, hemorrhage digestive).
Were excluded from the study all patients treated surgically for GERD or presenting symptoms of GERD less than once a week or presenting undercurrent factors that can cause dental erosion such as; disorders (bulimia, anorexia), professionals exposure to toxic agents (acid fumes and aerosols used in industry) and pregnant women.
Diagnosis of GERD
All patients of the study group were new patients seen at the Gastroenterology Department because of symptoms ⁄ signs suspicious of GERD. Gastro-esophageal reflux disease was diagnosed by esophagogastroduodenoscopy, 24-h esophageal pH-metry, esophageal manometry.
In fact all patients underwent a 24-h esophageal pH-metry to confirm the diagnosis with the exception of those who are carriers of reflux esophagitis (discovered during endoscopic examination). In our series, the characteristics of the disease (GERD), the eventual drug treatment and dietary habits were collected.
Oral involvement assessment
Medical history of potential oral symptoms associated with GERD was
carefully collected and the following parameters was evaluated; brushing method, dental erosion, dental sensitivity, loss of dental structure because of abnormal attrition (clenching or bruxing of one tooth surface against another), physical wear by extraneous objects such as toothbrushes, also known as tooth abrasion, alteration of the mucosa.
Thus, dental erosion was assessed in all the patients and by a single investigator under ideal lighting conditions, and to standardize this evaluation, patients were assigned a wear Index according to the classification scale erosion of Eccles and Jenkins (Table 1).
Tooth sensitivity was ranked on a subjective assessment by the dentist in 4 stages: no sensitivity, low sensitivity, moderate, and severe.
erosion of Eccles and Jenkins
Data entry and statistical analysis were performed using SPSS (software version 11.0). For the descriptive study, we calculated simple and relative frequencies, means, median and standard deviations for the analytical study, we used the Chi 2 test of Person for the comparison of percentages and the student t test for comparison of means. Only P-values <0.05 were considered statistically significant.
Clinical examination was carried out in 100 patients (Thirty-nine (39%) were men and Sixty-one (61%) were women) with sex’s ratio; 0.63% (mean age: 49.4; range: 20–75). (fig1)
The prevalence of dental erosion associated with GERD and distribution by score of Eccles and Jenkins are illustrated in (Fig. 2and table1).
The Predilection sites are the palatal surfaces of maxillary incisors followed by palatal surfaces of maxillary molars fig. 3 (a, b) and the occlusal surfaces of lower molars (protected by the tongue and saliva), fig 4.
incisors and molars
incisors and molars
A significant association was found between grade of erosion related to GERD and dental sensitivity (p=0.009).
A statistically significant associations between dental erosion related to GERD and the presence of abrasion or attrition was found (p<0.001) (fig5 ,fig 6,fig7).
related to GERD and the presence of abrasion
related to GERD and the presence of attrition
GERD and pathologic attrition (bruxism)
Horizontal brushing was found to affect dental erosion in our series (p = 0.02).
Concerning dietary hygiene we found a positive correlation between soft drink consumption and stage of erosion related to GERD (p=0.009) unlike the alcoholic beverage.
About factors related to medical antecedent; History of the presence of treated ulcer disease was significantly related to the presence of dental erosion (p=0.01).
On the contrary, no significant association was found between dental erosion related to GERD and diabetes (p =0.917) in our series.
The use of vitamin C and Beta-blockers: predisposes to dental erosions with a respective p 0.032et 0.045. (fig 8, fig9)
GERD and the use of Beta-blockers
GERD and the use of vitamin C
In contrast the effect of anti-reflux therapy (inhibitor of proton pump) reduced the percentage of erosion (p=0.038).
On the other hand we found statistically significant association between the age of the symptoms of GERD (≥ 12 months), the average number of episodes of GERD (mean 6.68 / week) , the prevalence of nocturnal GERD symptoms and the presence of erosion with a value of p=0.027; 0.001and 0.028 respectively.
Lazarchik and Filler (1997) , Groen and Smount (2003) revealed that dental erosion is the major lesion of GERD supraglottic. (2)
In fact research on tooth wear and related factors has received great interest in recent year.
The present study recorded the prevalence, location, severity and also to determine the effect of oral hygiene level, dietary behavior, dental behavior and GERD related medication and chronic illness in dental erosion.
According to the present results, dental erosion is a common disease with a prevalence that falls within the reported rates observed in previous studies. (8, 10)
However, no clear definitive data are available regarding the real prevalence of dental erosion in patients with GERD and prevalence varies widely among different studies This can be explained by several factors such as frequency of regurgitation, duration of untreated disease, buffering properties of saliva, diet, friction caused by tongue on teeth during mastication, deglutition , phonation, diagnostic difficulty of erosion at the early stage , lack of description of diagnostic criteria. (5,9,16,17,18)
The most affected dental surfaces were found to be the maxillary anterior teeth, a finding which is in agreement with other studies (14, 8, 6, 11) On the other hand, lower rates of erosion were found in the mandibular teeth, especially in their lingual surfaces, and this may be attributed to the protective effects of the saliva produced by submandibular and sublingual glands (3, 4, 5, 19), these findings are in accordance with those reported by Magdalini and co-workers. (8)
The present study has recorded a significant association between erosion related to GERD and dental sensitivity this finding is on contrast with the result found by Di Fede and al. who found that dental hypersensitivity was present in both sample and control group at the same prevalence. (5)
In our study the coexistence of attrition in these lesions was important as well as abrasion; which is in agreement with other studies witch explain the aggravating role of these lesions on the erosion linked to GERD (8, 10); some experimental findings support these observations and indicate that tooth wear under bruxism and gastric acid conditions can occur at an alarming rate, thus these findings point to the need for early preventive strategies. (3)
Tooth brushing is an important factor, in our series horizontal brushing was found to potentiates dental erosion, in fact it should be done carefully, using a soft tooth brush and a low-abrasive high sodium fluoride containing dentifrice not immediately after acid regurgitation, it should be avoided for approximately 2 h after a regurgitation episode to allow for the re-establishment of salivary pellicle and subsequent tooth surface remineralization. (3)
A positive correlation between soft drink consumption and stage of erosion related to GERD was found in our patient in fact this relationship was also quoted in the literature unlike the alcoholic beverage(4), this is can be explained by the majority of women in our sample.
In fact alcohol consumption may increase gastric acid secretion, delay gastric emptying and cause incompetence of the lower esophageal sphincter.
Thus patients should be advised to avoid such acidic foods and beverages and instead rinse their mouths either with water, milk, sodium bicarbonate solutions or sodium fluoride mouth rinses after each acid regurgitation episode. (3, 8)
As regards to medical history, the presence of treated ulcer disease was significantly related to the presence of dental erosion in our sample, the same observation has been cited by Frank Z (26) this observation could be explained by the restoration of a normal acid secretion after eradication of the bacterium (Helicobacter pylori) unlike the study of Munoz and al. (27)
For diabetic patients has not found a correlation with GERD in our sample in contrast to the literature. (28,29)
In our study we found that the use of vitamin C and Beta-blockers predisposes to dental erosions this finding is in accordance with the literature in fact physicians should be aware of any drugs or medicines consumed by patients that may cause or exacerbate hypo salivation and lead to xerostomia or being itself acid, in some instances, saliva substitutes may be prescribed or recommended.(3,8)
This fact is in accordance with the findings of Al-Malik et al who found that the use of vitamin C supplements is a predictive factor for dental erosion(22)
In contrast anti-reflux therapy reduced the percentage of erosion ;it is a protective factor ,Tantbirojn and colleagues have the same finding in their study where he observed a faster increase in the loss of tooth surface in patients in whom acid reflux is not controlled. (4,10,24)
In our study we found a significant correlation between the severity of dental erosion and the duration of the disease, frequency of regurgitation and the prevalence of nocturnal GERD symptoms witch is in agreement with literature. (1, 3)
The potential for erosive damage during sleep-related GERD can be explained by the fact that the anti reflux protective mechanisms present during the waking period like increasing salivary flow and swallowing mechanisms and localized esophageal peristalsis to buffer the acid and facilitate volumetric clearance are decreased during sleep. (4)
As regards the effect on the mucosa, in the literature GERD was recently reported to be associated with erythematous lesions on soft and hard palate mucosa and uvula. (5)
Some microscopic alterations in the palatal mucosa, such as epithelial atrophy and increased fibroblast numbers was found ;thus attention should be paid to mucosal inflammation in GERD patients on dental check-up. (15,12,5) but in our sample no such lesion was found.
As a result special attention must be given to prevention to avoid the loss of substance and alteration consecutive to GERD as well as on the soft and hard tissue of the oral cavity the principal method is to eliminate the primary cause requiring a close relationship with the patient’s medical practitioner. From the dental practitioner’s perspective, preventive measures may involve the stimulation or substitution of salivary secretions, providing dietary advice, placement of any physical barrier between the tooth surfaces and the endogenous acid like “metal ion” fluorides such as SnF, AgF, TiF4, and FeF3; the mechanism of action is probably not by the fluoride ion itself, but by the metal ion precipitate that forms a physical barrier to the acid.
Other dental products can be used as, often, temporary physical barriers like resin-based viscous varnishes, resin-based dentin bonding agents, glass-ionomer cement, sealant. (3,4,30)
According to many research publications, the association of tooth erosion and GERD is stronger than generally perceived by physicians. Dental practitioners should also determine whether a patient has erosive tooth surface loss and, if present, try to identify the cause. If the tooth surface loss is the result of acid reflux, the practitioner should advise the patient to see his or her family physician or internist for diagnosis and treatment of GERD or of another illness related to acid regurgitation. In addition, dental practitioners should educate their patients about the damage that acid reflux can cause to their teeth and ensure prevention of further tooth wear involving local prevention, restorative and maintenance phases.
As a result collaboration between gastroenterologist and dentists is strongly advocated to prevent or ameliorate possible adverse oral effects from endogenous acid.
By Dr. Ines kallel