Dental Enamel Defects (Defective Tooth Enamel)

What Are Dental Enamel Defects?

[dropcap]D[/dropcap]ental enamel defects (DED) comprise a variety of abnormalities in the dental enamel of the second or permanent teeth and of primary or baby teeth.

Teeth may appear with pits, thin or missing enamel, non-white enamel (yellow, orange, or gray colored teeth), and demarcated opacities (very white spots) even if teeth are white.

Q: What is enamel?

A: Dental enamel is the shiny, hard, white, dense, inorganic substance covering the crowns of the teeth. The crown is the tooth portion above the gum. Under the enamel is hard dentin which surround the living pulp. In teeth with missing enamel, the areas with exposed dentin appear dull and tan colored.

What Are Dental Enamel Defects In Celiac Disease and/or Gluten Sensitivity?

• Relationship between dental enamel defects and celiac disease. Dental enamel defects are a classic sign of celiac disease.
• Relationship between dental enamel defects and low blood calcium. Lower serum calcium significantly predicted celiac disease in children with dental enamel defects. Screening for celiac disease is highly recommended among those patients especially in presence of underweight and hypocalcemia.¹

• Relationship between dental enamel defects and small intestinal damage. A study of 125 children recruited by dental researchers showed that specific enamel defects seem to be genetically related to the histological damage and villous atrophy of the small intestinal lining.²

• Relationship between dental enamel defects and genes. The presence of the genetic HLA DR3 antigen significantly increased the risk of dental lesions, while genotype DR5,7 seemed to protect against enamel defects. A logistic regression analysis of the variables age, serum calcium concentrations, number of affected teeth, type of enamel defect and DR antigens showed that only DR antigens discriminated celiac disease patients with defects from those without enamel defects.³

• Relationship between dental enamel defects and tooth cavities. In a study of Turkish children, enamel defects were associated with an increased caries incidence. The number of caries-free subjects in the control group was higher (38%) than in the celiac disease group (17%).⁴

Celiac patients were found to have higher indexes of caries than healthy subjects, both in deciduous teeth and permanent teeth. The increase of caries in celiac patients is not a manifestation of celiac disease, but an explanation of this high frequency could be the co-presence of risk factors, like the fragility of hypoplasic enamel, alterations in salivary concentrations (too acidic with low calcium) and reductions in salivary flow. Moreover, the decrease of salivary flow, occurring in active phase of disease, determines alterations of oral protective factors and it could increase risk for dental caries.⁵.

How Prevalent Are Dental Enamel Defects In Celiac Disease and/or Gluten Sensitivity?

• In a prospective study of 125 children, 50 children with diagnosed celiac disease, 21 potential celiac patients, and 54 controls were recruited and the oral examination was performed to reveal clinical dental delayed eruption in 38% of the diagnosed celiac patients and 42.5% of the potential celiac patients versus 11.11% of the controls. The prevalence of specific enamel defects was 48% in diagnosed celiac patients and 19% in potential celiac patients versus 0% in controls.⁶

• In an Italian study, dental enamel defects were detected in 58 celiac subjects (46.4%) against seven (5.6%) controls. Furthermore, among celiac disease subjects the mean age at celiac disease diagnosis was significantly higher in the group with DED (3.41 +/- 1.27) than without DED (1.26 +/- 0.7). DED resulted more frequent (100%) in atypical and silent celiac disease forms than in the typical one (30.93%).⁷
• In a Turkish study of children, the prevalence of enamel defect in celiac disease subjects was found to be significantly higher (42.2%) than in healthy subjects (9.4%). Grade I type enamel defects were most commonly diagnosed in both groups (20.3% and 6.3%, respectively).⁴
• Demarcated opacities or hypoplasia occurred in 28% of children with celiac disease vs 14.8% of control.⁸
• Severe grade III or grade IV enamel defects occurred in 10.1% of study patients that included both children and adults with celiac disease.⁹ These dental enamel defects might be the only manifestation of celiac disease.
• Dental enamel defects occurred in 89% of patients with celiac disease and Sjogrens syndrome and 88% in celiac disease alone compared with only 25% in Sjogrens syndrome alone.¹⁰
• In the reverse, celiac disease was more diagnosed in patients with DEDs (17.86%) compared to controls (0.97%). The majority of non-celiac patients showed grade 1 DED compared to grades 1, 2, and 3 DED in celiac disease.¹

What Are The Symptoms Of Dental Enamel Defects?

Dental enamel defects in celiac disease are marked by:

• Demarcated opacities (very white spots.)
• Varying shades of yellow, orange or gray.
• Missing enamel.
• Thin enamel.
• Horizontal grooves.
• And/or pits in permanent teeth.¹¹
• Increased risk of developing dental cavities.¹².

How Do Dental Enamel Defects In Celiac Disease and/or Gluten Sensitivity Develop?

• Dental enamel defects result from celiac disease in patients with HLA DR3 genotype before the critical age of 7 years when the crowns of the permanent teeth have developed.⁸
• The pathogenesis of these oral abnormalities is not fully understood.⁹
• However, El-Hodhod et al. found that lower blood calcium (hypocalcemia) significantly predicted celiac disease in children with dental enamel defects. “Screening for celiac disease is highly recommended among those patients especially in presence of underweight and hypocalcemia.”¹³
• Dental enamel defects were detected in 58 celiac subjects (46.4%) against seven (5.6%) controls. An association was found between dental enamel defects (DED) and gluten exposure period. Among celiac disease subjects the mean age at celiac disease diagnosis was significantly higher in the group with DED than without DED. DED resulted more frequent (100%) in atypical and silent celiac disease forms than in the typical one (30.93%). The presence of HLA DR 52-53 and DQ7 antigens significantly increased the risk of dental enamel defects in celiac children.¹⁴

Do Dental Enamel Defects Respond To Gluten-Free Diet?

Yes. A nutritious gluten free diet with adequate calcium is protective against celiac disease-related dental enamel defects in children while the crowns are developing.³

Helpful hint: It has been shown that the sweetener erythritol can greatly reduce the build-up of plaque on teeth. Because plaque is the forerunner of tooth decay, it is very important to reduce it on defective enamel. Erythritol can be found in certain candies and can be used in most recipes in place of regular sugar.

6 Steps To Improve Dental Enamel Defects In Celiac Disease and/or Gluten Sensitivity:

• [dropcap]1[/dropcap]Remove the Trigger. Maintain a Strict, Nutritious Gluten Free Diet:

[box type=”shadow” ]Treatment. This condition responds to the complete elimination of gluten, which is the required treatment that improves both tooth and gut health.

• Gut health is the foundation to restore ALL health. Restored health will enable you to maintain a strict gluten free diet, just as other life tasks will be easier.
• A strict gluten free diet means removing 100% of wheat, barley, rye and oats from the diet.
• Cutting out bread and other obvious sources of gluten is not good enough for recovery. Even 1/8th teaspoon of flour or bread crumb is enough to sustain the inflammation that is damaging your small intestine, causing increased permeability (leaky gut) and allowing undigested gluten to enter your body where it can damage structures and function, and instigate immune inflammatory responses.

Correct Your Individual Nutritional Needs.

• Eat foods that can replenish missing nutrients. Find them under NUTRIENT DEFICIENCIES.
• Take nutritional supplements as needed. Find them under NUTRIENT DEFICIENCIES.

Recovery. You should begin to feel better within a week and notice more energy as inflammation subsides and the  absorbing cells that make up the surface lining of your small intestine are better able to function.

• Intestinal lining cells are replaced every 5 days. The healing process is like sunburn where the damaged surface layer of skin sloughs off and is replaced with new normal cells.
• Leaky gut normally resolves in two month after starting a gluten free diet and brings about a big improvement in health. Improvement in intestinal permeability precedes morphometric recovery (cell appearance and structure) of the small intestine in celiac disease.¹⁵
• The intestinal lining may take up to a year to heal.[/box]

• [dropcap]2[/dropcap] Reduce Inflammation. Foods to Eat and Foods Not to Eat:

Because gluten is inflammatory, eliminate OTHER inflammatory foods from your diet to reduce an additive effect to gluten. At the same time, try to eat foods that reduce inflammation (anti-inflammatory).

[box type=”shadow” ]Here Are Major Inflammatory Food Types That Reduce Healing:

• Damaging Foods. In susceptible persons, includes corn, dairy (cow), and soy. Lactose, the sugar in any animal milk disrupts intestinal permeability causing leaky gut.¹⁶
• Allergenic Foods. Includes foods that trigger the immune sytem to produce IgE antibodies. Allergy testing is the usual way to discover these offending foods.
• Shelf Stable Processed Foods. Includes any that contain additives and preservatives. Look for them on the nutrition label of the box or package. Additives and preservatives also disrupt intestinal permeability causing leaky gut.¹⁶
• Fats. Limit deep fried foods, trans-fats, saturated fats (animal fat/butter), and EXCESSIVE omega-6 fatty acid oils like corn oil. Rancid fats, sodium caprate (a medium chain fat), and sucrose monester fatty acid (a food grade surfactant) induce significant disruption of the intestinal barrier that causes leaky gut.¹⁶.
• Excessive Refined White Flours (bran layer removed). Includes products made from them such as cookies, bread, cakes, pies. Bran contains the vitamins and minerals that metabolize grains and slows the otherwise rapid entry of sugar from their digestion into the bloodstream. Also disrupt intestinal permeability causing leaky gut.¹⁶
• Refined Sugars.  Includes white sugar, corn fructose and high fructose corn syrup.
• Certain Spices. Includes paprika and cayenne pepper which disrupt intestinal permeability causing leaky gut.¹⁶
• Alcohol and Caffeine. Disrupt intestinal permeability causing leaky gut.¹⁶[/box]

[box type=”shadow” ]Here Are Important Anti-Inflammatory Food Types to Promote Health:

• Fruits. Contain ample amounts of vitamins, minerals and phytochemicals which are naturally occuring components in plants that detoxify toxins, carcinogens (reducing the risk by 50%) and mutagens.
• Non-Starchy Vegetables. Support intestinal integrity and provide ample amounts of vitamins, minerals and phytochemicals. Includes lettuce, kale, onion, broccoli, garlic, and others.
• High Quality Complex Carbohydrates. Provide vitamins, minerals, and fiber while boosting serotonin levels to help you relax and feel calm. Includes whole grains, legumes, and root vegetables such as carrots, parsnips, sweet potatoes, turnips, red beets, and others.
• Antioxidants. Protect the body from inflammatory oxidant molecules that continually occur and help us handle stress and reduce irritability. Includes vitamin C-containing foods such as lemon, grapefruit, apricot, Brussels sprouts and strawberries, and others. Also, includes vitamin E-containing foods such as nuts, seeds, avocado, olive oil, and others. Cocoa is good, too.
• Omega-3 Fatty Acids. Balance opposing omega-6 fatty acids and bad fats. Fish sources includes tuna, salmon, cod, and others. Plants sources include flax, chia seeds, canola oil, and others.
• Probiotics. Supply normal microbes needed for colon health and health of the body such as these fermented foods: yogurt, kefir, and unpasteurized apple cider vinegar.
• Prebiotics/ High Fiber Foods.  Food with fiber keeps our population of colonic microbes healthy.
• Protective Herbs and Spices.  See below #6 below for examples.[/box]

• [dropcap]3[/dropcap] Information Sheet You Can Take to Your Doctor or Other Health Professional:

Click here.

 

• [dropcap]4[/dropcap] Manage Your Medications Safely:

[box type=”shadow” ]

Certain prescription drugs cause deficiency of calcium that promote dental enamel defects. Ask your doctor or pharmacist about this possible adverse effect if you are taking any of the drugs listed below. Do not stop prescribed medications without supervision.

 This is not a complete listing.

ANTACIDS / ULCER MEDICATIONS

• Pepcid®, Tagamet®, Zantac® deplete Calcium.
• Magnesium and Aluminum Antacid preparations (Gaviscon®, Maalox®, Mylanta®) deplete Calcium.

ANTI-INFLAMMATORIES disrupt intestinal permeability.

• Aspirin and Salicylates deplete Calcium.

ANTICONVULSANTS

• Phenobarbital and Barbituates; and Dilantin®, Tegretol®, Mysoline®, Depakane/Depacon® deplete Calcium.

ANTIVIRAL AGENTS

• Foscanet depletes Calcium.[/box]

• [dropcap]5[/dropcap]Nutritional Supplements To Help Correct Deficiencies:

[box type=”shadow” ]

The type and quantity of nutritional supplements that may be needed depend on which nutrients are deficient.

• Multivitamin/mineral combination once a day is useful to improve overall nutrient levels. This is a safe dose, but always check with your doctor to avoid interactions with medications.
• Calcium citrate is the best absorbed of calcium supplements. Calcium carbonate is a poor choice.

Storage Note: Store container tightly sealed, away from heat, moisture and direct light to avoid loss of potency. That is, in a safe kitchen cabinet – not in the bathroom or on the kitchen table.[/box]

• [dropcap]6[/dropcap]Manage Natural Remedies: 

[box type=”shadow” ]Hydration:

• Eight glasses of water are recommended per day unless there is a contraindication such as kidney or heart disease. The Institute of Medicine recommends approximately 2.7 liters (91 ounces) of total water, from all beverages and foods, each day for women and 3.7 liters (125 ounces) daily of total water for men.
• If you are thirsty, drink water. Add fresh, squeezed lemon to water. Lemon is anti-inflammatory, alkalizing and provides vitamin C.
• Hydration Test: Urine should be pale yellow. Fingertips should be plump, without pruning but this may not be reliable when fingers are swollen with edema. Lips should be plump, without puckering. The feeling of thirst can be unreliable.
• What is wrong with soda, coffee, tea, and alcohol? These drinks are dehydrating, increase acid, and deplete nutrients.[/box]

[box type=”shadow” ]Carminatives. The following  anti-inflammatory plant sources called carminitives help heal the digestive tract. They also tone the digestive muscles which improves peristalsis, thus aiding in the expulsion of gas from the stomach and intestine to relieve digestive colic and gastric discomfort.

Carminative Food Remedies:

• Raspberry.
• Carrot is also a cleansing digestive tonic.
• Grape is also bile stimulating and a cleansing remedy for sluggish digestion and laxative.
• Redbeets also stimulate and improve digestion and are easily digested.
• Cabbage also stimulates and improves digestion and is also a liver decongestant.
• Lettuce also stimulates and improves digestion and is also an alterative, meaning it improves the function of organs involved with the digestion and excretion of waste products to bring about a gradual change.
• Potatoes are antispasmodic (due to atropine like properties) and a liver remedy.

Carminative Herb Remedies:

• Sage is also a digestive, astringent, bile stimulant and energy tonic that heals the mucosa.  Drink as tea or use in cooking.
• Chamomile, lemon balm, and fennel, (as a tea) also help relieve nervous tension.
• Parsley also relieves indigestion.
• Rosemary as a tea and in cooking also is a nervous system tonic for stress and fatigue, bile stimulant, and can relieve headaches and indigestion.
• Thyme is also soothing remedy useful for stimulating digestion of rich, fatty foods.

Carminative Spice Remedies:

• Cloves are also antispasmodic.
• Nutmeg is also useful for indigestion.
• Ginger.[/box]

[box type=”shadow” ]Exercise Helps:

Exercise improves circulation and rids the body of toxins.

• Walking is aerobic exercise that reconditions the whole body to improve stamina. Read more about Exercise and Fitness.
• Weight training builds muscle. Read more about Exercise and Fitness.
• Stretching improves flexibilty. Read more about Exercise and Fitness.

Note: Exercise is important, but the amount and type of exercise undertaken depends on your health. Your first priority is to heal. [/box]

What Do Medical Research Studies Tell About Dental Enamel Defects in Celiac Disease?

RESEARCH STUDY SUMMARIES

“Clinical Evaluation of Specific Oral Manifestations in Pediatric Patients with Ascertained versus Potential Celiac Disease: A Cross-Sectional Study.” This study investigating the oral hard and soft tissue lesions in potential and ascertained celiac children in comparison with healthy controls found that the overall oral problems were more frequently present in celiac disease patients than in controls and specific enamel defects seem to be genetically related to the histological damage and villous atrophy.

50 ascertained children, 21 potential celiac patients, and 54 controls were recruited and the oral examination was performed. Clinical dental delayed eruption was observed in 38% of the ascertained celiac and 42.5% of the potential celiac versus 11.11% of the controls. The prevalence of specific enamel defects (SED) was 48% in ascertained celiac and 19% in potential celiac versus 0% in controls.⁶

“Effect of three-year consumption of erythritol, xylitol and sorbitol candies on various plaque and salivary caries-related variables.” This study investigating the effects of erythritol, xylitol and sorbitol candies on the development of caries found that 3 year consumption of erythritol-containing candies by initially 7- to 8-year old children was associated with reduced plaque growth, lower levels of plaque acetic acid and propionic acid, and reduced oral counts of mutans streptococci compared with the consumption of xylitol or sorbitol candies.

Samples of whole-mouth saliva and dental plaque were collected from initially 7- to 8-year-old subjects who participated in a 3-year school-based programme investigating the effect of the consumption of polyol-containing candies on caries rates. The subjects were randomized in three cohorts, consumed erythritol, xylitol, or sorbitol candies. The daily polyol consumption from the candies was approximately 7.5 g.
A significant reduction in dental plaque weight from baseline (p<0.05) occurred in the erythritol group during almost all intervention years while no changes were found in xylitol and sorbitol groups.

After three years, the plaque of erythritol-receiving subjects contained significantly (p<0.05) lower levels of acetic acid and propionic acid than that of subjects receiving xylitol or sorbitol. Lactic acid levels partly followed the same pattern. The consumption of erythritol was generally associated with significantly (p<0.05) lower counts of salivary and plaque mutans streptococci compared with the other groups. There was no change in salivary Lactobacillus levels.¹⁷

“Screening for celiac disease in children with dental enamel defects.” This study investigating prevalence of celiac disease in 140 children with dental enamel defects (DED) found that celiac disease is more prevalent among children with DED than in the general population and that lower serum calcium significantly predicted celiac disease in them. “These DEDs might be the only manifestation of celiac disease.”

The children were tested for celiac disease. Gluten-free diet was instituted for celiac disease patients. A cohort of 720, age and sex-matched, normal children represented a control group. Both groups were evaluated clinically. Serum calcium, phosphorus, alkaline phosphatase, serum IgA, and tissue transglutaminase (tTG) IgG and IgA types were measured.

Celiac disease was more diagnosed in patients with DEDs (17.86%) compared to controls (0.97%). The majority of non-celiac patients showed grade 1 DED compared to grades 1, 2, and 3 DED in celiac disease. Five children had DED of deciduous teeth and remaining in permanent ones. After 1 year on gluten free diet, DED improved better in celiac disease compared to non-celiac patients. Gastrointestinal symptoms did not vary between celiac and non-celiac DED patients. Lower serum calcium significantly predicted celiac disease in this cohort. Screening for celiac disease is highly recommended among those patients especially in presence of underweight and hypocalcemia.¹⁸

“Implications of gluten exposure period, CD clinical forms, and HLA typing in the association between celiac disease and dental enamel defects in children. A case-control study.“ This study investigating the prevalence of dental enamel defects  (DED) in children with celiac disease and to specifically find the association of DED and gluten exposure period, celiac disease clinical forms, HLA class II haplotype confirmed a possible correlation between HLA antigens and DED.

This study was designed as a matched case-control study: 250 children were enrolled (125 coeliac children – 79 female and 46 male, 7.2 +/- 2.8 years and 125 healthy children). Data about age at celiac disease diagnosis, celiac disease clinical form, and HLA haplotype were recorded.

Dental enamel defects were detected in 58 celiac subjects (46.4%) against seven (5.6%) controls. We found an association between DED and gluten exposure period, as among celiac disease subjects the mean age at celiac disease diagnosis was significantly higher in the group with DED (3.41 +/- 1.27) than without DED (1.26 +/- 0.7). DED resulted more frequent (100%) in atypical and silent CD forms than in the typical one (30.93%). The presence of HLA DR 52-53 and DQ7 antigens significantly increased the risk of DED in celiac children.¹⁹

“Oral manifestations of celiac disease.: A clinical-statistic study.” This study investigating the prevalence of the different oral manifestations in a sample of celiac patients, in comparison with a control group of healthy subjects found that the celiac patients had higher indexes of caries than healthy subjects, both in deciduous teeth and permanent teeth.

Moreover, a second objective to determine if the clinical oral examination is useful as a diagnostic tool of screening for atypical forms of coeliac disease found that The clinical oral examination should be considered a diagnostic tool for the characterization of subjects affected by silent-atypical forms of celiac disease.

The enrolment of 300 celiac patients, aged between 4 and 13 years (mean age 8.16), was carried out at the Pediatric Dentistry Unit in patients sent from the Pediatric Gastroenterology Unit of the PTV Hospital, University of Rome Tor Vergata. The control group was composed of 300 healthy subjects, age-matched (mean age 8.29), enrolled from the Pediatric Dentistry Unit. The patients were examined for hard tissues (enamel hypoplasia, dental caries), soft tissues (recurrent aphthous stomatitis RAS, atrophic glossitis, geographic tongue) and delay dental eruption. Enamel defects were classified according to Aine’s criteria, while dental caries was recorded as dmft/DMFT indices. Statistical analysis was carried out by using SPSS/PC+ Software. Differences between case and control groups were tested using Paired samples T-test, and Chi-Square Test, depending on the variable considered. The minimal level of significance of the differences was fixed at p≤0.05 for all the procedures.

Statistical differences between groups were observed for the prevalence of enamel defects (p=0.0001), RAS (p=0.005), delay in dental eruption (p=0.0001), but not for the prevalence of atrophic glossitis (p=0.664). Differences in symmetrical distribution and a chronologic coherence of enamel defects were statistically significant between celiac and control groups (p=0.0001).²⁰

“The presence and distribution of dental enamel defects and caries in children with celiac disease.” This study investigating the presence and distribution of developmental enamel defects and caries in children with celiac disease and compare the results obtained with those of a control group of children without celiac disease showed that children with celiac disease  were at an increased risk of dental enamel defects compared with healthy subjects.

 A total of 64 subjects (mean age 8.2 years) selected from patients diagnosed and treated for celiac disease  were studied. Sixty-four age/ sex-matched healthy children were enrolled as a control group. Permanent dentition enamel defects were recorded according to Aine’s classification. The caries experience of the children was recorded according to the criteria of the World Health Organization (WHO). The prevalence of enamel defect in celiac disease subjects was found to be significantly higher (42.2%) than in healthy subjects (9.4%) (p < 0.001). Grade I type enamel defects were most commonly diagnosed in both groups (20.3% and 6.3%, respectively). The number of caries-free subjects in the control group was higher (38%) than in the CD group (17%). Enamel defects were associated with an increased caries incidence.²¹

“Celiac disease, enamel defects and HLA typing.” This study investigating 128 patients on gluten free diet revealed that changes in the permanent teeth may be the only sign of an otherwise symptomless celiac disease. It is important to study the oral cavity of patients suspected of having celiac disease, since no less than 66% of the patients in this study had oral symptoms. In a study by Aine et al., 3% of adult celiac disease patients had grade III – IV enamel defects. In this study, the figure was 10.3%, but this included pediatric patients. In the study of Aine et al., 30% of their children with celiac disease had grade III – IV enamel defects. The difference between the children and adults might indicate that the adults often develop celiac cisease after the critical age of 7 years when the crowns of the permanent teeth have developed.³

“Celiac disease, enamel defects and HLA typing.” This study investigating 82 children with celiac disease for the presence of dental enamel defects and their relation to hypocalcemia or a particular HLA class demonstrated that the presence of HLA DR3 antigen significantly increased the risk of dental lesions, while genotype DR5,7 seemed to protect against enamel defects. A logistic regression analysis of the variables age, serum calcium concentrations, number of affected teeth, type of enamel defect and DR antigens showed that only DR antigens discriminated celiac disease patients with defects from those without enamel defects.⁸

Sources:

1. El-Hodhod MA, El-Agouza IA, Abdel-Al H, Kabil NS, Bayomi KA. Screening for celiac disease in children with dental enamel defects. ISRN Pediatr. 2012;2012:763783. doi: 10.5402/2012/763783. [↩] [↩]
2. Bramanti E, Cicciù M, Matacena G, Costa S, Magazzù G. Clinical Evaluation of Specific Oral Manifestations in Pediatric Patients with Ascertained versus Potential Coeliac Disease: A Cross-Sectional Study. Gastroenterol Res Pract. 2014;2014:934159. doi: 10.1155/2014/934159. [↩]
3. Mariani P, Mazzilli MC, Margutti G, et al. Coeliac disease, enamel defects and HLA typing. Acta Paediatrica. Dec 1994;83(12):1272-5. [↩] [↩] [↩]
4. Avşar A, Kalayci AG. The presence and distribution of dental enamel defects and caries in children with celiac disease. Turk J Pediatr. 2008 Jan-Feb;50(1):45-50. [↩] [↩]
5. Costacurta M, Maturo P, Bartolino M, Docimo R. Oral manifestations of coeliac disease.: A clinical-statistic study. Oral Implantol (Rome). 2010 Jan;3(1):12-9. [↩]
6. Bramanti E, Cicciù M, Matacena G, Costa S, Magazzù G. Clinical Evaluation of Specific Oral Manifestations in Pediatric Patients with Ascertained versus Potential Coeliac Disease: A Cross-Sectional Study. Gastroenterol Res Pract. 2014;2014:934159. doi: 10.1155/2014/934159. [↩] [↩]
7. Majorana A, Bardellini E, Ravelli A, Plebani A, Polimeni A, Campus G. Implications of gluten exposure period, CD clinical forms, and HLA typing in the association between celiac disease and dental enamel defects in children. A case-control study. Int J Paediatr Dent. 2010 Mar;20(2):119-24. [↩]
8. Mariani P, Mazzilli MC, Margutti G, et al. Coeliac disease, enamel defects and HLA typing. Acta Paediatrica. Dec 1994;83(12):1272-5. [↩] [↩] [↩]
9. Lahteenoja H, Toivanen A, Viander M, Maki M, Irjala K, Raiha I, Syrjanen S. Oral mucosal changes in coeliac patients on a gluten-free diet. European Journal of Oral Sciences. Oct 1998;106(5):899,8p. [↩] [↩]
10. Patinen P, Aine L, Collin P, et al. Oral findings in coeliac disease and Sjogren’s syndrome. Oral Diseases. Nov 2004;10(Issue 6):330:5p. [↩]
11. Lahteenoja H, Toivanen A, Viander M, Maki M, Irjala K, Raiha I, Syrjanen S. Oral mucosal changes in coeliac patients on a gluten-free diet. European Journal of Oral Sciences. Oct 1998;106(5):899,8p. [↩]
12. Costacurta M, Maturo P, Bartolino M, Docimo R. Oral manifestations of coeliac disease: A clinical-statistic study. Oral Implantol (Rome). 2010 Jan;3(1):12-9. [↩]
13. El-Hodhod MA, El-Agouza IA, Abdel-Al H, Kabil NS, Bayomi KA. Screening for celiac disease in children with dental enamel defects. ISRN Pediatr. 2012;2012:763783. doi: 10.5402/2012/763783. [↩]
14. Majorana A, Bardellini E, Ravelli A, Plebani A, Polimeni A, Campus G. Implications of gluten exposure period, CD clinical forms, and HLA typing in the association between celiac disease and dental enamel defects in children. A case-control study. Int J Paediatr Dent. 2010 Mar;20(2):119-24. doi: 10.1111/j.1365-263X.2009.01028.x. [↩]
15. Cummins AG, Thompson FM, Butler RN, et al. Improvement in intestinal permeability precedes morphometric recovery of the small intestine in coeliac disease. Clinical Science. Apr 2001;100(4):379-86. [↩]
16. Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. [↩] [↩] [↩] [↩] [↩] [↩]
17. Runnel R, Mäkinen KK, Honkala S, Olak J, Mäkinen PL, Nõmmela R, Vahlberg T, Honkala E, Saag M. Effect of three-year consumption of erythritol, xylitol and sorbitol candies on various plaque and salivary caries-related variables. J Dent. 2013 Dec;41(12):1236-44. doi: 10.1016/j.jdent.2013.09.007. [↩]
18. El-Hodhod MA, El-Agouza IA, Abdel-Al H, Kabil NS, Bayomi KA. Screening for celiac disease in children with dental enamel defects. ISRN Pediatr. 2012;2012:763783. doi: 10.5402/2012/763783. [↩]
19. Majorana A, Bardellini E, Ravelli A, Plebani A, Polimeni A, Campus G. Implications of gluten exposure period, CD clinical forms, and HLA typing in the association between celiac disease and dental enamel defects in children. A case-control study. Int J Paediatr Dent. 2010 Mar;20(2):119-24. doi: 10.1111/j.1365-263X.2009.01028.x. [↩]
20. Costacurta M, Maturo P, Bartolino M, Docimo R. Oral manifestations of coeliac disease.: A clinical-statistic study. Oral Implantol (Rome). 2010 Jan;3(1):12-9. [↩]
21. Avşar A, Kalayci AG. The presence and distribution of dental enamel defects and caries in children with celiac disease. Turk J Pediatr. 2008 Jan-Feb;50(1):45-50. [↩]