Gastro-oesophageal reflux disease (GORD)

GERD is an increasingly common and potentially serious condition, with various extraesophageal adverse health effects that dental practitioners should be aware of. Clinicians should also be aware of the predisposing risk factors for GERD and its classical esophageal and extraesophageal symptoms and signs. However, not all affected persons will have the classical symptoms of gastric regurgitation.

An antireflux barrier at the gastroesophageal junction is formed by normal anatomical features, including the oblique course of the gastroesophageal junction and diaphragmatic curve. Of particular importance is a high-pressure gradient of 10-30 mm Hg maintained by tonic contraction of the circular muscles of the lower esophageal sphincter (LES).

With routine examination, your doctor can discover precancerous and cancer cells early, before they spread and when the disease is easier to treat. These beverages can increase the amount of acid in the stomach and aggravate the esophagus, triggering GERD symptoms.

These findings are supported by observations that fluoride-based and casein-based (amorphous calcium phosphate stabilized by casein-phosphopeptide) remineralizing agents provide some protection against erosion at pH 3.0 [70-73], but not at a highly erosive environment of pH 1.2 [74, 75]. Fortunately, several very large longitudinal studies suggest that only a minority of GERD sufferers develop Barrett’s esophagus [51, 52]. These studies found that Barrett’s esophagus developed in 0.0-1.8% of persons with nonerosive esophagitis and in 1.0-9.9% of persons with erosive esophagitis. Thus, the overall risk of development of Barrett’s esophagus in GERD sufferers is low, though generally increasing, with a slightly elevated risk in individuals with erosive esophagitis.

Endoscopy is also used to detect Barrett’s esophagus and hiatal hernia and for sampling for the presence of Helicobacter pylori from gastric mucosa [46, 48]. It has been elucidated that various factors are involved in the regulation of the mucus metabolism and each of these factors acts on some specific kind of mucus cells (Fig. 9). Among the endogenous regulatory factors of the stomach, gastrin, histamine and carbachol, which have an acid secretory action, EGF and HGF, which are growth factors and PG, which is an autacoid, are all able to increase the biosynthesis of the gastric mucin. However, a difference is seen in the mucin synthetic reactions based on these factors. Thus, the increase in mucin biosynthesis induced by gastrin among these acid secretagogues can be observed in the surface mucus cells of the gastric oxyntic mucosa, indicating that it occurs by way of specific gastrin receptors independent of the acid secretion mechanism (Ichikawa et al., 1993).

Most people with acid reflux don’t develop Barrett’s esophagus. But in patients with frequent acid reflux, the normal cells in the esophagus may eventually be replaced by cells that are similar to cells in the intestine to become Barrett’s esophagus. A recent systematic review involving 17 eligible mainly observational and case-control studies of GERD and dental erosion found a strong association between the two conditions [7]. The median prevalence of dental erosion in GERD patients was 24%, and the median prevalence of GERD in adults and in children with dental erosions was 32.5% and 17%, respectively.

Dentists may be the first persons to diagnose the possibility of GERD in these “silent refluxers,” particularly when observing unexplained instances of tooth erosion, which might be accompanied by coexisting hyposalivation. Numerous laboratory, and mainly case-control and observational clinical studies in adults and children, have shown a clear though variable relationship between GERD and tooth erosion. However, further randomized clinical trials are required to demonstrate that the progression of dental erosion reduces or ceases following gastric acid suppression therapy in patients with confirmed GERD.

protective barrier between cells and stomach acid

causes apoptosis, necrosis, and other oxidative damages [25]. When the lower esophageal sphincter is weak, the acid unnaturally moves up into the esophagus, causing gastroesophageal reflux disease (GERD), whose cardinal symptom is heartburn, mainly occurring postprandially. The adherent mucus gel layer is the functionally important component of the mucus barrier in the human stomach. However, it cannot be demonstrated by routine histological techniques because of its susceptibility to dehydration and shrinkage, which has hampered research.

  • In this context, further research is needed to clarify the roles of lifestyle factors and their interaction with GERD in causing Barrett’s esophagus and esophageal adenocarcinoma.
  • Parietal cells produce hydrochloric acid, a strong acid that helps to break down food.
  • Going to bed with a full stomach means there is an increased risk that acid in your stomach will be forced up into your oesophagus while you are lying down.
  • 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.
  • Oral antacids are given to raise the pH of the stomach’s contents by neutralizing gastric acid, but they increase gastric volume.
  • Protective antibodies are secreted by cells underlying the gastrointestinal lining.

Recently, attempts have been made to define GERD specifically for the pediatric population (including infants, children, and adolescents) in light of observations of a wider range of variability in the signs and symptoms in children compared with adults [18]. The increasing prevalence of gastroesophageal reflux disease (GERD) in children and adults, and of “silent refluxers” in particular, increases the responsibility of dentists to be alert to this potentially severe condition when observing unexplained instances of tooth erosion. Although gastroesophageal reflux is a normal physiologic occurrence, excessive gastric and duodenal regurgitation combined with a decrease in normal protective mechanisms, including an adequate production of saliva, may result in many esophageal and extraesophageal adverse conditions. Sleep-related GERD is particularly insidious as the supine position enhances the proximal migration of gastric contents, and normal saliva production is much reduced.

The maturation of mucus-secreting gastric epithelial progenitors into digestive-enzyme secreting zymogenic cells requires Mist1 . Development 134, 211-222 (2007). The intriguing relationship of Helicobacter pylori infection and acid secretion in peptic ulcer disease and gastric cancer .

There are also specific bacteria, called Helicobacter pylori, that may cause impairment of the stomach’s defenses and can also be responsible for ulcers. Parietal cells produce hydrochloric acid, a strong acid that helps to break down food. The acid in your stomach is so concentrated that if you were to place a drop on a piece of wood, it would eat right through it. ­The g-cells produce gastrin, a hormone that facilitates the production of hydrochloric acid by the parietal cells.

Though this same study of persons with and without GERD reported a lack of significant differences in salivary flow rates, buffering capacity, and pH values [61], the more recent large case-control study found a significant association between GERD and xerostomia [60]. However, a recent systematic review and meta-analysis of population-based studies found associations between frequent GERD symptoms and esophageal adenocarcinoma, with weekly and daily symptoms increasing the odds ratio of esophageal carcinoma by fivefold and sevenfold, respectively [3]. In a population-based case-control study investigating the association between obesity, GERD, and esophageal adenocarcinoma in White Australians, a greater risk of progression of adenocarcinoma was observed in men than in women [55].

Related to Heartburn / GERD

N. Engl. J. Med. 335, 242-249 (1996).

Luminal clearance of the esophagus is aided by gravity when upright, by physiological emptying (peristalsis) of the esophageal contents into the stomach and by salivary bicarbonate [14, 15]. Most microorganisms encountered in daily life are repelled before they cause detectable signs and symptoms of disease. These potential pathogens, which include viruses, bacteria, fungi, protozoans, and worms, are quite diverse, and therefore a nonspecific defense system that diverts all types of this varied microscopic horde equally is quite useful to an organism. The innate immune system provides this kind of nonspecific protection through a number of defense mechanisms, which include physical barriers such as the skin, chemical barriers such as antimicrobial proteins that harm or destroy invaders, and cells that attack foreign cells and body cells harbouring infectious agents. The details of how these mechanisms operate to protect the body are described in the following sections.

This chapter presents recent insights into the implication of the gastric mucus barrier as “no mucus, no protection”. Much like the control of salivary secretions, the gastric secretions (including mucus secretion) is largely controlled by neural influences.

protective barrier between cells and stomach acid

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