Parietal cells of the gastric mucosa contain receptors for gastrin (G) and acetylcholine (M2), both of which activate cellular mechanisms that increase intracellular calcium ion concentrations. In the presence of calcium ions, increased concentrations of cyclic AMP activate the proton pump (H+/K+‑ATPase) of parietal cells to secrete hydrogen ions against a large concentration gradient in the gastric lumen in exchange for potassium ions.
Histamine, released from mast cells, interacts with H2‑receptors on parietal cells and also activates adenylate cyclase resulting in increased concentrations of intracellular cyclic AMP and contributes to the secretion of hydrogen ions. In addition, under the influence of the neurotransmitter acetylcholine, the mucous neck cells and peptic (chief) cells secrete pepsinogen. Pepsinogen, following contact with gastric acid, is converted to pepsin, an active proteolytic enzyme.
The normal gastroduodenal mucosa resists injury from acid and pepsin in the gastric juice by several homeostatic defense mechanisms. Surface epithelial cells secrete mucus and bicarbonate creating a pH gradient in the mucus layer from the highly acidic gastric lumen to the nearly neutral surface of the mucosa. Gastric mucosal cells have a specialized apical-surface membrane, which resists the diffusion of acid back into mucosal cells.
Mucosal cells also resist injury by intrinsic mechanisms, such as extrusion of back-diffused acid by means of sodium-hydrogen or sodium-bicarbonate exchange. In addition, surface epithelial cells continually slough and proliferating cells rapidly repair mucosal injury. Prostaglandins also enhance mucosal resistance to injury by maintaining mucosal blood flow to remove acid that has diffused across the compromised mucosa and by stimulating the secretion of mucus and bicarbonate.
PUD is characterized by erosion of the gastric or duodenal mucosa by acid and pepsin.18,19 The principal symptom is pain. The patient often has periods of remissions, with complete freedom from symptoms for weeks or months.18,19 The patient with PUD is predisposed to hemorrhage, perforation, and pyloric stenosis.18,19 Hemorrhage may vary from slight bleeding to massive hemorrhage and the patient may vomit variable quantities of blood. Blood in the stool makes it black and tarry (melena).
Perforation of gastric or duodenal mucosa, results in the discharge of gastric or duodenal contents into the peritoneal cavity causing an inflammatory reaction (peritonitis) characterized by severe generalized abdominal pain and board-like rigidity of the abdominal muscles.18,19 Pyloric stenosis is the most common complication of duodenal ulcers and results from contraction of scar tissue laid down at the base of the ulcer.
Although PUD may be associated with increased secretion of acid (Zollinger-Ellison syndrome) and peptic activity is an indispensable component of the pathogenesis of ulcers, peptic ulcers generally develop only when mucosal defense mechanisms are also altered.18,19 Two major factors, Helicobacter pylori infection and NSAIDs appear to disrupt mucosal resistance to injury.18,19 Stress, alcohol, cigarette smoking, and genetic factors further exacerbate the injury.
The medical management of PUD associated with H. pylori includes various antibacterial combinations, which leads to rapid healing of active peptic ulcers and low recurrence rates.18,19 The antibacterial agents used most often include bismuth subsalicylate, tetracycline, metronidazole, amoxicillin, and clarithromycin. Two or three of these agents are usually given in combination with an H2‑receptor blocker (e.g., ranitidine) or a proton pump inhibitor (e.g., omeprazole).2,3,18,19
Sucralfate, a cytoprotective agent, is effectiveness in healing peptic ulcers and for prevention of relapse.2,3,19 Other strategies include antacids consisting of mixtures of magnesium hydroxide, aluminum hydroxide, and calcium carbonate.19 Sodium bicarbonate compounds can be effective in promoting the healing of duodenal ulcers and prostaglandin analogs can prevent gastric ulcers in patients on chronic NSAID therapy by increasing mucin and bicarbonate release.19
When documenting the medical history be cognizant that patients with PUD often have periods of remission, with complete freedom from symptoms for weeks or months. Patients in remission may respond negatively to questions related to PUD. Be specific, ask patients “do you now have or have you ever had PUD.” When managing odontogenic pain consider the well-established ulcerogenic effect of NSAIDs and use alternative analgesics, e.g., acetaminophen-containing formulations.