Biliary kinetics involve a series of complex interrelationships between gallbladder, cystic duct, common bile duct, sphincter of Oddi and upper small intestine, with control modulation by various cephalic, antral and neurohormonal mechanisms. Disorders of the biliary tract can affect any of these components and may lead to abdominal pain, dilation of bile and pancreatic ducts, elevation of liver and pancreatic enzymes, and ultimately, cholangitis or pancreatitis. The diagnosis of functional biliary disorders requires the exclusion of other conditions presenting with similar clinical signs and symptoms. The most common of these are gastroesophageal reflux disease (GERD), irritable bowel syndrome (IBS), functional dyspepsia and biliary lithiasis. The SO is a smooth muscle sphincter which when contracted, prevents biliary and pancreatic flow into the duodenum. It comprises three regions: The biliary sphincter, up to 10 mm long, that regulates bile flow, the pancreatic sphincter up to 6 mm long, that regulates the pancreatic juice flow and an approximately 6-mm long common sphincter that encircles the confluence of the common bile duct (CBD) and main pancreatic duct. Sphincter of Oddi dysfunction is a clinical entity characterised by symptoms of biliary and/or pancreatic obstruction in a patient with sphincter stenosis or malfunction, without other structural causes. The pathogenesis of sphincter of Oddi dysfunction is unknown. One possibility is the existence of primary disorders of motility, perhaps related to defects in the enteric nervous system. Secondary disorders also seem likely, either from direct damage or from the indirect effects on factors that control sphincter motility. Sphincter of Oddi manometry is usually performed at the time of ERCP. All drugs which relax (anticholinergics, nitrates, calcium channel blockers, and glucagon) or stimulate (narcotics or cholinergic agents) the sphincter should be avoided for at least 8-12 hours prior to manometry and during the manometric session. The current data indicate that benzodiazepines do not affect the sphincter pressure and therefore are acceptable sedation for SOM. Recent data suggested that meperidine, at a dose of 1 mg/kg does not affect the basal sphincter pressure. In 1884, Langenbuch suggested that stenosis of the sphincter of Oddi might cause biliary symptoms and described a transduodenal division of the biliary sphincter. Later, Kocher described a similar operation with sutures after division of the sphincter. Exploration of the common bile duct, once popular by the transduodenal route, is now usually undertaken througha supraduodenal route, although in some circumstances when supra duodenal access is difficult, a transduodenal approach may be used. Doubilet and Mullholland believed that gallstone-associated acute pancreatitis resulted from bile reflux into the pancreatic duct, and thus performed biliary sphincterotomy in a cohort of patients with acute pancreatitis in an attempt to prevent this, their sphincterotomy was only about 5 mm long, however. Bartlett and Nardi believed that pancreatic duct obstruction was the cause of acute pancreatitis and thus, in addition to a biliary sphincterotomy, divided the common septum between the ducts. Moody further extended the operation by excising the septum between the ducts. Endoscopic therapy for sphincter of Oddi dysfunction. This procedure is performed during ERCP and involves cutting the sphincter with electrocautery. Endoscopic pancreatic sphincterotomy prevents recurrent attacks of pancreatitis in patients with pancreatic sphincter dysfunction in more than 60% of cases.