For many restorative dentists, the classification and management of non-carious lesions can be difficult – especially with erosive lesions. The etiology is multifactorial and includes both intrinsic and extrinsic sources.

Gastroesophageal disorders like gastroesophageal reflux disease (GERD), bulimia and anorexia create intrinsically induced loss of tooth structure. This article introduces a new perspective on reflux and the possible triggering mechanisms that occur during sleep.

Classically, GERD has been described as a digestive condition caused by the backflow of acid into the esophagus often associated with discomfort or heartburn. A new model of reflux can be divided based on the location of the insult: esophageal or respiratory.

Esophageal reflux is the classic form of GERD, but respiratory reflux – also called laryngopharyngeal reflux (LPR) – is the introduction of acid and non-acidic contents into the larynx and/or pharynx past the upper esophageal sphincter. Non-acidic reflux includes stomach contents other than acid, like mucus, pepsin, bile and other digestive secretions that backflow.

Unlike the esophagus, the larynx is extremely sensitive to acid and pepsin assault. LPR is commonly called “Silent GERD.” The silence is from the fact that very few of the patients will have symptoms of heartburn. More commonly, patients present symptoms of hoarseness, chronic cough, frequent throat clearing, mucus in the throat, problems swallowing certain foods, or a lump in the throat. Dental erosive damage is most common in patients with respiratory symptoms.1

Interestingly, many of the symptoms are due to the pepsin rather than the acid. This means that treating the acid with proton pump inhibitors (PPI) may reduce acid exposure to the teeth but will do little to reduce pepsin-induced LPR symptoms.

During an obstructive sleep apnea event, thoracic and abdominal effort is increased in an effort to breath against a choke point in the pharynx. The exertion creates negative intrathoracic pressure. It has been proposed that the increase in respiratory effort associated with obstructive sleep apnea promotes additional stomach contents being expelled due to the negative pressure eventually overcoming the efforts of the lower esophageal sphincter. The contents are drawn and aerosolized into the larynx and pharynx during obstructive release into the upper airway. This model assists in explaining the older, overweight apnea patient but does little to explain why a common patient complaining of “GERD” is the upper airway resistance syndrome (UARS) patient.

The typical UARS patient is a young, fit female who has sleep fragmentation and insomnia due to inspiratory flow limitation (IFL) or respiratory effort-related arousals (RERA) rather than obstructive apnea. In a dental practice, these patients routinely present as the myofascial TMD or headache patient. Interestingly, chronic flow limitations do promote return of liquid past the upper sphincter, which creates a cyclic response between sleep and reflux.

It has been postulated that the respiratory reflux has an impact on sleep that goes beyond the traditional metric of the apnea-hypopnea index. First, the lining of the upper airway is not designed to withstand the insult of acid and pepsin. Acidic and non-acidic particulate harbored on the tissues in the nose and throat will cause erythema. The swelling and loss of tissue tone creates an airway that is more collapsible within normal flow limited breathing.

Second, the collapsible segment of the airway has neural receptors that signal the brain to changes in the airway closing pressure. These neural centers are damaged by repeated insult from respiratory reflux. The neural damage can deteriorate laryngeal dilator reflex mechanisms and cause respiratory effort.

Third, dysautonomia or autonomic dysfunction may cause an increase in respiratory reflux events and damage. Autonomic neuropathy may be induced by over-activity of the sympathetic nervous system during sleep. IFL and RERA create an increase in sympathetic sleep instead of parasympathetic healing sleep. These patients are more prone to multiple sympathetic arousals due to nasal and/or craniofacial limitations to air flow.

Every time they respond to a “minor” airway compromise, the sympathetic activity damages the autonomic nervous system. Patients with respiratory reflux demonstrate poor autonomic modulation and higher sympathetic activity. The lack of parasympathetic sleep seems to be involved in the pathogenesis of LPR.2

Finally, because of the location and nature of LPR, a more appropriate referral would be the otolaryngologist rather than the gastroenterologist.

In conclusion, examination of erosive tooth loss is a part of daily practice. Clinicians routinely ask “how” the damage occurred. The “why” of the disease is an important reminder that dentistry can detect many health issues far before the onset of the more serious damage related to obstructive apnea.

Jeffrey Rouse, D.D.S., is a member of Spear Resident Faculty.


1. Wang GR, Zhang H, Wang ZG, Jiang GS, Guo CH. Relationship between dental erosion and respiratory symptoms in patients with gastro-oesophageal reflux disease. J Dent. 2010;38:892–898.

2. Huang WJ, Shu CH, Chou KT, Wang YF, Hsu YB, Ho CY, Lan MY. Evaluating the autonomic nervous system in patients with laryngopharyngeal reflux. Otolaryngol Head Neck Surg. 2013;148:997–1002.