Oral sensory nerve damage: Causes and consequences

Abstract

Oral sensations (i.e., taste, oral somatosensation, retronasal olfaction) are integrated into a composite sense of flavor, which guides dietary choices with long-term health impact. The nerves carrying this input are vulnerable to peripheral damage from multiple sources (e.g., otitis media, tonsillectomy, head injury), and this regional damage can boost sensations elsewhere in the mouth because of central interactions among nerve targets. Mutual inhibition governs this compensatory process, but individual differences lead to variation in whole-mouth outcomes: some individuals are unaffected, others experience severe loss, and some encounter sensory increases that may (if experienced early in life) elevate sweet-fat palatability and body mass. Phantom taste, touch, or pain sensations (e.g., burning mouth syndrome) may also occur, particularly in those expressing the most taste buds. To identify and treat these conditions effectively, emerging clinical tests measure regional vs. whole-mouth sensation, stimulated vs. phantom cues, and oral anatomy. Scaling methods allowing valid group comparisons have strongly aided these efforts. Overall, advances in measuring oral sensory function in health and disease show promise for understanding the varied clinical consequences of nerve damage.

Sensory nerves regulate mesenchymal stromal cell lineage commitment by tuning sympathetic tones

“…Sensory nerves are innervated in various organs and tissues, such as skin, lung, kidney, liver, and bone. These nerves sense stimuli such as pain, itch, temperature, taste, and odor (1,2). The function of sensory nerves is essential for collecting information from both internal and external environments, helping individuals adapt to their surroundings and protect themselves from threats (3).…”

Structural equation modeling of associations among taste‐related risk factors, taste functioning, and adiposity

“…Variation in taste perception, from normal genetic variation to taste alterations, is associated with differences in dietary behaviors and adiposity status . Taste variation has been linked with differences in preferences for dietary sources that can influence total energy consumption, including sweets, high‐fat foods, vegetables, and alcoholic beverages .…”

“…Variation in taste perception, from normal genetic variation to taste alterations, is associated with differences in dietary behaviors and adiposity status . Taste variation has been linked with differences in preferences for dietary sources that can influence total energy consumption, including sweets, high‐fat foods, vegetables, and alcoholic beverages . Growing evidence suggests that taste receptors expressed along the gut regulate neurotransmitters and metabolic hormones involved in appetite, energy intake, and metabolism, further supporting taste‐adiposity linkages .…”

“…Growing evidence suggests that taste receptors expressed along the gut regulate neurotransmitters and metabolic hormones involved in appetite, energy intake, and metabolism, further supporting taste‐adiposity linkages . Some variation in taste perception has been explained by polymorphisms in taste receptor genes and density of taste receptors on the tongue . Environmental insults to taste‐related cranial nerves also may cause taste alterations, including diminished, intensified, or phantom (i.e., dysgeusia) sensations .…”

Individual differences in taste and their association with genes, dietary behaviour, and brain structure

“…This delivers an important message that, in addition to inborn variations, factors altering taste perception, such as disease status (e.g. middle ear infection) and medical treatment (radiotherapy on brain and neck) [212], may also modify our dietary behaviour. Given the popularity of these bitter beverages, future studies are necessary to investigate the underlying biology of how altered perception can potentially contribute to their addiction, which may shed light on the prevention and have public health implications.…”