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. 2021 Jun 23;46:bjab032. doi: 10.1093/chemse/bjab032

Positive Long-Term Effects of Third Molar Extraction on Taste Function

Dane Kim 1,2,✉, Richard L Doty 2
PMCID: PMC8286089  PMID: 34161573

Abstract

Taste and other neurosensory defects have been reported postoperatively in a number of patients who have undergone mandibular third molar extraction (TME). Although the taste deficits are generally believed to resolve within a year, the long-term effects of TME remain unknown. We retrospectively examined the whole-mouth taste function of 891 individuals who had received TMEs, on average, more than 2 decades earlier, and 364 individuals who had not undergone TME. All had been extensively tested for chemosensory function at the University of Pennsylvania Smell and Taste Center over the course of the last 20 years. The whole-mouth identification test incorporated 2 presentations each of 5 different concentrations of sucrose, sodium chloride, citric acid, and caffeine. Analyses of covariance (age = covariate) found those with histories of TME to exhibit better overall test scores for all 4 taste qualities than nonoperated controls. Such scores were not associated with the time since the TME. In both groups, women outperformed men and function declined with age. The basis of this phenomenon, which requires confirmation from prospective studies, is unknown, but could reflect sensitization of CN VII nerve afferents or the partial release of the tonic inhibition that CN VII exerts on CN IX via central nervous system processes.

Keywords: ageusia, hypergeusia, hypersensitivity, hypogeusia, iatrogenesis, psychophysics, taste

Introduction

Taste function can be adversely impacted by third molar extraction (TME) in some persons who have undergone such surgery (Shafer et al. 1999; Albuquerque et al. 2019). This reflects iatrogenic damage to taste sensory fibers from the anterior tongue which are carried via the chorda tympani division of the facial nerve to join the lingual branch of the mandibular nerve (CN V3) before its passage through the foramen ovale. Such sensory fibers are susceptible to damage given their close proximity to the retromolar pad (Leung and Cheung 2011). During TME surgery, neural damage can occur either through direct needle contacts, physical trauma, or neurotoxicity of the employed local anesthetics (Bromley and Doty 2015; La Monaca et al. 2017). When mild trauma occurs without axonal damage, a conduction nerve block can occur (neuropraxia). With more severe injury, significant dysesthesia/sensory distortions become more apparent (axonotmesis) and are accompanied by neural degeneration. When taste nerves are completely cut, total loss of function occurs (neurotmesis). Subtle damage from TME typically goes unnoticed and postoperative complaints are less common for taste than for somatosensation (Bui et al. 2003; Ridaura-Ruiz et al. 2012).

In addition to hyposensitivity, a number of studies have noted that nerve damage, in general, can lead to hypersensitivity (von Bischhoffshausen et al. 2015; Gallo et al. 2017; Yamaguchi et al. 2018). In most cases, such hyperalgesia is transient and reflects inflammatory processes (Gallo et al. 2017). Longer term hyperalgesia has been reported in cases of neuropathic pain, including allodynia, hyperalgesia, and hyperesthesia secondary to TME (Marbach et al. 1982; Campbell et al. 1990; Berge 2002). The mechanisms are poorly understood, but murine studies have shown that nerve crushing can lead to prolonged hyperexcitability and sprouting of new neuronal processes (Bedi et al. 1998). Moreover, murine brain-derived neurotrophic factor has been shown to contribute to spinal long-term potentiation and pain hypersensitivity following peripheral nerve injury (Li et al. 2017). Rats that received spinal nerve ligation (SNL) to simulate nerve damage exhibit long-term tactile hypersensitivity; however, thermal hypersensitivity is shorter lived. In 1 study, for example, the induced tactile hypersensitivity lasted for 580 days after SNL (42 years in human equivalent), while the thermal hypersensitivity disappeared in 35–40 days (Wang et al. 2013).

To our knowledge, general gustatory hypersensitivity has not been reported in cases of nerve damage from TME, although contralateral hypersensitivity has been noted following anesthetization of 1 chorda tympani nerve (Lehman et al. 1995; Yanagisawa et al. 1998). On the other hand, hyposensitivity is well established within 6 months of TME in participants with markedly impacted molars (Shafer et al. 1999). We now present evidence from a retrospective case–control study that TME may produce subtle enhancement of taste function years after the operation. Such findings contrast with the general view that TME only has the potential for adverse effects on afferent taste pathways.

Materials and methods

Participants

Data from 891 participants who had received TME and 364 who had not received TME were evaluated. Only 87 were smokers, of which 55 were in the TME group. All participants had visited the University of Pennsylvania Smell and Taste Center over the course of the last 20 years for chemosensory evaluation (see Table 1 for demographics). Most had presented with olfactory dysfunction (Deems et al. 1991)—dysfunction largely unrelated to the Center’s taste test measures (Stinton et al. 2010). None complained specifically of dental problems. In our experience, fewer than 1% of Center participants exhibit whole-mouth taste loss on the test employed in this study (Deems et al. 1991). Most complaints of such loss reflect the wide-spread confusion of taste with flavor dependent upon retronasal stimulation of the olfactory receptors via the nasopharynx during deglutition (Burdach and Doty 1987).

Table 1.

Demographics of study group

Etiology No TME TME
N Age (years) Sex (%F) Years of education Smoke (%) UPSIT N Age (years) Sex (%F) Years of education Smoke (%) UPSIT Years since TME
Idiopathic 163 53.49 (1.41) 42 13.73 (0.37) 8.08
(Missing 2)		 22.17 (0.77)
(Missing 2)		 388 55.04 (0.74) 64 15.54 (0.11)
(Missing 8)		 5.44
(Missing 2)		 25.70 (0.52) 26.79 (0.80)
URI 96 55.50 (1.31) 61 14.82 (0.24)
(Missing 2)		 5.32
(Missing 2)		 22.56 (0.86)
(Missing 1)		 252 56.46 (0.79) 63 15.74 (0.13)
(Missing 3)		 4.76 22.89 (0.551) 25.84 (1.01)
Head trauma 54 39.39 (2.12) 44 13.33 (0.52) 18.52 14.46 (1.05) 101 43.79 (1.52) 58 15.01 (0.20)
(Missing 1)		 13.00
(Missing 1)		 15.73 (0.81) 16.72 (1.32)
Allergy, sinusitis, rhinitis, polyps, nasal operation 10 52.10 (5.72) 70 13.90 (1.06) 0 20.60 (2.88) 47 52.70 (1.77) 66 15.51 (0.32)
(Missing 2)		 6.38 21.96 (1.36) 23.09 (2.14)
Others 41 49.49 (3.74) 51 13.31 (0.43)
(Missing 2)		 9.76 21.05 (1.59) 103 56.60 (1.74) 62 15.08 (0.25)
(Missing 1)		 5.26 26.07 (0.98)
(Missing 1)		 28.36 (1.78)
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All values are means (SDs) unless indicated otherwise. UPSIT, University of Pennsylvania Smell Identification Test (Doty et al. 1984); URI, upper respiratory infections. For education, 16 subjects who indicated “other” in the survey questionnaire were eliminated.

Information regarding each participant’s medical history, current health, and chemosensory complaint was obtained during participant interviews and medical examinations, as well as from an intake questionnaire the participant completed prior to visiting the Center. The questionnaire was comprised of 7 sections: 1) General Information (demographics, referral source, and drinking and eating habits); 2) Medical History (major illnesses and injuries, hospital admissions, dental extractions, and medications taken in the year prior to and since symptom onset); 3) History of Presenting Complaint (nature, onset date, duration, antecedent conditions, and treatments received); 4) Smell Symptoms (degree and type of dysfunction, general nasal health, and abnormal nasal sensations, e.g., nasal obstruction, rhinorrhea, and postnasal drip); 5) Taste Symptoms (abnormal oral sensations, problems with sweet, sour, bitter and salty taste perception, general oral health); 6) Endocrine Information (endocrine status, prior operations such as oophorectomy and thyroidectomy); and 7) Current Depression or Anxiety (the Beck Depression Inventory II; Beck Anxiety Inventory). This research was approved by the Institutional Review Board of the University of Pennsylvania’s Office of Regulatory Affairs (IRB#: 824251) and was performed in accordance with the ethical principles of the Declaration of Helsinki. All participants provided informed consent for the use of their data for research purposes.

Procedures

All Center participant intake questionnaires for which the third molar question was first inserted into the questionnaire (February 2000) were reviewed. We evaluated only data in which the participant clearly indicated either having no TME (control group) or the specific time frame when they had TME.

Whole-mouth taste identification test

Details of this sip-and-spit whole-mouth taste test are provided elsewhere (Soter et al. 2008; Doty et al. 2021). In brief, 5 concentrations of sucrose (0.08, 0.16, 0.32, 0.64, and 1.28 M), sodium chloride (0.032, 0.064, 0.128, 0.256, and 0.512 M), citric acid (0.0026, 0.0051, 0.0102, 0.0205, and 0.0410 M), and caffeine (0.0026, 0.0051, 0.0102, 0.0205, and 0.0410 M) were presented in 10 mL samples counterbalanced in presentation order. Each solution was sipped, swished in the mouth, and expectorated. The subject then indicated whether the solution tasted sweet, salty, sour, or bitter. After responding, the subject rinsed his or her mouth with purified water. Forty stimulus presentations were administered (4 tastants × 5 concentrations × 2 trials). The total possible identification score for a given tastant was 10.

Statistical analyses

The data for each of the four taste stimuli were subjected to separate sex by extraction group (extraction, no extraction control) analyses of covariance (ANCOVAs) with age as the covariate. Odds ratios (ORs) were computed using binary logistic regression adjusting for age and sex, after assigning each participant to “Better” and “Worse” category based on his or her performance relative to the corresponding average. To ensure that our primary findings were not meaningfully affected by deviations from normality of the frequency distributions, we also performed the nonparametric Kruskal–Wallis H-test between the taste test scores of the extraction and control groups on a subset of 994 age- and sex-matched participants.

To examine, in the TME group, whether either the time since extraction or the participant’s etiology influenced the test measures, the TME data alone were subjected to an etiology by sex by time since extraction ANCOVA with age as the covariate. For this analysis, the time since extraction was divided into 4 categories: ≤1, >1 to ≤5, >5 to ≤10, and >10 years. Because of the small number of participants in some of the etiology groups (Table 1), we confined this analysis to only those groups with at least 50 participants; that is, idiopathic (n = 551), upper respiratory infection (n = 348), head trauma (n = 155), and allergy or nasal sinus disease (n = 57). The idiopathic group was likely composed primarily of individuals with postviral olfactory deficits (Doty et al. 2021).

Results

TME versus control subject analyses

The least squares adjusted mean (SEM) test scores are shown in Table 2 for both the TME and non-TME control subjects. The TME group outperformed the control group for each of the 4 taste stimuli. In all cases, women outperformed men and performance was negatively related to age. The statistical details are as follows: Sucrose—Extraction Group F(1,1250) = 19.87, P < 0.0001; Sex F(1,1250) = 9.95, P < 0.002; Sex × Extraction Group F(1,1250) = 0.30, P = 0.582; Age F(1,1250) = 4.219, P < 0.04. Citric acid—Extraction Group F(1,1250) = 22.75, P < 0.0001; Sex F(1,1250) = 7.33, P < 0.007; Sex × Extraction Group F(1,1250) = 0.904, P = 0.342; Age F(1,1250) = 43.51, P < 0.0001. Sodium chloride—Extraction Group F(1,1250) = 12.95, P < 0.0001; Sex F(1,1250) = 3.60, P = 0.058; Sex × Extraction Group F(1,1250) = 0.50, P = 0.480; Age F(1,1250) = 43.41, P < 0.0001. Caffeine—Extraction Group F(1,1250) = 23.37, P < 0.0001; Sex F(1,1250) = 12.56, P < 0.0001; Sex × Extraction Group F(1,1250) = 0.57, P = 0.451; Age F(1,1250) = 34.86, P < 0.0001. Average—Extraction Group F(1,1250) = 39.04, P < 0.0001; Sex F(1,1250) = 15.77, P < 0.0001; Sex × Extraction Group F(1,1250) = 0.38, P = 0.54; Age F(1,1250) = 48.71, P < 0.0001.

Table 2.

Least squares adjusted mean (SEM) taste identification test scores of TME and control groups

Males Females
TME (n = 331) Controls (n = 184) Difference TME (n = 560) Controls (n = 180) Difference
Sucrose 9.37 (0.07) 8.96 (0.10) 4.38% 9.59 (0.06) 9.26 (0.10) 3.44%
Citric acid 7.70 (0.14) 6.79 (0.18) 11.82 % 7.97 (0.11) 7.37 (0.19) 7.53%
Sodium chloride 8.41 (0.10) 8.06 (0.14) 4.16% 8.72 (0.08) 8.21 (0.14) 5.85%
Caffeine 8.10 (0.13) 7.26 (0.18) 10.37% 8.52 (0.10) 7.90 (0.18) 7.28%
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Total correct possible per taste quality = 10. See text for details.

Influence of etiology and time since TME on taste identification scores

The ANCOVA examining the effects of etiology and the time since extraction found neither of these variables to be significant (Ps > 0.20). As reported in the aforementioned analyses, both sex and age were significant for all 4 taste qualities (Ps < 0.0001). Binary logistic regression controlling for age and sex found that the TME subjects were more likely, on average, to score significantly higher than the non-TME control subjects (OR: 2.03 [95% confidence interval, CI: 1.56, 2.64], P < 0.0001). The trend was consistent for all 4 taste stimuli: Sucrose—OR: 1.67 (95% CI: 1.30, 2.16, P < 0.0001). Citric acid—OR: 1.81 (95% CI: 1.40, 2.34, P < 0.0001). Sodium chloride—OR: 1.49 (95% CI: 1.15, 1.93, P = 0.0001). Caffeine—OR: 1.46 (95% CI: 1.13, 1.88, P < 0.0001). These findings were confirmed using the nonparametric Kruskal–Wallis H-test on the subset of 994 participants who were matched on the basis of sex and age: Sucrose—H(1) = 15.78, P < 0.0001. Citric acid—H(1) = 8.26, P < 0.004. Sodium chloride—H(1) = 3.31, P = 0.069. Caffeine—H(1) = 5.904, P = 0.015.

Discussion

This cross-sectional retrospective study suggests, for the first time, that persons who have received TME in the distant past experience, on average, a slight enhancement (typically 3–10%) in their ability to taste on a standardized and well-validated whole-mouth taste test. This phenomenon was present after controlling for the effects of sex and age, and was independent of these variables as well as the etiology of the chemosensory disorder for which they were seeking evaluation. In both the TME and control groups, women outperformed men, and age was inversely related to test performance, as occurs in subjects from the general population (Doty et al. 2021). The time when the TME improvement first appears is unknown, but such improvement was not progressive across the time periods assessed in this study.

Prior studies of the influences of TME on taste function have generally noted only adverse effects—effects that are most apparent within 6 months of the time of the TME (Scrivani et al. 2000; Valmaseda-Castellón et al. 2000; Graff-Radford and Evans 2003). In 1 study in which taste function was quantitatively evaluated in 17 participants before TME and at 1 and 6 months postoperatively, deficits were still present in a few persons—deficits that were not severe enough to result in participant complaints (Shafer et al. 1999). However, aside from the present study, studies beyond 9 postoperative months have not been performed and it has been generally believed that the adverse effects of TME largely dissipate over time. Our study provides the first insight into the possible long-term effects of TME on taste function. The degree to which such improvement has clinical meaning is not clear.

The mechanism or mechanisms responsible for the TME-related improvement in taste function seen in the present study are unknown. Two nonmutually exclusive hypotheses merit attention. The first comes from human taste nerve anesthetization research and the second from studies in which hypersensitivity is induced by directly or indirectly altering nerve function, as occurs in neuropathic pain. Regarding the first, unilateral anesthetization of the chorda tympani nerve (CN VII), which innervates the taste buds of the anterior tongue, enhances the sensitivity of taste buds located on the contralateral side of the rear of the tongue innervated by CN IX (Kveton and Bartoshuk 1994). This presumably reflects mitigation of a central inhibitory effect of CN VII on CN IX (Halpern and Nelson 1965). TME damage to both lingual nerves would therefore be expected to enhance whole-mouth taste sensitivity, particularly since most lingual taste buds are innervated by CN IX (Witt and Reutter 2015). Regarding the second, hypersensitivity after peripheral nerve injuries has been well documented in other contexts, and there is evidence from animal studies that repetitive light touch gradually accentuates pain responses from irritated tissue that can lead to progressive long-term tactile hypersensitivity. For example, in a murine model of crush injury to the sciatic nerve, progressive tactile hypersensitivity was induced by repeated low intensity mechanical stimulation over the course of several days which persisted after such stimulation was halted (Decosterd et al. 2002). Conceivably a similar process could occur in TME, given the repetitive nature of oral tactile stimulation from mastication, swallowing, and speech, and their potential influences on a compromised chorda tympani nerve.

Several experimental physiologic models for explaining hypersensitivity have been proposed. In a murine model using exposed sciatic nerve branches, downregulation of CIC-3 chloride channel/antiporter in dorsal root ganglia (DRG) induced a heightened level of mechanical sensitivity of DRG neurons (Pang et al. 2016). Endoplasmic reticulum stress in the DRG induced by peripheral nerve injury has also been found to result in pain hypersensitivity (Yamaguchi et al. 2018). Importantly, immune system components appear to be involved in some cases of neural hyperexcitability. For example, T lymphocytes utilize β-endorphin to mitigate the increase of neuropathy-related tactile sensitivity (Labuz et al. 2010).

The present study has both strengths and weaknesses. Among its strengths are its large sample size and the administration of a well-validated whole-mouth taste test with a high degree of reliability and sensitivity (Stinton et al. 2010; Doty et al. 2021). Among its weaknesses are: subjects that were not randomly sampled from the general population and who were seeking help for a chemosensory disorder; the reliance on self-report; the lack of detailed information regarding the specific nature of the TMEs (e.g., the degree of impaction/eruption, relation of tooth to second molar, radiographic signs of proximity to the inferior alveolar canal, degree of bone removal, etc.); and the lack of preoperative taste test scores. Prospective research is obviously needed in which such information is available before definitive assessments of the relationship between elements of TME and taste function can be made. Despite its shortcomings, however, the present study strongly suggests that, on average, TME likely has a positive long-term, albeit subtle, effect on the function of the lingual taste pathways of some persons.

Acknowledgments

We thank Crystal Wylie and Mark Potter for their comments on a previous version of the manuscript.

Funding

This work is based, in part, on a clinical database that was initiated by funding from National Institute on Deafness and Other Communication Disorders [PO1 DC 00161].

Conflict of interest

The authors have no disclosures or conflicts of interest to declare regarding this work.

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