Multimodal Management and Prognostic Factors in Post-Traumatic Trigeminal Neuropathic Pain Following Dental Procedures: A Retrospective Study

Abstract

Background: Post-traumatic trigeminal neuropathic pain (PTTNP) is a chronic condition often caused by dental procedures such as implant placement or tooth extraction. It involves persistent pain and sensory disturbances, negatively affecting the quality of life of patients. Methods: This retrospective observational study was conducted at Chosun University Dental Hospital and included 120 patients diagnosed with PTTNP involving the orofacial region. Patient data were collected between January 2014 and December 2023. Among them, 79 patients (65.8%) developed PTTNP following dental implant placement, with a total of 121 implants analyzed. The inferior alveolar nerve was most frequently involved. Clinical factors, including the time to treatment, removal of the causative factor, the Sunderland injury grade, and the type of treatment, were evaluated. Pain intensity and sensory changes were assessed using the visual analog scale (VAS). Results: Treatment initiated within the early post-injury period, commonly regarded as within three months, and implant removal tended to improve outcomes. Pharmacological therapy was the most commonly employed modality, particularly gabapentinoids (e.g., gabapentin, pregabalin) and tricyclic antidepressants such as amitriptyline. However, combined therapy, which included pharmacologic, physical, and surgical approaches, was associated with the greatest sensory improvement. Conclusions: Prompt, multidisciplinary intervention may enhance recovery in patients with PTTNP. Implant-related injuries require careful management, and multimodal strategies appear more effective than monotherapies.

1. Introduction

Post-traumatic trigeminal neuropathic pain (PTTNP) is a peripheral nerve injury that occurs following trauma to one or more branches of the trigeminal nerve, most commonly the inferior alveolar nerve (IAN) and the lingual nerve (LN) [1,2]. Among the various etiologies, dental procedures—particularly implant placement, tooth extraction, and endodontic treatment—are frequently implicated due to the anatomical proximity of these nerves to the surgical sites in the posterior mandible [1,2]. While dental implantology has achieved high technical success rates, the increasing number of procedures has led to a parallel rise in the reported cases of iatrogenic trigeminal nerve injuries, some of which progress to chronic neuropathic pain [3].

Pain is generally classified into three categories based on its underlying mechanisms: nociceptive, neuropathic, and nociplastic pain [4,5,6]. Nociceptive pain arises from the actual or potential damage to non-neural tissues and involves the activation of nociceptors, such as in trauma or inflammation [4,5,6]. Nociplastic pain, in contrast, results from altered nociceptive processing despite the absence of identifiable tissue or nerve injury and is commonly seen in functional pain syndromes such as fibromyalgia [4,5,6]. Neuropathic pain, the category under which PTTNP is classified, occurs as a direct consequence of a lesion or disease affecting the somatosensory nervous system [4,5,6].

The development of PTTNP involves complex pathophysiological mechanisms, including ectopic nerve firing, neuroma formation, peripheral and central sensitization, and maladaptive plasticity in the trigeminal system [7,8]. These changes contribute to the persistent pain and sensory disturbances that extend beyond the expected period of tissue healing [7,8].

PTTNP fulfills the diagnostic criteria for peripheral neuropathic pain, as it develops following trauma to the trigeminal nerve that causes a structural lesion and persistent sensory dysfunction [9,10]. Affected patients frequently exhibit both negative sensory signs—such as hypoesthesia and anesthesia—and positive sensory phenomena—including dysesthesia, allodynia, and hyperalgesia [9,10]. These symptoms are often chronic and significantly impair the patients’ oral function, psychosocial well-being, and overall quality of life [11,12].

Chronic orofacial neuropathic pain imposes a substantial burden on individuals and healthcare systems [13,14]. Patients may experience difficulty in eating, speaking, and engaging in social activities, while long-term pharmacologic treatment or surgical interventions incur considerable costs and emotional distress [13,14].

Several studies have identified the factors influencing the severity and prognosis of trigeminal nerve injury, including the trauma mechanism, the extent of the neural damage, and the timing of intervention [10,11]. The Sunderland classification stratifies nerve injuries into five grades based on their structural severity, from a temporary conduction block (grade I) to a complete transection requiring surgical repair (grade V), with the prognosis worsening at a higher grade [15]. The timing of intervention is another critical determinant of recovery. From a neuropathic pain perspective, delayed treatment may lead to central sensitization and persistent ectopic nerve activity, which contribute to chronic pain that is less responsive to therapy. Early intervention within three months may interrupt this progression and improve outcomes [7,8,9,16].

Clinical evidence strongly supports the value of early microsurgical repair [9,16]. Studies have shown that patients undergoing surgical exploration and nerve repair within a few days to three months of injury exhibit significantly better outcomes than those receiving delayed treatment [9,16]. Both Zuniga et al. and Susarla et al. emphasized that the optimal window for surgical intervention lies within 24–72 h post-injury, and that delaying a repair beyond three months markedly reduces the likelihood of meaningful sensory recovery [16,17]. While some degree of recovery may still occur with surgeries performed within six to nine months, the prognosis becomes increasingly poor with further delays [18].

In addition to timing, the preoperative pain intensity—often measured using the visual analog scale (VAS)—has been associated with postoperative outcomes [9]. Higher VAS scores before surgery predict poorer symptom resolution following nerve repair, underscoring the importance of an early and comprehensive clinical evaluation [9].

Despite these insights, the current evidence is primarily derived from case series or heterogeneous cohorts that include a variety of etiologies. There is a particular lack of well-structured research focusing on implant-induced neuropathy, despite its growing prevalence [3,9]. Moreover, the relationship between the early removal of the causative implant, the Sunderland grade, the treatment modality, and sensory recovery remains underexplored in this subgroup [2,16].

Although various treatment strategies have been proposed—including pharmacologic agents (e.g., anticonvulsants, antidepressants), microsurgical repair, and neuromodulation techniques—there is still no consensus regarding optimal management, particularly for implant-related injuries [13,14].

To address these gaps, this retrospective cohort study aimed to investigate the clinical characteristics, management strategies, and recovery patterns in patients who developed PTTNP following dental implant placement over 10 years. Using the VAS scores as a surrogate marker for sensory recovery and pain burden, we evaluated the impact of symptom onset timing, the Sunderland classification, causative factor removal, treatment duration, and treatment modality on outcomes. Additionally, by comparing implant-related cases with a broader dataset of PTTNP of other origins, we sought to elucidate the relative chronicity and severity of implant-induced neuropathy within the spectrum of trigeminal nerve injuries

2. Materials and Methods

2.1. Study Design and Participants

This retrospective observational study was conducted at Chosun University Dental Hospital and included patients diagnosed with trigeminal nerve injury involving the orofacial region between January 2014 and December 2023. The aim of the study was to investigate sensory changes and treatment outcomes over time, as well as to evaluate the influence of various clinical and therapeutic factors. This study was designed and reported in accordance with the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines [19]. A completed STROBE checklist is provided in Table S1 (Supplementary Materials).

Eligible patients were those who had sustained peripheral trigeminal nerve injury following trauma to the orofacial region, including both general facial injuries and procedure-related trauma, such as third molar extraction, dental implant placement, and endodontic surgery. Inclusion criteria were as follows: (1) the development of neurosensory symptoms such as hypoesthesia, allodynia, hyperalgesia, or dysesthesia after the traumatic event; (2) the availability of visual analog scale (VAS) scores at both the initial and final clinical visits; and (3) the receipt of at least one form of therapeutic intervention during the observation period. Patients were excluded if they had a prior history of neuropathic pain unrelated to orofacial trauma or if complete VAS data were not available.

Sensory function was evaluated using a normalized VAS ratio. Patients rated the intensity of tactile stimuli on the affected area relative to the contralateral normal side (defined as 100%), and the scores were divided by 100. A ratio of 1.0 represented normal sensation; values below 1.0 indicated hypoesthesia, while values above 1.0 reflected hyperesthesia or allodynia. Negative values were not permitted, as the sensory scores were calculated as ratios and could not fall below zero.

As this was a retrospective chart review, no randomization or blinding was implemented during the data collection or analysis. Demographic and clinical variables were obtained from the patient medical records, including the trauma etiology, the anatomical distribution of the nerve injury, and the treatment modality. A total of 122 patients were screened during the study period from January 2014 to December 2023. The mean follow-up (F/U) duration was 7.86 months (SD = 9.60). After excluding two patients (one for not meeting the inclusion criteria and one due to missing data), a final cohort of 120 patients was included in the analysis. The yearly and cumulative number of patients enrolled over the 10-year period is shown in Figure 1, indicating a gradual increase in case identification and referral. The patient inclusion process and the classification based on the etiology of the nerve injury are summarized in a STROBE-compliant flow diagram (Figure 2).

While all cases of orofacial trauma-related trigeminal nerve injury were reviewed to assess the overall epidemiological patterns—including anatomical distribution, sex differences, and trauma etiology—a focused subgroup analysis was performed for patients with implant-induced neuropathy, as this etiology represented the most frequent cause within the dataset. This allowed for a comparison of the clinical characteristics and treatment outcomes between the implant-related and non-implant-related cases.

This study was approved by the Institutional Review Board (IRB) of Chosun University Dental Hospital (Approval Number: CUDHIRB 2407 003). As this was a retrospective chart review study, all patient data were de-identified and anonymized prior to analysis. The requirement for informed consent was waived in accordance with the IRB regulations and institutional guidelines. All procedures adhered to the ethical principles outlined in the Declaration of Helsinki.

2.2. Data Collection

Data were retrospectively collected from the electronic medical records of patients diagnosed with trigeminal nerve injury. Extracted variables included the demographic information, clinical characteristics, and treatment-related data.

At the initial visit, all patients underwent a standardized clinical evaluation comprising a chairside neurosensory examination, qualitative sensory testing (QualST) using cotton swabs, ice sticks, and blunt probes, and, when applicable, quantitative sensory testing (QST) based on thermal and mechanical thresholds (

Table 1. Sensory testing protocol: qualitative and quantitative assessments performed at initial evaluation.

Test Type	Assessment Modality	Description	Tool/Device	Application Area	Purpose
QualST	Light touch detection	Detection of gentle tactile input	Cotton swab	Symptom area + contralateral control	Screening for hypoesthesia
	Pressure sensitivity	Response to blunt mechanical input	Tongue depressor or spatula	Symptom area	Evaluation of pressure perception
	Pinprick discrimination	Distinction between sharp and dull stimuli	Dental explorer or toothpick	Symptom area	Assessment of mechanical hyperalgesia
	Thermal response	Subjective reaction to cold stimuli	Ice stick	Symptom area	Screening for thermal hypoesthesia or dysesthesia
QST	Current perception threshold (CPT)	Electrical stimulation at 2000, 250, and 5 Hz to assess Aβ, Aδ, and C fibers	NeuroMeter	Facial skin (Mx., Mn. divisions)	Quantitative evaluation of sensory nerve function
	Two-point discrimination	Determination of the minimum distance between two distinct points	Caliper or blunt compass	Tongue	Spatial resolution and fine touch discrimination

Footnotes: The NeuroMeter ^® (Neurotron, Inc., Hanover, Germany) was primarily used for the current perception threshold (CPT) testing on cutaneous regions of the face. Measurements were performed on the skin overlying areas innervated by the maxillary (Mx.) and mandibular (Mn.) divisions of the trigeminal nerve. Intraoral areas such as the tongue or mucosa were not assessed using this device due to technical limitations. Two-point discrimination testing was selectively performed on the tongue, where the use of electrical or thermal devices was not feasible. This method served to evaluate the spatial tactile acuity in intraoral regions. Abbreviations: CPT, current perception threshold; Mx., maxillary; Mn., mandibular; QualST, qualitative sensory testing; QST, quantitative sensory testing.

) [20,21,22]. In addition, dental imaging studies were performed to assess the potential anatomical or iatrogenic causes of the nerve injury. These included panoramic radiographs, periapical X-rays, and cone-beam computed tomography (CBCT) when clinically indicated, to evaluate the spatial relationship between the dental structures and neural canals.

Demographic data included the patient age and gender. Clinical variables comprised the time from symptom onset to the first clinical visit (in months), the affected branch of the trigeminal nerve (inferior alveolar, lingual, or maxillary), the type of sensory disturbance (hypoesthesia, dysesthesia, allodynia, or hyperalgesia), and the anatomical location of the sensory dysfunction (chin, lip, labial mucosa, gingiva, anterior teeth, or tongue). The severity of the nerve injury was classified according to the Sunderland classification (grades I–V) (

Table 2. Sunderland classification of peripheral nerve injury [16].

Grade	Structural Damage	Functional Loss	Recovery Potential	Typical Clinical Features
Grade I	Local conduction block (neurapraxia); no axonal disruption	Temporary sensory/motor loss; no Wallerian degeneration	Complete recovery within days to weeks	Mild paresthesia; spontaneous resolution expected
Grade II	Axonal disruption; endoneurium intact	Wallerian degeneration distal to injury site	Good prognosis; axons can regenerate	Hypoesthesia; Tinel’s sign may progress distally
Grade III	Axonal and endoneurial damage; perineurium preserved	Disrupted axonal guidance and moderate conduction loss	Partial recovery; possible misdirection	Dysesthesia; prolonged or incomplete sensory return
Grade IV	Loss of axon, endoneurium, and perineurium; epineurium intact	Severe loss of continuity and conduction	Poor spontaneous recovery; often needs surgery	Chronic neuropathic symptoms; poor or absent regeneration
Grade V	Complete transection (neurotmesis) with loss of all nerve layers	Total sensory and motor loss distal to lesion	No recovery without surgical repair	Anesthesia; neuroma formation likely

) [16].

Sensory function was assessed using a VAS at both the initial and final clinical visits. In this study, a VAS ratio of 1.0 was defined as normal sensation. Ratios below 1.0 indicated hypoesthesia, whereas values above 1.0 were interpreted as hyperesthesia or allodynia. Negative values were not permitted, as ratios represent relative intensity and cannot be negative by definition.

Treatment-related variables included whether the causative factor (e.g., implant or prosthesis) was removed, the treatment modality applied (pharmacological, physical therapy, surgical, or no treatment), and the total duration of treatment, recorded in months.

2.3. Outcome Measures

2.3.1. Primary Outcome: Sensory Function Improvement

The primary outcome of this study was the degree of sensory function recovery, assessed by the change in the normalized VAS ratios between the initial and final clinical visits. VAS values were calculated by dividing the patient-reported sensory intensity on the affected side (relative to the contralateral, unaffected side, defined as 100%) by 100. A ratio of 1.0 indicated normal sensation; values below 1.0 reflected sensory loss (hypoesthesia), and values above 1.0 indicated sensory gain (hyperesthesia or allodynia).

To address distributional skewness, changes in the VAS ratios were log-transformed. Positive log-transformed values indicated an improvement toward normal sensation, whereas negative values indicated a persistence or worsening of the abnormal sensory perception

2.3.2. Secondary Outcomes

Secondary outcomes included the evaluation of various clinical and therapeutic factors that may influence sensory recovery. Specifically, we examined whether the timing of symptom onset, the removal of the causative factor (e.g., implant or prosthesis), the severity of the nerve injury based on the Sunderland classification, the total duration of treatment, and the type of treatment modality were associated with the degree of improvement in the VAS ratios.

In addition, exploratory analyses were conducted to assess the potential associations among the continuous variables, including the time from symptom onset to initial visit, the treatment duration, the Sunderland grade, and the VAS scores. Detailed results of these analyses are presented in the Results Section.

2.4. Statistical Analysis

All statistical analyses were performed using IBM SPSS Statistics version 29.0 (IBM Corp., Armonk, NY, USA). The continuous variables were summarized as the mean and standard deviation (SD), while the categorical variables were presented as frequencies and percentages. A two-tailed p-value of <0.05 was considered statistically significant.

For the group comparisons involving non-normally distributed variables—such as the symptom onset timing categories, the Sunderland grades, and the treatment modalities—the Kruskal–Wallis test was used. The Mann–Whitney U test was applied to compare two independent groups, such as the patients with versus without implant removal. Associations between the continuous variables (e.g., symptom onset time, treatment duration, and changes in VAS ratios) were evaluated using the Spearman’s rank correlation coefficient (ρ).

All analyses were conducted using complete-case analysis, with listwise deletion applied for missing data. Data distributions and intergroup differences were visually assessed using boxplots for the treatment modality comparisons and scatterplots to explore the correlations between the symptom onset time and treatment duration.

3. Results

3.1. Demographic and Clinical Characteristics (Total Cohort, n = 120) (

Table 3. Demographic and etiologic characteristics in the total study population (n = 120).

Category	Variable	Value
Demographics	Age (mean ± SD)	50.33 ± 13.33
	Age range	12–77 years
	Gender (Male/Female)	40 (33.3%)/80 (66.7%)
Cause of Injury	Implant Placement	79 (65.8%)
	Tooth Extraction	25 (20.8%)
	Endodontic Treatment	4 (3.3%)
	Other Trauma	12 (10.0%)
Injured Nerve	Inferior Alveolar Nerve (IAN)	107 (89.2%)
	Lingual Nerve (LN)	6 (5.0%)
	Maxillary Nerve	3 (2.5%)
	Mixed Nerve Involvement	1 (0.8%)
Sensory Disturbances	Hypoesthesia	55 (45.8%)
	Hypoesthesia + Allodynia	48 (40.0%)
	Other Combinations	17 (14.2%)

Data are presented as number (%) or mean ± standard deviation.

)

A total of 122 patients with suspected PTTNP were initially screened for this study. Of these, 2 patients were excluded: one due to not meeting the inclusion criteria and the other due to missing clinical data. Consequently, 120 patients were included in the final analysis (Figure 1 and Figure 2).

The mean patient age in the cohort was 50.3 years (SD = 13.3; range, 12–77 years). Among them, 40 patients (33.3%) were male and 80 (66.7%) were female, indicating a female predominance.

The most common cause of trigeminal nerve injury was dental implant placement (n = 79, 65.8%), followed by tooth extraction (n = 25, 20.8%), endodontic treatment—including conventional root canal therapy and apicoectomy—(n = 4, 3.3%), and other traumatic causes (n = 12, 10.0%). The other trauma group included facial bone fractures due to traffic accidents or blunt trauma, as well as inferior alveolar nerve (IAN) injuries associated with regional nerve block anesthesia prior to dental procedures.

The IAN was the most frequently affected branch (n = 107, 89.2%), followed by the lingual nerve (LN) (n = 6, 5.0%), and the maxillary nerve (n = 3, 2.5%). One patient experienced a combined injury to the IAN and the maxillary nerve following the extraction of teeth #28 and #38.

With respect to sensory symptoms, hypoesthesia was the most commonly reported (n = 55, 45.8%), followed by combined hypoesthesia and allodynia (n = 48, 40.0%). A minority of patients presented with additional symptoms such as dysesthesia, taste alterations, or hyperalgesia. Due to missing documentation, the Sunderland classification and complete baseline VAS scores were not available for all patients.

Among the study population, a wide range of systemic comorbidities were observed. Metabolic disorders—including hypertension, diabetes mellitus, and dyslipidemia—were the most common category (n = 32), followed by thyroid disorders (n = 7). Other less frequent systemic conditions included cardiovascular, musculoskeletal, autoimmune, hepatic, psychiatric, and neoplastic disorders (Figure 3). Of note, all the patients with diabetes had well-controlled blood glucose levels and did not exhibit any clinical history or symptoms of diabetic neuropathy. Therefore, they were included in the study, as the exclusion criteria specifically targeted patients with pre-existing neuropathic conditions that could confound the assessment of post-traumatic trigeminal nerve injury.

3.2. Subgroup Analysis of Patients with Implant-Related Nerve Injury

Among the 79 patients (65.8%) who developed PTTNP following dental implant placement, there were no significant changes in the VAS scores before and after treatment (Wilcoxon signed-rank test, p = 0.067). A significant negative correlation was observed between the symptom onset and the treatment duration (Spearman’s ρ = −0.349, p = 0.002), indicating that an earlier presentation was associated with a longer treatment duration. A marginally significant negative correlation was noted between the symptom onset and the log-transformed VAS change (Spearman’s ρ = −0.224, p = 0.050), suggesting that an earlier presentation may relate to a greater sensory improvement. No significant correlation was found between the Sunderland grade and the VAS change (Spearman’s ρ = 0.001, p = 0.996) or between the Sunderland grade and the treatment duration (Spearman’s ρ = 0.119, p = 0.296).

Implant removal was performed in 41% of cases, and pharmacologic treatment was provided in 58.2%, primarily with gabapentinoids. However, there were no significant differences in the VAS changes based on the implant removal status (p = 0.625) or pharmacologic treatment (p = 0.159) (

Table 4. VAS changes by clinical factor in implant subgroup.

Factor	Groups	N(%)	Mean VAS Change ± SD	p-Value
Onset to visit	0–3 mo	33 (41.8%)	−0.12 ± 0.23	0.9071 (Kruskal–Wallis)
	4–6 mo	13 (16.5%)	−0.09 ± 0.20
	7–12 mo	13(16.5%)	−0.05 ± 0.17
	>12 mo	20 (25.3%)	−0.04 ± 0.25
Implant removal	Yes	32 (40.5%)	−0.16 ± 0.22	0.625 (Mann–Whitney U)
	No	46 (58.2%)	−0.16 ± 0.22
Sunderland grade	I	39 (49.4%)	0.20 ± 0.12	0.0284 (Kruskal–Wallis)
	II	3 (3.8%)	0.53 ± 0.30
	III	14 (17.7%)	0.87 ± 0.40
	IV	23 (29.1%)	1.21 ± 0.61
	V	0	0
Treatment duration	0–3 mo	50 (63%)	−0.05 ± 0.15	ρ = −0.349, p = 0.002 * (Spearman correlation)
	4–6 mo	16 (20.3%)	−0.10 ± 0.17
	7–12 mo	11 (13.9%)	−0.16 ± 0.23
	>12 mo	2 (2.5%)	−0.20 ± 0.25

Footnote: Values are presented as mean ± standard deviation and n (%). p-values indicate comparisons by Kruskal–Wallis, Mann–Whitney U tests, or Spearman correlation as noted. * indicates a statistically significant difference (p < 0.05). mo, months.

).

When comparing the treated and untreated patients, there were no statistically significant differences in the log-transformed VAS changes (Mann–Whitney U test, p = 0.9873). Among those who received treatment, the log VAS changes varied by treatment duration group, but the differences were not statistically significant (Kruskal–Wallis H = 6.70, p = 0.1391). Notably, the 0–3 and 4–6 month groups showed positive mean changes, while the 7–12 month group showed a negative mean change, and the >12 month group showed a large positive change from a single case. These results reflect the substantial variability in individual recovery trajectories, despite overall trends (

Table 5. Comparison of log-transformed VAS changes by treatment duration and treatment status.

Treatment Group	Treatment Duration	N (%)	Mean Log VAS Change	Standard Deviation (SD)	p-Value
Treated	0–3 mo	18 (41.86%)	1.012	3.976	p = 0.1391 (Kruskal–Wallis H test)
	4–6 mo	14 (32.55%)	0.589	0.857
	7–12 mo	10 (23.25%)	−1.724	4.981
	>12 mo	1 (2.32%)	13.653	-
Total Treated	-	43 (100%)	0.607 (mean)	4.049	p = 0.9873 (Mann–Whitney U test)
No Treatment	-	36	0.312	0.890

Footnote: Values are presented as number and percentage [N (%)], mean log-transformed VAS change, and standard deviation (SD). SD was not calculated for the >12-month group due to a sample size of one. p-values indicate comparisons by Kruskal–Wallis or Mann–Whitney U tests as noted.

).

No significant differences were found across the treatment duration groups (Kruskal–Wallis H = 6.70, p = 0.1391) or between the treated and untreated patients (Mann–Whitney U test, p = 0.9873).

Treatment-related changes in the VAS are summarized, indicating a minimal improvement with no treatment, a modest reduction with pharmacologic and physical therapies, a greater reduction with surgical treatment, and the largest improvement with combined therapy, albeit with greater variability. This suggests that a combined treatment may offer enhanced symptom improvement in PTTNP management (Figure 4).

4. Discussion

4.1. Summary of Key Findings

This retrospective observational study included 120 patients diagnosed with PTTNP, aiming to evaluate the sensory changes over time and identify the clinical and therapeutic factors influencing recovery. Dental implant placement was the most common cause (65.8%), and the inferior alveolar nerve (IAN) was the most frequently affected branch (89.2%), with hypoesthesia alone or combined with allodynia being the most common symptom.

The primary outcome was sensory improvement, assessed using the VAS scores at the initial and final visits. Secondary outcomes included the evaluation of symptom onset timing, causative factor removal, Sunderland classification, treatment duration, and treatment modality in relation to VAS improvements.

In the implant-related subgroup (n = 79), although the patients presenting within three months showed a trend toward greater sensory improvement, there were no statistically significant differences across the onset-time categories (p = 0.9071). Patients who underwent implant removal showed a greater mean VAS improvement (−0.16) than those who did not (−0.08), though this difference was not statistically significant (p = 0.625). Sunderland grades were associated with differences in the initial VAS scores (p = 0.0284), reflecting the relationship between the anatomical severity and baseline symptoms; however, these grades did not correlate with VAS improvements (Spearman’s ρ = 0.001, p = 0.996).

A significant negative correlation was observed between the symptom onset and the treatment duration (Spearman’s ρ = −0.349, p = 0.002), indicating that an earlier presentation was associated with a longer treatment duration. A marginally significant correlation was also found between an earlier onset and a greater VAS improvement (Spearman’s ρ = −0.224, p = 0.050). Notably, patients with delayed presentation often did not receive active treatment due to the chronic nature of their condition or a reduced expectation of the benefit and were therefore classified within the short treatment duration groups. As a result, some of the shortest treatment durations were paradoxically associated with minimal or no improvement in the VAS scores, reflecting a subgroup that remained untreated (Table 4).

Since the analysis in Table 4 included all implant-related patients regardless of the treatment status, potential bias may have been introduced—particularly from the untreated patients grouped under the short treatment durations. To address this, a stratified analysis was conducted including only the 43 patients who actually received treatment (Table 5). When comparing the treated group (n = 43) with the untreated group (n = 21), no statistically significant differences in the log-transformed VAS changes were observed (Mann–Whitney U test, p = 0.9873). Among the treated group, the mean log VAS change varied by treatment duration: the 0–3 and 4–6 month groups showed an improvement, while the 7–12 month group showed a deterioration. However, these differences were not statistically significant (Kruskal–Wallis H = 6.70, p = 0.1391) (Table 5).

Among those patients who did undergo treatment, a meaningful VAS reduction was observed, particularly in those receiving multimodal therapy. Among the implant-related cases, implant removal was performed in 32 out of 79 patients (40.5%). The decision to remove the implants was based on persistent neurosensory symptoms, radiographic or clinical evidence of nerve compression, and shared decision-making between the patient and the clinician. No other surgical decompression procedures were performed in this cohort. Combined therapy showed the greatest VAS improvement (−0.35), while no treatment resulted in a minimal change (+0.01), though the differences were not statistically significant (p = 0.2154) (Table 4).

These findings align with the study’s aim of assessing sensory outcomes and identifying the associated clinical factors. They suggest potential benefits of early intervention, causative factor removal, and multimodal treatment, although the variability in nerve injury severity, presentation timing, and individual response may limit the detection of statistically significant effects.

4.2. Comparison with Previous Studies

Several prior studies have reported that PTTNP occurs more frequently in middle-aged to older female patients, especially with IAN involvement [23,24]. Our findings are consistent with this demographic pattern, which may be attributed to an increased implant placement in aging populations with atrophic jaws and reduced bone density [25,26].

The importance of early intervention has been emphasized in multiple studies [27,28,29]. Although our study did not reveal a statistically significant difference across the onset groups, earlier presentation tended to yield better sensory outcomes, likely due to a reduced risk of irreversible nerve damage and central sensitization.

The previous literature also supports early implant removal in cases of persistent symptoms, with our data demonstrating a similar trend despite the lack of statistical significance [25]. The association between the Sunderland classification and the baseline VAS scores observed in our study aligns with earlier findings, although this classification alone was not predictive of recovery [29].

Lastly, although the differences across the treatment modalities were not significant, the observed benefit of combined therapy supports the current recommendations favoring individualized, multimodal approaches to PTTNP management [30,31].

4.3. Clinical Implications

This study provides clinically relevant insights for the diagnosis and management of PTTNP, particularly in implant-related cases. The demographic distribution of middle-aged to older female patients with IAN involvement aligns with previous reports [23,24] and reflects the trends associated with increased dental implant placement in aging populations with atrophic jaws and reduced bone density [25,26].

Although not statistically significant, earlier presentation was associated with improved sensory recovery, consistent with the evidence that delays contribute to prolonged dysfunction and central sensitization [9,10,32]. The average delay exceeded five months in our cohort, likely impacting outcomes and emphasizing the importance of early recognition and prompt referral by general practitioners.

Implant removal demonstrated a trend toward better outcomes, supporting the literature recommending decompression for persistent sensory symptoms [25,29]. Sunderland classifications correlated with the initial VAS scores, reflecting the anatomical severity and subjective sensory loss [29], but was insufficient alone to predict recovery, highlighting the need for combined clinical, functional, and patient-reported assessments.

Patients receiving combined interventions, including pharmacologic, physical, and surgical treatments, demonstrated the greatest sensory improvement, aligning with the guidelines advocating multimodal, multidisciplinary care for PTTNP [13,18].

4.4. Treatment Considerations

The management of PTTNP requires a multimodal and individualized approach, particularly in cases involving implant-related injuries. The findings of this study underscore the clinical relevance of such a strategy (

Table 6. Clinical management of PTTNP (post-traumatic trigeminal neuropathic pain).

Phase	Recommendation
Diagnosis	Evaluate within one week of symptom onset. Perform detailed history and neurosensory testing (QST, brush test, pinprick, thermal). Use Sunderland classification to grade nerve injury.
Imaging	Obtain panoramic radiograph and/or CBCT to assess for foreign body, implant impingement, or bony compression.
Pharmacologic Treatment	Acute Phase (first few days to weeks): -Tapered corticosteroids (e.g., prednisone 40–60 mg/day for 5–7 days, then taper) -NSAIDs for inflammation and pain control Chronic Phase (>3 months): -Gabapentin 300–1800 mg/day -Pregabalin 75–300 mg/day -Amitriptyline 10–50 mg/day -Clonazepam 0.25–1.5 mg/day Topical Agents (adjunctive): -Lidocaine 5% patch -Capsaicin 0.025–0.075% cream
Physical Therapy	Adjunctive modalities: -Low-Level Laser Therapy (LLLT) -Transcutaneous Electrical Nerve Stimulation (TENS) -Desensitization techniques (e.g., cotton, cold/warm stimulation)
Surgical Consideration	If symptoms persist beyond 3–6 months or progressive worsening, consider the following: -Surgical decompression (if mechanical cause) -Neurorrhaphy or microsurgical repair (if laceration)
Referral	Refer to an orofacial pain specialist or oral/maxillofacial surgeon within one month if no improvement or diagnosis uncertain.
Monitoring & Follow-up	Reassess symptoms monthly using VAS, QualST/QST Monitor for changes in pain quality, spread, or new sensory deficits Adjust therapy based on response

Note: This table is based on the clinical recommendations from the American Academy of Orofacial Pain (AAOP), 7th Edition Guidelines.

). Patients who received combined interventions—including pharmacologic therapy, physical modalities (e.g., transcutaneous electrical nerve stimulation, TENS), and surgical management—demonstrated the greatest improvement in sensory function, although statistical significance was not achieved. Nevertheless, this trend aligns with the current guidelines advocating for interdisciplinary and multimodal care in neuropathic orofacial conditions [33].

4.4.1. Pharmacologic and Topical Treatment

Pharmacologic therapy remains the mainstay and first-line strategy for PTTNP. Commonly used agents include gabapentin, pregabalin, tricyclic antidepressants (e.g., amitriptyline), and benzodiazepines (e.g., clonazepam) [30,31,34]. Pharmacologic agents used in PTTNP target the aberrant neuronal excitability and aim to reduce the central and peripheral sensitization. Gabapentin (300–3600 mg/day) and pregabalin (150–600 mg/day) act on the α2δ subunit of the voltage-gated calcium channels, inhibiting excitatory neurotransmitter release. Amitriptyline (10–75 mg/day) exerts its effects via norepinephrine and serotonin reuptake inhibition and sodium channel blockade. Clonazepam (0.25–1.5 mg/day) may be beneficial for comorbid anxiety or insomnia but should be used cautiously due to the risk of dependence and cognitive side effects. Dose titration and adverse effect profiles must be considered, especially in elderly patients or those with renal or cardiovascular comorbidities [31,35].

In addition to the systemic agents, topical medications offer localized pain relief with minimal systemic burden. Lidocaine patches (5%) can be applied for 12 h/day and are useful for focal neuropathic pain. Capsaicin cream (0.025–0.075%) works by depleting substance P and desensitizing TRPV1 receptors, though it may cause an initial burning sensation. These topical agents are particularly beneficial in patients who are intolerant to systemic medications or for those with well-demarcated pain areas [31,36].

Careful monitoring of the treatment response, side effects, and comorbidities (e.g., renal or hepatic dysfunction) is critical in all cases. Patients should be educated on the gradual onset of therapeutic effects, the importance of adherence, and the need to avoid the self-adjustment of medications [30,31].

4.4.2. Physical Therapy

Physical therapies are frequently employed as adjuncts to pharmacologic treatment in PTTNP to enhance neural plasticity and reduce sensitization. Among these, low-level laser therapy (LLLT) exerts anti-inflammatory and analgesic effects via photobiomodulation, typically using 600–1000 nm wavelengths and 2–6 J/cm² doses. Transcutaneous electrical nerve stimulation (TENS) stimulates the Aβ fibers to inhibit nociceptive transmission and can be applied at varying frequencies depending on the patient response. Desensitization exercises, involving graded tactile and thermal stimuli, help to normalize somatosensory input in patients with dysesthesia. These modalities are generally safe and well-tolerated and may improve outcomes when combined with individualized medical therapy [31,33].

4.4.3. Surgical Decompression for Implant- or Prosthesis-Induced Nerve Compression

When radiographic or clinical evidence of nerve compression was present—typically due to implants, fixation screws, or ill-fitting prostheses—surgical decompression or removal was considered, especially in cases with persistent paresthesia or neuropathic pain. Early intervention within weeks to months post-injury led to better sensory recovery and pain relief, consistent with the literature emphasizing timely decompression to prevent irreversible nerve damage [9,10]. Delayed surgery, however, was linked to poorer outcomes.

Additionally, a longer treatment duration correlated with a greater VAS improvement, highlighting the importance of sustained multimodal management in chronic PTTNP [19,33]. Nonetheless, long-term care can be challenged by poor adherence, psychological comorbidities, and socioeconomic barriers. A multidisciplinary, patient-centered approach—emphasizing education, psychological support, and shared decision-making—is essential to optimize engagement and clinical outcomes [31,33].

4.5. Psychological and Sociocultural Factors

Persistent neuropathic pain, including PTTNP, is influenced not only by peripheral nerve injury but also by central and psychosocial mechanisms [36,37,38,39,40]. In the present study, several patients reported limited sensory improvement despite receiving appropriate pharmacologic and physical treatments. This may reflect the effects of central sensitization, as well as psychological comorbidities such as anxiety, depression, and sleep disturbances—all of which are known to amplify the subjective experience of pain and reduce compliance with rehabilitation protocols [38,39]. Psychological distress may also impair neuroplasticity and delay functional recovery. Although psychological status was not formally assessed in this study, future research could incorporate validated tools such as the Patient Health Questionnaire-9 (PHQ-9) or Generalized Anxiety Disorder-7 (GAD-7) to quantify the mental health burden and its prognostic impact [40,41].

In addition, sociocultural dynamics specific to South Korea should be considered. A significant subset of patients with nerve injury reportedly pursue legal compensation or official disability certification [42,43]. In such contexts, passive coping strategies or avoidance behaviors may emerge, potentially undermining treatment adherence and leading to suboptimal clinical outcomes. To address these challenges, clinicians should adopt a biopsychosocial treatment framework that includes early psychological screening, interdisciplinary consultation, and transparent communication regarding treatment expectations and goals. A patient-centered approach that fosters trust, motivation, and mental well-being may improve both objective and subjective outcomes in PTTNP management [39,42].

4.6. Study Limitations

This study has several limitations. First, its retrospective design precludes the establishment of causal relationships, and the absence of randomization introduces the possibility of confounding variables influencing the outcomes.

Second, while the VAS was used consistently to assess sensory changes, it is inherently subjective and does not capture the more nuanced functional impairments such as two-point discrimination or tactile threshold shifts.

Third, important psychological and socioeconomic factors that may significantly affect the treatment outcomes were not formally evaluated. The inclusion of validated psychometric instruments (e.g., PHQ-9, GAD-7) and socioeconomic profiling in future studies would enable a more holistic understanding of patient recovery trajectories [40,41].

Fourth, the relatively small sample sizes in certain subgroups, particularly those receiving surgical or combined therapies, may have limited the statistical power to detect significant intergroup differences. Furthermore, the treatment modalities were not standardized and were influenced by both patient preference and clinician judgment, which may have introduced a selection bias.

Lastly, as this investigation was conducted at a single academic institution, the findings may not be generalizable to the broader population or other healthcare systems. Future prospective, multicenter studies employing standardized diagnostic criteria, uniform treatment protocols, and comprehensive longitudinal follow-up—including both psychophysical and patient-reported outcomes—are warranted to refine the prognostic models and optimize the clinical management of PTTNP.

5. Conclusions

This study demonstrates that PTTNP following dental implant procedures remains a complex clinical challenge requiring timely diagnosis and a structured, multidisciplinary approach. The severity of the nerve injury and the duration of treatment were key factors associated with sensory recovery, while earlier intervention and the removal of causative factors showed trends toward improved outcomes despite not reaching statistical significance. These findings highlight the importance of early recognition, consistent monitoring, and patient-centered care to optimize recovery in PTTNP cases. Additionally, the integration of psychosocial factors such as patient motivation and mental health into treatment planning is essential, reflecting the multifactorial nature of PTTNP management. Future research should focus on establishing standardized protocols and early intervention strategies tailored to the sociocultural and healthcare contexts of South Korea to improve outcomes for patients with PTTNP.