Written by: Vivian Roknian, DMD
INTRODUCTION
Injury to the inferior alveolar nerve (IAN) is a recognized complication of mandibular implant placement, with reported incidence ranging from less than 1% to as high as 43.5%.1 Patients with neurosensory alterations (NSA) commonly report anesthesia, paresthesia, or stimulus-evoked pain, often with significant functional and psychological impact.2,3
The prognosis for recovery is closely tied to time. While some improvement may occur within the first 6 months following injury, deficits persisting beyond this period are generally considered to have a poor likelihood of meaningful recovery. As a result, patients with long-standing neurosensory deficits are frequently advised to accept permanent sensory loss.
Photobiomodulation (PBM), delivered via laser therapy, has been shown to support cellular metabolism, reduce inflammation, and promote neural repair mechanisms.6-11 However, clinical documentation demonstrating measurable recovery in chronic cases remains limited.
This report presents a case of a 7-year persistent neurosensory deficit following iatrogenic IAN injury, with serial visual mapping demonstrating progressive recovery following laser-assisted photobiomodulation therapy.
Case Presentation
A patient presented with a longstanding neurosensory deficit affecting the left mental nerve distribution following mandibular implant placement performed approximately 7 years prior. Records associated with ongoing legal proceedings indicated that the implant had violated the mandibular canal and remained in place for approximately 1 week before removal.
Since the time of injury, the patient reported complete anesthesia of the left chin and lower lip, with no measurable improvement over the intervening years. Multiple prior consultations concluded that recovery was unlikely due to the duration and nature of the injury, and no active treatment had been offered.
Baseline Neurosensory Assessment
At presentation, neurosensory testing demonstrated a complete absence of sensation across a broad region of the left chin and lower lip. There was no response to tactile stimulation, and a well-demarcated anesthetic boundary was identified that was consistent with the mental nerve distribution.
A standardized cutaneous mapping protocol was used to document the extent of sensory loss. The borders of the anesthetic region were traced directly on the skin and recorded photographically to allow reproducible comparison over time.
Intervention
The patient underwent laser-assisted PBM therapy using the PerioLase MVP-7 (Millennium Dental Technologies), utilizing the Nd:YAG wavelength (1064 nm).
Treatment Protocol
- Power Setting: 6 W (biostimulation mode)
- Energy Delivery: Approximately 2000 J per session
- Application Method: Extraoral sweeping motion from areas of intact sensation toward anesthetic regions along the course of the mental nerve
- Frequency: Weekly treatments were recommended
Energy delivery was intentionally maintained at a conservative level relative to higher-dose protocols described in the literature.
Initial PBM therapy was performed in September 2024 over 2 sessions. Following this initial intervention, treatment was paused. A structured treatment series was later resumed in January 2026 with serial neurosensory mapping performed at each visit (Figure 1).
Figure 1. (an and b) Patient presents at her consultation exam. She has a history of more than 7 years of complete paresthesia. Consults with various surgeons led her to the conclusion that surgery may create more harm than good. Traditional nerve mapping shows complete numbness within the brown lines. After the mapping, 2000 J of energy was applied to the site. Below the chin, there was scarring which was drawn in with the marker.
Observations and Clinical Course
Early Treatment Response: September 2024. Following the initial 2 PBM sessions in September 2024, the patient reported the onset of new sensory phenomena, including tingling and intermittent “electric” or “shooting” sensations within the previously anesthetic region.
Despite these subjective changes. upon mapping only the DAO was spared, yet the midline started to show dramatic changes in mapping (Figure 2).
Figure 2. (a to c) Nerve mapping done 1 week after the initial appointments. Notice the dramatic change in the midline, the lateral border is now medial to the DAO. Notice that the lower border now does not include the scarred area. At the end of the mapping, another 2000 J was applied to the area.
Treatment was subsequently paused. During the interval without continued therapy, the patient reported a return toward baseline symptoms, with no sustained improvement in sensory function (Figure 3).
Figure 3. (a and b) Patient did not return for approximately 15 months. She presented claiming that she felt that the area had grown in size. Mapping was done and while the area is now larger than the previous appointment, it is still smaller than the initial mapping. After the mapping was done, 2000 J of energy was applied to the area.
Baseline: January 3, 2025. A large, well-defined region of complete anesthesia was observed across the left chin and lower lip, indicating significant disruption of the mental nerve distribution (Figure 3).
Early Response: January 10, 2026. Within 1 week of resumed therapy, contraction of the anesthetic borders was observed, with sensory return beginning at the periphery of the affected region. The patient reported new onset of tingling and intermittent “shooting” sensations within hours of treatment. These findings were consistent with early neural reactivation (Figure 4).
Figure 4. (an and b) Patient returned 4 days later for a follow-up appointment. Mapping was done and she said that she was able to feel “the pokes as pokes, not pressure.” After the mapping was done, 2000 J of energy was applied to the area.
Intermediate Recovery: January 14, 2026. By day 11, the anesthetic region demonstrated a marked reduction in size, transitioning from a broad distribution to a narrower vertical band. Sensory return was noted in previously nonresponsive areas of the lip, and the patient reported improved facial symmetry during speech and animation. This phase corresponded clinically to a transition from anesthesia to paresthesia (Figure 5).
Figure 5. (a to c) The patient returned 2 weeks later and she said that when she wakes, she feels more of her face. She went on to say that she has been feeling a sense of heaviness in her chin “with occasional tingling.” After the mapping, 2000 J of energy was applied to the area.
Late Response: January 29, 2026. At this stage, the anesthetic field was reduced to a minimal residual area near the midline. The patient reported near-complete return of sensation, along with functional improvements including more symmetric facial movement and enhanced dynamic expression (Figure 6).
Figure 6. (a to c) Patient presents for a followup claiming, “there is definitely a very different feeling happening.” Nerve mapping was done, this time she said “ouch!” when a sharp stimulus was used and “I can feel that” when gentle pressure was applied.
Results. Serial neurosensory mapping demonstrated a progressive and measurable reduction in the anesthetic field over time (Table 1). Notably, this recovery occurred after a 7-year period of complete sensory loss with no prior improvement.
DISCUSSION
Injury to the inferior alveolar nerve is most commonly associated with implant placement in close proximity to, or within, the mandibular canal.1 The severity of injury may range from transient conduction block (neuropraxia) to axonal disruption (axonotmesis) or complete nerve transection (neurotmesis).4-5
The pattern of recovery observed in this case—characterized by progressive peripheral contraction of the anesthetic field—suggests a partial nerve injury rather than complete severance. This distinction is clinically relevant, as it implies preserved regenerative potential.
PBM has been shown to enhance mitochondrial activity, increase ATP production, reduce inflammatory mediators, and support axonal regeneration.6-12 These effects may create a biologic environment favorable for neural recovery.
Importantly, the timeline observed in this case deviates significantly from established expectations. Spontaneous recovery after such an extended duration would be considered unlikely based on known patterns of peripheral nerve healing.
Biphasic Response Pattern
An important feature of this case is the apparent biphasic response to therapy. Initial treatment in September 2024 resulted in subjective sensory changes with a moderate measurable reduction in the anesthetic field. In contrast, re-initiation of therapy in January 2026 resulted in rapid and quantifiable contraction of the anesthetic region.
This pattern may suggest that PBM first promotes neural activation or excitability, followed by more sustained structural or functional recovery with continued or repeated stimulation.
While further investigation is needed, this observation may have implications for the timing, frequency, and duration of treatment in managing chronic neurosensory deficits.
To the author’s knowledge, recovery of neurosensory function following a complete deficit of this duration (7 years) has not been well documented in the literature.
While causation cannot be definitively established in a single case report, the temporal relationship between initiation of PBM therapy and rapid neurosensory improvement suggests a clinically meaningful effect.
Clinical Implications
- Chronic neurosensory deficits may retain recovery potential beyond traditionally accepted timelines.
- Visual sensory mapping provides a simple and reproducible method for tracking changes over time.
- PBM represents a noninvasive adjunctive approach in the management of nerve injury.
- Early intervention may further enhance outcomes.
CONCLUSION
Meticulous surgical planning remains the most effective method for preventing neurosensory injury. However, for patients with established nerve damage—particularly those considered beyond the window for recovery—this case demonstrates that meaningful improvement may still be achievable.
The combination of serial neurosensory mapping and PBM therapy offers clinicians both an objective assessment method and a potential intervention pathway in otherwise refractory cases.
ACKNOWLEDGMENT
Special thanks to Ms. Madeline Mai for her help in gathering photos and research.
REFERENCES
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- Sunderland S. A classification of peripheral nerve injuries producing loss of function. Brain. 1951;74(4):491–516.
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- Chow RT, Johnson MI, Lopes-Martins RAB, et al. Efficacy of low-level laser therapy in the management of neck pain: a systematic review and meta-analysis. Lancet. 2009;374(9705):1897–1908.
- Gigo-Benato D, Geuna S, Rochkind S. Phototherapy for enhancing peripheral nerve repair: a review of the literature. Muscle Nerve. 2005;31(6):694–701.
- Khullar SM, Brodin P, Barkvoll P, et al. Preliminary study of low-level laser for treatment of long-standing sensory aberrations in the inferior alveolar nerve. J Oral Maxillofac Surg. 1996;54(1):2–7.
ABOUT THE AUTHOR
Dr. Roknian is a Beverly Hills–based general dentist, implant and laser educator, and national lecturer known for integrating surgical precision with advanced implant, laser, and restorative dentistry. She earned her BS in psychobiology from UCLA and her DMD from Temple University. Dr. Roknian has lectured and published nationally and internationally on implant complications, laser-assisted therapy, surgical risk management, and biologically driven treatment planning. She has helped train more than 2,500 dentists in advanced surgical and restorative workflows, including implant placement, extraction techniques, bone grafting, sinus augmentation, and prosthetic execution. A Fellow of the International College of Dentists and Diplomate of the International Congress of Oral Implantologists, Dr. Roknian is recognized for bringing practical, efficient, and biologically respectful protocols to advanced surgical and laser-based care. She can be reached at [email protected].
Disclosure: Dr. Roknian reports no disclosures.
