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The inferior alveolar and lingual nerves provide sensation to the structures of the lower face, including the teeth, skin, and oral mucosa. Injuries to these nerves can be caused by surgical procedures, trauma, or tumors involving the mouth and mandible. Such injuries can cause significant discomfort during daily activities, including chewing, eating, and speaking. Healthcare providers need to understand the anatomical course of the nerves to minimize the risk of injuries. However, if an injury occurs, clinicians should be able to recognize it and accurately assess the extent of the damage. Moreover, patients with nerve damage should be managed promptly to minimize the likelihood of long-term dysfunction. This activity will cover the etiology, presentation, diagnosis, and management of inferior alveolar and lingual nerve injuries. Objectives: Identify the possible causes of inferior alveolar nerve and lingual nerve injuries. Outline clinical presentations of inferior alveolar nerve and lingual nerve injuries. Review how to diagnose and classify inferior alveolar nerve and lingual nerve injuries. Summarize management of inferior alveolar nerve and lingual nerve injuries. Access free multiple choice questions on this topic.

The inferior alveolar nerve (IAN) and the lingual nerve are branches of the mandibular division (V3) of the trigeminal nerve (CN V). The IAN supplies somatic sensory innervation to the chin, lower lip, lower vestibular gingiva, molars, premolars, and alveolar bone. The lingual nerve supplies somatic sensory innervation to the lingual oral gingiva and the anterior two-thirds of the tongue.[1] See Image. Anatomical Dissection, Lingual Nerve. Although relatively uncommon, these nerves can be damaged during procedures performed near the mandible or lower face; certain mandibular fractures and tumors may also injure these nerves. Patients with these injuries may experience significant discomfort during daily activities, including chewing, eating, and speaking. Healthcare providers, especially dental professionals, should be able to identify and properly manage these injuries to minimize the risk of permanent neurosensory deficits.

It is important to understand the anatomy of the IAN and the lingual nerve to avoid injury to these nerves. The mandibular branch (V3) of the trigeminal nerve exits the skull through the foramen ovale to enter the infratemporal fossa, where the IAN and lingual nerve branch off from it. The IAN enters the mandibular foramen of the ramus. It runs within the body of the mandible to supply sensory innervation to the mandibular dentition, mandibular vestibular mucosa, and gingiva, as well as the skin of the chin and lower lip.[2] The lingual nerve travels inferiorly between the mandibular ramus and the medial pterygoid muscle, then passes anteriorly near the mandibular lingual alveolar crest. Once the lingual nerve has passed the retromolar region, it travels anteriorly, along the lateral aspect of the hyoglossus muscle, and deep to the mylohyoid muscle. The lingual nerve supplies somatic sensation to the lingual gingiva and anterior two-thirds of the tongue. Of note, the chorda tympani nerve, the branch of the facial nerve that provides gustatory sensation to the anterior two-thirds of the tongue, joins the lingual nerve at the level of the inferior border of the lateral pterygoid muscle.[2] This is important to bear in mind because damage to the lingual nerve is likely to injure the chorda tympani, resulting in altered taste and somatosensory sensation on the affected side. Local anesthetic injections are performed before most surgical procedures, and both the IAN and lingual nerve may be injured during attempts to place blocks around them (see Figure. Conventional Inferior Alveolar Nerve Block). It is very rare, but the needle or the local anesthetic can cause direct or indirect damage to the nerve. The risk is especially increased during the IAN block because the needle travels in proximity to both the IAN and the lingual nerve as they descend medial to the ramus of the mandible. Three theories may explain how nerve damage occurs in these situations.[3] The injection needle may cause direct axonal trauma if it comes in contact with or penetrates the nerve. Another theory is that the needle may damage the epineural blood vessels and cause a localized hematoma, causing a compression injury to the nerve or forming reactive fibrosis or scar. The final hypothesis is that the local anesthetic itself can cause cytotoxic injury during metabolism.

The injection needle may cause direct axonal trauma if it comes in contact with or penetrates the nerve. Another theory is that the needle may damage the epineural blood vessels and cause a localized hematoma, causing a compression injury to the nerve or forming reactive fibrosis or scar. The final hypothesis is that the local anesthetic itself can cause cytotoxic injury during metabolism. Another relatively common cause of IAN and lingual nerve injury is mandibular third molar extraction.[1] The inferior alveolar nerve can be damaged when the inferior alveolar canal is exposed or disrupted during surgery; surgical burs, elevators, or displaced tooth fragments may injure the nerve. The lingual nerve can be injured by surgical incisions or by crush or traction injuries resulting from aggressive retraction or suturing. Mandibular orthognathic surgery also involves fracturing the mandible, occasionally resulting in IAN damage secondary to exposure and manipulation of the nerve in its canal.[4] Likewise, mandibular fractures from trauma (frequently physical altercations or motor vehicle accidents) can lead to similar damage. Dental implant placement can cause IAN injury from either direct damage to the nerve within its canal or from thermal injury due to drilling.[3] Endodontic treatment can also lead to nerve damage from excessive instrumentation and from the chemicals that are used during the procedure.

The reported incidence of IAN and lingual nerve injuries varies within the literature and depends greatly upon the etiology of the injury. Local anesthetic injection-related nerve injuries are rare, and patients tend to recover nerve function spontaneously (85-94% of the time).[5][6] Mandibular third molar extraction is the leading surgical cause of IAN and lingual nerve injury, but rates fluctuate with operator experience and technique.[1] A 2012 study by Guerrero et al. reported incidences of IAN injury ranging from 0.4% to 13.4% and of lingual nerve injury ranging from 0% to 11% after third molar extractions.[7] The incidence of persistent IAN dysfunction ranged from 0% to 1.6%.[8] For lingual nerve injury, the majority recovered, but 0.5-0.6% had persistent dysfunction.[9] In dental implant surgery, the incidence of temporary nerve damage ranges from 0 to 24%, and that of persistent injury ranges from 0 to 11%. There is a widely varying incidence of nerve injury resulting from mandibular orthognathic surgery; a prospective study published by Poort et al. in 2009 reviewed 20 years of procedures and reported a 20-98% incidence of IAN injury with a 0 to 82% rate of persistent dysfunction.[8] Agbaje and colleagues' 2015 systematic review of IAN injuries following bilateral sagittal split osteotomy concluded that standardized assessment and further research are required to accurately assess the incidence.[4] With respect to non-iatrogenic injuries, the incidence of IAN damage due to traumatic mandibular fracture is 46 to 81%. The rates increase, however, after open reduction and internal fixation (77%-91%), with permanent dysfunction occurring in 0%-45% of cases.[8]

Two systems for classifying nerve injury severity based on histological changes are commonly employed: those of Seddon and Sunderland (see Table: Seddon and Sunderland Classification of Nerve Injury).[10][11] Seddon's classification system is simpler, dividing injuries into neuropraxia, axonotmesis, and neurotmesis. Neuropraxia is the mildest form of nerve injury, characterized by transient conduction block resulting from trauma to endoneurial capillaries, which leads to edema and potentially focal demyelination without axonal degeneration. This type of injury typically results in a full, spontaneous recovery. Axonotmesis occurs when there is an injury to the axons and potentially 1 or more of the internal connective tissue layers (endoneurium and perineurium). See Image. Neurology, Nerve Fascicle, Fasciculus, Epineurium. Although these injuries result in axonal degeneration, at least some recovery can be expected because axons can regenerate within the intact epineurium. If the endoneurium remains intact, complete recovery is expected; however, if the endoneurium or perineurium is violated, the prognosis is poorer. Neurotmesis is the most severe type of injury, characterized by complete transection of the nerve, including the axons and all of the connective tissue layers. In such cases, the likelihood of spontaneous recovery is low.[3] Sunderland's classification of nerve injury further characterizes injuries based on the involvement of each layer of neural connective tissue. The first degree corresponds to neuropraxia in Seddon's classification, which involves disruption of myelin sheaths but leaves axons and the rest of the neural architecture intact. Seddon's "axtonotmesis" category is divided in the Sunderland system into 3 distinct categories. Second-degree injury occurs when only the axons are damaged, but all the connective tissue layers remain intact; in these cases, as in first-degree injuries, full recovery is expected. The third-degree injury involves both axonal and endoneurial injuries.

Sunderland's classification of nerve injury further characterizes injuries based on the involvement of each layer of neural connective tissue. The first degree corresponds to neuropraxia in Seddon's classification, which involves disruption of myelin sheaths but leaves axons and the rest of the neural architecture intact. Seddon's "axtonotmesis" category is divided in the Sunderland system into 3 distinct categories. Second-degree injury occurs when only the axons are damaged, but all the connective tissue layers remain intact; in these cases, as in first-degree injuries, full recovery is expected. The third-degree injury involves both axonal and endoneurial injuries. Fourth-degree injury involves damage to all structures except the epineurium: the axons, the endoneurium, and the perineurium. Fourth-degree injuries, therefore, have worse prognoses than first, second, or third-degree injuries. Sunderland's fifth-degree injury is characterized by disruption of all nerve structures (nerve transection), corresponding to neurotmesis in Seddon's classification. First-, second-, and third-degree injuries are likely to recover spontaneously; however, fourth- and fifth-degree injuries are unlikely to achieve full sensory recovery.[3]

Patients with IAN and/or lingual nerve injury typically present with chief complaints of altered sensation in the lower lip, chin, mandibular teeth, gingiva, and tongue. Specifically, patients with lingual nerve injury are also likely to report altered taste on the ipsilateral anterior tongue due to concomitant chorda tympani damage. The ability to move the tongue and lower face should remain intact, though, as the hypoglossal and facial nerves are responsible for motor innervation of these areas. That said, a change in sensation in the region can interfere with numerous daily activities, including speech, eating, drinking, kissing, applying makeup, and shaving.[12] The quality and extent of altered sensations vary substantially among patients, who may experience paresthesias, hypo- or anesthesia, and dysesthesias.[3] Paresthesia is an abnormal sensation that is not necessarily unpleasant, such as a feeling of pins and needles. Hypesthesia is a decrease in sensation, and anesthesia is the complete absence of sensation. Anesthesia often leads patients to believe that the affected area is paralyzed because they cannot feel any movement, but this perception is readily corrected with a mirror. Dysesthesia, on the other hand, is an abnormal sensation that is unpleasant, such as pain. Examples of dysesthesias include hyperalgesia (increased pain response to painful stimuli), hyperpathia (a painful response to repeated stimuli), anesthesia dolorosa (pain in the area of anesthesia), and allodynia (pain from non-painful stimuli).

Evaluation of patients with IAN and lingual nerve injuries can be divided into subjective and objective evaluations. Perception of sensation varies among patients; therefore, documenting the neurosensory deficit's quality, extent, and location at each patient visit improves longitudinal assessment of recovery or lack thereof. Additionally, patient-reported outcomes, such as the McGill Pain Questionnaire and visual analog scales, are useful for outcome tracking.[8][13] After collecting subjective data, a variety of objective tests can be conducted to assess neurosensory deficits following IAN and lingual nerve injuries. These tests can be divided into 2 categories: mechanoreceptive and nociceptive.[8] Mechanoceptive testing evaluates non-painful stimuli, including static light touch, brush-directed stroking, and 2-point discrimination. Nociceptive testing typically involves pinprick and thermal discrimination. The precise location and extent of any positive findings should be carefully documented. The static light touch test assesses the integrity of A-beta fibers; a cotton wisp or a Semmes-Weinstein monofilament can be used to perform the test.[8] Brush directional discrimination assesses A-alpha and A-beta fibers, which detect vibration, touch, and flutter.[3] With eyes closed, patients are asked in which direction a brush or a filament is moving. Two-point discrimination can also assess A-alpha or C fibers if sharp instruments are used. Either blunt or sharp instruments can be used to determine the minimum distance between 2 stimuli at which a patient can appreciate 2 distinct points of contact; a normal value is roughly 5 mm.[14] The pinprick test assesses A-delta and C fibers by determining whether a patient perceives pressure and/or sharp pain from a needle. Thermal discrimination evaluates the integrity of A-delta fibers for detecting warmth and C fibers for detecting cold.[3] There is no universally accepted method for evaluating IAN and lingual nerve injury; however, the following grading system characterizes the extent of nerve injury based on responses to the aforementioned tests. This grading system divides neurosensory deficits into 3 levels: Level A (direction and 2-point discrimination; A-alpha and A-beta fibers), Level B (contact detection; A-beta and A-delta fibers), and Level C (pain sensitivity; C fibers).

There is no universally accepted method for evaluating IAN and lingual nerve injury; however, the following grading system characterizes the extent of nerve injury based on responses to the aforementioned tests. This grading system divides neurosensory deficits into 3 levels: Level A (direction and 2-point discrimination; A-alpha and A-beta fibers), Level B (contact detection; A-beta and A-delta fibers), and Level C (pain sensitivity; C fibers). In a patient without deficits, no altered sensation should be noted. For a patient with mild impairment, an abnormal response to level A testing, with intact responses to levels B and C, should be noted; such a constellation of findings indicates complete recovery. With moderate nerve injury, abnormal A and B test results are noted, whereas C test responses are normal; patients in this situation may recover partially or completely. With a severely impaired or severed nerve, abnormal responses are noted on all levels, and complete recovery should not be expected.[8] Patients are typically tested at level A first, then at level B, and finally at level C.

To minimize the risk of IAN and lingual nerve injuries, clinicians must have a thorough understanding of neural anatomy during procedures around the mandible or on the floor of the mouth (see Image. Lingual Nerve and its Anatomical Relations). Despite all reasonable preventive measures, however, nerve injury may still occur. This is why clinicians should weigh the risks and benefits of lower facial procedures and discuss them with patients to educate them, develop treatment plans, and obtain informed consent. Once IAN or lingual nerve injury is identified, the clinician should assess the extent of damage by performing the neurosensory testing detailed above. Unfortunately, there is no universally accepted standard for managing IAN and lingual nerve injury. Treatment strategies vary among clinicians depending on experience and comfort level. Listed below are some of the more commonly employed treatment options for IAN and lingual nerve injury. Conservative Management Corticosteroids: High-dose corticosteroid therapy may be initiated immediately after injury to reduce inflammation, potentially minimizing the extent of nerve damage. Evidence regarding the effectiveness of corticosteroids in preventing the development of nerve deficits is weak; however, steroids are widely used by neurosurgeons after intracranial surgery and have been shown to improve outcomes in facial nerve palsy.[9][15] Topical medications: For patients with pain due to nerve injury, there is some evidence that topical agents can help alleviate symptoms. Capsaicin, lidocaine, clonidine, and clonazepam can be applied to the affected areas.[9] Systemic pharmacologic agents: Oral medications can also be used to relieve pain from nerve injury. The use of tricyclic antidepressants and membrane stabilizers such as antiepileptics, lidocaine derivatives, and muscle relaxants has been described.[9] Surgical Management Surgical intervention should be considered when there is no improvement in neurosensory function for more than 3 months and the deficit is unacceptable to the patient.[1]

Systemic pharmacologic agents: Oral medications can also be used to relieve pain from nerve injury. The use of tricyclic antidepressants and membrane stabilizers such as antiepileptics, lidocaine derivatives, and muscle relaxants has been described.[9] Surgical Management Surgical intervention should be considered when there is no improvement in neurosensory function for more than 3 months and the deficit is unacceptable to the patient.[1] External nerve decompression: If nerve compression is suspected to cause the neurosensory deficit, surrounding structures may be released or removed to relieve pressure on the nerve. A 2012 study published by Bagheri et al. reported an 85% rate of sensory recovery after decompression.[16] Mozsary and colleagues also noted that decompression might lead to faster recovery than other nerve repair procedures.[17] Direct neurorrhaphy: A severed nerve may be repaired primarily via suture neurorrhaphy if there is not a significant amount of missing nerve and the ends can be brought together without tension. The reported likelihood of sensory recovery varies widely in the literature but may be as high as 90% with careful technique and optimal circumstances.[16] Sleeves: If the nerve stumps cannot reach each other in a tension-free manner, but the gap between them is small, collagen sleeves may be used to facilitate nerve regeneration in the absence of direct end-to-end coaptation. Success rates exceed 80%, particularly when the gap is ≤3 mm.[16][18]

Direct neurorrhaphy: A severed nerve may be repaired primarily via suture neurorrhaphy if there is not a significant amount of missing nerve and the ends can be brought together without tension. The reported likelihood of sensory recovery varies widely in the literature but may be as high as 90% with careful technique and optimal circumstances.[16] Sleeves: If the nerve stumps cannot reach each other in a tension-free manner, but the gap between them is small, collagen sleeves may be used to facilitate nerve regeneration in the absence of direct end-to-end coaptation. Success rates exceed 80%, particularly when the gap is ≤3 mm.[16][18] Nerve reconstruction with autogenous grafts: When the injury results in a gap between the nerve stumps >3 mm, nerve or vein grafts can be used to bridge the gap. Great auricular nerve or sural nerve grafts are most commonly harvested for this purpose, with the great auricular nerve being more convenient to use because of its location in the neck. In contrast, the sural nerve is better suited to providing longer graft segments, up to 40 cm if necessary. If no readily available nerves are available for harvest, or the patient refuses to permit nerve harvest, posterior facial or external jugular veins can be used instead. However, veins lack the structural architecture (endoneurium, perineurium, epineurium) of nerves.[1] Sensory recovery rates are notably higher when nerves are used (87.3%) compared to when veins are used (60%).[1][16] While veins appear to be less effective as interposition grafts than autologous nerves are, they can be used instead of collagen sleeves to wrap and protect neurorrhaphy or even to facilitate nerve coaptation with gaps ≤3 mm. Removal of the offending factor: When placement of a foreign body causes nerve dysfunction, the foreign body should be removed to limit inflammation and expedite recovery. For example, if dental implant placement results in damage to the inferior alveolar nerve, the implant should be removed, ideally within 36 hours of placement.[1]

Even though they are less common than iatrogenic injury or trauma, other conditions can alter trigeminal nerve sensation and lead to clinical presentations similar to IAN and lingual nerve injuries.[19] These include: Benign or malignant tumors involving the trigeminal nerve tract Autoimmune disorders: lupus erythematosus, dermatomyositis, progressive sclerosis, Sjögren syndrome, rheumatoid arthritis, and other connective tissue diseases Infections: herpes zoster, herpes simplex virus, syphilis, leprosy Multiple sclerosis Vertebrobasilar disease Sarcoidosis Amyloidosis Sickle cell anemia

Ideally, an IAN or lingual nerve injury would be identified at the time of injury, enabling immediate repair to maximize the likelihood of sensory recovery. If the injury is not identified until after the surgery, the likelihood of spontaneous recovery decreases, particularly if there is no improvement within 3 months. In these cases, surgical intervention should be considered. It remains unclear, however, what the optimal time point is for repairing an injured nerve identified after completion of the procedure in which it was injured. The prognosis for sensory recovery after surgical repair of an injured IAN or lingual nerve varies across studies; however, a 2021 systematic review and meta-analysis comparing outcomes at different time points after injury found a trend toward better recovery with earlier repair.[20] Ideally, the nerve would be reconstructed within 3 to 6 months of injury, as there appears to be a poorer prognosis for injuries older than 9 months at the time of repair.[1]

The main complications of IAN and lingual nerve injury are persistent or worsening neurosensory deficits. Dysfunction of these nerves can cause significant discomfort or distress during daily activities, including lip and tongue biting and drooling. More severe injuries are less likely to recover spontaneously and may require surgical intervention, which itself is not without risk.

Inferior alveolar nerve and lingual nerve injuries are rare but recognized complications of numerous oral and maxillofacial procedures. Clinicians should be familiar with risk factors that increase the risk of nerve injuries (e.g., complex anatomy or prior surgery) and be able to weigh the risks and benefits when deciding whether to undertake surgery on the lower face and which techniques to employ. Additionally, it is crucial to counsel patients on the risks of nerve injury and other potential operative sequelae when making shared decisions about treatment planning.

Injuries to the IAN and the lingual nerve most commonly result from dental procedures. If an affected patient does not demonstrate spontaneous sensory recovery with conservative management within 3 months of injury, the patient should be referred to a specialist, such as an oral and maxillofacial surgeon, who can determine whether other treatment modalities, including surgical repair or decompression, are appropriate. Early recognition of IAN and lingual nerve injury and prompt referral to clinicians who can evaluate and treat these complications increases the likelihood of functional sensory recovery. This may require coordination between dental providers and family practitioners, depending on who the patient first seeks out for care.