Damage to the alveolar nerves, which provide sensation to the lower face and mouth, can occur following dental procedures, leading to altered feeling. These nerves, primarily the inferior alveolar nerve and the lingual nerve, are branches of the trigeminal nerve and are located close to the teeth and jawbone. While most nerve injuries following dental work are temporary, a small percentage can result in persistent sensory deficits.
Anatomy and Function of the Alveolar Nerves
The Inferior Alveolar Nerve (IAN) and the Lingual Nerve (LN) originate from the mandibular division of the trigeminal nerve, the fifth cranial nerve responsible for sensation in the face. The IAN travels through the lower jawbone, or mandible, supplying sensory innervation to the lower teeth and the bone itself. This nerve continues as the mental nerve, which emerges onto the face to provide sensation to the lower lip, chin, and the gums on the cheek side.
The Lingual Nerve follows a different path, traveling near the inner surface of the mandible, close to where wisdom teeth are located. Its primary role is to provide somatic sensory innervation to the front two-thirds of the tongue, the floor of the mouth, and the gums on the tongue side. The Lingual Nerve also carries fibers from the chorda tympani, a branch of the facial nerve, which is responsible for the sense of taste in the anterior tongue.
Procedures That Lead to Injury
Nerve damage often results from procedures performed in the lower jaw due to the close anatomical relationship between the nerves and the surgical sites. The most common cause of Inferior Alveolar Nerve and Lingual Nerve injury is the surgical removal of impacted mandibular third molars (wisdom teeth). During this surgery, mechanical trauma such as stretching, crushing, or cutting can occur, particularly when a tooth is deeply impacted or positioned close to the mandibular canal housing the IAN.
Another cause of injury is the placement of dental implants in the posterior mandible. Damage can result from direct mechanical trauma if the drill or the implant itself violates the mandibular canal, or from thermal injury caused by the heat generated during drilling. Prompt recognition is necessary, as an implant violating the nerve canal may need immediate removal to prevent permanent damage.
Root canal therapy, or endodontic treatment, can also lead to nerve damage, typically from chemical injury. This occurs when filling materials, such as endodontic sealers, are inadvertently extruded beyond the root tip and into the mandibular canal where the IAN resides. The neurotoxic nature of certain chemicals in these sealers can cause inflammation and direct damage to the nerve fibers. Less commonly, nerve injury can result from local anesthetic injections, attributed to direct needle trauma or a neurotoxic reaction to the anesthetic solution itself.
Identifying Symptoms and Severity
The symptoms of alveolar nerve damage are characterized by altered sensation in the areas supplied by the affected nerve. A primary presentation is paresthesia, an abnormal but not necessarily unpleasant sensation often described as tingling, prickling, or a feeling of “pins and needles.” This can range from a partial loss of sensitivity (hypoesthesia) to a complete absence of feeling (anesthesia).
A more concerning symptom is dysesthesia, which describes an unpleasant, abnormal sensation. Dysesthesia often manifests as neuropathic pain, which can include a burning or crawling sensation, or an increased pain response to normally painful stimuli (hyperalgesia). Patients may also experience allodynia, which is pain caused by a stimulus that typically does not provoke pain, such as light touch.
Lingual Nerve injury specifically presents with altered sensation in the tongue, and often includes an altered or complete loss of taste due to the involvement of the chorda tympani fibers. These sensory deficits can lead to functional disturbances, such as:
- Lip or tongue biting.
- Drooling.
- Difficulty with speech.
- Difficulty controlling food while eating.
The severity of the injury is determined by the duration of symptoms; transient symptoms resolving within a few weeks are common, but symptoms persisting beyond six months are considered permanent.
Diagnosis, Prognosis, and Treatment
Initial evaluation of suspected nerve injury involves a thorough history and a neurosensory examination to map the area of altered sensation and quantify the degree of deficit. Diagnostic testing may include two-point discrimination tests, which assess the ability to distinguish two separate points of touch, and pin-prick tests, which evaluate the perception of sharp stimuli. Imaging, such as Cone-Beam Computed Tomography (CBCT), is often used to visualize the nerve canal and check for mechanical causes like a broken instrument fragment or an extruded root canal filling material.
The long-term outlook, or prognosis, is based on the severity of the initial nerve damage, often categorized using the Seddon classification system. The mildest injury, neurapraxia, is a temporary blockage of nerve conduction without structural damage to the axon; recovery is typically complete within days to weeks. Axonotmesis is more severe, involving damage to the axon while the nerve’s connective tissue sheath remains intact, allowing for eventual regeneration at a rate of approximately 1–3 mm per day.
The most severe injury, neurotmesis, involves complete division or disruption of the entire nerve structure, which has a poor prognosis for spontaneous recovery and usually requires surgical intervention. For all injuries, a period of observation, usually three to nine months, is recommended, as most temporary injuries will resolve within this timeframe.
If the sensory deficit persists, non-surgical treatment may involve pharmacological management, including anticonvulsant medications like pregabalin or gabapentin, which are used to control neuropathic pain. Other non-surgical approaches include the use of corticosteroids to reduce inflammation and vitamin complexes for neuroprotective benefits. If a persistent sensory deficit remains after the observational period, surgical repair, such as microsurgical nerve repair or decompression, may be considered. Early referral to a specialist, preferably within three months of injury, is associated with a higher likelihood of functional sensory recovery.