The mandibular nerve (V3 branch) is the third and largest division of the trigeminal nerve, the fifth cranial nerve. This nerve carries both sensory and motor fibers, controlling a range of functions in the lower face. Its sensory component provides feeling to the lower lip, chin, lower teeth and gums, and the anterior two-thirds of the tongue. The motor component sends signals to the muscles of mastication, which control chewing. Damage to this nerve interrupts both sensation and movement, leading to various difficulties in daily life.
Common Causes of Injury
The most frequent cause of mandibular nerve injury is damage occurring during dental procedures, accounting for approximately 60% of reported cases. The inferior alveolar nerve is particularly vulnerable during the extraction of impacted third molars (wisdom teeth) due to its close anatomical relationship to the tooth roots. Injury can also occur during dental implant placement from direct mechanical trauma by the drill or from thermal injury caused by inadequate cooling during bone preparation.
Other iatrogenic causes include the accidental extrusion of root canal filling materials, such as endodontic sealer, into the mandibular canal. This material can exert toxic or compressive effects on the nerve. Local anesthetic injections, especially those targeting the inferior alveolar nerve, can sometimes result in nerve damage due to direct needle trauma or the neurotoxicity of the anesthetic agent itself.
Physical trauma to the face and jaw is another significant cause of mandibular nerve damage. Fractures of the mandible, often resulting from motor vehicle accidents or physical altercations, can lead to compression, stretching, or laceration of the nerve where it travels through the bone. The nerve can become entrapped within the fracture site, leading to persistent symptoms even after the bone is set.
In a smaller number of cases, the nerve can be affected by pathological issues not caused by an external event. This includes the presence of tumors, cysts, or infectious processes that grow and exert pressure directly on the nerve tissue. Such lesions slowly compress the nerve over time, leading to a progressive loss of function and sensation.
Sensory and Motor Symptoms
Symptoms arising from mandibular nerve damage are categorized into sensory and motor deficits, reflecting the nerve’s dual function. Sensory symptoms are often the most noticeable, including abnormal sensations in the lower lip, chin, and sometimes the tongue. A common initial presentation is paresthesia, described as a tingling or “pins and needles” feeling in the affected area.
If the damage is more extensive, patients may experience anesthesia (complete loss of sensation) or hypoesthesia (reduced ability to feel light touch or temperature changes). Damage can also lead to dysesthesia, where a non-painful stimulus is perceived as unpleasant or painful. This neuropathic pain can manifest as a burning sensation or an electric shock-like feeling.
When the injury involves the lingual nerve, sensory deficits extend to the anterior two-thirds of the tongue. This can result in altered taste perception, as the chorda tympani nerve, which carries taste fibers, is often damaged concurrently. Patients with significant sensory loss in the lower lip and tongue may also report difficulty with speech articulation, chewing, and keeping food inside the mouth.
Motor symptoms occur when the nerve fibers controlling the muscles of mastication are compromised. This damage leads to weakness or difficulty when trying to chew or clench the jaw tightly. The inability to fully contract these muscles affects the efficient grinding of food. In severe, long-standing cases, the lack of nerve input can eventually lead to muscle atrophy, where the affected chewing muscles visibly decrease in size.
Diagnostic Testing and Severity Assessment
Healthcare providers confirm mandibular nerve damage and determine its extent using clinical examination and specialized testing. The initial assessment involves clinical sensory testing, which objectively measures the patient’s ability to perceive different stimuli in the affected area. This includes the pinprick test for pain perception and the two-point discrimination test, which measures the smallest distance between two points the patient can distinguish as separate.
Imaging studies are often necessary to rule out underlying structural causes or to visualize the nerve’s relationship to nearby structures. Computed Tomography (CT) scans identify fractures or foreign objects, such as extruded endodontic material, compressing the nerve within the bony canal. Magnetic Resonance Imaging (MRI), particularly Magnetic Resonance Neurography, provides a detailed image of the nerve tissue itself, helping to detect swelling, scarring, or a complete tear.
Electrophysiological testing, such as nerve conduction studies or electromyography (EMG), helps confirm the diagnosis by measuring the electrical activity of the nerve and the muscles it supplies. These tests distinguish between a nerve injury that blocks signal transmission and one that causes physical degeneration of the nerve fibers. The severity of the damage is classified using systems like the Seddon classification, which distinguishes three main types.
Seddon Classification of Nerve Injury
Neurapraxia is the mildest form, involving a temporary conduction block without physical damage to the axon, and has the best prognosis for full recovery. Axonotmesis involves damage to the nerve axon, but the protective outer sheath remains intact, allowing for potential regeneration along the preserved pathway. Neurotmesis is the most severe, representing a complete physical disruption or severing of the entire nerve trunk, which requires surgical intervention for meaningful recovery.
Treatment Pathways and Recovery Outlook
The management of mandibular nerve injury depends heavily on the severity classification and the time elapsed since the injury occurred. For the mildest injuries, such as neurapraxia or minor axonotmesis, the initial approach is expectant management. The patient is monitored closely over weeks to months, as many temporary injuries caused by compression or stretching resolve spontaneously as swelling subsides.
If the patient experiences persistent, unpleasant abnormal sensations like dysesthesia, medical management controls the neuropathic pain. Medications include anticonvulsants or tricyclic antidepressants, which stabilize the overactive nerve signals causing chronic pain. These drugs improve the patient’s comfort and quality of life while awaiting potential natural recovery, but they do not repair the nerve.
Surgical intervention is considered when there is no measurable improvement in sensation after three to six months, or if imaging indicates a complete nerve transection or severe compression. The goal of surgery is to explore the injury site and either remove scar tissue impeding regeneration or physically repair the nerve ends. This involves direct nerve repair (suturing nerve ends together) or nerve grafting (using a segment of a non-essential sensory nerve to bridge a gap).
The prognosis for recovery is influenced by the patient’s age, the cause of the injury, and the severity classification. Recovery is a slow process, as nerve fibers regenerate at about one millimeter per day, meaning functional return can take many months. While surgical techniques often achieve functional sensory recovery (a return of useful protective sensation), complete pre-injury sensation is not always fully restored.