Paresthesia

Paresthesia

Among the combination groups of irrigants are sodium hypochlorite mixed with a surfactant and EDTA or citric acid products mixed with surfactants and/...

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Among the combination groups of irrigants are sodium hypochlorite mixed with a surfactant and EDTA or citric acid products mixed with surfactants and/or antibacterial agents. The surfactants may improve the antibacterial or tissue-dissolving abilities of hypochlorite, but the studies conducted thus far are inconclusive. However, evidence seems to indicate considerable antimicrobial activity when surfactants and other antimicrobial materials are added to EDTA or citric acid. Combination products tend to simplify the irrigation process and eliminate the need to use NaOCl rinse after EDTA. Equipment.—Classic equipment consists of a syringe and needle. Needle irrigation applied with care is both effective and sufficient when done using small 27-gauge or preferably 30-gauge needles to access the apical canal. Irrigant exchange beyond the needle tip reaches 1 to 3 mm, depending on needle type and irrigant flow. Sidevented needles may be safer than open-ended needles with positive-pressure irrigation. Solutions tend to be more effective if the irrigant is agitated and constantly refreshed. A gutta-percha point in a size appropriate to the apical canal can be used if needed to facilitate irrigant exchange. Active needle irrigation, sonic activation, and ultrasonic activation are equally effective in increasing tissue dissolution speed using NaOCl and achieve levels up to 10 times those obtained with passive irrigation.

New equipment includes the EndoActivatory, Vibringe, and various ultrasonic devices that use a vibrating tip to direct the irrigant into the canal. The EndoVac uses negative pressure to safely irrigate the apical canal, applying the irrigant to the pulp chamber or coronal root canal, where it is sucked down into the canal and back via the needle.

Clinical Significance.—Root canal treatment includes both instrumentation and irrigation. The most important functions of irrigation are the dissolution of tissue and the antimicrobial effect. Apical irrigation can be especially challenging to achieve effective, safe cleaning. Use of a small 30-gauge side-vented needle and/or negative pressure with NaOCl and EDTA secures the best results in the apical canal.

Haapasalo M, Shen Y, Wang Z, et al: Irrigation in endodontics. Br Dent J 216:299-303, 2014 Reprints available from M Haapasalo, Div of Endodontics, Dept of Oral Biological and Medical Sciences, UBC Faculty of Dentistry, The Univ of British Columbia, 2199 Wesbrook Mall, Vancouver, BC, Canada, V6T 1Z3; e-mail: [email protected]

Paresthesia Background.—The sensations of burning, numbness, or twinging and/or the partial loss of sensitivity can indicate paresthesia, a disturbance of neurosensitivity caused by a neural tissue lesion. Endodontic-related paresthesia requires careful evaluation because of the close anatomic relationship between the root apex and nerve bundles, especially in the jaw. If the condition is severe, it may cause an irreversible condition. The literature on paresthesia as a complication of endodontic treatment was reviewed. Methods.—The literature review noted the causes of paresthesia, diagnostic issues, the nerves most often involved, and treatment choices. Forty cases of paresthesia related to endodontic treatment were identified in publications between 2002 and 2012. Causation.—The inferior alveolar nerve (IAN) and the mental nerve are the most often involved in paresthesia related to endodontic treatment. Usually paresthesia and endodontic infection are observed in teeth with large-

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diameter radicular lesions. The neural injury may result from compression mechanisms, but inflammatory mediators from injured tissue and bacterial products in the periradicular lesions may also be causative. Inflammatory mediators such as interleukin 1, tumor necrosis factor, and nitric oxide exert neurotoxic effects. Bacterial endotoxins such as lipopolysaccharide can also be harmful to neural tissues. Over-instrumentation can also cause damage to the nerve, but research tends to indicate that this form of paresthesia is temporary and resolves during healing. Extrusion of microorganisms can also cause paresthesia, but this has not been studied to date. The cytotoxicity and mechanical pressure exerted by the leakage of sealers into areas near the mandibular canal may cause nerve injury to the IAN and mental nerve. Materials that are most likely to be harmful contain paraformaldehyde. Few of the reported cases involved the innervation of the upper arch. Paresthesia occurring during retreatment of a maxillary central incisor was related

to the extravasation of sodium hypochlorite (NaOCl) into the periradicular tissues. This caused immediate pain and swelling, formation of a sinus tract, and paresthesia in the lower orbital and nasal areas. Excessive root canal preparation may also cause the apical formation to be enlarged and constriction to be lost, so that irrigation products or filling material can extravasate beyond the apex and cause neural injury of chemical or mechanical origin. Bone lesions of endodontic origin may have a large diameter, causing paresthesia usually in the premolar and molar area. The distance between the dental apex and mandibular canal can also contribute to paresthesia development. In the posterior area, the mandibular bone is not particularly dense and contains more trabecular bone. The IAN can act as a route for the dissemination of materials, microorganisms, and irrigating solutions into neural tissue. The apices of third molars can be very close to the IAN. In addition, vacuoles in the mandibular bone in the molar region offer areas where irrigation products and filling material can spread toward the inferior alveolar neurovascular set (Fig 2). Any periradicular infection present weakens the bone barrier between the apex and the neurovascular bundle. In addition, it is common for the neurovascular bundle to follow a path through cancellous bone, which makes the mandibular canal more vulnerable to elements coming from the root canal. Diagnosis.—A complete medical history combined with an assessment of the symptoms provides the diagnosis of paresthesia or neural anesthesia. Contributing findings include reactions of the area to thermal stimuli, mechanical influences, and electrical and chemical tests, although these responses are subjective. Periapical radiographs establish the dental apex–nerve ending relationships, especially in the mandible.

Clinical evaluation of patients who have lingual nerve lesions begins with observing nerve function during pronunciation and swallowing. Palpation of the involved region is also helpful. Clinical neurosensitivity testing includes mechanoceptive tests and nociceptive tests. It can be challenging to detect whether the effect on the nerve is mechanical or chemical. Cone-beam computed tomography (CBCT) is used in the prevention, diagnosis, and treatment of possible paresthesia of endodontic origin. Treatment.—No single approach is appropriate for all cases of paresthesia related to endodontic treatment. Treatment should reflect the causative agent. Paresthesia caused by overfilling of endodontic sealers or drug pastes may respond to surgical removal of the material. The success of this treatment can be altered depending on the time elapsed since the incident, the type of overfilling, and the extent and location of the extruded material. Paresthesia related to infection and inflammation may respond to endodontic treatment, periapical surgery, antibiotic treatment, or extraction. That related to local anesthesia or over-instrumentation usually resolves in a few days with no treatment. If the paresthesia is prolonged or permanent, laceration of the nerve fibers, prolonged pressure, or extrusion of toxic endodontic materials is usually to blame. Removal of the inciting factor is usually required. Surgery for cortical removal, then apical resection, will eliminate apically extruded endodontic sealers and pastes. When the alveolar nerve is involved, especially with compression of the nerve in the second and third molar region, sagittal split osteotomy can be helpful. Decompression of the IAN is achieved by first doing a sagittal mandibulectomy to better visualize the mandibular canal, then

Table 2.—Indications and Contraindications for Microsurgery to Treat Facial Paresthesia (Adapted from Zuniga and Labanca)32 Indications

Fig 2.—Schematic representation of the various causes of paresthesia due to endodontic problems. From the second premolar to the third molar, typical causes are extrusion or diffusion of intracanal medications, periradicular surgery, overfilling and over-instrumentation (beyond the apex), and apical periodontitis. (Courtesy of Alves FR, Coutinho MS, Gonc¸alves LS: Endodonticrelated facial paresthesia: Systematic review. J Can Dent Assoc 80:313, 2014.)

Contraindications

Observation or transection of the suspected nerve No remission of paresthesia after 3 months Pain caused by formation of neuroma Pain caused by foreign body or deformity of the canal Progressive decreasing sensation or increasing sensory pain

Central neuropathic pain Evidence of improvement in paresthesia Neuropraxia Acceptable paresthesia (determined by the patient) Metabolic neuropathy

Medical compromise Older age Very long interval since occurrence of initial trauma (Courtesy of Alves FR, Coutinho MS, Gonc¸alves LS: Endodontic-related facial paresthesia: Systematic review. J Can Dent Assoc 80:313, 2014.)

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removing extraneous materials along with or without a rootend resection. Microneurological techniques can restore function for certain sensory or motor nerve innervations (Table 2).

In addition to these measures, the endodontist should follow-up with the patient within 24 hours of the procedure. If symptoms are present, measures can be taken to identify the paresthesia and institute treatment.

Exploratory surgery done immediately after the diagnosis of trauma to the neural tissue and other diagnostic techniques does not help in defining the extent of nerve damage. Waiting to undertake interventions may be associated with less successful outcomes, although some evidence indicates interventions done up to 12 months after the trauma are successful. In extravasation cases, the cytotoxicity of sealers declines with time.

Discussion.—The literature review indicates that the nerves most often involved in endodontic treatment– related paresthesia are in the jaw. The IAN and mental nerve should be evaluated through anamnesis, nociceptive and mechanoceptive tests, periapical and panoramic radiographs, and CBCT if indicated. Treatment is geared toward the cause of the injury, the extent of the injury, the time that has passed since the injury, and the patient’s responses to the systemic administration of medications.

The use of low-power lasers can accelerate the repair of traumatized biologic tissues by promoting new vascularization. Spontaneous recovery from paresthesia tends to be unlikely after 3 to 6 months. Vitamin B complex supplements may promote myelin sheath development. Prevention.—The occurrence of paresthesia associated with endodontic treatment can be prevented. Among the precautions to take to avoid problems are the following: 

 





Perform a thorough radiographic examination, noting the distance between the radicular apices and/or periapical lesions and the nerve structures. Maintain an appropriate working length. Avoid over-instrumentation and excessive dilatation of the apical foramen. Irrigate using chlorhexidine if the apex is excessively broad or incompletely formed. Administer B vitamins immediately if filling material or solution is extruded close to the nerve.

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Clinical Significance.—Prevention is the most important approach with respect to paresthesia related to endodontic treatment. Taking the steps outlined offers the best chance to achieve an effective endodontic treatment without complications related to nerve injury.

Alves FR, Coutinho MS, Gonc¸alves LS: Endodontic-related facial paresthesia: Systematic review. J Can Dent Assoc 80:e13, 2014 Reprints available from FR Alves, Faculty of Dentistry, Estacio de Sa Univ, Av Alfredo Baltazar da Silveira, 580/cobertura, Recreio, Rio de Janeiro, RJ, Brazil 22790-710; e-mail: flavioferreiraalves@ gmail.com