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 Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 5  |  Issue : 2  |  Page : 138-145

Mental nerve paraesthesia: A review of causes and two endodontically related cases


1 Department of Dentistry, New Mowasat Hospital, Salem Al Mubarak St, Kuwait
2 Department of Restorative Sciences, Faculty of Dentistry, Kuwait University, Jamal Abdul Nasser St, Kuwait; School of Dentistry, University of Queensland, St Lucia, Queensland, Australia, Australia

Date of Web Publication20-Apr-2015

Correspondence Address:
Unni Krishnan
PO Box 9368, Salmiya - 22094
Kuwait
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1658-5984.155454

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  Abstract 

Mental nerve paraesthesia can occur as a result of a variety of reasons. Paraesthesia following endodontic treatment is an uncommon treatment complication. Causes of paraesthesia in the mental nerve region are reviewed and two cases involving endodontic treatment are discussed. In the first instance, a patient presented with difficulty in swallowing and severe pain localized to her right mandible, with numbness of her lower lip. Paraesthesia resolved quickly with endodontic treatment. In the second instance, a patient referred for treatment a mandibular second premolar developed profound paraesthesia in the distribution of the mental nerve after treatment. The local anesthetic used was 4% articaine by infiltration. CBCT imaging revealed two accessory mental foramen and slight extrusion of sealant into one of the neurovascular exits. Possible causes of paraesthesia are discussed in the light of the literature review. CBCT imaging may be useful in the diagnosis and management of these conditions.

Keywords: Articaine, accessory mental foramen, Cone beam computed tomography, endodontics, paraesthesia, root canal treatment


How to cite this article:
Krishnan U, Moule AJ. Mental nerve paraesthesia: A review of causes and two endodontically related cases. Saudi Endod J 2015;5:138-45

How to cite this URL:
Krishnan U, Moule AJ. Mental nerve paraesthesia: A review of causes and two endodontically related cases. Saudi Endod J [serial online] 2015 [cited 2019 Nov 13];5:138-45. Available from: http://www.saudiendodj.com/text.asp?2015/5/2/138/155454


  Introduction Top


Paraesthesia is an abnormal sensation, provoked or spontaneous, which is usually described by a patient as burning, pricking, tickling or tingling. [1] According to the taxonomy of the International Association of Study of Pain (IASP) paraesthesia, though abnormal, is not unpleasant. [2] The term dysesthesia is used to describe abnormal sensations which are painful. [2] However, for common clinical communication, the term paraesthesia is usually used to describe all abnormal sensations in skin and mucosa, whether pleasant or otherwise; it may be compounded by numbness. [1]

Paraesthesia can occur due to diseases and conditions affecting the peripheral nervous system such as nerve injury from trauma, osteomyelitis, polyneuropathy as in diabetes mellitus and infections such as shingles. It may also originate from the central nervous system as seen in disorders such as stroke, multiple sclerosis and migraine. [1] Paraesthesia in the face, particularly in the lower jaw, may result from dental causes. Mental and inferior alveolar nerve paraesthesia is an uncommon complication which can be associated with endodontic treatment. Careful consideration of all the possible causes is necessary for accurate diagnosis, management and prevention. Some aspects relating to paraesthesia of endodontic origin have been reviewed by Ahonen [3] and Mohammadi. [4] In this report the possible causes of paraesthesia in the mental nerve region are reviewed, and two cases which have involved endodontic treatment are discussed.


  Non-Dental causes of Mental Nerve Paraesthesia Top


There are a variety of non-dental causes for mental or inferior alveolar nerve (IAN) paraesthesia. Unilateral non-painful mental nerve numbness can be of viral origin. Such numbness is often of rapid in onset and usually lasts for 6-8 weeks with full recovery. Varicella zoster infection presenting with unilateral paraesthesia or facial or dental pain alone, without vesicular eruptions can be a diagnostic challenge as the initial presentation is suggestive of dental disease. [5],[6] Pain if present, can be intense. Vesicular eruptions, which usually occur within a few days, help confirm the diagnosis, but these can be delayed for some time. The possibility that numb - chin syndrome characterized by hypoesthesia or paraesthesia of the lower lip, chin and gingival mucosamight represent the initial manifestation of malignancy should always be considered. [7],[8],[9] Mental paraesthesia which is increasing in intensity or distribution over time warrants careful investigation. Hematological disorders, including sickle cell anemia, thalassemia and megaloblastic anemia has been associated with mental nerve paraesthesia. [10] As has multiple sclerosis, [11] diabetic neuropathy, [12] sarcoidosis, [13] Sjogren's syndrome, [14] trigeminal neuropathy, [15] Lyme's disease [16] and temporal arteritis [17] can also manifest as numb chin syndrome. Mental nerve nueropathy has also been reported to occur after hepatitis B vaccination. [18] Hyperparathyroidism may also be associated with paraesthesia but this is usually circum-oral in distribution, as is the case in hyperventilation syndrome and patients on the antiretroviral medication, Ritonavir. [19],[20]


  Dental causes of mental nerve paraesthesia Top


Procedural errors during endodontic therapy, mandibular third molar extraction, implant placement and rarely orthodontics can result in inadvertent physical, inflammatory or chemical injury to the neurovascular bundle. [21],[22] Periapical infection before and after endodontic therapy resulting in mental and inferior alveolar nerve paraesthesia is also well-documented. [23],[24],[25] The mechanism of induction of paraesthesia in infection may be three fold. The hemodynamic changes associated with periapical infection can result in mechanical pressure-induced neuropraxia depending on the anatomical proximity to the neurovascular bundle. [26] Secondly, the role of pro-inflammatory cytokine interluekin-2 andtumor necrosis factor- alpha in painful neuropathies is well-recorded, and paraesthesia is part of the spectrum of symptoms seen in such patients. [27] Finally, lowering of threshold of large myelinated nerves producing ectopic impulses has been shown in patients with paraesthesia. [28] The effect of altered microenvironment associated with infection in terms of decreased pH and elevated temperature can also sensitize the neurons. [26],[29]

From a radiological point of view, the intra osseous anatomical pathway of inferior alveolar nerve appears to be protected by the cortical lining of the inferior alveolar canal (IAC). However, the bony canal covering the neurovascular bundle is often absent, and is cribriform when present. [30],[31],[32] This explains how extruded material can easily seep into the IAC. Studies on the proximity of the root apices to the IAC have shown that the apices are closer to the IACin younger age group and females than in older patients. In young patients and females the apices of the mandibular second molar can be as little as 0.8mm from the canal and mandibular second premolars apices can be 1.7 mm away. [33],[34] This would explain the reported association of mental nerve paraesthesia with mandibular premolars and second molars, with one retrospective study reporting an incidence of 0.96% with mandibular premolars. [3],[31] Further, the presence of low-density trabeculations in cancellous bone along with numerous bony vacuoles in molar region favor the diffusion of extruded irrigant and obturation materials towards the IAC. [32] The destruction of peri-radicular bone and apical root resorption associated with lesions of endodontic origin, is often camouflaged in two-dimensional radiographs, preventing clinicians from realizing the extended of anatomical distortion in the region produced by infection. [35],[36] The contribution of individual endodontic treatment-related factors to paraesthesia should be evaluated against this backdrop. In this regard small field of view cone beam computed tomography provides better sensitivity and specificity in detection of periradicular changes, root resorption, canal morphology and anatomical proximity to the nerve bundle than conventional radiography. [37],[38]

In endodontics, physical trauma to the IAN, especially in mandibular second molars and premolars, can occur consequent to mistakes in working length determination. Overfilling, irrigant extrusion and sealant extrusion can result due to lack of an adequate apical seat or stop, binding of needle in the canal during irrigation and/or lack of apical control during obturation. [39],[40] Thermal injury to inferior alveolar nerve with overextension of thermoplasticized gutta-percha and possibility of bone necrosis with rise in root surface temperature has been reported. [41],[42]


  Local anesthetic as a cause of mental nerve paraesthesia Top


Nerve damage can occur from physical trauma to a nerve during administration or from neurotoxicity of the anesthetic solutions. The incidence of paraesthesia following local anesthesia in dentistry is reported to be in a wide range of 1 in 27,000 to 1 in 785,000 with a reported recent increase in incidence. [43],[44],[45],[46] Epidemiological studies reveal that 4% solutions of articaine and prilocaine are more often associated with paraesthesia than those containing 2% lignocaine. [47],[48],[49],[50] The reason for this increase is controversial. Some believe it to be due to concentration dependant neurotoxicity of articaine [51] whereas others consider it to be due to reporting bias. [52],[53] Unfortunately, though a widely quoted randomized controlled trial evaluating the safety of articaine compared to lignocaine reported 2% neurosensory disturbance toarticaine compared to 1.5% lignocaine, it failed to separate the procedure-related causes from drug-related causes. [53] Given the rarity of the event it is difficult to evaluate nerve injury to local anesthetics from clinical trials and hence it is no surprise that the recent meta-analysis had concluded that there is no difference in post-injection adverse effects with articaine compared to lignocaine. [54] However, the contribution of individual anesthetic solutions to paraesthesia cannot be discounted.


  CASE REPORTs Top


Case 1

A 35-year-old otherwise healthy female reported with severe pain localized to her right mandible with numbness of her right side of lower lip, and pain on swallowing. She had been to the emergency department the previous night and had anti-inflammatory injections without significant relief. On examination, the patient was apyrexic with normal vital signs, no evident facial asymmetry, painful inter-incisal mouth opening of 30 mm and pain on deglutition. Her lower right second molar had an occlusal temporary filling and was extremely tender to palpation. A small field of view CBCT (Kodak 900C, 70 kv, 8mA, 10.8 sec) revealed alarge periapical radiolucency involving the second molar extending into the inferior alveolar nerve canal and perforating the lingual cortex [Figure 1]. An inferior alveolar nerve block using 1.8 cc of 2% lignocaine with 1;100,000 adrenaline was used to achieve anesthesia followed by buccal infiltration with another 1.8cc. Drainage of purulent exudate was achieved through the root canals. In view of the dysphagia, the patient was hospitalized and placed on a slow intravenous infusion of Clindamycin (Dalacin Cphosphate), 600 mg in three divided equal doses on the first day. Theparaesthesia and dysphagia was completely resolved by the following day, allowing the patient to be discharged with oral antibiotics and ibuprofen. The obturation was done after a month of calcium hydroxide dressing. One year follow-up examination showed reconstitution of the apical region, lingual cortex and cortical lining of the inferior alveolar canal [Figure 2].
Figure 1: (a) Three-dimensional reconstruction of the lingual view of mandibular right molar second region (b) axial section through the region (c) coronal section though the distal root of second molar (c) showing perforation of lingual cortex (arrowed). (d) The extension of the periapical radiolucency into the inferior alveolar canal is evident in sagittal view

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Figure 2: (a) Axial section through the inferior alveolar canal showing destruction of the cortical lining of the inferior alveolar canal and perforation of the lingual cortex. (b) Axial section through the same region showing reconstitution of the cortical lining of inferior alveolar canal and lingual cortex after 1 year

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Case 2

A 45-year-old male was referred by his general dental practitioner for root canal treatment of his mandibular right canine and mandibular right first and second premolars after previous pulpectomy. The reason for the pulpectomies was recorded as being due to pulp exposures from deep non-carious cervical lesions. His medical history was non-contributory. On examination all the three concerned teeth were found to be asymptomatic with intact temporary restorations, both occlusally and cervically. An inferior alveolar nerve block was administered using 1.8cc of 2% lignocaine (1:200,000 adrenaline) using a traditional Halstead technique, and root canal treatment was completed for both canine and first premolar.

One week later, the patient was scheduled for asimilar procedure on the mandibular right second premolar. The patient was asymptomatic on this visit. 1.7ml of 4% Articaine (1:200,000 adrenaline) (Ubistesin, 3M ESPE, Seefeld, Germany) was administered using a 28-G needle near the apex of second premolar after negative aspiration without intentionally penetrating the mental foramen. Working length was determined usingan electronic apex locator (Dentaport Zx, J Morita Mfg.Corp, Kyoto, Japan). Sodium hypochlorite 2.5% was used carefully to irrigate the root canal space using a 30-G side-venting Max-I- probe (Dentsply, Detrey, GmbH, Konstaz, Germany). Cleaning and shaping was done with a combination of hand instruments and rotary ProTaper instruments (Dentsply, Detrey, GmbH, Konstaz, Germany) till F2 with a master apical file of size 35. Gutta-percha was used to obturate using continuous wave of condensation technique (Elements Obturation Unit, Sybron Endo Corporation, Orange, CA) with AH plus (Dentsply, Detrey, GmbH, Konstaz, Germany) as sealer [Figure 3]. The access was closed using micro hybrid composite resin as permanent restoration.
Figure 3: (a) Preoperative periapical radiograph showing previously accessed mandibular right second premolar, first premolar and canine-note accessory mental foramen is not visible. (b) Immediate post-obturation periapical radiograph showing minimal amount of sealant extrusion on mandibular second premolar. (c) Dental panoramic tomograph showing the sealant extrusion is not close to the inferior alveolar canal- note accessory mental foramen is not visible

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The patient returned the next day and complained of persistent numbness on the mucosal and skin surface of right side of lower lip from the mid line till the second premolar region. Two point discrimination, light touch and pin prick tests were done which confirmed persistent anesthesia. Perimeter mapping was difficult as the patient was heavily bearded. Electric pulp testing revealed an intact sensation in mandibular right central and lateral incisors. A small field of view (FOV) CBCT (Kodak 9000 C, 74 kv, 10 mA, 10.8 sec) was obtained, which revealed two additional accessory mental foramen (AMF), one anterior and another posterior to main mental foramen (MF). The anterior AMF was located 5.4mm from the MF and the posterior one was 6mm from the MF [Figure 4]. The pathway of posterior AMF was traced to the apex of second premolar and from there vertically down to the main IAN canal. Nearly 1 mm of sealant was found to have extruded beyond the apex of mandibular right second premolar on to the pathway of the posterior AMF [Figure 5]. The patient was given Vitamin B complex tablets for daily consumption and followed up every 2 weeks. The symptoms gradually improved and he completely recovered in 3 months.
Figure 4: Three-dimensional reconstruction of the mandibular premolar region showing mental foramen and two accessory mental foramen (small arrow)

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Figure 5: Coronal sections through second premolar showing the posterior accessory mental canal passing through its periapical region and exiting coronally (arrow). This image also shows the relation of extruded sealant (arrow) to the root apex and accessory mental canal

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  Discussion Top


Case 1

The quick recovery within 24 hours in this case shows that it likely resulted from compression-induced neuropraxia of the inferior alveolar nerve from the periapical abscess. Since dysphagia is an omnious sign denoting potential risk to airway, hospitalization and monitoring was considered advisable. The root of mandibular second molars is often situated close to the lingual cortex and drainage can occur lingually. If this occurs severe complications can develop including Ludwig's angina. In our case, vital signs remained stable and continuous monitoring allowed evaluation of the efficacy of the triage. The root canal treatment was completed uneventfully a month later.

Since incomplete root canal treatment is considered a major risk factor for future hospitalization, extraction of the offending tooth has been suggested as an alternative if patient compliance is questionable. [55]

Case 2

This patient went through a spectrum of symptoms from profound numbness to tingling sensations with complete recovery in 3 months. The previously enumerated causes for paraesthesia after endodontic treatment were carefully and individually considered in this case in an attempt to establish the exact etiology. Flare up-related paraesthesia was ruled out due to lack of other characteristic signs of infection, with no missed canals visible in CBCT imaging. Extrusion of sodium hypochlorite, if it occurs, usually results in more dramatic presentation with soft tissue necrosis, ecchymosis and sudden onset of severe pain. [56] Also, low-density air or fluid filled bubbles in soft tissue can also be visible in CBCT and usually a root apex fenestration can be confirmed. [57] Thus, extrusion of irrigant was not considered a likely cause. Mechanical over instrumentation of the main neurovascular bundle is unlikely in this case considering the meticulous attention to details and the significant distance from root tip to the main pedicle. Although continuous wave of condensation technique could potentially produce a higher root surface temperature, lack of bone necrosis, lack of tooth mobility and the previously uneventful root canal therapy on adjacent teeth makes it an unlikely cause. [58] The minimal amount of sealant extruded into the pathway of posterior AMF can be considered a confounding factor. Although AH plus releases less amount of formaldehyde than AH Plus, [59] both have poor osseous compatibility and, if extruded near a nerve bundle, can result in paraesthesia. [60] Considering the profoundness of the paraesthesia and small extend of the area involved it was concluded that extrusion of material was unlikely to be a sole factor. The CBCT imaging proved to be useful, as it confirmed that the small amount of extruded material was situated in an accessory canal and not near the main nerve trunk.

There was no evidence of associated medical reasons and the development of the paraesthesia appeared to be directly related in time to the treatment procedures. The contribution of 4% articaine infiltration in the region of mental foramen to paraesthesia was therefore considered. The possible role of articaine in the development of paraesthesia such as in this case is still considered controversial and has been the subject of several reviews. [46],[61],[62],[63] However, animal studies evaluating neurotoxicity of 4% articaine should be read carefully due to methodological differences before assumptions are made. [51],[64] The reduction in axon size and presence of new smaller axons with Schwann cells following intra neural injection of 4% articaine in Hillerup's study [51] represented degeneration of large myelinated axon. A clear concentration dependant difference between 2% and 4% articaine on the nerve, has been reported with higher concentration producing more degenerative changes in this study. [51] Unfortunately, a group with intranueral needle penetration alone, without local anesthetic administration, was not included in the above study. In contrast, the recent study by Baroni [64] failed to conclusively demonstrate difference in inflammatory response in rat's mental nerve following infiltration in the region with 4% articaine and 2% lignocaine. It is difficult to make clinical extrapolations from animal studies as cytotoxicity of different local anesthetics on different target cells will differ, and the mechanisms vary from direct cell necrosis to apoptosis. [65],[66]

Although some authors have recommended to avoid using 4% articaine for nerve block anesthesia, the predominant evidence of articaine associated paraesthesia is still based on epidemiological studies, case reports and in vitro studies and it is difficult to claim a cause and effect relationship. [46],[61] Since electric shock felt during injection is not a consistent symptom denoting physical trauma to nerve, it is difficult to separate the individual contribution of factors such as direct physical trauma to the nerve from needle, chemical/physical injury from ensuing hematoma and or toxicity of local anesthetic used. [21],[50]

Circumstantial evidence nevertheless points towards a possible role for 4% articaine in this case, with the possibility of the presence of accessory mental foramina providing more nerve contact and chances for intraneural administration. While it is difficult to detect the presence of these accessory mental foramen with periapical radiography and dental panoramic tomography, [67] the structures can nevertheless be clearly delineated with CBCT, as has been demonstrated in a variety of studies. [68],[69],[70] Its use is recommended as a diagnostic aid in examining causes of mental nerve paraesthesia. The distances between the MF and both anterior and posterior AMF in this case were within the reported range of 4.5-9.6 mm. [69] This highlights the difficulty in suggesting a safety zone for any procedure in the region and the advantage offered by small field of view CBCT with relatively lesser radiation. [71],[72]


  Management Top


The management of local anesthesia-associated paraesthesia depends on the cause of the paraesthesia and on the severity of the symptoms. Since paraesthesia includes a wide group of neuropathies, the choice of therapy would vary from no intervention to pharmacological therapy and surgical intervention in some situations. [46],[73],[74] Vitamin B complex, corticosteroids, benzodiazepines, tricyclic anti-depressants, anti-neuralgic medications such as carbamazepine or gabapentin are the main pharmacological options. [63],[73] The choice of vitamin B complex in this case was based on its safety profile and its ability to aid in functional recovery following nerve injury. [63] Further, vitamin B12 in particular, has been shown to up regulate expression of brain derived neurotropic factor (BDNF) in peripheral nerve injury by promoting regeneration of myelinated nerve fibres and proliferation of Schwann cells. [75],[76]


  Conclusion Top


In conclusion, the many possible causes of mental nerve paraesthesia have been reviewed and two cases have been presented illustrating two different etiologies associated with endodontic treatment. The idea that neurosensory disturbance is due to a single factor is oversimplification of the pathophysiological mechanism following nerve injury. While it is suspected in one case that the administration of articaine as a mental nerve block is a contributing factor, there is a lack of cause and effect relation between articaine and neurosensory disturbance; though a concentration-dependant association is possible. In addition to the non-dental causes, multiple physiochemical factors governing local anesthetic toxicity, anatomical aberrations, procedural contributions and periapical infection should be considered when evaluating neurosensory disturbance during and after root canal therapy. In this respect, CBCT imaging improves our understanding of the anatomy and can assist with the diagnosis and management of these conditions.

 
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    Figures

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Introduction
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