Neuropathic damage is a form of iatrogenic damage that is not common but, at the same time, frightening because of its rarity as well as the difficulty of its diagnostic and therapeutic approach. Most of the time, the damages are transitory conditions that tend to resolve autonomously within a certain time. In some cases, however, the damage may require invasive treatments of a neurological and neurosurgical nature. The variability of the type of damage is reflected in the clinical picture, which ranges from hypo-anesthesia, to different degrees of paresthesia, and to allodynia-hyperalgesia. In 70% of cases, a painful symptom is observed.
In the case of the inferior alveolar nerve, the possible causes of iatrogenic involvement in the field of dentistry can be traced back to four main categories: the damage caused by local injective anesthesia, that caused by endodontic therapy and that on a surgical basis, in turn essentially attributable to two types of procedures, implant surgery and the avulsion of the impacted lower third molar. According to the Renton and Yilmaz study of 2011, the latter is the most common cause (capable of covering 60% of cases on its own), followed by local anesthesia techniques (19%), on a par with implant surgery. Only 8% of the episodes would represent the complication of endodontic treatment.
Starting from these data and considering these same broad categories, Martinez and colleagues (2014) have conducted a review of the literature referring to the period 2008-2013. The evidence collected, the main points of which are reported below, refer to a corpus of 45 scientific articles, selected from an initial pool of almost 400.
As anticipated, neuropathic damage of the inferior alveolar nerve does not represent a common complication of root canal treatment. On the contrary, the rupture of an instrument is a dreaded but contemplated possibility for the endodontist, especially when it comes to rotating instruments and especially in the presence of thin channels and important curvatures. However, it is difficult for the instrument to go beyond the apex until it engages the mandibular canal where the nerve runs since the fracture follows precisely on contact with a sudden obstacle.
It is more likely that the complication follows the extrusion from the apex of canal cement, hot gutta-percha or other endodontic materials. It is, therefore, important to know the potential neurotoxicity of some of these products.
As regards to localization, the length of the roots of the lower first premolar and the lower first and second molars should be evaluated. A second aspect to be evaluated in the growing patient is the degree of patency of the apexes.
Anesthetic techniques at the level of the inferior alveolar nerve may represent a significant clinical problem, especially considering the rate of failure that affects the most common technique, namely the inferior alveolar block. However, cases are described, certainly rarer, in which the technique is associated with real complications, some of which are severe and not entirely imponderable.
This is the case of neuropathic damage secondary to the anesthetic procedure: as already mentioned in the first part of the text, it would be the cause of almost two out of ten episodes in this field.
Regardless of the anesthesiologic technique used—inferior alveolar nerve block, Gow-Gates technique or Vazirani-Akinosi technique—the repetition of anesthesia can be useless in a context of refractoriness to pharmacological action, as can be the acute pulpitis. More useful in these cases is the use of different additional techniques, primarily intraligamentary anesthesia.
A general rule is that any clinical act should be exposed to the risk of error and, therefore, the higher the number of injecting procedures, the higher the risk that one of them may favor the onset of a complication—even a remote one.
Although rare, cases of permanent damage to the inferior alveolar nerve have been reported. This structure would be at lower risk than the lingual nerve, which runs much more superficially and, therefore, would be more often affected. The painful symptom, however, would be systematically more severe in the case of the inferior alveolar nerve.
Equally true is that the anesthetic solutions currently used (with their molecules) ensure high standards of safety. According to the six-year study conducted by Progrel and colleagues, any molecule would be able to lead to paresthesia: the classic lidocaine would be linked to 25% of cases of paresthesia, articaine 33% and the now outdated prilocaine 34%. These differences would not be significant and, therefore, not useful to define the causal relationship with the individual species of anesthetic. Hillerup, on the contrary, indicates in the articaine the drug with the highest neurotoxicity.
It should be stressed that the complication referred to follows a procedure, at least in appearance, conducted regularly. Apart from possible secondary lesions to events such as needle rupture during injection, this possibility occurs more frequently in children and anxious subjects, being systematically secondary to sudden and unexpected patient movements.
In the final analysis, it should be considered that an anesthetic technique can lead to complications, including neuropathic damage, even in the presence of anatomical variations: the most significant, in this sense, is the possible bifid course of the nerve trunk.
The last cause treated is represented by the compartment of surgical damage which, in reality, represents the most numerically relevant possibility, able to cover almost eight cases out of ten of damage to the inferior alveolar nerve.
The traumatic outcome of implant surgery is, in many cases, the expression of deficient planning and, in particular, of an imperfect phase of radiological diagnosis. If, on the contrary, the planning is correct, the nerve damage is a rare complication and, if it occurs, it is not serious because it is secondary to the inflammatory state and to the bone remodeling following the surgery. Such involvement tends to resolve spontaneously, at the latest within a few months.
From an anatomical viewpoint, it is difficult to think that trauma of this type can manifest in a jaw, edentulous aside, that is healthy. More likely to be an acquired aspect, as typically happens in the presence of complete undefeated edentulousness, associated with severe bone base resorption. A process of this type leads to a relative approach of the mandibular canal to the alveolar crest.
In cases like this, the use of short implants may be a viable option for the prevention of alveolar nerve complications. It should be remembered that short implants are arousing clinical interest in wider fields of application than the one under examination: once again, therefore, the preventive measure is not justified solely based on complication, which remains in all cases a rare event.
In the surgical field and also in absolute terms, the main cause of involvement of the lower alveolar nerve (as, in fact, also of the aforementioned lingual nerve) is represented by the surgery of the third molar.
Smith observes that some of the most common procedures of aggression to the malpositioned third molar, ostectomy, dentistry or lingual separation of the element can induce excessive bleeding, which in turn can cause transient deficits in neurosensory conduction.
Jerjes has defined the anatomical risk factors underlying lower alveolar nerve paresthesia: horizontal position of the tooth and proximity to the alveolar canal. To this, the author adds little experience on the part of the clinician.
As far as the anatomical aspect is concerned, Park indicates as a critical factor the loss of cortical bone near the mandibular canal. Aspects concerning root morphology can also be added.
These indications also seem to underline the importance of the case study, especially from the radiographic viewpoint: in the face of a concrete suspicion of proximity between tooth and canal, deepening through the execution of a CT cone beam can correctly direct the surgical approach to the case.