Classification of nerve injury (Comparison of Sunderland and Seddon classifications)
Premature loss of posterior teeth in the mandible, failure to replace lost teeth as well as systemic factors may result in progressive resorption of the alveolar ridge. At present, oral and maxillofacial surgeons aim to reconstruct the lost bone and masticatory function via posterior mandibular grafting and/or implants. However, anatomic limitations such as the inferior alveolar nerve (IAN) may limit this. Various treatment methods are available for treatment of patients with posterior mandibular atrophy presenting with a superficial IAN; each has its own merits and drawbacks. [1,2] Use of removable or fixed prosthetics and reconstruction of the dentoalveolar system by dental implants are among the available treatment options; a superficial IAN often precludes use of the latter. Implant-based reconstruction has several advantages i.e. allows for placement of longer implants, bone preservation, better functionality etc. and is gaining more proponents. However, certain conditions should be met in order for an implant to be placed. The most important condition is the quality and quantity of the bone. The amount of resorption, density of the bone and level of the nerve may limit implant placement. Reconstruction and rehabilitation of the dentoalveolar system in cases with alveolar ridge atrophy is a challenge for maxillofacial surgeons and prosthodontists. To date, several treatment options such as augmentation techniques with bone grafts , cartilage  or hydroxylapatite , vestibuloplasty  and several osteotomy techniques  have been suggested. Such treatments are still indicated as alternatives for cases in which for some reason dental implants cannot be placed . In order to place an implant, we need adequate bone volume (both mediolaterally and mesiodistally) with optimal bone density. This condition is usually not met in atrophic areas of the posterior mandible especially in patients that have been edentulous for some time. As the alveolar ridge becomes atrophied, the bony height from the crest of ridge to IAN decreases and the bone height in this area is often not enough to place an implant. Due to the increasing demand of patients for dental implants, strategies have been presented to overcome the obstacle of deficient alveolar bone height. These include guided bone regeneration (GBR), onlay bone graft, inter-positional sandwich bone graft, distraction osteogenesis (DO), all-on-four technique, use of short implants, lateral ( or Lingual) positioning of implants and nerve transpositioning. Each of the aforementioned treatment options has its inherent advantages and disadvantages as well as indications and contraindications. In this chapter we discuss nerve transpositioning.
2. Nerve transpositioning
The first case of inferior alveolar nerve repositioning was reported by Alling in 1977 to rehabilitate patients with severe atrophy for dentures . Jenson and Nock in 1987 carried out IAN transposition for placement of dental implants in posterior mandibular regions . In 1992, Rosenquist performed the first case series study on 10 patients using 26 implants. He reported an implant survival rate of 96% for this procedure  and therefore, this technique was accepted as a treatment modality for reconstruction of the dentoalveolar system with dental implants in the posterior mandible. Consequently, research studies started to evaluate various surgical techniques developed for this procedure; their advantages, disadvantages, pitfalls and methods for preventing or decreasing complications were presented. As a result, this technique constantly improved. When looking at the history of different treatment modalities and surgical techniques in various academic fields we notice that most of them had limitations and complications at first but significantly improved with time and advancement of technology. Nerve transposition is a young procedure that needs further refinements in terms of technique and instrumentation to decrease complications.
2.2. Anatomy of the inferior alveolar nerve
The inferior alveolar nerve (IAN) is a branch of the mandibular nerve (V3) which is itself the third branch of the cranial nerve V (Figure 1). It runs downward on the medial aspect of the internal pterygoid muscle and passes inbetween the sphenomandibular ligament and the mandibular ramus entering through the mandibular foramen into the inferior alveolar canal innervating the teeth posterior to the mental foramen. At the mental foramen, the IAN divides into two branches namely the incisal and mental nerves (Figure 2). The incisal nerve is often described as the extension of the IAN innervating mandibular canines and incisors by passing through the bone .
The inferior alveolar nerve gives off 3 branches inside the canal: Ramus Retromandibularis, Rami Molares or Molar Branch and Ramus Incisivus or Incisal Branch.
In some cases, the IAN canal is unilaterally or bilaterally bifid [13,14]. Thus, it is necessary to pay close attention to radiographic and CT examinations before nerve transposition in order to detect such cases and decrease the related risks (Figure 3).
2.2.1. Inferior alveolar nerve canal in edentulous patients
On panoramic radiographs of edentulous patients, the IAN canal in the body of the mandible is not very clear; thus, its path through the ramus and the opaque lines above and below the canal may not be clearly visible. Also, the closer we get to the mental foramen, the less visible the canal becomes [15,16]. Cesar et.al in their studies offered 2 types of classification for the IAN canal in edentulous patients. Vertically, the canal is located either in the upper or in the lower half of the mandible. In 73.7% of males and 70% of females the nerve is located in the lower half of the mandible (therefore, presence of the canal in the inferior half of the mandible is the most common occurrence). Branching of the IAN in edentulous patients falls into one of the following patterns: Type 1: Presence of one single trunk with no branching. Type 2: Presence of a series of separate nerve branches (most common type). Type 3: Presence of a molar plexus. Type 4: Presence of proximal and distal plexuses. Type 2 is the most prevalent pattern where a main trunk along with several single branches is directed towards the superior border of the mandible. The second most prevalent pattern is the presence of a small molar plexus at the proximal half of the IAN or Type 3 (Figure 4) .
2.2.2. The mental nerve
The mental nerve emerges at the mental foramen and divides beneath the depressor anguli oris muscle into 3 branches namely a descending branch that innervates the skin of the chin and 2 ascending branches innervating the skin and mucous membrane of the lower lip . The patterns of emergence of the mental nerve at the mental foramen follows 1 of 3 patterns. Knowledge of these patterns is necessary for the surgeon before operating on this area. Type 1: The neurovascular bundle traverses anteriorly and then loops back to exit the mental foramen (anterior loop). Type 2: The nerve runs forward and exits the foramen along the canal path (absence of anterior loop). Type 3: The nerve exits the foramen perpendicular to the canal axis (absence of anterior loop). Type 1 is the most common pattern (61.5%) followed by type 2 (23.1%) and type 3 (15.4%) .
2.2.3. Contents of the mandibular canal and their location
Placing implants in areas adjacent to the IAN has increased significantly. Therefore, it is extremely important to know the contents of the canal and the exact location of components of the neurovascular bundle. According to histological examinations and MRI imaging, the inferior alveolar artery is located coronal to the nerve bundles inside the canal. Before entering the mandibular foramen, the artery is located inferior and posterior to the nerve. After entering the canal it changes its path at the mid length of the canal and runs superior and slightly medial to the nerve [18-20].The IAN usually has a round or oval cross section with a mean diameter of 2.2 mm. The mean diameter of the artery is 0.7 mm. The mean closest distance of the artery to a tooth apex is about 6 to 7 mm at the second molar area . Yaghmaie et al. in 2011 confirmed the presence of lymphatic vessels in conjunction with the nerve trunks and blood vessels in all directions .The neurovascular bundle and its branches are responsible for sensation of pain, temperature, touch, pressure and proprioception of their innervated areas. The nerve is comprised of 1 or multiple fascicles. A collection of nerve fibers forms a fascicle. Microscopic examination of neurovascular bundles usually shows 2 to 8 axon bundles. Each fascicle contains about 500 to 1000 nerve fibers. Epineurium wraps around the fascicles, protects them and contains blood vessels for nutrition (Figure 5) [18-20].
2.2.4. Fascicular patterns
There are 3 fascicular patterns: The mono-fascicular pattern includes one big fascicle along with perineurium and epineurium layers surrounding it (i.e. the facial nerve). The oligo-fascicular pattern includes 2 to 10 fascicles each covered by perineurium. Fascicles are interconnected through the epineurium layer inbetween them; in this pattern, fascicles are usually of the same size (nerve roots C6 and C7 have the oligo-fascicular pattern). The poly-fascicular pattern includes more than 10 fascicles of various sizes i.e. inferior alveolar and lingual nerves (Figure 6) [18-20].
As mentioned earlier, the IAN has a poly-fascicular pattern. The outer nerve fibers of the bundle are called “mantle bundle”. They usually innervate the proximal areas (molars). Following the administration of local anesthesia, this area is affected sooner and more efficiently since it is close to the side of the nerve bundle; whereas, core bundles innervate distal areas (central and lateral) and are affected later and less efficiently by local anesthetics. Various senses are affected when administering local anesthetics depending on the nerve diameter and presence or absence of a myelin sheath. For instance, signal transmission is slower in thinner non-myelinated nerve fibers. These fibers are affected more efficiently and more quickly by the local anesthetics than large diameter, myelinated fibers that have faster signal transmission. Non-myelinated fibers (sympathetic C fibers responsible for vascular tonicity and slow transmission of pain) and partially myelinated fibers (A delta fibers, fast transmission of pain) are affected sooner by the local anesthetics and also return to their normal state more quickly. On the contrary, thicker myelinated fibers (like A alpha and A Beta) that transmit deep sensations, pressure and proprioception are affected by local anesthetics later. In conclusion, general senses are affected clinically by the local anesthetics in the following order: First cold sensation through the autonomic nerves, then heat, pain, touch, pressure, vibration and eventually proprioception. Contents of the canal are responsible for innervation of dental pulps, periodontium, dental alveoli and soft tissues anterior to the mental foramen. Dental pulps receive unmyelinated sympathetic nerve fibers from the superior cervical trunk which enter the pulp accompanied by arterioles. Dental pulps also receive A delta myelinated sensory nerve fibers as well as unmyelinated nerve fibers (both from the trigeminal ganglion); together they form a large plexus below the odontoblastic layer in the pulp (Raschkow’s plexus). In the Raschkow’s plexus myelinated fibers lose their myelin sheath and penetrate into the odontoblastic layer. Today, they consider the phenomenon of fluid mobility inside the odontoblastic tubes (hydrodynamic theory) to be responsible for stimulation of nerve endings and sensing pain . There are 2 aspects in the sensation of pain namely, a physiologic aspect and a psychological aspect which together create the unpleasant psycho-physiologic and complex experience of pain. From the physiologic point of view, stimulation of specific nerves (like A delta and C fibers) and transmission of the signal to the trigeminal ganglion is called “transduction”. Passing over the signal from this site to upper centers (thalamus and cortex) is called “transmission” and “modulation”. The three mentioned pathways comprise the physiologic aspect of pain that combined with the psychological aspect (previous experience, cultural behaviors, psychological state and medical status) create the unpleasant complex experience of pain .
2.2.5. Inferior alveolar nerve injury
Various factors can traumatize the IAN ranging from simple accidents like trauma from a needle during injection, bleeding around the nerve and even the local anesthetic drug itself, to maxillofacial traumas, pathologic lesions and surgical operations. Generally, the main nerve injuries are usually due to trauma or surgical operations among which, the most frequent ones are surgical extraction of mandibular third molars, endodontic treatment, implant placement, osteotomies (visor, sagittal, body of the mandible and subapical osteotomies), genioplasty, resection of mandibular cysts and tumors, partial mandibulectomy, fracture of the angle, ramus or body of the mandible, D.O. and IAN transpositioning. The nerve trunk is composed of 4 connective tissue sheaths. These membranes from the outermost to the innermost include mesoneurium, epineurium, perineurium and endoneurium. The mesoneurium suspends the nerve trunk within the soft tissue and contains vessels. The epineurium is a dense irregular connective tissue that protects the nerve against mechanical stress. The larger the epineurium (it usually measures 22 to 88% of the nerve diameter), the higher the nerve resistance against compressive forces compared to tensile forces. It should be mentioned that most nerve injuries are usually of a transient nature and will recover partially or completely. Epineural tissue wraps around nerve bundles and protects them against mechanical stress. Also, in many cases pressure due to severe inflammation or retention of fluid around the nerve trunk and subsequent development of transient ischemia in the epineurium cause clinical symptoms of neural dysfunction and disturbances. It is worth noting that the IAN is a poly-fascicular nerve. The smaller the number of nerve fascicles and the thicker the epineurium the more resistant the nerve is to pressure and vice versa (the greater the number of fascicles and the thinner the epineurium, the less resistant the nerves are towards pressure)[12,21-23]. It should be mentioned that poly-fascicular nerves like the IAN have a large number of small fascicles and therefore are more resistant to tensile forces compared to mono-fascicular or oligo-fascicular nerves .Perineurium wraps around the axon, Schwann cells and endoneurial sheath ; each nerve fiber is covered by the endoneurium sheath. Schwann cells are necessary for the axon to stay alive. They are the most sensitive cells to ischemia and radiation  (Figure 5).
2.2.6. Classification of nerve injury
There are 2 classifications available for nerve injury. The first was introduced by Seddon in 1943. He classified nerve injury into 3 types: Neuropraxia, Axonotmesis and Neurotmesis (from minor to major injury). The other classification was described by Sunderland  in 1987. He categorized 5 degrees of nerve injury : First degree where the axon and the covering sheath are intact. Epineural ischemia is probably the cause of the conduction block. Recovery is usually complete. Second degree where the axon is injured but endoneurium, perineurium and epineurium are intact. Recovery is often satisfactory. Third degree where the axon is injured but endoneurium is disrupted. However, of recovery. Fifth degree where there is complete transection with loss of continuity and less chance of spontaneous epineurium and perineurium are intact. Partial recovery may be achieved. Fourth degree where the axon, endoneurium and perineurium are all interrupted. However, epineurium is intact. There is a small chance recovery. Microscopic surgery is recommended (Table 1) .
Grade 1 (Sunderland)
|Compression, traction, small burn, acute infection||Neuritis, paresthesia, conduction block, no structural damage||Spontaneous recovery in less than 2 months||Not necessary unless a foreign body interrupts the process of nerve repair|
Grade 2 (Sunder.)
|Partial crushing, traction, burn, chemical trauma, hematoma, chronic infection||Intact epineurium, isolated axon loss, episodic dysesthesia||Spontaneous recovery within 2-4 months||Not indicated unless for decompression due to a foreign body or perineural fibrosis|
|Grade 3 (Sunder.)||Traction, crushing, contusion, burn, chemical trauma||Wallerian degeneration of axon, some internal fibrosis, peripheral pain||Poor sensory recovery, neuropathy for more than a year||Decompression and repair in case of poor function and continuous pain for 3 months|
|Grade 4 (Sunder.)||Complete crushing, severe traction, severe burn, direct chemical trauma||Neuroma-in-continuity, hypoesthesia, triggered hyperpathia||Permanent damage, minimal spontaneous recovery||Repair, resection of neuroma in case of unbearable pain after 3 months|
Grade 5 (Sunder.)
|Transverse incision on the nerve, laceration, laceration of the main nerve trunk||Neuroma at the site of incision, anesthesia, evolving deafferentation pain||Permanent damage, low spontaneous recovery||Resection of neuroma by neurorrhaphy or graft in case of poor function and lasting neuropathic pain|
2.2.7. Nerve changes following injury
Before discussing the clinical examinations, we explain the definition of common clinical terms (Table 2).
|Anesthesia||Absence of any sensation|
|Paresthesia||Abnormal sensation even spontaneously or for no reason|
|Analgesia||No pain in response to a normally painful stimulus|
|Dysesthesia||An unpleasant abnormal sensation that can be spontaneous or for a reason|
|Hyperalgesia||Hypersensitivity to harmful stimuli|
|Hyperesthesia||Hypersensitivity to all stimuli except for special senses|
|Hypoalgesia||Decreased sensitivity to stimuli|
|Hypoesthesia||Decreased sensitivity to all stimuli except for special senses|
|Allodynia||Pain due to a stimulus that does not normally cause pain|
|Neuralgia||Pain that is distributed in one or several nerve fibers|
|Deafferentation pain||Pain due to decreased sensory afferents into the CNS|
|Neuropathic pain||Pain due to a primary lesion or nervous system dysfunction|
|Causalgia||Burning pain immediately or several months after injury|
|Anesthesia dolorosa||Pain felt in an area which is completely numb to touch|
|Synesthesia||Stimulation of one sensory or cognitive pathway leads to experience in a second cognitive or sensory pathway due to misdirected axonal buds resulting in misperception of the location of touch or pain|
|Central pain||Pain due to a primary lesion or central nervous system dysfunction|
|Hyperpathia||A painful syndrome characterized by hyper-responsiveness to a stimulus. Hyperpathia may be associated with hyperesthesia, hyperalgesia or dysesthesia|
2.2.8. Clinical tests
The length of bone above the canal, anomalies, distance of the canal from the buccal cortex and also thickness of the cortex for ostectomy are all evaluated on panoramic radiography. Exact location and precise anatomy of the mental foramen and anterior loop can also be evaluated . In rare cases, the IAN canal may be completely attached to the medial or lateral cortex on CBCT. In such cases, implants can be easily placed buccally or lingually to the canal with no need for extensive surgery. Additionally, by analysis and reconstruction of scanned images using CAD-CAM, it is feasible to determine the path of the canal and place the implants in atrophic areas.
2.3. Indications, contraindications and limitations
Babbush mentioned several indications for nerve transpositioning; namely placement of removable prosthetics, stabilizing the remaining anterior teeth, stabilizing the temporomandibular joint, and establishing muscular balance following reconstruction of the dentoalveolar system. He also discussed some related limitations. This procedure is technically difficult and requires adequate expertise. The surgeon should have adequate experience, sufficient anatomical knowledge and necessary skills to fully manage peri-operative and post-operative complications. Accordingly, the most significant risk of surgery is nerve injury due to surgical manipulations and the surgical procedure itself. Although rare, mandibular fracture should also be considered as a risk factor especially in cases with severe mandibular atrophy (Figure 8) .
Resenquise et al. in their studies on nerve transpositioning procedure mentioned the following indications and contraindications for this operation:
According to author’s personal experience, nerve transpositioning in cases where the bone height over the canal is less than 3 mm is still feasible. We can transpose the nerve from the alveolar crest laterally, and after placing the implant with bone graft material. More details in this regard will be discussed subsequently.
2.4. Surgical procedure of nerve transpositioning
Inferior alveolar nerve transpositioning for implant placement is usually performed by 2 techniques:
2-Retracting the mucoperiosteal flap is done so that the mental foramen is totally exposed and the dissection is extended towards the inferior border. Considering the radiographic and CBCT evaluations along with the fact that the neurovascular canal is usually located 2 mm below the mental foramen, it is necessary to expose the lateral surface of the body of the mandible and release the periosteum around the mental nerve (Figure 10) [1,36]. 3-Bone removal on the lateral surface of the canal is done while preserving the maximum thickness of buccal bone as this especially important. Presence of adequate bone thickness in this area results in better and faster healing of the bone defect adjacent to the implant where nerve transposition has been performed. Bone can be removed using a diamond round bur or piezosurgery device [1,6].
In the first technique which is usually performed for treatments other than dental implants a piece of bone is removed as a block and then the canal is exposed. This method can be indicated for simultaneous implant surgery when there is adequate bone height over the canal. In such cases, even after resecting a bone block, a sufficient amount of bone still remains at the lateral side of the implant . Rosenquist reported that in this method, it is difficult to maintain a proper angulation when placing the implant because a great extent of buccal bone has been removed for nerve transposition and accessing the canal . In patients who are candidates for implants, cortical bone preferably should not be removed as a block because in such patients there is limited amount of bone available in the superior and lateral sides of the canal which should be preserved. If the surgical technique does not include manipulation of the mental nerve, bone is removed using a round bur number 700 or 701, a straight handpiece and copious normal saline for irrigation or a piezosurgery device. Bone removal is initiated 3-4 mm distal to the mental foramen and follows the canal path posteriorly and superiorly. Bone removal should extend 4-6 mm posterior to the intended location of the last implant. We should try to remove the smallest amount of bone possible from the buccal cortex. Excessive bone removal along with extensive drilling for implant placement can result in temporary mandibular weakening followed by increased risk of mandibular fracture which has been reported in the literature. Bone preservation helps in primary and final implant stability and shortens the recovery time. After removing the cortical bone, a curette may be used for removal of spongy bone and cortical layer of the canal in cases where the cortical layer surrounding the canal is not dense or thick. A special instrument (Hassani nerve protector) is required to protect the nerve while the cortical layer has to be removed using surgical burs or piezosurgery device. Bone removal in close vicinity to the neurovascular bundle should be performed patiently and thoroughly. This is usually performed using special curettes parallel to the surface of nerve bundles in an antero-posterior direction. Tiny bone spicules around the nerve should be removed. The area should be thoroughly irrigated so that the nerve bundle can be clearly seen (Figure 11 A - D) [1,2,4,9,10].
Another method that has been suggested is drilling the bone surrounding the canal using a hand piece and a round bur. The surgeon carefully enters a probe (round end with no sharp edge) into the canal through the mental foramen and determines the canal path. Then according to this test and after evaluating the canal path on the radiographs, the surgeon inserts the tip of the nerve protector into the canal. This instrument has been designed, patented and manufactured by the author (Hassani nerve protector). This instrument should be placed in between the nerve and the bone in order to protect the nerve. The buccal bone is drilled using a bur. By directing the bur distally, the nerve protector is also moved distally inbetween the nerve and bone to protect the nerve at all times. The bone chips are collected by a bone collector in the process. In this technique, while the nerve is protected minimum amount of bone is removed from the buccal cortex and the maximum amount of bone is preserved in an atrophic ridge for implant placement which results in maximum primary stability of the implant. Also, mandibular bone weakening is minimal in this method which is a great advantage of this technique. The neurovascular bundle inside the canal is freed using special curettes and is moved laterally using a nerve hook (Figure 12). Then a 10 mm wide gauze cord or elastic band is passed below it retracting the nerve away from the surgical site decreasing ischemic trauma to the nerve. It also retracts the nerve away from the surgical site during the operation reducing the risk of nerve damage (Figure 13) [9,34,24,35].
Some studies recommend piezosurgery for bone removal in nerve transposition surgery. This device causes vibrations in the range of 20-200 micrometers and cuts through the mineralized tissue completely and smoothly. If soft tissue or the neurovascular bundle comes in contact with this device it stops to function because the device is made in a way that it stops working when it is in contact with unmineralized tissue. This device is especially beneficial when a small osteotomy is going to be performed . Among the disadvantages of this device we can mention the long duration of time that it takes to remove bone. Also, there is still controversy regarding the indications of this device and some believe that vibrations may damage the nerve. Further investigations are required regarding indications of using this device in nerve transposition surgery [9,10].
In patients with an atrophic alveolar ridge involving the premolar area or those with an edentulous mandibular ridge along with alveolar crest atrophy who need implant placement IAN transposition in the posterior mandible and mental nerve transposition is also necessary most of the time. This transposition is usually associated with incisal nerve transection. In such cases, the patients will not have any problems related to incisal nerve transection but in cases where transposition of the nerve is intended and the patient has vital anterior mandibular teeth, nerve transection may result in patient having an unpleasant sensation in these teeth. In some cases, even root canal therapy may be required. However, several studies have reported that no problems related to anterior mandibular teeth were seen [1,9,35].
Sectioning the incisal branch of the inferior alveolar nerve, releasing the neurovascular bundle and moving it backwards in order to avoid traction is called nerve distalization . Based on the author’s experience, in many cases it is possible to transpose the mental nerve without sectioning the incisal nerve. In the method of nerve transposition without releasing the mental nerve, great traction force is exerted on the nerve when keeping it out of the surgical site. According to the literature, the highest number of nerve injuries occurs during anterior osteotomy because the nerve trunk becomes thinner at mental foramen and is therefore more susceptible to injury. That is why nerve transposition without involving the mental foramen has the least sensory complications and side effects. According to the literature, by preserving 3-4 mm bone distal to the mental foramen during nerve transposition we can reduce inferior alveolar nerve damage because the nerve is thinner and more susceptible to injury at this specific location .
Vasconcelos et al. believes that at least 5 mm bone height above the canal is necessary in case selection for nerve transposition whereas, Kahnberg and colleagues believe that 2 to 3 mm bone thickness above the canal is adequate [9,10]. In cases where minimum requirement of bone height above the canal does not exist some authors suggest to do a bone graft before nerve transposition and implant placement . However, fixing the grafts especially blocks of autogenous bone to the limited remaining bone above the canal is difficult and is associated with a risk of nerve injury by the screws. Based on the author’s experience in such cases we can transpose the nerve from the alveolar crest laterally. Bone is removed from the alveolar crest, and when the nerve is exposed we move it upward and outward and start drilling for implant placement from inside the canal while the nerve is retracted laterally from the buccal cortex. Bone graft is placed inside the canal anterior and posterior to the implant. The nerve is placed into a newly formed groove from the posterior area of the last implant (Figure 19).
Research demonstrates that bone formation around the implant surface sand blasted with aluminum oxide was 2.5 times greater than a smooth titanium surface. Bone formation around the neurovascular bundle prevents the implant from having direct physical contact with the bundle and therefore the nerve structure will be protected from mechanical or thermal trauma. Microscopic sections show the formation of a vascular network in the adjacent tissues which proves that there is no need for placing a barrier or any kind of graft material to separate the nerve from the implant .
In Kahnberg et al. study on a dog, healing was not complete after 14 weeks but none of the implants were exposed. Histological examination showed that in cases where membrane had not been placed a small contact was present between the nerve bundle and the implant. Plasma cells, macrophages, polymorphonuclears, and granulocytes were alternately seen next to the membrane. Several giant cells and macrophages were also seen. Vascular buds were seen where membrane had been placed (compared to areas where no membrane had been used). In some cases, a capsule with less than 10 µm thickness was seen in some areas between the implant and the nerve. When membrane is used the distance between the nerve bundle and the implant will be 4 to 8 times greater. The mean distance between the implant and the nerve was 348.3 µm when using a membrane and 39.8 µm when not using it. There is no contact between the nerve and the implant when using a membrane but the bone was not seen around the implant either .
2.5. Important considerations in nerve transposition surgery
2.5.1. Patient selection
The surgical process is complicated and occurrence of sensory disturbances is definite. Therefore, the surgeon should evaluate the patient’s mental condition. Some people are stressed out and over sensitive even towards the smallest surgical complications. Such patients do not have tolerance and compatibility skills and therefore are not good candidates for nerve transposition surgery. Providing data and acquainting the patient with phases of surgery and probable complications: Thorough explanation should be provided for the patient in an understandable and comprehendible manner regarding surgical and neural complications. The sense of anesthesia that may occur should be well described for the patient and it also should be mentioned that the anesthesia may be permanent and irreversible.
CBCT should be obtained for precise evaluation of the canal and bone thickness around it.
Dexamethasone should be administered before the surgery
The surgeon should have full knowledge regarding anatomy and physiopathology of nerve injury and be able to evaluate the clinical course of nerve dysfunction after the surgery.
The surgeon’s skill and expertise are very important and magnification loops should be used.
Delicate instruments required for this type of surgery should be available (for minimal injury). Also, the surgeon should have the knowledge and skills for repairing the nerve in case serious damage is done to the nerve during surgery.
In cases where the canal is located in the center or lingually on CBCT, the surgeon should expect a more complex surgery.
In cases where the nerve transposition surgery extends further posterior and involves the 2nd molar area, the surgery can be more complicated due to the thicker cortical bone and limited access to the area.
Using low level laser after surgery reduces the inflammation and improves recovery.
The surgeon should be familiar with and have adequate skills regarding nerve reconstruction surgery and the instruments required for it.
2.5.2. Post-operative measures
Antibiotic therapy and administration of analgesics and NSAIDs post-operatively are similar to that of implant surgery and there are no specific recommendations in this regard in the literature. Antibiotic and corticosteroid prophylaxis is recommended because of the extensiveness and duration of surgery. Using corticosteroids pre- and post-operatively helps in decreasing the symptoms. However, there is no consensus in this regard but since inflammation can be among the causes of nerve dysfunction, corticosteroid therapy can be beneficial.
The most common sensory complications following nerve transposition are hypoesthesia, paresthesia and hyperesthesia. The most common causes of nerve dysfunction include the mechanical trauma to the nerve and ischemia following extracting the bundle from the canal, nerve traction during surgery, edema and probable hematoma and or chronic compression after the surgery [9,10]. According to Hirsch and Branemark, the main cause of sensory disturbances is nutritional impairment of the nerve due to injury to the microvascular circulation of nerve fibers as the result of mechanical trauma. Thermal and pain sensation nerve fibers are more resistant to compressive traumatic forces and ischemia than larger fibers responsible for touch sensation . Therefore, great attention should be paid during and after surgery to minimize the factors responsible for ischemia and mechanical trauma such as;
Avoiding exerting too much traction upon the nerve and when lateralizing the nerve and during nerve transposition, try to transform the contact point to a contact area.
During ostectomy care must be taken not to injure the nerve with rotary instruments, curette or elevator. When removing the bone cortex over the nerve, the author recommends using the nerve protector designed specifically for this purpose by the author himself; it fits inside the nerve canal over the nerve (Figure12 C and D'). Direct contact of rotary or other surgical instruments with the nerve is among the most serious injuries in this type of surgery.
In order to lateralize the nerve, use instruments with minimal traction and prevent ischemia to the nerve. Instruments that have large contact area with the nerve and minimum thickness are preferred to be placed between the nerve and the location of drilling for implant placement.
The retracted bundle should be constantly moistened by normal saline.
Prevent development of hematoma because it applies pressure on the nerve trunk.
After inserting the implant, autogenous bone powder or collagen membrane should be placed between the implant and the nerve bundle (as discussed earlier).
Use of anti-inflammatory drugs before and after surgery: Some articles have recommended administration of corticosteroids pre- and post-operatively or high dose ibuprofen 800 mg TDS for 3 weeks .
Using vitamin B complex supplements (studies have shown that B complex and vitamin E supplementation improves nerve function and decreases neuropathy. Vitamin B family especially B1 and B12 can prevent nerve injury and improve natural growth of the nerve by preserving and protecting the lipid-rich covering of nerve terminals. Alcohol consumption causes vitamin B deficiency and therefore should be avoided .
Use of low level laser (LLL) immediately after surgery 4 times a week for 10 sessions. Studies suggest using LLL as a non-invasive non-surgical method for faster recovery from paresthesia may obviate the need for surgery in nerve injuries. Use of GaA1As laser causes the patient’s subjective and objective symptoms to disappear. Low level laser increases nerve function and capacity of myelin production [10,41]. Bleeding inside the canal can cause a hematoma or compartment syndrome . The incidence of post-operative neuropraxia, permanent anesthesia and paresthesia decreases when only the thicker parts of the neurovascular bundle are manipulated compared to the manipulation of thinner parts or terminal branches. Therefore, although nerve transposition in more posterior areas like the 2nd molar area is technically more complex, it is usually associated with smaller risk of serious and long term injuries to the nerve because the neurovascular bundle is thicker in this region. Regeneration process of nerve following mild compression or crushing takes several weeks to 6 months . If recovery does not occur in this time period, we should consider the possibility of permanent anesthesia. Some researchers believe that sensory changes following implant placement and nerve transposition should be considered as a normal consequence of treatment and not a sequel or complication [10,43].
2.5.3. Pharmaceutical therapy and treatment of traumatic nerve injuries
Course of nerve recovery and symptoms vary based on the type and severity of the primary injury. In most cases, only time and regular patient visits are required. Other cases may need drug therapy or microscopic reconstructive neural surgery (
How to decide about the treatment and management of inferior alveolar nerve injury
Fluphenazine 1 mg, 3 times a day along with Amitriptyline 75 mg before bedtime
Doxepin (tricylic antidepressant) 25 mg 3 times a day
Carbamazepine up to 100 mg/day
Baclofen up to 80 mg/day
For sympathetical pain we can do injections for stellate ganglion block. Alpha 2 adrenergic blockers (clonidine 0.1 to 0.3 mg/day based on tolerance) 5 times a week for 3 weeks; sympathectomy can also be used.
In case of acute pains fast-acting anticonvulsants (like clonazepam) 2 to 10 mg/day may be useful.
Titrated Gabapentin anticonvulsant 600 to 3000 mg is beneficial for chronic pains following traumatic injuries. If the patient also suffers from sleep disorders, antidepressants may be used at bedtime.
Anti-inflammatory drugs, analgesics, anti-anxiety medications and sleeping pills can also be used in addition to the above mentioned medications.
Topical lidocaine gel (for mucus membrane) and 5% lidocaine patches (for skin) which are released slowly within 12 hours are used for the mucous membrane and skin of the irritated areas or trigger zones.
Intravenous injection of lidocaine may be used sometimes for diagnostic purposes. In such cases, first normal saline is injected as a placebo and then the patient’s symptoms are evaluated and then 1 mg/kg lidocaine is slowly injected intravenously within 2 minutes and the patient is asked about its effects every 30 seconds. Pain relief (more than 30%) indicates the effectiveness of intravenous lidocaine injection which shows the neuropathic origin of the pain and we should consider the probable efficacy of medications with central effects such as anticonvulsants [12, 22].
In case of requiring inferior alveolar nerve reconstructive surgery, it is important to maintain the integrity of the nerve. First, the nerve is exposed and the surrounding tissues are released so that the extensiveness of injury is evident. Compression injuries result in development of fibrosis. In such cases, first lactate ringer’s solution is subcutaneously injected in the fibrotic area with a 30 gauge needle to separate the epineurium from the fascicles and determine the extension of fibrous tissue. Then the fibrous tissue is eliminated by a fine longitudinal incision over the epineurium. If the fibrous tissue is extensive and has penetrated into the fascicles we have to dissect this area and suture the free ends of the nerve together. Inferior alveolar nerve is usually composed of 12 to 30 small fascicles with scattered epineurium wrapped around them. Therefore, extensive fibrosis between the fascicles rarely occurs unless in case of major injury. If there is a neuroma, similar to extensive fibrosis the lesion has to be removed and the two free ends should be sutured together. No traction should be applied to the free ends when suturing in order to avoid future fibrous formation. Approximation of the two ends of the nerve regardless of the direction of fascicles and placing the fascicles alongside each other is called coaptation. Since inferior alveolar nerve is a sensory nerve, often only approximation is sufficient. Sutures are applied to the epineural layer. If neural graft is intended, the most similar nerve to the inferior alveolar nerve in terms of diameter and consistency is the sural nerve and the second most similar is the greater auricular nerve [12,22].
Surgical intervention for a patient suffering from nerve injury has 2 main objectives: resuming the sensory function and managing the pain and discomfort due to nerve injury.
Presence of foreign body around the nerve
No change in anesthesia or hypoesthesia 2 months after nerve injury
Uncontrollable neuropathic pain
Signs of improved sensory function based on quantitative sensory testing (QST) which is a method for determining the exact threshold of sensory stimulation with the use of oscillatory, touch, thermal or painful stimuli)
Patient admission based on remaining dysfunction or present discomfort
Signs of central sensitivity (regional dysesthesia, secondary hyperalgesia)
Presence of clinical symptoms with autonomic origin (erythema, swelling, hypersensitivity, burning sensation) which are indicative of autonomic nerve dysfunction rather than sensory nerve injury)
Old age, presence of an underlying systemic or neuropathic disease
A long time has passed since the injury
Patient has unrealistic expectations (demands immediate full recovery or resuming of sensory function with no pain)
Neural pains that are not alleviated by local anesthesia 
The main goal of primary treatment of nerve injury is to eliminate the progressive cause, and prevent secondary nerve injury to allow formation of a peripheral tissue for maximum recovery of the nerve and avoid secondary neuropathic hypersensitivity. If the injured nerve is exposed, pressure from the foreign body, bony and dental chips, toxic materials or implant if present should be eliminated. The exposed nerve should be washed with isotonic solution and sutured with temporary epineural sutures. Infection and inflammation should be controlled precisely both locally and systemically. Anti-inflammatory medications, opioid analgesics and sedatives should be extensively used in order to control anxiety and minimal stimulation of the CNS. An appropriate method for this purpose is administration of a long acting local block anesthesia. A course of systemic corticosteroids like dexamethasone 8 to 12 mg/day can decrease the perineural inflammation in the first week following surgery . Fast acting anticonvulsants like clonazepam in divided doses of 2 to 10 mg/day can further protect the CNS . Topical lidocaine in the form of gel or 5% patch which is released and absorbed subcutaneously within 12 hours can also be used . Basic examinations should be performed using QST and the injured nerve should be under follow up. The patient should be informed about the nature of nerve injury, importance of tests and examinations, constant and immediate care, possibility of requiring secondary consultation and microscopic reconstructive surgery and possibility of prolonged recovery.
Nerve surgery is categorized into 3 types based on the time of surgery following nerve injury:
Primary and immediate surgery: within the first few hours following injury.
Delayed surgery: within 14 to 21 days after injury.
Secondary surgery: 3 weeks after injury.
The high capacity for maximum recovery within the first week after surgery
Quick intervention can prevent traumatic neuroma from extension and subsequent chronic neuropathic hypersensitivity or fibrosis
Technical simplicity of the reconstruction (after a long delay, microscopic surgery would be very difficult due to the contraction and progressive atrophy of the nerve segments, increased collagen precipitation inside and outside the nerve and scarring of Schwann cells)
Decompression of the injured nerve by extracting the foreign bodies and releasing the scar tissues and other tissues compressed around the nerve.
Detection of the injured area, incision and transection of the traumatic neuroma
Repair with microscopic sutures through neurorrhaphy ( repeated direct anastomosis)
Reconstruction through an interstitial graft if neurorrhaphy is not feasible due to the extensive loss of nerve tissue.
An alternative strategy for nerve graft is to use skeletal muscles . To date, there is no definite report regarding the level of sensory recovery of the inferior alveolar nerve. Also, use of arteries and veins has been reported with varying levels of success clinically . Use of vasculature for grafting has been considered because of the minimum tissue invasion and ease of access. However, this method has not shown acceptable results thus far. At present, some have suggested using alloplastic grafts which have caught great attention for their availability and avoiding the morbidity of the donor site. Their biocompatibility and efficacy are for the short grafts only. However, acceptable results have not been reported in this regard either.
Inferior alveolar nerve transposition for implant placement almost in 100% of cases results in sensory impairment immediately after surgery [10,31,32]. Sensory disturbances are resolved in 84% of cases and in only 16% of patients may this complication be permanent and irreversible [10,24,32,33]. The important issue in management of nerve injury is to inform and educate the patient in this respect. The patient should be educated before and after the surgery and should be well aware that nerve reconstruction may take a long time and he/she may experience paresthesia or dysesthesia for a long period of time. The patient may be taught to massage the area (with lanolin or a moisture absorbing ointment). Massage should be started with mild movements and then the intensity is increased to improve the sense of touch. Massaging is indicated 4 to 6 times a day for 10 to 15 minutes. The first sense that resumes is the sense of cold followed by pain. At this time the patient still has paresthesia in the area. After 4 to 5 months, the patient would be able to differentiate between cold and heat sensations and feels the sharpness of needle with 25 to 30 g pressure. After 6 months, touch, pain and thermal sensations will resume more efficiently . All patients should undergo treatment with low level laser for 10 sessions (4 times a week). The sessions start from the day of surgery. The sensitive area is detected using a simple anesthesia needle and is controlled monthly. The percentage of recovery is calculated by the proportion of the primary area suffering from paresthesia to the final area after 6 months. Researches indicate that chance of spontaneous recovery of the nerve is smaller in women compared to men . As mentioned earlier, most surgeons believe that sensory disturbances should be considered as a normal predictable state following nerve transposition surgery and not a complication or sequel of treatment [10,32].