Sensory impairment of the skin and mucosa innervated by branches of the trigeminal nerve is a potential concern in association with dental implant surgery. The most common nerves traumatized in implant dentistry are the inferior alveolar nerve (IAN) and its mental branch. Other nerves at risk include the lingual nerve, long buccal nerve and the infraobital nerve because of the anatomic location of these structures. Neurosensory impairment may occur during all phases of dental implant surgery, including anesthetic administration, incisions, soft tissue reflection, osteotomy preparation, bone augmentation, implant placement, suturing and/or soft tissue swelling after surgery. The reported incidence of such nerve injuries following dental implant procedures is highly variable (0%-44%).1-5
When a nerve injury occurs, the dentist should be able to recognize the type and extent of injury and provide the most appropriate post-operative care. Traumatic and iatrogenic nerve complications may involve total or partial nerve resection, crushing, stretching, or entrapment injuries. The resulting sensory deficits may range from a non-painful minor loss of sensation to a permanent and severe debilitating pain dysfunction. Presently, no standardized protocol exists for the dentist in the management of nerve injuries after implant surgery. Yet, surveys at the Misch International Implant Institute™ indicate 87% of dentists have encountered situations of neurosensory impairment within their practices.6 Yet , no organized approach to evaluate and/or treat this condition has been presented. The purpose of this paper is to present guidelines for the dentist in the diagnosis and possible management of mandibular nerve neurosensory deficits (including referral) following dental implant surgery that is dependent on the history, type, and nature of the injury.
PERIPHERAL NERVE ANATOMY/HISTOLOGY
The trigeminal nerve is the largest of the cranial nerves and has three major divisions: the opthalamic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3). A nerve outside of the central nervous system is called a peripheral nerve. The mandibular nerve is a peripheral nerve which is the largest of the trigeminal branches and, as previously stated, is the most common branch that is involved with neurosensory disturbances following dental implant surgery. This division carries sensory information from the lower lip, chin, lower teeth (and associated soft tissues), the mandibular bone, and parts of the external ear.
The mandibular nerve also contains motor fibers for supply of the muscles of mastication, tensor tympani muscles of the ear and tensor veli palatine muscles of the soft palate.6 However, these motor branches and many of the sensory fibers to the external ear are not injured during implant surgery, since the motor fibers are separated from V3 prior to its exit from the foramen ovale of the skull and many of the sensory fibers enter the nerve above the lingula of the ramus. A V3 injury in implant surgery usually occurs after the nerve enters the lingula of the mandibular ramus and anywhere along its pathway in the body and/or its exit from the mental foramen.
The histology of the mandibular nerve consists of connective tissue and neural components. The smallest functional unit in the trigeminal nerve is the nerve fiber. These nerve fibers can be either myelinated or unmyelinated. Myelinated nerve fibers, the most abundant, consist of a single axon that is encased individually by a single Schwann cell. The individual nerve fibers and Schwann cells are surrounded by a protective endoneurial connective tissue layer (endoneurium), which is made up of a basal lamina, collagen fibers and endoneurial capillaries.7
The individual nerve fibers of the trigeminal nerve are situated in multiple groups termed fascicles. Surrounding the bundles of fascicles is a thin, dense, multilayered connective tissue sheath called the perineurium. The perineurium maintains intrafascicular pressure and acts as a diffusion barrier in the protection of the individual fibers. If any of these extra neural tissues are injured, impaired neural transmission of the individual nerve fibers may result in a sensory disturbance.11 The neurosensory impairment is dependent on the extent of damage to the individual tissue type.
A main concern related to injury of the IAN is the altered sensory functions (i.e. touch, pressure, temperature or pain) following implant related surgeries. Loss of sensation of the cheek and/or mandibular lip may lead to traumatic injury to the soft tissues during chewing and mastication and may affect the ability to drink. Significant pain may also be associated with these sensory functions, which may be debilitating to the patient.
TERMINOLOGY OF SENSORY DISTURBANCES
The literature related to peripheral nerve injuries is abundant; however there exists great variation in the nomenclature used to describe the clinical signs and symptoms. Several common terms are used, often with overlapping meanings. The most commonly used term to describe an altered sensation is paresthesia. For years, paresthesia has been used to describe any altered sensation including pain, numbness, tingling, aching, warmth, cold, and burning.12 Recently, the Association for the Study of Pain has standardized a nomenclature system that defines the most frequently used neurosensory descriptive terms.13 There now exists three distinct categories with related subcategories describing neurosensory deficits. The most significant change is paresthesia which is limited to an altered sensation that is not unpleasant. Dysesthesia is defined as any altered sensation that is unpleasant. Anesthesia is the total loss of feeling or sensation. These three main categories are used to describe, diagnose and treat (including referral) the nerve injury in the protocol suggested in this paper. Table 1 describes the most commonly used terms for neurosensory deficits. (Table 1).
RELATED HOST AND LOCAL FACTORS
Many factors, both local and host-related, will determine the neurologic response to an injury. The type of injury is the most significant local factor relating to the neurologic response. In general, injuries that occur at the proximal site of the peripheral nerve are more significant (i.e. ramus region) than those that occur at distal sites (i.e. the mental foramen area). The more proximal the nerve injury site, the higher the risk of trigeminal ganglion cell damage and the initiation of retrograde differentiation effects into the central nervous system.16
Less traumatic injuries often are associated with early paresthesia or dysesthesias. When a nerve is stretched or compressed, the perineurium will protect the nerve fibers within the fascicles. With greater tension, the fascicles will begin to elongate, thus elevating the intrafascicular pressure. Further pressure will lead to axon damage and if elongation is greater than 30%, structural failure with possible severance may occur.17 Partial or incomplete nerve injuries will have different responses than complete nerve lacerations or resections. In contrast, more severe injuries are initially anesthetic lesions with poor orofacial function and associated referred, radiating forms of paresthesia. Although they may not be painful initially, they may eventually lead to formation of dysfunctional chronic neuroma formation.18,19
The most significant host factors related to implant dentistry are the patients age and gender. It is well documented, for all types of nerve injuries that both females and increasing age are at greater risk of neurosensory deficits.20,21 In older individuals, cell body regeneration has been shown to be slower and less dramatic than in younger individuals.
The pharmacologic therapies for acute nerve injuries include the use of corticosteroids and non-steroidal anti-inflammatory agents. The use of adrenocorticosteroids (e.
g., Dexamethasone) has been shown to minimize neuropathy following nerve injuries if administered in high doses within one week of injury.22,23 Additionally, adrenocorticosteroids have been shown to inhibit axon sprouting centrally and ectopic discharges from injured axons and prevention of neuroma formation.24,25 Dexamethasone (8–12 mg) is specifically recommended because of its greater anti- inflammatory effects in comparison to other corticosteroids.26,27 It has been advocated that a tapering dose of a corticosteroid for 5–7 days be prescribed following trigeminal nerve injury.28
Further pharmacologic therapy includes the use of Nonsteroidal Anti-Inflammatory agents (NSAIDs). NSAIDs have been shown to be excellent inhibitors of prostaglandin synthesis from damaged peripheral nerve endings.29 Prostaglandins released as a result of peripheral nerve damage sensitize peripheral nociceptor fibers and central spinal tract neurons.30 Accordingly, maintaining therapeutic blood levels of NSAIDs as an adjunct to the corticosteroid usage for one to three weeks after the injury is highly beneficial for the acute and intermediate stages of trigeminal nerve recovery.31 Since any altered sensation may be due to an inflammatory reaction, a post-operative course of steroid treatment followed by a high dose of nonsteroidal anti-inflammatory medication (such as ibuprofen 600 to 800 milligrams three times per day for three weeks) is used as soon as possible following any nerve injury. If necessary at two to three weeks after the injury on the basis of a repeated neurosensory examination, the clinician can prescribe an additional three weeks of nonsteroidal anti-inflammatory drug treatment, if no signs of gastric disturbances are present.
Additional pharmacologic agents that have been advocated include antidepressants, anticonvulsants, antisympathetic agents and topical medications. Precaution should be taken with these types of pharmacologic treatments as they should be prescribed and managed by a clinician familiar with the side effects of these drugs and experienced in treatment of nerve injuries.
INITIAL MANAGEMENT OF NEUROSENSORY IMPAIRMENT
Various surgical and pharmacologic treatments have been advocated in the literature for nerve injury with varying degrees of success.30 The management of the neurosensory deficits presented in this paper (Table 2) should first include recognition and documentation of the type of injury and associated signs and symptoms. Initially, physiologic and pharmacologic nonsurgical therapies are indicated followed by surgical evaluation and/or treatment.
If the patient experiences an electric shock feeling to the tongue (lingual nerve) or chin, lip, and/or gingival region (IAN), the anesthetic needle may have perforated the nerve. This is more an issue for the lingual nerve, since it is smaller in diameter. Although more than 75% of altered feelings from this type of nerve injury resolves within threeweeks when this happens, a pharmacologic protocol of immediate dexamethasone 4 mg/ml injection into the site, followed by three days of decreasing corticosteroid doses is beneficial (Fig. 1).
If, during surgery, known or observed trauma (including traction or compression of the nerve trunk) has occurred, the topical application of Dexamethasone is suggested. One to two ml of the intravenous form of Dexamethasone (4mg/ml) may be topically applied for 1-2 minutes32 (Figs. 2-4). The direct application of adrenocorticosteroids will reduce neural inflammation and reduce compression from swelling, which may enhance recovery from neurosensory deficits. No morbidity has been associated with topical steroid application at the nerve injury site, yet significant improvement in post surgery recovery has been observed. This is followed by a six day regimen of oral dexamethasone (4 mg two tabs AM for three days, one tab AM for three days). If known nerve trunk transection is clinically observed during the surgery, immediate referral to a nerve repair specialist is highly recommended.
The most important physiologic therapy at the time of surgery includes removal or repositioning of any irritant (implant, bone screw) in close approximation to the neurovascular bundle. A radiograph or CT scan immediately after implant placement is warranted to insure the nerve is not violated. If a post operative radiograph indicates the implant may encroach upon the IAN, it may be removed, a steroid introduced into the osteotomy site and then a shorter length implant replaced in the same site in a more ideal location.32 No bone grafting materials should be placed in the osteotomy site, since it may invade the mandibular canal and interfere with nerve repair.
Cryotherapy should be applied extraorally to most any implant or bone graft site, but especially when nerve injury is suspect. The paraneural tissues should have ice applied intensely for the first 24 hours post operatively and then episodically for the first week. Cryotherapy has been shown to minimize secondary nerve injury from edema-induced compression, decrease the metabolic degeneration rate of trigeminal ganglion cells from undergoing degeneration, and slow potential neuroma formation.33 Ice, when applied to the tissues, has been shown to significantly improve postsurgical recovery.
POST-OPERATIVE MANAGEMENT OF MEUROSENSORY DEFICITS
When the dentist discovers a neurosensory deficit has occurred (often at the suture removal) a comprehensive sensory evaluation should be completed. The purpose of this initial examination is to ascertain whether a sensory deficit exists, to define and quantify the extent of nerve injury, record a baseline for recovery, and to determine if referral for microneurosurgery is indicated.11
There are several accepted protocols for neurosensory testing. Ideally, a range of tests are performed ranging from light mechanical to noxious stimuli. The authors have advocated two categories of clinical neurosensory testing, nociceptive and mechanoreceptive. Each test is specific for various neural receptors and axons. The responses are recorded and quantitatively compared with responses from contralateral uninjured tissues (control). The following are the more common tests suggested for the neurosensory evaluation:
“Pin-Prick” Test: A 27-gauge needle is utilized to test for pressure detection and anesthesia/paresthesia/dysthesia. A cosmetic pencil is used for mapping and photographs are used to evaluate the recovery period (Fig. 5).
Temperature Sensitivity Tests: Ice chips or ethyl chloride spray and a heated mirror handle (warmed to 43 degrees) are used to determine the patient’s ability to feel cold and hot. Alternatively, test tubes may be filled with hot (43°C) water and/or cold water.
Static Touch Detection Tests: A cotton tip applicator is used to determine sensation.
Direction of Movement Test: The sensory modalities of mandibular nerve fibers are touch and vibration. A soft brush is used (with the patient’s eyes closed) to determine the patient’s ability to detect both sensation and direction of movement.
Two-Point Discrimination Test: With the patients eyes closed, the patient’s ability to discriminate varying distances between two points is determined. A caliper with the ability to vary the distance between two points can be used. The normal distance at which most patients can discriminate two separate points is 6 mm.34
If the initial exam is within one week of the surgery, a course of steroids (decadron) is prescribed followed by three weeks of high dose NSAID’s (600 mg – 800 mg ibuprofen). If paresthesia is reported after a two week period, only high doses of NSAID’s should be prescribed (600 mg to 800 mg ibuprofen TID for three weeks). If necessary, an additional three
weeks of NSAID’s may be prescribed. If paresthesia is present, the neurosensory exam is repeated every two to three weeks. The patient should be periodically re-examined to evaluate if nerve repair is occurring, signified by reduced symptoms and less soft tissue area involvement. Neurosensory improvement most often occurs by two to three months. If significant sensation has not improved by three to four months after the surgery, the prognosis typically is poor.
REFERRAL OF NEUROSENSORY DEFICITS
In certain situations, patients need to be referred to a practitioner experienced in nerve injury assessment and repair (Table 2). As previously mentioned, if known transection of the nerve occurs during surgery, Dexamethasone should be applied and following surgery, an immediate referral to a specialist in microsurgical repair. Likewise, if the patient has dysesthesias or complete anesthesia at the initial exam after surgery, the patient should be referred to a nerve specialist. Prompt surgical intervention may allow for the best chance of neurosensory recovery.
The decision post operatively to refer should be based on the patient’s signs and symptoms and the type of injury. A paresthesia should be given sufficient time for neurosensory recovery. However, referral to a nerve injury specialist is suggested after three months if the paresthesia has not improved during this time frame.
Additional physiologic therapies have shown successful results in the treatment of nerve impairments, and include transcutaneous electric nerve stimulation (TENS),35 acupuncture36 and low-level laser therapy.37 It is suggested these physiologic therapies be used as indicated by a nerve specialist.
Various techniques to surgically treat nerve impairments have been advocated with varying results. This includes decompression, direct anastamosis,38 autogenous nerve grafts,39 and alloplastic grafts.40 Successful surgical intervention, when indicated, is generally agreed to be most predictable if performed prior to the onset of Wallerian degeneration (approximately three months).28 This early, aggressive treatment may prevent transition to chronic refractory neuropathies.41,42
The suggested treatment of mandibular nerve neurosensory deficit is summarized in Table 2. The protocol during surgery is divided into two aspects: nerve injury suspected (most often after a radiograph is made), or known nerve transection during surgery. Corticosteroids, NSAID’s, and cryotherapy are prescribed following surgery. The post operative protocol is divided into the one week, initial treatment and the 12 week period. During this time frame a paresthesia is documented and mapped every two to three weeks to monitor the condition. NSAID’s are prescribed for up to three weeks after the initial corticosteroid therapy. If dysesthesias or anesthesia is found at the initial post operative appointment, a referral to a nerve specialist is suggested. Referral is also suggested to a specialist in nerve damage after three months if the paresthesia is not improved.
With the popularity of dental implants and associated bone grafting, peripheral trigeminal nerve branch impairments may become more frequent. It is not expected that the practitioner make a definite neurosensory diagnosis. However, one must be sufficiently knowledgeable in the causes, prevention and treatment of such injuries to make an appropriate diagnosis and treatment and timely referral when necessary. Neurosensory changes in the orofacial region on rare occasions may be devastating. A protocol has been presented which emphasizes early treatment with a wide range of modalities and guidelines for treatment — based on type and degree of neurosensory impairment. OH
*Clinical Professor, Temple University, PA,
+Misch International Implant Institute, Beverly Hills, MI
∞Private Practice, Beverly Hills, MI
‡Private Practice, Pittsburgh, PA
◊ Faculty, Misch Implant Institute, Beverly Hills, MI.
Oral Health welcomes this original article.
1. Bartling, R., Freeman, K., Kraut, RA: The incidence of altered sensation of the mental nerve after mandibular implant placement, J Oral Maxillofac Surg 57:1408 – 1410, 1999.
2. Gregg, MJ: Neuropathic complications of mandibular implant surgery: review and case presentation, Ann Roy Australas Coll Dent Sur 15:176-180, 2000.
3. Van Stenberghe, D., Lekholm, U., Bolender C., et al: Applicability of osseointegrated oral implants in the rehabilitation of partial edentulism: A prospective multicenter study of 558 fixtures, Int J Oral Maxillofac Implants 5:272-281, 1990.
4. Ellies, L., Hawker, P.: The prevalence of altered sensation associated with implant surgery, Int J Oral Maxillofac Implants 8: 674-679, 1993.
5. Smith, MH., Lung KE.: Nerve injuries after dental injection: A review of the literature, J Can Dent Assoc 72: (6). 559-564, 2006.
6. Misch International Implant Institute, 16231 W. 14 Mile Rd., Beverly Hills, MI 48025, Carl E. Misch, DDS, MDS, Director
7. Sharawy, M.: Applied anatomy for dental implants. In Misch, CE: Contemporary Implant Dentistry, St. Louis, Mosby Elsevier, 353-358, 2008.
8. Assael, LA.: The nerve under the microscope, J Oral Maxillofac Surg. 60:5, 483-484, 2002.
9. Svane, JT, Wolford, LM., Milam, SB., Bass, RK: Fascicular characteristic of human inferior alveolar nerve. Oral Maxillofac Surg. 44: 431-431, 1986.
10. Pogrel, MA., Schmidt, BL., Sambajon, V., Jordon, RC.: Lingual nerve damage due to inferior alveolar nerve blocks, J Am Dent Assoc, 134: (2) 195-199, 2003.
11. Day, RH.: Diagnosis and treatment of trigeminal nerve injuries, J Calif Dent Assoc 22 (6): 48-51, 53-4., 1994.
12. Girad, Kenneth R: Considerations in the management of damage to the mandibular nerve, JADA, 98: 65-71, 1970.
13. Classification of Chronic Pain, Second Edition: International Association for the Study of Pain Task Force on Taxonomy, ed.: H Merskey and N. Bogduk. IASP Press IASP Council in Kyoto, November 29-30-2007.
14. Seddon, JJ.: Three types of nerve injury, Brain 66:237-240, 1943.
15. Sunderland, S.: A classification of peripheral nerve injuries produced by a loss of function, Brain 74:491-505, 1951.
16. Cooper, BY, Sessle, BJ.: Anatomy, Physiology and Pathophysiology of Trigeminal System Paresthesia and Dysesthesias, Oral Maxillofac Surg Clin of North America. 4:2, 297-322, 1992.
17. Hubbard, JH.: The quality of nerve regeneration. Factors independent of the most skillful repair. Surg Clin North Amer, 52:1099-1105, 1972.
18 Jaaskelainen, SK, Teerjoke-Oksa, T, Forssell, H.: Neurophysiologic and quantitive sensory testing in the diagnosis of trigeminal neuropathy and neuropathic pain. Pain, 117 (3): 349-356, 2005.
19 Rasmussen, PV, et al.: Symptoms and signs in patients with suspected neuropathic pain, Pain 110: 461-464, 2004.
20. Bruce, RA. Frederickson, GC, Samll, GS.: Age of patients and morbidity associated with mandibular third molar surgery, J Am Dent Assoc, 101:204-251, 1980.
21. Haas, DA, Lennon, D.: A 21 year retrospective study of reports of paresthesia following local anesthetic administration, J Can Dent Assoc. 61:319-320, 1995.
22. Galloway EB; Jensen RL; Dailey AT; Thompson BG; Shelton C.: Role of topical steroids in reducing dysfunction after nerve injury. The Laryngoscope 110(10):1907-10, 2000.
23. Jansco, G. Kiraly, E., Jansco-Gabor, S.: Pharmacologically induced selective degeneration of chemo sensitive primary sensory neurons, Nature 270:741-756, 1977.
24. Kohnelein, KE, Ocker, K. Seitz, HD: Experimental trails to inhibit neuroma formation. Chir Plast (Berlin) 5:207-211, 1980.
25. Seo, K. et al.: Efficacy of steroid treatment for sensory impairment after orthognathic surgery. J Oral Maxillofac Surg, 62: 1193-1201, 2004.
26. Devor, MR., Govrin-Lippman, R.: Corticosteroids suppress ectopic neural discharge originating in injured experimental neuromas, Pain 22:127-135, 1985.
27. Vecht, ChJ, Haakma-Reich, H., Van Putten, WLJ.: Conventional versus high dose dexamethasone in metastatic spinal cord compression, Neurology 39 (Suppl 1): 220-228, 1989.
28. Kraut, RA, Chanal, O.: Management of patients with trigeminal nerve injuries after mandibular implant placement, JADA 133: 1351-1354, 2002
29. Devor, M.: Pathophysiology of damaged peripheral nerves. In Wall PD, Melzack, R. (eds): Textbook of Pain, ed 2. London, Churchill Livingstone, 63-66, 1989.
30. Muller, HW., Stoll, G.: Nerve injury and regeneration: basic insights and therapeutic interventions. Cun Opin Neurol, 11: 557-559, 1998.
31. Devor, M., Govrin-Lippman, R., Raber, P.: Axoplasmic transport block reduces ectopic impulse generation in injured peripheral nerves, Pain, 16:73-77, 1983.
32. Misch, CE: Root Form Surgery in the Edentulous Anterior and Posterior Mandible: Implant Insertion, In Misch, CE: contemporary Implant Dentistry, St. Louis, 2008, Mosby Elsevier, 221-226.
33. Olson, J.: A review of cryotherapy. Phys Ther. 52:840-844, 1972.
34. Kawamura, P. Wessberg, Ga.: Normal Trigeminal Neurosensory Responses, Hawaii Dent J, 16:8-11, 1985.
35. Bates, JAV., Nathan, PW.: Transcutaneous electrical nerve stimulation for chronic pain, Anesthesia. 35-817-824, 1980.
36. Sung, YF, Kutner, MH, Cerine, FC.: Comparison of the effects of acupuncture and codeine on postoperative dental pain, Anesth Analg Curr Res, 56:473-481, 1977.
37. Poole, TE., Holland, I., Peterson, LJ.: Clinical efficacy of low level laser treatment of oro-facial neurosensory deficits, J Oral Maxillofac Surg, 51 (suppl. 3), 182-186, 1993.
38. Colin, W. Donoff, RB.: Restoring sensation after trigeminal nerve injury: a review of current management. JADA 123 (12), 80-85, 1992.
39. Ruggiero, S.: Trigeminal nerve injury and repair, NY State Dent J, 62:36-40, 1996.
40. Pogrel, MA: The results of micro neurosurgery of the inferior alveolar and lingual nerve. J Oral Maxollofac Surg, 60 (5): 485-489, 2002
41. Hegedus, F. Diecidue, FJ.: Trigeminal nerve injuries after mandibular implant placement- Practical knowledge of clinicians, Int J Oral Maxillofac Implants 21: 111-116, 2006.
42. Nazarian, Y., Eliav, E., Nahlieli, O.: Nerve injury following implant placement: Prevention, diagnosis and treatment modalities. Refuat Hapeh Vehashinayim. 20:44-50, 2003.