The overall goal of this article is to provide the reader with information on achieving profound local anesthesia.
On completion of this course, the participant will be able to do the following:
1. List the factors that the clinician must be aware of when providing local anesthesia for endodontic emergencies.
2. Describe the inflammatory and degenerative processes that occur in the presence of pulpal disease.
3. Describe the anatomical considerations in the maxilla and mandible that can complicate the achievement of profound local anesthesia.
4. Identify the alternative techniques that can be utilized for local anesthesia, where and how each of these may be used.
5. Utilize tips provided in this article for evaluating the degree of anesthesia for the symptomatic mandibular molar.
The ability to achieve profound local anesthesia for patients in general, and endodontic patients in particular, can be impacted by
many factors. These include the inflammatory process, anatomical structures and neural variations. In order to efficiently and effectively manage endodontic emergencies in a relatively painless manner, the clinician must understand all of these considerations.
Local anesthetic techniques for the maxillary and mandibular arches that included both inferior mandibular nerve blocks and maxillary infiltrations are usually sucessful, however, at times supplemental or alternative approaches to achieve profound anesthesia are necessary for total patient comfort and clinician achievement.
How often have you heard a patient say, “On my last dental visit it took 5 shots of Novocain to do the dental work and I still could feel pain” or something akin to this scenario; or if you are an endodontist, the comment is as follows, “My dentist can never get me numb and it always takes 5-6 shots and now I dread having this root canal.” These are common, daily scenarios that often contribute to patient avoidance of dental procedures, no matter how small. The alleviation and prevention of dental pain resulting from pulpal or periradicular pathoses are prime objectives for the dental professional.
The attainment of these goals is predicated on three major factors that must be addressed in every clinical case:
• The clinician must thoroughly understand the inflammatory disease processes that affect the dental pulp and periradicular tissues.
• The clinician must make a thorough subjective and objective assessment of the patient’s chief complaint and integrate these findings with the spread of inflammation, infection, and degenerative processes in the pulp and periradicular tissues.
• A repair-predictive, treatment-oriented approach must result from these findings.
Once acute pulpal pain, acute periradicular pain, acute alveolar abscess, or cellulitis is identified/diagnosed, one of the greatest problems in managing the patient’s discomfort is the inability to provide adequate anesthesia. However, endodontic emergencies can be efficiently and effectively managed in a relatively painless manner when the clinician is aware of the following:
• Inflammatory and neural considerations in the pulp and periradicular tissues
• Osseous and neural variations in the area to be anesthetized
• Variable approaches to achieving anesthesia in both dental arches
• Patient-specific considerations
• Obtaining anesthesia in the most challenging clinical scenario
Normal pulp tissue has a relatively high blood flow that is minimally influenced by vasodilator substances (products of irritation). This results, therefore, in minor increases in localized blood flow during irritation and inflammation.1 In the inflamed environment, capillary permeability appears to be more significant than blood flow with regard to the inflammatory response of the pulp. This set of circumstances rules out the concept of generalized pulpal edema, in spite of the low compliance environment within the tooth. Localized inflamed tissues undergo an increase in tissue pressure, which results in focal vascular stasis, ischemia, and tissue necrosis. These focal areas of necrosis serve as additional insults within the pulp, and the subsequent cyclical episodes of inflammation and cellular death result in incremental and circumferential spread of tissue destruction.2
The periodic irregular inflammation and destruction of local tissues coupled with bacterial invasion partially explain the clinical experience of episodic pain. Further explanations for this episodic phenomenon may include neural fluctuation with cycles of increased and decreased nerve fibers and peptide cytochemicals; this is perhaps associated with cycles of intrapulpal abscess expansion and repair.3-6 Interestingly, the sprouting of new nerve fibers and alterations in neuropeptides associated with a painful carious attack have been identified. 6,7 Likewise, sustained severe pain might be interpreted as multiple areas of tissue simultaneously undergoing demise. In many patients episodes of severe pain are often followed by the absence of symptoms, indicating the presence of either pulpal necrosis or an effective avenue of drainage from the inflammatory process.
The inflammatory and degenerative processes that occur in the presence of pulpal disease are basically the same as elsewhere in the body’s connective tissue.8 When coupled with root canal procedures, coronal leakage of bacteria, products from inferior dental restorations, and/or toxic root canal filling materials, the periradicular tissues will reflect a complex of both inflammation and repair. Histologically, the lesion consists predominantly of granulation tissue (exhibiting significant angioblastic activity), many fibroblasts, connective tissue fibers, an inflammatory infiltrate, and often a connective tissue encapsulation.9 The inflammatory infiltrate consists of plasma cells, lymphocytes, mononuclear phagocytes, and neutrophils. Occasionally, cholesterol clefting is seen with foreign body giant cells. If adjacent strands of epithelium or rests of Malassez have been stimulated by the inflammatory response to form a squamous epithelium-lined cavity filled with fluid or semisolid material, a cyst will develop.
As long as there is an egress of tissue irritants and bacteria from the root canal system, or there is a failure of the phagocytic macrophage system to control this irritation, the histologic pattern of the periradicular lesion will be one of concomitant repair and destruction.10 Often this variable tissue response is subjected to superimposed inflammatory, infective or immunological processes. These changes will be reflected by the patient’s signs and symptoms, moving from a chronic clinical state of minimal-to-no symptoms to an acute state with painful characteristics. It is this environment that the astute clinician must control with properly chosen and administered anesthetic solutions. Table 1 provides typical clinical signs and symptoms that usually exist with irreversible pulpitis with symptomatic periapical/periradicular periodontitis.
The inflammation that accompanies pulpal and periradicular degenerative-infective changes results in a reduced pH in tissues over variable areas, depending on the extent and acuteness of the process. This has been suggested as the explanation for the difficulty in achieving quality anesthesia, as the ability of the weak anesthetic base (pKa 7.5 to 9.0) to dissociate is significantly affected.11 Others have suggested that the inflammation alters peripheral sensory nerve activity,12 possibly due to neurodegenerative changes along the inflamed neural element distal from the inflammatory site.13,14 As suggested by Wong and Jacobsen, 15 an increase in anesthetic concentration (not necessarily volume) is required to lower the neural action potential when attempting to achieve complete anesthesia in the presence of inflamed tissues. An alternate approach would be to administer the local anesthetic away from the area of inflammation, such as the use of a regional nerve block,16,17 especially in the case of extensive cellulitis or acute periapical abscess.
Variations in the osseous anatomy surrounding the tooth roots and aberrant neural structures have received renewed attention as potential impediments to the administration of successful anesthesia. Common variations relative to the maxilla and mandible are discussed below.
Maxillary Arch
Generally, the outer cortical plate of an adult’s maxillary bone is thin and sufficiently porous to infiltrate anesthesia effectively. However, in areas of the zygomaticoalveolar crest (Figure 1), penetration of anesthetic solution to the middle superior alveolar nerve may be restricted,18 especially in children.16 Likewise, the absence of this neural branch has been reported—requiring more extensive placement of the anesthetic solution to manage the first molar and premolars.19,20 The prominence of the anterior nasal spine (Figure 2) and floor of the piriform aperture may preclude approximation of the root apices of the incisors. In the premolar and molar regions, the position of the palatal roots relative to the buccal cortical plate may require palatal infiltration anesthesia (Figure 3).
Mandibular Arch
The mandibular foramen is the primary target for the deposition of anesthetic solution for profound anesthesia of the mandibular teeth (Figure 4). While the foramen’s position is variable, it is usually found anterior to the midpoint of the ramus of the mandible when the anterior border of the mandible is the internal oblique ridge.21 This position is slightly above the occlusal level of the molars,22 although Nicholson 21 defines it as being below the occlusal surface in 75% of the mandibles studied. The importance of this variability cannot be overemphasized to the clinician, as the angle and level of needle penetration must be reassessed and altered accordingly in many cases in which profound anesthesia is not readily achieved with a standard approach. Rare, extreme variability in the course of the mandibular canal has also been reported—even to the extent of bifidity.23-25 Conventional attempts at mandibular blocks in these cases may lead to failure. Two- or three-dimensional examination of panoramic views of the mandible or the use of Cone Beam CT scans are extremely helpful to anticipate such variations when necessary.26 Of all the variables that create controversy in achieving profound anesthesia in the mandible, the presence of accessory innervations has received the most attention.27 This ranges from the presence of well-defined foramina higher on the internal surface of the ramus (Figure 4), in the coronoid or mandibular notch (Figure 5), and in the retromolar fossa (Figure 6),23,28-31 to the extension to and innervation of both posterior and anterior teeth by branches of the mylohyoid nerve,29,32,33 the median symphyseal crossover from branches of the incisive nerve,9,33,34 and the transverse cervical cutaneous nerve that may intermingle with fibers of the mental nerve or enter the mental foramen and continue posteriorly, innervating the premolars or molars.12,18,35,36 Support for this speculated phenomenon is primary empirical.37-39 In-depth discussions of the complexities of mandibular innervations can be found in the literature.39,40
There are a number of approaches that can be used for the maxillary and mandibular arches to achieve anesthesia.
Maxillary Arch
Considering the potential impediments to achieving profound anesthesia in the maxillary teeth, the suggested sequence for administering anesthetic is as follows: 1. Supraperiosteal injection: Infiltrate the facial tissues with the needle tip in the immediate area of the root apex at an angle of 45 to 90 degrees
2. Palatal injection: Use to supplement facial infiltration when necessary
3. Regional injection or block: Use when infiltration fails or when extensive infection/swelling is present
4. Intraligamentary ligament (periodontal ligament) injection: Use multiple injection sites (may be limiting in scope when extensive discomfort is present)
5. Intraseptal injection: Use when bone is less dense
6. Intraosseous injection: Use a rotary instrument for osseous penetration and be careful with the amount of solution injected. Use as an adjunct with intrapulpal injection.
Mandibular Arch
The suggested sequence for achieving profound anesthesia for mandibular teeth is as follows:
1. Inferior alveolar injection: Administer by the traditional method, taking into account the following possible variations:
• Gow-Gates Injection*
• Akinosi-Vazirani Closed-Mouth Injection:*
2. Buccal Infiltration: Use of soft tissue anesthesia.
3. Mylohyoid infiltration: Use if teeth continue to be inaccessible endodontically.
4. Mental foramen infiltration: Use if teeth continue to be inaccessible endodontically. Consider as an adjunct to any inferior alveolar nerve block (IANB), especially when the tooth is symptomatic. (Note the discussionabove on the cervical transcutaneous nerve.)
5. Intraligamentary injection (Periodontal Ligament): Use multiple injection sites (may be limited in scope when extensive discomfort is present).
6. Intraseptal injection: Use when bone is less dense.
7. Intraosseous injection: Use a rotary instrument for osseous penetration and be careful with the amount of solution injected. Use as adjunct with intrapulpal injection. *The use of these two alternative injections has received renewed interest in the dental community.27
They can be used for any type of dentistry performed in the mandibular arch and their use can be advantageous when the patient reports a history of failed IANBs or when oral opening is limited. However, present dental curricula do not afford the dental student the opportunity to learn these techniques at a level of competency. For the practicing dentist, the ability to learn these techniques and achieve success in their application is available through continuing educational courses.
Assessment of the patient’s pain level and perception of pain is essential in the provision of pain-free dental treatment. A history of a patient’s inability to be anesthetized to the proper level must be noted, especially when considering an IANB. Furthermore, following the administration of any anesthetic the clinician must wait for an adequate amount of time for anesthesia to occur before initiating emergency treatment. Early treatment intervention that results in pain only lessens the patient’s confidence, while decreasing the pain threshold. Every effort should be made to determine that profound anesthesia is present before initiating any dental, and certainly any endodontic, emergency procedure (see section below on tips for evaluating the degree of anesthesia for the symptomatic mandibular molar).
The clinical challenge in obtaining profound anesthesia that has received significant attention in the dental literature is the mandibular molar (in particular the first molar) when the diagnosis is irreversible pulpitis with acute (symptomatic) periapical (periradicular) periodontitis.41 Achieving profound and lasting anesthesia in this situation is possibly the most difficult task for both the neophyte and the experienced clinician. Failure rates for the IANB can reach as high as 30-45% when proper technique is used.42 Even when patients are asymptomatic, failure to achieve profound anesthesia in the first mandibular molar may run as high as 15-20%.40,42,43 Multiple studies have recommended the use of supplemental infiltrations in both symptomatic and asymptomatic patients 43-46 or the use of alternative anesthetic solutions.43,46-51 When considering both clinically advocated alternatives, neither has been fully successful. Moreover, studies from both the USA and other countries have shown a higher incidence of paresthesia following the administration of these alternative solutions (4% prilocaine and 4% articaine) for the IANB,52 although in select areas it did not differ much from the use of 2% lidocaine.53
The numerous reasons cited for the high failure rate encountered with the IANB include the thickness of the cortical plate of bone, soft tissue thickness and accessory or cross innervations,54 as previously discussed. Physiological reasons that have been identified include a decrease in local pH, tachyphylaxis of anesthetic solutions and activation of nociceptors (including tetrodoxtin and capsaicin-sensitive transient receptor potential vanilloid type).55 From a clinical perspective, the cause of failure is more often attributed to failure in the technique of needle placement,56 time of delivery of the solution 50 and failure to give the anesthetic sufficient time to penetrate into the target zone before starting any procedure.57
Three alternative techniques for the administration of anesthetic solution for mandibular molar anesthesia in the case of the symptomatic tooth are:1) the intraligamentary injection,58-61 2) the intraosssseous injection, 61-65 and 3) the intrapulpal injection.66-68 Prior to considering these injections, consider a mental injection as in many clinical situations this may be sufficient to achieve the desired profound anesthesia.
The intraligamentary injection can be used as a primary or secondary technique.58,61 However this approach may have some limitations, such as anesthesia of short duration, pain at the time of injection (if a primary injection), pain or soreness following the loss of anesthesia, elevation of the tooth in its alveolus and an elevated heart rate.59,60,69 A 27- or 30-gauge needle is recommended for this injection and should be placed in the gingival sulcus on the mesial and distal aspects of the tooth (Figure 7). With the bevel oriented toward the root surface, the needle is advanced into the periodontal ligament between the root surface and the adjacent alveolar bone. The solution must be placed under pressure so that it will be redirected into the surrounding cancellous bone through fenestrations in the alveolar socket. Anesthesia is usually rapid, but even here the clinician is cautioned to wait a few minutes prior to commencing treatment.
The intraosseous injection can be performed using standard or specialized equipment. Radiographs are necessary to locate the site of injection — the interradicular bone. Initially, the soft tissue over the site of planned penetration is infiltrated with a few drops of local anesthetic solution. The site is usually considered to be within the attached gingival about 2-3 mm below the gingival margin of adjacent teeth (or 5 mm below the marginal gingiva) in a vertical plane bisecting the interdental papilla.57,61 Subsequently, the bone is penetrated slowly with a small, sterile round bur. Once penetrated, a small needle is placed in the opening and a minimal amount of anesthetic solution (with no vasopressor, such as mepivacaine) is injected under pressure. Clinicians have noted that when this injection is used there is rapid attainment of anesthesia with sufficient duration for use with mandibular molars.63,69-72 Recent in vivo research in animals has identified the concentration of lidocaine around the root apices following the intraosseous injection, which would explain the clinical observations.73 There are some potential dangers associated with the intraosseous technique,64 including damage to root structure, a persistent sinus tract opening at the site of injection, breaking of a needle in the bone during delivery of the anesthetic solution under pressure, postoperative pain, swelling and infection. This technique should not be used in the presence of acute periapical infections or gross periodontal disease. Even when appropriate attempts have been made to anesthetize a painful tooth, failure may occur. In these cases an intrapulpal injection can be used, which achieves pain control due to the pressure applied during its placement. 68 This technique may initially evoke a painful response until the pulp has been penetrated. Therefore, attention to proper technique is mandatory. If the pulp is pathologically or traumatically exposed, the procedure is simple. However, if the pulpal chamber has not been penetrated, it will be necessary to gain entrance to the chamber with the least amount of patient discomfort. A No. 1 or 2 round bur is used in short incremental strokes to cut into the center of what would normally be the outline of the access opening preparation (or directed to the highest pulp horn). If the bur penetrates a few tenths of a millimeter at a time into the tooth, severe discomfort is minimized, and access to the pulp is achieved. A 30-gauge needle is passed into the small opening in the roof of the pulpal chamber, and the anesthetic agent is injected during penetration (Figure 8a). Often only a few drops of solution are necessary to anesthetize the pulpal tissue (Figure 8b). It should be noted, however, that the intrapulpal technique may anesthetize only the coronal pulpal tissue and vital tissue in the canals may not have been properly anesthetized. Further injections into the canal orifices may be necessary prior to a painless pulpectomy. In cases of acute pulpal pain without excessive pain to percussion or biting, an alternative treatment is to limit the emergency procedure to a pulpotomy, and to reschedule the patient for the pulpectomy procedure.67 Tips for evaluating the degree of anesthesia for the symptomatic mandibular molar Following proper delivery of the anesthetic solution used in an IANB and a mental injection, patients generally report a tingling sensation followed by numbness of the lip. However, these responses may not indicate profound pulpal anesthesia or complete anesthesia of the supporting, periradicular tissues. Two easy ways to determine the depth of anesthesia are to test the tooth with a cold stimulus(especially if pain to cold was a chief complaint) and to percuss the tooth with a mirror handle. The absence of abnormal responses would indicate that is it clinically acceptable to begin treatment. If the patient experiences any pain during the evaluation, the clinician must reassess the techniques used, redo the same injections, or alternatively go immediately to one of the injections discussed above (preferably using the intraligamentary injection first and if necessary the intraosseous injection).
Many factors impact the ability to achieve profound local anesthesia for patients in general, and endodontic patients in particular. Local anesthesia techniques are available for use in the maxillary and mandibular arches to help overcome these challenges, either as alternative or supplemental local anesthesia. Profound local anesthesia is necessary to efficiently and effectively manage endodontic emergencies in a relatively painless manner, and the clinician must understand the considerations involved and be familiar with available anesthesia techniques.
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