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Written by James K. Bahcall, DMD, MS, FICD Thursday, 01 May 2003 00:00
If you graduated from dental school in the last few years, you need not read any further, but if you graduated from dental school more than 5 years ago, I invite you to please read on. The field of endodontics has seen great technological advances and changes in thought process over the last decade. Unfortunately, this has made it very difficult for the general dentist to keep up with these changes in everyday practice.
As I lecture about endodontics to general dentists across the country, I have noticed a common theme of overall confusion about today’s endodontic practice. I felt that with approximately 80% of the general dentists in this country providing endodontic treatment to their patients, it was important to try to clear up some of this confusion.
Providing the best high-tech endodontic treatment on the wrong tooth does not do you or your patient any good. This is why good endodontic treatment begins with proper diagnosis. It is of utmost importance that etiology be identified prior to any endodontic treatment. Dental school education of the past never reinforced the fact that listening to the patient’s perception of the problem (subjective) and a dentist’s clinical testing (objective) to reproduce a patient’s subjective pain symptoms must correlate before any treatment is rendered. Integrated into the diagnosis is thorough review of a patient’s medical and dental history.
There is often confusion among practitioners as to the correlation of objective clinical tests with endodontic diagnosis. There are 5 objective clinical tests that need to be incorporated in the diagnostic evaluation: (1) cold, electric pulp tester (EPT), and heat test for pulp vitality; (2) percussion tests for the status of the periodontal ligament; (3) palpation tests of the gingival tissue and cortical and medullary bone for infection or inflammation; (4) periodontal examination, to include probings and tooth mobility; and (5) current radiographic examination with multiple angle periapical films and bite wing films as indicated.
It should be noted that heat and cold tests do not jeopardize the health of the pulp.1 Also, there seems to be a belief among clinicians that porcelain or metal crowns cannot transfer temperature to the underlying dentin. Teeth with crowns can be tested for vitality with cold or hot. The use of the electric pulp tester can establish pulp vitality, but the numerical readings cannot be used to determine the overall health of the pulp.2 An example of this is if tooth No. 8 has an EPT of 12 and tooth No. 9 has an EPT of 24, tooth No. 8 is not considered twice as healthy. When using an EPT, be aware that teeth with metal restorations can give false positive or negative readings.
Basic inflammatory pulp diagnosis is reversible or irreversible pulpitis. Reversible pulpitis is pain from an inflamed pulp that can be treated without the removal of the pulp tissue. It should be noted that this is not a disease, but a symptom of inflammation. Classic clinical symptoms are sharp, quick pain that subsides as soon as stimulus is removed. Physiologically, it is the A-Delta fibers that are firing, not the C-fibers of the pulp. A-Delta fibers are the myelinated, low-threshold, sharp/pricking pain nerve fibers that reside principally in the pulp-dentin junction. They are stimulated by cold and EPT and cannot survive in a hypoxic environment. Reversible pulpitis does not involve unprovoked (spontaneous) response.
Irreversible pulpitis is an inflamed pulp that cannot be treated except by the removal of the pulp tissue. Classic clinical symptoms are lingering of cold/hot stimulus greater than 5 seconds and/or patient reporting of spontaneous tooth pain. Physiologically, it can be the A-Delta fibers and/or the C-Fibers firing neural impulses. C-fibers are the unmyelinated, high-threshold, aching pain nerve fibers. They are distributed throughout the pulp. They are stimulated by heat and can survive in a hypoxic environment.
It is important to note that there are many nonodontogenic pain symptoms that mimic endodontic type symptoms.3 If a patient’s subjective description of pain is “tingling,” “electric-like,” “burning,” or “hurts on both sides of my face,” the etiology may be nonodontogenic in origin.
The gray areas of diagnosis appear when there are inconsistencies between a patient’s subjective description and the clinician’s diagnostic tests. If a clinician feels the diagnosis is odontogenic, but cannot localize the etiology, consider prescribing medication(s) to help localize the symptoms, or refer the patient to a dental specialist for another evaluation. Prescribing anti-inflammatory or antibiotic medications, then having the patient back for reevaluation, can sometimes help in definitive diagnosis. The difficulty with this is that some dentists believe that prescribing medication is not treating the patient unless a high-speed drill is involved. Yet, in the field of medicine, if physicians prescribe medicine, they are treating their patients properly. A dentist who renders treatment without identifying etiology is more likely to have a patient quickly lose confidence because of treatment that does not relieve symptoms.
A dentist should never feel defeated or any less of a practitioner if a referral is made to an endodontist for further evaluation. Patients will respect and appreciate dentists who know their limits in a particular case.
The use of selective anesthesia can also be a helpful aid in diagnosis. Although there are exceptions, if local anesthesia dissipates the patient’s pain, the etiology is generally odontogenic. If local anesthesia is not effective in eliminating pain, the etiology is usually nonodontogenic. When a dentist implements selective anesthesia in diagnostic procedures, it should be the last test performed because the tooth or teeth involved will not be able to be further tested for sensitivity at this appointment.
Another helpful aid in diagnosis is to have the patient keep a short daily diary. Remember, we were all dental-illiterate before we attended dental school! Patients often describe pain in generalities. It is not until they are asked to make notes of specific incidences of pain that they can better communicate to the dentist. Examples that I have seen in patient diaries are describing pain waking them up at night (spontaneous; diagnosis: irreversible pulpitis) or when they have coffee in the morning (C-fibers stimulation; diagnosis: irreversible pulpitis), but the pain is quickly relieved when they drink cold orange juice. The patient is usually requested to keep such a diary for a week.
If, after thorough review of diagnostic tests, the dentist feels that the etiology is nonodontogenic, the dentist should refer the patient to a physician (usually a neurologist) or a dental specialist (oral surgeon or maxillofacial pain specialist).
Anesthesia is one of the most important pain medications given in endodontics. Because in a clinical situation the anesthetic cannot be applied directly to a nerve membrane, a local anesthetic’s ability to diffuse through the tissue surrounding a nerve is of critical significance. The dissociation of local anesthesia and the relative proportion of each form in solution depend on the pH of the solution and surrounding tissues. If high pH (fewer H+ ions) exists, the chemical dissociation reaction is driven to the right, thus providing more base than cation. If low pH (more H+ ions) exists, the chemical dissociation is driven to the left, thus providing more cation than base4 (See Table).
Profound anesthesia is achieved with diffusion of the base through the nerve sheath, which then binds to specific receptors in the ion channel. Clinically, inflammation, infection, and vasoconstrictors lower the surrounding tissue pH. This can delay or prevent local anesthetics from taking effect. Providing profound anesthesia prior to endodontic treatment is paramount, yet our dental school training of the past has taught us the long road to achieve such profound anesthesia. I was taught that the more vasoconstrictor I can get on board, the faster I can get a patient comfortable. As stated above, a vasoconstrictor like epinephrine is acidic, and although it will provide constriction of the blood vessels, it will also delay the uptake of anesthetic when large quantities are placed, because less amount of base will be available to penetrate the nerve sheath.
Profound anesthesia is really obtained in the endodontic patient by using more Carbocaine (mepivacaine) without vasoconstrictor. I recommend using one carpule of anesthetic with vasoconstrictor, then switching over to Carbocaine. Mepivacaine is not as acidic, and therefore will allow more base to penetrate the nerve sheath. Injections should be given slowly to prevent inflammation of the surrounding tissue. This inflammation can also help to lower the tissue pH.
It is important to test the vitality of the tooth that is to be endodontically treated prior to administering local anesthesia. Many clinicians only determine the level of anesthesia from a patient’s subjective signs. The problem with this method is that although patients will tell you that they are numb, in many instances, the tooth being treated is not. Therefore, you should test the tooth to cold or EPT to determine the level of anesthesia (objective tests). Even if a tooth is going to have endodontic treatment for prophylactic reasons, it still should be objectively tested preoperatively and after local anesthesia is given to determine if profound anesthesia has been achieved.
|Figure 1. The “bull’s-eye” administration of anesthesia for endodontic treatment.|
It is also important to give what I call the “bull’s-eye” administration of anesthesia (Figure 1). Administer local anesthesia from a regional block and then work your way to an intrapulpal injection if indicated. Many dentists have been taught that an intraosseous injection or a mental block alone will suffice. It may work for a short period of time, but a patient’s discomfort level will quickly increase without the support of a regional block.
When giving an intraosseous anesthetic, do not use any epinephrine, as this most likely will cause tachycardia and an uncomfortable feeling for the patient. Mepivacaine should be used. This anesthetic will give you a 3- to 5-minute window of anesthesia to allow the practitioner to access a tooth and remove the inflamed or infected pulp tissue.
MECHANICAL CANAL DEBRIDEMENT
Over the last 10 years, we have seen the advent of nickel-titanium files and rotary instrumentation. Along with the change in metallurgy (stainless steel to nickel-titanium), there have been changes in the tapers and shapes of files. We have gone from the traditional step-back filing technique we learned in dental school to a crown-down technique that creates continual taper canal preparations.
During this time, we have been inundated with various file systems that are touted as the latest and greatest. Yet, from an in vivo evaluation of these systems with the aid of a fiberoptic endoscope,5 no file manufacturer to date has created the perfect file system. Although each of the systems has advantages and disadvantages, the combination of certain file systems has proven to provide the ideal file system. This system takes into account the biological (science) and a clinician’s (art form) requirements for state-of-the art endodontic treatment.
|Figure 2. Canal sections for instrumentation.||Figure 3. Apex locator.|
It is important to understand the physical principles of canal preparation. A clinician should think of a canal preparation in sections. These sections are the coronal two thirds, transition zone, and the apical one third (Figure 2). Hand files should be used at the start of the case to determine working length and obtain an initial tactile feel of the canal morphology. Working length should be confirmed radiographically or with an apex locator (Figure 3) prior to further canal preparation.
|Figure 4. File sequence for canal preparation.|
A file system that I recommend is the Orifice Shapers (DENTSPLY Tulsa Dental) 0.50/0.07, 0.40/0.06, and 0.30/0.06 for the coronal two thirds. The files should be used in a modified crown-down technique. This modified technique uses small to large Orifice Shapers (0.30/0.06, 0.40/0.06 and 0.50/0.07). If a larger Orifice Shaper is required, use the 0.60/0.08 and/or 0.80/0.08. The GT (DENTSPLY Tulsa Dental) 0.20/0.10 and 0.20/0.08 are used for the transition zone, and the 0.04 or 0.06 taper Profile (DENTSPLY Tulsa Dental) or K3 (Sybron Endo) files are used for the apical one third (Figure 4). The apical third files should be taken to working length and increased to the largest size the canal will permit. The largest file size to go to working length is the master apical file.
|Figure 5. Electric torque slow-speed handpiece.|
When using rotary instrumentation, do not force instruments past what the canal morphology will allow, replace files frequently (single use is ideal, but no more than 3 uses per file), and use a torque electric slow-speed handpiece (Figure 5) that will reverse a file out of the canal when binding of dentin is detected. These techniques will help prevent file separation.
CHEMICAL CANAL DEBRIDEMENT
|Figure 6. RC-Prep.|
Today’s conventional endodontic thought is that files shape and irrigants clean. Root canal systems in 3 dimensions are more complicated than a 2-dimensional radiograph may demonstrate. It is virtually impossible to thoroughly clean a root canal system with instrumentation alone. The use of chemical debridement enables removal of vital or nonvital pulpal tissue in areas the file cannot reach. Sodium hypochlorite should be used during canal instrumentation. The literature supports the use of sodium hypochlorite from 1% to 5.25% (full-strength bleach).6 The common clinical usage is 2.5% sodium hypochlorite. The simple formula is taking 50% bleach and mixing it with 50% water. RC-Prep (Premier Dental Products, Figure 6) should be used in conjunction with sodium hypochlorite during instrumentation. RC-Prep is made up of 15% EDTA (ethylenediamine tetra-acetic acids) and 10% urea peroxide. The EDTA is a chelating agent (removes calcium ions) that helps remove the smear layer (dentin debris and pulp tissue left on the canal walls from instrumentation) in combination with sodium hypochlorite.7 The removal of the smear layer allows the antibacterial irrigants and intracanal medicaments into the dentinal tubules. The combination of RC-Prep and sodium hypochlorite acts as a lubricant and effervescent to aid in the flotation of dentinal particles from the root canal.8 The urea peroxide produces hydroxyl radicals that can cause cell death.
It is a common misnomer among clinicians that RC-Prep should only be used in the instrumentation of necrotic root canal systems. It is important to use RC-Prep with vital cases too. The RC-Prep prevents collagen plugs from occurring during instrumentation in vital cases. A collagen plug is the result of an instrument packing down the pulp into the root canal. This collagen blockage can be just as hard to negotiate through as a dentinal chip blockage.
Recent literature has suggested the use of chlorhexidine as an endodontic irrigant in nonvital (necrotic) teeth. Chlorhexidine has a broad-spectrum antimicrobial action and relative absence of toxicity. Its major disadvantage is that it does not dissolve pulp tissue. A study by Kuruvilla and Kamath9 demonstrated that the combination use of 2.5% sodium hypochlorite and 0.2% chlorhexidine gluconate had significant reduction of microbial flora as compared to the use of 2.5% sodium hypochlorite alone.
Many dentists who perform multiple-visit treatments on vital pulp cases leave the canal(s) dry between appointments. Today’s thoughts regarding this clinical technique have changed. In vital cases that are multiple appointments, sodium hypochlorite should be left in the canal (not pulp chamber) between appointments. The rationale is that the sodium hypochlorite will continue to dissolve vital pulp tissue in the areas of the canal system that were inaccessible to the files.11 Sodium hypochlorite will not increase postoperative pain when used as an intra-appointment medicament.12
In nonvital cases, many dentists also leave the canal(s) dry between appointments. The problem is this will allow for continued growth of the bacteria. The dry canal is a warm and low-oxygen (anaerobic bacteria) environment that provides the bacteria an incubator-type environment in which to grow.
|Figure 7. Calcium hydroxide.|
The recommended medicament to be placed intra-appointment in the canal(s) is calcium hydroxide (Figure 7). A recent study has demonstrated the antimicrobial effects of calcium hydroxide.13 The calcium hydroxide should be placed for 7 to 10 days for best effectiveness.14 The advantage of calcium hydroxide is that it can have an effect on microorganisims in the absence of direct contact.15 It is the hydroxyl ions derived from the calcium hydroxide dressing that diffuse through the dentinal tubules.16 The mechanism of effect of calcium hydroxide on bacteria is its alkaline pH of 12.5 and the ability to absorb CO2 required for bacterial growth.
In part 2 of this article, I will discuss obturation, the use of anti-inflammatory and antibiotic medications, and the endodontic-restorative relationship.
1. Rickoff B, Trowbridge H, Baker J, et al. Effects of thermal vitality tests on human dental pulp. J Endod. 1988;14:482-485.
2. Lado EA, Richmond AF, Marks RG. Reliability and validity of a digital pulp tester as a test standard for measuring sensory perception. J Endod. 1988;14:352-356.
3. Okeson JP, ed. Orofacial Pain: Guidelines for Assessment, Diagnosis, and Management. Carol Stream, Ill: Quintessence Publishing Co, Inc; 1996:89.
4. Malamed SF. Handbook of Local Anesthesia. 4th ed. St. Louis, Mo: CV Mosby; 1997:14-17.
5. Bahcall JK, Barss JT. Understanding and evaluating the endodontic file. Gen Dent. 2000;48:690-692.
6. Baumgartner JC, Cuenin PR. Efficacy of several concentrations of sodium hypochlorite for root canal irrigation. J Endod. 1992;18:605-612.
7. Baumgartner JC, Mader CL. A scanning electron microscope evaluation of four root canal irrigation regimens. J Endod. 1987;13:147-157.
8. Heling I, Irani E, Karni S, et al. In vitro antimicrobial effect of RC-Prep within dentinal tubules. J Endod. 1999;25:782-785.
9. Kuruvilla JR, Kamath MP. Antimicrobial activity of 2.5% sodium hypochlorite and 0.2% chlorhexidine gluconate separately and combined, as endodontic irrigants. J Endod. 1998;24:472-476.
10. Inamoto K, Kojima K, Nagamatsu K, et al. A survey of the incidence of single-visit endodontics. J Endod. 2002;28:371-374.
11. Harrison JW, Svec TA, Baumgartner JC. Analysis of clinical toxicity of endodontic irrigants. J Endod. 1978;4:6-11.
12. Harrison JW, Baumgartner JC, Svec TA. Incidence of pain associated with clinical factors during and after root canal therapy. Part 1. Interappointment pain. J Endod. 1983;9:384-387.
13. Behnen MJ, West LA, Liewehr FR, et al. Antimicrobial activity of several calcium hydroxide preparations in root canal dentin. J Endod. 2001;27:765-767.
14. Safavi KE, Nichols FC. Effect of calcium hydroxide on bacterial lipopolysaccharide. J Endod. 1993;19:76-78.
15. Kontakiotis EG, Wu MK, Wesselink PR. Effects of calcium hydroxide dressing on seal of permanent root filling. Endod Dent Traumatol. 1997;13:281-284.
16. Nerwich A, Figdor D, Messer HH. pH changes in root dentin over a 4-week period following root canal dressing with calcium hydroxide. J Endod. 1993;19:302-306.
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