Local anesthetics (LAs) form the backbone of pain control techniques in dentistry. “Modern” dentistry began with the introduction of cocaine in 1885 and procaine (Novocain) in 1905, allowing dentists and surgeons to painlessly carry out procedures that previously had been impossible to do or were excruciatingly painful.

From the early 1900s until the mid-1940s, the “ester-type” LAs were used: Procaine, propoxycaine, and tetracaine were the most popular. In 1948, the first “amide-type” LA, lidocaine (Xylocaine), was introduced, quickly becoming the gold standard.

The 1960s and 1970s saw the introduction of other amides: mepivacaine (1960), prilocaine (1965), and bupivacaine (1972).

In dentistry, amide LAs have replaced the esters; indeed, in North America today, ester LAs are no longer marketed in dental cartridges.

Annually, more than 300 million cartridges are administered by dentists in the United States, another 30 million in Canada, and 1.96 billion worldwide.

With Dentistry Today celebrating its 40th anniversary this year, it was my thought to review the significant advances that have been made in the area of dental pain control over these past 40 years.

THE EARLY YEARS (1980 to 1999)      

By the 1980s, in North America, 4 [more than 4 are mentioned] excellent LAs were available: mepivacaine and prilocaine, “plain” (no vasoconstrictor), for procedures of up to 30 minutes; mepivacaine, lidocaine, and prilocaine, with a vasoconstrictor, for procedures of up to 1 hour; and bupivacaine with epinephrine for post-surgical pain control.

With few exceptions (eg, infected mandibular molars), effective pain control for dental procedures was achievable. Still, consistently effective pain control with the traditional inferior alveolar nerve block (IANB, “mandibular block”) proved vexing to many dentists and dental hygienists, even for simple procedures. In response to the high failure rate associated with the IANB, alternative techniques of mandibular anesthesia were developed or reintroduced, including the Gow-Gates mandibular block, the Vazerina-Akinosiclosed-mouth mandibular block, the periodontal ligament injection (PDL), and intraosseous (IO).

Gow-Gates mandibular block: The Gow-Gates mandibular block technique had been introduced in 1973. Taught at many—but not all—dental schools, its rate of successful anesthesia, once learned, is considerably greater than the IANB.¹

Another area of concern was palatal anesthesia. The density and sensitivity of palatal soft tissues and their adherence to bone made palatal injections one that most patients and, in many cases, their dentists reticent to receive or administer. The use of topical anesthetic, pressure, and slow injection served, to some degree, to minimize discomfort, but to put it simply, palatal injections hurt!

C-CLAD (computer-controlled local anesthetic delivery): In 1997, Dr. Mark Hochman published the first paper describing the use of a local anesthetic delivery system employing a computer to control the rate and pressure of LA delivery.² That device, the Wand (Milestone Scientific), represented an evolution in LA delivery, moving away from the traditional metal aspirating dental syringe.

C-CLAD devices permit the precise administration of LA at a steady rate and pressure, providing a more comfortable injection experience for the patient. Though designed for those injections deemed more uncomfortable, palatal, PDL- C-CLAD devices may be employed for any and all intraoral injections.

Hochman compared palatal injections with a traditional syringe and the Wand and found 96% of subjects preferred the C-CLAD instrument.² Visual analog scale (VAS) measurements were significantly lower for C-CLAD vs traditional syringes.

Subsequent research with C-CLAD led to the development of 2 new LA techniques: anterior, middle superior alveolar (AMSA) nerve block and palatal-approach anterior superior alveolar (P-ASA) nerve block.

Since the introduction of the Wand in 1997, other C-CLAD systems have been introduced, including the Wand STA (Milestone Scientific) and Dentapen (Septodont).

Published research trials have demonstrated the utility of C-CLAD in all patients,³ especially in the pediatric population.

RECENT DEVELOPMENTS (2000 to 2021)      

From 2000 to the present, the years have seen the development and introduction of a number of valuable adjuncts to pain control.

Articaine HCl (2000): In 1999, in the United States, 3 excellent, highly effective, and safe LAs were available (lidocaine, mepivacaine, and prilocaine) that, with the addition of a vasoconstrictor, provided pulpal anesthesia for approximately 1 hour. Bupivacaine, a long-duration LA, is primarily used for post-surgical pain control.

A fifth LA—articaine—was available worldwide, but not yet in the United States in 2000. Synthesized in Germany in 1969, articaine was introduced into clinical practice there in 1976, representing the first, and still only, LA designed for dentistry. Its clinical characteristics (eg, onset, duration) are similar to those of the other intermediate-duration LAs. Marketed as a 4% solution with epinephrine in 1:100,000 and 1:200,000 concentrations, articaine has become the preferred LA in most countries (Table 1).

In June 2000, the Food and Drug Administration (FDA) approved articaine for use in the United States in patients aged 4 and up, and it quickly become popular—but why?

Anecdotal reports from dentists beginning to use articaine stated that: “it works faster,” “it works better,” “I don’t miss as often,” and “hard-to-numb patients are easier to numb.” Of course, anecdotal reports are not science.

In phase 3, randomized, controlled, double-blinded trials (RCT) in the United States, it was concluded that articaine was “as safe and as effective as lidocaine,”⁴ the drug to which it was compared.

Articaine does possess chemical and clinical characteristics that make it, in this author’s opinion, the preferred LA in many situations. These characteristics, articaine’s advantages, and the “controversy” regarding an increased risk of paresthesia following IANB are discussed in a subsequent section.    

Phentolamine mesylate—the LA “off switch” (2008): The addition of a vasoconstrictor confers the following benefits on the LA: (1) increased depth, (2) increased duration, and (3) increased safety (by decreasing the LA blood level). Associated with these benefits is an increase in the duration of soft-tissue anesthesia to 3 to 5 hours. Following surgical procedures, residual soft-tissue anesthesia (RSTA) is appreciated; however, most dental procedures do not require post-treatment pain control. In some instances, self-inflicted soft-tissue injury (SISTI) may result from chewing or biting on the still-numb lip or tongue. Though most common in younger children, the incidence of SISTI is significant in special needs and geriatric patients. Additionally, many patients would appreciate having soft-tissue anesthesia “go away” more quickly so that they could return to their usual lifestyles—eating, social gatherings, business meetings, etc, where RSTA can be an embarrassment or lead to soft-tissue injury.

Phentolamine mesylate (PM), an alpha-adrenergic antagonist (eg, vasodilator), available in dental cartridges and injected at the end of the “painful” part of the dental treatment (eg, drilling or root planing) into the same location that the LA was deposited earlier, significantly decreases the duration of RSTA.

In a study by Malamed et al,⁵[ ref 5 is Malamed alone, wrong ref?] complete loss of anesthesia in the upper lip at 30 minutes following PM administration occurred in 26.7% vs 1.7% of controls; at 60 minutes, it was 59.2% vs 11.7%. In the lower lip, at 30 minutes, 17.2% of PM subjects had complete loss of anesthesia vs 0.8% of controls, and at 60 minutes, it was 41% PM vs 7.4% controls.

PM (OraVerse [Septodont]) has been approved by the FDA for administration to patients age 3 and up.

Buffered local anesthetics—The LA “on switch” (2010): Vasoconstrictor-containing LAs are highly acidic, with a pH ranging from 3.0 to 4.0. Injection of this acidic solution is associated with a “stinging” or “burning” sensation and a slower onset of anesthesia (compared to plain LAs). Addition of a defined volume of 8.4% sodium bicarbonate to a dental cartridge—raising its pH to approximately 7.35 to 7.4—provides a more comfortable injection experience for the patient. Additional benefits of buffering include (1) more rapid onset of pulpal anesthesia,⁶ more profound anesthesia,⁷ and decreased post-injection soreness. 

In an RCT comparing lidocaine 2%, epinephrine 1:100,000, buffered to a pH of 7.35, with unbuffered (pH 3.5) for IANB, the onset of pulpal anesthesia was 1 minute, 51 seconds (buffered), vs 6 minutes, 37 seconds unbuffered.⁶   

The methods of buffering are (1) DIY (do it yourself) and (2) onset (the original dental buffering system). DIY is more cost-effective but runs the risk of the resulting pH of LA solution being higher than desired (7.35 to 7.4). With an elevated pH (> 7.5), edema (swollen lip and/or cheek) at the injection site is a common occurrence. With the dental buffering system, the pH consistently ranges from 7.35 to 7.4.

In a 2019 Journal of the American Dental Assosiation paper,⁷ buffered LAs were reported to be more effective than nonbuffered LAs both by mandibular and maxillary injection in pulpally involved teeth. Buffered LAs had a 2.29 greater likelihood of achieving successful anesthesia.

Though not all assessments of buffering have produced similar results, it is this author’s recommendation that all LA injections be buffered.

ARTICAINE: AN IN-DEPTH LOOK

As mentioned earlier and illustrated in Table 1, articaine is a popular LA. Worldwide, 600 million articaine cartridges are administered annually, exceeded only by lidocaine’s 1 billion cartridges.⁸

There are 2 distinct pharmacokinetic and chemical characteristics that make articaine popular: (1) more rapid elimination from the cardiovascular system (elimination half-life) and (2) lipid solubility.

More rapid elimination leads to increased safety, and it’s being a preferential drug, in this author’s opinion, in patients who are pregnant, nursing, geriatric, and pediatric, while being more lipid-soluble leads to more rapid onset and greater depth of anesthesia. Additionally, articaine’s greater lipid solubility enables it to be successful using injection techniques that have been uniformly unsuccessful with other LAs.

Elimination half-life: Classified as an amide-LA, articaine is actually a hybrid molecule, possessing both amide and ester bonds (Figure 1).

Anesthesia “stops” when LA diffuses out of the nerve and into the cardiovascular system (CVS): to capillaries, veins, the heart, and then arteries, circulating the LA throughout the body. This process is called “redistribution.” The LA—not yet metabolized—is an active drug upon entering the CVS. A measurable blood (plasma) level of the LA occurs.

The significance of LA blood level is LAST (local anesthetic systemic toxicity), also known as overdose or toxic reaction. An overly high plasma level of any drug in its target organ(s) produces overdose. Target organs for LAs are the brain (central nervous system) and myocardium. The higher the plasma level, the greater the overdose risk. Plasma levels of LAs decrease primarily through metabolism (biotransformation, detoxification).

Amide LAs undergo metabolism almost entirely in the liver (hepatic microsomal enzymes), whereas ester LAs are metabolized in the blood by plasma esterases.

The elimination half-life of a drug—the time for its plasma level to decrease by 50%—for most amide LAs is approximately 90 minutes (hepatic metabolism). Esters have a considerably shorter half-life (plasma esterase metabolism). For procaine, it’s 6 minutes; for tetracaine, it’s 20 minutes.

Between 90% to 95% of articaine metabolism is plasma esterase. In adults, articaine’s elimination half-life is 20 to 27 minutes; for geriatric patients, it’s 27 minutes; in pediatric patients, it’s 18.5 to 23.6 minutes⁹ (Figure 2).

LAST resulting from “proper” administration (aspirate 2 times, administer slowly) of an overly large LA dose is considerably less likely with articaine than other amide LAs. One must always remember that one cartridge of any LA administered rapidly intravascularly will produce LAST.

Lipid solubility: For LA to diffuse through a nerve membrane, it must be lipid-soluble. Lipid solubility is conferred through an aromatic ring—part of the drug’s chemical configuration. Most LAs possess a benzene ring (Figure 1). Articaine possesses a more lipid-soluble thiophene ring.

The anecdotal significance of increased lipid solubility is “I don’t miss as often,” “hard-to-numb patients are easier to numb with articaine,” and “it works better.” Randomized, controlled clinical trials have proven these claims true.

Articaine by Mandibular Buccal Infiltration (BI) in Adults

Research has demonstrated the efficacy of articaine mandibular BI in adults. Robertson et al¹⁰ infiltrated 1.8 mL of either lidocaine or articaine by the first mandibular molar as the primary injection for pain control. Pulpal anesthesia for lidocaine was 45% second molar, 57% first molar, 67% second premolar, and 61% first premolar. Articaine results were 75%, 87%, 92%, and 86%.[“, respectively”?] Lidocaine onset times ranged from 6.3 minutes (first premolar) to 11.1 minutes (second molar); onset for articaine ranged from 4.2 to 4.7 minutes.[“, respectively”?]

Buccal infiltration of articaine as a supplement to IANB significantly increases IANB success rates. Kanaa et al¹¹ showed a 55.6% success rate for IANB on the first molar with lidocaine and epinephrine. When articaine BI was administered, the success rate went to 91.7%, not showing any decrease by the end of the 45-minute study.

It is this author’s recommendation that all IANBs, regardless of the LA used, be followed by BI of articaine (0.9 mL) at the tooth being treated. 

Articaine by Maxillary Buccal Infiltration for Palatal Soft-Tissue Anesthesia in Adults

Palatal injections are dreaded by dental patients and by most dentists and hygienists. Yet palatal anesthesia is frequently necessary for dental procedures.

Clinical trials comparing the efficacy of articaine and lidocaine in providing palatal soft-tissue anesthesia following maxillary BI have demonstrated articaine’s superiority. Gholami et al12 repeated the infiltration of 0.6 mL of LA at 2-minute intervals and evaluated palatal anesthesia. At 4 minutes (1.2 mL), 65.4% of articaine patients and 0.65% of lidocaine patients had palatal anesthesia. At 6 minutes (1.8 mL), values were 82.7% vs 1.3%. Results were similar in the anterior, premolar, and posterior maxillary regions.

Though not all studies demonstrated this same success rate, it is this author’s recommendation that BI of 1.2 or 1.8 mL articaine be administered, with palatal anesthesia evaluated after 4 (1.2 mL) and 6 minutes (1.8 mL). If palatal anesthesia proves less than ideal at 6 minutes, administer a palatal infiltration. Some degree of palatal anesthesia should be present, making the palatal infiltration more comfortable for the patient.  

Controversy: Does Articaine, Administered By IANB, Have a Greater Risk of Paresthesia Than Other LAs?

In 1995, Haas and Lennon¹³ reported on the incidence of paresthesia following LA administration in Ontario, Canada. Most reports involved the lingual nerve (70.6%). The calculated incidence of paresthesia following LA injection (all drugs) was 1 in 785,000; for articaine by IANB, the incidence was 1 in 440,000. In a subsequent paper by Garisto et al,[is this not a ref?] the calculated risk of paresthesia for articaine in the United States was 1 in 4.1 million injections, with an overall risk (all LAs) of 1 in 13.8 million. Other published case reports of paresthesia following articaine[injections?] recommended that articaine not be administered by IANB.

It is estimated that in a 20-year practice career, approximately 30,000 IANBs will be administered.¹⁴ Pogrel and Thamby,¹⁴ in a paper published prior to articaine’s arrival in the United States, estimated the risk of permanent nerve damage following IANB at 1 in 26,762 injections, stating: “it is reasonable to suggest that during a career, each dentist may encounter at least one patient with an IANB resulting in permanent nerve involvement. The mechanisms are unknown, and there is no known prevention or treatment.” 

Recent research on LA neurotoxicity using human neuroblastoma cells (precursor nerve cells) has shown that (1) all LAs are neurotoxins and (2) amongst dental LAs, articaine and ropivacaine demonstrate the “lowest toxicity”; mepivacaine, prilocaine, and lidocaine were “medium toxicity”; and bupivacaine had the “highest toxicity.”¹⁵

There is no scientific evidence demonstrating that articaine is more neurotoxic than other LAs. Almost all publications present case reports or opinion papers—the lowest form of scientific evidence. Meta-analyses and systematic reviews—the most reliable science—have confirmed that articaine is a “better” LA and no more neurotoxic than other LAs.¹⁶

Addressing the controversy regarding articaine paresthesia, Dr. Gordon Christensen, a well-respected dental educator and clinical researcher, stated: “Studies have not shown that to be true. The controversy is unfounded.”¹⁷ 

FORTY YEARS LATER: RECOMMENDATIONS

As we celebrate 40 years of Dentistry Today and complete our review of the evolution of dental pain control, I leave you with several recommendations:

1. Articaine has been clearly demonstrated to be more effective than other dental LAs.  

• Routinely administer 0.9 mL by BI at the apex of a mandibular molar being treated following IANB with any LA.
• Articaine maxillary BI, 1.2 to 1.8 mL (waiting 4 to 6 minutes), provides palatal soft-tissue anesthesia in a large majority of adult patients.

2. Buffer LA injections. Buffering LA solutions provides faster onset of more profound anesthesia and is more comfortable on injection and less uncomfortable for the patient postoperatively. Though all injections—maxillary and mandibular—can, and should, be buffered, it is in the mandible where the greatest benefit is noted. 

3. C-CLAD: The ability to provide a painless injection is the No. 1 criteria patients use when evaluating their doctors. C-CLAD devices enable significantly more comfortable injections to be administered.

4. PM: Post-treatment RSTA is, at a minimum, uncomfortable and undesirable and potentially a source of trauma. The ability to significantly decrease the duration of soft-tissue anesthesia will be desirable for many patients.

Here is one final note:

In 1981, only 10 states permitted the administration of LAs by dental hygienists. Today, LA administration is permitted in 45 states.¹⁸ Only 5 to go.

REFERENCES

1. Gow-Gates GA. Mandibular conduction anesthesia: a new technique using extraoral landmarks. Oral Surg Oral Med Oral Pathol. 1973;36(3):321–8. doi:10.1016/0030-4220(73)90208-9

2. Hochman M, Chiarello D, Hochman CB, et al. Computerized local anesthetic delivery vs. traditional syringe technique. Subjective pain response. N Y State Dent J. 1997 Aug-Sep;63(7):24–9.

3. Flisfisch S, Woelber JP, Walther W. Patient evaluations after local anesthesia with a computer-assisted method and a conventional syringe before and after reflection time: A prospective randomized controlled trial. Heliyon. 2021;7(2):e06012. doi:10.1016/j.heliyon.2021.e06012

4. Malamed SF, Gagnon S, Leblanc D. Efficacy of articaine: a new amide local anesthetic. J Am Dent Assoc. 2000;131(5):635–42. doi:10.14219/jada.archive.2000.0237

5. Malamed SF. Local anesthesia reversal. Dent Today. 2010;29(3):65–6, 68, 71-2 passim; quiz 74. 

6. Malamed SF, Tavana S, Falkel M. Faster onset and more comfortable injection with alkalinized 2% lidocaine with epinephrine 1:100,000. Compend Contin Educ Dent. 2013;34 Spec No 1:10-20. 

7. Kattan S, Lee SM, Hersh EV, et al. Do buffered local anesthetics provide more successful anesthesia than nonbuffered solutions in patients with pulpally involved teeth requiring dental therapy?: A systematic review. J Am Dent Assoc. 2019;150(3):165-177. doi:10.1016/j.adaj.2018.11.007 

8. Communication with Septodont Holding. Saint Maur des Fosses Cedex, France. May 2017. 

9. Cazaubon Y, Mauprivez C, Feliu C, et al. Population pharmacokinetics of articaine with 1:200,000 epinephrine during third molar surgery and simulation of high-dose regimens. Eur J Pharm Sci. 2018;114:38-45. doi: 10.1016/j.ejps.2017.11.027

10. Robertson D, Nusstein J, Reader A, et al. The anesthetic efficacy of articaine in buccal infiltration of mandibular posterior teeth. J Am Dent Assoc. 2007;138(8):1104–12. doi:10.14219/jada.archive.2007.0324

11. Kanaa MD, Whitworth JM, Corbett IP, et al. Articaine buccal infiltration enhances the effectiveness of lidocaine inferior alveolar nerve block. Int Endod J. 2009;42(3):238–46. doi:10.1111/j.1365-2591.2008.01507.x

12. Gholami M, Banihashemrad A, Mohammadzadeh A, et al. The Efficacy of 4% Articaine Versus 2% Lidocaine in Inducing Palatal Anesthesia for Tooth Extraction in Different Maxillary Regions. J Oral Maxillofac Surg. 2021;S0278-2391(21)00195-6. doi:10.1016/j.joms.2021.02.019

13. Haas DA, Lennon D. A 21 year retrospective study of reports of paresthesia following local anesthetic administration. J Can Dent Assoc. 1995;61(4):319–20, 323–6, 329–30. 

14. Pogrel MA, Thamby S. Permanent nerve involvement resulting from inferior alveolar nerve blocks. J Am Dent Assoc. 2000;131(7):901–7. doi:10.14219/jada.archive.2000.0308.

15. Malet A, Faure MO, Deletage N, et al. The comparative cytotoxic effects of different local anesthetics on a human neuroblastoma cell line. Anesth Analg. 2015;120(3):589–96. doi:10.1213/ANE.0000000000000562.

16. Stirrup P, Crean S. Does articaine, rather than lidocaine, increase the risk of nerve damage when administered for inferior alveolar nerve blocks in patients undergoing local anaesthesia for dental treatment? A mini systematic review of the literature. Br Dent J. 2019;226(3):213-223. doi: 10.1038/sj.bdj.2019.98.

17. Christensen GJ. Observations on Current Controversies in Dentistry. Dent Today. 2015;34(11):100, 102, 104-5. 

18. American Dental Hygienists’ Association. States that permit dental hygienists to administer local anesthetics. https://www.adha.org/resources-docs/7521_Local_Anesthesia_by_State.pdf. Accessed 15 May 2021.

ABOUT THE AUTHOR

Dr. Malamed graduated from the New York University College of Dentistry in 1969 and completed a dental internship and residency in anesthesiology at Montefiore Hospital and Medical Center in the Bronx, NY, before serving for 2 years in the US Army Dental Corps. In 1973, Dr. Malamed joined the faculty of the University of Southern California School of Dentistry in Los Angeles where today he is a professor of anesthesia and medicine. Dr. Malamed is a Diplomate of the American Dental Board of Anesthesiology as well as a recipient of the Heidebrink Award (1996) from the American Dental Society of Anesthesiology and the Horace Wells Award (1997) from the International Federation of Dental Anesthesia Societies. He has authored more than 120 scientific papers and 16 chapters in various medical and dental journals and textbooks in the areas of physical evaluation, emergency medicine, local anesthesia, sedation, and general anesthesia. He authored the textbooks Handbook of Local Anesthesia (fifth edition), Emergency Medicine in Dentistry (sixth edition), and Sedation: A Guide to Patient Management (fourth edition). Dr. Malamed speaks and writes extensively on the subjects of emergency medicine, physical evaluation, local anesthesia, sedation, and general anesthesia. He can be reached at malamed@usc.edu.

Disclosure: Dr. Malamed is a consultant to OnPharma

RELATED ARTICLES

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Figure 1. Acquiring thought of event and emotional context for 30 to 40 seconds.

Every dentist has been confronted with the challenge of the anxious or phobic patient. Recent literature describes several approaches to making these individuals more comfortable and easier to treat. Those papers focus on the anxiety itself and attempt to down-regulate the fear response. Currently, 3 approaches are routinely used to address the concerns of the patient. First are the talk therapies, such as Cognitive Behavioral Therapy.¹ This approach involves an interaction and a relationship between a trained therapist and a client. Second is Systematic Desensitization/Exposure, where the individual is slowly introduced to the feared situation.² Third, medication can be used to alter the brain’s neurochemical response to the exposure.³
This paper introduces a new therapeutic modality and suggests a neurobiological mechanism for its effectiveness. We call this Havening Therapy, as in “find a safe haven.” This approach utilizes the extrasensory aspect of touch to alter pathways that create distress.

WHAT IS A PHOBIA AND WHY DO SOME PEOPLE HAVE THEM?
A phobia (from Greek: phobos, “fear”) is generally defined as “an irrational, intense and persistent fear of certain situations, activities, things or persons.”⁴ Phobic anxiety is distinguishable from other forms of anxiety only in that it occurs specifically in relation to a certain object or situation. Anxiety is a physiological and psychological state characterized by cognitive, somatic, emotional and behavioral components. The physiological symptoms of fear include a rapid pounding heartbeat, widening of the eyes, pupil dilation, peripheral muscle activation and increased respiration.⁵ These symptoms are the observed responses to a complex neurobiological event generated within the mind of an individual.
This response, produced involuntarily by the brain, has only one objective: to flee from or defend against a fearful object or situation. These primitive responses were needed to increase muscle strength, increase blood flow and decrease the experience of pain. Over millions of years, evolution has perfected a cascade of neurochemicals such as norepinephrine, epinephrine, dopamine, and cortisol that are released into our bodies to prepare for flight or fight.⁶
For nonprimates, where predator and prey battle, there are 2 options: escape or die. In the primate/human species, a third option exists. Survive and not escape (abused child, traumatic dental experience). This third outcome can, for some people, become encoded as a phobia, which is one type of traumatization. Phobias are the response to a perceived encoded threat. How they form is beyond the scope of this paper, but suffice it to say that certain criteria must be met.
The most critical of these requirements is that escape is not to be perceived as possible. Without escape, there is no closure on the event. Cues and content by overlapping with the original event can reactivate feelings (ie, white coat syndrome). A stimulus that reactivates the emotional (fear) component of the traumatic event does so as if it were being experienced for the first time. This response to a previous event provides the opportunity to de-link the emotional component and find a safe haven.

Table. Havening Sequence

Figure 2. Initial counting backwards with gentle collarbone tapping—eyes closed. Figure 3. Softly tapping and lightly rubbing the forehead with fingertips while humming a song—eyes closed. Figure 4. Gently tapping while counting backwards from 30 by 3s—eyes closed. Figure 5. Gently caress outside of the hands with eyes open—patient is rolling eyes: upper and lower right, upper and lower left, rolling clockwise and then counter clockwise then closing eyes. Figure 6. Gently glide hands up and down on arm while using auditory distracting approach (counting, humming a song). Figure 7. Rest period 15 seconds after each round prior to asking for subjective unit of distress. Obtain an subjective unit of distress (SUD) and have the patient write the number on a slip of paper and close her eyes again (Figure 1). Tap on the collarbone and perform other havening processes while the individual counts backwards from 20 while visualizing walking down stairs or some other visual task (such as removing cups from a dispenser) with each number (Figure 2). Have the patient open her eyes and look down to the left, down to the right, look up, look down, roll her eyes in a circle and then roll them in an opposite direction. Close eyes. Have the patient hum a song out loud with eyes closed (eg, “Take Me Out to the Ballgame,” “Old MacDonald Had a Farm,” “Happy Birthday,” etc). Apply a havening stroke, eg, stroking forehead, arms, hands, and head simultaneous with the humming (Figures 3 to 6). Have the patient open her eyes and follow your finger up, down, and to both sides, then up again. Have the patient take a deep breath, exhale with an “ommm” and move your hand downward as she closes her eyes. Ask her to lower her shoulders and relax her jaw and stroke gently downward on the arms. Sit with the patient for 10 seconds with hands in lap (Figure 7). With the patient’s eyes still closed, ask her to look at the back of her eyelids and listen only to your voice. Obtain another SUD. Repeat process until the SUD is zero or remains fixed at another number after 3 rounds.

When a nonhuman escapes a predator, the brain is flooded with serotonin.⁷ This primitive neurochemical allows for the brain to become calmer and inhibits a fear response, thus allowing for normative behavior. In humans, rising serotonin (meaning a safe place is found) on recall of the trauma allows for a disconnect between the emotions and memory. Thus, serotonin extinguishes the phobia.

HAVENING
Havening makes it possible to alter the response to a stimulus that would normally generate a fear response by using the extra sensory aspects of touch. It is well known that touch increases serotonin in the brain.⁸ Swedish massage has been shown to create physically and mentally relaxed states by increasing serotonin and dopamine. It is this connection between serotonin and touch that forms the basis for treatment.

ACTIVATION AND DISPLACEMENT OF THE PHOBIA/ANXIETY
History taking is the key to removing the unwanted traumatically encoded pathway. Early traumas set the stage for current circumstances. To start the displacement, the initial sensitizing event must be found and activated. In dental phobias, the event quite often occurs at a fairly young age. Usually the patient can give a narrative of the experience and can see quite clearly the whole context of the event. The fact that the memory is still so significant after so many years speaks to the high emotional content at the time of encoding.

PREHAVENING PROTOCOLS
If the patient cannot bring to mind a specific event, then have the patient focus on the current situation and feelings.
Have the patient bring to mind the entire circumstance involved with the memory or moment. The sights, sounds and smells should fill the subject’s mind until she approaches being in that moment. The patient’s eyes should be closed (Figure 1). The patient should also experience the emotional content of the moment. The “experience of fear” is the response to an unresolved trauma.

HAVENING PROCEDURES
Allow 30 to 40 seconds to have the patient recall and “feel” the moment with eyes closed. Request a subjective unit of distress (SUD), which is a number from zero to 10 which the patient will indicate the degree of “being in the moment.” Ten represents being right there; zero represents its disappearance. She should open her eyes and write down the number that she feels. The sequence that I find effective is found in the Table.
During this process I use an unmodulated, somewhat monotonous voice that is never hurried. I am always encouraging and never correcting when simple mistakes are made (Figure 2). I say, “Listen to the sound of my voice.” Additionally, phrases in the same unmodulated tone, such as, “Almost home,” and “You are excellent at this,” are interjected while other sensory components are being stimulated.
This process is called havening. It includes kinesthetic components (touch and posture) that raise serotonin, as well as the distractive elements (humming, counting, eye rolling, and so on⁹) that cause displacement of the thought (emotional core).

THE KINESTHETIC COMPONENT (TOUCH AND POSTURE)
The touch is meant to be comforting, soothing, gentle, supportive, and produces a dramatic surge of serotonin in the brain. Light touch is best and the movements should create a bond between the doctor and the patient. The patient should always be seated in a comfortable position. During the therapy, one can use different hand and arm positions such that it appears that the patient is either praying (Figure 3) or hugging oneself gently (Figure 4). During the havening touch component, the patient should be encouraged to allow the shoulders to drop and the jaw to become slack. This postural approach is useful for calming both the body and the mind. Light, sensitive stroking of the arms, hands, and head is the somatic aspect of the havening (Figures 5 and 6).

THE DISTRACTIVE COMPONENT
At the same time, distracting thoughts and tasks are introduced to the moment displacing the present mindset. Try it yourself. Hum “Happy Birthday” out loud and count backwards from 20 in your mind. So only one thought can exist at a time! Eye rolling, humming a tune, counting backwards by multiple numbers causes an intense focus on the task at hand and slowly displaces the originally held thought. Sit with the patient for 10 seconds with palms up and your hand on top of palms (Figure 7). Repeat the process 3 times and obtain the SUD after the third round. After 3 rounds say “when you are ready, open your eyes.”
This combination of activation of the memory and its emotional core, along with the increase in serotonin, creates the window for disrupting the linkage which has been encoded at the time of traumatization. The distraction displaces the thought from working memory and inhibits further responsiveness. Since the exact circumstances of the previous traumatizing moment cannot be replicated, the memory fades and becomes a simple memory without emotional context and is unable to produce a fear response.
After havening, the patient feels calm. Following the havening process to ensure the memory and the stimulating cues are removed, the patient is asked to attempt to recapture the same feelings she had at the start of the process. Invariably, the patient will be unable to recall the previously thought experience and may present in one of 3 ways: (1) the thought is gone, (2) the thought is looked at from above with no emotional content, or (3) the thought is fuzzy. The patient finds a safe haven. When this is accomplished, the phobia disappears forever.
It is the authors’ experience that these techniques work extremely well when used with patients who present with varying degrees of anticipatory anxiety. Most of the therapy can easily be done in the dental chair using the above protocol. You will find that the patient is more relaxed and ready to accept care. One or 2 repetitions should be sufficient to achieve significant results. After years of experience this nondrug therapy has been shown to be safe and effective. For further information, scientific foundation, and testimonials visit healingthemind.net.

CONCLUSION
A technique has been demonstrated that utilizes the patient’s thoughts, emotions, and the extrasensory components of touch to modify encoded pathways to disrupt and eliminate unwanted responses from previous traumatic experiences.

References

1. Choy Y, Fyer AJ, Lipsitz JD. Treatment of specific phobia in adults. Clin Psychol Rev. 2007;27:266-286.
2. Marks I. Exposure therapy for phobias and obsessive-compulsive disorders. Hosp Pract. 1979;14:101-108.
3. Tolksdorf W, Siefert S. Drug-related methods for alleviation of stress in dentistry. Anesth Pain Control Dent. 1992;1:34-40.
4. Bourne EJ. The Anxiety & Phobia Workbook. 4th ed. Oakland, Calif: New Harbinger Publications; 2005.
5. Seligman MEP, Walker EF, Rosenhan DL. Abnormal Psychology. 4th ed. New York, NY: WW Norton and Co; 2000.
6. Fellous J-M, Arbib MA, eds. Who Needs Emotions? The Brain Meets the Robot. New York, NY: Oxford University Press; 2005.
7. Weisstaub NV, Zhou M, Lira A, et al. Cortical 5-HT2A receptor signaling modulates anxiety-like behaviors in mice. Science. 2006;313:536-540.
8. Field T, Hernandez-Reif M, Diego M, et al. Cortisol decreases and serotonin and dopamine increase following massage therapy. Int J Neurosci. 2005;115:1397-1413.
9. Shapiro F. Efficacy of the eye movement desensitization procedure in the treatment of traumatic memories. Journal of Traumatic Stress. 1989;2:199-223.

Dr. Steven Ruden graduated from New York University in 1971. He is the director of the Sea Cliff Health Center. His education includes 2 years of training in periodontics at Albert Einstein College of Medicine, advanced studies at The LD Pankey Institute, and continuing education at Lund University in Malmo, Sweden. As director of the dental implant program at Nassau University Medical Center (1986 to 1998), he created and developed many of the procedures in use today and trained a generation of implant dentists. Dr. Ruden is a certified hypnotherapist, which enables him to address many phobias that interfere with patients’ ability to accept optimal dental treatment. He can be reached at drruden@seacliffdentist.com.

Dr. Ronald Ruden started his academic career in 1971 when he earned his PhD in organic chemistry. He then joined Nobel Laureate E.J. Corey at Harvard where they developed new advanced synthetic methods and pioneered computer modeling in chemical synthesis. Two years later, he was asked to join the faculty of Rutgers University. At Rutgers, he became interested in medical research and received his MD from Mt. Sinai School of Medicine in 1979. He took a Fellowship in Nutrition at Sloan Kettering Cancer Center, and during his first year he chaired an international symposium on cancer and nutrition. He is a published author, and his first book, The Craving Brain, is in its second edition and addresses issues pertaining to addiction and obesity. Dr. Steven Ruden is the contact author for this article.

Disclosures: Drs. Steven and Ronald Ruden report no conflicts of interest.

Dentistry Today is pleased to present our Practice Pyramid Series, to assist today’s practitioners. Various leading clinicians will be featured, demonstrating the application of new technologies. Dr. Lou Shuman and Amy Morgan, both of the Pride Institute, will provide technological product introductions and practice management implications in each article. All technologies presented in this series are 2009 Pride Institute “Best of Class” Technology Winners, chosen through an unbiased assessment selection process in conjunction with a known technology expert, Dr. Larry Emmott.

I can’t tell you how many times I have heard from my patients: “Dr. Ruiz, can you do my work without anesthesia? I hate the feeling of being numb.” One of the best practice builders is painless anesthesia, and with proper technique, pain during the anesthetic injections should be very little. However, still remaining is the other really unpleasant part of being anesthetized, the 4 to 5 hours of postoperative numbness. We all dislike this part, and this unpleasantness is in many cases responsible for keeping our patients away from doing necessary dental treatment. In some cases, patients may even cancel an appointment if they suspect it may interfere with an important activity after their dental visit. Well, now we have a cutting-edge new drug, phentolamine mesylate (OraVerse [Novalar]), that may be the solution to these problems.

Figure 1. Supragingival preparation for a partial coverage all-ceramic onlay replacing the fractured cusp.	Figure 2. Restoration after cementation with a resin cement.
Figure 3. Preoperative view showing 2 old veneers with staining and poor morphology.	Figure 4. Immediate postoperative view of gingivectomy and temporary veneers.

Figure 5. One-week postoperative view of 2 bonded porcelain veneers.

WHAT IS ORAVERSE AND HOW IS IT USED
OraVerse is an FDA-approved anesthesia reversal drug which cuts the postoperative numbness time in half, and often even faster, without any known serious side effects. It is injected in a 1:1 ratio to the anesthetic quantity administered, after the procedure is finished.
OraVerse can be used for the most basic dental procedures where we would expect a minimum postoperative pain, such as hygiene procedures, fillings, and the preparation and cementation of supragingival indirect restorations (ie, porcelain onlays, veneers, and all-ceramic crowns). It should not be used on procedures where considerable post-operative pain is expected, such as after a crown preparation with deep retraction cord placement, periodontal surgery, endodontic procedures or oral surgery. In these cases, a longer postoperative numbness is desirable for the patient’s comfort. In all cases, it would be wise to recommend that the patient take 400 mg to 800 mg of ibuprofen to minimize any discomfort after the anesthesia is reversed.

How Phentolamine Mesylate Is Used in Our Practice
I have a busy private practice and implementation of new procedures or new things learned are important keys to success. OraVerse can be a great adjunctive service and practice builder which will enhance the patient’s perception of the practice and the value received for fees charged. It is important to understand that, although there is a small profit associated with it, its true value is as a practice builder in providing a new way to improve the overall dental experience for our patients.
Educating and informing our patients is always vital in implementing any new technique or technology, so in my practice we have placed a large display informing our patients that “Having a ‘fat lip’ for hours after your dental appointment is a thing of the past! Ask us about OraVerse.” We have also included quotes in our reception area slide presentation from satisfied patients who have experienced the positive effects of OraVerse. In our practice, anesthesia reversal is offered as an optional procedure. We charge a nominal fee to cover the cost of the drug and the additional time it will take to do the injection. The following clinical examples demonstrate how successful this additional service can be within the scope of many clinical procedures.

CASE 1
A very successful and busy 40-year-old TV producer was scheduled to do a porcelain onlay preparation on tooth No. 18 due to caries and a fractured disto-bucal cusp. After being seated, the patient stated that the only reason she was present at her appointment was because we offered the anesthesia reversal procedure. This is because she had an important meeting that evening, approximately 4 hours later, and she did not want to be numb for the event. I was careful not to promise that the anesthesia would be completely gone by the time of the meeting, but she was assured that with OraVerse, she should experience at least a 50% reduction the time she would feel the effect of the local anesthetic. We performed the supragingival preparation (Figure 1), and the following day she sent us an e-mail thanking us for offering OraVerse. Furthermore, she said that she wanted to have OraVerse administered after every subsequent procedure. Two weeks later, the restoration was cemented (Figure 2). If we had performed a traditional PFM crown, we would have had to place retraction cord in the gingival sulcus. If the patient had had considerable postoperative pain, this would have made the use of OraVerse less desirable, and as a result she may not have had a positive experience. Supragingival bonded restorations have many advantages, are typically easier to perform with less postoperative pain, and are much more gentle to the gingival tissue than any traditional subgingival PFM crown and bridge procedure.¹

CASE 2
The next case was an actress and dancer in her late twenties who wanted to replace 2 porcelain veneers because of marginal staining and to improve form (Figure 3). The treatment plan included gingivectomy on the 2 centrals to improve gingival symmetry. She had been informed about OraVerse, and although she had requested to have it used at the time of the veneer preparations, I recommended against it. This is because I knew she would have postoperative pain after the gingivectomy (Figure 4). After the gingiva healed, the restorative work was finished. OraVerse was used during the final impressions and for final cementation of the supragingival veneers. The patient was very happy with the aesthetic results and the much reduced post-treatment anesthesia time (Figure 5).

CASE 3
It is rare when I can use myself as an example of a satisfied patient, but this is one of those cases. Recently, I had to have a minor bilateral procedure on the maxillary arch. I was anesthetized for the procedure with one carpule of Septocaine (1:100,000 epinephrine) (Septodont) in each side. Immediately after the procedure was finished, I received one injection of OraVerse on the right side, and (by choice) nothing on the left. The left side was numb for 5 hours while the right side was back to normal within 1 hour. I had slight pain on the OraVerse side at the injection site (this is normal and expected) and took 2 (200 mg) ibuprofen tablets that took care of the pain in about 20 minutes. I wanted to experience first-hand the benefits of phentolamine mesylate. I am one of those patients who hates the feeling of being numb long after the treatment is done, and would use OraVerse every time that it is indicated.

CONCLUSION
When used as indicated, this new anesthesia reversal agent is an effective way to reduce the amount of time a patient feels numbness related to the administration of local anesthetics. It is a practice builder giving doctors an effective way to help their patients realize a more comfortable dental experience.

REFERENCE

1. Ruiz JL. Supragingival dentistry using metal-free restorations. Dent Today. 2008;27:104-109.

Dr. Ruiz is course director of the USC Advanced Esthetic Dentistry Continuum and clinical instructor at USC, associate instructor and mentor at PCC Utah, teaching with Dr. Gordon Christensen, and is an independent evaluator of dental products for CRA. He is a Fellow of the AGD and practices general dentistry in the Studio District of Los Angeles, where he treats many stars and entertainers. He lectures both nationally and internationally on aesthetic dentistry and leadership. He can be reached at (818) 558-4332 or via email at ruiz@drruiz.com.

Disclosure: Dr. Ruiz reports no conflicts of interest.

Dr. Shuman is president of Pride Institute and is well known in the dental community for his leadership and expertise in the areas of strategic relations, emerging technologies, Internet strategy, practice management, and marketing. The Pride Institute’s goal is to utilize their reputation of integrity and fairness as a foundation in educating the community within the field of emerging technologies. He previously served as vice president of clinical education and then vice president of strategic relations for Align Technology for 7 years. He is a member of Dentistry Today’s Dental Advisory Board and has been listed in Dentistry Today’s Leaders in Continuing Education from 2004 to 2008, and is currently listed as a Leader in Dental Consulting. He is proud to be collaborating in this exciting new Dentistry Today article series. He can be reached via e-mail at lshumani@msn.com. Follow Dr. Lou Shuman on Google+, on Twitter (@LouShuman) or subscribe to Lou Shuman’s posts on Facebook.

Disclosure: Dr. Shuman reports no conflicts of interest.

Ms. Morgan serves as the CEO of Pride Institute. She is a dental consultant and international lecturer. Over the years, Ms. Morgan has facilitated the successful revitalization of thousands of dental practices using Pride Management Systems. She can be reached at amym@prideinstitute.com.

Disclosure: Ms. Morgan reports no conflicts of interest.

THE LA CARTRIDGE

Figure 1. LA cartridge.

Figure 2. Chemical structure of Articaine HCI.

The LA cartridge is a glass cylinder (plastic cartridges of LA are available in some countries) capable of holding 2.0 mL of solution (Figure 1). A thick silicone rubber stopper (plunger) seals one end of the cartridge. As a result, a filled cartridge contains 1.8 mL of anesthetic solution. (In some countries, such as Great Britain, Australia, and South Africa, LA cartridges contain 2.2 mL). The opposite end of the cartridge has a thin latex membrane through which the needle penetrates into the cartridge.

ALLERGY

LA Allergy

Figure 3. Basic management of all medical emergencies.11

True, documented, and reproducible allergy to ester-type LAs is relatively common, while with amide-type LAs allergy is such a rarity as to be virtually nonexistent³ (Table 2). Reports of “alleged” allergy (eg, “Doctor, I am allergic to Novocain”) are more frequent. Confronted with an alleged LA allergy, the clinician must: (1) always believe the patient and not administer any LA, including (or perhaps, especially) topical anesthetic, and (2) determine what actually happened during their “allergic reaction.” Questions to ask of the patient (dialogue history) are presented in Table 3.

Allergy to Components of a LA Cartridge

Though allergy to a LA drug is highly unlikely, allergy may occur to one of the components included in the cartridge.

Specific mention must be made of articaine HCl, an amide local anesthetic that contains a sulfur molecule in its chemical structure (Figure 2). As the sulfur molecule is an integral part of the thiophene ring of articaine HCl, it is not available to act as an allergen. Articaine HCl may safely be administered to patients with sulfur allergy. Introduced in 1975, and presently available in approximately 131 countries, there have been no reported cases of allergy to articaine HCl.⁵

Epinephrine Allergy
Allergy to epinephrine cannot occur. Questioning of the “epinephrine-allergic” patient (see dialogue history, above) immediately reveals signs and symptoms related to increased blood levels of circulating catecholamines (tachycardia, palpitation, sweating, nervousness), likely the result of fear of receiving injections (release of endogenous catecholamines [epinephrine and norepinephrine]).

Latex Allergy

The thick plunger (also known as the “stopper”) on one end of the LA cartridge and the thin diaphragm on the other end of the cartridge (Figure 1) through which the needle penetrates may contain latex. As latex allergy is of growing concern among all healthcare professionals, the risk of provoking an allergic reaction in a latex-sensitive patient must be considered. A recent review of the literature on latex allergy and local anesthetic cartridges by Shojaei and Haas⁶ demonstrates that latex allergen can be released into the LA solution as the needle penetrates the diaphragm, but there were no reports or case studies in which an allergic response to the latex component of the cartridge containing a dental local anesthetic was documented.

OVERDOSE (TOXIC REACTIONS)
Overdose (also known as toxic reaction) occurs when the blood (serum) level of LA in either the central nervous system (CNS) or myocardium is elevated to a point where the drug produces potentially life-threatening events. The overdose reaction persists until the blood level of the drug in these “target” organs falls below the toxic level. Table 4 lists ways in which overly high blood levels can be produced. 

(1) Treatment plan. In interviews with trained pediatric dentists, I have found that when presented with the patient described above (young, light-weight, well-behaved), the pediatric dentist will not treat all 4 quadrants at one visit using LA. Limiting treatment to 1 or 2 quadrants per visit represents a more rational approach to this patient’s needs, and increased safety.

(2) Choice of LA. In most instances where serious LA overdose has occurred in children, the LA administered has been a “plain” drug, either mepivacaine HCl 3% or prilocaine HCl 4%. Both of these are excellent LAs when used properly. The rationale behind the clinician’s selection of a short-acting drug for children includes: (a) most pediatric appointments are of short duration, and (b) plain LAs have a shorter duration of posttreatment soft tissue anesthesia, minimizing the likelihood of inadvertent soft tissue injury as the child bites or chews his/her numb lip or tongue.

(3) Volume of LA administered. Pain control for the entire primary dentition can be achieved with approximately 2 cartridges of LA. In the child patient, there is never a compelling reason to administer a full 1.8 mL cartridge of LA for any 1 injection. Yet, when children receive LA administered by nonpediatric dentists, full cartridges tend to be routinely administered. In many of the instances where death resulted, a total of 5, 6, or 7 cartridges were administered.⁸

(4) LA administered to all 4 quadrants at one time. The administration, over 1 or 2 minutes, of 4 or more cartridges of a LA without a vasopressor to all 4 quadrants makes little therapeutic sense, while increasing the likelihood of an overdose. Administration of LA to one quadrant, treating that area, then anesthetizing the next quadrant, and so on, makes considerably more sense both from a therapeutic and safety perspective. For equal amounts of LA, administration over a longer timeframe (1 to 2 hours) will result in a lower blood level of the LA as compared to the entire dose being administered at one time.
(5) Exceeding the maximum dosage based on patient’s body weight. An important factor, especially when managing younger, lighter-weight patients, is maximum dosage. Determine the weight of the patient (in pounds [lb] or kilograms [kg]) prior to the start of treatment. It is preferable to weigh the child on a scale, as parents frequently can offer only a rough estimate of the child’s weight.

CONCLUSION
LAs are the foundation of pain control in dentistry and are used to reversibly block peripheral nerve conduction. It must always be remembered that all drugs have the potential to do harm. All dentists and hygienists permitted to administer LAs must be aware of these potential problems and be prepared to manage them expeditiously and effectively.

References

1. Malamed SF. What’s new in local anaesthesia: dentistry’s first line in pain control. Independent Dentistry. 2001;4:43-46.
2. Haas D, Lennon D. Local anesthetic use by dentists in Ontario. J Can Dent Assoc. 1995;61:297-304.
3. Jastak JT, Yagiela JA, Donaldson D. Local Anesthesia of the Oral Cavity. Philadelphia, Pa: Saunders; 1995.
4. Haas DA. An update on local anesthetics in dentistry. J Can Dent Assoc. 2002;68:546-551.
5. Malamed SF, Gagnon S, Leblanc D. Articaine hydrochloride: a study of the safety of a new amide local anesthetic. J Am Dent Assoc. 2001;132:177-185.
6. Shojaei AR, Haas DA. Local anesthetic cartridges and latex allergy: a literature review. J Can Dent Assoc. 2002;68:622-626.
7. Malamed SF. Morbidity, mortality and local anaesthesia. Primary Dental Care. 1999;6:11-15.
8. Finder RL, Moore PA. Adverse drug reactions to local anesthesia. Dent Clin North Am. 2002;46:747-757.
9. Malamed SF. Handbook of Local Anesthesia. 4th ed. St Louis, Mo: C.V. Mosby Inc; 1997:191, 218, 265.
10. Malamed SF. Report of a case. Unpublished data. 2002.
11. Malamed SF. Handbook of Medical Emergencies in the Dental Office. 5th ed. St. Louis, Mo: C.V. Mosby Inc; 2000:51-52.

Dr. Malamed is a professor of anesthesia and medicine at the School of Dentistry at the University of Southern California.

Figure 1. The pattern of the numbers of reported cases of paresthesia in Ontario, Canada. * *Reproduced with permission of the publisher from Figure 1: The pattern of the numbers of reported cases of paresthesia in Ontario, Canada, by Haas and Lennon. 4

LITERATURE REVIEW AND ANALYSIS
Because of voluntary medical-legal reporting of the occurrence of paresthesia in Ontario, Canada, and the publication of these data by Haas, Miller, and Lennon, information has been collected regarding the occurrence of paresthesia following administration of mandibular local anesthesia, which is not related to surgical trauma.^4,10,11 Data from three reports indicate that articaine and prilocaine show a very high rate of mandibular paresthesia (usually of the lingual nerve), while lidocaine and mepivacaine were rarely associated with this untoward side effect.^4,10,11

Because all reported paresthesias were of the lingual nerve, inferior alveolar nerve, or both, maxillary injections are not considered in this analysis. The assumption is that half of all injections are for the maxillary arch,6 and the total number of cartridges was divided in half.

Analysis of the data indicates that articaine has a 4% higher occurrence of paresthesia than prilocaine, though they are both 4% solutions. Although they may not be causative factors, articaine is the only local anesthetic with sulfur or a thiophene ring and an ester bond.¹ It is also the only local anesthetic having both an ester and amide bond. The relationship of chemical structure to the occurence of paresthesia should be investigated. A number of recent publications suggest that articaine is associated with a higher rate of paresthesia for mandibular block injections than was calculated in this paper. While the Canadian data were for voluntary reporting of paresthesia, recent data reported all occurrences. Two cases of paresthesia were reported following treatment of 13,000 patients with articaine.¹² If half of these were for mandibular procedures, the rate would be two cases for 6,500 mandibular injections, or 1:3,250. Considering that infiltration anesthesia could also have been employed for the mandible, the paresthesia rate may have even been higher. The product insert for articaine, and the publications associated with the study of articaine reported to the Food and Drug Administration (FDA), indicate a paresthesia rate much higher than one in 3,250 usages.^13-16 The FDA study reported twenty-one cases of paresthesia in 882 patient treatments, or one in every fourty-two patient treatments. The product insert¹⁴ and one publication16 indicate a 1% paresthesia rate. Another publication¹⁵ lists paresthesia as one of the minor adverse events found in the study.

CONCLUSIONS
Because paresthesia associated with the use of local anesthetics as part of dental care in the United States has been an infrequent event, many dentists and patients are not aware of the potential problem. Besides the range of altered sensations considered as paresthesia (perceived numbness, swelling, tingling, itching), there can be oral dysfunction4 and pain.^4,7,17 The dysfunctions include tongue biting, drooling, loss of taste, and speech impediment.⁴ Pain (dysesthesia or hyperesthesia) is usually not considered when discussing local anesthesia-induced paresthesia. The pain of dysesthesia can severely impact the quality of life,^7,17 causing some patients to seek treatment at pain management clinics.^6,7,17 The life changes patients experience from these alterations are significant.^6,7,17 Minimizing the chance of paresthesia is the best approach. The analysis of data from the study in Canada presented here indicates that 4% articaine has a twenty-fold higher rate of paresthesia compared to 2% lidocaine. Data from more recent studies suggest an even greater disparity in this untoward side effect when comparing articaine and lidocaine.^12-16 These data suggest a rate of paresthesia (using articaine for lingual or mandibular block injections) as high as 2% to 4%. As evidenced by the Canadian data from 1993, there were no reported cases of paresthesia with the use of more than 3 million cartridges of lidocaine. Furthermore, there were only five confirmed cases of paresthesia with lidocaine in 21 years. One study of permanent nerve injuries associated with inferior alveolar nerve blocks found the same number of injuries associated with lidocaine (41) as with prilocaine (41). However, national sales figures indicate that lidocaine was used 4.7 times more than prilocaine.⁷ It should be noted that this study⁷ was conducted prior to the FDA approval of articaine in the United States.

The paresthesia rates listed for articaine, and to a lesser extent prilocaine, raise questions regarding the use of these local anesthetics:

(1) Does the risk of paresthesia warrant use of articaine and prilocaine for lingual nerve, inferior alveolar nerve, and other mandibular block injections?
(2) Does the risk of paresthesia with articaine and prilocaine for mandibular block or lingual block injections warrant the use of special informed consent? Based on this analysis of data it appears informed consent is merited in performing mandibular block and lingual block injections with articaine or prilocaine. The risk of paresthesia is so remote in all other administrations of local anesthesia that consent seems unnecessary. Previously, the medicolegal environment has not considered the issue in this context. In 1989, the Ontario High Court¹⁸ ruled that informed consent was not necessary before administering local anesthesia because the expert witnesses said the risk was infinitesimal, minimal, extremely small, or in order of magnitude of 1:800,000. Based on the Canadian study,⁴ the rate of paresthesia in Ontario for 1993 was estimated to be 1:785,000. Although this was true, ten of the fourteen cases were associated with the use of articaine in mandibular block injections and the other four were from the use of prilocaine with mandibular block injections.
(3) The Canadian data do not provide information regarding the duration of paresthesia in the cases reported. This would certainly be one important consideration when deciding on the use of these agents for local anesthesia. Analysis of the available data indicates that there are areas for future studies, and more specific data needs to be collected. For example, improved clinical monitoring/recording of extent, degree, and duration of paresthesia; clear definition of terms; the specific type of injections administered, and; differentiating paresthesia from minor adverse events related to administration of anesthesia. These data would improve our understanding of the problem. In summary, the incidence of paresthesia of the lingual nerve and inferior alveolar nerve should be considered when selecting a local anesthetic agent for anesthetizing the mandible and its associated structures.

References
1. Malamed SF. Handbook of Local Anesthesia. 4the ed. St. Louis, Mo: C.V. Mosby Co; 1997: 248;249;63-64.
2. Jastak JT, Yagiela JA, Donaldson D. Local Anesthesia of the Oral Cavity. Philadelphia, Pa: W.B. Saunders Co; 1995:301.
3. Haas DA. Localized complications from local anesthesia. J Calif Dent. 1998;26:677-682.
4. Haas DA, Lennon D. A 21-year retrospective study of reports of paresthe sia following local anesthetic administration. J Can Dent Assoc. 1995;61:319-330.
5. Pogrel MA, Kaban LB. Injuries to the inferior alveolar and lingual nerves. J Calif Dent. 1993;21:50-4.
6. Pogrel MA, Bryan J, Regezi J. Nerve damage associated with inferior alveolar nerve blocks. J Am Dent Assoc. 1995;126:1150-1155.
7. Pogrel MA, Thamby S. Permanent nerve involvement resulting from inferior alveolar nerve blocks. J Am Dent Assoc. 2000;131:901-907.
8. Harn SD, Durham TM. Incidence of lingual nerve trauma and postinjection complications in conventional mandibular block anesthesia. J Am Dent Assoc. 1990;121:519-523.
9. Kalichman MW, Moorhouse DF, Powell HC, Myers RR. Relative neural toxicity of local anesthetics. J Neuropathol Exp Neurol. 1993;52:234-240.
10. Miller PA, Haas DA. Incidence of local anesthetic-induced neuropathies in Ontario in 1994. J Dent Res. 1996;75SI:247.
11. Miller PA, Haas DA. Incidence of local anesthetic-induced neuropathies in Ontario from 1994-1998. J Dent Res. 2000;79Sl:627.
12. Clinical Research Associates Newsletter. 2001;25(6):1-2.
13. Septodont application to United States Food and Drug Administration for approval of articaine local anesthetic (NDA 20-971). 1998;256-259.
14. Septocaine (articaine hydrochloride 4% (40 mg/ml) with epinephrine 1:100,000 injection) product insert 04/2000.
15. Malamed SF, Gagnon S, Leblanc D. Efficacy of articaine: a new amide local anesthetic. J Am Dent Assoc. 2000;131:635-642.
16. Malamed SF, Gagnon S, Leblanc D. Articaine hydrochloride: a study of the safety of a new amide local anesthetic. J Am Dent Assoc. 2001;132:177-184.
17. Pogrel MA, Thamby S. The etiology of altered sensation in the inferior alveolar, lingual, and mental nerves as a result of dental treatment. J Calif Dent. 1999;27:531-538.
18. Supreme Court of Ontario. Trial proceedings No. 158/89; Vol 3:494-497,1989.

Dr. Dower is an associate professor in the Department of Restorative Dentistry at University of the Pacific’s School of Dentistry. He has been director of the Local Anesthesia courses since 1979 and implemented a local anesthesia curriculum at UOP that includes three rotations in local anesthesia during students clinical years. Dr. Dower has presented local anesthesia courses, lectures, and table clinics to regional, state, and national dental meetings. His publications and research articles have appeared in Anesthesia Progress, Journal of the American Dental Association, Quintessence International, Journal of General Dentistry, and Journal of the California Dental Association. Dr. Dower also holds a master’s degree in Educational and Counseling Psychology.

Topical anesthetics used prior to infiltration and block injections for dental treatment commonly come in the form of sprays, liquids, or gels. The clinical efficacy of these agents in averting discomfort on needle penetration is questionable at best, with notably little difference between these agents, tissue vibration (“cheek tugging”) with or without concomitant topical anesthetic use, and even placebo.^6-8 Even the use of electronic anesthesia as a topical agent produces comparatively insignificant reductions in pain on needle penetration.²

I believe that it is the form in which the majority of topical anesthetics are applied, and to some degree their composition, that accounts for the relative inadequacy of most topical agents. A principal factor in the effectiveness of topical anesthetics is tissue penetration.9 While not allowing adequate time for diffusion of the topical anesthetic into the mucosa is a mistake often made by practitioners, poor localization and retention of the agent on the soft tissue can negatively affect its success, as well.¹⁰ The oral cavity pre-sents considerable challenges with respect to these parameters because salivary flow and pooling can be a hindrance to these objectives. This is evidenced by the fact that topical efficiency on the mandible is relatively higher in the mucobuccal fold area for mental blocks than at the pterygo-mandibular raphe for inferior alveolar blocks, where a greater accumulation of saliva could be expected.¹¹ While this is not the only issue relating to the pain associated with these blocks, it is a key one.

Some agents have been convincingly shown to almost eliminate needle insertion pain.12 From personal experience, I know the Denti-Patch (Noven Pharmaceuticals) to be a highly efficacious topical agent if given sufficient time to act. It uses a fairly high concentration of lidocaine in an adhesive patch that clings firmly when applied to attached soft tissue, allowing targeted dispersion of the active ingredient. Adhesive patches and cellulose discs would seem to be more successful vehicles in terms of maintaining and concentrating the topical agent at the intended site.¹⁰

Figure 1. Anaesthesie Tab 5-mm cellulose disc.	Figure 2. Blue “bull’s eye” left by Anaesthesie Tab to mark the site of injection.
Figure 3. The Syrijet anesthetic injector.	Figure 4. Red macule marks the spot where anesthesia has entered.

It also appears that some anesthetic agents have a greater potential than others to be correlated with a higher level of topical anesthesia. Tetracaine hydrochloride and dibucaine hydrochloride are among the most potent in this regard.¹³ Both of these anesthetics can be found in Anaesthesie Tabs (Voco, Germany), which are cellulose discs about 5 millimeters in diameter (Figure 1) that leave a blue “bull’s eye” on the tissue upon removal, to mark the eventual injection site (Figure 2). Gently extend the mucosal surface taut and insert your needle into the center of the bull’s eye. I have been using these tabs for several years now and have found them to be just as effective as the Denti-Patch, while being more cost-effective on a per-injection basis. They reach full effect in 90 to 120 seconds, and the blue marking disappears a few hours after use. They have a somewhat higher-than-average rate of allergic contact dermatitis,¹⁴ but it has been my experience that most patients comment on the appearance of this reaction more than any related sensations.

The tabs are effective in any mucobuccal fold where they can be held in place with a cotton roll. It is critical that enough time be allowed to elapse after the tab has been inserted before the injection is attempted, or the full effects possible with this product will not be realized. I use the Anaesthesie Tabs for all injections save for inferior alveolar blocks and palatal infiltrations. For the latter, I use the transpapillary technique following a buccal infiltration.¹⁵ At the pterygo-mandibular raphe, of course, there is no fold, and until the year 2000 I had used gels, liquids, and sprays with erratic success at best. Then I discovered the Syrijet (Keystone Industries). The Syrijet (Figure 3) is a needleless, jet anesthetic injector that I have found provides excellent topical and, more importantly, subtopical anesthesia for inferior alveolar blocks. To deposit the contents of a carpule of anesthetic at the lingula for inferior alveolar blocks, needle penetration must reach significantly greater depths into soft tissue than with an infiltration injection in most instances. The subtopical anesthesia that the Syrijet provides is ideal for this purpose.¹⁶ The breadth and depth of anesthetic penetration achieved with this device¹⁷ gives the dentist wide latitude to manipulate the cannula in the soft tissue with little or no patient discomfort. Typical of the comments I have heard when using this procedure, one of my patients remarked to me that she did not feel the needle insertion, “any of the way in.” Standard dental carpules may be used in the Syrijet with jet volumes up to 0.20 cc having been shown to be well tolerated by dental patients, even children.^16,18

First, place a cotton roll in the mucobuccal fold of the upper arch on the side where you will be working for moisture control, have the patient open as wide as possible, and dry the pterygo-mandibular raphe with your suction. Now place the injector head’s nozzle (arrow) snugly against the tissue where you will be injecting, and press the trigger. A red macule (Figure 4) will then appear on the tissue surface where the jet of anesthetic entered. Use this as the target point for your injection.

I use a 0.05-cc volume of articaine hydrochloride in my Syrijet and wait 2 to 3 minutes before performing the inferior alveolar block injection, to allow for full efficacy. Again, allowing sufficient time for complete effect is crucial. I use this small volume of articaine hydrochloride because that anesthetic’s chemical composition affords it a greater solubility in lipids,19 which increases its penetration into fatty tissues. Also, unlike other anesthetics reported to cause a burning sensation on immediate infusion,²⁰ I have heard no such complaints from my patients with this one. Even though using the same carpule on multiple patients in the Syrijet should present a minimal risk of cross-infection,²¹ I always use one carpule for one patient. After using the Syrijet, I remove the articaine carpule and place it in my traditional syringe for the block, as articaine has been observed to be more effective in these injections because of its aforementioned chemical characteristics.²² In my office, the rubber sheaths supplied with the Syrijet that cover its injector head are always changed between patients and sterilized after each use. I also prime the Syrijet with a carpule of distilled water before each patient use, even though the manufacturer only recommends this on a weekly basis. Priming is imperative as crystalline residue from anesthetics can clog the Syrijet after repeated use.

CONCLUSION

I have always felt that if when providing a patient with dental treatment I cause that patient discomfort such that he or she becomes apprehensive about future treatment, I have failed that patient. Discomfort from administration of local anesthesia is a significant source of such apprehension.¹ I have found that the use of the methods and materials described in this article greatly minimizes the patient’s discomfort from, and therefore fear of, local anesthetic injections. This is a practice builder that will reduce the doctor’s stress level, promote patient loyalty, and increase case acceptance. It is important to remember that when providing local anesthesia, as in most other phases of direct patient care, it is deeply appreciated when doctors really take the time to make their patients comfortable.

References

1. Glassman P, Peltier B. Guidelines for the administration of local anesthesia in fearful dental patients. J Calif Dent Assoc. 1995;23:23-26.

2. Quarnstrom F, Libed EN. Electronic anesthesia versus topical anesthesia for the control of injection pain. Quintessence Int. 1994;25:713-716.

3. Hochman M, Chiarello D, Hochman CB, et al. Computerized local anesthetic delivery vs. traditional syringe technique. Subjective pain response. NY State Dent J. 1997;63:24-29.

4. Krochak M, Friedman N. Using a precision-metered injection system to minimize dental injection anxiety. Compend Contin Educ Dent. 1998;19:137-143.

5. Goodell GG, Gallagher FJ, Nicoll BK. Comparison of a controled injection pressure system with a conventional technique. Oral Surg Oral Med Oral Pathol Radiol Endod. 2000;90:88-94.

6. Kinchloe JE, Mealiea WL Jr, Mattison GD, Seib K. Psychophysical measurement on pain perception after administration of topical anesthetic. Quintessence Int. 1991;22:311-315.

7. Martin MD, Ramsay DS, Whitney C, et al. Topical anesthesia: differentiating the pharmacological and psychological contributions to efficacy. Anesth Prog. 1994;41:40-47.

8. Hutchins HS Jr, Young FA, Lackland DT, Fishburne CP. The effectiveness of topical anesthsia and vibration in alleviating the pain of oral injections. Anesth Prog. 1997;44:87-89.

9. Maddi R, Horrow JC, Msrk JB, et al. Evaluation of a new cutaneous topical anesthsia preparation. Reg Anesth. 1990;15:109-112.

10. Holst A, Evers H. Experimental studies ofnew topical anesthetics on the oral mucosa. Swed Dent. 1985;9:185-191.

11. Nakanishi O, Haas D, Ishikawa T, et al. Efficacy of mandibular topical anesthesia varies with the site of administration. Anesth Prog. 1996;43:14-19.

12. Houpt MI, Heins P, Lamster I, Stone C, Wolff MS. An evaluation of intraoral lidocaine patches in reducing needle insertion pain. Compend Contin Educ Dent. 1997;18:309-310.

13. Yokoyama S. Correlation between pharmacological potency and micellar surface potential of local anesthetic. Toxicol Lett. 1998;100-101:365-368.

14. Amano K. [Clinical study of patients with positive reactions in patch tests with local anesthetics]. Nippon Ika Daigaku Zasshi. 1997;64:139-146.

15. McArdle BF. Painless palatal anesthesia. J Am Dent Assoc. 1997;128:647.

16. Greenfield W., Karpinski JF. Needleless Jet injection in comprehensive pain control and applications to oral surgery. Anesth Prog. 1972;19:94-97.

17. Bennett CR, Mundell RD, Monheim LM. Studies on tissue penetration characteristics produced by jet injection. J Am Dent Assoc. 1971;83:625-629.

18. Saravia ME, Bush JP. The needleless syringe: efficay of anesthesia and patient preference in child dental patients. J Clin Pediatr Dent. 1991;15:109-112

19. Malamed SF, Gagnon S, Leblanc D. Articaine hydrochloride: a study of a new amide local anesthetic. J Am Dent Assoc. 2001;132:177-185.

20. Strupp W. A clinical Technique for giving painless injections. Dent Today. 1998;17:34-37.

21. Suria H, Van Enk R, Gordon R, Mattano LA Jr. Risk of cross-patient infection with clinical use of a needleless injector device. Am J Infect Control. 1999;27:444-447.

22. Friedman MJ. New advances in local anesthesia. Compend Contin Educ Dent. 2000;21:432-440.

Dr. McArdle is cofounder of the Seacoast Esthetic Dentistry Association (SEDA) (www.dentalesthetics.org) and is on the Board of Directors of Priority Dental Health, Inc (www.prioritydental.com). Visit his website at www.mcardledmd.com.

In the majority of cases of toothache, the tooth is the source of the pain. In a small percentage of cases, however, the site of the pain is not the specific source. The literature suggests that 6% of the population suffers from persistent periodontal pain,2 and 3% to 5% of patients have persistent pain after endodontic treatment.3,4 The purpose of this article is to explore the differential diagnosis of patient complaints of pain that feels like a toothache, but is not related to the teeth. If all appropriate diagnostic tests focusing on the tooth in question are negative (including referral to an endodontist), this information will enhance the clinician’s ability to provide the appropriate care for patients who experience such pain.

ATYPICAL TOOTHACHE

In a limited number of cases, pain is referred from a source other than a tooth to the region of a tooth. An analogy of a commonly referred pain in which the site and source are different is when a myocardial infarction presents as indigestion.

The differential list for atypical toothache is a list of disorders that should be considered when the diagnosis of tooth-related pain, ie, pulpal hyperemia or cracked tooth, is not clear. This list should be considered when tooth-directed diagnostic tests are negative, additional treatment is not indicated, and there is a clear sense that pain relief will not result from treatment of the tooth.

Diagnosis of these disorders is not difficult if a logical diagnostic scheme is followed. The list of disorders in their frequency of occurrence is shown in the Table.5-7

Muscle

The most common cause of atypical tooth pain is referral of pain from muscles of mastication. Muscle pain tends to be deep pain, which is not location-specific. The two most common pain referral patterns from muscles of mastication are the masseter muscle referring to mandibular posterior teeth, and the temporalis muscle referring to maxillary posterior teeth.8 A common cervical muscle referral pattern is when the sternocleidomastoid (SCM) refers pain to the ipsilateral periorbital area. The trigeminal nerve travels primarily to the trigeminal ganglion, but some of the neurons synapse with the superior-cervical ganglion, which can elicit a response from cranial nerves Nos. 7, 9, and 10. Atypical pains in the head region referred from the SCM can be mistaken for vascular headaches or atypical facial neuralgias.9 Furthermore, nociceptive input from virtually the entire head and neck converge on the trigeminal spinal nucleus, which can also lead to unusual pain referral patterns.10,11 Nociception from deep structures (muscle, vasculature, and joint) is generally non-topographic in nature and often difficult for a patient to localize.12 Regardless of the exact mechanism, referred tooth pain does occur.8 Thus, many patients with pain of muscular origin are misdiagnosed with other conditions.13

It has been reported that between 75% and 85% of the patients with atypical toothache also have pain and dysfunction in the cervical region.14 The connection is the stabilization kinetic chain (muscles are used to keep joints in place at rest, resist gravity, and stabilize a joint when a structure is moved in a certain direction or held in a certain position). An example is when the abdominal muscles are contracted, the back muscles contract to keep the person upright. The muscles in the shoulders and upper chest must contract to stabilize the torso, and the muscles of the neck contract to stabilize the shoulder. Considering normal daily activity, the muscles of mastication (masseter, medial pterygoid, lateral pterygoid, and temporalis) are among the most frequently used of all muscles, and contraction of the neck muscles plays a role in stabilizing the jaw. Trauma, hyperextension, hyperflexion injuries, and prolonged opening of the mouth have been related to discomfort reported by more than 50% of all patients with temporomandibular dysfunction.15

Injury to Periodontal Ligament

Injury to the periodontal ligament (PDL) is the second most likely cause of tooth pain.16 Tooth innervation and vascular supply can be pulpal or periodontal, and insult, infection, or injury can be signaled from either source. Heavy occlusal forces can create the symptoms of pulpitis.17 If there is no reason for pulpal pain, the next thing to consider is the PDL that surrounds the tooth, generally protecting it from excessive chewing forces. During the day, the fast reactive two-neuron protective loop keeps a patient from injuring the tooth, PDL, and bone complex when biting.18 At night the protective reflex mechanisms are reduced, and a major force such as clenching or grinding teeth can cause injury to the PDL. These forces can also contribute to alveolar bone loss,19,20 and cause hot and cold sensitivity, cervical erosion,21 masseter muscle enlargement, bony exostosis, and tooth fractures.22 Parafunctional causes of injury to the PDL include the following:

•grinding—lateral movement of the teeth

•clenching—static holding of the teeth in maximum intercuspation

•tooth bracing—locking of upper and lower teeth together in any position outside of centric relation, especially a forward or forward lateral position.

Each of these nonfunctional activities of the masticatory apparatus can damage or injure bone, muscles, joints, or teeth. The discomfort associated with injury to the PDL can feel like pulpal pain.17 Injury to the PDL may be associated with tooth mobility,23 which may lead to further confusion. If endodontic treatment is provided in situations where the pain is related to the PDL, no relief will be reported. When a general dentist or an endodontist rules out the teeth as the cause for pain, occlusal trauma should be considered.2 A diagnostic anesthetic injection is not usually helpful because it will block both the pulpal and PDL innervation. The occlusal trauma may be reduced by simple adjustment of a tooth, but in moderate cases occlusal appliance therapy and medication are necessary. In more complicated cases, referral to an orofacial pain specialist is required. Note that in some cases of PDL-related pain, endodontic therapy may be performed in the course of care. However, if the pain is not relieved, no further dental treatment should be initiated until the cause of the pain is properly identified.

Temporomandibular Joint

The temporomandibular joint (TMJ) can directly or indirectly refer pain to the dentition. The concept of the three-legged stool presented by Pankey and Dawson,24 where instability in one leg leads to instability in the whole system, is a helpful analogy.24,25 If the sum of all the muscular forces lies in the triangle of support formed by the two condyles and bitepoint, then the force system is said to be stable. If the bitepoint is more posterior, the resultant force will create stress on the working side condyle and muscles.25 The most common problem with the TMJ is internal derangement (disc displacement), and this can lead to indirect referral of pain to the teeth. Of 200 patients diagnosed as having internal derangement of the joint, 67% had disc displacement with reduction (recapturing the central non-innervated thin area of disc by the condyle head as you open), 22% had disc displacement without reduction, and 10% had osteoarthritis.26 Pathology of the joint induces muscle splinting (a protective mechanism by the muscle to restrict joint activity), which when added to bruxism, chewing, and increased muscle tone related to stress, can induce referred pain. According to Hilton’s Law (Dorland’s medical dictionary), the nerve that innervates muscles of a given joint also supplies the joint,27 allowing the muscles surrounding an injured joint to protect the joint. This increase in loading force to an already unstable joint, or increase in muscle activity to that joint, can lead to referred pain.

Neuropathic Pain

Neuropathic pain is not often encountered by general dentists, but may be seen by endodontists. Neuropathic pain must be included in the differential diagnosis, especially after the tooth, muscle, PDL, and joint have been evaluated and ruled out as a cause. The neuropathies are considered when no obvious local pathology is identified, there is a history of trauma or surgical intervention, and the patient is depressed. Neuropathies occur most commonly in the fifth or sixth decade of life, and the pain can be severe.28 A neuropathy may be central or peripheral. The location of the neuropathic pain needs to be determined by history of what triggers the pain, and if diagnostic anesthesia blocks the pain. If the pathology is a result of surgery or trauma, described as burning, and blocked at the foramen ovale (by providing a Gow-Gates injection, blocking the entire third division of trigeminal nerve), then a peripheral neuropathy is suspected. The peripheral neuropathies include postherpetic neuralgia, neuroma-related neuropathy, and trigeminal neuropathy. The central neuropathies include trigeminal neuralgia, glossopharyngeal neuralgia, postherpetic neuralgia, and tumors of the mid-cranial fossa.29

Postherpetic neuralgia is caused by a viral infection of one or more branches of the trigeminal nerve. In 10% of cases involving patients over 50 years of age, the nerve pain remains after resolution of the acute viral infection.30 The patient will report a vesicular lesion, moderate to severe pain, with a burning sensation. The pain can occur in any of the divisions of the trigeminal nerve; maxillary distribution (V1 or forehead) is the most common.30 The herpes virus selectively infects large diameter fibers, leaving the C fibers to dominate the gating mechanism of pain.31

The second type of neuropathic pain is nerve injury, leading to a neuroma. Nerve injury is associated with inflammation and release of nerve growth factor (NGF) from cells participating in the repair response, including mast cells.32 NGF stimulates growth of sympathetic nerve tissue.32 A neuroma, then, represents ineffective healing of a nerve, and is associated with excessive production of NGF and benign overgrowth of nerve tissue.33 Some neuromas develop ectopic nerve impulses as a result of release of the cytokine tumor necrosis factor from activated macrophages.25 Concurrently, the pain fibers in a neuroma develop adrenoceptors sensitive to stress-related neurotransmitters.31 A neuroma may result from the trauma of an anesthetic syringe needle injuring a nerve, or as a result of damage during surgery. Chronic neuropathic pain can result.34

The central neuropathies include trigeminal neuralgia, glossopharyngeal neuralgia, and tumors in the mid-cranial fossa. Trigeminal neuralgia is a neurological condition that may manifest as a toothache, but is not related to tooth pathology.35 If the burning pain is not blocked by anesthetic injection and is relieved by the drug Tegretol, a central neuropathic lesion is inferred.34 The central neuropathies are considered to be nerve dysfunction associated with a sensory impulse that crosses over to a pain impulse pathway, which in turn is caused by an artery abrading the myelin sheath of a nerve bundle or pressure from an expanding tumor.36 This is found in association with the trigeminal nerve (cranial nerve No. 5) or the glossopharyngeal nerve (cranial nerve No. 9).

Neurovascular Pathology

The neurovascular pathologies are classified into two groups which have some similarities and certain differences. The first type is now referred to as atypical odontalgia. The patient describes the pain as throbbing, crawling, constant discomfort in the teeth, bone, or gingiva. The problem is thought to be a microconstriction of the blood vessels in a particular area, caused by autonomic dysfunction.2 Women 30 to 50 years of age, who suffer from depression and have a history of a recent surgical dental procedure seem to be predisposed to this condition.37 Although atypical odontalgia has symptoms very similar to pulpal pain, endodontic procedures will not relieve the pain. A clinical course of an antidepressant (Tofranil) will confirm the diagnosis.38

The second neurovascular pathology is called neuralgia-inducing cavitational osteonecrosis (NICO), and is thought to be related to trauma to bone with improper healing.39 The typical patient is female, 40 to 60 years of age, and describes the pain as throbbing or burning, which is not elicited by any specific activity. The diagnosis is usually confirmed by an unusual anesthetic response to lidocaine (variant anesthetic responses), such as blocking (partial anesthesia up to a certain point, then it stops), bridging (zone of complete anesthesia-zone of partial anesthesia-zone of complete anesthesia), or divergence (zone of anesthesia in another nerve distribution) instead of a complete nerve block of nerve.40 After the exact location of the bone cavity is determined, the area can be probed with an aspirating syringe to locate the thin area of cortical bone.39 A technetium 99 scan may reveal an area of active bone turnover.41 The technetium scan may not reveal the cavity if it is an older lesion without significant metabolic activity. These disorders are quite rare, and should be considered only when other causes of nondental toothache have been ruled out. Nevertheless, in an attempt to provide relief, patients suffering from atypical odontalgia and NICO may receive unnecessary and ineffective treatment. It is essential for the dentist and the physician treating facial pain to be aware of these conditions.38

Other Disorders

Other disorders that can manifest as a toothache include sinus pathology and psychological problems. Only 4% of headaches or toothaches are related to sinus infections.42 Nevertheless, upper respiratory infections and allergies can manifest as tooth pain in the maxillary posterior regions. A clinical course of decongestants and/or antihistamines, or referral to an otolaryngologist, would confirm the diagnosis.

Toothaches associated with psychological disorders are sometimes difficult to diagnose because of difficulty in taking a complete and accurate history. These patients often present with impaired cognitive ability, inability to focus, and inability to reason. As a result, it is difficult to maintain continuity and clarity during the diagnostic phase of care. Because the history is an important part of the diagnostic process, if the reporting is compromised the dentist or the physician may begin treatment when there is no basis for such treatment. This is more likely to happen when a patient with a psychiatric problem presents with a poor dentition. This unnecessary treatment may even exacerbate the psychological condition. Patients with this condition seen in the dental office are most often suffering from severe depression.43

DISCUSSION

When a clinician suspects that the cause of a toothache may not be strictly dental in origin, referral to an appropriate specialist (orofacial pain specialist, neurologist, otolaryngologist) is often indicated. If endodontic therapy is the initial approach to treatment, but some doubt remains, the patient should be informed that diagnostic tests for endodontic disease are not always conclusive, and that this therapy may not eliminate the pain associated with the tooth. The fully informed patient should participate in the choice of treatment and be told about the reason for referral.

Reasons for not initiating endodontic therapy (and possibly for referral) include negative test results for pulpal pathology; the diagnostic anesthetic injection does not provide pain relief; and the masseter or temporalis muscle is tender to palpation. A careful diagnostic phase of care is essential. The differential diagnostic process helps the clinician decide to refer an informed patient for additional consultation. This is a valuable service, and helps avoid overtreatment.

CONCLUSION

Having a defined diagnostic plan for atypical toothache based on a differential list of causes is an essential first step in providing appropriate care for patients with these challenging problems. Using the differential diagnostic list described in this article, the clinician can conduct a variety of tests, provide treatment, or suggest referral. Such a process can help prevent or limit treatment that does not resolve the problem, and can better focus the clinician on the true cause of the patient’s pain. To be effective, treatment must be directed at the source of the pain, not the site of the pain.2

References

1. Mahan P. Facial Pain. 3rd ed. Philadephia, Pa: Fea & Febiger; 1991:4-143.

2. Brunsvold MA, Nair P, Oates TW, Jr. Chief complaints of patients seeding periodontal treatment. JADA. 1999;130:359-364.

3. Campbell RL, Parks KW, Dodds RN. Chronic facial pain associated with endondontic neuropathy. Oral Surg, Oral Med, Oral Path. 1990;69:287-290.

4. Marbach JJ, Hulbrock J, John C, Segal AG. Incidence of phantom tooth pain, an atypical facial neuralgia. Oral Surg. 1982;53:190-193.

5. Okeson J. Chronic pain. AAOP Convention. San Antonio, Texas, 2002.

6. Gremillion H. Epidemiology of chronic pain. Parker Mahan Study Cub, Parker E. Mahan Facial Pain Center at University of Florida, April 1997.

7. Yount K. Seven Reasons for Atypical Toothache. Academy of General Dentists of North Carolina Convention. Hilton Research Triangle. Raleigh, NC, June 2000.

8. Travel J, Simon D. Myofascial Pain and Dysfunction, Trigger Point Manual. Vol 1. Baltimore, Md: Williams & Wilkins; 1983.

9. Travel J. TMJ Pain from muscles of the head and neck. J Pros Dent. 1960;10:745-763.

10. Yu XM, Mense S. Somatotopical arrangement of rat spinal dorsal horn cells processing input from deep tissues. Neuroscience Lett. 1990;108:43-47.

11. Schaible HG, Schmidt RF, Willis WD. Enhancement of the responses of ascending tract cells in the cat spinal cord by acute inflammation of the knee joint. Exp Brain Res. 1987;66:479-499.

12. Sessle BJ, Hu JW, Amano N, Zhong G. Convergence of cutaneous, tooth pulp, visceral, neck, and muscle afferents onto nociceptive and non-nociceptive neurons in trigeminal subnucleus caudalis and its implications for referred pain. Pain. 1986;27:219-235.

13. Hubbard D, Jr. Clinical Overview and Pathogenesis. Practical Pain Management. Haworth Press; 1996:123-143.

14. Gremillion H. Multidisciplinary diagnosis and management of orofacial pain. Gen Dent. 2001;3:179-186.

15. Harkins SJ, Martiney JL. Extrinsic trauma: a significant factor in temporomandibular dysfunctions. J Pros Dent. 1985;54:271-272.

16. Burgett F. Trauma from occlusion. Dental Clinics NA. 1995;39:301-311.

17. Ikeda, Nakano, Brando, The effect of traumatic occlusal contact on tooth pain threshold. J Dent Res. 1991;70:330.

18. Melzack R, Wall P. Pain mechanisms. Pain Forum. 1996;5:3-11.

19. Waerhaug J. Pathogenesis of pocket formation in traumatic occlusion. J Perio. 1952;26:107-118.

20. Roberts WE. Bone physiology, metabolism, and biomechanics in orthodontic practice. Current Principles and Technique. St Louis, Mo: Mosby; 1994:193-234.

21. Garro, Stephenson, Good. Chronic illness of TMJ as experienced by support-group members. J Gen Intern Med. 1994;9:372.

22. Cannistraci AJ, Fredrich JA. A multidimensional approach to bruxism and TMD. NYS Dent J. 1987;53:31-34.

23. Hirt, Muhleeman. Diagnosis of bruxism by measurement of the tooth mobility. Dent Abst. 1956;1:356.

24. Dawson P. Evaluation, Diagnosis, and Treatment of Occlusal Problems. 2nd ed. St Louis, Mo: Mosby; 1989:275.

25. McNeil C. Science and Practice of Occlusion. Chicago, Ill: Quintessence Books; 1997:180.

26. Hoffman DC, Cubillos L. The effect of arthroscopic surgery on mandibular range of motion. J Cranio Prac. 1992;12:11-18.

27. Webster Medical Dictionary, 25th ed. Saunders.

28. Rosenkopf K. Current concepts concerning the etiology and treatment of trigeminal neuralgia. J Cranio Prac. 1989;7:312-318.

29. Hupp J. Facial neuropathology. Temporomandibular Disorders and Facial Pain. 697-712.

30. Currey TA, Dalsania MD. Tx for herpes zoster ophthalmicus: stellate ganglion  block as a tx for acute pain and prevention of postherpetic neuralgia. Ann Ophthalmol. 1991;23:188-189.

31. Fields HL, Rowbotham M, Baron R. Postherpetic neuralgia: Irritable nociceptors and  deafferrentation. Neurbiology of Disease. 1998;5:209-226.

32. Merrill RL. Neuropathic Pain. Seminars in Anesthesia. 1997.

33. Leon A, Buriani A, Toso R, et al. Mast cell synthesize, store, and release nerve growth factor. Proc Natl Acad Sci. 1994;91:3739-3743.

34. Dalessio D. Wolfe’s Headache. 6th ed. New York, NY: Oxford University Press; 1993:345.

35. Merrill RL, Graff-Radford SB. Trigeminal neuralgia. J Am Dent Assoc. 1962;123:63-68.

36. Puca A, Meglio M, Tamburrini GT, Vari R. Trigeminal Involvement in intracranial tumours. Acta Neurochir. 1993;125:47-51.      

37. Schnurr R, Brooke R. Atypical odontalgia. Oral Surg, Oral Med, Oral Path. 1992;73:445-448.

38. Reik L. Atypical Odontalgia: Localized form of atypical facial pain. Headache. 1984;24:222-224.

39. Ratner EJ, Person P, Kleinman DJ. Jawbone cavities and trigeminal and atypical facial neuralgis. Oral Surg, Oral Med, Oral Path. 1979;48:3-20.

40. McMahon RE, Adams W, Spolnik KJ. Diagnostic anesthesia for referred trigeminal pain. Comp Cont Ed Dent. 1992;13:870-997.

41. Bullough PG, Dicarlo EF. Subchondral avascular necrosis. Annals Rheu Dis.1990;49:412-420.

42. Couch J. Sinus headache: a neurologist’s viewpoint. Seminars Neurology. 1988;8:298-302.

43. Vimpari SS, Knuutila ML, Sakki TK, Kivela SL. Depressive symptoms associated with symptoms of the temporomandibular joint pain and dysfunction syndrome.  Psychom Med. 1995;57:439-444.

Dr. Yount is a diplomate of the American Board of Orofacial Pain and a fellow of the Academy of General Dentistry. He is a graduate of The Pankey Institute and Dawson Advanced Studies (Occlusion), and received a fellowship in cranio-facial pain from the University of Florida. He lectures on topics related to chronic pain and myofacial pain dysfunction, atypical toothache, and trigeminal neuropathies.

BACKGROUND

In 1996 the National Institutes of Health (NIH) recognized the enormous diversity of treatments being offered to TMD patients. It would not be uncommon for a patient with TMD symptoms to have one doctor suggest full-mouth rehabilitation, another recommend a bite plate, another suggest occlusal equilibration, and another give the patient a jaw exercise program. It is not unusual for one dentist to prescribe medication and another to recommend surgery. In April of 1996, The National Institute of Dental Research and the NIH Office of Medical Applications of Research convened a Technology Assessment Conference on Management of Temporomandibular Disorders to provide the dental community and the general public with a “responsible assessment of management approaches to TMD.”3 More than 1,000 people attended this landmark conference. It brought together specialists in dentistry, medicine, surgery, cellular and molecular biology, biostatistics, epidemiology, immunology, behavioral and social sciences, pain management, tissue engineering, as well as representatives of the public, including TMD patients and advocacy groups. An independent, unbiased panel of accomplished scientists and doctors evaluated all of the information that was presented, and issued a conference statement summarizing the data and offering several conclusions.3

Some of the important conclusions included the following: “Because most individuals will experience improvement or relief of symptoms with conservative treatment the vast majority of TMD patients should receive initial treatment using noninvasive and reversible therapies.” “The efficacy of most treatment approaches for TMD is unknown, because most have not been adequately evaluated in long-term studies and virtually none in randomized controlled group trials.” “Therapies that permanently alter the patient’s occlusion cannot be recommended on the basis of current data.”3 These conclusions were not greeted with enthusiastic support by the profession, but remain valid.

Following are the conservative, noninvasive modalities, adhering to the recommendations set forth by the NIH that will serve dentists and their patients well.

PRINCIPLES OF TREATMENT

Although the popularity of specific treatments comes and goes, the basic principles of treatment do not change. Before discussing specific treatments, several guiding principles require explanation.

Noninvasive and Reversible Modalities

The first rule of treatment is “Do no harm.” Simple modalities, which are both noninvasive and reversible, should always initiate TMD treatment.2,4 These modalities carry very little risk, and the overwhelming majority of patients respond very well.3-6

The second rule of treatment is “Do know harm.” It is important to recognize when treatment is either not indicated because the diagnosis is not TMD related or the treatment itself is not reversible and may lead to unnecessary dental procedures. Many bite-plate appliances are used inappropriately and cause an inadvertent or unintentional change in the occlusion. Bite plates used properly should not permanently alter the dentition. Altering the occlusion by equilibration is not considered reversible, yet it is one of the most common procedures performed by dentists when confronted with a TMD patient.2 One objective of this article is to provide the clinician with alternatives to occlusal equilibration that carry little or no risk and are reversible.

Understanding Success

The treatment of TMD is often successful, and seemingly contradictory treatments can work equally well. There are many factors, other than treatment, which lead to a successful outcome, such as the cyclical nature of TMD, reduction of anxiety, adaptive capacity of joints and muscles, the placebo effect, and the doctor-patient relationship. All of these factors influence outcome.

A patient who meets with the doctor needs to receive an explanation for their pain. They should receive reassurance that they do not have a life-threatening disease, and they are often relieved to find a doctor who is knowledgeable about their condition and is concerned about them. Patients are comforted to know that others with similar problems have successful outcomes, and that they are not alone. The patient’s anxiety prior to coming to the doctor’s office is reduced, and the patient develops a more hopeful attitude toward recovery. All of these factors influence patient care prior to the rendering of any treatment. It is humbling to think of factors, in addition to treatment, that help patients improve. Sometimes patients get better because of the treatment that is provided, and sometimes they get better for reasons that are unclear. Randomized clinical trials are being conducted to more precisely identify the determinants for a successful outcome.

Management Versus Cure

Acute pain following trauma can be treated and cured. Chronic pain, where tissue damage occurred long ago, can be managed. With chronic conditions “cure” is not a useful term—management is more appropriate. Chronic pain can be reduced and can go into remission, but over the long term it should be managed. Patients learn to avoid certain activities which exacerbate symptoms, and learn what to do to minimize symptoms when they occur.

Continuous Reevaluation of Diagnosis

Many serious medical problems mimic TMD symptoms. Salivary gland tumors, intracranial lesions, and nasopharyngeal carcinoma are three examples. If a patient fails to respond to treatment in a reasonable time period the clinician must be vigilant and reevaluate the diagnosis. There is a great responsibility placed on the clinician who treats TMD patients; continuous reevaluation of the diagnosis is mandatory to avoid mistreatment.

INITIAL, REVERSIBLE, NONINVASIVE TMD MANAGEMENT

Establish a Diagnosis and Provide an Explanation

Explanation of the diagnosis to the patient is a simple yet often overlooked aspect of treatment.7 Patient anxiety stems from a misunderstanding of what the symptoms indicate and what may exacerbate those symptoms. When the doctor can provide a concise explanation of the diagnosis that the patient can understand, it serves to alleviate the patient’s anxiety and helps them understand the rationale for their treatment. An explanation of the diagnosis and placing it in proper perspective is the first step toward helping the patient improve. A patient who is told that they have an internal derangement of the joint may indicate to the patient that the damage is permanent and the situation hopeless. Explaining the diagnosis in these terms is not sufficient. The diagnosis must be placed in the proper perspective by explaining that up to one third of the population has evidence of internal derangement,1 and even when the disc is fully displaced, healing without surgery is possible and even likely.

TMD is too broad a term to be useful as a diagnosis. TMD involves problems with the masticatory muscles, the joint(s), or both. A specific diagnosis should be established for each patient. Myalgia, arthralgia, myospasm, synovitis, and internal derangement are examples of specific diagnoses.      

The Soft Diet

Mastication of hard food places loading forces on the TM joints and involves contraction of the masticatory muscles used for chewing. By changing to a soft diet the TM joint is relieved of its load and less muscle activity is required. The soft food diet encompasses a spectrum that ranges from a liquid diet in severe cases to minor changes in consistency. A practical recommendation is to avoid chewy food. Substitute softer foods for chewy foods, such as fish instead of steak. Cutting food into smaller pieces also helps to decrease masticatory load.

Reducing Parafunctional Habits

Habits are usually an unconscious behavior. Breaking a habit first requires the person to become aware of the habit, then take steps to eliminate the behavior. Tooth grinding and jaw clenching are common habits that aggravate TMD symptoms. When these habits occur during waking hours it is possible to reduce or eliminate them by taking the unconscious jaw activity and making the person aware of it. Increasing cognitive awareness of tooth grinding and jaw clenching can be done using reminders. “Lips together teeth apart” (LTTA) is a refrain taught to clenchers and bruxers. The neutral, relaxed position for the jaw is with the lips together and the teeth slightly apart. The patient is told to put reminders, such as placing notes with the letters “LTTA,” in obvious places. Some patients use small clocks with an alarm set to go off at frequent intervals to serve as a reminder not to clench. These habit-breaking strategies are useful for habits that occur when the patient is awake but will not carry over to habits that occur during sleep. Other habits such as chewing gum and biting nails can be similarly addressed.

Self-directed Home Physical Therapy

Orthopedic treatment used to rehabilitate musculoskeletal problems can easily be applied to TMD. Both muscle and joint problems respond well to physical therapy. The role of mobilization of joints to promote healing has been  studied extensively.8 Older concepts of immobilization have been abandoned. Joints must move in order to produce synovial fluid.9 Production of synovial fluid provides the joint with nutrition and lubrication. Joint mobilization promotes joint healing. Physical therapy can readily be used to treat TMD.

Application of hot or cold compresses, exercise, and massage form the basis for self-directed home physical therapy (Table 1). Applying heat or cold to the affected area is a matter of personal preference. This can be accomplished with ice in a plastic bag, a hot washcloth, electric heating pads, microwavable packs, and/or chemical hot/cold packs. For acute injuries cold is recommended, yet most TMD problems are not acute. The hot or cold application is left in place for 2 to 3 minutes, and then massage and exercise can begin.

Massage of the painful muscles is the next step. The patient uses the fingers to massage the tender muscles, usually the masseter or temporalis, for 5 to 10 seconds. Massage stops and the patient stretches the mouth open to the point where it is comfortable and not painful, and it is held stretched open for 5 to 10 seconds. This helps to stretch the masticatory muscles to their full length. The patient then alternates between massage and stretching for 5 to 10 repetitions, and can then go back to hot/cold packs. This regimen should be repeated frequently throughout the day.

When muscle pain is widespread (involving the cervical and shoulder musculature) it may be appropriate to refer the patient to a physical therapist. However, if the problem is restricted to the masticatory muscles and TM joint, then self-directed home physical therapy should be initiated.

Muscle Relaxation and Stress Reduction

Gaining control over tight sore muscles and producing relaxation can be accomplished with a variety of methods. Motivated patients with mild anxiety-related muscle tension may do well on their own with proper guidance. Before seeking professional help, patients may try reading a book about relaxation,10 listen to a relaxation tape, or do exercises (eg, yoga). For patients with more advanced problems referral to a psychologist or psychiatrist may be appropriate. A psychologist can teach biofeedback and stress- reduction skills, tools which are very helpful in reducing muscle tension and destructive habits.

Pharmacologic Management

Pharmacologic intervention serves an important role in the initial management of TMD. Numerous categories of medications are useful, including nonsteroidal anti-inflammatory drugs (NSAIDs), muscle relaxants, antianxiety agents, antidepressants, antiepileptics, and opioids. Initial management generally requires only NSAIDs and muscle relaxants (Table 2).

The NSAIDs are a large group of drugs which have the ability to inhibit cyclooxygenase, thereby preventing the formation of prostaglandins. No single NSAID has been shown to be superior to all others. Because there is a wide range of individual responses to different NSAIDs, if one drug is not working it is wise to try another. Newer COX-2 inhibitors (ie, Celebrex, Vioxx, Bextra) are more selective in their action and may cause less gastric disturbance. For the majority of patients, over-the-counter preparations are successful, such as ibuprofen (Motrin or Advil), naproxen (Aleve), or ketoprofen (Orudis).

Muscle relaxants are another type of medication useful in initial TMD treatment. There are several to choose from, and they differ in their strengths and side effects. Strong muscle relaxants produce more sedation. Sedation may be a welcome side effect if taken at night and a patient has difficulty sleeping. This may be an adverse side effect if someone takes the drug during the day and then cannot function. The dosage may need to be titrated to the therapeutic level. Several common muscle relaxants are provided in Table 2.

This brief mention of medications is not meant to be a substitute for a more complete description of pharmacologic management for TMD. Understanding benefits and risks, adverse effects, patient education, compliance, and potential for abuse are concepts that need to be explored when prescribing medications. The interested reader should refer to more in-depth discussions.11,12

Occlusal Appliances: Bite Plates

Occlusal appliances are known by numerous names, including bite plates, mouth guards, splints, and night guards. There are dozens of different designs, each one with its own group of advocates. Collectively they all do the same thing, that is, provide an acrylic platform to bite against. The effectiveness of bite plates to relieve TMD symptoms is well documented although there is no agreement as to why they work. Even placebo bite plates, which do not cover the occlusal surface, are effective.

No one bite plate design has been shown to be consistently more effective than any other. Some bite plates are designed to move the mandible to a new position. Unintended problems associated with these appliances include inadvertent movement of teeth. Partial coverage appliances have the potential to depress teeth under the appliance and cause super-eruption of the teeth that are not covered. Soft (rubbery) appliances can be deformed by clenching and may unintentionally move teeth and open interproximal contacts. Given these concerns the simplest design is desirable.7,13

The design that provides the least chance of producing an unexpected change in the occlusion is a hard appliance covering all the teeth in the arch, utilizing a flat occlusal surface adjusted to provide even contact in habitual closure (Table 3). In general it should not be worn 24 hours a day. It can be made for the maxilla or mandible. Maxillary bite plates have an advantage over mandibular appliances because occlusal contact can be distributed over the entire surface of the appliance. Mandibular appliances cannot adequately include contact with the maxillary central incisors without the risk of pushing these teeth labially.

SUMMARY

The existing dental literature does not support the superiority of any one type of treatment to manage TMD. Few studies meet rigorous scientific standards of the randomized clinical trial. This has led to enormous controversy.

The initial management of TMD does not have to be controversial. Noninvasive, reversible modalities can be employed that carry very little risk and a high degree of success (Table 4). The success rate of this approach has been studied and determined to be 75% to 90%.4-6

Of course, not every patient will get better with this approach. For those who do not improve more advanced techniques must be used, and referral to specialists in TMD, neurology, and rehabilitation medicine may be required. A few patients will need surgery.

Initial treatment of TMD requires relatively simple modalities, such as patient education, adherence to a soft diet, reducing oral habits, self-directed home physical therapy, muscle relaxation, the use of medication, and the proper use of bite plates. The majority of TMD patients will respond successfully to these basic treatments.

Author’s Note

For dentists and other professionals who would like to learn more about TMD and orofacial pain, the book Orofacial Pain by Lund et al13 is recommended.

References

1. American Academy of Orofacial Pain. JP Okeson, ed. Orofacial Pain: Guidelines for Assessment, Diagnosis, and Management. Chicago, Ill: Quintessence Publishing Co, Inc; 1996.

2. Stohler CS, Zarb GA. On the management of temporomandibular disorders: a plea for a low tech, high-prudence therapeutic approach. J Orofacial Pain. 1999;13:255-261.

3. Management of Temporomandibular Disorders. NIH Technology Assessment Statement. 1966;Apr 29-May1:1-31.

4. Greene CS. The etiology of temporomandibular disorders: implications for treatment. J Orofacial Pain. 2001;15:93-105.

5. Greene CS, Laskin DM. Long-term evaluation for myofascial pain dysfuction syndrome: a comparative analysis. J Am Dent Assoc. 1983;107:235-238.

6. Okeson JP, Hayes DK. Long-term results of treatment for temporomandibular disorders: an evaluation by patients. J Am Dent Assoc. 1986;112:473-478.

7. Syrop SB. In: Peterson LJ, ed. Principles of Oral and Maxillofacial Surgery. Philadelphia, Pa: JB Lippincott Co; 1992:1905-1931, Chapter 67.

8. Israel HA, Syrop SB. The important role of motion in the rehabilitation of patients with mandibular hypomobility: a review of the literature. J Craniomandibular Pract. 1997;15:1-10.

9. Israel HA. Current concepts in the surgical management of temporomandibular joint disorders. J Oral Maxillofac Surg. 1994;52:289-294.

10. Benson H. The Relaxation Response. New York, NY: Avon Books; 1976.

11. Ganzberg S, Quek SYD. Pharmacotherapy. In: Pertes RA, Gross SG, eds. Clinical Management of Temporomandibular Disorders and Orofacial Pain. Chicago, Ill: Quintessence Publishing Co, Inc; 1995: Chapter 13.

12. Syrop SB. Pharmacologic therapy. In: Kaplan AS, Assael LA, eds. Temporomandibular Disorders. Philadelphia, Pa: WB Saunders Co; 1991: Chapter 25.

13. Lund JP, Lavigne GJ, Dubner R, et al. Orofacial Pain: From Basic Science To Clinical Management. Chicago, Ill: Quintessence Publishing Co, Inc: 2001.

Dr. Syrop is an associate professor of clinical dentistry in the Division of Oral and Maxillofacial Surgery at Columbia University and Weil Medical College. Currently he is the section chief of Temporomandibular Disorders Service, Division of Dentistry, New York Presbyterian Hospital. He is the former director for 15 years of the Temporomandibular Joint Facial Pain Clinic at Columbia University. He is active in teaching and has been a member of the part-time faculty at Columbia University School of Dental and Oral Surgery for the past 20 years. Dr. Syrop is a member of the American Academy of Orofacial Pain, a diplomate of the Board of Orofacial Pain, and has written numerous chapters and articles on the nonsurgical management of TMD. Dr. Syrop has extensive experience in the clinical management of patients with TMD and has been in private practice for 21 years in New York, NY.

DEFINING PAIN

Pain, as defined by the International Association for the Study of Pain, is “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.”¹ 

ACUTE PAIN MANAGEMENT
The majority of dental pain is an acute response to inflammation. The acute pain associated with dental trauma, infection, or surgery is usually predictably managed pharmacologically. The key to pharmacologically managing pain is to provide a sufficient dose of a particular drug to minimize pain onset and give the patient comfort. The drug should be administered frequently to prevent the pain from becoming severe. The most effective way to maintain analgesia is to administer doses on a regularly scheduled basis for a specified period after the trauma. For example, after periodontal surgery, inflammation and pain usually peak 48 hours later. Thus, postoperative analgesic medication can be administered on a regular schedule, depending on the half-life of the drug (eg, every 4 hours), for 48 hours, then given as necessary (prn).

CLASSIFICATION OF ANALGESICS
Analgesics are classified as antipyretic analgesics, nonselective nonsteroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase-2 (COX-2) selective NSAIDs, and opioids.

Antipyretics
Acetaminophen is an antipyretic analgesic with no real attributable anti-inflammatory effect. Its mode of action has never been totally determined. It is provided as an oral or rectal dose form. Although acetaminophen is eliminated through the kidneys, part of the therapeutic dose is broken down in the liver. However, doses in the excessive range of 10 g can cause hepatic damage. Also, consumption of alcohol and acetaminophen can cause liver damage. Over­dosing is not difficult, as the patient may not be cognizant that other OTC products contain acetaminophen. The maximum recommended dose is 2 to 4 g daily.

The analgesic potency of a NSAID is largely related to its ability to inhibit pros­taglandin synthesis. NSAIDs block prostaglandin production by the inhibition of the COX enzyme in the arachidonic acid pathway. Two forms of COX have been identified. The constitutive form (COX-1), which is present in most tissues, including the gastrointestinal (GI) tract, kidneys, and platelets, plays a protective role in these organs. The inducible form (COX-2) is found in small amounts in inflammatory cells (macrophages), endothelial cells, synovial cells, and chondrocytes (un­less an inflammatory process is occurring).² Inhibition of COX-2 in these tissues is probably responsible for the anti-inflammatory effects of NSAIDs. Each NSAID in­hibits COX-1 and COX-2 to varying degrees. The inhibition of COX-1 causes undesirable effects including gastric complications, depression of renal function, and inhibition of platelet aggregation. This inhibition of platelet aggregation is dose/drug dependent. Aspirin and nonselective NSAIDs exert their antiplatelet effect by inhibiting COX which blocks the formation of thromboxane A2. When a NSAID comes into contact with the platelet cell membrane, it binds to and inhibits the release of COX, thereby altering platelet function. The antiplatelet effect of aspirin is irreversible, lasting for the half-life of the platelet (approximately 7 days). How­ever, NSAID derivatives reversibly bind to the platelet membrane causing a transitory antiplatelet effect. Re­covery of platelet function may occur within 1 to 4 days after discontinuation of the drug.

COX-2 NSAIDs
The most recent advances in NSAIDs have been the development of selective COX-2 inhibitors. An advantage of these NSAIDs is a more favorable GI, renal, and platelet side-effect profile. Rofecoxib (Vioxx) is FDA approved for acute pain (including dental pain) in adults, primary dysmenorrhea, and osteoarthritis.³ Celecoxib (Celebrex) is only FDA approved for the long-term treatment of osteo­arthritis and rheumatoid arthritis and not for acute dental pain. Thus, rofecoxib is a good choice for patients with prior or present GI problems.

ADVERSE SIDE EFFECTS/CONTRAINDICATIONS TO NSAID USE
Because serious GI effects have been associated with nonselective COX inhibitors, these medications should be avoided in patients who present with a history of peptic ulcer disease or GI bleeding. Additionally, all NSAIDs are highly protein-bound and have the potential to displace coumadin and potentiate its anticoagulant effect. 

Along with the analgesic effects, all opioids have similar profiles of toxic side effects, which should be considered when prescribing these medications. Respira­tory depression may occur in a patient taking an opioid for the first time. Tolerance to opioids can develop over time so that regular increases in the dosage may be required in order to provide a sustained analgesic effect. How­ever, side effects will continue to occur including constipation, sexual impairment, and nausea. Opioids can create a physical dependence and addiction, which is termed a psychological loss of control resulting in compulsive use. Opioids may cause sedation and/or drowsiness.

SELECTION CRITERIA: DECISION TREE FOR MANAGEMENT OF ACUTE PAIN
A decision tree (Figure) is proposed for the management of acute dental pain. Initially, a maximally effective dose of a NSAID should be prescribed, (eg, rofecoxib, ibuprofen, or acetaminophen), with the patient in­gesting the loading dose in the office. 

References

1. Mersky H. Pain terms: a list with definitions and notes on usage, IASP Subcommittee on Taxonomy. Pain. 
2. Fu JY, Masferrer JL, Seibert K, et al. The induction and suppression of prostaglandin H2 synthase (cyclooxygenase) in human monocytes. J Biol Chem. 1990;265:16737-16740.
3. Matheson AJ, Figgitt DP. Rofecoxib: a review of its use in the management of osteoarthritis, acute pain and rheumatoid arthritis. Drugs. 2001;61:833-865.
4. Ament PW, Bertolino JG, Liszewski JL. Clinically significant drug interactions. Am Fam Physician. 2000;61:1745-1754.
5. McEboy GK, ed. AHFS Drug Information 2001. Bethesda, Md: American Society of Health-System Pharmacists; 2001.
6. Noble SL, King DS, Olutade JI. Cyclooxygenase-2 enzyme inhibitors: place in therapy. Am Fam Physician. 2000;61:3669-3676.
7. Moore PA, Hersh EV. Celecoxib and rofecoxib. The role of COX-2 inhibitors in dental practice. J Am Dent Assoc. 2001;132:451-456.
8. Agency for HealthCare Policy and Research. Acute Pain Management in Adults: Operative Procedures. Rockville, Md: Department of Health and Human Services, Agency for Health Care Policy and Research; 1992: AHCPR Publication no. 92-0019. 
9. Carpenter RL. Optimizing postoperative pain management. Am Fam Physician. 1997;56:835-844, 847-850.
10. Vogel RI, Desjardins PJ, Major KVO. Comparison of presurgical and immediate postsurgical ibuprofen on postoperative periodontal pain. J Periodontol. 1992;63:914-918.
11. Dionne RA, Cooper SA. Evaluation of preoperative ibuprofen for postoperative pain after removal of third molar. Oral Surg Oral Med Oral Pathol. 1978;45:851-856.

Dr. Weinberg is clinical associate professor of periodontics and director of the second-year periodontic program at New York University College of Dentistry, David B. Kriser Dental Center in New York. She is a member of the American Dental Association. Dr. Weinberg can be reached at (212) 998-9506 or maw2@nyu.edu.

Dr. Fine is presently associate professor of clinical dentistry and postdoctoral director of the Division of Periodontics at the School of Dental and Oral Surgery of Columbia University and associate attending dental surgeon on the Presbyterian Hospital Dental Service. He is a diplomate of the American Board of Periodontology. Dr. Fine has served on the Research, Science, and Therapy Committee of the American Academy of Periodontology, and has been the recipient of several teaching awards and fellowships. He has authored or coauthored numerous articles in the periodontal literature, and was an author of the text, Clinical Guide to Periodontics. He can be reached at ms14@columbia.edu.

About half of the US population does not receive yearly dental care. Between 6% and 14% of these individuals avoid treatment because of fear.2 This phenomenon is not unique to the United States. Similar statistics have been reported in Sweden and Japan.2,3,4 In an attempt to help patients manage fear and anxiety, many practitioners utilize nitrous oxide and oxygen analgesic. It is estimated that approximately 50% of dentists have the equipment needed to administer nitrous oxide, and more than 424,000 dental personnel are exposed to trace amounts of the gas as a result.5

Many dental schools and dental hygiene schools urge students to have a very cautious attitude toward the use of nitrous oxide. This is a result of reports concerning the effect of trace amounts of gas on office personnel, particularly on pregnant women.6-8 This paper discusses the issue of safety of nitrous oxide for dental personnel.

HISTORY OF THE USE OF NITROUS OXIDE

Nitrous oxide was discovered by Joseph Priestley in 1776. Humphry Davey wrote about the effect of nitrous oxide on diminution of pain associated with extraction of his third molar. In the 1840s Gardner Quincy Colton, a chemist and intinerant lecturer, introduced nitrous oxide to the public after reading Davey’s account. Colton introduced nitrous oxide to Horace Wells, a dentist who was the first to use gas inhalation for relief of pain. On December 11, 1844 Wells had a local dentist, Dr. John Riggs, extract one of Wells’ teeth while under the effects of nitrous oxide.9

Following this, nitrous oxide was used in dentistry as a general anesthetic until the advent of local anesthesia. With local anesthesia, dentistry had another option for controlling pain. In the early part of the twentieth century, nitrous oxide was reported as a sedative/analgesic. In the 1950s Langa and others popularized its use as an antianxiety agent by demonstrating that it could be used as a sedative in conjunction with local anesthesia. If the percentage of gas delivered was limited to 25% to 40%, few side effects were seen.10

OCCUPATIONAL SAFETY

Occupational exposure to certain chemicals, materials, and ionizing radiation has been shown to cause serious health effects. As examples, liver disease is a toxic effect of exposure to carbon tetrachloride in the dry-cleaning industry; benzedrine has been associated with bladder cancer in the chemical industry; and occupational exposure to x-rays has been associated with a variety of problems including cancer and spontaneous abortions.11

The first indication that trace amounts of anesthetic gas might be associated with side effects was a report in 1968 by Vaisman12 who reported problems in Russian female anesthesiologists, including irritability, headache, fatigue, nausea, pruritis, and spontaneous abortion. Studies by Askrog and co-workers13 indicated that women who worked in operating rooms faced similar problems. In 1956 Lassen and colleagues14 observed that nitrous oxide was associated with pronounced bone marrow depression when patients were exposed to 50% nitrous oxide for 14 days. The marrow returned to normal within a few days after treatment was stopped.

ANIMAL STUDIES

Figure 1. Nitrous oxide deactivates vitamin B12. Two tests can be performed to determine the level of vitamin B12 suppression. Methionine synthetase and deoxyuridine levels can be measured and are an indication of the effect of nitrous oxide exposure.

Anesthetic agents have been shown to be associated with teratogenic effects in animal studies.15 These effects were observed at low concentrations. Eger7 demonstrated teratogenic changes, fetal skeletal changes, reduced fetal weight, and miscarriage when rats were exposed to nitrous oxide during pregnancy. Abdul-Kareem and co-workers16 exposed rats to nitrous oxide at 50, 500, or 5,000 parts per million (ppm) for 6 hours a day, 5 days a week, for 2 and 13 weeks, and showed changes in neurotransmitters. In a similar study, Healy and colleagues17 exposed mice to 50, 500, or 5,000 ppm for 5 days a week for 2 or 13 weeks. The weight of the liver was lower for all three concentrations at 13 weeks, but not at 2 weeks. The number of circulating leukocytes was lower at the highest concentration at 2 weeks, and at all concentrations at 13 weeks. The bone marrow also demonstrated a dose-related reduction in deoxyuridine uptake. Fujinaga et al18 demonstrated rat fetal mortality when pregnant rats were exposed to 75% nitrous oxide. Viera and co-workers19 demonstrated spontaneous abortions in rats with exposure to nitrous oxide at 1,000 ppm. Similarly, testicular damage was observed after a minimum of 2 days exposure to 20% nitrous oxide,20 and rat bone marrow was depressed with exposure to 80% nitrous oxide,21 but not at 1% exposure even after 6 months.22 Furthermore, nitrous oxide at 1,000 ppm decreases the vitamin B12 component of the enzyme methionine synthetase by interfering with folate metabolism, and this can impair DNA synthesis23 (Figure 1).

In a study intended to simulate operating room conditions, rats were exposed to 1 ppm halothane and 50 ppm nitrous oxide, or 10 ppm halothane and 500 ppm nitrous oxide for 7 hours a day, 5 days a week, for 104 weeks. No increase in tumor incidences was found.24,25 Several studies showed increased fetal mortality or small litter size when rats were exposed to 1,000 ppm nitrous oxide if the rats were exposed to this concentration for a number of days. No effect was observed at lower concentrations.19 In addition, studies have failed to demonstrate teratogenic effects for rats or mice exposed to 0.5%, 5%, or 50% nitrous oxide for 8 hours a day throughout gestation.26 In summary, the animal studies suggest potential problems associated with exposure to nitrous oxide. They also indicate that if the exposure levels are low, problems can be lessened or not observed.

RETROSPECTIVE HUMAN STUDIES

The dental office is an ideal location to study the effects of occupational exposure to nitrous oxide as some offices use nitrous oxide, and others do not. Cohen and colleagues,27,28 conducted two important studies demonstrating changes associated with higher levels of exposure to nitrous oxide. These studies demonstrated a higher incidence of hepatic, renal, and neuralgic disorders among exposed personnel. In addition, there was an increase in spontaneous abortions seen among chairside assistants and the dentists’ wives. There was also an increase in congenital abnormalities in children of assistants. There are, however, several problems associated with these studies. There is concern that respondents might not have accurately recalled events in the past. Furthermore, 18.7% of the respondents were also exposed to other anesthetic gases, and no attempt was made to identify recreational users of nitrous oxide.29 These studies did identify a problem for pregnant females who worked in dental offices where nitrous oxide was used. The studies did not suggest at which level exposure became a problem.

OCCUPATIONAL SAFETY AGENCIES

There are three governmental agencies responsible for establishing appropriate levels of exposure to chemicals: the American Conference of Governmental Industrial Hygienists (ACGIH), Occupational Safety and Health Administration (OSHA), and the National Institute for Occupational Safety and Health (NIOSH). The ACGIH publishes a set of suggested maximum exposure levels for many chemicals. It is clear in their literature that these levels are only suggestions and guidelines to be used as a guide by industrial hygienists, and they should not be used to set regulations. OSHA sets minimum guidelines for employers to assure a safe workplace in the United States. NIOSH is the occupational safety and health research arm of the federal CDC that makes recommendations to OSHA.30 The NIOSH publication, Alert, suggests that the recommended exposure limit is 25 ppm on a time-weighted average (usually an average exposure over an 8-hour day of 25 ppm). These levels were recommended based on two studies by Bruce.31,32

THE BRUCE STUDIES

In the first study, effects were seen when subjects were exposed to 50 ppm nitrous oxide with 1 ppm halothane, but not to 500 ppm nitrous oxide. Changes were seen in audiovisual tasks, tachistoscopic tasks, memory passages, and digit span tests.31 The second study showed a slight effect when subjects had been exposed to 500 ppm nitrous oxide for 4 hours, and were asked to recall a series of numbers and were given a digit span test.32 It is important to note that in two letters Bruce later claimed this study was flawed.33,34 He stated that the conclusions of the study were wrong, derived from data subject to sampling bias and not applicable to the general population. He called for the NIOSH standards to be revised.

Many papers have been published in the dental literature which mention the effect of nitrous oxide on motor skills, but this effect has not been demonstrated for nitrous oxide acting alone. Furthermore, no study has been published that demonstrates a detrimental effect of 50 ppm nitrous oxide. One study demonstrated an effect at 500 ppm, but it has been retracted by the author because neither he nor others have been able to duplicate the findings.31,32 In spite of these problems with the data, the NIOSH standards have not been revised.

WHAT IS A SAFE LEVEL OF EXPOSURE?

Figure 2. The Sweeney et al study measured deoxyuridine suppression. They suggested that 450 ppm of nitrous oxide was a safe occupational level. This is much higher than what has been adopted.

Ahlborg35 reported that Swedish midwives exposed to nitrous oxide did not have difficulty becoming pregnant unless they were exposed to nitrous oxide 30 or more times a month. In another study of midwives, he did not observe an increase in spontaneous abortions with exposure to nitrous oxide, but this was seen with night shifts and increased work load and no nitrous oxide exposure.36 Sweeney37 studied 20 practicing dentists by having them wear a nitrous oxide monitor. At the conclusion of the study, bone marrow samples were collected. The exposures ranged from 50 ppm to more than 5,000 ppm on a time-weighted average. All but three participants were above 400 ppm. Bone marrow depression was seen in three dentists with exposures over 1,800 ppm. Some participants showed no change even with an exposure of over 5,000 ppm. To set levels that would assure safety, Sweeney suggested exposure should not exceed 450 ppm on an 8-hour time-weighted average (Figure 2). Nevertheless, Nunn38 showed that 450 ppm of nitrous oxide exposure had no effect on operating room personnel or experimental animals. In addition, Karakaya and colleagues39 concluded that chronic exposure to halothane and nitrous oxide does not affect serum immunoglobulin levels, white blood cell counts, or lymphocyte subpopulations of anesthetists, anesthetic assistants, or anesthetic nurses.

Figure 3. The Roland et al study showed no change in ability of dental assistants to become pregnant provided scavenging is used or the office uses nitrous oxide on a limited basis.

Rowland et al8 examined pregnancy in female dental assistants (facundability). They first looked at exposure to mercury vapor and found no effect. They reevaluated the data, taking into consideration whether the assistants had been exposed to nitrous oxide. The assistants were divided into five groups: a control group that was not exposed to nitrous oxide; two groups in offices that used scavenging devices to remove traces of nitrous oxide and had either an exposure of less than 5 hours per week or greater than 5 hours per week; and two groups with no scavenging devices and again grouped by high or low usage. Only the group with no scavenging devices and high utilization had a statistically significant decrease in facundability (Figure 3). These studies strongly suggest that if scavenging is used and nitrous oxide levels are kept below 450 ppm, the dental office staff is not at risk.

HOW CAN ENVIRONMENTAL EXPOSURE BE REDUCED?

Figure 4. The Brown Mask results in levels of exposure in the 50 ppm range. This led to the suggestion by OSHA that 50 ppm should be the goal. Suction is applied to the space between masks to scavenge any gas that may escape around the seal.	Figure 5. Donaldson and Orr showed that scavenging devices were effective in reducing the trace levels of nitrous oxide.

Donaldson and Orr have shown that many scavenging devices being used in dental offices can result in environmental levels in the 40 to 60 ppm range.40 (Figures 4, 5) Nevertheless, NIOSH has stated that exposure should be limited to 25 ppm, and if this level of exposure could not be achieved then self-contained respirators were required.6

It is clear that dental offices using nitrous oxide analgesia should have one of the available scavenging systems on each machine. The systems that deliver the gases come in three basic forms: semi-open, open, and semi-closed systems.

Semi-open Systems

Figure 6. The semi-open system allowed gas to escape from a pop-off valve on the mask and into the breathing space of the dentist and dental assistant. This led to nitrous oxide levels as high as 5,000 ppm.	Figure 7. Some older masks had pop-off valves that directed exhaust gases into the breathing area of the dentist.

Prior to scavenging, all systems could best be described as semi-open systems (Figure 6). The gas left the machine and went to a connector attached to a hose and a reservoir bag. The hose carried gas to a Y-shaped connector and two smaller hoses that went around the patient’s head and attached to either side of the nose mask. The nose mask had a pop-off valve that vented exhaust gas into the dental operatory (Figure 7).

Open Systems

Some machine manufacturers placed a one-way valve downstream from the reservoir bag. With this valve, the system was now fully open and permitted no rebreathing. All exhaled gas was blown out through the valve of the mask into the breathing zone of the dentist and assistant who were treating the patient. With open and semi-open systems, trace gas levels have been reported as high as 5,000 ppm of nitrous oxide in the dentist’s and assistant’s breathing zone.41

Semi-closed Systems

Figure 8. Semi-closed or circle system with a CO2 absorbing canister. The gas is reused, removing CO2 each time the gas passes through the soda lime granules in the absorber canister. This system requires a nitrous oxide machine that can deliver low flow volumes.

A third system that is common in hospital operating rooms is the semi-closed, circle system. Here a CO2 absorbing canister is placed in the system. The patient inhales, pulling gas from the reservoir bag through the CO2 absorber, thus removing CO2. The gas goes through a hose to one side of the mask. There is a one-way valve that prevents the exhaled gas from returning back down this tube. The tube on the other side of the mask carries the exhaled gas back to the reservoir bag where the cycle starts again. Each pass through the CO2 absorber removes the CO2 produced by the patient and exhaled (Figure 8). These systems have a pop-off valve to allow excess gas to escape. Suction is applied to this valve to remove the exhaust gases from the room.

CURRENT SCAVENGING SYSTEMS

Figure 9. This mask has a vacuum applied between the two shells. Exhaled gas enters the space between the two shells and is removed from the space by suction.	Figure 10. Mask insert for a Brown mask system. Suction is applied to the space between the masks.

Today’s scavenging systems are predominantly open systems with suction placed at the pop-off valve on the mask. Some systems also attempt to remove the air that is around the mask, which may contain traces of nitrous oxide that the patient has exhaled through their mouth or that has leaked from around the mask (Figure 9). One of the earliest (and still excellent) systems is a mask within a mask, or the Brown Mask. The space between the inner and outer masks is under vacuum (Figure 10). Another current system has a mask with a disk that sits over the pop-off valve. The plastic disk (about 3 inches in diameter) removes the exhaust gas from the pop-off valve and brings in surrounding air via a slit in the disk. Unfortunately, this mask is rather noisy.

Figure 11. In the open system, gas is drawn from the bag and exhaled through a second hose, or into a space around the mask. Suction then removes the waste gas.	Figure 12. By adding a hose, two one-way valves, and suction, a semi open system can be converted to a scavenging system.

In one current and inexpensive system (Figures 11 and 12), the hose from the bag goes to one side of the mask. The mask has no pop-off valve. Exhaled gas leaves the mask from the opposite side and goes into a second hose that is approximately 1 m long. There is a one-way valve that only allows gas to flow away from the patient. The end of this hose is open to the air, but suction is applied to the hose just downstream from the one-way valve, and the exhaled gas is removed. The suction from a typical saliva ejector that is part of a high-volume suction system is adequate. In practice, there is fresh air flowing into the open end of the exhaust hose, and this is removed with the exhaled gas. All the systems now on the market can be expected to keep levels of nitrous oxide in the 50 ppm range.40

Conclusion

Figure 13. By altering the shape and size of the nose hole, a pediatric mask can be used by adults.

Every nitrous oxide/oxygen machine must have a scavenging system with adequate suction. Furthermore, there must be a reasonable exchange of air in the operatory. Outside air should be brought into the office by heating and cooling systems. This will help clear trace amounts of gas, and it is suggested that the minimum air exchange is 5 per hour, with 15 to 20 changes being better. Hoses and connectors should be routinely checked for leaks, and masks should be selected that fit the patient (Figure 13). The patient should also be discouraged from speaking while using nitrous oxide sedation. If all these suggestions are followed, trace amounts of nitrous oxide will be in the 50 ppm range.

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Dr. Quarnstrom has received fellowships in the Academy of General Dentistry, American Dental Society of Anesthesiology, and the International College of Dentists, and is a diplomate of the American Board of Dental Anesthesiology. He is a clinical assistant professor in the Department of Dental Public Health Sciences at the Univers