Figure 1. The maxillary DNA appliance that was used in this case. Note the 3-dimensional axial springs for anterior development, the midline expansion screw for transverse development and the occlusal coverage for vertical development, including the temporomandibular joint. Also note the posterior extension to guide the tongue anteriorly, and the labial bow to train the upper lip. Figure 2a. The pretreatment upper study model has a minimum intermolar width of 34 mm at the cervical margin of the mesiopalatal cusp of the first maxillary molar. Figure 2b. In the post-treatment upper study model, the minimum intermolar width at the cervical margin of the mesiopalatal cusp of the first maxillary molar has increased to 39 mm. Figure 3a. The pretreatment mandibular trajectory requires advancement by 2.9 mm, according to the jaw-tracking data. Figure 3b. Post-treatment, the mandible appears to have been repositioned correctly, according to the jaw-tracking data.

INTRODUCTION
Surgical approaches to the management of obstructive sleep apnea (OSA) include uvulopalatopharyngoplasty (UPPP) and similar procedures. For example, Pang and Woodson¹ assessed the efficacy of expansion sphincter pharyngoplasty (ESP) in the treatment of OSA. They reported that the apnea-hypopnea index (AHI) decreased from 44 to 12 events/hour following ESP and from 38 to 19 events/hour in a similar group that had UPPP. But, it appears that these surgical techniques were unable to eradicate OSA entirely. Similarly, Bertoletti et al² found a significant reduction in continuous positive airway pressure (CPAP) levels 3 months after minimally invasive pillar placements, but the underlying OSA remained unresolved. On the other hand, Conley and Legan³ demonstrated the importance of surgical transverse expansion of the maxillary and mandibular arches in patients with severe OSA. They found a marked improvement in the degree of OSA, but the severity of the surgical procedure, which included distraction osteogenesis, cannot be overlooked. Similarly, Bonetti et al⁴ reported a case of severe OSA in which an increase in the transverse dimensions by surgically-assisted rapid maxillary expansion and mandibular symphyseal distraction osteogenesis dramatically decreased the AHI to 9 events/ hour. Therefore, it appears that surgical techniques are able to moderate but not eliminate OSA entirely.
A possible alternative to surgical intervention might be nonsurgical manipulation of the upper airway. In a recent study,⁵ the upper airway was evaluated following midfacial treatment in adults who had never had been tested for OSA. Pre- and post-treatment lateral cephalographs of 99 patients (mean age 42.9 ± 1.5 years: treatment time 21.3 ± 6.2 months) were analyzed using appropriate software. Using 2-dimensional finite-element analysis, a relative 22% increase in nasopharyngeal airway area was found above and behind the soft palate.⁶ It was concluded that upper airway changes in nongrowing adults are similar to those of actively growing children undergoing functional orthodontic corrections,7 and these findings suggested that genetically-encoded developmental mechanisms might be modulated by maxillary appliances to enhance the upper airway in adults. A new case is described here to substantiate these implications in the management of adults diagnosed with OSA.

Figure 4a. The patient’s upper airway segmented from the level of the posterior nasal apertures to the level of the hyoid bone. The reconstruction indicates the pretreatment upper airway volume is 12,889 mm3. Figure 4b. The patient’s post-treatment upper airway segmented from the level of the posterior nasal apertures to the level of the hyoid bone. The reconstruction indicates the upper airway volume has increased by 58.5% from 12,889 mm3 pretreatment to 22,024 mm3 post-treatment. Note also the mediolateral change in the shape of the post-treatment upper airway. Figure 5. Plot to show the minimum cross-sectional area of the pretreatment upper airway (red) and the corresponding increases post-treatment (blue). Figure 6a. Lateral aspect to show patient profile post-treatment. Note that inappropriate mandibular prognathism has not been induced. Figure 6b. Frontal aspect to show smile aesthetics post-treatment. Note that the spacing has been camouflaged and closed by the judicious placement of veneers.

CASE REPORT
Diagnosis and Treatment Planning
A 36-year-old male diagnosed with OSA following overnight polysomnography (PSG) presented, seeking a nonsurgical alternative to bimaxillary advancement for the correction of his condition. The PSG report indicated an AHI of 24 events/hour and a mean oxyhemoglobin saturation of 90%. He was on CPAP therapy at an average pressure of 16.5 cm H₂O and was taking 30 mg mirtazapin (Remeron), 500 mcg melatonin, and one mg klonopin, as needed, which was almost every night.
Upon intraoral examination, his maxillary minimum intermolar width was recorded as 34 mm at the cervical margin of the mesiopalatal cusps of the first permanent molars. His maxillary and mandibular first premolars were missing, and the patient volunteered that these had been extracted as part of an earlier orthodontic procedure. Diagnostic records were taken, including facial photographs, a 3-dimensional cone-beam computed tomography scan (iCAT [Imaging Sciences]), as well as impressions for study models. His mandibular trajectory was recorded using a jaw-tracking device (Myotronics). All treatment procedures were carried out by Dr. Wendling.

Treatment
After reaching a differential diagnosis of midfacial underdevelopment, the treatment objectives were listed as follows: to increase the maxillary transverse direction, to reposition the mandible anteriorly, and to reduce the AHI to within normal limits. A customized maxillary appliance (Figure 1) was fabricated (as well as a mandibular appliance). After insertion, the patient was instructed to wear the maxillary appliance during the evening and every night for at least 12 to 16 hours, and to return for periodic adjustments every 3 to 4 weeks. In the interim, the patient was instructed to turn the appliance’s midline expansion screw when the appliance became loose. After 10 months, the patient was studied using type IV monitoring device (ApneaLink [ResMed Corp]).

Outcome
The patient reported that he wore the maxillary appliance each evening and every night for an average of approximately 16 hours. The patient did not wear the appliance for approximately 8 hours during the day. The midline expansion screw was advanced approximately twice a week (0.25 mm on each turn). The patient reported that he gradually reduced the CPAP pressure by about 70% as the treatment proceeded. He also reduced the dosage of Remeron from 30 mg to 7.5 mg. By 10 months of treatment, the patient reported that he no longer took any klonopin but continued with melatonin at a dose of 250 mcg because he believes he is sensitive to changes in his sleep schedule.
Upon intraoral examination, the minimum intermolar width had increased from 34 mm to 39 mm (Figures 2a and 2b). The patient reported that the development of his upper arch seemed to have helped him breathe through his nose. In addition, the mandible repositioned itself further forward by 2.9 mm with the mandibular appliance, according to the jaw-tracking data (Figures 3a and 3b).

Cone Beam Computed Tomography Results
The patient’s upper airway was segmented and reconstructed from the level of the posterior nasal apertures to the level of the hyoid bone, using appropriate software. The upper airway volume increased by 58% from 12,889 mm³ to 22,024 mm³ (Figures 4a and 4b), and the minimum cross-sectional area showed corresponding increases (Figure 5).

Sleep Architecture
The patient was studied using a type IV monitoring device from 22:00 pm to 04:58 am for a flow evaluation period of 2 hours and 24 minutes and SpO₂ evaluation period of 6 hours and 37 minutes. The patient had an AHI of zero events/ hour. The oxygen desaturation index was 95%. The lowest oxygen saturation was 88%. Approximately 3 minutes were spent with an oxygen desaturation between 85% to 90%. Therefore, some flow limitation was noted, although this was within normal parameters. Extended pulse, oxygen saturation, and limb movement profile were not available. However, the cardiac profile showed a minimum pulse frequency of 47 beats per minute, while the maximum pulse frequency was 161 beats per minute, with an average pulse frequency of 63 beats per minute.

DISCUSSION
Current, nonsurgical, dental management of OSA typically deploys the use of mandibular advancement devices. However, side effects associated with this modality include: unwanted tooth movements8; the precipitation of anterior crossbite,⁹ and temporomandibular changes in some cases.¹⁰ Therefore, maxillary appliances that putatively induce renewed midfacial development might provide an alternative approach, by permitting nonsurgical remodeling (pneumopedics) of the upper airway. A type IV monitoring device was used to detect changes in respiratory events such as apneas and hypopneas post-treatment. Using this device, the evidence for sleep disordered breathing appears to be within a normal range for this particular case study. However, the scored AHI may possibly underestimate the severity of sleep-disordered breathing in this patient as other history and physical details were not available. Therefore, further evaluation and treatment should be discussed with the patient because a normal ApneaLink study does not rule out sleep disordered breathing, and a full diagnostic PSG should be obtained if clinically indicated. However, the ApneaLink is an ambulatory sleep monitor that can detect OSA and/or hypopnea with acceptable reliability.¹¹
A recent study suggests that both the maxillary and the mandibular dental arches are smaller in adults with OSA.¹² Therefore, maxillary appliances that putatively induce midfacial development might provide an alternative approach, by permitting nonsurgical (pneumopedic) remodeling of the upper airway. According to Stellzig-Eisenhauer and Meyer-Marcotty,¹³ it is not disputed that expanding the maxilla improves not only nasal volume and nasal flow, but also the subjective sensation of patients, and this seems to be our experience in this particular case. Indeed, in the opinion of Posnick and Agnihotri,¹⁴ in patients with a dentofacial deformity, treatment of the maxillary dysplasia with a specific emphasis on transverse expansion appears to address the chronic difficulties with nasal breathing, inter alia. Therefore, in patients with normal craniofacial architecture, one might anticipate a similar outcome, and an improvement in nasal breathing appears to be the case in this particular patient also. In support of these findings, Rose and Schessl¹⁵ reported that enlarging the upper airway and preventing its collapse using orthodontic means in children with craniofacial anomalies serves to successfully treat OSA. However, the response of children with no craniofacial abnormalities remains unaddressed. In this regard, Villa et al¹⁶ assessed rapid maxillary expansion (RME) in the treatment of OSA in children devoid of other craniofacial abnormalities. Polysomnography showed a significant decrease in the AHI, and the authors concluded that RME is an effective appliance for treating children with OSA. Similarly, Pirelli et al¹⁷ investigated whether RME could improve the patency of the nasal airways and OSA. They reported that RME therapy widens the nasal fossa, releases the nasal septum, restores nasal airflow, and that these functional improvements are associated with a reduction of sleep disordered breathing in children. In addition, Miano et al18 also evaluated REM sleep microstructure in children with OSA before and after one year of RME treatment. They also found that after one year of treatment, the AHI in children with OSA decreased significantly compared to controls. Therefore, RME appears to improve sleep architecture in children. We believe that the adult case reported here showed a similar response.

CONCLUSION
Maxillary appliances that putatively induce renewed midfacial development might provide an alternative approach to managing OSA, by permitting nonsurgical remodeling of the upper airway. However, a normal ambulatory sleep study does not rule out sleep disordered breathing or upper airway resistance, and the scored AHI may underestimate the current severity of OSA in this patient and further follow-up to obtain a full diagnostic PSG is warranted. Nevertheless, the facial and dental outcomes for this particular patient (Figures 6a and 6b) seem to provide further support for the protocol described here.

Acknowledgements
The authors would like to thank Quint Whipple, Phoenician Dental Studios for the cosmetic veneers.

References

1. Pang KP, Woodson BT. Expansion sphincter pharyngoplasty: a new technique for the treatment of obstructive sleep apnea. Otolaryngol Head Neck Surg. 2007;137:110-114.
2. Bertoletti F, Indelicato A, Banfi P, et al. Sleep apnoea/hypopnoea syndrome: combination therapy with the Pillar palatal implant technique and continuous positive airway pressure (CPAP). A preliminary report. B-ENT. 2009;5:251-257.
3. Conley RS, Legan HL. Correction of severe obstructive sleep apnea with bimaxillary transverse distraction osteogenesis and maxillomandibular advancement. Am J Orthod Dentofacial Orthop. 2006;129:283-292.
4. Bonetti GA, Piccin O, Lancellotti L, et al. A case report on the efficacy of transverse expansion in severe obstructive sleep apnea syndrome. Sleep Breath. 2009;13:93-96.
5. Singh GD, Krumholtz JA. Epigenetic Orthodontics in Adults. Chatsworth, CA: SMILE Foundation; 2009.
6. Singh GD, McNamara JA Jr, Lozanoff S. Morphometry of the cranial base in subjects with Class III malocclusion. J Dent Res. 1997;76:694-703.
7. Singh GD, Garcia-Motta AV, Hang WM. Evaluation of the posterior airway space following Biobloc therapy: geometric morphometrics. Cranio. 2007;25:84-89.
8. Ueda H, Almeida FR, Lowe AA, et al. Changes in occlusal contact area during oral appliance therapy assessed on study models. Angle Orthod. 2008;78:866-872.
9. Korngut R. Case study: A persistent positive outcome treating OSA with a MAD following the treatment protocol. Dialogue. 2010;1:26-27.
10. Almeida FR, Lowe AA, Sung JO, et al. Long-term sequellae of oral appliance therapy in obstructive sleep apnea patients: Part 1. Cephalometric analysis. Am J Orthod Dentofacial Orthop. 2006;129:195-204.
11. Chen H, Lowe AA, Bai Y, et al. Evaluation of a portable recording device (ApneaLink) for case selection of obstructive sleep apnea. Sleep Breath. 2009;13:213-219.
12. Banabilh SM, Suzina AH, Dinsuhaimi S, et al. Dental arch morphology in south-east Asian adults with obstructive sleep apnoea: geometric morphometrics. J Oral Rehabil. 2009;36:184-192.
13. Stellzig-Eisenhauer A, Meyer-Marcotty P. Interaction between otorhinolaryngology and orthodontics: correlation between the nasopharyngeal airway and the craniofacial complex [in German]. Laryngorhinootologie. 2010;89(suppl 1):S72-S78.
14. Posnick JC, Agnihotri N. Consequences and management of nasal airway obstruction in the dentofacial deformity patient. Curr Opin Otolaryngol Head Neck Surg. 2010;18:323-331.
15. Rose E, Schessl J. Orthodontic procedures in the treatment of obstructive sleep apnea in children [in English, German]. J Orofac Orthop. 2006;67:58-67.
16. Villa MP, Malagola C, Pagani J, et al. Rapid maxillary expansion in children with obstructive sleep apnea syndrome: 12-month follow-up. Sleep Med. 2007;8:128-134.
17. Pirelli P, Saponara M, Attanasio G. Obstructive Sleep Apnoea Syndrome (OSAS) and rhino-tubaric disfunction in children: therapeutic effects of RME therapy [in English, Italian]. Prog Orthod. 2005;6:48-61.
18. Miano S, Rizzoli A, Evangelisti M, et al. NREM sleep instability changes following rapid maxillary expansion in children with obstructive apnea sleep syndrome. Sleep Med. 2009;10:471-478.

     

Dr. Singh is currently president of BioModeling Solutions, director of continuing education for the SMILE Foundation, senior instructor/consultant/Fellow for the International Association for Orthodontics, academic Fellow of the World Federation of Orthodontists, and chair of research for the Academy of Sports Dentistry. Previously, he was adjunct professor at Portland State University, visiting professor in Orthodontics (Malaysia), and associate professor at the University of Puerto Rico. He has been published extensively in orthodontic and dental literature, and is co-author of the book entitled Epigenetic Orthodontics in Adults. Dr Singh has lectured internationally. He holds several US patents with international patents pending. He can be reached at (503) 430-7529/7536 or at drsingh@drdavesingh.com.

Disclosure: Dr. Singh is president of BioModeling Solutions, LLC, and holds all patents for the DNA Appliance System.

Dr. Wendling graduated at Oregon Health & Sciences University School of Dentistry, Portland, Ore. She attended Portland State University for her predental studies. Prior to that, she graduated from West Liberty State College, West Virginia School of Dental Hygiene with an associate in science in dental hygiene. She also attended Eastern Kentucky University, Richmond, Ky, for her predental hygiene requirements. Dr. Wendling’s current professional affiliations include: the American Academy of Dental Sleep Medicine, the AGD (Fellow), the American Academy of Cosmetic Dentistry (active member), and the International Congress of Cranio Mandibular Orthopedics. She can be reached at (503) 636-4069 or at drsue@drwendling.com.

Disclosure: Dr. Wendling reports no disclosures.

Dr. Chandrashekhar was born in Bangalore, India, and has been residing in the United States since early childhood. He attended the State University of New York at Buffalo where he received a BS in electrical engineering and a minor in mathematics. He worked in industry at NASA in Houston, Tex, as well as Alcatel Telecom. Dr. Chandrashekhar earned a MS in electrical engineering at the University of Texas at Dallas. Upon completion of his internal medicine residency, he went straight into a competitive sleep medicine Fellowship at the New Jersey Neuroscience Institute at the JFK Medical Center in Edison, NJ. He can be reached at (760) 843-0100 or via e-mail at rc@eusomnia.com.

Disclosure: Dr. Chandrashekhar reports no disclosures.

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Within the past 10 years, there has been a huge increase in the diagnosis and treatment of sleep disorders, such as obstructive sleep apnea (OSA), by the medical community. Because there are many patients who are unable to tolerate continuous positive airway pressure (CPAP) therapy (Figure 1) prescribed by medical doctors, dentistry has a tremendous new opportunity to help patients in the treatment of sleep disorders. The American Academy of Sleep Medicine (AASM) has designated dental sleep appliances as the top nonsurgical alternative for the CPAP intolerant patient. In addition, in February of 2006, the AASM designated dental sleep appliances to be a viable treat­ment for mild to moderate sleep apnea.¹ This has opened the door for dentists who are trained to treat snoring/mild-moderate sleep apnea, and who want to help CPAP intolerant patients.
Dentists now have more advanced appliance choices for sleep breathing disorders. The purpose of this article is to introduce an example of a new concept in sleep therapy using a single-arched mandibular (or maxillary) oral appliance. In addition, it is important to note that we have better techniques for diagnostics and the fitting of these appliances, including the use of 3-dimensional (3-D) dental imaging. Using such techniques, dentists are capable of achieving high success rates consistently with their snoring and CPAP-intolerant patients.

SNORING
Snoring is caused by a restriction in the size of the airway with rapidly moving air vibrating the tissues in the oropharyngeal airway. If the tongue is restrained from closing the airway, the snoring dissipates.
Fifty-two percent of all Americans age 40 years or older snore.² Twenty-seven percent of all couples more than 40 years old sleep apart because of snoring problems. A recent article in the Wall Street Journal stated that new housing construction was beginning to include 2 master bedrooms in new homes.³ In fact, the problem of bothersome snoring within households has become so widespread that separate sleeping quarters are frequently desired.
Without a reliable and broad-based remedy in use, snoring has become a ubiquitous American cultural phenomenon.

CONTINUOUS POSITIVE AIRWAY PRESSURE: HIGHLY SUCCESSFUL, HIGHLY REJECTED

Figure 1. Patient sleeping using continuous positive airway pressure (CPAP) therapy.	Figure 2. Diagrams show how CPAP functions.

After weight loss, the number-one medical treatment for snoring and OSA is CPAP therapy. It is an extremely successful treatment modality for these problems. (Figure 2 shows how the CPAP device functions.)
However, CPAP therapy presents its own difficulties since it is not tolerated by 50% to 60% of the patients who are treated with it.^4,5 Some of these difficulties include dry/stuffy nose, irritated facial skin, sore eyes, and headaches. If the CPAP device is not properly adjusted, the patient may get stomach bloating and discomfort while wearing the mask. Without the ability to wear the CPAP device, these patients are left to “fall through the cracks” untreated. Where do they go, and what hope do they have for the successful treatment of their condition?

ORAL SLEEP APPLIANCES

Figure 3. The Tap appliance, an example of a double-arch appliance that opens the bite and positions the mandible/tongue forward.	Figure 4. The SUAD appliance, another example of a double-arch appliance.

Figure 5. Tongue-retaining appliance that holds the tongue forward with suction.

The answer for people who are CPAP intolerant lies with dental sleep appliances. In the proper diagnosis and use of oral sleep appliances, dentistry has a workable solution for sleep apnea and snoring. With this, dentistry has been handed a major responsibility in the treatment of snoring and OSA.
For the most part, the dental devices currently available for the treatment of snoring and OSA are double-arched appliances. Success is achieved by opening the vertical dimension and advancing the mandible forward.⁶ The advancement can be from edge-to-edge to, as much as, a full protrusive position. With some patients, the vertical is opened as much as 10 to 15 mm. In this way, the tongue is pulled forward and the airway opened.
Two popular double-arched sleep appliances that advance the mandible and open vertical are illustrated in Figure 3, the Tap appliance, and Figure 4, the SUAD appliance.
Another option is the tongue-retaining device (Figure 5). It holds the tongue forward by suction, created when the tongue is inserted into a rubber bubble in the front of the appliance.
Appliances like these can be successful, however, a large percentage of them can be uncomfortable since mandibular advancement can lead to jaw pain, changes in occlusion, and tempromandibular disease problems. Furthermore, what can be done once the dentist has opened the vertical, and moved the jaw forward as far as possible, without accomplishing the reduction of snoring and apneic events? The treatment is finished, unsuccessfully.

SINGLE-ARCHED APPLIANCES
In September, 2006, a new maxillary single-arch oral sleep appliance was introduced to dentistry called the Full Breath Solution (FBS). It allows the clinician to take a very different approach to treatment. Rather than pulling the tongue forward by advancing the mandible, it works by utilizing a “tail” that restrains the tongue from moving upward and backward. The tail is expanded posteriorly and inferiorly, depressing the tongue in the same manner in which the medical doctor utilizes a wooden tongue blade in an exam. The tongue is gently depressed in order to open and view the airway. In the same way, dentists can utilize the tail on the single-arch FBS oral appliance to open the airway.
In June, 2009, the mandibular single-arch FBS oral appliance was granted FDA certification, and subsequently introduced into patient care. This was the fifth FDA certification granted to the FBS appliance since 2004.
The CPAP is almost 100% successful, when tolerated, because the positive pressure of the continuous air stream pushes the tongue forward keeping the airway open. Similarly, the FBS oral appliance is successful because it depresses and restrains the tongue, inhibiting the tongue from moving up/backward and blocking the airway. An oral device that controls the tongue is able to control and open a patient’s airway, allowing more oxygen to enter the lungs, dramatically improving nighttime breathing.

Figure 7. The tail of the lower FBS which can be seen here depresses the tongue and prevents it from moving posteriorly.	Figure 8. An underside view of a mandibular FBS appliance. Two to 4 clasps are placed for retention.

Figures 6a and 6b show the maxillary FBS oral appliance, and Figures 7 and 8 show the mandibular FBS oral appliance. The man­dibular FBS single-arched appliance utilizes a posterior tongue restrainer (PTR), or “tail” to depress the tongue.
The FBS appliance gains its clinical success by small additions of acrylic to get posterior and inferior extension of the PTR (tail). This allows for more leverage in re­straining the tongue. The formation of the tail, which acts exactly like a tongue depressor, prevents the tongue from its upward and backward movement resulting in an open airway and reduced/eliminated snoring.

Figure 9. Blue wax has been added to the tail of the maxillary FBS appliance.	Figure 10. Blue wax has been added to the tail of the mandibular FBS appliance.

With either the maxillary (Figure 9) or mandibular appliance (Figure 10), wax is incrementally added to the tail, a little at a time, to clinically test for patient comfort and tolerance. If comfortable, the wax is removed and acrylic is added in the same approximate size and shape as the wax-up (Figures 11 and 12). In this way, the tail is expanded (from its original lab-fabricated starting point) to adequately depress the tongue.
Depression can be slight, or much deeper, depending on the patient. The question that invariably comes up is the comfort of the tail. Approximately 5% of patients complain of discomfort or irritation. In those cases, the tail is cut off. Then, approximately 3 weeks later, the tail is added back on in small increments of acrylic extensions. This approach produces a uniform success rate with patients (breathing and comfort) in the 99th percentile. When desired, acrylic can also be removed from the superior surface of tail to keep it thinner and more comfortable.
Despite the tail, the properly fabricated and adjusted FBS appliance will not cause gagging. The reason lies with the physics and effects of snoring. When a person is snoring, the tongue falls back and closes the airway from 80% to 90%. As the air flows through the constricted airway, it picks up speed as it moves through the reduced opening. This constantly speeding air desensitizes the nerve endings on the posterior section of the tongue. As a result, there is a reduction or elimination of the normal gagging reflex due to a reduction of tactile nerve endings on the tongue.

3-D IMAGING

Figure 13. In these CAT scan views, the lateral cervical view (upper right) shows the small airway caused by the posterior position of a large tongue. The lower right image is the same individual with the FBS appliance in place.	Figure 14. These images show the increase in the size of the airway achieved with the FBS appliance. Compare the pretreatment image (upper right) with the post-treatment (lower right) image. Again, note the tongue depressing effect of the tail to depress the tongue and open the airway.

Figure 15. In the upper right, the superior posterior tip of the tail is touching the soft palate and can be a cause of discomfort. Also, the tail needs to be repositioned downward to better control the tongue. The lower right image shows the changes made to the appliance and the increased airway.

The tail, which is the key to successfully treating the patient, is incrementally elongated and thickened in depth until the snoring is eradicated. The elongation of the tail with acrylic is done by adding a little length and slowly increasing the depth inferiorly, gauging clinical success by the lack of snoring. The pace of addition is based on the comfort/tolerance of the patient with each addition.
The most efficient and precise method of increasing tail size is provided by one of dental radiology’s new diagnostic tools, 3-D cone beam. 3-D imaging allows detailed viewing of appliance tail placement, tongue position, and the size of the airway. It also makes precise adjustments possible to maximize the airway opening. We can easily analyze how and where we should add acrylic to the tail to maximize the opening of the airway. We are able to observe the original restricted airway, and then to see the improved airway with use of the FBS appliance. 3-D dental imaging clearly illustrates the ability of the appliance’s tail to control the tongue and open the airway (Figures 13 to 15).

Figure 16. CASE 1: Upper left and right im­ages: Pretreatment AHI of 33. Pretreatment frontal (left) view showing the narrow airway. Note the small oropharyngeal airway obvious in the lateral (right) view. Lower left and right images: Post-treatment AHI of 2 with FBS treatment. See increased oropharyngeal airway with tongue restrained by the tail of the FBS appliance.

Figure 17a. CASE 2: Pretreatment AHI of 20.1. Note the narrow airway shown with both the frontal (left) and lateral (right) pretreatment views.

Figure 17b. Post-treatment AHI of 2.4. Note the increased width of the airway in the frontal (left) and lateral (right) post-treatment views.

Figure 18. CASE 3: Upper left and right images: Pretreatment AHI 109.9. Frontal (left) and lateral (right) pretreatment views of airway appear good-sized. Lower left and right images: Post-treatment AHI of 22. Note airway opening has been dramatically improved using the FBS oral sleep appliance.

CASE EXAMPLES: USINGTHE FBS ORAL APPLIANCE

CASE 1

A 31-year-old male patient presented with a history of severe snoring, moderate sleep apnea, and resulting fatigue. The patient had been previously treated with somnoplasty and an uvuloectomy, resulting in only minimal improvement. CPAP had been prescribed by the medical doctor, but the patient was found to be CPAP intolerant.
Treatment would consist of a pretreatment PSG (lab or hospital sleep test) to determine the Apnea Hypopnea Index (AHI) (the number of times the oropharygeal airway is blocked by the tongue per hour), FBS oral appliance therapy, and a post-treatment AHI.
Including the initial visit, delivery appointment, and subsequent visits to adjust the appliance, treatment consisted of 5 appointments. It was successful in correcting the patient’s sleep problems. AHI went from 33 to 2. (See Figure 16 for the pre-and post-treatment images associated with this case.)

CASE 2
A 67-year-old male patient presented with snoring that was disturbing to his wife, and fatigue upon awakening. CPAP therapy had been previously prescribed by his medical doctor and he was found to be CPAP intolerant. Treatment would consist of a pretreatment PSG, FBS oral appliance therapy, and a post-treatment PSG.
Treatment involved 5 appointments and was successful. AHI went from 20.1 to 2.4. (See Figures 17a and 17b for the pre-and post-treatment images associated with this case.)

CASE 3
A 67-year-old male patient with a history of severe sleep apnea presented with fatigue and morning headaches. CPAP had been previously prescribed by a medical doctor, and the patient was very unhappy with it, still waking fatigued with morning headaches.
The patient wanted a FBS oral appliance to open the airway so he could reduce the high airflow setting of the CPAP device. Treatment would consist of a pretreatment PSG, a FBS oral appliance therapy with continued use of CPAP, and a post-treatment PSG.
In this case the lateral and frontal views of this patient’s airway appear good-sized. Pretreatment AHI was 109.9. (See Figure 18 for the pre- and post-treatment images associated with this case.) This patient’s sleep study showed that he stopped breathing 109.9 times an hour. Why? The real culprit in OSA reared its head in this case: the tongue was falling back 109.9 times an hour and blocking his airway.
Treatment success was achieved with the FBS appliance. The patient was very happy because he was able to reduce the CPAP airflow needed. His AHI went from a 109.9 (pretreatment) to 22 (post-treatment). This post-treatment AHI represented a large
reduction from the pretreatment AHI using an oral appliance.

DISCUSSION
In all 3 of the above cases, controlling the tongue resulted in increased airways and successful results. The oral appliance tail depressed the tongue and prevented the tongue from moving posteriorly to block the airway. This resulted in reduced AHI readings and the elimination of snoring. All 3 cases demonstrated an increase of the oropharygeal airway from the lateral view. In addition, we got a very pleasant surprise when we viewed the frontal view of the same airways: the lateral width of the 3 airways all increased with minimal advancement using the expanded tails of the FBS.

CONCLUSION
The best treatment available for OSA is CPAP therapy, but its rejection rate has been estimated by some to run as high as 75%. After weight loss, the best nonsurgical treatment for snoring/OSA is an oral appliance.
The FBS sleep appliance differs from other sleep appliances in that it has a posterior transpalatal/translingual bar and a Posterior Tongue Restrainer (tail). This controls and restrains the tongue in a manner that could not be previously achieved. In addition, utilizing 3-D imaging allows the dentist to view treatment progress and to make the appropriate changes to ensure clinical success. Utilizing these advanced oral and imaging techniques, dentistry can now realize success in treating snoring and OSA patients in the 99th percentile range, far beyond the low tolerance rates of CPAP, and well beyond the hit-and-miss success rate of the mandibular advancing technique.
In the author’s opinion, dentists are now able to offer an option for the treatment of snoring, mild to moderate OSA, and CPAP intolerance, that can dramatically improve the quality
and longevity of life for our patients.

References

1. Kushida CA, Morgenthaler TI, Littner MR, et al. Practice parameters for the treatment of snoring and Obstructive Sleep Apnea with oral appliances: an update for 2005. Sleep. 2006;29:240-243.
2. Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. 3rd ed. Philadelphia, Pa: Saunders; 2005:33-34.
3. Mapes D. When happily ever after means separate beds. Available at: http://www.huffingtonpost.com/2008/09/16/when-happily-ever-after-m_n_126810.html. Accessed July 26, 2009.
4. Redline S, Adams N, Strauss ME, et al. Improvement of mild sleep-disordered breathing with CPAP compared with conservative therapy. Am J Respir Crit Care Med. 1998;157(3 pt 1):858-865.
5. Engleman HM, Kingshott RN, Wraith PK, et al. Randomized placebo-controlled crossover trial of continuous positive airway pressure for mild sleep Apnea/Hypopnea syndrome. Am J Respir Crit Care Med. 1999;159:461-467.
6. Millman RP, Rosenberg CL, Carlisle CC, et al. The efficacy of oral appliances in the treatment of persistent sleep apnea after uvulopalatopharyngoplasty. Chest. 1998;113:992-996.

Dr. Keropian is the founder of the Center for Snoring and Continuous Positive Airway Pressure (CPAP) Intolerance, which provides nonsurgical treatment for patients who suffer wit mild or moderate sleep Apnea, CPAP-intolerance, and snoring. He can be reached at (818) 344-7200 or via e-mail at bk@cpapalternative.com or tmjrelief@msn.com.

Disclosure: Dr. Keropian is the inventor and patent holder of the Full Breath Solution sleep appliance, and CEO of Full Breath Corporation located in Tarzana, Calif.

BTX A acts as a presynaptic neurotoxin that blocks neuromuscular transmission by binding to receptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles located within nerve endings. When BTX A is injected intramuscularly in therapeutic doses, it produces partial chemical denervation of the muscle, resulting in a localized reduction in muscle activity. This causes dose-dependent weakness or paralysis in skeletal muscle. The effect of BTX A can last from 3 to 6 months, and local paralysis is reversed chiefly by neural sprouting with reinnervation of the muscle. In addition, when injected intradermally, BTX A produces temporary chemical denervation of the sweat glands, resulting in local reduction of sweating.

The Food and Drug Administration (FDA) first approved BTX for use in focal dystonia  in 1989. Following completion of clinical trials, the FDA approved BTX A use in treating cervical dystonias, primary axillary hyperhidrosis, blepharospasm, and strabismus. These clinical problems have been challenging to clinicians and generally treated surgically with poor results. BTX has been widely adapted for these applications because it provides a minimally invasive approach to treating these challenging clinical problems. One of the most popular and successful applications of BTX has been in the treatment of hyperkinetic facial lines.

BTX A is produced by Allergan and is supplied in 100-unit vials. One unit of BTX corresponds to the calculated median intraperitoneal lethal dose (LD50) in mice. Unopened BTX must be stored in a refrigerator (2º to 8ºC), and preservative-free normal saline is used for reconstitution. In general, 1 to 8 mL of saline is added to 1 vial, producing a concentration of 10 to 1.25 units per 0.1 mL. Once reconstituted, the effectiveness of BTX begins to diminish after 4 hours. Therefore, immediate administration of BTX is recommended. The recommended doses range from 5 units to 25 units per muscle. The cumulative dose of BTX treatment in a 30-day period should not exceed 200 units.¹

TEMPOROMANDIBULAR DISORDERS (TMD)

Temporomandibular disorders (TMD) are a broadly defined group of nonodontogenic facial pain/disorders associated with the temporomandibular joint (TMJ) and/or associated muscles. Often, proper diagnosis of TMD problems can be challenging to clinicians as a result of the overlap of symptoms with other oral/dental/craniofacial disorders. Usual TMD symptoms can include but are not necessarily limited to the following: jaw pain, difficulty with jaw opening, earaches, headaches, pain behind the eyes, jaw joint popping and clicking, dizziness, and difficulty chewing food or occluding the teeth.

In recent years, there have been reports describing the use of BTX for several subcategories of TMD: bruxism, clenching, masseteric hypertrophy, recurrent dislocation of the temporomandibular joint, oromandibular dystonias, and chronic myogenous orofacial pain.2-12 Although BTX is not a panacea for  the listed problems, this drug appears to be an important treatment option for many patients. This article will review the clinical problems for which BTX has been used, and the indications and reported effectiveness will be discussed.

TMJ Dislocation

Recurrent TMJ dislocation may be the result of one of several underlying problems. Often it is the result of a steep articular eminence and ligamental laxity. Patients with such an anatomic variance will often report that after yawning, the mandible cannot be closed. In some cases, these events resolve spontaneously, and in other situations a visit to the emergency room is necessary. With conservative therapy and restricted jaw-opening exercises, many patients can fully control TMJ dislocation. In a small percent of patients, the dislocation recurs, especially among elderly patients with neurologic disorders or tardive dyskinesia secondary to medications (eg, antidepressants).

Figure. Masseteric hypertrophy and myalgia successfully treated with BTX A injection.

In the past, limited use of intermaxillary fixation or invasive surgery was used to treat recurrent dislocation of the TMJ. Currently, with electromyography-guided delivery of BTX A to the lateral pterygoid muscles, extreme range of motion of the mandible may be prevented for 3 to 4 months. Several case reports have been published that support the use of BTX A for recurrent dislocation of the TMJ.^2-4

Masseteric Hypertrophy

Masseteric hypertrophy may be unilateral or bilateral. It is often associated with excessive chewing of gum or food and clenching habits while awake or asleep. It presents as a unilateral condition when the habit favors asymmetric use of the jaw. It may be associated with myogenous facial pain (usually the masseteric or temporalis) or may present alone as a cosmetic complaint. Several studies have shown that the use of BTX A at the masseteric bulge can result in significant reduction of the muscular mass, which results in a more ovoid appearance of the lower face. Furthermore, the reduction in muscle mass is accompanied by less myogenic pain and discomfort. Again, these effects usually last 3 to 4 months. However, with repeated treatments some patients do not require additional treatment due to a satisfactory reduction in masseteric muscle bulge and a reduced clenching habit. An adverse side effect of facial muscle weakness has been reported in some patients. This is most likely due to diffusion of BTX A to superficial muscles during masseteric injection.^5-6

Chronic Myogenous Facial Pain/Myofacial Pain

Orofacial pain of muscular origin is often referred to as myofacial pain. The current conservative treatment approach includes the use of nonsteroidal anti-inflammatory medications, soft diet, and occlusal splint. Other medications such as muscle relaxants and tricyclic antidepressants have been used. Some clinicians advocate the use of other modalities such as massage therapy, ultrasound therapy, and transcutaneous electric nerve stimulation. More than 80% of patients respond to conservative therapy.¹³

For those patients who are refractory to these treatments and continue to suffer significant pain and dysfunction, treatment with BTX has been proposed. As mentioned previously, patients with masseteric hypertrophy and pain often respond well to BTX A administration to the affected muscles. In a randomized, blinded, placebo-controlled study by Von Linden, et al⁷, 90 patients with chronic facial pain were treated (60 BTX A, 30 placebo). Patients received on  average 35 units of BTX A to affected muscles (masseter, temporalis, or medial pterygtoid), and 0.9% normal saline was used as a control. The data indicated that 91% of those who received BTX A reported improvement, with a significant mean reduction of approximately 3.2 on the visual analog pain scale (VAS 0 to 10).

It is believed that BTX A hinders trigeminal nerve activity not only by preventing the release of acetylcholine but also preventing the release of substance P. Substance P is a potent neurotransmitter that plays a role during neurological inflammation.⁷ Furthermore, BTX A therapy can indirectly alleviate pain of arthrogenic origin. This is achieved with the prolonged “joint-sparing” effect of diminished loading secondary to the decreased ability of the musculature to affect joint loading.⁸

A study by Freund, et al⁹ also supports the effectiveness of BTX A in the reduction of myogenic pain associated with the TMJ. Forty-six patients with TMD were treated with a total dose of 150 units of BTX A (50 units per masseter and 25 units per temporalis). During the following 8 weeks these patients had a mean 3-point reduction in the 0 to 10 VAS pain score. There were no controls in this study.⁹

A study by Nixdorf, et al10 of 15 patients (10 completed the study) examined the use of BTX A for chronic myogenous orofacial pain. This report did not show a statistically significant improvement in the group that received BTX A versus normal saline. In the discussion, they acknowledged the small number of patients in the study.¹⁰

Bruxism and Clenching

Bruxism is a diurnal or nocturnal parafunctional habit of the jaws that includes clenching or grinding of teeth. Bruxism is thought to be a dystonia, although its origin in the central nervous system is not understood.11 Severe bruxism has been reported in anoxic brain injury and in patients with neurological disorders such as Rett syndrome. Certain medications can cause tardive dyskinesia and bruxism habits. Other etiologies for bruxism are head trauma, Parkinsonism, and neurodegenerative disorders.

A study by Tan and Jankovic11 successfully treated severe bruxism with BTX A. Approximately 65 units were injected per masseteric muscle in patients with long-standing (14±10 years) bruxism habits. The mean duration of response was 19 weeks, and the mean peak effect on a scale of 0 to 4 (in which 4 equals to total abolishment of grinding) was 3.4± 0.9. Only one subject reported having dysphagia following injection of BTX A.¹¹

Oromandibular Dystonia

Oromandibular dystonia (OMD) refers to involuntary spasms of masticatory, lingual, and pharyngeal muscles resulting in tongue protrusion, persistent jaw opening and closing, or jaw deviation. OMD can be idiopathic or can be caused by a wide range of neurological disorders. A study by Tan and Jankovic¹² examined the effect of BTX A on OMD; 202 patients were treated with injection of the masseter and submentalis complex. On a zero to 4 scale, with 4 being complete abolition of dystonia, the authors reported a mean reduction of 3.1. The best results were seen in patients with jaw-closing oromandibular dystonia. This report did observe that 31.5% of patients had adverse side effects, which included dysarthria and dysphagia. The high incidence of adverse side effects may be due to BTX A overdosing.

DISCUSSION

There is a growing body of evidence that supports the use of BTX A as a treatment modality for various TMD. Several subcategories of TMD including bruxism, clenching, masseteric hypertrophy, recurrent dislocation of the TMJ, oromandibular dystonias, and chronic myogenous orofacial pain have been effectively treated with BTX. However, without FDA approval, using BTX for treatment of TMD (with the exception of oromandibular dystonia) is an off-label application.

BTX has become a treatment modality in many healthcare disciplines. Its effects are reversible, and administration is minimally invasive. Adverse side effects such as dysarthria and dysphagia are observed when overdosing occurs or the injection misses the target muscle and the medication diffuses into adjacent structures. In addition, this treatment can be expensive ($474 for a 100-unit vial; adding a professional fee can bring the cost to more than $1,100 for a therapy that lasts up to 4 months). For off-label application, insurance does not cover BTX injections. Injection of BTX A should be performed by a clinician with knowledge of its pharmacology and the relevant anatomy of the sites receiving the injection. Finally, Allergan  offers a comprehensive manufacturer’s package insert, which includes FDA-approved use of the medication as well as contraindications for its use, such as hypersensitivity, pre-existing neuromuscular disorders (eg, muscular dystrophy), and dysphagia. Although there has been no fatal hypersensitivity/allergic reaction to BTX, severe dysphagia, which resulted in aspiration pneumonia and death, has been reported.¹

References

1. Botox [package insert]. Irvine, Calif: Allergan Inc; 2004.

2. Daelen B, Thorwirth V, Koch A. Treatment of recurrent dislocation of the temporomandibular joint with type A botulism toxin. Int J Oral Maxillofac Surg. 1997;26:458-460.

3. Aquilina P, Vickers R, McKellar G. Reduction of a chronic bilateral temporomandibular joint dislocation with intermaxillary fixation and botulinum toxin A. Br J Oral Maxillofac Surg. 2004;42:272-273.

4. Moore AP, Wood GD. Medical treatment of recurrent temporomandibular joint dislocation using botulinum toxin A. Br Dent J. 1997;183:415-417.

5. Bentsianov B, Francis A, Blitzer A. Botulinum toxin treatment of temporomandibular disorders, masseteric hypertrophy, and cosmetic masseter reduction. Oper Tech Otolaryngol Head Neck Surg. 2004;15(2):110-113.

6. Park MY, Ahn KY, Jung DS. Botulism toxin type A treatment for contouring of the lower face. Dermatol Surg. 2003;29:477-483.

7. von Lindern JJ, Niederhagen B, Berge S, et al. Type A botulinum toxin in the treatment of chronic facial pain associated with masticatory hyperactivity. J Oral Maxillofac Surg. 2003;61:774-778.

8. Schwartz M, Freund B. Treatment of temporomandibular disorders with botulinum toxin. Clin J Pain. 2002;18(6 suppl):S198-S203.

9. Freund B, Schwartz M, Symington JM. Botulinum toxin: new treatment for temporomandibular disorders. Br J Oral Maxillofac Surg. 2000;38:466-471.

10. Nixdorf DR, Heo G, Major PW. Randomized controlled trial of botulinum toxin A for chronic myogenous orofacial pain. Pain. 2002;99:465-473.

11. Tan EK, Jankovic J. Treating severe bruxism with botulinum toxin. J Am Dent Assoc. 2000;131:211-216.

12. Tan E, Jankovic J. Botulinum toxin A in patients with oromandibular dystonia: long-term follow-up. Neurology. 1999;53:2102-2107.

13. Peterson LJ, ed. Principles of Oral and Maxillofacial Surgery. 2nd ed. Hamilton, Ontario, Can: B.C. Decker; 2004:chap 48.

Dr. Chang completed her dental degree at Columbia University School of Dental and Oral Surgery and her medical degree at the University of Connecticut Health Center. She completed her residency in oral and maxillofacial surgery in June of 2004. At the 2004 annual American Association of Oral and Maxillofacial Surgeons meeting, she presented her work, “Analysis of Inflammatory Mediators in TMJ Synovial Fluid Lavage Samples of Symptomatic Patients and Asymptomatic Controls,” which won the best abstract award for the session. In May of 2005 she joined Columbia University as a full-time faculty member in the division of oral and maxillofacial surgery. She can be reached at (212) 305-7626 or hkc3@columbia.edu.

THE “UGLY DUCKLING” STAGE
The ugly duckling stage is an awkward period in a child’s life when newly erupted maxillary incisors appear to be “snow shovels” in a small face. This is a particularly hazardous time for traumatic dental injuries because of the size and protruding nature of the front teeth, the softness of the alveolar bone, the lack of completed radicular formation, and the lack of ability to splint to adjacent teeth.
Frequently, avulsed teeth occur in young patients with predisposing orthodontic conditions such as thumb-sucking and/or class II malocclusion with excessively flared maxillary central incisors. These patients have maxillary incisors that hang over the lower lip, and when the child falls down, his or her teeth strike first without lip cushion to soften the blow.
I’ve known orthodontists who routinely extract a tooth with a history of avulsion. These teeth frequently ankylose and often fail long term. They feel it is better to correct the problem in the patient’s teens than to retreat the problem in the patient’s 30s or 40s.
When I saw the child described in the opening paragraph, the next day after trying to splint avulsed teeth Nos. 9 and 10 to teeth Nos. 8 and 11, I realized there was no hope. The orthodontic wire and composite were removed from the hanging teeth, and the patient was fitted with an occlusal guide. The appliance was inserted over the loose teeth.

THE OCCLUSAL GUIDE
The occlusal guide is a preformed polypropylene orthodontic positioner. For decades, orthodontists have used custom-made positioners to fine-tune orthodontic detail into their fixed orthodontic cases. Orthodontic labs manufacture custom-made positioners by cutting out every tooth from a plaster cast of a nearly completed orthodontic case. The cut-out plaster teeth are reassembled into perfect occlusion in ideal tip, torque, and angulation at Angle class I interdigitation. Then a polypropylene, football-style mouth guard is fabricated over the ideally reset plaster cast.
Dr. Earl Bergersen, an orthodontist and developer of the occlusal guide, realized how extremely uniform the human dentition is. This is why preformed denture teeth can precisely restore ideal aesthetics to an edentulous patient and why aesthetic dentistry has adopted the “golden proportions” in cosmetic makeovers. Prefabricating the positioner by duplicating different sizes of denture teeth set to ideal class I occlusion eliminated the need for orthodontists to remove the last upper and lower wires, take an impression, replace the same wires, send the poured models to the lab for positioner fabrication, and have the patient return for debonding, debracketing, and appliance insertion. Orthodontists could now select the size needed and insert the best-fitting appliance immediately after fixed appliance removal. The patient needs to do heavy biting exercises for a prescribed length of time, say 2 hours per day for one week, prior to final retention.
Dr. Bergersen soon realized that his device with a motivated child could do far more than provide fine detail to a near-finished orthodontic case. He found that the occlusal guide was capable of correcting severe orthodontic malocclusions with sustained use in a motivated child. Huge overjet/overbite cases could be corrected 1 mm per month. Severely crooked teeth with absence of crowding could be straightened over several months of heavy biting exercises. The flexible but firm polypropylene rims can catch misaligned teeth and slowly force them into place. The occlusal guide became the most frequently used orthodontic appliance worldwide.

THE AVULSED TOOTH STABILIZING APPLIANCE
The problem with using an occlusal guide to stabilize avulsed teeth is that it is both an upper and lower bulky, football-style rubber mold. The patient has to eat and drink, necessitating early removal during the crucial 7- to 10-day period for avulsed teeth. Early removal could possibly remove the teeth with the appliance, because dried blood and contaminants cake to the very loose teeth, and the appliance slots grasp tooth curvatures, making removal risky.
However, if the mandibular half was eliminated from the appliance, leaving only the upper, then with some difficulty the patient could eat and drink for days, perhaps weeks, before removing the occlusal guide (see Figure). Longer-term wear may allow complete reattachment of the avulsed teeth. Intermittent biting exercises would place an apically directed force, maintaining the terminal root in the depth of socket position at an ideal tip, torque, and angulation. I estimate that 3 sizes of the appliance would fit 90% of patients: small, medium, and large. The size is determined by arch width and central incisor width.
Frequently, pediatric patients age 6 to 8, in their ugly duckling stage, have teeth ectopically positioned with flared centrals and huge diastemas. Because of the very flexible material used to fabricate the occlusal guide, these teeth can still be stabilized by the appliance even if the central incisors overlap into the lateral slots. Again, the occlusal guide was designed to straighten crooked teeth. Different size appliances may be inserted to determine the best fit, although this appliance will not fit all mouths.

Figure. Eliminating the mandibular half from the occlusal guide appliance, leaving only the maxillary, will allow the patient with some difficulty to eat and drink for days, maybe weeks, before removal. Long-term continuous wear will allow complete reattachment.

The patient should be instructed to wear the appliance continuously for 7 to 10 days including eating, drinking, and sleeping, while intermittently biting hard into the appliance throughout the waking hours as much as possible. Sleep could be difficult, especially the first night, and as with any oral appliance, temporary excessive salivation is a frequent problem.
After 7 to 10 days, the child should be re-examined. Then the dentist should peel back the phlanges of the appliance labially and palatally, detaching any dried blood and contaminants. The teeth should be examined for stability and firmness. If after 7 to 10 days a firm reattachment is not evident, the teeth should be removed.
Besides being useful for tooth reimplantation in the ugly duckling stage, this device could be used for multiple avulsed teeth that are difficult to stabilize. For example, I had a patient who avulsed all 4 maxillary incisors when his teeth caught the net while dunking a basketball. The attempt to reimplant and stabilize them by an oral surgeon was unsuccessful. Stabilizing multiple teeth avulsions in a bloody operating field with composite and orthodontic wire can be very difficult. The patient now has 4 implants.
This device could also remedy other traumatic dental injuries, such as accident victims where the incisors are crushed palatally or are very loose but not fractured. These teeth could be repositioned to close to an ideal position and the appliance inserted for 7 to 10 days.
Perhaps this device could be useful for fractured teeth; broken teeth stabilized precisely may allow successful root canal treatment, especially with current perforation sealing techniques. I propose the hypothesis that sustained, apically directed pressure on the crown into the bony socket of a mid root fracture would more likely correctly align a fractured root than a dentist bonding a loose crown haphazardly to adjacent teeth with orthodontic wire.

DISCUSSION

Many gaps exist in current treatment for successful reimplantation of avulsed teeth, even if the accident victim arrives to a medical professional within the narrow window of time needed. For example, general dentists see these cases so infrequently that they are often ill-suited to treat a screaming, bloody, ugly duckling child with no adjacent teeth to which to bond. They often refer them to an oral surgeon across town.
In car accidents with multiple avulsed teeth, medical per-sonnel are rarely prepared to handle anything dental. Even large trauma centers with around-the-clock general surgery, orthopedic, and cardiovascular residency coverage often call in oral surgeons to handle tooth avulsions. What if every paramedic had 3 sizes of the avulsed tooth stabilizing splint on board his vehicle and was trained to reimplant and insert the appliance even as a temporary means to stabilize? What if every emergency room physician/resident or general dentist had these appliances on hand ready to use?
Perhaps unconscious accident victims could be stabilized by reimplanting the teeth, selecting and fitting the appropriate appliance, relining the splint with cold care liquid gel polypropelene, and reinserting the appliance over avulsed teeth until the material was hardened and secure.

CONCLUSION

How many avulsed teeth are lost by holes in the healthcare system? How many avulsed teeth are lost by poor stabilization of multiple avulsed teeth with little to which to bond? How will prolonged, intermittent, apically directed biting force affect reimplantation success in the short term and long term? Can nondental, first-arriving healthcare professionals be trained to reimplant avulsed teeth with a preformed polypropylene mold? Will mid root fractures have a greater chance of success if the broken fragments are compressed over each other for 7 to 10 days? Will this device help other dental injuries such as subluxation and tooth loosening?
The answers to these questions won’t be known for perhaps years. However, how many thousands of avulsed teeth are failing currently? Failure to reimplant an avulsed tooth correctly can doom a young child and the family to a long emotional, financial, and aesthetic tragedy. This article has discussed a new treatment ap-proach that the author feels has promise for stabilizing avulsed teeth and for certain other dental trauma situations as well. Additional clinical experience is needed to determine how successful this approach will be.

(Note: Currently, the Nebraska Medical Center Trauma Center is investigating this appliance.)

Dr. Brosnihan is a 1981 graduate of Creighton University Dental School. He is currently practicing in Oakland, Neb. He has previously been published in Dentistry Today, JADA, Dentistry (England), The Irish Dentist, and the Journal of Clinical Orthodontics. He can be reached at (402) 685-5677.

TREATMENT

Treatment goals for TMDs are decreasing pain, restoring normal range of motion, and restoring normal masticatory and jaw function. Many TMDs can be cyclical and self-limiting, with periods of complete remission of symptoms. Thus, initial treatment should emphasize a conservative and reversible approach. Primary treatment options include (1) home care (self-care), (2) medical care (nonsurgical care), and (3) surgical care

HOME CARE (SELF-CARE)

Home care generally represents the initial approach to TMD management, at least as part of a more extensive treatment plan. Patient education is a crucial aspect of home care and is one of the most subtle and under-appreciated yet effective treatments for TMDs. Informing and reassuring patients regarding their condition and presenting symptoms may alleviate a great deal of anxiety. In fact, a number of patients report feeling less pain immediately after their initial patient education/counseling visit, perhaps attributable to an immediate reduction in tension-related parafunctional activity.

A successful home care program consists of resting the masticatory muscles by limiting jaw movements, parafunctional habit modification, emphasizing a soft diet, and moist heat and/or ice therapy.2 Muscle rest may involve limited jaw activity (eg, reduced talking, chewing, and yawning) for the treatment duration and perhaps even after symptoms have resolved as a preventative measure. Patients may have a diurnal (daytime) parafunctional habit (clenching, grinding, posturing) that often is not conscious. Patient education and understanding of the physiological rest position (lips together, teeth apart) is imperative in reducing and eventually halting the daytime activity that contributes to the progression of TMDs. If asked to pay attention to their jaw position over time, many patients will return for follow-up with the recognition that they are in fact engaging in some jaw activity that contributes to their symptoms. Additionally, suggesting habit-controlling cues may be helpful in reminding patients throughout the day to check the position of their bite. As an example, saying the letter n throughout the day can remind patients to unclench or discontinue grinding their teeth. Also, a soft diet is crucial to muscle and temporomandibular joint (TMJ) pain management so that the condition is not exacerbated while treatment is provided. Finally, a trial of moist heat and/or ice therapy overlying the painful areas of the face, head, and neck can be recommended. Usually, moist heat tends to work better for muscle pain or tension by increasing circulation and relaxing involved muscles, and ice tends to work better for TMJ capsulitis by reducing inflammatory symptoms.

MEDICAL (NONSURGICAL) CARE

Physical Therapy

Physical therapy can be performed by an experienced physical therapist or can be provided by a qualified clinician who is treating the TMD. The consistency and regularity of the exercises are critical for achieving a therapeutic effect. Thus, at the outset of treatment planning, an agreement between practitioner and patient regarding compliance will aid in patients understanding of their roles and responsibilities in treatment. Primary goals of the physical medicine component of treatment are to stretch chronically fatigued and contracted muscles, increase range of motion, and reduce muscular trigger point activity.3,4 Some commonly used exercises to treat TMJ-associated muscle disorders include (1) n-stretching (placing the tip of the tongue on the roof of the mouth and stretching the jaw), (2) chin-to-chest exercises (gently pulling the head forward, bringing the chin toward the chest), and (3) head tilts (turning the head to one side and then tilting it posteriorly). These exercises are most effective if done regularly (4 to 6 times per day). In addition, moist heat application for 10 to 15 minutes followed by ethyl chloride or fluoromethane spray prior to stretching the muscles is helpful. The vapo-coolant spray provides a temporary anesthesia effect to the muscles so a more intense stretch can be achieved without pain. Patients can expect an even higher likelihood of treatment success if biofeedback training or transcutaneous electrical nerve stimulation (TENS) is added to a strict stretching regimen.

Pharmacotherapy

Commonly used pharmacological agents for the treatment of TMDs include analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), local anesthetics, corticosteroids, muscle relaxants, and antidepressants.5-7 The analgesics and corticosteroids are indicated for acute TMD pain; the NSAIDs, local anesthetics, and muscle relaxants are indicated for both acute and chronic conditions; and tricyclic antidepressants are usually indicated more for chronic TMD pain with associated muscle tension headaches.5,7 Clinicians should always consult the Physicians Desk Reference for proper dosing, side effects, and drug interactions, and make decisions regarding pharmacological treatment based on individual patient medical history and comorbidity. Also, referral to the proper specialist should be made in complex TMD cases.

NSAIDs

NSAIDs are indicated for mild-to-moderate acute inflammatory conditions. Commonly used NSAIDs are ibuprofen (Motrin) and naproxen (Naprosyn). NSAIDs may be prescribed for a minimum of 2 weeks with time-contingent usage as opposed to a dosing based on the presence of pain.6 Long-term NSAID use is not recommended as long as the parafunctional activity causing the inflammatory process can be reduced. In some chronic arthritic cases, long-term NSAIDs such as the COX-2 inhibitors (Celebrex, Vioxx), may be considered. However, possible side effects (ie, GI upset) should be taken into account.

Local Anesthetics

Local anesthetics are primarily used when a myofascial trigger point is present. Myofascial trigger points are usually detected in the muscles of mastication but can also be found in numerous other muscles such as splenius capitus and upper trapezius. One percent Procaine (1 cc) is recommended due to its low toxicity to muscles. However, studies have shown that dry needling of the muscle site may play a prominent role in breaking up the trigger point, with the anesthetic functioning more for pain control. Muscles may be sore for the first 48 hours after the injection, but generally should be less tender after that. The efficacy of trigger-point injections is highly variable and dependent for the most part on the patients compliance with a strict physical therapy regimen in conjunction with the injection. In addition, local anesthetics can be used to block the suspected source of pain in order to confirm a diagnosis.

Corticosteroids

Corticosteroids may be used for acute and chronic TMD symptoms. These medications are used enterally as well as injected directly into the joint space. Systemic steroids may be prescribed for the duration of a week. It is suggested that a steroid TMJ injection should be performed when all previous conservative treatments have not worked and the joint is still acutely inflamed.9 Tomograms of the TMJ or other radiographic studies are required prior to injecting into the joint space. A long-term study has shown that intra-articular corticosteroid injection has demonstrated a significant reduction in pain.10 However, the number of steroid injections should be carefully considered due to the possibility of bone resorption in the site of injection.

Muscle Relaxants

Muscle relaxants may be prescribed for muscle tension associated with TMDs. Commonly, they are taken at night before bed because of associated drowsiness. Thus, for patients with poor sleep patterns, these drugs are particularly helpful in alleviating insomnia in addition to their muscle-relaxing effects. A commonly used muscle relaxant is cyclobenzaprine (Flexeril), started at lower dosages and gradually increased until the patient starts noticing relief of symptoms or starts developing side effects. Muscle relaxants tend to be used for the more acute presentation of muscle tension.

Antidepressants

Tricyclic antidepressants like amitriptyline (Elavil) and nortriptyline (Pamelor) may be used for more chronic myofascial pain syndrome. In addition, they can be prescribed for the TMD patient that has tension-type headaches, depression, poor sleep, and/or poor appetite. It is important to inform the patient that the medication will not usually have antidepressive effects when prescribed at the dosages that are usually necessary to treat muscle pain and/or headaches. Nortriptyline or amitriptyline should be gradually tapered up until the desired therapeutic effect is achieved or side effects such as drowsiness, dry mouth, or weight gain develop. Caution should be used in patients who have comorbid heart conditions, concurrent psychotropic use, and/or psychiatric illness (eg, bipolar disorder).

Orthopedic Appliance Therapy Stabilization Appliance

Stabilization appliances (flat-plane splints) are utilized for the purpose of unloading the joints, equally distributing the forces, reducing the forces placed on the masticatory muscles, and protecting the occlusal surfaces of the teeth from chronic nocturnal bruxing. Usually, the patient is instructed to wear the splint only at night as long as parafunctional activity is controlled during the day with education and bite relation awareness. The splint should cover all of the maxillary or mandibular teeth and have bilateral posterior contacts with little to no anterior contacts. In addition, bilateral ball clasps may be incorporated into the splint for added retention. The stabilization appliance should feel comfortable to the patient at the time of try-in and be re-evaluated in a week. Adjustments should continue every 3 to 6 months because of changes that may result in the form and function of the splint from chronic bruxing.

Anterior Repositioning Appliance

Anterior repositioning splint prescription varies among clinicians, but is usually utilized for the chronic, intermittent closed-locking patient. With the possibility of permanent occlusal and bite changes with long-term use of repositioning appliances, short-term (6 weeks) use of this appliance is strongly recommended. If bite changes start to develop, the patient should be instructed to discontinue the use of the splint, and the splint may need to be converted to a stabilization nonrepositioning appliance. A few patients may experience increased pain with the use of a splint. In this case, the splint as well as the initial diagnosis should be re-evaluated. If the pain persists, discontinuation of splint therapy is recommended.

Surgical Therapy

Surgical therapy for TMD patients is recommended primarily for those that have tried conservative treatments without resolution of symptoms. Surgical recommendations (ie, arthrocentesis, arthroscopy) will depend on the degree of pathology as well as the result of previous conservative treatments. Also, consideration should be given to the patients extent of impairment and their compliance with previous non-surgical treatment modalities. Working closely with an oral and maxillofacial surgeon who has expertise with TMJ surgery is strongly recommended.

Arthrocentesis

Arthrocentesis involves irrigation of the joint with lactated Ringers solution or saline. In certain acutely inflammatory joint conditions, steroid injection may follow arthrocentesis. This procedure is often followed by mandibular manipulation and is recommended for patients who have unresolving joint restrictions and for those individuals who have developed an acute or chronic closed lock.11 It is recommended that the patient have a stabilization or repositioning splint ready to be delivered immediately following the procedure. The procedure may need to be repeated if the lock recurs, and the patient must be reminded to avoid activities that cause locking.

Arthroscopy

Arthroscopy is direct visualization of a joint with an endoscope. It is performed by an oral and maxillofacial surgeon mainly in the upper joint space and is recommended primarily for lysis and lavage and also for ablation of adhesions and biopsy.12 An MRI of the joint is needed prior to the arthroscopic procedure. It is crucial to keep the procedure as brief and atraumatic as possible.

Arthrotomy

TMJ arthrotomy is an open surgical intervention performed by an oral surgeon. It is recommended for severe osseous pathology involving the TMJ, such as ankylosis and severe osteoarthritis that has not responded to conservative treatments.13 It is crucial to work closely with an experienced TMJ surgeon to assess the necessity of this procedure. Open surgical procedures include disk repair (diskoplasty), disk removal (diskectomy) with or without replacement and disk repositioning, and arthroplastic procedures such as condylar repair and removal (condylectomy).

SUMMARY

TMDs are only one of a host of different conditions that are part of the broader category of chronic orofacial pain disorders and dysfunctions. Due to multifactorial etiologies, it is imperative to adopt a multidisciplinary approach when evaluating and treating these patients. Table 1 lists the various conditions to consider in the differential diagnosis of orofacial pain disorders.

References

1. Okeson JP. Orofacial Pain: Guidelines for Assessment, Diagnosis, and Management. Chicago, Ill: Quintessence Publishing; 1996.

2. Randolph CS, Greene CS, Moretti R, et al. Conservative management of temporomandibular disorders: a posttreatment comparison between patients from a university clinic and from private practice. Am J Orthod Dentofacial Orthop. 1990;98:77-82.

3. Carlson CR, Okeson JP, Falace DA, et al. Stretch-based relaxation and the reduction of EMG activity among masticatory muscle pain patients. J Craniomandib Disord. 1991;5:205-212.

4. Clark GT, Adachi NY, Dornan MR. Physical medicine procedures affect temporomandibular disorders: a review. J Am Dent Assoc. 1990;

121:151-162.

5. Gangarosa LP, Mahan PE. Pharmacologic management of TMJ-MPDS. Ear Nose Throat J. 1982;

61:670-678.

6. Gregg JM. Pharmacologic management of myofascial pain dysfunction.  Am Dent Assoc. 1983:167-173. 

7. Gregg JM, Rugh JD. Pharmacological therapy. In: Mohl ND, Zarb GA, Carlsson GE, et al, eds. A Textbook of Occlusion. Chicago, Ill: Quintessence; 1988:351-375.

8. Kopp S, Carlsson GE, Haraldson T, Wenneberg B. Long-term effect of intra-articular injections of sodium hyaluronate and corticosteroid on temporomandibular joint arthritis. J Oral Maxillofac Surg. 1987;45(11):929-935.

9. Kopp S, Carlsson GE, Haraldson T, et al. Long-term effect of intra-articular injections of a glucocorticosteroid into the TMJ: a clinical and radiographic 8-year follow-up. J Craniomandib Disord. 1991;5:11-18.

10. Dimitroulis G, Dolwick MF, Martinez A. Temporomandibular joint arthrocentesis and lavage for the treatment of closed lock: a follow-up study. Br J Oral Maxillofac Surg. 1995;33:23-27.

11. American Association of Oral and Maxillofacial Surgeons. Position paper on TMJ arthroscopy. Rosemont, Ill: American Association of Oral and Maxillofacial Surgeons; 1988. 

12. Buckley MJ, Merrill RG, Braun TW. Surgical management of internal derangement of the temporomandibular joint. J Oral Maxillofac Surg. 1993;51(suppl 1):20-27.

Dr. Uyanik completed his DDS degree at SUNY Buffalo School of Dental Medicine and then went on to a 2-year post-doctoral residency program in orofacial pain at UCLA. Upon completion of his post-doctoral training, he obtained boardcertification from the American Board of Orofacial Pain and is currently a member of the house staff at St. Barnabas Hospital working with residents in the diagnosis and treatment of orofacial pain disorders. He was recently appointed as clinical assistant professor at Columbia School of Dental and Oral Surgery in the Division of Oral and Maxillofacial Surgery as well as director of the Center for Oral, Facial and Head Pain. Dr. Uyanik is currently investigating the effects of low-level diode laser therapy on TMJ arthralgia and myofascial pain syndrome. He can be reached at (212) 305-7626 or e-mail jmu2101@columbia.edu.

HISTORY AND EVOLUTION OF THE MANAGEMENT OF TMD (TABLE 1)

As a result of Costen’s work, awareness of the TMJ and its relationship to facial pain increased greatly among practitioners.² He noted that a number of his patients with pain in the TMJ region seemed to experience a reduction of symptoms following therapeutic alteration in their occlusion. These findings were significant on 2 fronts. Firstly, Costen’s writings introduced hypotheses that occlusion and TMD may be linked. Secondly, he emphasized the practitioner’s role in providing treatments aimed at affecting the TMJ region. Thus, in the first half of the century, generally accepted concepts of patient management focused on occlusal adjustment as the major treatment modality for TMD.^3-7

The concept of internal derangement of the TMJ was introduced by Ireland15 in 1953 but was not widely accepted until the 1970s, following imaging techniques such as arthrography. Also in the late 1970s and 1980s, surgical intervention with disk repositioning started gaining popularity. Subsequently, TMJ disk removal procedures were recomended, with some surgeons choosing to maintain the joint complex without a disk while others opted for prosthetic TMJ disk implant placement. Unfortunately, use of certain prosthetic implants such as Vitek proplast/teflon resulted in severe complications such as giant cell foreign body reactions. In some implant cases, this led to extremely painful joint conditions with limited range of motion (ROM). Less-invasive surgical techniques such as arthrocentesis and arthroscopy proved to be highly effective for chronic TMJ conditions (eg, unresolving joint pain and closed lock).^16-18

Figure 1. Structure of the temporomandibular joint.	Figure 2. Palpating the temporalis muscle.
Figure 3. Palpating the superficial and deep masseter muscles.	Figure 4. Bilateral palpation of the TMJs.
Figure 5. Evaluating mandibular range of motion using a millimeter ruler.	Figure 6. A crude measure of reasonably normal interincisal distance is approximately the width of 3 of the patient’s fingers.

STRUCTURE AND FUNCTION (FIGURE 1)
TMJ has been a source of interest since the fifteenth century, when this anatomical structure was studied by Leonardo da Vinci. Other notable contributors include Vesalius in the sixteenth century, Meyers in the nineteenth century, and Sicher19 and Rees20 in the early twentieth century. The TMJ has been described as a ginglymoarthrodial synovial compound paired joint. A compound joint consists of 3 bones; however, in the case of the TMJ, the functional disk operates as the third nonossified bone and therefore fulfills the criteria. As a synovial joint, it is governed by the same basic orthopedic principles that apply to other human synovial joints, ranging from pathologic disorders to treatment protocols. The TMJ, however, has many unique features that distinguish it from other synovial joints. These include (1) rigid end point of closure; (2) one side cannot function without movement of the opposite joint; (3) both joints act as one functional unit; (4) any movement or functional alteration in one joint will affect the other joint; and (5) no hyaline cartilage is present.

NATURAL HISTORY AND EPIDEMIOLOGY
In a study on symptoms associated with TMD, Rasmussen²¹ found that most patients with a clicking TMJ usually did not evolve into an open or closed locking state. According to his findings, acute TMD symptoms lasted a mean of 5 years, and although joint noises generally did not disappear, most painful and disabling symptoms subsided in time. Similar results were shown by Könönen and colleagues, who followed 128 Finnish adults over 9 years.²² They found that the incidence of clicking in these patients increased with age. However, none of the patients developed locking. These studies demonstrate the importance of reversible and noninvasive treatments for the acute TMD patient. In an epidemiological study by Solberg,²³ 76% of subjects aged 18 to 25 had one or more signs associated with TMD and 26% had at least one symptom associated with TMD. Of this group, only 10% had symptoms that were considered by the subjects to be severe enough to seek treatment.

CLASSIFICATION (TABLES 3 AND 4)

Internal Derangement (ID)
Internal derangement of the TMJ is characterized by an anatomical disturbance in the relationship of the components of the disk-condyle complex. This term encompasses a number of clinical entities, including the following:

Inflammatory Joint Disorders
Arthralgia: This describes a joint that displays increased tenderness on palpation. Osseous changes are usually not noted on radiographic examination. Various terms have been used to specifically characterize this condition depending upon the location of the pain (eg, capsulitis, retrodiscitis, and synovitis).

Muscular Disorders
Myalgia/Myofascial Pain (MFP): This is a dull, aching pain varying in intensity. The primary difference between MFP and myalgia is that MFP produces pain referred to other satellite muscle trigger points upon palpation, whereas myalgia results in pain that is localized to the muscle that is being palpated. MFP tends to be seen in more chronic muscle pain conditions compared to the usually acute presentation of myalgia. Palpation of the trigger points should duplicate the patient’s pain complaint, thus confirming the diagnosis. In addition, blocking the source of the pain (ie, masseter muscle) utilizing a vapo-coolant spray or local anesthetic injection can also provide a definitive diagnosis.

PATIENT EVALUATION
TM disorder assessment should include a general examination of the head and neck, a detailed examination of the masticatory muscles, an evaluation of the temporomandibular joints, an evaluation of mandibular range of motion, and a detailed intraoral examination.²⁴

Evaluation of the Muscles of Mastication
The muscles of mastication are palpated bilaterally for firmness and tenderness utilizing approximately 2 to 3 pounds of pressure. A pain pressure algometer may be used to reproduce reliable palpation pressure²⁵ or the amount of pressure needed to cause blanching of the fingernail. Upon muscle palpation, the patient is asked to report the severity of the tenderness, pain referral to multiple sites or single-site pain localization, and replication of the chief complaint. The primary muscles to be palpated include the temporalis (Figure 2), the superficial and deep masseter (Figure 3), the medial and lateral pterygoid, the suprahyoid, and the upper cervical muscles. Note that palpation of the lateral pterygoid from an intraoral perspective is difficult.²⁶ It may be pertinent to ask patients about their use of analgesic prior to palpation in order to account for reduced symptoms upon examination.

Evaluation of the TMJ
The TMJs are palpated bilaterally for tenderness or swelling with slightly less pressure than used for muscle palpation, especially in the presence of an existing capsulitis (Figure 4). The clinician should palpate the preauricular region as well as the anterior walls of the external auditory canal. Lateral palpation may be utilized to assess joint pain in the lateral capsule, whereas the intrameatal approach via the external auditory canal is better for locating pain emanating from retrodiscal tissues.¹

Evaluation of Mandibular Range of Motion (ROM)
Initially, patients’ opening and closing patterns are closely observed to note any mandibular deviations. Evaluation of mandibular ROM consists of measuring with a millimeter ruler the (1) comfort opening, (2) active opening, (3) passive opening, (4) protrusion, and (5) left and right lateral excursions while noting the severity and location of pain with jaw movement (Figure 5). This can be particularly helpful in differentiating between joint and muscle pain. Comfort opening is determined by (1) the patient opening as wide as possible without any pain, (2) active opening with the patient opening as wide as possible with pain, and (3) passive opening with the clinician gently stretching the patient presumably past active opening while noting a soft or hard end feel. A reasonably normal interincisal distance is approximately 40 mm or the width of 3 of the patient’s fingers as a crude measure (Figure 6). Usually, with proper questioning, the patient will reliably reveal any recent limitations in ROM. The occurrence of TMJ clicking, crepitus, or jaw opening interferences with or without pain should also be noted at the initial examination. These baseline findings will aid in establishing the differential diagnosis and treatment options as well as providing a comparison for future change in TMD symptoms.

Evaluation of the Cervical Spine
Often, patients who present with TMD may have a coexisting pain complaint in the neck, shoulder, or upper back region. Poor posture may lead to a forward head position, rounded shoulders, and/or added tension in the head, neck, or back. Thus, an evaluation of the cervical spine may aid in assessing the patient’s head ROM in flexion, extension, and rotation. In addition, if range of motion is limited, it is pertinent to note any areas of pain that the patient experiences while performing various head and neck movements. This may help in localizing additional trigger areas that may have been missed on the palpatory exam.

SUMMARY
The study of temporomandibular disorders has undergone many changes throughout its history. Focus on the structure and function of the TMJ continues to improve our understanding of these complex disorders. A more standardized classification system allows practitioners and researchers to discuss findings in a common language. With improved patient evaluation techniques, the clinician can establish a proper working differential diagnosis and begin focusing attention on treatment planning.

References

1. Okeson JP. Orofacial Pain: Guidelines for Assessment, Diagnosis, and Management. Chicago, Ill: Quintessence Publishing; 1996.
2. Costen JB. A syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann Otol Rhinol Laryngol. 1934;43:1-15.
3. McCollum BB. Factors that make the mouth and teeth a vital organ (articulation orthodontia). J Am Dent Assoc. 1927;14:1261-1271.
4. Stallard H. Functions of the occlusal surfaces of the teeth. J Am Dent Assoc. 1930;13:401.
5. Stuart CE, Golden IB. The History of Gnathology. Ventura, Calif: CE Stuart Gnathological Instruments; 1981.
6. Shore N. Temporomandibular Joint Dysfunction and Occlusal Equilibration. Philadelphia, Pa: JB Lippincott; 1976.
7. Ramfjord SP. Dysfunctional temporomandibular joint and muscle pain. J Prosthet Dent. 1961;11:353-374.
8. Travell J, Rinzler SH. The myofascial genesis of pain. Postgrad Med. 1952;11:425-434.
9. Schwartz LL. A temporomandibular joint pain dysfunction syndrome. J Chronic Dis. 1956;3:284-293.
10. Laskin DM. Etiology of the pain-dysfunction syndrome. J Am Dent Assoc. 1969;79:147-153.
11. Wilkes CH. Arthrography of the temporomandibular joint in patients with the TMJ pain-dysfunction syndrome. Minn Med. 1978;61:645-652.
12. Farrar WB. Diagnosis and treatment of anterior dislocation of the articular disk. N Y J Dent. 1971;41:348-351.
13. Farrar WB, McCarty WL. A Clinical Outline of Temporomandibular Joint Diagnosis and Treatment. Montgomery, Ala: Normandie Study Group Publications; 1982.
14. Rugh JD, Solberg WK. Psychological implications in temporomandibular pain and dysfunction. Oral Sci Rev. 1976;7:3-30.
15. Ireland VE. The problem of the clicking jaw. J Prosthet Dent. 1953;3:200-212.
16. Ohnishi M. Clinical application of arthroscopy in the temporomandibular joint diseases. Bull Tokyo Med Dent Univ. 1980;27:141-150.
17. Sanders B. Arthroscopic surgery of the temporomandibular joint: treatment of internal derangement with persistent closed lock. Oral Surg Oral Med Oral Pathol. 1986;62:361-372.
18. Nitzan DW, Dolwick MF, Martinez GA. Temporomandibular joint arthrocentesis: a simplified treatment for severe, limited mouth opening. J Oral Maxillofac Surg. 1991;49:1163-1167.
19. Sicher H. Temporomandibular articulation in mandibular overclosure. J Am Dent Assoc. 1948;36:131-139.
20. Rees LA. The structure and function of the temporomandibular joint. Br Dent J. 1954;96:125-133.
21. Rasmussen OC. Description of population and progress of symptoms in a longitudinal study of temporomandibular arthropathy. Scand J Dent Res. 1981;89:196-203.
22. Kononen M, Waltimo A, Nystrom M. Does clicking in adolescence lead to painful temporomandibular joint locking? Lancet. 1996;347:1080-1081.
23. Solberg WK, Woo MW, Houston JB. Prevalence of mandibular dysfunction in young adults. J Am Dent Assoc. 1979;98:25-34.
24. Clark GT, Seligman DA, Solberg WK, et al. Guidelines for the examination and diagnosis of temporomandibular disorders. J Craniomandib Disord. 1989;3:7-14.
25. Ohrbach R, Gale EN. Pressure pain thresholds, clinical assessment, and differential diagnosis: reliability and validity in patients with myogenic pain. Pain. 1989;39:157-169.
26. Johnstone DR, Templeton M. The feasibility of palpating the lateral pterygoid muscle. J Prosthet Dent. 1980;44:318-323.

Dr. Uyanik completed his DDS degree at SUNY Buffalo School of Dental Medicine and then went on to a 2-year post-
doctoral residency program in orofacial pain at UCLA. Upon completion of his post-doctoral training, he obtained board certification from the American Board of Orofacial Pain and is currently a member of the house staff at St. Barnabas Hospital working with residents in the diagnosis and treatment of orofacial pain disorders. He was recently appointed as clinical assistant professor at Columbia School of Dental and Oral Surgery in the Division of Oral and Maxillofacial Surgery as well as director of the Center for Oral, Facial and Head Pain. Dr. Uyanik is currently investigating the effects of low-level diode laser therapy on TMJ arthralgia and myofascial pain syndrome.

Dr. Murphy currently works in private practice in Cork, Ireland. He is a part-time lecturer in the Anatomy Department and Dental School in University College Cork and the Eastman Dental Institute in London, England. He graduated from the UCLA orofacial pain residency programin 2001 and also completed a master of science in oral biology. He is a diplomate of the American Board of Orofacial Pain. His private practice is exclusive to orofacial pain and temporomandibular disorders.

Until recently, all avulsed teeth were treated in the same way, which involved reimplantation of the tooth immediately or as soon as possible after the avulsion. This approach was followed regardless of how much time had passed since the avulsion accident and was attempted even if the avulsed tooth was dehydrated and the periodontal ligament (PDL) cells were no longer viable. This philosophy became pervasive, and practitioners did not recommend any other treatment. This occurred despite evidence in the literature that did not support this approach.^2-4

Each patient who has suffered an avulsed tooth arrives at the dentist’s office with a specific set of circumstances. The history is evaluated, a diagnosis is made, then treatment is instituted. The treatment of avulsed teeth should, therefore, be dependent upon the specific clinical conditions that present to the dentist. These clinical factors are the following: the physiologic status of the PDL, the stage of root development, and the length of time since avulsion (extraoral time). The availability and use of a specialized storage and preservation medium, a cushioning and retrieval system, topical antibiotics, and enamel matrix protein promoters can increase reimplantation success.¹

BIOLOGIC RATIONALE FOR TREATMENT RECOMMENDATIONS

Status of the Development of the Root Apex

In certain instances, it is possible for the pulp tissue in immature avulsed teeth to completely revascularize.4 Researchers differ as to which factor is most influential regarding the incidence of revascularization. Important parameters include the width of the apical foramen, duration of time the tooth is outside the socket, and storage conditions. However, there is agreement that bacterial contamination can prevent revascularization of the pulp. Soaking avulsed teeth in a 1-mg/20-mL solution of doxycycline for 5 minutes prior to reimplantation has been shown to decrease root resorption and—of greater significance—to increase the frequency of pulpal revascularization.⁴

Physiologic Status of the PDL Cells

The status of PDL cells remaining on the root surface of an avulsed tooth determines the development of replacement root resorption.⁸ If the PDL cells are healthy, a new attachment to the surrounding alveolar bone is possible. If the PDL cells are metabolically stressed or damaged physically, the root cementum will experience necrosis. A new PDL will not form, and the surrounding alveolar bone will view the root surface as foreign and resorption will occur.^9-11 In order for optimum physiologic conditions to be maintained, the PDL cells on the avulsed tooth require nutrients and the proper pH.^1,12 In order for proper structure and physiology to be maintained, the cells must be in an appropriate osmotic environment and must be protected from physical damage.^13,14

Figure 1. The beneficial effect of soaking vs nonsoaking of avulsed teeth in Hank’s Balanced Salt Solution.

Many studies have demonstrated the damaging effects that storage can have on PDL cells. It is clear that dry storage, storage in water, and even storage in saliva are damaging to these cells. Water and saliva have a low osmolality and cannot replace lost cell nutrients.¹³ Even milk, which has received much attention as a storage medium, does not preserve PDL cells well.¹ A fluid that has been shown to have the necessary characteristics for preserving cell viability is Hank’s Balanced Salt Solution (HBSS), which is a cell culture medium. HBSS is a pH-balanced cell preserving fluid, not a salt-water solution. It maintains the ideal osmotic pressure for PDL cells and replaces depleted cell metabolites.2 Its use has been shown to maintain cell vitality, reconstitute cells that would otherwise die, and prevent or reduce resorption^2,6,7 (Figure 1).

Length of Time the Tooth Is Outside the Socket

The focus of research concerning the treatment of avulsed teeth has been on the length of time elapsed from avulsion to reimplantation. If the avulsed teeth are stored in a supportive medium such as HBSS, the length of time out of the socket is less important then physiologic status of the PDL cells.^15,16 Studies have indicated that storage for 4 days in dogs and 2 weeks in monkeys results in <30% resorption following reimplantation.^17-19

CLINICAL TREATMENT OF AVULSED TEETH

The treatment of avulsed teeth can be divided into 3 stages: pre-reimplantation, reimplantation, and post-reimplantation. Successful long-term retention of reimplanted avulsed teeth involves a wide range of factors, including treatment directed toward the PDL cells (ie, use of a biologic storage medium and maintenance of PDL cell vitality), timing of pulp extirpation, and splinting of the involved tooth or teeth. Every step in this process is important, and ultimate success is dependent to some degree on all 3 stages. Nevertheless, the pre-reimplantation stage is of primary importance.

Pre-reimplantation Stage

Patients with avulsed teeth can be categorized into one of 8 categories (Tables 1 and 2). Only patients with avulsed teeth in category 1 benefit from immediate reimplantation. Patients in the other 7 categories benefit from prereimplantation conditioning of affected teeth.

The clinician reimplanting the tooth must be concerned with maintaining the PDL cells in their original state or returning the cells to as healthy a condition as possible. By so doing, the remaining PDL cells will be able to differentiate and reestablish a new PDL. The PDL cells that remain on the root following the avulsion do not have a blood supply and begin to deplete their stored metabolites. In order to maintain optimal cell metabolism, the depleted metabolites must be replaced within 1 hour after avulsion.¹ After this time, the untreated PDL cells will undergo necrosis, the cementum will be lost, and root resorption will occur following reimplantation.

 Since teeth are rarely reimplanted within this time frame, biologic storage of the avulsed teeth and protection of the PDL cells from physical damage are of paramount importance.²⁰ Many methods of storage have been proposed.^6,21 Except for the pH-balanced cell culture media, all of these methods either damage the PDL cells (water and saliva²²), or at best are of limited benefit (milk). Milk has been shown to be a compatible short-term storage medium if the avulsed teeth are placed in milk within 15 to 20 minutes following avulsion.⁴ However, milk only prevents cell death; it does not restore normal cell morphology or the ability of these cells to differentiate and undergo mitosis.²³ More significantly, the studies of milk as a storage medium have been performed under ideal conditions.4 In most of these studies, teeth were extracted, immediately placed in milk, and then left for variable periods of time.4 The conclusions regarding milk as a storage medium were thus based on conditions that did not mimic actual clinical conditions.

Teeth that have been outside the mouth for 15 minutes or more should not be immediately reimplanted but rather soaked in a pH-balanced cell-reconstituting medium such as HBSS for 30 minutes and then reimplanted.^1,2 Once the teeth have been placed in HBSS, they can remain in that solution for up to 24 hours.¹ Some studies have suggested that 70% of PDL cells can remain viable for as long as 4 days in HBSS.⁴

Even if avulsed teeth are stored in saline or milk from the moment of the avulsion accident, the teeth should still be soaked in HBSS for 30 minutes prior to reimplantation. PDL cells that are stored in milk remain vital but lack the capacity for mitosis and reformation of the PDL.

Figure 2. Save-A-Tooth System.

Figure 3. Use of the Save-A-Tooth System.

Figure 4. Avulsed tooth on soft sponge.

Successful reimplantation of avulsed teeth can be achieved if the teeth are stored in an optimal storage environment (OSE) such as the Save-A-Tooth system²⁰ (Figures 2, 3, 4).  Save-A-Tooth is a 6-part system that was designed to prevent damage to the PDL cells of avulsed teeth. Each part of the system addresses a potentially damaging situation that can occur between the time of avulsion and reimplantation. Among these situations are (1) removal of debris from the root surface, (2) spillage of storage medium, and (3) removal of the avulsed tooth from the storage container. All of these situations can lead to PDL damage and thus to increased root resorption following reimplantation. The 6 parts of the Save-A-Tooth system and their functions are the following:

(1) Shatterproof container to prevent leakage of HBSS.

(2) Tightly fitting top to prevent spillage during transport.

(3) Removable basket that permits atraumatic removal of teeth.

(4) Suspension net with divider fins that permits atraumatic washing of debris from the tooth surface and prevents bumping of the avulsed tooth against the walls of the container or against another tooth.

(5) Sponge on underside of lid that allows for atraumatic removal of the avulsed tooth.

(6) HBSS, which provides optimum osmotic pressure and replacement of PDL cell metabolites.

There is space on the Save-A-Tooth container  to write the patient’s name. One suggested use of this system is in ambulances. If the accident victim has severe injuries and several teeth avulsed, emergency personnel are often reluctant to take the time to find the avulsed teeth and reimplant them. If the Save-A-Tooth system is utilized, a friend or family member can gather the teeth and place them in the container and bring it to the hospital, where the teeth can be reimplanted when the patient is stabilized.

There is little difference in clinical resorption rates of teeth reimplanted within 15 minutes and those reimplanted after many hours of storage in a Save-A-Tooth system, with less than 9% of the teeth stored in the system demonstrating moderate or severe root resorption.^1,20 The use of a Save-A-Tooth system is now considered the standard of care for avulsed teeth and is recommended for use by dentists, in ambulances, in emergency rooms, in schools, and at home.^1,18

Avulsed teeth with immature roots present a different clinical problem. These teeth are subject to root resorption but also possess the potential for pulpal revascularization.²⁴ The width of the apical foramen is not the most important factor, but rather the prereimplantation conditioning procedures. Teeth with an open apex must be treated differently than teeth with a closed apex.^1,18 Avulsed teeth with an open apex should be soaked for 5 minutes in a 1-mg/20-mL doxycycline solution to increase the chance of pulpal revascularization.^1,18 Complete revascularization appears to be dependent on the absence of bacteria in the pulpal lumen.⁴

Therefore, when treating  avulsed immature teeth, one must consider the physiologic status of the PDL cells and the potential for pulpal revascularization. If an avulsed immature tooth has been outside the mouth for 15 minutes or less, it should not be reimplanted immediately but should be soaked in the doxycycline solution for 5 minutes, then reimplanted.^1,18 In each of these situations, the teeth should be monitored every month for signs of pulpal necrosis and root resorption. If there are signs of resorption, the pulp should be immediately extirpated and apexification procedures instituted.

As an alternate approach for teeth that have been outside the mouth for more than 1 hour in a nonphysiologic medium, a regenerative therapy can be used.18 Since the PDL cells will be necrotic, they are scraped from the root surface and the tooth placed in a sodium hypochlorite solution to remove cellular debris. The root surface is then treated with Emdogain (Biora), an enamel matrix protein solution.¹⁸ Emdogain should also be placed in the socket prior to reimplantation. Emdogain has been shown to stimulate the formation of new cementum on root surfaces.^25,26

TRANSPORTATION AND CLINICAL MANAGEMENT OF AVULSED TEETH

The means by which an avulsed tooth is transported to the dentist and is then removed from the transportation device can affect the success of reimplantation.¹ Consensus recommends against touching the root surface of the avulsed tooth. This recommendation can be difficult to follow. Transport devices such as a paper tissue, handkerchief, and cotton gauze should not be used. If the tooth is transported in a glass or plastic container, the container should have a tightly fitting top so that the contents do not spill.

Retrieving an avulsed tooth from a transportation container without damaging or traumatizing the root can be difficult. The tooth may be covered in debris, which can cause the transport media to be opaque. If it is difficult to see the tooth, reaching for it blindly with a forceps will cause crushing damage to PDL cells. If the container is tipped to remove the liquid, the avulsed tooth can inadvertently fall to the counter top or floor. If the liquid is suctioned, there may not be a medium in which to place the tooth should a delay occur in reimplantation (eg, modifying the socket). The Save-A-Tooth system has a removable basket that permits atraumatic retrieval of the avulsed tooth while also retaining the storage medium if it is needed later.

Crushing damage to the PDL cells of an avulsed tooth has been shown to cause severe root resorption following reimplantation.²⁷ If a dentist is called by a patient or parent regarding transportation of an avulsed tooth, the patient should be told to place the tooth in a Save-a-Tooth, or if not available, a jar with a lid filled with cold, fresh, whole milk, and to try to avoid dry storage.

Reimplantation Stage

Prior to reimplantation, a radiograph is taken to rule out the presence of a root tip or foreign body in the socket. The presence of an alveolar fracture can also be identified. Local anesthesia is administered, and the socket is gently irrigated with sterile water, saline, or an anesthetic solution. If a clot has formed in the socket, it can be gently removed by curettage. The previously treated avulsed tooth is grasped by the clinical crown and inserted into the socket. Steady, gentle pressure should be exerted in an apical direction. It may require as long as 30 to 60 seconds to completely seat the tooth. If the tooth will not seat completely, remove it, place it in a Save-A-Tooth container, and once again curette and irrigate the socket. Surgical removal of the tooth apex is not indicated.

Figure 5. Improper splint.	Figure 6. Physiologic splint.

When the tooth is in place, it must be stabilized. There are a variety of approaches that can be used, but splinting should place the tooth in physiological function (ie, the splint should hold the tooth firmly in position while allowing slight movement; Figures 5 and 6). The occlusion should be carefully checked prior to finalizing the splint. The ideal splint utilizes orthodontic brackets and a 0.06 wire on the avulsed tooth and one tooth mesial and distal to it.

If orthodontic brackets cannot be placed, GC Fuji Ortho (GC Corporation), a resin reinforced glass ionomer, placed on the facial surface of the teeth is a good substitute. Splints involving arch bars and nylon fishing line or splints that require a channel to be cut in the teeth should be avoided. After the splint is completed, the occlusion should be checked to confirm that excessive force is not being exerted on the reimplanted tooth. In addition, a radiograph with the avulsed tooth splinted into position should be taken to ensure proper placement. Endodontic treatment should not be instituted at this time. The patient is reappointed for the following week. The patient should be prescribed a systemic antibiotic such as Augmentin 250 mg qid or doxycycline 100 mg bid for 7 to 10 days.¹⁸ A chlorhexidine rinse is used twice a day for 2 weeks, and an appropriate analgesic such as ibuprofen 600 mg q4h is prescribed. In addition, the patient is referred to a physician to determine if a tetanus prophylaxis injection should be administered. 

Since treatment of a patient with tooth avulsion is always an emergency, the following items should be available on notice (ie, on a prepared tray):

•Save-A-Tooth System (888-788-6684; Save-A-Tooth.com)

•Doxycycline capsules (100 mg)

•Orthodontic wire (0.06) and brackets

•Light-cured composite

•5-cc irrigating syringe

•Long-necked spoon excavator

•Emdogain (Biora.com). Periodontists and possibly oral surgeons are more likely to have this product in their office.

Post-reimplantation Stage

The patient should return 7 to 10 days after the reimplantation. At this appointment, the splint is checked for integrity and stability, and the tooth is anesthetized using local anesthesia. Endodontic therapy is performed in the usual fashion. A calcium hydroxide mixture such as Calasept (JS Dental) is placed in the cleansed canal, filling it completely.

CONCLUSION

Radiographic root resorption of avulsed teeth decreases dramatically when (1) the teeth are stored in an enclosed protective environment such as Save-A-Tooth and (2) the roots are conditioned prior to reimplantation. This improved success is due to a number of factors, including the recognition of different conditions of avulsed teeth and different approaches to treatment based on different clinical conditions. An appreciation of the importance of the residual PDL cells on the root surface has helped to reduce the incidence of root resorption following reimplantation of avulsed teeth.

Reference

1. Krasner P, Rankow H. New philosophy for the treatment of avulsed teeth. Oral Surg Oral Med Oral Pathol. 1995;79:616-623.

2. Matsson L, Andreasen JO, Cvek M, et al. Ankylosis of experimentally reimplanted teeth related to extra-alveolar period and storage environment. Pediatr Dent. 1982;4:327-9.

3. Cvek M, Granath LE, Hollender L. Treatment of non-vital permanent incisors with calcium hydroxide: III. Variation of occurrence of ankylosis of reimplanted teeth with duration of extra-alveolar period and storage environment. Odont Revy. 1974;25:43-6.

4. Cvek M, Cleaton-Jones P, Austin J, et al. Effect of topical application of doxycycline on pulp revascularization and periodontal healing in reimplanted monkey incisors. Endod Dent Traumatol. 1990;6:170-6.

5. Andreasen J.O. Relationship between cell damage in the periodontal ligament after replantation and subsequent development of root resorption. A time-related study in monkeys. Acta Odontol Scand. 1981;39:15-25.

6. Andreasen J.O, Reinholdt I, Dybdahl R, et al. Periodontal and pulpal healing of monkey incisors preserved in tissue culture before replantation. Int J Oral Surg. 1978;7:104-112.

7. Trope M, Friedman S. Periodontal healing of replanted dog teeth stored in ViaSpan, milk and Hank’s Balanced Salt Solution. Endod Dent Traumatol. 1992;8:183-8.

8. Lindskog S, Pierce AM, Blomlof L, et al. The role of the necrotic periodontal membrane in cementum resorption and ankylosis. Endod Dent Traumatol. 1985;1:96-101.

9. Lenstrup K, Skieller V. A follow-up study of teeth replanted after accidental loss. Acta Odontol Scand. 1959;17:503-509.

10. Kemp WB, Phillips J. Evaluation of 71 replanted teeth. J Endodon. 1977;3:30-35.

11. Andreasen JO, Hjorting-Hansen E. Replantation of teeth. I. Radiographic and clinical study of 110 human teeth replanted after accidental loss. Acta Odontol Scand. 1966;24:287-306.

12. Andreasen JO. Effect of extra-alveolar period and storage media upon periodontal and pulpal healing after replantation of mature permanent incisors in monkeys. Int J Oral Surg. 1981;10:43-53.

13. Blomlof L. Milk and saliva as possible storage media for traumatically exarticulated teeth prior to replantation. Swed Dent J. 1981;Suppl. 8.

14. Blomlof L, Otteskog P, Hammarstrom L. Effect of storage in media with different ion strengths and osmolalities on human periodontal ligament cells. Scand J Dent Res. 1981;89:180-187.

15. Lindskog S, Blomlof L. Influence of osmolality and composition of some storage media on human periodontal ligament cells. Acta Odontolog Scan. 1982;40:435-43.

16. Trope M. Clinical management of the avulsed tooth: present strategies and future directions. Dent Traumatol. 2002;18:1-11.

17. Andreasen JO. Exarticulations in “traumatic injuries of the teeth.” 2nd ed. Copenhagen, Denmark: Mungsgaard, 1981.

18. Pathways of the Pulp, Cohen S, Burns R. eds.  Trope M. Traumatic Injuries Chapt 16, p 636-37 8th Ed. Mosby, 2002 St. Louis.

19. Andreasen JO, Reinholdt J, Riis I, et al. Periodontal and pulpal healing of monkey incisors preserved in tissue culture before replantations. Int J Oral Surg 1978;7:104-10.

20. Krasner P, Person P, Preserving avulsed teeth for replantation.  J Am Dent Assoc 1992;123:80-88.

21. Haracz OM, Carnes DL, Walker WA. Determination of periodontal ligament cell viability in the oral rehydration fluid Gatorade and Milks of varying fat content. J Endodon 1997;23:687-90.

22. Andreasen JO, Andreasen FM. Essentials of traumatic injuries of the teeth, ed2, Copenhagen Denmark, 2000, Munksgaard International Publishers.

23. Courts M, Mueller WA, Tabeling JH. Milk as in interim storage medium for avulsed teeth. Pedatr Dent 1983;5:183-6.

24. Kling M, Cvek M, Mejare I. Rate and predictability of pulp revascularization in therapeutically reimplanted permanent incisors. Endo Dent Traumatol 1986;2:83-8.

25. Filippi, A, Pohl Y, von Arx T.  Treatment of replacement resorption with Emdogain preliminary results after 10 months.  Dent Traumatol 2001;17:134-138.

26. Iqbal MK. Effect of Emdogain on periodontal healing after replantation of permanent incisors in dogs.  Dent Traumatol  2001;1736-45.

27. Andreasen JO. Luxation of permanent teeth due to trauma: a clinical and radiographic follow-up of 189 injured teeth. Scand J Dent Res 1970;78:273-8.

Dr. Krasner is in private practice of endodontics in Pottstown, Pa. He is a professor in the Department of Endodontology at Temple University, School of Dentistry. He is a co-author with Dr. Sam Seltzer of the second edition of the textbook “Endodontology: Biologic Aspects of Endodontics.” He can be received at endsurg@aol.com.

THE AUTOMATED EXTERNAL DEFIBRILLATOR

AEDs are sophisticated, battery-operated (the batteries in AEDs last up to 5 years, according to the manufacturers), computerized devices that have been shown to be reliable and easy to operate. Their availability, prior to the arrival of EMS, enables lay rescuers with minimal training to administer the critically important step of defibrillation. AEDs are employed by flight attendants,¹ security personnel,² family members,³ and school-age children⁴. They are found in airports, airplanes, casinos, high-rise office buildings, shopping malls, recreational facilities and are used by healthcare professionals⁵ in ambulances, hospitals, physicians’ offices, and dental clinics.^6-8

AEDs are actually semiautomated, because the AED advises the operator that a shock is (or is not) indicated, but will not deliver the shock without the rescuer activating the unit (eg, pushing the shock button). The AED records and analyzes the ECG signal to determine if it is consistent VF (ventricular fibrillation) or pulseless VT (ventricular tachycardia), 2 conditions associated with cardiac arrest (Figures 1 and 2).⁹ The AED then advises a shock when an ECG signal consistent with these rhythms is detected. These devices are extremely accurate in their ability to analyze cardiac rhythms.¹⁰

AEDs should be employed only when cardiac arrest has been confirmed and only when all movement has ceased¹¹ (see Table 1). Failure to follow manufacturer’s instructions for use has—on rare occasions (<0.1%)—resulted in the delivery of an inappropriate shock.¹²

Before applying the AED electrodes, the rescuer must determine if any special situations exist that require modification of—or contraindicate the use of—the AED. Such situations include the following: (1) victim is <8 years of age or <25 kg (55 lb, athough recently introduced AEDs may be used in children); (2) victim is in or near standing water (eg, edge of swimming pool); (3) victim has an implanted pacemaker or ICD (implanted cardioverter/defibrillator); and (4) victim is wearing a transdermal medication patch of any type on skin where the AED electrode is to be placed. The patch should be removed and the area thoroughly dried.¹³

Although numerous manufacturers market AEDs in the United States, most operate in the same way and have similar components. The American Heart Association (AHA) recommends that AEDs be stored beside a telephone, permitting the rescuer to activate EMS rapidly and deliver the AED to the scene of the cardiac arrest promptly. Once available, the AED should be placed close to the victim’s left ear. Table 2 presents the 4 universal steps in AED operation.

Once the power is turned on (step 1), the AED’s voice prompt directs the rescuer to attach electrodes to the patient (step 2). Each adhesive pad has a diagram of the chest indicating its proper placement location (Figure 3). One electrode is placed on the upper-right sternal border directly below the clavicle; the other lateral to the left nipple, with the top margin of the pad a few inches below the axilla (Figure 4). If wet, the chest should quickly be dried. If the chest is excessively hairy, the pad may not achieve contact with the skin. The AED will indicate this by repeating “check electrodes” or “attach electrodes.” Applying firm pressure may correct this problem. If not, quickly remove the electrode (taking hair with it) and reapply a new electrode. Once properly attached, the AED prompt will state “analyzing rhythm, do not touch patient” (step 3). No one should be touching the patient as any movement might influence the rhythm analysis by the AED. Rhythm analysis takes between 5 and 15 seconds (depending upon AED brand and rhythm present). If VT or VF is detected, the AED will prompt “shock advised,” then “charging,” and finally “charged.” The next prompts will be “stand back” and “press shock button.” Before pressing the shock button, it is important to clear all persons from contact with the victim. The lead rescuer should look and say, “I’m clear, you’re clear, everybody’s clear.” Delivery of the shock should only occur after all responders are clear of the victim.¹⁴ The shock button is pressed and a sudden contraction of the victim’s musculature will be noted (step 4).

After delivery of the first shock, CPR is not restarted. It is important to deliver the second and third shocks (if needed) as promptly as possible. The AED will automatically re-analyze the rhythm, and if VF/VT is still present, the AED will announce it (“shock indicated”) and it will go through the same sequence for a second and (if needed) third shock. Following delivery of a third shock, the AED immediately prompts the rescuer to “check airway, check breathing, check pulse. If no pulse, continue CPR.”

POTENTIAL OUTCOMES AFTER DEFIBRILLATION

There are 3 potential outcomes of defibrillation: (1) VT or VF is still present; (2) VT or VF is no longer present, but there is no palpable pulse; and (3) VT or VF is no longer present and a palpable pulse is present. The following text examines these 3 outcomes individually.

(1) “Shock indicated.” VF or VT is still present. Following 3 shocks, the AED prompts the rescuer to resume CPR for 1 minute, after which the AED prompts a check for breathing and pulse and an analysis of the rhythm. If VF or VT persists, the AED will deliver additional sets of 3 shocks alternating with 60 seconds of CPR until the AED gives a “no shock indicated” message or until ACLS (advanced cardiovascular life support) becomes available.¹⁵

(2) “No shock indicated; check airway, check breathing, check pulse. If no pulse, continue CPR.” No pulse is detected. If, after delivery of any shock, the AED detects a rhythm that is neither VF nor VT, it will state that no shock is indicated. Following the delivery of 3 sets of shocks, there is a low probability that the detected rhythm can be corrected

(eg, asystole has probably occurred). CPR is resumed, but the prognosis for these victims is poor. In this situation, rhythm analysis should only be performed every 1 to 2 minutes.

(3) “No shock indicated; check airway, check breathing, check pulse. If no pulse continue CPR.” Pulse is detected. When a palpable pulse is present, but the unconscious adult victim is still apneic, rescue breathing at a rate of 1 ventilation every 5 seconds (12 per minute) is provided. If the victim is breathing adequately, place him on his side (recovery position), keeping the AED attached until the arrival of EMS personnel. Should VF or VT recur (which happens frequently) the AED will prompt the rescuer to check for signs of circulation, then proceed through the sequence described above.

TYPES OF AED

The concept underlying defibrillation is that the unit should deliver the lowest effective energy needed to terminate VF. If the energy and current are too low, VF will not be terminated; if it is too high, myocardial damage may result.

AEDs use 1 of 2 waveforms: monophasic or biphasic. Monophasic AEDs deliver current in one direction (from one electrode pad to the other). Biphasic waveforms deliver current that flows in a positive direction for a specified duration, then reverses to the negative or opposite direction in the second phase. As compared to biphasic units, more energy must be delivered with monophasic units. For monophasic AEDs, the recommended first-shock energy is 200 J (joules), second shock is 200 or 300 J, and the third shock is 360 J.¹⁶ The goal of escalating the energy dosage is to maximize success at terminating VF while minimizing myocardial damage.¹⁷ The higher shock energies (300 J and 360 J) are delivered only if the lower doses (200 J and 300 J) fail to convert the dysrhythmia. The AED automatically provides the appropriate dosage. Biphasic AEDs have been available in the USA since 1996, delivering nonescalating shocks of 150 J. Most currently introduced and available AEDs deliver biphasic waveform shocks.¹⁸

AEDS IN THE DENTAL OFFICE

Basic life support (BLS) certification is a requirement for dental licensure in many states. BLS for healthcare providers, as now defined, includes defibrillation.¹⁹ Nevertheless, no state dental board has mandated the availability of AEDs in the dental office (except where the doctor is permitted to administer parenteral conscious sedation or general anesthesia).

AEDs are easy to use, safe, have been proven to save lives, and are relatively inexpensive. (Some models are presently under $1,500.) In addition, AEDs are portable and can be taken home. (Approximately 70% to 80% of cardiac arrests occur in the home.)

In November 2002, the United States Food and Drug Administration approved the sale of AEDs to laypersons who live in home environments in which the likelihood of cardiac arrest is high.²⁰ A prescription from a medical doctor is required before a layperson can obtain an AED, which can be purchased at some pharmacies.^21,22

A CASE SCENARIO

In your office or in your home, a member of your office staff or a family member collapses. Trained in BLS, you quickly come to the victim’s side, shake the victim and yell at him, determining that he is unconscious. You yell to someone to call 9-1-1 as you start assessing the airway (head tilt-chin lift) and breathing (look, listen, feel). Noting no spontaneous respiratory efforts, you start rescue breathing—2 full, complete ventilations, seeing the victim’s chest rise each time. You next check for the carotid pulse for 10 seconds, but it is absent. Chest compression is started at a compression/ventilation ratio of 15 to 2. You yell to the person on the phone that the victim is in cardiac arrest.

When 9-1-1 is called, the primary EMS operator answers the phone within 5 to 10 seconds. You state that you have a medical emergency, then you are transferred to an EMS medical emergency operator (another 5 to 10 seconds passes). Table 3 lists the information that the caller should make available to the EMS operator.²³

You are informed that the ambulance has been dispatched. Approximately 1 minute has elapsed. The ambulance requires a variable length of time to arrive, depending on your location and local response time.

Once the ambulance arrives at the scene, the EMS personnel gather their equipment and walk into the office or house, assessing the situation. They arrive at the victim’s side and prepare the AED for use. From ambulance arrival to initiation of defibrillation is probably an additional 2 minutes.

In the preceding scenario, in all likelihood the elapsed time from the moment of collapse to the delivery of the first shock is in excess of 10 minutes. Even with the delivery of ideal BLS, the expected survival rate in this scenario is 10% or less (at 9 to 11 minutes), and between 2% and 5% (beyond 12 minutes).^24,25 These percentages could be markedly improved if the first shock was delivered after a shorter time interval following collapse. Wouldn’t you like to have a greater chance at survival if you were the victim?

Table 4.

Company Name of Unit Picture of Unit American Heart Science, Burbank, CA 91502-3115 (800) 927-9917 americanaed.com Criticare Systems, Inc. Waukesha, WI 53186-4054 (262) 798-8282 csiusa.com AccessAED Cardiac Science, Irvine, CA 92606 (949) 587-0357 (888) 274-3342 Fax: (949) 951-7315 cardiacscience.com PowerHeart AED Survivalink / FirstSave AED HeartSine Technologies, Inc. San Clemente, CA (949) 218-0092 or (866) 478-7463 heartsine.com Samaritan AED Medical Research Laboratories, Inc., Buffalo Grove, IL 60089 (800) 462-0777 (847) 520-0300 (847) 520-0303 mrlinc.com MRL JumpStart AED MRL LifeQuest AED MRL JumpStart AED MRL LifeQuest AED Medtronic Physio-Control, Redmond, WA 98073-9706 (800) 442-1142 or (425) 867-4000 medtronic.com Lifepak 500 (Philips) Heartstream, Bothell, WA 98041-3003 (800) 722-7900 Ext. 0 heartstream.com HeartStart FR2+ HeartStart Home Defibrillator HeartStart FR2+ HeartStart Home Defibrillator ZOLL Medical, Burlington, MA 01803-4420 (800) 348-9011 (781) 229-0020 zoll.com AED Plus

Table 4 lists many of the manufacturers of AEDs in the United States. Online sites offering different AEDs include aedsuperstore.com and medekit.com.

Figure 1. Ventricular tachycardia (VT).

Figure 2. Ventricular fibrillation (VF).

Figure 3. AED electrodes (adult).

Figure 4.Placement of AED pads (courtesy of Cardiac Science, Inc).

CONCLUSION

The most frequent initial rhythm in witnessed sudden cardiac arrest is ventricular fibrillation, and the most effective treatment for VF is electrical defibrillation. The probability of successful defibrillation diminishes rapidly over time; therefore, reducing the elapsed time between cardiac arrest and defibrillation is critical for successful resuscitation. The use of new automated external defibrillators in cases of out-of-hospital cardiac arrest can significantly decrease the time between collapse and defibrillation.

References

1. Wolbrink A, Borrillo D. Airline use of automatic external defibrillators: shocking developments [see comments]. Aviat Space Environ Med 1999;19:179-186.

2. Valenzuela TD, Roe DJ, Nichol G, et al. The Casino Project: implications for public access defibrillation. Academic Emerg Med. 2000;7:426.

3. Eisenberg MS, Moore J, Cummins RO, et al. Use of the automatic external defibrillator in homes of survivors of out-of-hospital ventricular fibrillation. Am J Cardiol. 1989;63:443-446.

4. Gundry JW, Comess KA, DeRook FA, et al. Comparison of naïve sixth-grade children with trained professionals in the use of an automated external defibrillator. Circulation. 1999;100:1703-1707.

5. Weisfeldt ML, Kerber RE, McGoldrick RP, et al. Public access defibrillation: a statement for healthcare professionals from the American Heart Association Task Force on Automatic External Defibrillation. Circulation. 1995;92:2763.

6. O’Rourke MF, Donaldson E, Geddes JS. An airline cardiac arrest program [see comments]. Circulation. 1997;96:2849-2853.

7. Valenzuela TD, Roe DJ, Nichol G, et al. Outcomes of rapid defibrillation by security officers after cardiac arrest in casinos. N Engl J Med. 2000;343:1206-1209.

8. Kaye W, Mancini ME. Improving outcome from cardiac arrest in the hospital with a reorganized and strengthened chain of survival: an American view [editorial]. Resuscitation. 1996;31:181-186.

9. Stults KR, Cummins RO. Fully automatic vs shock advisory defibrillators: what are the issues? J Emerg Med Serv. 1987;12:71-73.

10. Cummins RO, Eisenberg M, Bergner L, et al. Sensitivity, accuracy, and safety of an automatic external defibrillator. Lancet. 1984;2:318-320.

11. Dickey W, Dalzell GW, Anderson JM, et al. The accuracy of decision-making of a semi-automatic defibrillator during cardiac arrest. Eur Heart J. 1992;13:608-615.

12. Sedgwick ML, Watson J, Dalziel K, et al. Efficacy of out of hospital defibrillation by ambulance technicians using automated external defibrillators. The Heartstart Scotland Project. Resuscitation. 1992;24:73-87.

13. American Heart Association. BLS for Healthcare Providers. Dallas, Tex: American Heart Association; 2001:95.

14. Gibbs W, Eisenberg M, Damon SK. Dangers of defibrillation: injuries to emergency personnel during patient resuscitation. Am J Emerg Med. 1990;8:101-104.

15. American Heart Association. BLS for Healthcare Providers. Dallas, Tex: American Heart Association; 2001:101.

16. Weaver WD, Cobb LA, Copass MK, et al. Ventricular defibrillation – a comparative trial using 175-J and 320-J shocks. N Engl J Med. 1982;307:1101-1106.

17. Kerber RE, Martins JB, Kienzle MG, et al. Energy, current, and success in defibrillation and cardioversion: clinical studies using an automated impedance-based method of energy adjustment. Circulation. 1988;77:1038-1046.

18. Bardy GH, Gliner BE, Kudenchuk PJ, et al. Truncated biphasic pulses for transthoracic defibrillation. Circulation. 1995;91:1768-1774.

19. Cummins RO, Hazinski MF, Kerber RE, et al. Low-energy biphasic waveform defibrillation: evidence-based review applied to emergency cardiovascular care guidelines: a statement for healthcare professionals from the American Heart Association Committee on Emergency Cardiovascular Care and the Subcommittees on Basic Life Support, Advanced Cardiac Life Support, and Pediatric Resuscitation. Circulation. 1998;97:1654-1667.

20. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care: part 4: the automated external defibrillator: key link in the chain of survival. Circulation. 2000;102(suppl I)I-60–I-76.

21. Anonymous. A shock at home can save a life. For some people it makes sense to have an automated external defibrillator. Harv Heart Lett. 2003;13(5):6-7.

22. Anonymous, Home Defibrillation, from http://www.cvs.com.

23. Chandra NC, Hazinski MF, Stapleton E. Instructor’s Manual for Basic Life Support. Dallas, Tex: American Heart Association; 2000.

24. McIntyre KM. Cardiopulmonary resuscitation and the ultimate coronary care unit [editorial]. JAMA. 1980;244:510-511.

25. Larson MP, Eisenberg MS, Cummins RO, et al. Predicting survival from out-of-hospital cardiac arrest: a graphic model. Ann Emerg Med. 1993;22:1652-1658.

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

Figure 1. Normal sinus rhythm (NSR).	Figure 2. Premature ventricular contractions (PVCs).
Figure 3. Ventricular tachycardia (V-tach or VT).	Figure 4. Coarse ventricular fibrillation (VF).
Figure 5. Fine ventricular fibrillation.	Figure 6. Myocardial contraction ceases (asystole, “silent heart”).

SUDDEN CARDIAC ARREST
Fifty percent of people in Western society with serious coronary artery disease (CAD) experience their first signs of the disease in a dramatic way—sudden cardiac arrest.⁷ The first sign of a progressive narrowing of the coronary arteries from a decades-long development of an atheroma (intra-arterial plaque) can be a rapid sequence of plaque rupture or erosion and formation of an occluding thrombus. This arterial obstruction leads to ischemia, an irritable myocardium, a sudden generation of ventricular fibrillation, collapse, and death. Whether the victim lives or dies at this point depends on whether the collapse has been witnessed; whether the people who respond are trained in basic life support, resuscitation, and defibrillation; and whether they access an emergency response system that can bring about early arrival of BLS (basic life support) and ACLS (advanced cardiovascular life support) resources.⁸

ACUTE CORONARY SYNDROMES (INCLUDING ACUTE MYOCARDIAL INFARCTION)
Though the mortality rate from coronary heart disease has steadily declined in the United States for the past 30 years, it remains the number one cause of death.⁷ Acute myocardial infarction (AMI, aka “heart attack”) occurs in approximately 1,100,000 Americans annually.¹ As described above, an AMI usually develops when a plaque ruptures and a blood clot forms in a coronary artery, compromising blood flow to a portion of myocardium—most commonly located in the left ventricle. Deprived of blood, these now ischemic myocardial cells can no longer function normally (contracting synchronously with other myocardial cells) to pump blood out of the heart into the systemic circulation. The heart has been weakened. The victim of an AMI usually retains consciousness, but exhibits symptoms associated with decreased cardiac output as well as complaining of retrosternal pain, described variably as crushing, burning, and constricting “like there is a heavy weight on my chest” and exhibiting the classical radiation patterns associated with AMI (eg, upper epigastric region, left arm, left neck, left mandible).

Figure 7. The adult chain of survival.

Figure 8. Defibrilation converts VF to a NSR.

AMI MAY PROGRESS TO CARDIAC ARREST
From 4% to 18% of AMI’s progress to cardiac arrest.¹² Ischemia makes the myocardium irritable and more likely to depolarize prematurely, provoking irregularities in the rhythm of the heart. Frequently noted at this time are premature ventricular contractions (PVCs) (Figure 2). In a PVC, the ischemic myocardium depolarizes prematurely, before the ventricles have refilled with blood following the previous contraction. No blood is ejected from the heart into the systemic circulation with a PVC, therefore no peripheral pulse is palpable. Cardiac output decreases and the symptoms described above increase in intensity. Since the majority of heartbeats are still normal, consciousness is retained, although at a diminished level (eg, “dizzy,” “lightheaded,” “faint”).

SUDDEN CARDIAC DEATH
Fifty-two percent of deaths associated with acute coronary syndromes, including AMI, occur within the first hour following the onset of symptoms, prior to the victim reaching the hospital.⁷ In 17% of patients, ischemic pain is the first, last, and only symptom.16 Seventy to 80% of cardiac arrests occur in the home.¹⁷

SURVIVAL FROM OUT-OF-HOSPITAL CARDIAC ARREST
In the United States, fewer than 5% of victims of out-of-hospital cardiac arrest are resuscitated and survive to be discharged from the hospital neurologically intact.¹⁵ Restoration of a perfusing cardiac rhythm requires prompt implementation of BLS followed by defibrillation within a few minutes of the initial arrest. As noted, from the time of collapse until defibrillation, survival rates decrease at about 7% to 10% per minute. When defibrillation is delayed, survival rates decrease to approximately 50% at 5 minutes, 30% at 7 minutes, approximately 10% at 9 to 11 minutes, and 2% to 5% beyond 12 minutes.^23,24

References

1. 2002 Heart and Stroke Statistical Update. Dallas, Tex: American Heart Association; 2002.
2. Caffrey SL, Willoughby PJ, Pepe PE, et al. Public use of automated external defibrillators. New Engl J Med. 2002;347:1242-1247.
3. State-specific mortality from sudden cardiac death–United States, 1999. MMWR Morb Mortal Wkly Rep. 2002;51:123-126.
4. Huikuri HV, Castellanos A, Myerburg RJ. Sudden death due to cardiac arrhythmias. N Engl J Med. 2001;345:1473-1482.
5. White RD, Hankins DG, Bugliosi TF. Seven years’ experience with early defibrillation by police and paramedics in an emergency medical services system. Resuscitation. 1998;39:145-151.
6. Becker LB, Pepe PE. Ensuring the effectiveness of community-wide emergency cardiac care. Ann Emerg Med. 1993;22:354-365.
7. Gillum RF. Trends in acute myocardial infarction and coronary heart disease death in the United States. J Am Coll Cardiol. 1994;23:1273-1277.
8. International Consensus on Science. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2000;102(suppl):I-5-6.
9. Calle PA, Verbeke A, Vanhaute O, et al. The effect of semi-automatic external defibrillation by emergency medical technicians on survival after out-of-hospital cardiac arrest: an observational study in urban and rural areas of Belgium. Acta Clin Belg. 1997;52:72-83.
10. Malamed SF, Handbook of Medical Emergencies in the Dental Office. 5th ed. St. Louis, Mo: CV Mosby;2000: 000.
11. Tan WA, Moliterno DJ. Aspirin, ticlopidine, and clopidogrel in acute coronary syndromes: underused treatments could save thousands of lives. Cleve Clin J Med. 1999;66:615-618,621-624,627-628.
12. Antiplatelet Trialist’ Collaboration. Collaborative overview of randomized trials of antiplatelet therapy, part I: prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Brit Med J. 1994;308:81-106.
13. Kern KB, Hilwig RW, Berg RA, et al. Efficacy of chest compression-only BLS CPR in the presence of an occluded airway. Resuscitation. 1998;39:179-188.
14. Eisenberg MS, Hallstrom AP, Copass MK, et al. Treatment of ventricular fibrillation: emergency medical technician defibrillation and paramedic services. JAMA. 1984;251:1723-1726.
15. Weaver WD, Copass MK, Bufi D, et al. Improved neurologic recovery and survival after early defibrillation. Circulation. 1984;69:943-948.
16. Kannel WB, Schatzkin A. Sudden death: lessons from subsets in population studies. J Am Coll Cardiol. 1985;5(suppl):141B-149B.
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Dr. Malamed is a professor of anesthesia and medicine at the School of Dentistry at the University of Southern California.