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editorial

Health of the Dental Profession is Shared Concern

Facebook posting sparks conversation about what the future of dentistry looks like.

recently shared a photo on Facebook from an online card service that showed a man slapping the side of his head. The caption read “Just heard that a few Walmarts will be opening dental offices inside their stores. I bet there will be an express lane for people with 12 teeth or less.” I thought it was funny, which was why I shared the photo. You know, a little dental humor to lighten the day. As far as what impact it had on the readers of my feed, two people “liked” it; one person left a comment; and two people shared it on their pages—so it kind of went viral. Following that post, I received an e-mail from a Facebook friend, also a dentist. Saying the post rang a bell for him, he lamented the fact that dentistry is becoming more of a commodity than a health service or health profession. He spoke to the continued corporatization of dentistry and how more and more dental offices are opening in malls. And trying to discover who the dentist is in the office is getting more difficult, as these offices all have “dentist” or “dentistry” in their names, but no 4

November 2013 • The New York State Dental Journal

identification of who the dentist is. Again, lessening the personal and professional touch, making it more corporate like. My friend, who has been in dental education for most of his career, observed that the new dental schools are more involved in producing clinical dentists and in turning a profit. They seem to be eschewing the scientific basis of dentistry in favor of producing more clinically proficient dentists to address the access-to-care issue. He said basic medical sciences, research, academic inquisitiveness and standards were being downgraded, overlooked and even ignored. He hoped that dentistry was not reverting back to a time when it was considered merely a technical field and not a branch of medicine. I wrote back to him, thanking him for his thoughts. I told him I agreed that dentistry was being marketed as a commodity and that I didn’t like the trend. I explained I had written two editorials concerning both corporate dentistry and how advertising by dentists on the radio and TV seem to

NYSDA

A b st r a c t A case report on the orthodontic management of a 10-year-old female patient with Angle’s Class II Division I malocclusion, 12 mm overjet, incompetent lips, a deep bite and a lower midline shift to the right using the Twin Block of Clark is presented. Treatment objectives included reduction of the overjet and overbite, obtaining a Class I molar and canine relationship, and improving the patient’s profile. After a thorough patient assessment, a two-phase orthodontic treatment plan was chosen with myofunctional therapy using the Twin Block constituting the first phase of treatment. Second phase of treatment was to be carried out using a preadjusted edgewise appliance system. Active treatment with the Twin Block lasted for nine months. Patient’s compliance with the appliance was good, and an overjet reduction to 4.5 mm was achieved with an improvement in facial profile after the first phase of treatment. The Twin Block of Clark is a very good treatment alternative in managing selected cases of Angle’s Class II Division I malocclusion.

november 2013 • The New York State Dental Journal

Class II malocclusion presents in a wide variety of skeletal and dental configurations.1 The most consistent diagnostic finding in these patients is mandibular skeletal retrusion.2 Several treatment options are available for managing Class II malocclusions; among these is the use of functional appliances. Functional appliances encompass a range of removable and fixed devices that are designed to alter the position of the mandible, both sagittally and vertically, to induce supplementary lengthening of the mandible by stimulating increased growth at the condylar cartilage.3 The Twin Block (TB) appliance, originally developed by Clark,4 is a widely used functional appliance for the management of Class II malocclusion. Its popularity is attributed to its high patient adaptability and ability to produce rapid treatment changes.5 The appliance consists of maxillary and mandibular acrylic plates with bite blocks, which interlock at a 70-degree angle on closure, while posturing the mandible forward.6,7 Two main schools of thought exist with regard to the timing and choice of orthodontic treatment for children presenting with Angle’s Class II Division I malocclusion. One advocates an early or two-phase treatment in which the first phase commences in the mixed dentition using appliances such as the TB or other functional appliances to achieve growth modification while a second phase of treatment commences in the permanent dentition using fixed appliance therapy. The other school of thought advocates a one-phase or delayed/late treatment in which treatment is delayed until the early permanent dentition, when fixed appliance

Figure 2. Frontal view and profile view showing increased overjet.

Figure 1. Frontal view and profile view.

Figure 2. Right lateral view and left lateral view.

Figure 3. Pre-treatment study models.

Figure 4. Twin block in place in patient’s mouth.

therapy is used. A two-phase treatment plan reduces the risk of maxillary incisor trauma and need for orthognathic surgery at a later stage. In addition, the time spent in fixed appliance therapy is much shorter in children who undergo the two-phase treatment.8-10 This case report demonstrates management of a patient with a Class II Division I incisal relationship, using a two-phase treatment plan, with successful completion of the first phase of treatment using the TB appliance. Case Report The patient is a Pakistani girl, aged 10 years, 7 months. She was referred to the orthodontic clinic of the Child Dental Health Department of the Lagos University Teaching Hospital, Idi-araba. Her chief complaint was that she was unhappy with her teeth, as the top ones “stuck out.” On extraoral examination, the patient presented with a skeletal base II. She had a convex soft tissue profile with mandibular retrusion. Her lips were grossly incompetent (Jackson’s classification 1/0) with a prominent mentolabial depression. There was no transverse asymmetry when viewed frontally (Figure 1). On intraoral examination, the patient was in mixed dentition. The oral hygiene was fair. She had a Class II Division I incisor relationship, while her molar relationship was Angle’s Class II Division I, sub-division left. She had a 12 mm overjet, and her overbite was incomplete and increased. She presented with mild

spacing of the upper labial segment (4 mm) and very mild crowding of the lower labial segment (1 mm). The upper and lower posterior segments were in normal alignment. With respect to the arch width, the upper arch was constricted, while the lower arch was normal; however, there were no crossbites. Both maxillary canines were mesiopalatally rotated, and she had a lower midline shift to the right of 3 mm (Figure 2). The upper right first maxillary molar was carious. The patient had a digit sucking habit, which she started when she was toddler, but stopped when she was 4 years old. Teeth present:

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Cephalometric findings were compared to normal values for a Pakistani population.11 The cephalometric analysis confirmed the clinical finding of a Class II skeletal base relationship with a retrusive mandible and ANB of 9 degrees. Both upper and lower incisors were proclined (Table 1). Treatment Objectives l Restoration of carious lesion on the upper right first maxillary molar. l Reduce the overjet. l Reduce the overbite. l Improve the facial profile.

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l l l l l

Improve lip competence. Correct the spacing in the upper labial segment. Resolve the crowding in the lower labial segment. Correct the lower midline shift. Obtain Class I molar and canine relationships.

Treatment Alternatives l Commencing treatment immediately using “2-by-4” fixed appliance therapy (preadjusted edgewise system) while waiting for exfoliation of the second primary molars. l Delaying treatment for a few months, after which comprehensive fixed appliance therapy is commenced with two-unit extraction and reinforced anchorage in the upper arch. l Two-phase treatment consisting of removable appliance (Roberts retractor with an anterior bite plane) and then fixed appliance therapy using the preadjusted edgewise system. l Two-phase treatment consisting of functional appliance and then fixed appliance therapy. Treatment After consultation with the patient, the last option, two-phase treatment with functional appliance and fixed appliance therapy,

TABLE 1 Pre-Treatment Cephalometric Analysis

was selected. The carious lesion on the upper right maxillary molar was restored and oral prophylaxis carried out. The following treatment records were obtained: clinical photographs, study and working models (Figures 1-3). Occlusal registration for construction of the TB (squash bite) was obtained using a wax wafer of 4 mm thickness, with the mandible in a protruded position and the incisors biting edge-to-edge. Working models were sent to the lab with the squash bite in place. The appliance was fitted satisfactorily and post-insertion instructions were given. The patient was advised to wear the appliance for 24 hours a day and while eating, if possible (Figure 4). Treatment Progress A gradual reduction in the overjet was observed after a period of time, with an average overjet reduction of 1 mm per month commencing from the first month of treatment. The bite planes of the TB appliance had to be trimmed intermittently to allow for eruption of the lower first mandibular molars. After nine months of treatment, the following was achieved (Figures 5, 6): l Overjet reduction to 4.5 mm. l Normal overbite achieved. l Improvement in patient’s facial profile. l Appliance left in the mouth for retention, pending commencement of second phase of treatment.

Discussion This case shows a good treatment outcome for the first phase of treatment, which was achieved with the TB appliance. The success o o 82 SNA 80 can be attributed to three factors, namely, proper patient selection— o o pubertal growth spurt, timing of treatment and patient compliance. 80 SNB 71 Current wisdom suggests that any attempt at growth o o 2-4 ANB 9 modification should be undertaken at the peak of the pubertal growth spurt.10 The optimum timing for functional/orthoo o 111.5 UI to Frankfort plane 127 pedic treatment of Class II malocclusion is during or slightly o o after the pubertal growth spurt.12,13 From the point of view of 95.4 LI to Mandibular plane 106 occlusal development, this period correlates in most patients with the late mixed or early permanent dentition.6 The patient in this TABLE 2 case was in the late mixed dentition Cephalometric Analysis: Comparison of Pre- and Post-Treatment Cephalometric Values and, thus, at an ideal age to comMeasurement Pre-treatment Normal Post-treatment mence treatment. Considering the fact that the o o o 82 78 SNA 80 TB appliance worn by the patient o o o was a removable appliance, patient 80 72 SNB 71 compliance was also a key factor to o o o 2-4 6 ANB 9 treatment success. A major advantage of the TB appliance is its relatively o o o 111.5 115 UI to Frankfort plane 127 smaller size—it comes in two parts rather than as a mono bloc—como o o 95.4 107.5 LI to Mandibular plane 106 pared to other functional appliances. MEASUREMENT

PATIENT

NORMAL11

november 2013 • The New York State Dental Journal

Figure 5. Post-treatment extraoral views.

Figure 6. Post-treatment intraoral views.

Figure 8. Diagramatic representation of cephalometric changes after first phase of treatment. Red outline: Pre-treatment cephalometric tracing. Blue outline: Post-treatment cephalometric tracing. Figure 7. Post-treatment dental casts.

This may also enhance patient compliance and minimize speech disturbance.14 The positive outcome at the end of treatment can be attributed to skeletal and dentoalveolar changes produced by the TB appliance. Post-treatment, the patient experienced an increase in the SNB angle by one degree, from 71 degrees to 72 degrees; this was most likely a result of increased mandibular growth. In contrast, the patient experienced a slight inhibition of forward maxillary growth as the SNA reduced to 78 degrees at the end of treatment, from the pre-treatment value of 80 degrees (Table 2). This reduction in the SNA angle can be attributed to the “headgear effect” produced by the TB appliance.10 Mills and McCulloch,13 in a cephalometric study of the treatment effects of the TB appliance, reported a 1.9-degree increase in the SNB angle of the treatment group as compared to almost no change (0.3-degree increase) in the control group, while a 0.9-degree reduction was observed in the SNA, as compared to a +0.1-degree increase in the control subjects. Post-treatment, a lingual tipping of the maxillary incisors was observed in this patient, with a reduction of incisor proclination from 127 degrees to a post-treatment value of 115 degrees (Table 2). This lingual tipping may be due to the labial bow in the TB appliance, which comes in contact with the maxillary incisors during sleep, causing them to retract.15 Others have also attributed it to the contact of the lip musculature during treatment.16 Lund and Sandler17 achieved significant maxillary incisor retraction by incorporating a maxillary labial bow in the TB ap-

pliance, in contrast to Mills and McCulloch,14 who did not use a labial bow and found little change in the maxillary incisor position. Thus, the labial bow in the TB appliance plays an important role in the lingual tipping of the maxillary incisors. A slight degree of mandibular incisor proclination was observed (2.5 degrees), with an increase in angulation from 106 degrees to a post-treatment value of 107.5 degrees (Table 2). This proclination is probably due to the mesial force on the mandibular incisors produced by protrusion of the mandible.1,16 Toth and McNamara16 reported a comparable value of mandibular incisor proclination of 2.8 degrees. Other authors14,17 have also reported values of 3.8 degrees and 7.9 degrees, respectively, after TB appliance therapy. However, lower incisor proclination, although helpful in achieving the initial overjet correction, is not a goal of functional appliance treatment. The more the lower incisors are proclined, the less possibility there is for skeletal correction of the overjet. In addition, labial tipping of lower incisors is not stable over the long term and is liable to relapse.8 For these reasons, lower incisor proclination is considered a limitation of using the TB appliance. The reduction in overjet from 12 mm to 4.5 mm (Figure 8) can be attributed to the skeletal and dental changes highlighted above. Active treatment for this patient lasted for nine months, which is comparable to that reported in the literature of 6 to 15 months.8,14,18 The appliance was left in place for three months following treatment to act as a retainer, pending commencement of the second phase of treatment. At the end of the first phase of

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treatment, due to the asymmetric molar relationship present at the start of treatment, the patient had a Class 1 molar relationship on the right, but was tending toward a Class III molar relationship on the left. This would be corrected during fixed appliance therapy in the second phase of treatment. A second phase of treatment, using fixed appliance therapy, would be necessary to correct all other occlusal irregularities present and to obtain minor detailing of the occlusion. However, the use of a TB appliance in the first phase of treatment has reduced the expected duration of fixed appliance therapy in the second phase of treatment. The high risk of fracturing the maxillary incisors has also been reduced, while the patient’s facial aesthetics have been greatly improved within a reasonably short period of time without having to delay treatment until the early permanent dentition. In addition, the risk of external apical root resorption, which has been reported to be higher in one-phase than in two-phase treatments, has been reduced.9,19 Furthermore, the need for a two-unit extraction in the upper arch as part of the fixed appliance therapy or orthognathic surgery has been eliminated. Conclusion This case has demonstrated the successful management of the first phase of treatment of a patient with Angle’s Class II Division I malocclusion using the Twin Block of Clark. p Queries about this article can be sent to Dr. Isiekwe at [emailprotected].

References 1.

Jena AK, Duggal R, Parkash H. Skeletal and dentoalveolar effects of Twin Block and bionator appliances in the treatment of Class II malocclusion: a comparative study. Am J Orthod Dentofacial Orthop 2006;130-694. 2. McNamara JA Jr. Components of a Class II malocclusion in children 8-10 years of age. Angle Orthod 1981;51:177202. 3. Marsico E, Gatto E, Burrascano M, Matarese G, Cordasco. Effectiveness of orthodontic treatment with functional appliances on mandibular growth in the short term. Am J Orthod Dentofacial Orthop 2011;139:24-36. 4 Clarke WJ. The Twin Block traction technique. Eur J Orthod 1982; (4):129-138. 5. Gill DS, Lee RT. Prospective clinical trial comparing the effects of conventional Twin Block and mini block appliances: Part 1. Hard tissue changes. Am J Orthod Dentofacial Orthop 2005; 1:27:465-72. 6. Jacobson A. Book review: Twin-block Functional Therapy-Applications in Dentofacial Orthopaedics. 2nd Ed. Clark WJ. St Louis: Mosby, 2002 . Am J Orthod Dentofacial Orthop 2004;126:262-3. 7. Bacetti T, Franchi L, Toth LR, McNamara JA. Treatment timing for Twin-Block therapy. Am J Orthod Dentofacial Orthop 2000;118:159-70. 8. Mills CM, McCulloch KM. Post-treatment changes after successful correction of Class II malocclusions with the Twin Block appliance. Am J Orthod Dentofacial Orthop 2000;118:24-33. 9. Justus R. Are there any advantages of early Class II treatment? Am J Orthod Dentofacial Orthop 2008;134:717-8. 10. Gianelly AA. One-phase versus two-phase treatment. Am J Orthod Dentofacial Orthop 1995; 108:556-9. 11. Hammed A, Khan JI, Ijaz A. Soft tissue facial profile analysis in patients with Class I and Class II skeletal pattern, visiting Children’s Hospital Lahore, Pakistan. Pak Oral and Dent J 2008;Vol 28(2):183-8. 12. Hägg U, Pancherz H. Dentofacial orthopaedics in relation to chronological age, growth period and skeletal development: an analysis of 72 male patients with Class II Division 1 malocclusion treated with the Herbst appliance. Eur J Orthod 1988;10:169-76. 13. Pancherz H, Hägg U. Dentofacial orthopedics in relation to somatic maturation: an analysis of 70 consecutive cases treated with the Herbst appliance. Am J Orthod 1985;88:273-87. 14. Mills CM, McCulloch KM. Treatment effects of the Twin Block appliance: a cephalometric study. Am J Orthod Dentofacial Orthop 1998;114:15-24. 15. Gafari J, Shofer FS, Jacobsson-Hunt U, Markowitz DL, Laster LL. Headgear versus functional regulator in the early treatment of Class II Division 1 malocclusion: a randomized clinical trial. Am J Orthod Dentofacial Orthop 1998;113:51-61. 16. Toth LR, McNamara JA. Treatment effects produced by the Twin Block appliance and the FR-2 appliance of Fränkel compared with an untreated Class II sample. Am J Orthod Dentofacial Orthop 1999;116:597-609. 17. Lund DI, Sandler PJ. The effects of Twin Blocks: a prospective controlled study. Am J Orthod Dentofacial Orthop 1998;113: 104-10. 18. Gill DS, Lee RT. Prospective clinical trial comparing the effects of conventional Twin Block and mini block appliances: Part 1. Hard tissue changes. Am J Orthod Dentofacial Orthop 2005;127:465-72. 19. Brin I, Tulloch JFC, Koroluk L, Phillips C. External apical root resorption in Class II malocclusion: a retrospective review of 1-versus 2-phase treatment. Am J Orthod Dentofacial Orthop 2003; 124: 151-6.

november 2013 • The New York State Dental Journal

Transplant Patient Care

Medical and Dental Standardization for Solid Organ Transplant Recipients Mea A. Weinberg, D.M.D., R.Ph., M.S.D.; Stuart L. Segelnick, D.D.S., M.S.; Lawrence B. Kay, D.D.S.; Vinay Nair, D.O.

A b st r a c t Communication between the organ transplant team and dentist is important in formulating individualized care plans to reduce the incidence of pre- and post-transplant complications. Periodontal diseases and other oral infections may present serious risks that could compromise the success of a solid organ transplant. This article reviews why dentistry is an important component of total transplant care while the patient is on the waiting list for a transplant and after the transplantation. Recommendations regarding the care of the organ transplant patient are given. Dental clearance is the action or process of removing all acute dental disease and chronic dental conditions that can become acute. Dental clearance includes conducting pre- and post-treatment, comprehensive oral and radiographic examinations and providing a full written report that the patient has been treated. This report will be required by the medical team to inform its members that the patient’s dental status should have no effect on his or her medical treatment. There are several important factors to be considered by both the organ transplant team and the dentist before a patient can undergo a major organ transplant, including heart, kidney, lung,

liver, intestine and pancreas. Patients who are immunosuppressed due to the antirejection medications needed for successful organ transplant surgery may be at greater risk of developing systemic complications and transplant rejection relating to odontogenic inflammation and infections.1-3 Histologically, gingival connective tissue in patients taking cyclosporine, an antirejection drug, has been reported to have high levels of interleukin-6 (IL-6), which is a destructive pro-inflammatory cytokine produced by cells in the presence of inflammation.1 It has been documented that renal transplant recipients with chronic periodontitis had significantly higher serum IL-6 levels.2 Thus, inflammation and elevated serum IL-6 levels may increase the risk of organ transplant dysfunction. The dentist becomes an important part of the transplant team in controlling the cause of the inflammation (e.g., infection) before and after the surgery. Compared to being on dialysis, having a kidney transplant decreases long-term mortality and improves the quality of life.4 Therefore, it is strongly advocated for transplantation as soon as possible unless there is a direct contraindication.5 Chronic inflammation is not a direct contraindication and does not need to be eliminated before the actual transplant surgery, but it is more important to the organ’s future survival. Thus, based on the time of the actual transplant surgery, the dentist must first expedite elimination of active acute inflammation (e.g., periodontal and endodontic abscesses) by performing periodontal surgery, endodontics or extraction, and then, as best as possible, in the re-

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maining time, eliminate chronic inflammation (e.g., dental caries, periodontal disease). In addition, long-standing deep caries must be treated to prevent an acute dental “flare-up.” Knowing the relative timeframe for the impending transplant surgery will help the dentist formulate a care plan so that any acute inflammation can be eliminated as soon as possible. The main concerns of a transplant physician are whether the patient can tolerate the surgery and whether he or she is at risk for any severe infections immediately post-transplant.4,6 A care plan must be developed while the patient is on the wait list and following transplant surgery. This is universal in terms of chronic inflammation and disease. For example, transplant patients with active chronic hepatitis C and even HIV have an improved survival as compared to patients remaining on dialysis.7,8 However, although patients with chronic disease benefit from transplantation, this benefit may be less than if they did not have a chronic disease. Currently, a patient on a waiting list for an organ transplant must be evaluated by the dental professional for diagnosis and treatment of oral disease, with the objective of stabilizing his or her oral health prior to transplantation.9 Unfortunately, there is no definitive criteria assessment between the physician and the dentist regarding the level of inflammatory disease of the patient

november 2013 • The New York State Dental Journal

and the scope of therapy required to eliminate or reduce oral inflammation in the pre- and post-transplant patient.10,11 Criteria must be standardized so that all transplant centers/ clinics and dentists can communicate effectively with each other. Unfortunately, it may be years after the initial exam that the transplant physician will see the patient again. The minimal level of dental health must be defined and achieved so that medical treatment can be started. Additionally, the physician must assess whether the dental evaluation meets the requirements for transplant surgery. Currently, there are no definitive criteria for physicians and dentists to follow to determine the level of dental care needed for individual patients both pre- and post-transplant surgery. Organ-specific Dental Considerations Pre-transplant patient Dental care for the pre-transplant patient differs from that of the post-transplant patient. General dentists also need to be cognizant of the specific underlying end-stage disease in the pre-transplant patient and how to deal with it. Consultation with the patient’s physician is necessary if antibiotics or anti-inflammatory/analgesics have to be prescribed to a patient with end-stage liver or kidney disease. Several of these medications may require a decrease in dosage or an increased dosing interval, and some drugs, such as NSAIDs, should be avoided in patients with chronic kidney disease and liver cirrhosis to prevent renal failure. In addition, narcotics should be avoided or prescribed with limitations to prevent encephalopathy.12 The amount of acetaminophen should be limited to less than or equal to 2 to 3 g/d in patients with liver disease (cirrhosis) but without renal failure, and these patients monitored for adverse drug events.12 The severity of chronic kidney disease is determined by the glomerular filtration rate (GFR). These values are obtained from the patient’s physician. There may be comorbid systemic diseases that the dentist has to be aware of before rendering dental care. Dentists must take into consideration the compromised health and immune system in pre-transplant patients, which places them at increased risk for systemic and oral infections. Managing oral health before organ transplantation involves obtaining a medical consultation from the patient’s medical team regarding the need for antibiotic prophylaxis to prevent systemic infections from dental procedures. Dental management involves obtaining a dental and medical history and a dental and periodontal examination. It is best to avoid procedures that cause bleeding until a physician’s consult is obtained. The pre-transplant patient is usually taking several medications, including anticoagulants such as warfarin and antihypertensives such as beta blockers or calcium channel blockers. The dentist should know all the adverse effects of these medications, including xerostomia, orthostatic hypotension, gingival enlargement (with calcium channel blockers) and drug interactions and be prepared to avoid and manage

them.13 INR (international normalized ratio) and platelets values must be obtained in anticoagulated patients or in patients with end-stage liver disease within 24 but not more than 72 hours of performing invasive dental procedures to determine if the dental procedure can be done without complications of bleeding. After formulation of a treatment plan, any active infections Table 1 Pre-treatment Transplant Questions (answered by transplant team when assessing an organ recipient patient for referral to the dentist) 1.

What type of transplant is the patient being listed for?

What is the cause of organ failure?

List chronic medical conditions

Does the patient have any known contraindications to anesthesia or dental procedures? ( ) No ( ) Yes 5. ( ) ( ) ( )

How imminent is the transplant surgery? Within the next: Less than 1 year Greater than 1 year Unknown

6. ( ) ( ) ( )

The highest risk for infections will be during: 1-6 months Up to 1 year Indefinitely

7. ( ) ( ) ( )

The level of immunosuppression of this patient post-transplant will be: Low Moderate High

After transplantation the medical status of the patient will allow dental care: ( ) Immediately ( ) After post-transplant month ( ) Unknown Exceptions to treatment 9. ( ( ( ( ( (

) ) ) ) ) )

After transplantation the necessary medical precautions to be taken prior to dental treatment will include: Prophylactic antibiotic therapy suggested medication: Corticosteroid supplementation: Medications to be stopped: Limitations on the use of local anesthetics: Limitations on the use of epinephrine: Other suggestions:

10. Other suggestions:

must be eliminated if time allows; periodontal treatment, including surgeries, should be completed before transplantation and extraction of unrestorable teeth. The patient should be instructed about the importance of maintaining optimum oral hygiene. If the patient is undergoing hemodialysis, it is recommended that the patient have dental treatment one day after dialysis. Sometimes surgical procedures may have to be performed in a hospital setting. Post-transplant Patient Dental care of the post-transplant patient is different from that of the pre-transplant patient. Essentially, all dental treatment, except for emergencies, must be avoided for at least three and up to six months following organ transplantation, as well as in patients with organ rejection.14 This is the time it takes for the graft to be stabilized and the immune system to partially recover. If emergency dental treatment is needed before the six months are up, the patient must have antibiotic prophylaxis. The impact of organ transplantation on the general health status, including systemic low-grade inflammation, must be recognized in the post-transplant patient. The post-transplant patient will be taking many immunosuppressive medications, including cyclosporine, tacrolimus, prograf, azathioprine and corticosteroids. Cyclosporine, an immunosuppressive drug, may cause gingival enlargement, which makes oral hygiene more difficult for the patient.15-17 Additionally, patients taking a calcium channel blocker for hypertension may further aggravate the gingival enlargement.14 There are a few dental drug interactions with cyclosporine. These are: 1. erythromycin, clarithromycin (Biaxin) and fluconazole (Diflucan) may increase cyclosporine levels and can cause toxicity; 2. carbamazepine (Tegretol) may decrease cyclosporine levels; and 3. nonsteroidal and anti-inflammatory drugs such as ibuprofen should be avoided with cyclosporine because of kidney damage. Dental drug interactions with tacrolimus include erythromycin and clarithromycin, which may increase tacrolimus levels, and nonsteroidal anti-inflammatory drugs, which may cause oliguria or anuria. Tacrolimus has not been documented to cause gingival enlargement.17 Azithioprine (Imuran) is an antimetabolite that can cause bone marrow suppression by inhibiting the production of boneforming cells. Azithioprine causes leukopenia (inhibits production of white blood cells) and thrombocytopenia (decreased platelets). The complete blood count (CBC) value must be known before the start of dental treatment.13 Over the years, the rate of organ transplant success has increased due to improved screening and evaluation, as well as to newer surgical procedures and immunosuppressive drugs.18 However, oral infections can be a cause of patient morbidity and transplant dysfunction.19 The importance of treating inflammatory periodontal and dental diseases cannot be overemphasized. Knowing the degree of immunosuppression of the patient, the

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nature and severity of the oral inflammation present and the amount of time before the transplant surgery will help the dentist develop a dental treatment care plan. For example, if a patient is going to die in a few months if a transplant is not performed, or if finding a compatible donor is becoming very tenacious, then a compromise must be reached where oral disease may not be totally eliminated. Some patients may require a high level of dental treatment, including periodontal surgery and extractions, whereas other patients may require a less invasive level of care, including scaling and root planing, local drug delivery and antimicrobial mouthrinses.20 Once it has been established that the patient’s graft is stable, the following steps should be performed:13 1. The dentist must obtain a medical consultation from the patient’s transplant team to ascertain the patient’s immunosuppressive state, adrenal suppression and bone marrow suppression. There is a definite risk for infection with bone marrow suppression, and an appropriate antibiotic may be necessary after consultation with the patient’s physician. The patient usually will be taking steroids, such as prednisone, which is an immunosuppressant that prevents the body from rejecting the transplanted organ and could result in adrenal insufficiency, especially with stressful surgical procedures. Symptoms of an adrenal crisis include weakness, nausea and vomiting, and hypertension. This is a medical emergency and can be avoided with a comprehensive medical consultation. Laboratory blood values are important in evaluating the patient’s immune system and risk for infection due to immunosuppression and bone marrow suppression. Important lab values consist of: l Total white blood cell count (WBC) Normal: 4,000-10,000/ mm3 Leucopenia: < 4,000/mm3 l Absolute neutrophil count (ANC) Normal: 1,500-7,200 cells/mm3 Values below 1,500 cells/mm3 predict the risk for infection 2. Obtain INR and platelet values to determine the risk of bleeding. The patient is usually taking anticoagulants. l International Normalized Ratio (INR) Normal (not on an anticoagulant): INR 1 In order to perform invasive dental procedures the INR must be < 3.5. l Platelet count21 Normal: 150,000-400,000/mm3 For dental procedures: > 50,000/mm3 3. The patient’s blood pressure should be monitored before and after dental treatment. 4. The patient should bring in all medications taken, including over-the-counter, to avoid any potential adverse event. 5. Check for any drug interactions that could occur with the

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medications the patient is taking. In addition, many medications given to an organ transplant patient or patients with end-stage renal or liver dysfunction can cause further organ damage. Consult with the patient’s physician before prescribing any antibiotic, analgesic or anti-inflammatory agent that may require a dosage adjustment either in the amount or increase in the interval of administration. Most infections during the first month post-transplant are associated with surgical complications. Opportunistic infections usually occur from the second to the sixth month post-transplant. Beyond six months or during the late post-transplant phase, transplantation recipients suffer from the same infections seen in the general community.22 Fever secondary to odontogenic infections following successful renal transplantation has been reported.23 Complications and failures after renal transplant may be due to active viral infections.24 Nowzari et al. found the presence of cytomegalovirus (CMV) in saliva and gingival crevicular fluid of these patients with associated periodontal disease.25 Controlling oral inflammation is also important during the post-transplant period to improve organ survival.26 How to Use Data Collection Worksheets The physician should follow specific guidelines and criteria relating to the patient’s pre-transplant inflammatory state and then forward the results to the treating dentist. This information will help the dentist formulate an individualized treatment plan for the patient. Furthermore, the dentist can then inform the physician about the patient’s post-transplant dental/periodontal inflammatory condition and how the patient can be maintained. Periodontal inflammation is extremely important in controlling both the morbidity and mortality rates in patients on hemodialysis as well as in post-transplant patients.27,28 This is accomplished by identifying the inflammatory oral risk factors and other non-oral risk factors, such as heart conditions, obesity and tumors.29 The dentist needs to know how much inflammatory disease is acceptable for the surgery to proceed and what is the level of disease or what level of dental health can be attained that is acceptable for medical treatment. In order to answer these questions a risk assessment must be performed. We are proposing a series of easy-to-follow care plan recommendations for the preand post-transplant patient that are based on the medical and dental expertise of the authors of this article. These recommendations should be utilized for clinical assessment and as guidelines by the organ transplant team and referring general dentists and periodontists. Physicians generally do not have the same in-depth understanding of dental disease and how to treat it as dentists do. Therefore, they may have difficulty relaying to the dentist their pre- and post-medical/dental requirements. These care plan recommendations are designed to bridge this gap. They will provide

the dentist with knowledge of what the physician feels is the minimal dental health the transplant patient may have prior to transplant surgery, the timeframe the dentist has to work within and the medical restrictions placed on the dental treatment. Once a dentist has this information, he or she will be able to develop a tailored treatment plan for the patient. If the physician’s expectations cannot be attained, then further consultation with the physician and dentist is necessary. Table 1 lists specific questions that are answered by the transplant coordinator and sent with an introductory referral letter to the dentist. Table 2 contains selective questions that need to be filled out by the dentist and sent back to the transplant coordinator. The answers to these questions will determine the care plan while the patient remains on the wait list and post-transplant. Additionally, a standardized form (Table 3) pertaining to dental care for the post-transplant patient should be recorded by the dentist and communicated to the transplant team. Conclusions Prudent management of transplant patients is essential prior to their surgery, postsurgically and over the remainder of their lives. Currently, there is no definitive guidance from the transplant physician and dentist regarding the dental needs of transplant patients. The development of care plan recommendations will enable more comprehensive medical and dental treatment of immunosuppressed patients through better communication between the transplant physician and dentist. These recommendations will help treating doctors formulate a comprehensive patient management program. The guidelines presented here were developed in response to a lack of direction with regard to the dental needs of transplant patients. The forms are based upon our clinical experiences and the result of communication between dentists and transplant physicians. To date there are no studies linking patients’ dental health and complications with transplants. At this time we really do not know what constitutes “clearance” for these patients or how much inflammation is tolerable. Future work needs to be done, including surveying multiple transplant centers to better understand what the transplant physician is asking for. We need to educate physicians as to what is practical for the dentist to accomplish. A recent article found that there was a major concern regarding underutilization of preventive dental services in medically transplant children undergoing renal and liver transplants.15 Many dentists may not feel comfortable in pre- and postoperative monitoring and treating these patients as well as other transplant patients. The intent of these forms is to ease the responsibility of the dentist and improve preventive care by providing better communication with the physician and by giving the physician a better understanding of what the dentist must accomplish during patient care. It is just as important to recognize that when the dentist is communicating with the physician, the dentist is actually requesting a

Table 2 Pre- and Post-transplant Patient Assessment. To be filled out by the dentist (check in the box after procedure is completed) and sent to the transplant physician. 1. Recommended therapies prior to transplantation: a. b. c. d. 2.

Expected time until completion of treatment:

Recommended ongoing care for patient (pre- or post-transplant) a. b. c. d.

Full mouth radiograph taken: date:

Treating Acute Dental Disease Presence of dental caries: Tooth number and surface: Treated (tooth # & restoration): Endodontically treated? Endodontically involved teeth (e.g., acute or chronic abscess) Tooth number: Treated: Teeth requiring extraction # Treating Chronic Dental Disease Root caries Tooth number: Treated (tooth # & treatment) Ailing, failing or failed implants Tooth number: Treated: Periodontal Diseases Treating Acute Periodontal Conditions Necrotizing ulcerative gingivitis or necrotizing ulcerative periodontitis Periodontal abscess Treating Chronic Periodontal Conditions Chronic gingivitis (localized or generalized; severity: mild, moderate or severe) Circle: plaque-induced, medication-induced, systemic disease-induced Treatment: Is patient adherent to plaque control ( ) NO ( ) YES Periodontal abscess o Chronic periodontitis Circle: localized or generalized Circle: severity: mild, moderate or severe risk factors Circle all that apply: plaque-induced; smoking; diabetes or other treatment: Is patient adherent to plaque control ( ) NO ( ) YES Aggressive periodontitis Circle: localized or generalized Circle: severity: mild, moderate or severe o Status of third molars Impacted third molars should be extracted List tooth number: Treatment:

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medical consultation rather than a medical clearance from the transplant physician. Essentially, the dentist needs to know about the patient and how well he or she will be able to get through a dental procedure.30 These recommendations or guidelines give the dentist an idea of the patient’s medical status, timelines and postsurgical needs prior to the transplant surgery. The dentist will be able to assess whether he or she can meet the physician’s expectations. If not, then further communication needs to be initiated between the dentist and the physician. Once the transplant physician and dentist come to a consensus, they will be able to inform the transplant patient what is expected of them both before and after transplant surgery. Post-transplant dental care is often overlooked. These guidelines give the dentist follow-up guidelines for postsurgical care. Periodontal diseases and dental caries must be monitored in these patients to lessen the incidence of life-threatening postsurgical infections. Furthermore, post-transplant patients are usually severely immunosuppressed from medications taken to prevent rejection of the organ. p Queries about this article can be sent to Dr. Segelnick at [emailprotected].

Table 3 Dental Care Guidelines for Post-transplant Recipients 1. Medical history a. Consult with transplant physician b. Medications (e.g., cyclosporine, calcium channel blockers) c. Antibiotic prophylaxis for periodontal maintenance visits o Medication usage ( ) Presence of medication-induced gingivitis Circle: cyclosporine, nifedipine, tacrolimus, sirolimus Dosage: o Antibiotic prophylaxis required ( ) Yes Antibiotic & dosage: ( ) No 2.

Radiographs as needed

Oral a. b. c.

Reinforce oral hygiene a. Devices used (e.g., soft-bristled toothbrush, interdental) b. Technique (e.g., modified Bass)

Gingival and periodontal assessment (gingival evaluation, bleeding, probing depths)

Caries assessment a. Fluoride application

Prescribe antimicrobial mouthrinse, if needed

Three-month maintenance schedule

hygiene assessment Nonadherent Good Improving

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References 1.

Atilla G, Kutukculer N. Crevicular fluid interleukin-1beta, tumor necrosis factor-alpha, and interleukin-6 levels in renal transplant patients receiving cyclosporine A. J Periodontol 1998;69(7):784-790. 2. Ioannidou E, Kao D, Chang N, et al. Elevated serum interleukin-6 (IL-6) in solid organ transplant recipients is positively associated with tissue destruction and IL-6 gene expression in the periodontium. J Periodontol 2006;77(11):1871-1878. 3. Raasveld MH, Bloemena E, Wilmink JM, Surachno S, Schellekens PT, ten Berge RJ. Interleukin-6 and neopterin in renal transplant recipients: A longitudinal study. Transpl Int 1993;6:89-97. 4. Wolfe RA, Ashby VB, Milford EL, Ojo AO, Ettenger RE, Agodoa LYC, Held PJ, Port FD. Comparison of mortality in all patients on dialysis, patients on dialysis awaiting transplantation, and recipients of a first cadaveric transplant. N Engl J Med 1999;341:1725-1730. 5. Meier-Kriesche HU, Prort FK, Ojo AO, Rudich SM, Hanson JA, Cibrik DM, Leichtman AB, Kaplan B. Effect of waiting time on renal transplant outcome. Kidney International 2000;58:1311-1317. 6. Silverstein DM. Inflammation after renal transplantation: role in the development of graft dysfunction and potential therapies. J Organ Dysfunction 2009;5(4):233-241. 7. Stock PG, Barin B, Murphy B, Hanto D, et al. Outcomes of kidney transplantation in HIVinfected recipients. N Engl J Med 2010 Nov 18;363(21):2004-14. Erratum in: N Engl J Med 2011 Mar 17;364(11):1082. 8. Roth D, Gaynor JJ, Reddy KR, et al. Effect of kidney transplantation on outcomes among patients with Hepatitis C. J Am Soc Nephrol 2011 Jun;22(6):1152-60. Epub 2011 May 5. 9. Segelnick SL, Weinberg MA. The periodontist’s role in obtaining clearance prior to patients undergoing a kidney transplant. J Periodontol 2009;80 (6):874-876. 10. Cochran D. Shifting the paradigm of treatment of periodontal diseases – implications for patient care. AAP News 2009; April-June:11. 11. Guggenheimer J, Mayher D, Eghtesad B. A survey of dental care protocols among US organ transplant centers. Clin Transplant 2005;19:15-18. 12. Chandok N, Kymberly DS. Pain management in the cirrhotic patient: the clinical challenge. Mayo Clinic Proc 2010, 85(5): 451–458. 13. National Institute of Dental and Craniofacial Research. Dental Management of the Organ Transplant Patient. www.nidcr.nih.gov (Accessed August 15, 2011). 14. Ganda K. Organ transplants, immunosuppressive drugs, and associated dental management guidelines. In: Dentist’s Guide to Medical Conditions and Complications. 1st Ed. Wiley-Blackwell 2008:467-472. 15. Shiboski CH, Kawada P, Megan G, Tornabene A, Krishnan S, Mathias R, Den Besten P, Rosenthal P. Oral disease burden and utilization of dental care patterns among pediatric solid organ transplant recipients. J Public Health Dent 2009;69(1);48-55. 16. Kilpatrick NM, Weintraub RG, Lucas JO, Shipp A, Byrt T, Wilkinson JL. Gingival overgrowth in pediatric heart-lung transplant recipients. J Heart Lung Transplant 1997;16:1231-1237. 17. Greenberg KV, Armitage GC, Shiboski CH. Gingival enlargement among renal transplant recipients in the era of new-generation immunosuppressants. J Periodontol 2008;79:453:460. 18. Provenzano R. The importance of dental care for transplant recipients. Renalife 2005;21(1):12. 19. Schander K, Jontell M, Johansson P, Nordén G, Hakeberg M, Bratel J. Oral infections and their influence on medical rehabilitation in kidney transplant patients. Swed Dent J 2009;33(3):97-103. 20. Cerveró AJ, Bagán JV, Soriano YJ, Roda RP. Dental management in renal failure: patients on dialysis. Med Oral Pathol Oral Cir Bucal 2008;1:13(7):E419-426. 21. Radmand R, Schilsky M, Jakab S, et al. Pre-liver transplant protocols in dentistry. Oral Surg Oral Med Oral Pathol Oral Radiol 2013;115:426-430. 22. Patel R, Paya CV. Infections in solid-organ transplant recipients. Clin Microbiol Rev 1997;10(1): 86-124. 23. Wilson RL, Martinez-Tirado J, Whelchel J, Lordon RE. Occult dental infection causing fever in renal transplant patients. Am J Kidney Dis 1982;2(3):354-356. 24. V. Jha. Post-transplant infections: an ounce of prevention Indian J Nephrol. 2010 October; 20(4):171–178. 25. Nowzari H, Jorgensen MG, Aswad S, Khan N, Osorio E, Safarian A, Shidban H, Munroe S. Human cytomegalovirus-associated periodontitis in renal transplant patients. Transplant Proc 2003;35(8):2949-2952. 26. Naugle K, Darby ML, Bauman DB, Lineberger LT, Powers R. The oral health status of individuals on renal dialysis. Ann Periodontol 1998; 3:197-205. 27. Yeun JY, Levine RA, Mantadilok V, Kaysen GA. C-reactive protein predicts all cause and cardiovascular mortality in hemodialysis populations. Am J Kidney Dis 2000;35: 469-476. 28. Lobo SM, Lobo FR, Bota DP, Lopes-Ferreira F, Soliman HM, Mélot C, Vincent JL. C-reactive protein levels correlate with mortality and organ failure in critically ill patients. Chest 2003;123: 2043-2049. 29. Jofre´ R, Rodriguez-Benitez P, Lo´pez-Go´mez JM, Pe´rez-Garcia R. Inflammatory syndrome in patients on hemodialysis. J Am Soc Nephrol 2006;17: S274–S280. 30. Gary CJ, Glick M. Medical clearance: an issue of professional autonomy, not a crutch. J Am Dent Assoc 2012 Nov;143(11):1180-1.

Trauma Treatment

Surgical Exposure and Crown Lengthening for Management of Complicated Fractures of Maxillary Anterior Teeth A Case Report Pradeep S. Anand, M.D.S.; Sukumaran Ashok, M.D.S.; K. Nandakumar, M.D.S.; N.O. Varghese, M.D.S.; Kavitha P. Kamath, M.D.S. A b st r a c t When a tooth fracture occurs, the fracture line can extend in a variety of directions, and the direction of the fracture line often dictates the treatment plan. In cases where fracture lines extend apical to the gingival margin, exposure of fractured margins becomes necessary. And management of such tooth fractures often requires an interdisciplinary approach involving endodontic, periodontic and restorative procedures. This article describes a case in which severely traumatized maxillary anterior teeth were managed by a combined approach involving surgical exposure and crown lengthening, endodontic and restorative procedures. Dental injuries are a common occurrence in patients who have suffered trauma to the middle-third of the face. These injuries to the teeth can range from minor craze lines in enamel to avulsion of the tooth. The most commonly affected teeth are usually the maxillary incisors.1 When fracture of a tooth occurs, the fracture line may extend in a variety of directions, and the direction of the fracture line often dictates the treatment plan. A crown fracture with a subgingivally

located fracture line poses a significant challenge to the dentist. This is because a subgingival fracture presents problems in completing endodontic and restorative procedures.2 Problems encountered in endodontic therapy include difficulty in establishing adequate isolation, which, in turn, can affect the cementation of endodontic posts. Moreover, as preparation of adequate margins for a crown becomes difficult in cases of a subgingival fracture, such a fracture may contribute to future periodontal breakdown if the margins of the restorations are placed apical to the gingival margin. Hence, in cases where fracture lines extend apical to the gingival margin, exposure of fractured margins becomes necessary and management of such tooth fractures often requires an inter-disciplinary approach involving endodontic, periodontic and restorative procedures. Exposure of tooth margins can be achieved by various techniques. These include surgical crown lengthening,2-4 orthodontic extrusion2,5-8 and surgical repositioning.2,9,10 Crown lengthening is a periodontal resective procedure that removes supporting periodontal structures to expose sound tooth structure coronal to the alveolar crest level. Traditionally, endodontic, crown lengthening and restorative procedures are performed in a staged manner, with the crown-lengthening procedures usually performed after completion of endodontic treatment and prior to finalization of tooth preparation. However, in situations where the fracture lines are entirely subgingival, the execution of the endodontic treatment may be difficult unless the tooth margins are exposed by surgical procedures.

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Figure 1. Preoperative view; labial aspect.

Figure 4. Incisions for crown-lengthening procedure.

Figure 2. Preoperative view; occlusal aspect.

Figure 5. After ostectomy.

Crown-lengthening procedures are performed in cases of subgingival tooth fractures to expose the tooth margins and, also, in situations in which a tooth has a short clinical crown considered inadequate for the retention of cast restorations.3 This report describes a case in which surgical exposure and crown lengthening were performed prior to endodontic treatment for management of fractured maxillary anterior teeth. Case Report A healthy 24-year-old male patient was referred to the Department of Periodontics from the Department of Oral and MaxilloFacial Surgery of the Government Dental College, Trivandrum, India, with the complaint of fractured maxillary anterior teeth. The injury had occurred as a result of an alleged assault seven days prior. Clinical examination revealed complicated crown fractures of the maxillary right first premolar, canine, lateral and central incisors, and maxillary left central incisor, with complete loss of coronal tooth structure (Figures 1, 2). The fracture lines were located entirely subgingivally. The maxillary left lateral incisor had been stabilized to the adjacent canine with a stainless steel wire splint at the Department of Oral and Maxillo-Facial Surgery. Radiographic examination revealed the extent of the fracture lines and the level of the alveolar crest (Figure 3). The patient was informed about the prognosis of the teeth and the available treatment options. After having been given the options of either an inter-disciplinary approach to retain the

november 2013 • The New York State Dental Journal

Figure 3. Preoperative periapical radiographs.

Figure 6. Flap displaced apically.

Figure 7. Suturing done.

teeth or extraction of fractured teeth followed by prosthetic replacement with removable or implant-supported prostheses, the patient opted for the former. Hence, after consultation with the Department of Conservative Dentistry and Endodontics, a treatment plan was arrived at that included surgical crown lengthening for exposure of the fractured margins, followed by endodontic and restorative treatment procedures. The patient was informed in detail about the treatment plan, and written consent was obtained prior to initiating the treatment procedures. Crown lengthening was performed under local anesthesia. After removal of the stainless steel wire splints, sulcular and vertical incisions were placed and a full thickness flap was raised on the labial aspect in relation to the fractured teeth (Figure 4). On the palatal aspect, an internal bevel incision was placed to resect the gingival tissue to obtain adequate exposure of the fracture margins. Ostectomy and osteoplasty were performed using rotary instruments to achieve exposure of sufficient tooth structure coronal to the alveolar crest to facilitate placement of the restoration without violating the zone of supra-crestal gingival tissues. Bone removal was performed on the labial and palatal aspect of the roots, as well as from the inter-dental regions (Figure 5). The labial flap was displaced apically (Figure 6), and the flaps were sutured at the level of the alveolar crest with interrupted silk sutures (Figure 7). The surgical site was covered with a periodontal dressing, and the patient was prescribed postoperative systemic antibiotics (amoxicillin 500 mg three times a day for 7 days), analgesics

Figure 8. Three weeks after crown lengthening.

Figure 9. After placement of cast post and core; labial view.

Figure 10. After placement of cast post and core; palatal view.

Figure 12. Post-treatment view; labial aspect.

Figure 13. Post-treatment view; palatal aspect.

Figure 14. Extraoral photograph before placement of restorations (A) and after placement of restorations (B).

(combination of aceclofenac 100 mg and paracetamol 500 mg twice daily for 5 days) and 0.2% chlorhexidine gluconate oral rinse for two weeks. The patient was also advised to avoid brushing at the surgical site until the removal of sutures, which was done 10 days after the surgery. Adequate exposure of the tooth structure to perform endodontic and restorative procedures was achieved (Figure 8). Following the crown-lengthening procedure, the teeth had become mobile. However, this mobility subsided four weeks after surgery. Endodontic treatment was performed on the teeth, and the root canals were obturated with gutta-percha by the sectional technique. Due to the subsequent development of a periapical abscess, endodontic treatment was performed on the maxillary left lateral incisor also. Following endodontic treatment, the teeth were restored with cast post and core restorations (Figures 9-11), and vitallium crowns with ceramic facings were placed four months after surgery (Figures 12-14). Favorable tissue healing had occurred and there was no mobility or pocket formation in relation to the restored teeth. The patient was satisfied with the results of the treatment. Discussion Traumatic injuries with loss of tooth structure in the incisor region are common, especially among children and young individuals. In certain situations, the fracture line may extend apical to the gingival margin or crest of the alveolar bone. In these instanc-

Figure 11. Radiograph after placement of cast post and core.

es, in order to facilitate proper restoration of the teeth, surgical intervention in the form of a crown-lengthening procedure is required. Other treatment options for exposure of the fracture lines include orthodontic extrusion and surgical repositioning. Anterior teeth with coronal fractures can be managed without surgical invasion if the biologic width of the tooth is not violated by the apical extent of the fracture, provided the residual root structure possesses an adequate ferrule. In such clinical situations, orthodontic extrusion can be employed to expose the fractured margins.7 Orthodontic extrusion has also been termed forced eruption, orthodontic eruption and assisted eruption. It can be achieved with either fixed or removable appliances.11 It is a conservative procedure that, unlike surgical crown lengthening, does not involve loss of bone or periodontal support and does require application of tractional forces in all regions of the periodontal ligament to simulate marginal apposition of crestal bone.5 When a root is orthodontically erupted, the attachment apparatus and gingiva may follow to a further coronal position at the adjacent teeth.6 This may necessitate periodontal surgical procedures to correct any discrepancy in the levels of periodontium at adjacent teeth.5 In rapid extrusion, where higher forces are used, the coronal migration of the supporting tissues may be reduced. But this carries the risk of injury to the periodontium and root resorption.5 Surgical extrusion refers to repositioning of the root to the desired position coronally and securing it with simple sutures in

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the soft tissues.2,9,10 The limitations of this procedure include the difficulty of surgically luxating a fractured tooth without damaging the periodontal ligament, as any damage to the periodontal ligament on the root surface may prevent reattachment.2 Orthodontic or surgical extrusion can be performed in cases of isolated tooth fractures. When multiple adjacent teeth are involved, clinical crown-lengthening procedures need to be performed to expose sufficient tooth structure for restorative purposes.12 In the case presented here, the patient was given an alternative option of extraction and prosthetic replacement of the teeth. As the patient opted not to undergo extraction, a treatment plan was formulated involving exposure of tooth structure, followed by endodontic and restorative procedures. As multiple teeth were involved in the esthetic zone, a decision was made to perform crown lengthening to achieve the desired exposure of tooth structure. Crown lengthening is a periodontal resective procedure aimed at removing supporting periodontal structures to gain sound tooth structure coronal to the alveolar crest. Crown-lengthening procedures are performed in cases of subgingival or subcrestal root fracture; perforations of the root at the coronal third; caries with subgingival extension; excessive wear of the dentition; or presence of previous subgingival margins of restoration.12,13 Clinical crown lengthening is indicated in these situations to gain additional tooth structure to meet the mechanical need of the restorative procedures.14 Besides these functional and biological reasons, crown-lengthening procedures can be performed for esthetic reasons in cases where there are short clinical crowns, excessive wear, uneven gingival contours or an excessive gingival display.15,16 Although crown-lengthening procedures are usually performed after completion of endodontic treatment, as in the case here, where the fracture lines are entirely subgingival, surgical exposure and crown lengthening can be performed as the initial procedure to facilitate both endodontic and restorative procedures. Periodontal health is of paramount importance for all teeth, both sound and restored. Crown-lengthening procedures are based on biologic principles that can be determinants for successful treatment. These procedures enable the clinician to develop an adequate area for crown retention without extending the crown margins deep into the periodontal tissues, an area referred to as the biologic width,14 the portion of the root surface occupied by the junctional epithelium and gingival connective tissue. Gargiulo et al., in their study of human cadavers, reported that the connective tissue attachment occupies 1.07 mm of space coronal to the crest of the alveolar bone and that the junctional epithelium occupies another 0.97 mm of space coronal to the connective tissue attachment.17 Vacek et al. reported the dimension of epithelial attachment to be 1.14 mm and that of the connective tissue attachment to be 0.77 mm.18 According to their

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study, the biologic width of the anterior teeth was 1.75 mm; for premolars it was 1.97 mm; and for molars it was 2.08 mm. If the restoration margin is placed into this area, the crestal bone will be lost to re-establish the biologic width.19 It may also lead to gingival inflammation and pocket formation.12,19 Crown-lengthening procedures enable the clinician to expose adequate clinical crown in order to prevent the placement of the crown margin into the area of the biologic width. Besides the biologic width, prevention of violation of a zone known as supracrestal gingival tissue (SGT) is also considered important.20 SGT refers to the tissues located coronal to the alveolar crest extending up to the gingival margin, that is, connective tissue attachment, junctional epithelium and sulcular tissue. Gargiulo et al. reported in their study that the sulcular depth was approximately 0.69 mm. When combined with the biologic width, the dimension of the SGT comes out to be approximately 2.73 mm.17 Vacek et al. reported the value of SGT to be approximately 3.23 mm.18 In a recent study to determine the dimensions of SGT among 100 dental students, Barboza et al.21 reported that the dimensions of the SGT ranged from 1 mm to 6 mm, with a mean value of 3.3 mm (3.4 mm in males and 3.2 mm in females). They also reported that there were no significant differences between contra-lateral measurements, suggesting that the SGT dimension at a fractured tooth can be determined preoperatively by examining the contra-lateral tooth. Causes for the violation of the SGT include root fracture, restorative procedures and dental caries. As violation of SGT can result in gingival inflammation and bone loss to re-establish this dimension, prevention of this violation is critical to the maintenance of a healthy periodontium. Although gingivectomy can be performed to eliminate the soft tissue that forms the pocket or sulcus wall, it cannot increase the clinical crown length, as no bone removal is done. The fact that traumatically fractured teeth usually have a healthy periodontium makes it difficult to achieve crown lengthening by a simple gingivectomy.2 Hence, bone margin must also be removed to achieve lengthening of the clinical crown. As a minimum width of attached gingiva is desirable for the long-term success of the restored tooth, care should also be taken to preserve the width of attached gingiva. This can be performed by a flap surgery where ostectomy can be performed for crown lengthening in combination with an apically displaced flap.22 Thus, crown-lengthening procedures aid in bone removal and apical repositioning of soft tissues to permit formation of a new SGT complex. Bone removal can be done using rotary instruments in the presence of copious irrigation. During the osseous recontouring, care should be taken to establish a positive osseous architecture.20 Requirement for bone removal is often greater in the inter-proximal areas than on the buccal and lingual surfaces, and this interproximal bone height reduction should be accompanied by reduction of bone height on the buccal and lingual surfaces so that

bone levels in these areas will remain apical to the inter-proximal bone level. The amount of bone removal required depends upon the future position of the restoration margins and the SGT dimension for that particular patient.12 A sufficient amount of bone has to be removed to create a 3 mm zone of SGT around the tooth to be restored. Herrero et al., in a study to compare the actual amount of supracrestal tooth length obtained during surgical crown-lengthening procedures with the presurgically desired amount, reported that a proposed minimally desired 3 mm distance from planned restoration margin to alveolar crest was not routinely achieved, irrespective of the experience of the clinician.23 However, in a 12-month radiographic study evaluating the results of crownlengthening surgery, Diniz et al.24 reported that the overall mean distance from the restorative margin to the alveolar crest achieved after osseous resection was 3.28 mm at mesial and 2.81 mm at distal sites. They also reported that no significant radiographic changes in the bone crest were observed during a 12-month healing period. The time interval between the surgical procedure and final preparation and placement of restoration is also critical. It is determined by the stability of the postsurgical position of the marginal periodontal tissues. Pontoriero and Carnevale, in a 12-month clinical study of wound healing following surgical

crown lengthening, reported that the marginal periodontal tissue showed a tendency to grow coronally from the level defined at surgery.25 The postsurgical growth of the gingival margin at various time intervals after surgery was more in the inter-proximal region than at buccal or lingual sites. The postsurgical coronal displacement of the gingival margin observed at both sites was statistically significant when compared to the level achieved after surgery. It has also been reported that the closer the flap margin is sutured to the alveolar crest, the greater the tissue rebound during the postsurgical period. Studies have shown that there is a significant tissue rebound following crown-lengthening surgery; the amount of tissue rebound seems related to the position of the flap relative to the alveolar crest at suturing.26 Hence, it is important that proper crown height be established during surgery without over-reliance on flap placement at the osseous crest. Although it is recommended that preliminary preparation of the teeth with placement of temporary restorations be performed prior to the crown-lengthening procedure, it has also been suggested that, on account of this postsurgical coronal growth of the marginal periodontium, the final preparation and restoration be delayed for 12 months after the crown-lengthening procedure and that any intermediate preparations be delayed for at least six weeks after surgery.12 In situations where the final restorations cannot be delayed, it has been recommended that,

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during the first three to six months of the postsurgical period, the restoration margins can be placed minimally coronal to the gingival margin so that when the tissues grow coronally, the restorations margins may be located at an acceptable subgingival position.20 A technique of crown lengthening with simultaneous tooth preparation has been suggested as a method for a more accurate placement of the restoration margin in relation to the alveolar crest.4 This technique also offers the additional advantage of reducing the treatment time. In the case presented here, because of the complicated nature of the tooth fractures, which necessitated surgical exposure to facilitate endodontic treatment, crown lengthening was also performed as an initial procedure without any preliminary tooth preparation or placement of temporary restorations. Potential complications of crown-lengthening procedures include the possibility of furcation involvement in the case of molars27 and migration of teeth.28 Although crown lengthening is a useful technique in managing teeth with short clinical crowns, decisions regarding use of this approach should be made judiciously. Due to the invasive and irreversible nature of the procedure, this approach should be used with caution. Crown-lengthening procedures are contraindicated in teeth with deep carious lesions or fractures that result in nonrestorable situations, in teeth with unfavorable crown-toroot ratio because of short roots or reduced bone support, and in posterior teeth where exposure of the furcation region may occur as a result of the procedure.29 Since crown lengthening is a surgical procedure, other factors to be considered include the potential for damage to surrounding anatomic structures, as well as the systemic health of the patient. Conclusion Proper management of fractured teeth with extensive loss of coronal tooth structure often requires an interdisciplinary approach. The location of the fracture line, as well as the periodontal status of the involved teeth, play important roles in proper treatment decisions. In cases of multiple tooth fractures occurring apical to the gingival margin, crown-lengthening procedures are a valuable treatment approach for exposure of the fracture lines. In an interdisciplinary approach, although the various treatment procedures are generally performed in a staged manner, which usually involves endodontic therapy followed by crown lengthening and finally restorative therapy, the sequence of treatment may be altered in accordance with the clinical situation. As in the case presented here, when surgical exposure and crown lengthening are performed as initial procedures, they will enable the clinician to perform endodontic and restorative procedures properly and contribute to the long-term retention of such teeth. p Queries about this article can be sent to Dr. Anand at [emailprotected].

november 2013 • The New York State Dental Journal

References 1. Bastone EB, Freer TJ, McNamara JR. Epidemiology of dental trauma: a review of the literature. Aust Dent J 2000 Mar;45(1):2-9. 2. Lovdahl PE. Periodontal management and root extrusion of traumatized teeth. Dent Clin North Am 1995 Jan;39(1):169-179. 3. Takei HH, Azzi RR, Han TJ. Preparation of the Periodontium for Restorative Dentistry. In: Newman MG, Takei HH, Carranza FA, editors. Clinical Periodontology. 9th ed. Pennsylvania: Saunders; 2003, p. 943-948. 4. Park JB. Restoration of the severely decayed tooth using crown lengthening with simultaneous tooth-preparation. Eur J Dent 2010 Apr;4(2):197-201. 5. Bach N, Baylard JF, Voyer R. Orthodontic extrusion: periodontal considerations and applications. J Can Dent Assoc 2004 Dec;70(11):775-780. 6. Kozlovsky A, Tal H, Lieberman M. Forced eruption combined with gingival fiberotomy. A technique for clinical crown lengthening. J Clin Periodontol 1988 Oct;15(9):534-538. 7. Valerio S, Crescini A, Pizzi S. Hard and soft tissue management for the restoration of traumatized anterior teeth. Pract Periodontics Aesthet Dent 2000 Mar;12(2):143-150; quiz 152. 8. Spear FM, Cooney JP. Periodontal-Restorative Interrelatioships. In: Newman MG, Takei HH, Carranza FA, editors. Clinical Periodontology. 9th Ed. Pennsylvania: Saunders; 2003. p. 949-964. 9. Kim SH, Tramontina V, Passanezi E. A new approach using the surgical extrusion procedure as an alternative for the reestablishment of biologic width. Int J Periodontics Restorative Dent 2004 Feb;24(1):39-45. 10. Kim CS, Choi SH, Chai JK, Kim CK, Cho KS. Surgical extrusion technique for clinical crown lengthening: report of three cases. Int J Periodontics Restorative Dent 2004 Oct;24(5):412421. 11. Aggarwal V, Logani A, Shah N. Complicated crown fractures - management and treatment options. Int Endod J 2009 Aug;42(8):740-753. 12. Camargo PM, Melnick PR, Camargo LM. Clinical crown lengthening in the esthetic zone. J Calif Dent Assoc 2007 Jul;35(7):487-498. 13. Hempton TJ, Esrason F. Crown lengthening to facilitate restorative treatment in the presence of incomplete passive eruption. J Calif Dent Assoc 2000 Apr;28(4):290-291, 294-296, 298. 14. Levine DF, Handelsman M, Ravon NA. Crown lengthening surgery: a restorative-driven periodontal procedure. J Calif Dent Assoc 1999 Feb;27(2):143-151. 15. Ravon NA, Handelsman M, Levine D. Multidisciplinary care: periodontal aspects to treatment planning the anterior esthetic zone. J Calif Dent Assoc 2008 Aug;36(8):575-584. 16. Chu SJ, Karabin S, Mistry S. Short tooth syndrome: diagnosis, etiology, and treatment management. J Calif Dent Assoc 2004 Feb;32(2):143-152. 17. Gargiulo AW, Wentz FM, Orban B. Dimensions and relations of the dentogingival junction in humans. J Periodontol 1961;32:261-267. 18. Vacek JS, Gher ME, Assad DA, Richardson AC, Giambarresi LI. The dimensions of the human dentogingival junction. Int J Periodontics Restorative Dent 1994 Apr;14(2):154-165. 19. Kois JC. The restorative-periodontal interface: biological parameters. Periodontol 2000 1996 Jun;11:29-38. 20. Smukler H, Chaibi M. Periodontal and dental considerations in clinical crown extension: a rational basis for treatment. Int J Periodontics Restorative Dent 1997 Oct;17(5):464-477. 21. Barboza EP, MonteAlto RF, Ferreira VF, Carvalho WR. Supracrestal gingival tissue measurements in healthy human periodontium. Int J Periodontics Restorative Dent 2008 Feb;28(1):55-61. 22. Sims TN, Ammons Jr WF. Resective Oseeous Surgery. In: Newman MG, Takei HH, Carranza FA, editors. Clinical Periodontology. 9th Ed. Pennsylvania: Saunders; 2003, p. 786-803. 23. Herrero F, Scott JB, Maropis PS, Yukna RA. Clinical comparison of desired versus actual amount of surgical crown lengthening. J Periodontol 1995 Jul;66(7):568-571. 24. Diniz DE, Okuda KM, Fonseca CR, Gonzalez MK, Greghi SL, do Valle AL, et al. Surgical crown lengthening: a 12-month study - radiographic results. J Appl Oral Sci 2007 Aug;15(4):280-284. 25. Pontoriero R, Carnevale G. Surgical crown lengthening: a 12-month clinical wound healing study. J Periodontol 2001 Jul;72(7):841-848. 26. Deas DE, Moritz AJ, McDonnell HT, Powell CA, Mealey BL. Osseous surgery for crown lengthening: a 6-month clinical study. J Periodontol 2004 Sep;75(9):1288-1294. 27. Dibart S, Capri D, Kachouh I, Van Dyke T, Nunn ME. Crown lengthening in mandibular molars: a 5-year retrospective radiographic analysis. J Periodontol 2003 Jun;74(6):815821. 28. Smidt A, Ziskind D, Venezia E. Migration following crown-lengthening procedure—a case report. Quintessence Int 2004 Jul-Aug;35(7):514-518. 29. Yeh S, Andreana S. Crown lengthening: basic principles, indications, techniques and clinical case reports. N Y State Dent J 2004 Nov;70(8):30-36.

Dental Economics

New York State after Last Recession Dentists and Dental Establishments H. Barry Waldman, D.D.S., M.P.H., Ph.D.; Aaron G. Segal, D.D.S.

A b st r a c t Data from the U.S. Census Bureau and the New York State Office of the Professions indicate an increase in emigration and immigration, resulting in slowing in the overall growth of New York State’s population, with accompanying modifications in the numbers of dentists and dental establishments in state counties. In addition, ADA data suggest that per capita dental spending has not rebounded since the end of the last recession. While there have been many changes at the county level, there does not seem to have been dramatic changes in the overall state numbers of dental practitioners and establishments through the early years of the current decade. As a result of a decline in fertility rates and the aging of the postWorld War II baby-boom generation, the nation as a whole got older between 1990 and 2010. New York State got older, too, but with striking regional variations. While the median age of the nation’s population rose 4.3 years between 1990 and 2010, it increased by 1.9 years in New York City, 5.2 years in downstate suburbs and 6.6 years upstate.3

These dramatic demographic changes are occurring at a time when the country continues to struggle out of the last recession, which officially ended almost four years ago. “The Business Cycle Dating Committee of the National Bureau of Economic Research…determined that …the recession that began in December 2007 … (had ended) in June 2009. The recession lasted 18 months, which makes it the longest of any recession since World War II.”4 Specifically, Dentistry In 2013, the ADA’s Health Policy Resources Center suggested “… very strongly that the dental economy is in a major transition… Dental spending has not rebounded since the end of the Great Recession and has been stagnant, on a per capita basis, since 2008… the declines in both dental spending and visits predate the economic crisis of 2008.”5 Dentists, Residents and Economics A previous article in the NYSDA News indicated that between 2000 and 2006 (prior to the last recession), the number of registered dentists decreased in 27 New York counties. The greatest decrease occurred in the counties of Albany, Bronx, Niagara, Suffolk and Westchester.6 Regional Differences Reports for 2012 from the New York State Office of the Professions emphasized a continuing decrease in the overall number

The New York State Dental Journal • november 2013

of dentists in the state, in New York City and in the rest of the state. The combination of these decreasing numbers of dentists and changes in the population in different sections of the state resulted in slight increases in the number of residents per dentist in New York City and in the rest of the state. Nevertheless, the population per dentist remained greater in New York City than in the rest of the state (Table 1). County Differences In 2012, reflecting the changing population numbers and the decrease in the number of dentists, there were dramatic differences in New York State counties in terms of the number of residents per dentist. These differences range from fewer than 1,000 residents per dentist in New York (Manhattan), Nassau, Westchester and Rockland counties, to more than 4,000 residents per dentist in Allegany, Washington, Lewis, Hamilton and Tioga counties. In most counties, however, the number of residents per dentist ranged between 1,000 and 2,999 residents per dentist (Table 2). Economics While there are a great range of factors that enter into consideration when selecting practice and living locations, one issue can be a critical factor in the final determination, that is, the economics of a community. In this computer age, these data are readily available. For example, in 2010, while the average per capita income of New York State residents was $30,948, it ranged from $17,575 in Bronx County, $19,807 in Franklin County and $20,058 in Allegany County, to $41,387 in Nassau County, $47,814 in Westchester County and $59,149 in New York County (Manhattan). More locally, among more than 1,000 locations, the per capita income ranged from $4,355 in Kiryas Joel in Orange County, to $113,320 in Hewlett Bay Park in Nassau County.11 In terms of expenditures for dental services, at the end of the recession in 2009, national per capita spending for dental care was $333, ranging from $223 in Mississippi, to $507 in Washington State. New York State ranked 28th (1= lowest, 51= highest) in spending $338 per capita for dental services.12 Dental Establishments In a series of previous reviews in The NYSDJ, the increasing numbers and size of dental establishments(1) in New York State were reported, with emphasis on the decreasing proportion of facilities with fewer than five employees.13-17 This trend continued through 2007, prior to the recession, with the proportion of “smaller” es-

Table 1. Population per New York State Dentists by Region: 2007, 20127-10 Population (in 000s) Year

New York City

Rest of State

New York State

2007

8,274

11,023

19,297

2012

8,337

11,233

19,570

Number of Dentists 2007

6,357

9,051

15,408

2012

6,298

8,982

15,280

Population per Dentist 2007

1,301

1,217

1,252

2012

1,323

1,250

1,280

Note: Location reflects licensee’s primary mailing address on record with Office of Professions and is not necessarily licensee’s practice location or is in active practice. In addition, 2,903 registered dentists are in residence in other states, 34 out of U.S.

tablishments (fewer than five employees) continuing to decrease. (Employees may include dentists, dental hygienists, dental assistants, office staff, etc.) In 2011, after the recession: l 51.9 thousand individuals were employed in New York State dental establishments. l 52.2 percent of New York State establishments had fewer than five employees, compared to 40.7 percent in the United States. l The “average” New York City dental establishment had 4.6 employees, compared to 6.3 employees in the “average” dental facility in the rest of the state. Overall, there were 5.6 employees statewide in the “average” establishment, compared to 6.5 employees in the “average” establishment in the United States.(2) l The “average” full-time dental establishment employee’s annual salary was $42,100 in New York State, compared to $45,200 in the United States.19 Between 2007 and 2011: l There was a statewide increase of 162 dental establishments, reflecting an increase in each of the New York City counties and gains and losses in the number of dental facilities in other state counties, including larger decreases in Erie and Monroe counties and large increases in Onondaga and Westchester counties (Table 3).

(2) (1)

An establishment is a single physical location where services are performed. It is not necessarily identical to a company or enterprise, which may consist of one or more establishments. In addition, one or more practitioners may be present in an establishment. Throughout this presentation, except where specified, the term “dental establishment” refers to those facilities 1. with employees and 2. subject to federal income tax. Government agency programs (hospitals and health department clinics) are not included.18

november 2013 • The New York State Dental Journal

While there is no such thing as an “average” dental establishment, comparisons between averages (over time and between locales) do provide a picture of the evolving practice of dentistry. The “average” number of employees in New York State was determined by dividing the total number of dental employees (51,908) by the number of dental establishments (9,237). The “average” salary was determined by dividing the total annual state payroll figure for dental establishment employees ($2,187,415,000) by the total number of employees (51,908 individuals).19

“New York lost 2.9 million residents to other states between 1990 and 2010—the biggest

l There was a decrease in population per establishment in New York City and an increase in population per dental establishment in the rest of the state (Table 4).

domestic outflow, relative to population,

Dental Establishments with No Employees In 2010, there were an additional 4,420 (an increase from 4,373 of any state during the 20-year period. An in 2007) New York dental establishments that were subject to federal income tax but with no employees. These non-employee influx of foreign immigrants, mainly to New dental facilities represented almost one-third (32.5%) of the total York City and its suburbs, reduced the state’s number of dental establishments in the state that year (i.e., 9,181 dental establishments with employees and 4,420 establishments net migration loss during that period ….”1 with no employees). Between 2007 and 2010, there was no change in the proportional representation of establishments Table 2. with any employees among all dental estabPopulation per Licensed and Registered Dentist in New York State Counties: 20127,9 lishments in the state. The New York dental Pop. per Dentist County Pop. per Dentist County facilities with no employees in 2010 reported a < 1,000 (606) New York (Manhattan) 2,500-2,999 Cattaraugus total of $344 million in gross receipts ($77,850 (657) Nassau Franklin per establishment). Nationally, in 2010, there (826) Westchester Fulton were 40,897 (an increases from 39,455 in (897) Rockland Genesee Greene 2007) dental establishments with no employees that reported more than $3.1 billion in 1,000-1,499 Albany St. Lawrence gross receipts (an annual average of $75,800 Dutchess Schuyler Erie Wayne in gross receipts per establishment). Monroe Wyoming In 2010, more than half (52%) of den Onondaga tal establishments in New York State (2,310 Queens 3,000-3,499 Bronx Richmond Chenango facilities) with no employees were located in Saratoga Delaware New York City, compared to 58% in 2007. The Schenectady Herkimer combination of the number of no-employee Suffolk Oswego Warren Schoharie facilities in New York City and those in Nassau County (679) and Suffolk County (352) 1,500-1,999 Broome 3,500-3,999 Cortland on Long Island represented 76% of all non Chemung Delaware Clinton Orleans employee facilities in the state, compared to Jefferson Seneca 83% in 2007. In 2010, there were 363 den Kings Montgomery 4,000-4,490 Allegany tal establishments with no employees in Oneida Washington Westchester County, 84 in Erie County and Ontario 89 in Monroe County. Orange >4,500 (4,537) Lewis Putnam (4,778) Hamilton During 2010, in New York State, most non Tompkins (6,309) Tioga employee dental establishments were individual Ulster proprietorships with average annual gross re2,000-2,499 Cayuga Total New York State ceipts of $69,800. A smaller number of corpo Chautauqua rate arrangement facilities had average annual Columbia Population – 19,501,616 gross receipts of $139,000; partnerships had av Essex Dentists – 15,280 Livingston Pop. per dentist – 1,280 erage annual gross receipts of $254,800.17,22 Madison Given the increasing numbers of employees Niagara Note: Location reflects licensee’s primary per dental establishment with employees, how Otsego mailing address on record with Office Rensselaer of Professions & is not necessarily licensee’s does one account for the great number of fa Steuben practice location or is in active practice. cilities with no employees? It was suggested in Sullivan In addition, 2,903 registered dentists are the previous NYSDJ review that non-employee in residence in other states, 34 out of U.S. establishment arrangements might include:

The New York State Dental Journal • november 2013

l Recent graduates just starting practices. l Older practitioners who are decreasing their time commitment to practice as they prepare for eventual retirement. l An establishment that serves as a secondary activity for an individual who works full time for someone else. l Contracts with independent outside firms for auxiliary personnel. l Use of family members as auxiliary personnel and where no reports are made for Social Security and income tax purposes. l Establishments of independent corporate arrangements for in-house auxiliaries. l Any number of other alternative practice arrangements, including practice in private homes and other locations that do not file required quarterly payroll tax reports.17 Overview The April 2013 lead article in the ADA News highlighted the finding that, “…our results suggest very strongly that the dental economy is in a major transition. Dental spending has not rebounded since the end of the Great Recession and has been stagnant on a per capita basis since 2008.” (sic)23

“Although New York State grew by 87,092 people in the 15 months after the 2010 census, 37 upstate counties lost population…”2 “Because its population growth did not keep pace with other regions of the United States, New York State lost two congressional seats following the 2010 census.”2

Table 3. New York State Dental Establishment by County: 2007, 201119 2007 2011

Change 2007 – 2011

Total State

9,075

9,237

162

New York City Bronx Kings New York Queens Richmond

3,684 265 875 1,374 980 190

3,869 273 917 1,438 1,031 210

185 8 42 64 51 20

Rest of State

5,391

5,368

- 23

Albany Dutchess Erie Monroe Nassau Onondaga Orange Rockland Suffolk Westchester

137 142 438 342 1,083 191 147 211 773 657

136 133 421 323 1,079 204 137 211 782 676

-1 -9 - 17 - 19 -4 13 -10 9 19

Total >100 estab./county

4,121

4,102

- 19

Counties (100 establishments in 2007

Table 4. Population per New York State Dental Establishments by Region: 2007, 201118-21

november 2013 • The New York State Dental Journal

Year

New York City

Rest of State

New York State

2007

2,246

2,044

2,126

2011

2,131

2,094

2,109

Data from the U.S. Census Bureau and the New York State Office of the Professions indicate an increase in emigration and immigration, resulting in the slowing of the overall growth of New York State’s population, with accompanying modifications in the numbers of dentists and dental establishments in state counties. While ADA data suggest that per capita dental spending has not rebounded since the end of the last recession, there does not seem to have been dramatic changes in the overall numbers of New York State dental practitioners and establishments through the early years of the current decade. p Queries about this article can be sent to Dr. Waldman at [emailprotected].

References 1. McMahon EJ, Scardamalia R. The graying of the Empire State. Research Bulletin 7.2 August 2012. Empire Center for New York State Policy. Web site: http://empirecenter.org/ pb/2011/08migration1080311.cfm/ Accessed April 21, 2013. 2. Cornell University. Most upstate New York continues to lose people. Web site: http://phys. org/print253428695.html/ Accessed April 19, 2013. 3. Empire Center for New York State Policy. The graying of the Empire State. Web site: http:// www.empirecenter.org/pb/2012/08/migration3081612.cfm/ Accessed April 23, 2013. 4. The Business Cycle Dating Committee of the National Bureau of Economic Research. The recent recession. Web page: http://www.nber.org/cycles/sept2010.html/ Accessed April 22, 2013. 5. American Dental Association. National dental spending flat since 2008. April 18, 2013. Web site: http://www.noodls.com/view/3F1A30966AA6C833A799B7C0BBD4A768C8534 A05?9531xxx1366388107/ Accessed April 23, 2013. 6. Waldman HB. Upstate areas experience shortfall in dental professionals. New York State Dental Association News 19:1-2, October 2006. 7. Census Bureau. Estimates of resident population change and rankings: 2012 population estimates. Web site: http://factfinder2.census.gov/faces/tableservices/jsf/pages/productview. xhtml?src=bkmk/ Accessed April 19, 2013. 8. Census Bureau. Population data. Web site: http://factfinder.census.gov: 2007 population estimates. Accessed January 17, 2010. 9. New York State Office of the Professions. License statistics. Web site: http://www.op.nysed. gov/prof/dent/dentcounts.htm/ Accessed April 19, 2013. 10. New York State Office of the Professions. License statistics. Web site: http://www.op.nysed. gov/dentcounts.htm/ Accessed June 1, 2007. 11. Wikipedia. New York locations by per capita income. Web site: http://en.wikipedia.org/ wiki/New_York_locations_by_per_capita_income/ Accessed April 23, 2013. 12. Kaiser Family Foundation. Statehealthfacts.org. Health care expenditures per capita by services by state of residence, 2009. Web site: http://www.statrehealthfacts.org/comparetable. jsp?cat=5&ind=597/ Accessed April 24, 2013. 13. Waldman HB. Dental establishment business activity in New York State Counties. NYSDJ 2000;66:26-29. 14. Waldman HB. New York State dental establishment keep getting larger. NYSDJ 2001;67:1618. 15. Waldman HB. Stabilizing the number of NY State dental establishments. NYSDJ 2004;70:3436. 16. Waldman HB. Dental establishment business activity in New York State counties at the start of millennium. NYSDJ 2006;72:42-45. 17. Waldman HB, Cannella D. Mapping dental establishments in New York State just before the recession. NYSDJ 2010;76:22-25. 18. Census Bureau. County Business Patterns: 2007. Web site: http://censtats.census.gov/cgibin/cbpnaic/cbpsel.pl/ Accessed January 19, 2010. 19. Census Bureau. County Business Patterns 2011. Web site: http://censtats.census.gov/cgibin/cbpnaic/cbpdetl.pl/ Accessed May 1, 2013. 20. 2010 Census State Population and the Distribution of Electoral Votes and Representatives. Web site: http://www.thegreenpapers.com/Census10/HouseAndElectors.phtml/ Accessed April 29, 2013. 21. New York http://City Department of Planning. 2011 population. Web site: http://www.evi. com/q/what_is_the_population_of_new_york_state_2011/ Accessed May 1, 2013. 22. Census Bureau. Nonemployer statistics. Web site: http://censtats.census.gov/cgi-bin/nonemployer/nonsect.pl/ Accessed April 22, 2013. 23. Soderlund K. Baby boomers boost utilization. ADA News 2013;44(8):1,4.

The New York State Dental Journal • november 2013

Smoking Cessation

The Relationship between Smoking and Periodontal Disease Review of Literature and Case Report Gene B. Sherwin, D.D.S.; Diana Nguyen, D.D.S.; Yaakov Friedman, D.D.S.; Mark S. Wolff, D.D.S., Ph.D.

A b st r a c t Cigarette smoking has been associated with tooth loss from periodontal disease for a long time. Smoking cessation has been shown to reverse these effects. The purpose of this paper is to review the current literature regarding the possible mechanisms for destruction of the periodontium caused by smoking and to present a protocol for the implementation of a smoking cessation program at New York University College of Dentistry. Periodontal disease is the most common cause of tooth loss among adults.1 Risk factors for periodontitis include smoking, genetic predisposition, probably psychosocial stress, diabetes and several uncommon systemic diseases.2 Of all the environmental factors known to be associated with periodontitis, cigarette smoking may be the most important, as it has been shown to significantly increase the risk of tooth loss.3 Papapanou outlined the manner in which this occurs as follows: Evidence for the role of smoking in periodontitis includes 1. A higher prevalence of disease among smokers in cross-sectional studies; 2. A higher incidence of periodontitis among smokers in longitudinal studies; 3. A statistically significant association even after controlling for other risk factors; 4.

november 2013 • The New York State Dental Journal

Increased prevalence and incidence of disease with increased amounts of smoking; and 5. Biologically plausible mechanisms that can explain how smoking is involved in the destruction of periodontal tissues.4 A review of the literature over the past 20 years has demonstrated a positive correlation between cigarette smoking and a higher risk for periodontal disease. Mullally noted that as long ago as 1848, John Burdell, an American dentist, described the oral changes associated with tobacco chewing and commented on the difficulties he had experienced in providing dentures for this group.5 Van Winkelhoff has suggested that smoking is a determining factor for the composition of the subgingival microflora in adult patients with periodontitis and may select for a specific cluster of periodontal pathogens, notably, Bacteroides forsythus, Peptostrptococcus micros, Fusobacterium nucleatum and Campylobacter rectus. Antibiotic therapy may be effective against smoking-associated periodontal bacteria.6 Kubota has demonstrated in smokers a statistically significant association between having a probing pocket depth of greater than or equal to 4 mm and detection of T. denticola, P. intermedia, T. forsythia or C. rectus.7 Haffajee concludes that the relationship between cigarette smoking and the composition of the subgingival microbiota is not clear. The major difference between the subgingival microbiota in subjects with different smoking history was in the prevalence of species rather than the counts or proportions. The greater extent of colonization in smokers appeared to be due to greater colonization at pocket depths

less than 4 mm.8,9 Fullmer found that microbial profiles differed significantly between smokers and quitters at 6 and 12 months following smoking cessation. The microbial community in smokers was similar to the baseline, while quitters demonstrated significantly more divergent profiles. Changes in bacterial levels contributed to this shift. These findings reveal a critical role for smoking cessation in altering the subgingival biofilm and suggest a mechanism for improved periodontal health associated with smoking cessation.10 Early Evidence of Damage Cigarette smoking has been shown to be associated with a greater increase in probing depth and attachment loss, as well as greater tooth loss at an earlier age. Mullally found a high prevalence of cigarette smoking among young individuals with aggressive periodontitis and that tobacco use increases the risk of periodontal destruction most significantly in young populations.11 It is clear from the evidence that environmental exposure to cigarette smoking has been associated with two- to three-fold increases in the odds of developing clinically detectable periodontitis.12 The noxious effect of smoking has been shown to be dosedependent and to be particularly marked in younger individuals. Baljoon notes that cigarette smoking is associated with increased prevalence and severity of destructive periodontal disease in terms

of periodontal pocketing, bone and tooth loss. The destructive effect of smoking on periodontal bone may be of the horizontal and vertical “angular” pattern.13 Preshaw has demonstrated the importance of smoking cessation in that it has a beneficial effect in reducing probing depths following nonsurgical treatment.14 Current literature identifies the harmful effects of smoking, including interference with the vasculature and immunologic reactions. This results in a destruction of the supportive functions of the periodontal tissues. The local host response to bacteria, which initiates periodontitis, includes the recruitment of leukocytes and the subsequent release of inflammatory mediators and cytokines such as interleukin (IL-1,6,8,10,12) and tumor necrosis factor (TNF- alpha). Researchers have tried to examine a possible relationship between smoking, stress and cytokine production. Giannopoulou studied cytokines in the pathogenesis of periodontal disease and suggests they may be used as markers in its diagnosis. His data implies that in smokers, higher levels of crevicular interleukins IL-1beta and IL-8 levels reflect the activity of periodontal destruction, whereas, conversely, nonsmokers have higher levels of IL-4 but lower amounts of IL-8.15,16 Erdemir evaluated the effects of smoking on clinical parameters such as plaque index (PI), gingival index (GI), bleeding on probing (BOP), probing depth (PD) and clinical attachment loss (CAL). Gingival crevicular fluid samples were collected for IL-6

The New York State Dental Journal • november 2013

Figure 1A. Right bite wing.

2A.

Figure 1B. Right bite wing.

2B.

Figure 1C. Left bite wing.

2C.

Figure 1D. Left periapical showing caries on tooth #12. 2D.

Figure 2A.-2D. Intraoral photographs at presentation.

and TNF-alpha in patients with chronic periodontitis. Results show that only attachment loss was significantly higher at the third month among smokers compared with nonsmokers. GI and BOP were higher in nonsmokers than in smokers. The study demonstrated that cigarette smoking increases the amount of dental plaque over time in smokers and does not influence GCF contents of IL-6 and TNF-alpha. Better oral hygiene must be applied, as well as initiation of nonsurgical periodontal therapy.17 Kamma concluded that smoking influences host-related factors, including the cytokine network; however, the relative importance of smoking and stress-related alterations and their precise mode of action in increasing the risk of aggressive periodontitis remain to be elucidated.18 Leide studied salivary proteolytic enzyme activity and found that smoking may significantly lower both general proteolytic enzyme activity and matrix metalloproteinase-8 (MMP-8) levels in saliva when smokers who had quit were compared with those still smoking. The data suggests that periodontal status and oral mucosa are better in those who have quit compared to current smokers.19 Johnson cites evidence that smoking has a negative effect on host response, such as neutrophil function and antibody production. An encouraging finding is that periodontal disease progression slows in patients who quit smoking and that these individuals have a similar response to periodontal therapy as nonsmokers.20 In summary, even though there may be conflicts in the research, especially regarding smoking’s effect on the microflora, there is very strong evidence of more severe dose-related peri-

november 2013 • The New York State Dental Journal

odontal destruction among smokers and a return to a healthier status once periodontal therapy and smoking cessation counseling have been given and accepted. Johnson, in 2004, recommended the use of the five A’s as follows: l Ask—identify tobacco users. l Advise—advise them to quit. l Assess—evaluate the patient’s readiness to quit. l Assist—offer assistance in cessation. l Arrange—follow up on the patient’s cessation efforts. The addition of pharmacotherapy to the behavioral therapy, including nicotine replacement therapy (NRT) and bupropion (Wellbutrin), can increase cessation rates. The most popular form of NRT is the patch; its use has been shown to double cessation rates compared to behavioral therapy alone. Use of bupropion in combination with NRT may be particularly helpful for heavy smokers or smokers who have experienced multiple failed attempts at cessation.21 During the last several years, tobacco cessation counseling has become a standard part of treatment planning at New York University College of Dentistry (NYUCD) with all patients who are current smokers. Case Report The female patient, JT, presented to NYUCD in September 2011. She is 27 years old, 5-feet, 3-inches tall and weighs 130 pounds. Her blood pressure was measured at 128/89, with a pulse of 87. JT reports she has been smoking about five or six cigarettes daily since the age of 16 and drinks alcohol socially, less than one drink a day. She presented with poor periodontal health, including multiple

Figure 3. Charting of dental findings.

The New York State Dental Journal • november 2013

sites of pocket depths measuring 5 mm, especially in the maxilla. There was mild plaque buildup, some recession, clinical attachment loss, generalized bleeding on probing, as well as moderate radiographic bone loss. This is the first time she has been to see a dentist in a while, so it is unclear how long the periodontal disease has been present. Based on clinical findings and history, she was categorized as having chronic generalized moderate periodontitis. A review of the medical history shows that the patient has had asthma since childhood. It is well controlled and attacks are rare, the last occurring more than five years ago. She carries an albuterol inhaler in case of an unexpected attack. Smoking cigarettes places her at high risk for chronic lung diseases, including the possibility that her asthma could take on a more severe form. She is also at risk for cardiovascular disease and stroke, especially with her family history of high blood pressure. The risk of cancer, oral and lung cancer in particular, is increased. The risk of periodontal disease is confirmed by findings of bleeding upon probing, periodontal pocketing and bone loss. JT’s dental examination revealed that teeth #4, #17, #18 and #19 were missing due to extensive caries, rendering them unrestorable. Caries is present on tooth #12, which places her in a high-caries risk as well. Endodontic and restorative treatments have been performed on several teeth. The patient brushes daily with fluoride toothpaste and flosses occasionally. The extraoral exam was unremarkable. In order to decide on a treatment plan to optimize the patient’s health, the appropriate risk factors must be identified. Furthermore, the treatment plan must focus not only on removing disease and restoring health, but also on health promotion, giving the patient the knowledge and tools necessary to maintain a healthy status. In this case, the first focus was to restore her periodontal health with scaling and root planing, followed by a re-evaluation in four to six weeks. The treatment plan also includes asking about smoking cessation at every visit; restoration of the carious lesions; and reinforcing oral hygiene, including the proper way to brush with the modified Bass technique and the use of dental floss. Prevident 5000-plus toothpaste will be prescribed, along with MI paste, to promote remineralization to prevent future caries. The patient will be placed on a three-month recall to monitor her oral health status. Smoking Cessation Protocol The importance of a smoking cessation program should not be underestimated. Quitting smoking is not only critical for one’s overall health and well-being, it is also specifically beneficial with regard to one’s dental and periodontal health. Smoking cessation therapy is broken up into the “5 A’s”: Ask, Advise, Assess, Assist and Arrange. Smoking cessation begins with “asking” patients about their smoking habit. This includes how much and how often they smoke, when they started smoking and have they ever thought about quitting. After “advising” the patient to quit smoking, the patient’s readiness to quit is “assessed.” For example, is the patient thinking of quitting, as in the “contemplation stage?” Or has he or

november 2013 • The New York State Dental Journal

she not even thought about it—the “pre-contemplation stage?” Is the patient motivated and confident? Or has he or she tried, failed and even given up hope? Patients who have failed or give up hope should be encouraged to try to quit again. Proper “assistance” is provided to the patient. Patients receiving some form of assistance have a greater likelihood of success in quitting. At NYUCD, all patients who smoke receive information enabling them to contact the New York State Smokers Quitline (1-866-NY-QUITS), which provides free telephone counseling and a free starter kit for NRT. In addition, all patients are referred to the NYU Nurse Faculty Practice for the option of face-to-face personal or group counseling and assistance if that better suits the patient’s needs. It is important to get the patient to commit to a program of tobacco cessation at the moment he or she indicates interest. Offering counseling and putting the information in their hands is helpful, but providing NRT with dentist-supplied instruction at that moment further increases the chance the patient will actually quit. Patients who smoke 10 to 15 cigarettes a day qualify for NRT in the dental clinic. They are started on either the 14 mg patch for two weeks or the 4 mg gum or lozenge every one to two hours for two weeks. If cravings persist, the patch may be increased to 21 mg, or the frequency of the gum or lozenge can be increased. If patients smoke more than 15 cigarettes a day, combination therapy should be instituted. This means they should be started on the 21 mg patch, along with either the gum or the lozenge. The use of NRT is very safe, but it is not recommended for people with underlying cardiovascular disease, pregnant women or children under the age of 18. Another route to assist in quitting smoking, especially for patients who have tried NRT unsuccessfully, is non-nicotine pharmacotherapy. The two drugs that are recommended are varenicline and bupropion. For varenicline, the prescription is to dispense a 12-week supply of 0.5/1mg tablets. The patient should start with 0.5 mg once a day for the first three days, then 0.5 mg twice a day for the next four days, then 1 mg twice a day after that. Varenicline binds with high affinity to specific nicotinic acetylcholine receptors and, in effect, reduces symptoms of nicotine withdrawal and cravings. For bupropion, the prescription is to dispense a 7- to 12-week supply of 150 mg tablets. The patient should begin taking the medication one to two weeks prior to the quit date. For the first three days it should be taken once a day. After that it should be taken twice a day. Bupropion is a type of anti-depressant that affects the levels of dopamine and norepinephrine in the brain. Despite their benefits, these drugs do have contraindications. Bupropion is not recommended for patients with seizure disorders or patients taking certain anti-depressants. Varenicline is contraindicated in patients with renal impairment and who have been associated with mood changes, including suicidal ideation. Whichever smoking cessation therapy is instituted, it should be one designed for the specific patient and his or her needs. The final step is to “arrange” for follow-up. This is to make sure that the smoking cessation program the patient is on is suitable and is

providing the help and support needed to make the transformation from an addicted state to one of health and well-being. Conclusion The existing evidence shows that individuals with a smoking habit will eventually damage their periodontium and immune systems. Implementation of periodontal treatment, home care instruction and smoking cessation guidance can overcome and reverse the destructive effects of smoking. During their dental school education, dental and hygiene students should be taught these skills in order for them to be better equipped to provide optimum care in dental practice. Toward this end, we have prepared a protocol for treatment at New York University College of Dentistry that we expect will become a standard for instruction globally. p Queries about this article can be sent to Dr. Sherwin at [emailprotected].

References 1.

Periodontal (gum) disease (Internet), NHI National Institute of Dental and Craniofacial Research (US): Last Updated 2010 Mar 10 Available from: http://www nidcr.nih.gov/DataStatistics/FindDataByTopic/GumDisease/. 2. Research, Science and Therapy Committee of the American Academy of Periodontology. Position Paper: Epidemiology of periodontal diseases. J Perio 2005;76:1406-1419. 3. Newman MG. Caranza’s Clinical Periodontology. 10th Ed. Takei H, Carranza FA Saunders; 2006. 4. Papapanou PN. Risk assessments in the diagnosis and treatment of periodontal diseases. J Dent Edu 1998;62:822.

5. Mullally BH. The influence of tobacco smoking on the onset of periodontitis in young persons. Tobacco Induced Diseases 2004 Jun 15; 2(2):53-65. 6. van Winkelhoff AJ, Bosch-Tijhof CJ, Winkel EG, van der Reijden WA. Smoking affects the subgingival microflora in periodontitis. J Perio 2001 May;72(5):666-71. 7. Kubota M, Tanno-Nakanishi M, Yamada S, Okuda K, Ishihara K. Effect of smoking on subgingival microflora of patients with periodontitis in Japan. BMC Oral Health 2011;Jan 5;11:1. 8. Haffajee AD, Socransky SS. Relationship of cigarette smoking to attachment level profiles. J Clin Perio 2001Apr;28(4):283-95. 9. Haffajee AD, Socransky SS. Relationship of cigarette smoking to the subgingival microbiota. J Clin Perio 2001 May;28(5):377-88. 10. Fullmer SC, Preshaw PM, Heasman PA, Kumar PS. Smoking cessation alters subgingival microbial recolonization. J Dental Research 2009 Apr; 88(6):524-528. 11. Mullally BH. The influence of tobacco smoking on the onset of periodontitis in young persons. Tobacco Induced Diseases 2004 Jun 15; 2(2):53-65. 12. Tonetti MS. Cigarette smoking and periodontal diseases: etiology and management of disease. Ann Periodontology 1998 Jul;3(1):88-101. 13. Baljoon M. Tobacco smoking and vertical periodontal bone loss. Swed Dental J; Suppl 2005;(174):1-62. 14. Preshaw PM, Heasman L, Stacey F, Steen N, McCracken GI, Heasman PA. The effect of quitting smoking on chronic periodontitis. J Clin Perio 2005 Aug;32(8):869-79. 15. Giannopoulou C, Kamma JJ, Mombelli A. Effect of inflammation, smoking and stress on gingival crevicular fluid cytokine level. J Clin Perio 2003 Feb;30(2):145-53. 16. Giannopoulou C, Cappuyns I, Mombelli A. Effect of smoking on gingival crevicular fluid cytokine profile during experimental gingivitis. J Clin Perio 2003 Nov;30(11):996-1002. 17. Erdemir EO, Duran I, Haliloglu S. Effects of smoking on clinical parameters and the gingival crevicular fluid levels of IL-6 and TNF-alpha in patients with chronic periodontitis. J Clin Perio 2004 Feb; 31(2): 99-104. 18. Kamma J J, Giannopoulou C, Vasdekis V G, Mombelli A. Cytokine profile in gingival crevicular fluid of aggressive periodontitis: influence of smoking and stress. J Clin Perio 2004 Oct; 31(10):894-902. 19. Liede KE, Haukka JK, Hietanen JH, Matilla MH, Ronka H, Sorsa T. The association between smoking cessation and periodontal status and salivary proteinase levels. J Perio 1999 Nov; 70(11):1361-8.

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The New York State Dental Journal • november 2013

Pharmacotherapy

Role of Topical Drugs in Treatment of Oral Mucosal Diseases A Literature Review Soheyl Sheikh, M.D.S.; Deepak Gupta, M.D.S.; Shambulingappa Pallagatti, M.D.S.; Isha Singla, M.D.S.; Rajesh Gupta, M.D.S.; Varun Goel, M.D.

A b st r a c t Few topical formulations have been designed specifically to treat oral mucosal diseases. Local drug delivery may provide a more targeted and efficient option than systemic delivery for diseases of the oral mucosa. The permeability to the topical drugs differs according to the thickness of the epithelium and the extent of keratinization. The loss of the permeability barrier in the oral mucosa, due to ulceration or erosion, leads to rapid diffusion of the drug into tissues as compared to the intact areas of the mucosa. Oral mucosal delivery has the potential to treat many different conditions and diseases, such as oral cancer, mucositis, lichen planus, herpes simplex, candidiasis, recurrent aphthous stomatitis, vesiculo-bullous diseases, neuropathic pain and salivary dysfunction. Each therapy requires distinct penetration and drug retention profiles in order to optimize treatment and minimize side effects. In this paper, topical medications are discussed, as these are advantageous for the treatment of oral mucosal lesions with fewer side effects.

november 2013 • The New York State Dental Journal

Oral mucosal delivery has the potential to treat many different conditions and diseases, such as pre-malignant lesions, mucositis, lichen planus, herpes simplex, candidiasis, recurrent aphthous stomatitis, vesiculo-bullous diseases, neuropathic pain and salivary dysfunction.1 There are few topical formulations that have been designed specifically to treat oral mucosal diseases. Most topical therapies currently used by oral medicine specialists are those that are used to treat dermatological conditions.1 Still, mucosal therapy requires distinct penetration and drug retention profiles in order to optimize treatment and minimize side effects.1 The permeability to these topical drugs differs according to the thickness of the epithelium and the extent of keratinization.2 Keratinized tissues display a lower permeability than non-keratinized tissues because of the lipid composition of the membrane-coating granules in keratinized tissues rather than the presence of keratin alone.3 However, the permeability of topically applied agents is greater in the sublingual region.2 But its surface is constantly washed by saliva and tongue activity, which makes it difficult to keep the dosage form in contact with the mucosa. The buccal mucosa is also a useful route for the treatment of either local or systemic therapies. It is more tolerant of potential allergens, which have a reduced tendency to irreversible irritation or damage. But the palatal mucosa is keratinized and intermediate in thickness with less permeability.3 In this review, we discuss the potential for using topical drugs in the treatment of oral mucosal diseases and the possible reduction in drug side effects.

Local Drug Delivery and Therapeutics for Specific Oral Diseases Potentially Malignant Oral Diseases Potentially malignant oral disease is morphologically altered tissue that is present on clinical examination in which cancer is more likely to occur than in normal tissue.4 It is recognized that occasionally non-dysplastic lesions may turn into cancer, while not all dysplastic lesions become malignant.5 Over the years, many topical medications have been used to treat potentially malignant oral diseases. Piattelli et al., in 1999, advocated 13-cis-Retinoic acid (iso-tretinoin) to induce remission of oral leukoplakia and to prevent the development of cancer in patients with oral leukoplakias. It inhibits the development of second primary tumors in patients with previous head and neck cancer. All patients treated with the active medication showed a significant improvement of the oral lesions, and no side effects from use of the gel were observed.6 5-aminolevulinic acid (ALA) is the only photosensitizer that can be given orally or applied topically. All other photosensitizers have to be given intravenously. In 1998, Kubler et al. used 20% ALA cream applied to the leukoplakia lesion of the oral mucosa for two hours. During the healing period, none of the patients felt any pain. During nine months of follow-up, no changes in the clinical appearance of the treated lesions were observed. ALA-PDT seems to be a promising means of treating oral leukoplakia, with long-term follow-up.4 Epstein et al., in 1999, evaluated the use of topical 1% bleomycin in dimethylsulfoxide for the treatment of dysplastic oral lesions. It was applied once daily for 14 consecutive days to lesions of the oral mucosa in 19 patients. Immediate post-treatment biopsies and the clinical response were evaluated. The results revealed that topical bleomycin may prevent the potential progression of leukoplakia through dysplasia to carcinoma.7 There are other drugs that can also be used to treat oral leukoplakia with limited effects. Epstein et al., in 1999, used topical 0.05% vitamin A (tretinoin) acid gel four times a day for the treatment of oral leukoplakia. In case of local oral tissue sensitivity and burning sensation, a less concentrated gel (0.01% vitamin A acid gel) was prescribed.8 The use of topical vitamin A acid showed a limited effect in controlling oral leukoplakia.8 Aggressive treatment regimens associated with significant morbidity are used to treat later stage oral cancers.1 There are no reliable treatments to prevent malignant transformation of dysplastic lesions or the development of recurrent ⁄ new disease in patients with a history of oral cancer.9 The difficulty in developing such a reliable treatment is that each cancer is unique, carrying its own blend of mutations and, thus, not all patients will benefit from the same therapy.1

Oral Mucositis Oral mucositis is a common complication of cancer treatments such as chemotherapy and radiotherapy. It is characterized by erythema, inflammation, pain and ulceration, which can occur in up to 100% of patients undergoing stem cell transplantation, radiotherapy to the head and neck, and chemotherapy.10 Labial and buccal mucosa are most commonly affected by chemotherapy; the uvula and soft palate respond more intensely to irradiation.11 Benzydamine hydrochloride is a non-steroidal drug that has topical anti-inflammatory, analgesic, anesthetic and antimicrobial activities.12 The effectiveness of benzydamine hydrochloride for managing oral mucositis was assessed mainly in patients undergoing radiotherapy for head and neck cancer.11,13 In 1989, Prada et al. proved that the topical application of benzydamine resulted in a reduced incidence and significant alleviation of symptoms associated with radiotherapy- and chemotherapy-induced oral mucositis, as compared with a placebo.14 In 2001, Epstein et al. used 0.15% benzydamine oral rinse to prevent the oral mucositis that occurs during radiation therapy in patients with head and neck cancer. Subjects were asked to rinse with 15 mL for two minutes four to eight times daily before and during radiation therapy, and for two weeks after completion of therapy. The results revealed that benzydamine oral rinse was effective, safe and well tolerated for prophylactic treatment of radiation-induced oral mucositis.13 Franzen et al. and Allison et al., in 1995, found a statistically significant reduction in the severity of oral mucositis in patients who were using topical sucralfate during radiotherapy.15,16 Immunologically Mediated Diseases Immunologically mediated diseases constitute one of the most common groups of disorders to affect the oral mucosa. And they present a therapeutic challenge to contemporary oral medicine practice. These diseases affect the oral mucosa, presenting with inflammation and loss of epithelial integrity, through cellular and humoral immunity-mediated attack on epithelial connective tissue targets.17 Disorders that usually center upon T-cells include oral lichen planus; those centering upon the B-cell involve pemphigus and mucous membrane pemphigoid.1 Oral lichen planus: Oral lichen planus is a chronic inflammatory condition that is probably of multifactorial origin, often idiopathic, with an immunopathogenesis involving T- cells.1 A range of treatments have been proposed for oral lichen planus. They include topical and systemic corticosteroids; topical cyclosporine; topical and systemic retinoids; antimicrobials; azathioprine; photochemotherapy; and surgery. In recent years, tacrolimus ointment 0.1% and cream 0.1% have received approval from the U.S. Food and Drug Administration on the basis of their demonstrated efficacy in the treatment of atopic dermatitis refractory to conventional

The New York State Dental Journal • november 2013

treatment.18 Tacrolimus is an immunosuppressive agent. This substance is produced by Streptomyces tsukubaensis, which belongs to the macrolide family. It has a greater capacity to penetrate the mucosa.18 In 2002, Morrison et al. conducted an open-label study with six patients administered topical tacrolimus. This treatment proved to be effective in controlling the symptoms of erosive lichen planus.18 Triamcinolone acetonide is among the most commonly used topical corticosteroids for the treatment of immunologically mediated diseases. The concentration ranges between 0.05% and 0.5%, and is applied 3 to 10 times a day for a period of 3 to 5 minutes.19 Laeijendecker et al., in 2006, compared the efficacy of topical tacrolimus ointment versus triamcinolone acetonide 0.1% ointment. The most commonly reported side effect in both groups was temporary burning or stinging at the site of application. Topical tacrolimus 0.1% ointment induced a better initial therapeutic response than triamcinolone acetonide 0.1% ointment.20 Pimecrolimus is a derivative of the macrolide ascomycin that was developed specifically for the treatment of inflammatory disorders of the skin.18 Dissemond et al., in 2004,21 prepared this ointment by mixing 1% cream 1:1 with a hydrophilic adhesive gel base. It was applied twice daily. It represents a new topical selective inflammatory cytokine-release inhibitor. Pimecrolimus binds to macrophilin-12 and inhibits the calcium-dependent phosphatase calcineurin. By blocking the transcription of early cytokines and thus down regulating synthesis of both T-helper 1and 2-type cytokines, pimecrolimus inhibits T-cell activation.21 In 2007, Gorouhi et al.22 and in 2008, Volz et al.23 carried out a study showing pimecrolimus cream at a concentration of 1% results in a significant reduction in oral erosions.18 According to Sardella in 1998,24 Carbone in 1999,25 Muzio in 200126 and Gonzalez-Moles in 2006,27 Clobetasol propionate, in the form of orabase ointment or aqueous solution, has been effective in the treatment of oral lichen planus.28 Lozada et al., in 1994,29 and Carbone et al., in 1999,30 using concentration ranges between 0.025% -0.05%, applied two to three times day for three to five minutes,19 induced vasoconstriction followed by a reduction of the inflammation due to an alteration of histamine levels and to the effects of the catecholamines on peripheral blood vessels. Clobetasol has demonstrated superior therapeutic effects compared to other topical corticosteroids.17 For severe erosive gingival lesions, Clobetasol-17- propionate orabase paste 0.05%, plus 100,000 IU/ml of nystatin, is efficacious treatment.28 Fluocinonide is considered to be a moderate to high potency corticosteroid. Lozada et al., in 1994,29 used this drug at concentrations ranging between 0.025% and 0.05%. The medication is applied 5 to 10 times a day for 3 to 5 minutes. It is a milder topical corticosteroid than clobetasol propionate and is less effective in reducing pain. When used at a 0.025% concentration, a 60

november 2013 • The New York State Dental Journal

complete resolution of lesions is achieved in 25% of patients with oral lichen planus.19 In symptomatic oral lichen planus, Carbone et al., in 1999,30 using 0.025% fluocinonide in an adherent vehicle, produced complete remission of lesions and symptoms in 25% of patients.17 Hydrocortisone hemisuccinate in aqueous solution is often of little benefit in treating oral lichen planus. Fluticasone propionate spray and betamethasone sodium phosphate mouthrinse have been used effectively in the short-term management of symptomatic oral lichen planus.28 Pemphigus: Pemphigus vulgaris is the most common form of oral mucosal pemphigus. Topical agents are likely to have a role in management of this oral disease, although this will depend upon the severity of disease.1 Topical corticosteroids may suffice for a time if there are only localized oral lesions with low titre serum antibodies; otherwise, systemic immunosuppressants are essential.31 Systemic corticosteroids are the first-line therapy for severe oral and/or cutaneous Pemphigus vulgaris.1 These corticosteroids remain the mainstay of therapy for patients with oral lesions, transforming an invariably fatal disease into one whose mortality is now below 10%.31 But, in such cases, if steroidal topical ointments are used in conjugation with the systemic steroids therapy, it will lead to a reduction in side effects of systemic drugs by reducing dosage. Mucous membrane pemphigoid (MMP): Mucous membrane pemphigoid is a chronic autoimmune subepithelial disease that primarily affects the mucous membranes of patients over the age of 50, resulting in mucosal ulceration and subsequent scarring.32 In patients who are at low risk and with lesions confined only to the oral mucosa, topical corticosteroids, such as 0.1% triamcinolone acetonide, 0.05% fluocinolone acetonide or 0.05% clobetasol propionate in orabase, are applied 3 to 4 times a day for 9 to 24 weeks to resolve the lesion.33 Recurrent apthous stomatitis (RAS): Recurrent aphthous stomatitis is a common condition characterized by multiple, recurrent, small, round or ovoid ulcers with circumscribed margins, erythematous haloes, and yellow or gray floors. It appears first in childhood or adolescence.34 Topical corticosteroids are the mainstay of RAS treatment in most countries.35 Several different topical corticosteroids may reduce symptoms and hasten healing.34 The most common treatment involves the use of topical agents to provide symptomatic relief. These include antibiotics, analgesics, non-steroidal anti-inflammatory drugs and immunosuppressants.35 The most common topical therapy involves use of glucocorticoids—including hydrocortisone—triamcinolone, fluocinonide, betamethasone and flumethasone. These medications can reduce symptoms and will not cause hypothalamic-pituitary-adrenal axis suppression when used for less than three weeks.36

Of all the topical agents available to treat recurrent aphthous ulceration, amlexanox appears to be one of the best. It is 2-amino-7isopropyl-5-oxo-5H-(1) benzopyrano-(2,3-b)-pyridine-3-carboxylic acid, a topical anti-inflammatory and anti-allergic drug.35 It is available as a 5% paste in the U.S. for the treatment of RAS. According to Greer et al., in 1993, and Khandwala et al., in 1997,37,38 5% amlexanox paste is very useful in the management of recurrent aphthous ulceration. In 2005, Murray et al. showed that 5% amlexanox paste is more effective in accelerating the healing of ulcers and resolving pain.39 Alternative regimens include dexamethasone 0.05 milligrams/5 mL rinse three times a day, or a high-potency topical corticosteroid such as clobetasol ointment 0.05 percent in Orabase (1:1). Fluocinonide ointment 0.05 percent in Orabase (1:1) can also be used.40 Orofacial Neuropathic Pain Neuropathic pain is defined as a condition that is initiated or caused by a primary lesion or by dysfunction in the nervous system.41 In the orofacial region, pain can be caused by traumatic neuroma, trigeminal or glossopharyngeal neuralgia. Neuropathic pain has a severe psychosocial impact on the quality of life and mood of affected patients and causes substantial societal costs.

Topical Drugs for Recurrent Apthous Stomatitis34

Topical corticosteroids

Hydrocortisone hemisuccinate (pellets) Triamcinolone acetonide (in adhesive paste) Fluocinonide (cream) Betamethasone valerate (mouthrinse) Betamethasone-17-valerate (mouthrinse) Flumethasone pivolate (spray) Beclomethasone diproprionate (spray) Clobetasol proprionate (cream) Mometasone furoate (cream)

Antimicrobials

Chlorhexidine gluconate (mouthrinse) Triclosan (mouthrinse) Topical tetracyclines (e.g.aureomycin, chlortetracycline, tetracycline)

Topical analgesics

Benzydamine hydrochloride (spray or mouthrinse) Topical anaesthetics (gel)

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