Earn

3 CE creditsThis course was

written for dentists, dental hygienists,

and assistants.

Supplement to PennWell Publications

Go Green, Go Online to take your course

The Management of Oral Lichen PlanusA Peer-Reviewed Publication Written by Kimberly M. Parsons, EdD, CDA, EFDA, RDH

© R

ober

t Kne

schk

e | D

ream

stim

e.co

m

AbstractOral lichen planus is an immune-mediated and chronic inflammatory condition that can cause erosion of the oral mucosa. The disease is described as reticular, erosive, atrophic, or bullous in nature, and it typically develops in women in their fifth and sixth decades. Reticular oral lichen planus, absent erythema, is asymptomatic and does not usually need intervention. However, as there is potential for conversion to carcinoma, reticular oral lichen planus associated with erythema or erosion needs treatment and periodic re-evaluation. The literature suggests that erosive and ulcerated oral lichen planus is best managed with topical corticosteroid preparations and, in refractory cases, systemic steroids. Several other immunosuppressive medications and non-medication based interventions are also available, but at greater cost and with greater potential for adverse reactions and side effects. This educational review article focuses on best practices in the management of oral lichen planus.

Educational ObjectivesAt the conclusion of this educational activity, participants will be able to:1. Describe interventions used to manage oral

lichen planus2. Identify the appropriate medications to be

prescribed for managing erosive and ulcerative oral lesions

3. Implement treatment strategies for managing oral ulcers associated with the disease

4. Identify interventions discussed in the litera-ture that are supported by limited evidence

Author ProfileKimberly M. Parsons, EdD, CDA, EFDA, RDH, is the Program Chair of the Dental Assisting and Dental Hygiene Programs and an Assistant Professor of Dental Assisting/Dental Hygiene at the University of Southern Indiana. Her scholarly activities include research in the areas of educa-tional technology, treatment of special needs patients, and allied dental education. Dr. Parsons has been a dental hygienist for 15 years, practicing in Arizona, Indiana, Kentucky, and Michigan. She has also worked as a dental educator in Arizona and Indiana.

Author DisclosureKimberly M. Parsons, EdD, CDA, EFDA, RDH, has no commercial ties with the sponsors or the providers of the unrestricted educational grant for this course.

Publication date: Feb. 2015 Review date: Apr. 2016Expiration date: Mar. 2019

This educational activity has been made possible through an unrestricted grant from PerioSciences.This course was written for dentists, dental hygienists and assistants, from novice to skilled. Educational Methods: This course is a self-instructional journal and web activity. Provider Disclosure: PennWell does not have a leadership position or a commercial interest in any products or services discussed or shared in this educational activity nor with the commercial supporter. No manufacturer or third party has had any input into the development of course content.Requirements for Successful Completion: To obtain 3 CE credits for this educational activity you must pay the required fee, review the material, complete the course evaluation and obtain a score of at least 70%.CE Planner Disclosure: Heather Hodges, CE Coordinator does not have a leadership or commercial interest with products or services discussed in this educational activity. Heather can be reached at hhodges@pennwell.comEducational Disclaimer: Completing a single continuing education course does not provide enough information to result in the participant being an expert in the field related to the course topic. It is a combination of many educational courses and clinical experience that allows the participant to develop skills and expertise.Image Authenticity Statement: The images in this educational activity have not been altered.Scientific Integrity Statement: Information shared in this CE course is developed from clinical research and represents the most current information available from evidence based dentistry. Known Benefits and Limitations of the Data: The information presented in this educational activity is derived from the data and information contained in reference section. The research data is extensive and provides direct benefit to the patient and improvements in oral health. Registration: The cost of this CE course is $59.00 for 3 CE credits. Cancellation/Refund Policy: Any participant who is not 100% satisfied with this course can request a full refund by contacting PennWell in writing.

PennWell designates this activity for 3 continuing educational credits.

Dental Board of California: Provider 4527, course registration number CA# 03-4527-15076“This course meets the Dental Board of California’s requirements for 3 units of continuing education.”

The PennWell Corporation is designated as an Approved PACE Program Provider by the

Academy of General Dentistry. The formal continuing dental education programs of this

program provider are accepted by the AGD for Fellowship, Mastership and membership

maintenance credit. Approval does not imply acceptance by a state or provincial board of

dentistry or AGD endorsement. The current term of approval extends from (11/1/2015) to

(10/31/2019) Provider ID# 320452.

1606de_91 91 6/1/16 9:00 AM

92 06.2016 | DENTALECONOMICS.COM

Educational ObjectivesAt the conclusion of this educational activity participants will

be able to:

1. Describe interventions used to manage oral lichen planus

2. Identify the appropriate medications to be prescribed for

managing erosive and ulcerative oral lesions

3. Implement treatment strategies for managing oral ulcers

associated with the disease

4. Identify interventions discussed in the literature that are

supported by limited evidence

AbstractOral lichen planus is an immune-mediated and chronic inflam-

matory condition that can cause erosion of the oral mucosa. The

disease is described as reticular, erosive, atrophic, or bullous

in nature, and it typically develops in women in their fifth and

sixth decades. Reticular oral lichen planus, absent erythema, is

asymptomatic and does not usually need intervention. However,

as there is potential for conversion to carcinoma, reticular oral

lichen planus associated with erythema or erosion needs treat-

ment and periodic re-evaluation. The literature suggests that

erosive and ulcerated oral lichen planus is best managed with

topical corticosteroid preparations and, in refractory cases, sys-

temic steroids. Several other immunosuppressive medications

and non-medication based interventions are also available, but

at greater cost and with greater potential for adverse reactions

and side effects. This educational review article focuses on best

practices in the management of oral lichen planus.

IntroductionOral lichen planus (“lichen planus,” “OLP,” “oral LP,” or

simply “LP”) is an immune-mediated and chronic inflamma-

tory condition that can cause erosion of the oral mucosa. Based

primarily on clinical presentation, it can be characterized as

reticular, erosive, atrophic, and/or bullous. Rare in children,

this condition typically develops in the fifth or sixth decade of

life and is more common in women. Prevalence of LP ranges

from 1%1 to 6.3%.2

While the occurrence of reticular LP is higher, other types

of LP that cause mucosal erosion or erosive/bullous lesions are

more frequently reported due to the severity of the symptoms

associated with these types. Reticular LP without adjacent er-

ythema is usually asymptomatic. Erosive/ulcerative LP (ELP)

is associated with significant inflammation, tissue erosion, and

sometimes bullous oral lesions. Patients with ELP are likely to

experience a continuous moderate to severe aching pain that

may be accompanied by burning.3 This pain worsens when

eating, particularly when hot or spicy foods are consumed, and

when lesions contact alcohol. Generalized distribution of oral

lesions can be debilitating.4 LP fluctuates between periods of

remission and episodes of recurrence.

The cause of LP is unknown, but considerable research

suggests the primary disease mechanism to be immune medi-

ated.5 It is believed that in most cases mucosal pathology is

triggered by keratinocytes or modified Langerhans cells in

either antigen-specific reactivity involving keratinocyte killing

by CD8 cytotoxic cells or antigen non-specific reactivity in-

volving mast cell degranulation and matrix metalloproteinase

activation.6 It has also been proposed that in some cases of LP

refractory to immunologic intervention, the underlying cause

may be partly neurogenic.7

Other factors or conditions reported in relation to the de-

velopment of mucosal LP include the following: genetics;8 in-

fection such as the hepatitis C virus9 even though magnitude

of the association may be minimal;10 effects of medication

termed lichenoid drug reaction;11 vitamin or mineral defi-

ciencies, such as B-12 deficiency or iron deficient anemia;12

systemic disease, such as the autoimmune disease Sjogren’s

syndrome, rheumatoid disease, pemphigus, or graft versus

host disease;13 and amalgam hypersensitivity.14 (See also Table

1.) The origination of LP stemming from an immune system

abnormality informs most treatment considerations related to

patient care. If underlying disease or a lichenoid drug reaction

is strongly suspected as the cause of LP, the patient should

be referred for additional medical evaluation or consultation.

However, regardless of the association of LP with a number

of medical problems, the treating clinician should not assume

that the patient with LP has one of these conditions. It has

been proposed that patients with LP should not be routinely

screened for systemic disease without a strong indication of

possible disease.15

Table 1: Factors/conditions reported in mucosal lichen planus development

Factor/Condition

Genetics

Infection

Lichenoid drug reaction

Vitamin/mineral deficiencies

Systemic disease

Amalgam hypersensitivity

Reticular LPReticular LP is typically asymptomatic and does not routinely

require intervention. However, due to the white striations and

plaques associated with reticular LP and their similar appear-

ance to oral cancer, all lesions should be documented in the

patient chart, including recording of the the location(s), tak-

ing photographs, and other pertinent descriptions of the le-

sions. In addition, lesions associated with reticular LP should

be monitored for changes, such as size, thickness, coloration

of mucosa, ulceration or erosion, and emergent symptoms

such as pain, that may be indicative of potential dysplastic

1606de_92 92 6/1/16 9:00 AM

DENTALECONOMICS.COM | 06.2016 93

conversion.16,17 Dysplastic transformation of lichen planus is

relatively rare, as is evidenced by a systematic review of over

7,000 subjects with LP where malignant transformation was

reported in only 3.7% of cases. Transformation to malignancy

is reported to occur more frequently in female patients, with

the tongue serving as the most common site of expression.

Fitzpatrick, Hirsch, and Gordon’s research demonstrated

that cancer develops a mean of 51.4 months after the initial

discovery of the condition, with the average age of onset of

malignancy being 60.8 years old.18 If transformation to a

premalignant lesion (dysplasia) is suspected, histopathologic

evaluation is indicated.

In patients with lichenoid lesions caused by hypersensitiv-

ity to amalgam or other restorative materials, or those with

lesions that suggest a lichenoid drug reaction, treatment con-

sists of removal of the associated restoration(s) or discontinu-

ation of the offending medication under the guidance of the

patient’s physician. The following medications are associated

with lichenoid drug reactions: antihypertensives, including

beta-blockers, angiotensin converting enzyme (ACE) in-

hibitors, and diuretics; antibiotics, such as penicillin, ami-

nosalicylate sodium, isoniazid rifampin, streptomycin, and

tetracyclines; non-steroidal anti-inflammatories (NSAIDs);

oral hypoglycemic agents; antiretroviral medications; antima-

larials, such as hydroxychloroquine; anticonvulsants, such as

carbamazepine, oxacarbazepine, phenytoin, valproate; antidi-

arrheals, such as bismuth; antifungals, such as amphotericin

B and ketoconazole; and antihistamines, such as cimetidine,

cinnarizine, and triprolidine40.Lichenoid reactions tend to be

widespread over the mucosa, while lesions associated with

dental restorative material will be confined to mucosa that is

in close contact with the material. At present, there appears to

be little reason to remove all amalgam restorations in patients

with generalized reticular lichen planus.19

Erosive/Ulcerative Lichen PlanusSimilar to other forms of lichen planus, erosive/ulcerative

lichen planus (ELP) is a chronic disease with no known cure.

Regardless of therapy, complete resolution of lesions is dif-

ficult to achieve. Future research may identify cellular and

genetic mechanisms that prove useful in the development of

effective long-term treatment strategies and a possible cure.

Until that time, the clinician treating ELP must utilize either

pharmacotherapy known to suppress immune function and

pain and promote healing or non-pharmacological interven-

tions that have previously shown promise in managing the

disease. Most medication strategies used to treat ELP have

limited supportive evidence, as few of these are supported by

studies using rigorous scientific methodology.20 There is even

less evidence-based support for non-pharmacological inter-

ventions such as photochemotherapy, photodynamic therapy,

or laser therapy, which have also been suggested as treatment

for ELP.

Figure 1

PharmacotherapyIn a Cochrane Database Systematic Review published in 2012,

Cheng et al.21 reviewed studies up to September 2009 from

multiple databases. These databases included the Cochrane

Central Register of Controlled Trials, MEDLINE, EMBASE,

and LILACS, as well as the registries for ongoing trials. Cheng

et al. selected a randomized control trial to report results of

treatment of lichen planus with topical or systemic medication.

They identified 15 randomized control trials with 473 total

participants having erosive LP. However, they were not able

to pool data due to the small number of subjects, heterogeneity

of the interventions, design methods, and different outcome

variables found between the studies. Meta-analysis could not

be performed. Nonetheless, the authors reported that in one

study with 50 subjects, 0.025% clobetasol propionate adminis-

tered as a liquid microsphere significantly reduced pain when

compared to the delivery of a placebo ointment.21 In another

study, significant pain reduction occurred with a cyclosporine

solution, when contrasted to a 0.1% triamcinolone acetonide in

orabase formulation.21 In a third study, aloe vera gel was shown

to be six times more likely to result in at least a 50% reduction

in pain when compared with a placebo.21 Additionally, it was

noted that pimecrolimus cream was more effective in improv-

ing ELP than a vehicle cream.21

Another Cochrane Database Systematic Review assessed

28 clinical ELP trials that used “pain-report” as an outcome

variable following medication application. 21 Similar results

to those found in the aforementioned review were reported,22

and authors from both reviews asserted that evidence on the

effectiveness of treatment for ELP is weak.

Regardless, topical corticosteroirds continue to be widely

utilized as a first-line therapy for erosive/ulcerative LP in both

medicine and dentistry.23 Additionally, high-potency topical

steroids are thought to be the most effective strategy for reduc-

ing symptoms and minimizing disease in patients with severe

pathology. One example of this is a double-blind placebo-con-

trolled clinical study where a 75% improvement was reported

following the application of fluocinonide in an adhesive base.24

High-potency topical treatments include clobetasol (Temo-

vate®), fluocinonide (Lidex®), and halobetasol (Ultravate®), all

three of which are dispensed as 0.05% creams or ointments. Clo-

1606de_93 93 6/1/16 9:00 AM

94 06.2016 | DENTALECONOMICS.COM

betasol propionate and fluocinonide are also provided in a 0.05%

solution, but the FDA has recommended that these products only

be used externally25 because of the possibility of hypothalamus-

pituitary-adrenal inhibition.26 Gels can be mixed with equal parts

orabase to make an adhesive paste for application to small- or

medium-sized lesions. It is recommended that lesions should be

coated with the gel or cream after each meal and at bedtime.27

Broader coverage can sometimes be achieved through the use of

an acrylic appliance that holds the gel or cream against the mucosa.

Dexamethasone, another potent corticosteroid, is effec-

tive in treating generalized erosive or ulcerative lesions. It is

prescribed as a rinse that is held in the mouth for a short time.

When used three or four times daily, maximum coverage is pro-

vided. Two prescriptions are presented: Rx: Dexamethasone

(Decadron) elixir 0.5mg/5ml (Disp 320 mls; Sig [1] For 3 days,

rinse with 1 tablespoonful (15ml) qid and swallow. Then [2], for

3 days, rinse with 1 teaspoonful (5ml) qid and swallow. Then

[3], for 3 days, rinse with 1 teaspoonful (5ml) qid and swallow

every other time. Then [4], rinse with 1 teaspoonful (5ml) qid

and expectorate). Another prescription is: Rx: Dexamethasone

elixir 0.5mg/5ml (Disp 100mls; Sig: Rinse with 1 teaspoonful

(5ml) for 3-4 minutes qid and spit out); discontinue when le-

sions become asymptomatic. Either approach may be consid-

ered reasonable intervention as published research comparing

these two prescriptions of dexamethasone is not available.28

Even with topical application of corticosteroid to mucosa,

there is potential for systemic, as well as local side effects. Close

collaboration with the patient’s physician is recommended, par-

ticularly when these medications are prescribed for a prolonged

period of time.28 Systemic prednisone can also be prescribed, but

its use should be considered only in cases involving severe recal-

citrant lesions where topical approaches to therapy have failed.

If systemic corticosteroid is considered, it should be prescribed

at the lowest possible dosage and only for a short time. There are

a number of prescribing regimens that are effective such as: Rx:

Prednisone tablets 5mg (Disp: 40 tabs;Sig: Take 5 tablets in the

morning for five days, then 5 tablets in the morning every other

day until gone.) Medrol dose packs are also available.

Any patient using corticosteroids should be monitored for

the emergence of fungal infection (candidiasis), that can occur

with application of this class of drugs. If the LP patient is prone

to fungal infections or has experienced candida infection in the

past following steroid administration, prophylactic antifungal

therapy should be pursued as concurrent therapy.

Additional immunosuppressant medications and immuno-

modulatory agents that may be considered to manage severe re-

calcitrant erosive/ulcerative LP include calcineurin inhibitors

such as cyclosporine, tacrolimus, and pimecrolimus. However,

these drugs are expensive and there are few studies supporting

the use of cyclosporine. Further, local and systemic side effects

can be problematic.29

Pimecrolimus and tacrolimus, indicated for the treatment of

atopic dermatitis, have a number of studies supporting their use

in treating LP. These drugs inhibit T-cell activation and cyto-

kine release from mast cells. Systematic review of five double-

blind studies and ten prospective studies, as well as numerous

case reports, suggest that topical tacrolimus ointment 1% may

be equal to topical clobetasol propionate 0.05% ointment and

topical triamcinolone acetonide 0.1% paste, in terms of treat-

ment outcome.30 Treatment with topical tacrolimus appears

to result in measurable blood levels but, according to Swift et

al.,31 this medication has not been associated with significant

adverse effects. However, prolonged use of tacrolimus may

increase cancer risk, and therefore, should only be applied for

a short period of time. The FDA recommends against oral ap-

plication of this medication to mucosa41.

Other medications, such as retinoids, dapsone, azathioprine,

mycophenolate mofetil, acitretin, and enoxaparin, that have

been recommended for use with ELP have limited scientific

support and should not be routinely utilized. The use, particu-

larly long term, of some of the aforementioned drugs may result

in adverse reactions. For example, two common side effects of

dapsone use are hemolysis and hypersensitivity reactions in the

form of fever and jaundice, typically occuring within the first

six weeks of therapy.32 Finally, all of the abovementioned drugs

are more expensive relative to the cost of corticosteroids.

Non-pharmacological Treatment ModalitiesThere are several non-pharmacological interventions sug-

gested for treatment of ELP. These include PUVA therapy,

where uses are application of the sensitizing drug psoralen

followed by ultraviolet light; photodynamic therapy, which

includes a photosensitizer, light source, and tissue oxygen;

and laser therapy. Only the latter is likely to be utilized in the

dental office. These strategies have limited supportive evidence

for treating LP but might be considered for severe recalcitrant

cases.33 When 21 atrophic/erosive LP patients who were treat-

ed with laser phototherapy (LPT) three times a week for three

months were compared to 21 atrophic/erosive LP patients who

used clobetasol propionate 0.05% applied three times a day

for three months. The LPT group was found to have a higher

percentage of complete lesion resolution at 60 and 90 days with

no recurrence of lesions.34 In contrast, the clobetasol group was

reported to have experienced worsening of all the variables ana-

lyzed.34 Although this suggests that LPT may be quite effective

in the treatment of recalcitrant ELP, an in-office application

three times a week might be difficult for some patients to man-

age.34 PUVA therapy has been associated with adverse events,

including nausea, dizziness, and 24-hour photosensitivity.35

Although not considered “treatment,” patients with LP

should be advised to maintain good oral hygiene and instruc-

tion in appropriate care should be considered to reduce injury

to involved tissues. Dietary recommendations should include

instructions to eat soft nutritious food during outbreaks, the

avoidance of caffeine, and cessation of smoking and alcohol.

Since ELP may be aggravated by stress and can be associated

1606de_94 94 6/1/16 9:00 AM

DENTALECONOMICS.COM | 06.2016 95

with depression, activities that reduce stress and modify de-

pression should be suggested. Another novel approach to treat-

ment that has not been extensively studied but may be useful is

antioxidant application (e.g., AO ProVantageGel). In one case

study, the gel was applied three times daily for eight weeks with

symptom improvement continuing for over a year. There is also

published evidence that the saliva of a patient with LP exhibits

increased levels of oxidative stress and lower antioxidant capac-

ity compared to the saliva of healthy patients.37–39

ConclusionDental professionals are likely to encounter one or more cases of

LP during clinical practice. Since it is probable that they will en-

counter reticular LP, the importance for the clinician to differenti-

ate between this disease and other more serious problems, such as

dysplasia, is high.36 However, it is the erosive/ulcerative LP that

will require direct clinical intervention and careful monitoring.

This course has presented several pharmacologic approaches to

treatment that are evidence-based or common practice for man-

aging erosive/ulcerative LP. In addition, the course provided sug-

gestions for non-pharmacologic interventions, which may have

limited use. Although a number of new drugs have been suggested

for the treatment of ELP, at the present time, topical application

of corticosteroid medication followed by systemic administration

in severe refractory cases remains the standard of care.

Bibliography1. McCartan BE, Healy CM. The reported prevalence of oral lichen planus: Areview

and critique. J Oral Pathol Med. 2008;37:447–53. 2. Oliveira Alves MG, Almeida JD, Balducci I, Guimarães Cabral LA. Orallichen

planus: A retrospective study of 110Brazilian patients. BMC Res Notes. 2010;3:157).3. Patil A, et al. Oral bullous lichen planus: Case report and review ofmanagement

Contemp Clin Dent. 2012 Jul-Sep; 3(3): 344–348. 4. Usatine R, Tinitigan M. Diagnosis and Treatment of Lichen Planus. Am Fam

Physician. 2011 Jul 1;84(1):53-60.5. Usatine R, Tinitigan M. Diagnosis and Treatment of Lichen Planus. Am Fam

Physician. 2011 Jul 1;84(1):53-60. 6. Radwan-Oczko M.Topical application of drugs used in treatment of oral lichen

planus lesions. Adv Clin Exp Med. 2013 Nov-Dec;22(6):893-8.7. Guarneri F, Guarneri C, Marini H. Oral lichen planus and neurogenic inflammation:

new observations and therapeutic implications from four clinical cases. Dermatol Ther. 2014 Jul-Aug;27(4):206-10.

8. Stanimirovic D, et al. TLR2, TLR3, TLR4, ad CD14 gene polymorphisms associated with oral lichen planus risk. Eur J Oral Sci. 2013; 121(5):421-6.

9. Carrozzo M, Scally K.Oral manifestations of hepatitis C virus infection. World J Gastroenterol. 2014 Jun 28;20(24):7534-43

10. Petti S, et al. The magnitude of the association between hepatitis C virus infection and oral lichen planus: meta-analysis and case control study. Odontology. 2011 Jul;99(2):168-78.

11. Romanelli M, Rhodes A. Guanfacine-induced lichenoid drug eruption in a child with autism and attention deficit hyperactivity disorder. Pediatr Dermatol. 2014 Sep;31(5):614-5.

12. Wu YC, et al. Oral manifestations and blood profile in patients with iron deficiency anemia. J Formos Med Assoc. 2014 Feb;113(2):83-7.

13. Findler M, Garfunkel AA Images in clinical medicine. Oral lichen planus as a clinical sign of graft-versus-host disease. N Engl J Med. 2003 Dec 4;349(23):2223.

14. Gowri Pendyala. Oral Lichen Planus: A Report and Review of an Autoimmune-Mediated Condition in Gingiva. Compendium September 2012, Volume 33, Issue 8. Published by AEGIS Communications.

15. Vučićević Boras V. The Significance of Oral and Systemic Factors in Australian and Croatian patients with Oral Lichen Planus. Acta Dermatovenerol Croat. 2014 Jul;22(2):97-102.

16. Otero-Rey EM, et al. Malignant transformation of oral lichen planus by a chronic inflammatory process. Use of topical corticosteroids to prevent this progression? Acta Odontol Scand. 2014 May 22:1-8.

17. Safadi RA. Oral lichen planus shows higher expressions of tumor suppressor gene products of p53 and p21 compared to oral mucositis. An immunohistochemical study. Arch Oral Biol. 2010 Jun;55(6):454-61.

18. Fitzpatrick SG, Hirsch SA, Gordon SC. The malignant transformation of oral lichen planus and oral lichenoid lesions: a systematic review. J Am Dent Assoc. 2014 Jan;145(1):45-56.

19. Baccaglini L, et al. Urban legends series: lichen planus. Oral Dis. 2013 Mar;19(2):128-43.

20. Cheng S. et al. Interventions for erosive lichen planus affecting mucosal sites. Cochrane Database Syst Rev. 2012 Feb 15;2:CD008092.

21. Cheng S. et al. Interventions for erosive lichen planus affecting mucosal sites. Cochrane Database Syst Rev. 2012 Feb 15;2:CD008092.

22. Thongprasom K, et al. Interventions for treating oral lichen planus. Cochrane Database Syst Rev. 2011 Jul 6;(7):CD001168.

23. Usatine R, Tinitigan M. Diagnosis and Treatment of Lichen Planus. Am Fam Physician. 2011 Jul 1;84(1):53-60.

24. Voûte AB, Schulten EA, Langendijk PN, Kostense PJ, van der Waal I. Fluocinonide in an adhesive base for treatment of oral lichen planus. A double-blind, placebo-controlled clinical study. Oral Surg Oral Med Oral Pathol. 1993;75(2):181–185.

25. h t t p : / / d a i l y m e d . n l m . n i h . g o v / d a i l y m e d / a r c h i ve s / f d a D r u g I n f o.cfm?archiveid=10779)(http://dailymed.nlm.nih.gov/dailymed/archives/fdaDrugInfo.cfm?archiveid=8186). Accessed 9/23/14.

26. Gonzalez-Moles MA, Scully C. HPA-suppressive effects of aqueous clobetasol propionate in the treatment of patients with oral lichen planus. J Eur Acad Dermatol Venereol. 2010 Sep;24(9):1055-9.

27. Silverman S, and Eversole R. Immunopathologic Mucosal Lesions. Chapter 21 in Essentials of Oral Medicine. Eds. Sol Silverman, L Roy Eversole, and Edmond Truelove. BC Decker Inc. London 2001.

28. Clinician’s Guide to Treatment of Common Oral Conditions. Ed. Michael A Siegel, Sol Silverman, Thomas P Sollecito. Fifth edition. The American Academy of Oral Medicine, 2001 and 1997.

29. López-Jornet P, Camacho-Alonso F, Salazar-Sanchez N. Topical tacrolimus and pimecrolimus in the treatment of oral lichen planus: an update. J Oral Pathol Med. 2010 Mar;39(3):201-5.

30. Samycia M, Lin AN.Efficacy of topical calcineurin inhibitors in lichen planus. J Cutan Med Surg. 2012 Jul-Aug;16(4):221-9.

31. Swift JC, et al. The effectiveness of 1% pimecrolimus cream in the treatment of oral erosive lichen planus. J Periodontol. 2005 Apr;76(4):627-35).

32. Lavanya N, et al. Oral lichen planus: An update on pathogenesis and treatment. J Oral Maxillofac Pathol. 2011 May-Aug; 15(2): 127–132.

33. Trehan M, Taylor CRLow-dose excimer 308-nm laser for the treatment of oral lichen planus. Arch Dermatol. 2004 Apr;140(4):415-20.

34. Dillenburg CS, et al. Efficacy of laser phototherapy in comparison to topical clobetasol for the treatment of oral lichen planus: a randomized controlled trial. J Biomed Opt. 2014 Jun;19(6):068002.

35. Lundquist GPhotochemotherapy of oral lichen planus. A controlled study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1995 May;79(5):554-8.

36. Gorouhi F, et al. Cutaneous and Mucosal Lichen Planus: A Comprehensive Review of Clinical Subtypes, Risk Factors, Diagnosis, and Prognosis. ScientificWorldJournal. 2014; 2014: 742826. Published online Jan 30, 2014.

37. Shovna Shivani Mishra, et al. Evaluation of oxidative stress in oral lichen planus using malonaldehyde: A systematic review. DOI: 10.1016/j.jssdds.2014.01.002.

38. Iffat Hassan, et al. Evaluation of the antioxidant status in patients of lichen planus in Kashmir valley – A hospital based study. DOI: 10.1016/j.jssdds.2012.12.002.

39. Miricescu D, et al. The antioxidant potential of saliva: clinical significance in oral diseases.Therapeutics, Pharmacology and Clinical Toxicology. 2011 Jun;15(2):139-143.

40. Kalmar JR. Oral manifestations of drug reactions. Medscape. August 2014. Retrieved from http://emedicine.medscape.com/article/1080772-overview

41. US Food and Drug Administration. Safety labeling changes approved by FDA Center for Drug Evaluation and Research (CDER). November 2011. Retrieved from http://www.fda.gov/safety/medwatch/safetyinformation/ucm283160.htm

Author ProfileKimberly M. Parsons, EdD, CDA, EFDA, RDH, is the Program Chair of the

Dental Assisting and Dental Hygiene Programs and an Assistant Professor of Den-

tal Assisting/Dental Hygiene at the University of Southern Indiana. Her schol-

arly activities include research in the areas of educational technology, treatment of

special needs patients, and allied dental education. Dr. Parsons has been a dental

hygienist for 15 years, practicing in Arizona, Indiana, Kentucky, and Michigan.

She has also worked as a dental educator in Arizona and Indiana. Author DisclosureKimberly M. Parsons, EdD, CDA, EFDA, RDH, has no commercial ties with the

sponsors or the providers of the unrestricted educational grant for this course.

1606de_95 95 6/1/16 9:00 AM

Questions

Online CompletionUse this page to review the questions and answers. Return to www.ineedce.com and sign in. If you have not previously purchased the program select it from the “Online Courses” listing and complete the online

purchase. Once purchased the exam will be added to your Archives page where a Take Exam link will be provided. Click on the “Take Exam” link, complete all the program questions and submit your answers. An

immediate grade report will be provided and upon receiving a passing grade your “Verification Form” will be provided immediately for viewing and/or printing. Verification Forms can be viewed and/or printed anytime

in the future by returning to the site, sign in and return to your Archives Page.

1. Which of the following statements most accurately characterizes lichen planus:a. The condition develops in the third and forth

decadeb. Men are most likely to express the diseasec. It is most prevalent in childrend. It is an immune mediated condition

2. Which of the following statements is accurate:a. Reticular lichen planus occurs more frequently than

other forms of the diseaseb. The prevalence rate for all forms of oral LP range

from 1 to 6.3 percentc. Both a and bd. Neither a or b

3. Oral lichen planus is characterized as:a. Reticularb. Erosivec. Atrophicd. All of the above

4. Which of the following statements is not accurate:a. Lichen planus is curableb. Lichen planus is chronic with episodes of remission

and reoccurrencec. Erosive LP is associated with significant inflamma-

tion d. Patients with erosive LP often say their mucosal is

painful

5. Identify the correct statement regarding erosive lichen planus:a. Lichen planus associated with erosive lesions is not

debilitating for the patientb. Erosive lichen planus is associated with moderate to

severe aching painc. Eating does not worsen pain experienced with

erosive lichen planusd. Medications containing alcohol are not likely to

exacerbate erosive lichen planus lesions

6. The mucosal pathology of LP is thought to include:a. Antigen specific activity involving keratinocyte

killing by CD8 cytotoxic cellsb. Antigen non-specific reactivity involving mast

cell degranulation and matrix metalloproteinase activation

c. Both a and bd. Neither a or b

7. Which of the following statements is most accurate:a. A neurogenic etiology has been proposed to explain

LP refractory to immunologic interventionb. Langerhans cells have little to do with disease

pathology in LPc. Both a and bd. Neither a or b

8. Which of the following factors has been linked with lichen planus:a. Vitamin A deficiencyb. Hepatitis C virusc. Both a and bd. Neither a or b

9. When medications cause lichen planus the condition is termed:a. Medication lichen planusb. Medicamentosac. Erosive LP diseased. Lichenoid drug reaction

10. Medical conditions that have been associ-ated with oral lichen planus include:a. Pemphigusb. Graft versus host diseasec. Rheumatoid diseased. All of the above

11. If a drug reaction is strongly suspected as the cause of oral LP the patient should be:a. Immediately removed from the drugb. Referred for medical consultation prior to

withdrawal from the drugc. Both a and bd. Neither a or b

12. Which of the following statements is accurate:a. If a patient has lichen planus he/she is likely to have

one of the medical conditions associated with the disease.

b. As a general rule patients with LP should not be routinely screened for systemic disease.

c. Both a and bd. Neither a or b

13. If a patient is found to have oral reticular LP a dentist should:a. Aggressively treat the conditionb. Chart the condition for location and followc. Immediately biopsyd. Assume that every lesion is precancerous

14. Dysplastic transformation of lichen planus, while rare, may occur in what percent of cases per reported research:a. 3.7b. 5.1c. 12.2d. 1.0

15. Which of the following statements ac-curately describes dysplastic conversion:a. It occurs more frequently in female patientsb. The most common site of conversion is the tonguec. The average age at conversion is around 60d. All of the above

16. Which of the following statements is most accurate:a. Non-medication interventions used to treat

erosive/ulcerative LP have been extensively researched

b. Few studies involving medication treatment are supported by rigorous science

c. Both a and bd. Neither a or b

17. Which class of medication is the most useful for treating erosive/ulcerative LP:a. The antifungalsb. The anxiolyticsc. The corticosteroidsd. None of the above

18. The clinician treating erosive/ulcerative LP should consider which of the following as first line therapy:a. High potency corticosteroidsb. Low potency corticosteroidsc. An immunosuppressive such as Cyclosporined. None of the above

19. A dentist treating erosive/ulcerative LP should not use which type of corticosteroid preparation:a. Clobetasol (Temovate®) ointmentb. Fluocinonide (Lidex®) ointmentc. Halobetasol (Ultravate®) creamd. Fluocinonide (Lidex®) solution

20. What is the percentage of corticosteroid in high-potency topicals used to treat LP:a. 0.20%b. 0.05%c. 0.10%d. 0.75%

21. When corticosteroid gels are used it is recommended that they be:a. Applied four times a dayb. Applied before each mealc. Applied twice a day after mealsd. None of the above

22. The correct way to prescribe dexametha-sone is:a. 0.5 mg/5mls; Disp 320 mls; Sig – for 3 days rinse

with 1 tablespoonful (or 15mls) qid and swallow; then for 3 days rinse with 1 teaspoonful (or 5mls) qid and swallow; then for 3 days rinse with 1 tsp qid and swallow; then rinse with 1 tsp qid with expectoration

b. 0.5mg/5ml; Disp 100 mls; Sig – Rinse with 1 teaspoonful (5mls) for 3-4 minutes qid and spit out; Discontinue when lesions are asymptomatic

c. Both a and bd. Neither a or a

23. When should systemic prednisone be prescribed:a. Immediately after lesions are diagnosedb. Only in cases involving severe recalcitrant lesions

where topical therapy has failedc. When the patient has both reticular as well as

erosive/ulcerative lesionsd. None of the above

24. What is the most accurate approach to prescribing systemic prednisone:a. It should be prescribed at the lowest possible

dosageb. It should be prescribed for a long period of timec. It should be prescribed using an increasing dose

strategyd. None of the above

25. Adverse reactions to prescribed systemic prednisone include:a. Hypothalamus-pituitary-adrenal inhibitionb. Fungal infection (candidiasis)c. Both a and bd. Neither a or b

26. Additional immunosuppressant medica-tions and immunomodulatory agents that can be considered to manage recalcitrant erosive/ulcerative LP include:a. Cyclosporineb. Tacrolimusc. Pimecrolimusd. All of the above

27. Which statement is accurate regarding Tacrolimus use for erosive/ulcerative LP:a. The US Food and Drug Administration recom-

mends against oral application of this medicationb. Tacrolimus may increase cancer riskc. Tacrolimus treatment can result in measurable

blood levelsd. All of the above

28. Which statement accurately reflects medications such as the retinoids, dapsone, azathioprine, mycophenolate, mofetil, and acitretin:a. There is limited scientific support for their useb. These drugs have few side effects or adverse

reactionsc. Dapsone has not been associated with hemolysis

and hypersensitivity reactionsd. All of the above

29. Of the following non-pharmacological interventions suggested as treatment of erosive/ulcerative LP, which therapy has been contrasted with Clobetasol:a. PUVA therapyb. Photodynamic therapyc. Laser phototherapyd. None of the above

30. PUVA therapy has been associated with which of the following:a. Nauseab. Dizzinessc. Photosensitivityd. All of the above

1606de_96 96 6/1/16 9:00 AM

Customer Service 800-633-1681

ANSWER SHEET

The Management of Oral Lichen PlanusName: Title: Specialty:

Address: E-mail:

City: State: ZIP: Country:

Telephone: Home ( ) Office ( )

Lic. Renewal Date: AGD Member ID:

Requirements for successful completion of the course and to obtain dental continuing education credits: 1) Read the entire course. 2) Complete all information above. 3) Complete answer sheets in either pen or pencil. 4) Mark only one answer for each question. 5) A score of 70% on this test will earn you 3 CE credits. 6) Complete the Course Evaluation below. 7) Make check payable to PennWell Corp. For Questions Call 800-633-1681

Educational Objectives

1. Describe interventions used to manage oral lichen planus

2. Identify the appropriate medications to be prescribed for managing erosive and ulcerative oral lesions

3. Implement treatment strategies for managing oral ulcers associated with the disease

4. Identify interventions discussed in the literature that are supported by limited evidence

Course Evaluation1. Were the individual course objectives met?

Objective #1: Yes No Objective #2: Yes No

Objective #3: Yes No Objective #4: Yes No

Please evaluate this course by responding to the following statements, using a scale of Excellent = 5 to Poor = 0.

2. To what extent were the course objectives accomplished overall? 5 4 3 2 1 0

3. Please rate your personal mastery of the course objectives. 5 4 3 2 1 0

4. How would you rate the objectives and educational methods? 5 4 3 2 1 0

5. How do you rate the author’s grasp of the topic? 5 4 3 2 1 0

6. Please rate the instructor’s effectiveness. 5 4 3 2 1 0

7. Was the overall administration of the course effective? 5 4 3 2 1 0

8. Please rate the usefulness and clinical applicability of this course. 5 4 3 2 1 0

9. Please rate the usefulness of the supplemental webliography. 5 4 3 2 1 0

10. Do you feel that the references were adequate? Yes No

11. Would you participate in a similar program on a different topic? Yes No

12. If any of the continuing education questions were unclear or ambiguous, please list them.

________________________________________________________________

13. Was there any subject matter you found confusing? Please describe.

_________________________________________________________________

14. How long did it take you to complete this course?

_________________________________________________________________

15. What additional continuing dental education topics would you like to see?

_________________________________________________________________

For IMMEDIATE results, go to www.ineedce.com to take tests online.

Answer sheets can be faxed with credit card payment to 918-831-9804.

Payment of $59.00 is enclosed. (Checks and credit cards are accepted.)

If paying by credit card, please complete the following: MC Visa AmEx Discover

Acct. Number: ______________________________

Exp. Date: _____________________

Charges on your statement will show up as PennWell

If not taking online, mail completed answer sheet to

PennWell Corp.Attn: Dental Division,

1421 S. Sheridan Rd., Tulsa, OK, 74112 or fax to: 918-831-9804

PLEASE PHOTOCOPY ANSWER SHEET FOR ADDITIONAL PARTICIPANTS.

MOLP0616DE

COURSE EVALUATION and PARTICIPANT FEEDBACKWe encourage participant feedback pertaining to all courses. Please be sure to complete the survey included with the course. Please e-mail all questions to: hhodges@pennwell.com.

INSTRUCTIONSAll questions should have only one answer. Grading of this examination is done manually. Participants will receive confirmation of passing by receipt of a verification form. Verification of Participation forms will be mailed within two weeks after taking an examination.

COURSE CREDITS/COSTAll participants scoring at least 70% on the examination will receive a verification form verifying 3 CE credits. The formal continuing education program of this sponsor is accepted by the AGD for Fellowship/Mastership credit. Please contact PennWell for current term of acceptance. Participants are urged to contact their state dental boards for continuing education requirements. PennWell is a California Provider. The California Provider number is 4527. The cost for courses ranges from $20.00 to $110.00.

PROVIDER INFORMATIONPennWell is an ADA CERP Recognized Provider. ADA CERP is a service of the American Dental association to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, not does it imply acceptance of credit hours by boards of dentistry.

Concerns or complaints about a CE Provider may be directed to the provider or to ADA CERP ar www.ada.org/cotocerp/

The PennWell Corporation is designated as an Approved PACE Program Provider by the Academy of General Dentistry. The formal continuing dental education programs of this program provider are accepted by the AGD for Fellowship, Mastership and membership maintenance credit. Approval does not imply acceptance by a state or provincial board of dentistry or AGD endorsement. The current term of approval extends from (11/1/2015) to (10/31/2019) Provider ID# 320452

RECORD KEEPINGPennWell maintains records of your successful completion of any exam for a minimum of six years. Please contact our offices for a copy of your continuing education credits report. This report, which will list all credits earned to date, will be generated and mailed to you within five business days of receipt.

Completing a single continuing education course does not provide enough information to give the participant the feeling that s/he is an expert in the field related to the course topic. It is a combination of many educational courses and clinical experience that allows the participant to develop skills and expertise.

CANCELLATION/REFUND POLICYAny participant who is not 100% satisfied with this course can request a full refund by contacting PennWell in writing.

IMAGE AUTHENTICITYThe images provided and included in this course have not been altered.

© 2016 by the Academy of Dental Therapeutics and Stomatology, a division of PennWell

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

AGD Code 739

1606de_97 97 6/1/16 9:00 AM