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Ce400/Ce400.Aspx Actinic Cheilosis: Etiology, Epidemiology, Clinical Manifestations, Diagnosis, and Treatment Michaell A. Huber, DDS; Géza T. Terézhalmy, DDS, MA Continuing Education Units: 2 hours Online Course: www.dentalcare.com/en-US/dental-education/continuing-education/ce400/ce400.aspx Disclaimer: Participants must always be aware of the hazards of using limited knowledge in integrating new techniques or procedures into their practice. Only sound evidence-based dentistry should be used in patient therapy. This continuing education course presents the etiology, epidemiology, clinical manifestations, diagnosis, and treatment of actinic cheilosis. Conflict of Interest Disclosure Statement • Dr. Huber reports no conflicts of interest associated with this course. • Dr. Terézhalmy has done consulting work for Procter & Gamble and is a member of the dentalcare.com Advisory Board. ADA CERP The Procter & Gamble Company 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, nor 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 at: http://www.ada.org/cerp 1 ® ® Crest Oral-B at dentalcare.com Continuing Education Course, Revised December 9, 2015 Approved PACE Program Provider The Procter & Gamble Company is designated as an Approved PACE Program Provider by the Academy of General Dentistry. The formal continuing education programs of this program provider are accepted by 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 8/1/2013 to 7/31/2017. Provider ID# 211886 Overview Actinic cheilosis is a chronic degenerative disorder primarily of the lower lip caused by long-term exposure to sunlight. It is premalignant and usually occurs in fair-skinned men over 40 years of age. Reducing exposure to sunlight is the single most important measure in preventing actinic cheilosis. Diagnosis is predicated on histological examination of biopsy specimens. Topical chemotherapy may be used in early lesions. Prophylactic ablation or vermilionectomy may be performed in cases where malignant transformation has not yet occurred. The treatment of malignancy is primarily surgical. Learning Objectives Upon completion of this course, the dental professional should be able to: • Discuss the etiology and epidemiology of solar cheilosis. • Recognize the clinical manifestations of solar cheilosis. • Diagnose solar cheilosis. • Develop preventive and treatment management strategies for patients with solar cheilosis. Course Contents and mucous membrane of the inner labia.2 The • Introduction epidermis is characterized by a highly developed • Etiology and Epidemiology stratum lucidum and a very thin stratum corneum. • Clinical Manifestations Hair and sweat glands are absent but dermal • Diagnosis papillae are abundant, leading to the rich vascular • Prevention supply that imparts the characteristic red color • Therapeutic Strategies (vermilion). In dark-complected individuals, the red • Conclusion hue is camouflaged by increased melanin deposits.3 • Course Test • References SC is a precancerous neoplasia found primarily • About the Authors on the lower lip of light-skinned individuals. Given the high risk for the progression of SC to SCC of Introduction the lip vermilion and the high rate of discordance Exposure to sunlight leads to the development of between clinical and histologic findings, a sunburn, premature aging of the skin, cataracts, biopsy is indicated in the presence of clinically immune suppression, and skin cancer. Actinic discernable degenerative changes.1 Prevention, keratosis (AK) of the skin represents an early early diagnosis, effective therapeutic intervention, stage of a continuum that may ultimately and close long-term follow-up are paramount. progress to squamous cell carcinoma (SCC). Actinic cheilosis is the labial equivalent of AK. Etiology and Epidemiology The term actinic cheilitis is often used; however, The etiologic factors associated with SC are the actinic or solar cheilosis (SC) is more accurate same as those associated with AK and cutaneous because this sun-induced neoplastic disease is SCC, namely the cumulative effect of exposure primarily non-inflammatory.1 to ultraviolet radiation (UVR), skin phenotype, genetic predisposition, increasing age, male The highly developed lip vermilion exists only gender, outdoor occupation and leisure activities, in man and is bounded by the keratinized skin geographic latitude of residence, failure to use 2 ® ® Crest Oral-B at dentalcare.com Continuing Education Course, Revised December 9, 2015 lip-protective agents, and host immune status.1,4 skin phenotype (Table 1) is an important The risk associated with smoking, alcohol predisposing factor and it is important in consumption, and poor oral hygiene is unclear.1 assessing the risk for SC.4,8,12,13,18,19 The increased melanin in the lip vermilion of dark-complected Chronic exposure to UVR is the most important individuals appears to provide increased cause of SC.1,5-10 Ultraviolet-B (UV-B) radiation protection from the harmful effects of UVR.4,11 It is (wavelength 280-320 nm) is principally of note that SCC of the lower lip occurs 30 times responsible, but ultraviolet-A (UV-A) radiation more frequently in white than in black individuals.4 (wavelength 320-400 nm) adds to the risk.7,11,12 AK and SC serve as clinical dose-meters for chronic Individuals whose sun exposure habits began UVR exposure.13 UV-B reaches the epidermal early in life are at greatest risk for developing cell layer to induce very specific mutational SC.13,20 Persons with SC tend to be over the age changes which serve to both initiate and promote of 40 years and men are afflicted more frequently dysplastic changes in the epidermis. than women by a 12 to 1 ratio.21,22 This correlates closely with a 10.7 to 1 male to female ratio of SCC UV-B damages the DNA at adjacent pyrimidines of the lip.23 It has been postulated that women are resulting in double cytosine (CC) to double at lesser risk because they experience less chronic thymidine transition mutations.6,14 This mutation is sun exposure and are more likely to use a lip so specific that it is referred to as “UV signature” protective agent such as lipstick or sunblock.1 or “UV fingerprint.”6,14-16 The characteristic UV-B mutations target tumor suppressor genes, the While the association between tobacco use and most notable being p53.10,11,17 Normal p53 acts SC is unclear, the habit of leaving a cigarette on the to allow repair of damaged DNA or induces lip has been reported to increase the risk of labial apoptosis (controlled cell death) when the DNA SCC.10,24 As well, there is a paucity of data on the damage is nonrepairable.6,11,16 association between a patient’s immune status and SC. However, the association between a patient’s UVR-induced mutations to the p53 gene lead to immune status and the frequency of developing AK impaired tumor suppressor activity. Other UVR- and SCC of the lip is profound.24-28 Consequently, induced molecular alterations affect the normal a patient’s immune status is likely to worsen the activity of cyclooxygenases, signal transducer severity of SC and promote its progression to SCC. and activator of transcription proteins, fibroblast growth factor, cytokeratin, and cytotoxic killer The true incidence of SC is unknown; however, cells.1 While these effects contribute to the the likelihood that SC will progress to SCC of the molecular evolution of SC to SCC, their reliability lip vermilion is 2.5 times higher than the risk of as clinical markers with predictive or staging AK progressing to cutaneous SCC.29,30 SCC of value remains unclear.1,11 the lip tends to be more severe in those patients who develop SC at a younger age and in those Since SC occurs more frequently in light- with severe clinical and histologic evidence of complected than darker-complected individuals, inflammatory infiltrates at the time of diagnosis.1 The progression of SC to SCC of the lip may take 18 Table 1. Skin Phenotypes. 2 to 3 decades.31 It is estimated that in the United States there are 3500 new cases of SCC of the lip diagnosed annually.32 This represents approximately 50% of all oral cancers. The overall incidence rate of SCC of the lip in Canada is 2.7 per 100,000.33 The incidence rate of labial SCC in persons with skin types I and II in Canada has been reported to be 12 per 100,000.34 It is of import that approximately 15% of the patients with SCC of the lower lip will develop a second primary on the lip vermilion.30,35 3 ® ® Crest Oral-B at dentalcare.com Continuing Education Course, Revised December 9, 2015 Clinical Manifestations The clinical appearance of SC does not always UVR-induced damage to the lip may be acute, correlate directly with underlying histological resulting in sunburn, blistering or peeling; chronic changes and an apparently suspicious lesion exposure leads to SC, primarily of the lower may prove to be benign, while a perceived benign lip.1,2,12,21,22,36 In its early stages, SC presents as a lesion may in fact represent severe dysplasia or dry, scaly unobtrusive “chapped lip.” Palpation even SCC.1 Waxing and waning of erythematous provides a sense of rubbing the fingers over or ulcerative areas with evidence of induration and sandpaper.37 At later stages small nodules; pain are ominous signs.21,39 Figures 1-8 document marked parallel fissuring; mottled, opalescent the progression of labial UVR damage from acute white or gray plaques; erosion or ulceration along sunburn to primary and recurrent invasive SCC.
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