1999 JOURNAL OF THE CALIFORNIA DENTAL ASSOCIATION
Feature Story
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Lip Cancer

Prevention and Detection of Lip Cancer -- The Dentist's Role

George E. Kaugars, DDS;
Louis M. Abbey, DMD, MS;
Dennis G. Page, DDS, MS;
John A. Svirsky, DDS, MEd;
James C. Burns, DDS, MEd, PhD; and
Todd Pillion, BA


Copyright 1999 Journal of the California Dental Association.

With their attention to the oral area, dentists are in an excellent position not only to diagnose lip cancer, but also to counsel patients in its prevention. Patients need to be educated on the dangers of ultraviolet radiation and the measures available to decrease exposure to it. This article discusses the circumstances that increase the chance of developing lip cancer, the variety of ways to decrease that chance, and the recognition and treatment of premalignant and malignant lip lesions.

Evaluation of the lips should be a part of every oral examination. The purpose of this article is to discuss recommendations for the prevention of lip cancer, the clinical recognition and diagnosis of suspicious changes of the lip, and follow-up care for patients with a history of premalignant or malignant lip lesions.

Lip cancer

The link between lip cancer and sunlight was first noted in 19231; and exposure to sunlight, particularly in fair-skinned individuals, is widely accepted as the principal cause of lip cancer.2 An overwhelming percentage of premalignant and malignant changes of the lips affect the lower lip because of its greater exposure to sunlight. An estimated 3,500 cases of lip cancer are diagnosed every year in the United States.2 Lip cancers are generally painless, which explains the average time of patient delay of from five months to two years before seeking professional help.3,4 One study noted that almost half of the patients with lip cancer had lesions greater than 1.5 cm in diameter at the time of their diagnosis.3 The time needed for solar-induced changes of the lip to evolve into cancer is generally 20 to 30 years, but it can occur in less time.5 The profile of a patient at high risk for lip cancer is a tobacco-using Caucasian male older than 40 with a fair complexion and a history of chronic exposure to the sun.6

The Lip

The lip is clinically divided into "wet" and "dry" components. The wet lip, which extends from the oral mucosa to the contact line between the upper and lower lip, is rarely the site of malignant change. The dry lip or exposed portion, which is unique to humans, is the transition between the wet lip and the skin.1,2 The dry lip contains some sebaceous glands but usually does not have hair follicles or sweat glands.1 The dry lip appears reddish because the blood vessels are in a superficial location and the overlying epithelium is thin. The term "vermilion," which is often used for the dry part of the lip, simply means a reddish appearance.7

The epidermis of the skin provides some natural protection against the damaging effects of the sun. About 5 percent to 10 percent of ultraviolet (UV) radiation is reflected from the skin, and as much as 70 percent is absorbed.6 The thicker the epidermis and the higher the melanin content, the better the skin's ability to absorb UV radiation without damaging epithelial cells. The lip has less protection than the skin because the lip epithelium is thinner, has a thinner keratin covering, has less melanin, and has fewer secretions from sebaceous and sweat glands.8

Diagnosis


Figure 1. This fairly well-defined white lesion of the right lower lip was noted in this Caucasian male. The lesion was of variable thickness and demonstrates a number of fissures. This large lesion illustrates the difficulty in deciding which area should be biopsied to get a representative sample. The left side of the lower lip also shows subtle changes consistent with chronic sun exposure.

Figure 2. The epidermis in this photomicrograph is covered by a thin layer of parakeratin, which would correspond to a subtle white color found in many of these lesions. The abnormal maturation pattern and variation in cellular size indicate mild epithelial dysplasia within the epidermis. The underlying fibrous connective tissue contains enlarged vascular spaces and chronic inflammatory cells, which would cause erythematous foci to become clinically apparent. (Hematoxylin and eosin stain, 100x)

Figure 3. The right side of the photomicrograph shows normal epidermins with an abrupt change to epithelial dysplasia on the left side. It is typical to have a sharp transition from normal to affected epidermins in sun-damaged lips and to have several affected foci with interspersed areas of normal epidermis. (Hematoxylin and eosin stain, 100x)
The early clinical changes of a sun-damaged lip, usually referred to as actinic cheilitis, are subtle and not directly related to the histologic degree of either epithelial or connective tissue change. Generally, the sun-damaged lip has a white lesion of variable thickness with interspersed red foci, and it may be either well- or ill-defined (Figure 1). Although the lesions are usually unilateral, it is also common to see lesions that cross the lip almost from commissure to commissure. Actinic cheilitis is usually asymptomatic and will often have been present for months or years. Palpation is an important clinical test because actinic cheilitis feels like fine sandpaper as one slides a gloved finger across the lesion. Induration and a noticeable thickening are rarely present in the early stages of the lesion. Almost all cases of a sun-damaged lip will be noted on the lower lip; the upper lip is rarely involved. Histologically, the sun damage on the lip can be a reactive change called hyperkeratosis, premalignant changes ranging from mild epithelial dysplasia to carcinoma in situ, or even invasive carcinoma (Figures 2 and 3).

The decision as to whether a biopsy is necessary is difficult to make for an asymptomatic, subtle lesion of the lip because it is not possible to determine the degree of cellular damage based solely on clinical appearance.5 To ask a patient to return in six months for re-evaluation carries the risk that the lesion may increase in histologic severity or even metastasize during that time. An incisional biopsy has the advantage of providing a definitive diagnosis and minimizing the amount of tissue removed. The biopsy can easily be done with a punch; and if the diameter is small enough, sutures may not even be necessary. Usually the lip heals quickly after a punch biopsy, and rarely do the patients need anything stronger than over-the-counter analgesics for a day or two afterward. The patient should be informed that it takes about a week to get the results of the biopsy and that after obtaining the histopathologic diagnosis, the appropriate follow-up care can be determined. If the diagnosis is hyperkeratosis, the patient should be monitored and additional incisional biopsies considered if the clinical appearance of the lesion changes or the patient becomes symptomatic. It is the authors' recommendation that if the diagnosis is either epithelial dysplasia (premalignant) or carcinoma that the lesion be removed entirely unless there are mitigating circumstances. The drawback to an incisional biopsy is that only a small area of the lesion is sampled, and other affected areas may have a greater degree of cellular damage. It is reasonable to assume that because the entire lip has been exposed to the same amount of sunlight, areas that appear clinically normal may also have histologic abnormalities. In spite of the disadvantages of an incisional biopsy, the authors' recommend one to rule out the possibility of malignant change and to reassure the patient.9 Unfortunately, exfoliative cytology and toluidine blue staining are generally not useful in assessing these lip lesions because of the keratinization that is present.4

Ultraviolet Radiation

Sunlight consists of radiation that varies in wavelength from 200 to 1,800 m (Table 1). The infrared spectrum is from 760 to 1,800 um and is responsible for the heat associated with sunlight. Visible light is from 400 to 760 um and UV rays are from 200 to 400 um.

Table 1.

Radiation from Sunlight

Type

Wavelength

Effect

Infrared

760-1,800 um

Heat

Visible light

400-760 um

 

Ultraviolet A

320-400 um

Aging of skin, probably some role in skin cancer

Ultraviolet B

290-320 um

Causes sunburns, significant factor for skin cancer

Ultraviolet C

200-290 um

Blocked by earth's atmosphere

     

 

UVA radiation makes up 90 percent of the UV radiation that reaches the earth's surface and is associated with connective tissue changes that accelerate aging of the skin. Initially, UVA radiation was thought to be harmless, but it now has been implicated in cellular DNA changes and probably participates with UVB radiation in the development of cancer. One widespread use of UVA radiation is in tanning salons. The radiation emitted by a tanning bed consists of 98 to 99.5 percent UVA rays, but chronic exposure carries with it an increased risk of developing either cutaneous basal cell carcinoma or melanoma.

UVB radiation causes sunburns and is the form of UV radiation responsible for lip and skin cancer. The atmosphere filters only some UVB rays, and the time of greatest UVB radiation exposure is from 11 a.m. to 2 p.m.6 Clouds do little to block UVB rays,6 and even being in the shade does not provide complete protection because the rays are scattered by the ground and water. For example, dry sand reflects 17 percent of UVB rays at 300 m and fresh snow reflects as much as 85 percent.6

UVC radiation has the shortest wavelength and the greatest potential to cause skin damage, but its rays are blocked by the ozone layer and the earth's atmosphere.

Sunscreen Products

There are two types of sunscreens: chemical and physical. Chemical sunscreens act by absorbing UV radiation, especially in the UVB range. Some chemical sunscreens contain either para-aminobenzoic acid (PABA) or one of its esters such as Padimate O.10 Many sunscreens are now being sold that utilize other chemicals and advertise themselves as being PABA-free. Oxybenzone is a popular UVA sunscreen, but it blocks only 50 percent of the UVA rays.11 Eusolex 8020 and Parsol 1789 are also used for UVA protection, but contact sensitivity is an occasional side effect.11 Physical sunscreens reflect rather than absorb UV radiation, which provides maximum protection.12 Zinc oxide and titanium dioxide are examples of physical sunscreens. The physical sunscreens have not been as popular as chemical ones because of their opaque white appearance. A good sunscreen should contain a combination of ingredients that will protect against both UVA and UVB radiation and have a sun protection factor of at least 15.

Some sunscreens are specifically designed for use on the lips because there is a need for the vehicle to be physically retained after exposure to fluids, to be cosmetically acceptable, and to not taste bad. Coppertone, Banana Boat, Hawaiian Tropic, ChapStick, and Panama Jack offer fruit-flavored lip balms that contain a waxy or petroleum-based ointment that aids in retaining moisture. Gel-based lip sunscreens provide the longest retention: More than 90 percent of the protection is still present three hours after application.6 Because of the large variety of lip sunscreens available, dentists should encourage patients to try more than one brand to find the one they would be most likely to use consistently. Cost, availability, cosmetic appearance, and taste will influence the patient's decision. Because of these personal variables, the authors do not recommend one specific lip sunscreen but instead encourage patients to find one with a minimum SPF of 15 that they like. Lip sunscreens should be applied at least 15 minutes before exposure to the sun and reapplied at hourly intervals while in the sun and right after swimming.6,13 Lip sunscreens need to be applied more frequently than the ones for the skin because of removal by licking the lips and the need for greater protection for the lips.

Sun Protection Factor

The sun protection factor (SPF) is determined by taking the time needed to reach a minimum erythema dose (MED) in sunscreen-protected skin and dividing it by the time required to reach MED in unprotected skin.6 These tests are usually done by exposing the skin on the backs of 10 to 20 subjects with laboratory light sources and then averaging the results.10,11 A sunscreen is given an SPF of 15 if it takes 15 times longer for the skin to turn red in the protected area than in unprotected areas. The SPFs determined with natural sunlight are generally lower than those done with artificial laboratory light.10 A minimum SPF of 15 is recommended for most people. There is not a proportional increase in protection with greater SPFs. For example, an increase in SPF from 15 to 34 only increases the protection by 4 percent.10 The long-term benefit of using a sunscreen with an SPF of at least 15 is that there is a 78 percent lifetime reduction in the incidence of cutaneous basal cell and squamous cell carcinomas if there is regular application during the first 18 years of life.11 Although SPF is a popular way to compare sunscreens, it has been shown that suberythemal doses cause skin damage without any apparent reddening of the skin.11

The effective SPF of a sunscreen is reduced by incorrect application. Correct application of sunscreens in adults who have been diagnosed with skin cancer is remarkably low, with only 34 percent of these patients using sunscreens effectively.14 The true SPF of a sunscreen can be as little as 50 percent of the stated SPF if it is incorrectly applied.11

Lip sunscreens and balms usually have an SPF of at least 15 and even a few lipsticks have an SPF of that high.

Adverse Reactions to Sunscreens

Contact dermatitis can occur with chemical sunscreens and is usually due to one of the preservatives or fragrances used in the formulation rather than the active ingredient.10 Clinically, it is difficult to distinguish redness of the skin caused by sun exposure from contact dermatitis, and allergic reactions are probably underdiagnosed for that reason. One other drawback to the use of sunscreens is that patients may spend more time in the sun because they feel protected. Some authors have discussed the possibility that sunscreen use might increase the risk for melanoma because carcinogenic compounds are produced when sunscreens are exposed to sunlight.11 At present, an increased risk for melanoma because of sunscreen use is unproven, and a recommendation for the routine usage of sunscreens is prudent until evidence to the contrary becomes available.

Patient Education

It may be that skin cancer is perceived by many as being a minor nuisance because most basal cell and squamous cell carcinomas are effectively treated as an office procedure and have little impact on the patient's life. However, an estimated 41,600 new cases of melanoma will be diagnosed in 1998; and while the prognosis for melanoma has considerably improved, there are still unfortunate cases that cannot be successfully treated.15 For prevention to be maximally effective, it must be directed toward preadolescents and adolescents, which is a group that may not readily accept the importance of a problem that may not appear for at least several decades.14 Because a tan is associated with good looks and general health, it is difficult to persuade some patients to reduce their time in the sun and to use sunscreens. As health professionals, dentists should encourage their patients to use sunscreens to protect their lips as well as their skin. The physical sunscreens, zinc oxide and titanium dioxide, are the most effective because they reflect UV radiation. These should be recommended to patients with unavoidable chronic exposure to the sun, such as fishermen, farmers, and sailors.12 If there is a cosmetic objection to the "whiteness" of zinc oxide, then one of the many lip balms should be recommended. The use on the lips of sunscreen intended for the skin is not as effective as true lip sunscreens because of the diminished physical retention.

One study showed that only 62 percent of patients with nonmelanoma skin cancer started using sunscreen after their diagnosis.14 For patients with a history of a sun-damaged lesion of the lip, there must be an increased emphasis on prevention and education because of the possibility of developing another lesion. If sun exposure is unavoidable, a physical sunscreen should be recommended for daily use on the parts of the body that cannot be covered. If sun exposure is sporadic, then one of the chemical sunscreens that protects against both UVA and UVB radiation is acceptable. Patient education should stress the need for more frequent application of lip sunscreens as compared to the ones for the skin and the need to apply them even on cloudy days. Although people tend to think of sunscreen use only in the summer, patients must also understand the need for protection during the remainder of the year.

Conclusions

A dentist should examine the lips of every patient at every visit and periodically emphasize the use of sunscreens for both the skin and lips. The clinical signs of sun damage to the lip may be subtle, but a biopsy should be considered so that a diagnosis and appropriate follow-up care can be determined. Patients with a biopsy-proven premalignant or malignant change of the lip must be educated about the need for eliminating sun exposure to the lips. They should be clinically monitored for any other changes of the lips and counseled on the possible need for future diagnostic biopsies. Consistent use of lip sunscreens beginning at an early age and early diagnosis of sun-damaged areas of the lips may help in reducing the number of lip cancers diagnosed each year in the United States.


Authors

George E. Kaugars, DDS, is a professor in the Department of Oral Pathology at the Medical College of Virginia, Virginia Commonwealth University, in Richmond, Va.

Louis M. Abbey, DMD, MS, is a professor in the Department of Oral Pathology at the Medical College of Virginia.

Dennis G. Page, DDS, MS, is an associate professor in the Department of Oral Pathology at the Medical College of Virginia.

John A. Svirsky, DDS, MEd, is a professor in the Department of Oral Pathology at the Medical College of Virginia.

James C. Burns, DDS, MEd, PhD, is a professor in the Department of Oral Pathology at the Medical College of Virginia.

Todd Pillion, BA, is a dental student at the Medical College of Virginia.


References

1. Picascia DD, Robinson JK, Actinic cheilitis: a review of etiology, differential diagnosis, and treatment. J Am Acad Dermatol 17:255-64, 1987.

2. Million RR, Cassisi NJ, Mancuso AA, Oral cavity. In, Million RR, Cassisi NJ, eds, Management of Head and Neck Cancer: A Multidisciplinary Approach. JB Lippincott Co, Philadelphia, 1994, pp 321-400.

3. Batsakis JG, Squamous cell carcinomas of the oral cavity and the oropharynx. In, Tumors of the Head and Neck: Clinical and Pathological Considerations. Williams & Wilkins, Baltimore, 1979, pp 144-76.

4. Silverman S Jr, Epidemiology. In, Oral Cancer. BC Decker, Hamilton, Ontario, 1998, pp 1-6.

5. Cataldo E, Doku HC, Solar cheilitis. J Dermatol Surg Oncol 7:989-95, 1981.

6. Lundeen RC, Langlais RP, Terezhalmy GT, Sunscreen protection for lip mucosa: a review and update. J Am Dent Assoc 111:617-21, 1985.

7. Woolf HB, Webster's New Collegiate Dictionary, 1980.

8. Nicolau SG, Balus L, Chronic actinic cheilitis and cancer of the lower lip. Br J Dermatol 76:278-89, 1964.

9. Marks VJ, Actinic keratosis: a premalignant skin lesion. Otolaryngol Clin North Am 26:23-35, 1993.

10. Habif TP, Clinical Dermatology: A Color Guide to Diagnosis and Therapy. Mosby-Year Book Inc, St. Louis, 1996, pp 1-859.

11. Rapaport MJ, Rapaport V, Preventive and therapeutic approaches to short- and long-term sun damaged skin. Clinics Dermatol 16:429-39.

12. Main JHP, Pavone M, Actinic cheilitis and carcinoma of the lip. Can Dent Assoc J 60:113-6, 1994.

13. Payne TF, An evaluation of actinic blocking agents for the protection of lip mucosa. J Am Dent Assoc 92:409-11, 1976.

14. Koblenzer CS, The psychology of sun exposure and tanning. Clinics Dermatol 16:421-8, 1998.

15. Landis SH, Murray T, et al, Cancer statistics, 1998. CA Cancer J Clinicians 48:6-29, 1998.

To request a printed copy of this article, please contact/George E. Kaugars, DDS, Department of Oral Pathology, Medical College of Virginia, P.O. Box 980566, Richmond, VA 23298-0566.



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