actinic keratosis: from the skin to the lip

15
J Oral Maxillofac Surg 66:1162-1176, 2008 Actinic Keratosis: From the Skin to the Lip Michael F. Zide, DMD* Purpose: Actinic keratoses are commonly the result of intense sun damage to the skin and lips of susceptible patients. The purposes of this 2-section article are to familiarize the surgeon with options for care and to suggest methods of incorporation into practice as a true benefit to patients. Patients and Methods: The first section discusses the options chosen for patients who were referred to the Facial Lesion Clinic in a county hospital for precancerous or cancerous facial lesions; the second section reviews ramifications for precancerous sun-damaged lips with clinical leukoplakia. Results: Methods are available to aid patients with precancerous facial and lip lesions. Choices have been presented with patient examples. Conclusion: Patients with precancerous facial and lip lesions should receive therapy that diagnoses or treats these lesions. Long-term avoidance or mere observation of these lesions will portend future cancer. © 2008 American Association of Oral and Maxillofacial Surgeons J Oral Maxillofac Surg 66:1162-1176, 2008 Actinic keratoses (AK) are the premalignant form of squamous cell carcinoma (SCC) of the skin. They are described as irregular scaly lesions of sun-exposed skin that may itch or burn. Over 10% of the average dermatologic practice is expended freezing, electro- desiccating and curetting, chemo medicating, biopsy- ing, or excising these lesions. Literature has exposed that the outlay is valid, 1 as progression of AK to SCC in high risk individuals may approach 12% to 30% over 3 years. Indirect evidence suggests that 2% of SCC originating in AK metastasize, and 7% recur lo- cally. Over the course of a year, 20% to 25% of AK may regress, 85% permanently. Rates of AK occurrence vary with geographic loca- tion and susceptible patient skin type. As expected, excluding Hawaii, the highest incidence in the United States is for men of the South and Southwestern states. Accepted data show 2 that men have a 9% to 14% risk of developing SCC of the skin, and women a 4% to 9% risk. SCC of the skin has the potential to metastasize and may account for 35% to 55% of all skin cancer deaths over 65 years of age. Because more than 1 million new nonmelanoma skin cancers are diagnosed yearly in the United States, and the validity of AK treatment is undeniable; our patients need and deserve the diagnostic skills of surgeons educated in skin evaluation. Although the modalities of therapy for single and multiple AK may confuse the uninitiated, the methods espoused in this article have proved effective for greater than 15 years. On the lower lip, AK may show itself as a scaly spot or with leukoplakia. In this location, wishful observa- tion is also not warranted. Our standard criterion is that any suspicious area, present for greater than 1 month under our personal observation receives a small incisional biopsy. The lip will be discussed in more detail in the second part of this article. This first part of this article will review the results of 1 year of biopsies for head and neck skin AK in Facial Lesion Clinic at John Peter Smith Hospital (Fort Worth, TX) and will suggest an effective treatment scheme. Patients and Methods During the course of a single year, 75 to 150 patients are referred to the Facial Lesion Clinic for malignancies or premalignancies. All patients were referred from fam- ily practice department personnel, urgent care facilities, or the dermatology service. Some patients arrived with biopsy in hand whereas others arrived with provisional diagnoses. Approximately 50% of patients with known malignancies received more biopsies before definitive malignancy therapy. Exact epidemiologic data were ir- relevant because they were noncontributory to the ulti- mate choices of therapy. Each patient was evaluated for skin type and history, medically contributory factors, and had a complete head and neck examination. No excisional biopsies with lay- ered closures were carried out on suspected AKs. 3 Indi- *Director of Facial Lesion Clinic and Vice Chair of Oral and Maxil- lofacial Surgery, John Peter Smith Hospital, Fort Worth, TX; and Clin- ical Faculty, University of Texas Health Sciences Center, Dallas, TX. Address correspondence and reprint requests to Dr Zide: John Peter Smith Hospital, 1625 St Louis Ave, Fort Worth, TX 76104; e-mail: [email protected] © 2008 American Association of Oral and Maxillofacial Surgeons 0278-2391/08/6606-0012$34.00/0 doi:10.1016/j.joms.2008.01.047 1162

Upload: michael-f-zide

Post on 05-Sep-2016

234 views

Category:

Documents


6 download

TRANSCRIPT

Page 1: Actinic Keratosis: From the Skin to the Lip

J6

AsdsdditioScr

teSs14ms

s

l

i

P

e

©

0

d

Oral Maxillofac Surg6:1162-1176, 2008

Actinic Keratosis:From the Skin to the Lip

Michael F. Zide, DMD*

Purpose: Actinic keratoses are commonly the result of intense sun damage to the skin and lips ofsusceptible patients. The purposes of this 2-section article are to familiarize the surgeon with options forcare and to suggest methods of incorporation into practice as a true benefit to patients.

Patients and Methods: The first section discusses the options chosen for patients who were referredto the Facial Lesion Clinic in a county hospital for precancerous or cancerous facial lesions; the secondsection reviews ramifications for precancerous sun-damaged lips with clinical leukoplakia.

Results: Methods are available to aid patients with precancerous facial and lip lesions. Choices havebeen presented with patient examples.

Conclusion: Patients with precancerous facial and lip lesions should receive therapy that diagnoses ortreats these lesions. Long-term avoidance or mere observation of these lesions will portend future cancer.© 2008 American Association of Oral and Maxillofacial Surgeons

J Oral Maxillofac Surg 66:1162-1176, 2008

apsmca

ottmsm

1LT

P

aoiobdmmrm

ma

ctinic keratoses (AK) are the premalignant form ofquamous cell carcinoma (SCC) of the skin. They areescribed as irregular scaly lesions of sun-exposedkin that may itch or burn. Over 10% of the averageermatologic practice is expended freezing, electro-esiccating and curetting, chemo medicating, biopsy-

ng, or excising these lesions. Literature has exposedhat the outlay is valid,1 as progression of AK to SCCn high risk individuals may approach 12% to 30%ver 3 years. Indirect evidence suggests that 2% ofCC originating in AK metastasize, and 7% recur lo-ally. Over the course of a year, 20% to 25% of AK mayegress, 85% permanently.

Rates of AK occurrence vary with geographic loca-ion and susceptible patient skin type. As expected,xcluding Hawaii, the highest incidence in the Unitedtates is for men of the South and Southwesterntates. Accepted data show2 that men have a 9% to4% risk of developing SCC of the skin, and women a% to 9% risk. SCC of the skin has the potential toetastasize and may account for 35% to 55% of all

kin cancer deaths over 65 years of age.Because more than 1 million new nonmelanoma

kin cancers are diagnosed yearly in the United States,

*Director of Facial Lesion Clinic and Vice Chair of Oral and Maxil-

ofacial Surgery, John Peter Smith Hospital, Fort Worth, TX; and Clin-

cal Faculty, University of Texas Health Sciences Center, Dallas, TX.

Address correspondence and reprint requests to Dr Zide: John

eter Smith Hospital, 1625 St Louis Ave, Fort Worth, TX 76104;

-mail: [email protected]

2008 American Association of Oral and Maxillofacial Surgeons

278-2391/08/6606-0012$34.00/0

eoi:10.1016/j.joms.2008.01.047

1162

nd the validity of AK treatment is undeniable; ouratients need and deserve the diagnostic skills ofurgeons educated in skin evaluation. Although theodalities of therapy for single and multiple AK may

onfuse the uninitiated, the methods espoused in thisrticle have proved effective for greater than 15 years.

On the lower lip, AK may show itself as a scaly spotr with leukoplakia. In this location, wishful observa-ion is also not warranted. Our standard criterion ishat any suspicious area, present for greater than 1onth under our personal observation receives a

mall incisional biopsy. The lip will be discussed inore detail in the second part of this article.This first part of this article will review the results of

year of biopsies for head and neck skin AK in Facialesion Clinic at John Peter Smith Hospital ( Fort Worth,X) and will suggest an effective treatment scheme.

atients and Methods

During the course of a single year, 75 to 150 patientsre referred to the Facial Lesion Clinic for malignanciesr premalignancies. All patients were referred from fam-

ly practice department personnel, urgent care facilities,r the dermatology service. Some patients arrived withiopsy in hand whereas others arrived with provisionaliagnoses. Approximately 50% of patients with knownalignancies received more biopsies before definitivealignancy therapy. Exact epidemiologic data were ir-

elevant because they were noncontributory to the ulti-ate choices of therapy.Each patient was evaluated for skin type and history,edically contributory factors, and had a complete head

nd neck examination. No excisional biopsies with lay-

red closures were carried out on suspected AKs.3 Indi-
Page 2: Actinic Keratosis: From the Skin to the Lip

ve

newtfr

aAcss

M

ocgs

ewsgfws

mcht

ssefitwtcos

M

MICHAEL F. ZIDE 1163

idual choices were formulated based on the history,xamination, and permanent histologic (biopsy) results.Biopsy was relevant because predictive clinical recog-

ition is flawed, even through the eyes of an experi-nced dermatologist4 or plastic surgeon.5 Cryosurgeryith liquid nitrogen, an effective method of inexpensive

orso and extremity control of AK, was never chosen foracial lesions because hypopigmentation, scar, and er-atic lesion control are common6 with this method.

Shave biopsy results influenced therapy significantly,s somewhat identical-looking lesions were read out asK (of differing subtypes), noninvasive AK, AK butannot rule out deep SCC, AK with moderate toevere dysplasia, SCC in-situ, SCC with localized inva-ion, and superficial basal cell carcinoma.

ethods of Therapy

SINGLE LESIONS

Electrodesiccation and CurettageElectrodesiccation and curettage (E&C) involve 2

r 3 sequences of curettage (with a dermatologicurette) followed by electrodesiccation with arounded Hyfrecator (ConMed, Utica, NY) of the le-ion. E&C was well-suited for some superficial lesions,

FIGURE 1. A, Actinic keratosis (3 mm) outlined. B, Curetted with tiss

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

g, most AK and some superficial skin cancers thatere well-defined and in areas of easy continual ob-

ervation for the patient. The procedure was abro-ated if the E&C encroached subcutaneous fat or hairollicles because of the high rate of recurrence.7 E&Cas never chosen for initial biopsy/therapy for the

calp, behind the ears, or the back of the head.

Method of E&CPatients in generally good condition without pace-akers and implanted cardio defibrillators were good

andidates. A nonalcohol skin prep such as chlor-exidine or povidone-iodine was chosen in preferenceo alcohol, which is flammable. Jewelry was removed.

Nonsterile gloves were donned. The assistanttretched the adjacent tissues so the surgeon couldcrape the soft lesion out until normal tissue wasncountered. Because higher rates of cure for super-cial lesions occur when experienced clinicians tensehe skin peripherally and curette aggressively, lesionsere curetted 3 times with light force with cautery in

he intervals. The electrocautery (or Hyfrecator) tipontacted the skin and superficial skin dehydrationccurred secondary to the Ohmic heating. Minimalcarring occurred with low power settings (Fig 1).

hed. C, Cauterized first round shows actual involvement of �5 mm.

ue stretc
Page 3: Actinic Keratosis: From the Skin to the Lip

iaEid

as

Aaiow

fc

Aaci(sa

((cltoca

wbs

R

rtttrr

D

toco

rbiii

bhcsAS

FBw

M

1164 ACTINIC KERATOSIS

The scrapings were sent for biopsy and the cauter-zed area was dressed with antibiotic ointment on

small circular bandage (Bacitracin Zinc ointment;. Fougera and Co, Melville, NY). The patient wasnstructed to shower as usual and change the bandageaily until all stickiness to touch was gone.

Liquid NitrogenOur clinic does not use liquid nitrogen on the face

nd neck because of the potential for depigmentation,carring, and lack of hair regrowth.

ExcisionAfter initial confirmatory biopsy, eyelid, ear, and lip

Ks were removed surgically. Additionally, AKs withhigh propensity to convert to SCC, such as those in

mmunocompromised patients or histologically readut as severely dysplastic in one area of a larger AKere considered for excision (Fig 2).

SINGLE OR MULTIPLE LESIONS

Chemo-MedicalMultiple medications eliminate superficial AKs ef-

ectively. Selection of one over the other is based onost, frequency of application, and symptoms.

IGURE 2. A, A 60-year-old man with 2 biopsies of AK on skin of lip., After excision and lip-shave, permanent pathology returned SCCith minimal invasion in lesion at skin.

richael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

5-Fluorouracil is the prototype topical remover forK. Although tube microsphere preparations arevailable in 0.5%, 1%, and 5%, our clinic uses the 5%omposition routinely because all seem to cause vary-ng degrees of irritation. Commonly, Efudex 5%Valeant Pharmaceuticals, Costa Mesa, CA) was pre-cribed to be applied 2�/day after washing affectedrea for 3 to 4 weeks (Fig 3).

CO2 Laser/Chemical Peel/DermabrasionThe Facial Lesion Clinic routinely uses the CO2 laser

Fig 4) and 35% trichloracetic acid (TCA) chemical peelFig 5). Dermabrasion has been eliminated because ofoncern over heavy particle aerosolization. When CO2

aser or chemical peel were selected, patients preparedheir skin with a retinoid (0.1% tretinoin for 2� weeks,r 0.05% for 4 weeks when tolerance of the higheroncentration is difficult). Routinely documented pre-nd postoperative regimens are followed.

35% TCA PeelDeep 35% TCA peels (preceded with mild abrasionith an electrocautery pad, or scraping with a #10lade, or Jessner’s solution) reduced the number ofuperficial AK significantly (Fig 5).8

esults

Results of therapy were effective. Patients wereeferred back to their primary care doctor or derma-ologist in most cases within 1 year of therapy. Pa-ients were informed that permanent cures might beemporary because the skin/patient history are onecord. The need for sun avoidance, sunscreen, andepeat therapy should be expected.

iscussion

The terminology, actinic keratosis, is a clinicalerm9,10 that does not take the histologic appearancer pathogenesis into consideration. As such, AKs areommonly destroyed unceremoniously without bi-psy confirmation.Histologically, AK is a proliferation of atypical cells

estricted to the lower level of the epidermis. If theasement membrane is encroached and neoplastic cells

nvade the dermis, the diagnosis of invasive SCC is reg-stered. In truth, it may be impossible to draw a mean-ngful distinction to what is and is not cancer.11,12

Even more confusing is the fact that when shaveiopsies of clinical AKs are submitted for routineistology, diagnostic readings between pathologistsonfound therapy. Pathology reports of seeminglymall AKs may be read as nonpathogenic or benignK, AK, AK with dysplasia, AK with severe dysplasia,CC in-situ (Fig 6), AK but biopsy not deep enough to

ule out SCC (that is classic for a hypertrophic exo-
Page 4: Actinic Keratosis: From the Skin to the Lip

pma

tal

os5wdc

MICHAEL F. ZIDE 1165

hytic AK) (Fig 7) invasive SCC, invasive SCC withargins clear (questionable from a biopsy specimen),

nd basal cell carcinoma (BCC).Medical therapy for AK varies in the hands of prac-

itioners. Carac (Dermik, Berwyn, PA) (30-gm tube,pply once a day after washing; apply sunscreen 2 h

ater), 0.5% fluorouracil may also be prescribed for a

nce a day use for 4 weeks. This lower concentrationeems to be almost equivalent in efficacy to Efudex%. No fluorouracil should ever be used on pregnantomen or women who intend to become pregnanturing therapy. Imiquimod 5%13 (Aldara; 3M Pharma-euticals, St Paul, MN) is a slightly more expensive

URE 3. A, Scalp and forehead of 70� year-old male withltiple AKs. B, After 2 weeks of 5-FU applied twice a day aftershing. The patient also used 1% hydrocortisone OTC to help with

hing. C, Result 3 months later shows general lesion clearance.

chael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

FIGmuwaitc

Mi

lternative, applied 2 to 3 times per week for several

Page 5: Actinic Keratosis: From the Skin to the Lip

FfCp

M

1166 ACTINIC KERATOSIS

IGURE 4. A, A 50-year-old transvestite male, irradiated for teen acne with multiple SCC and AK proven by biopsy (right side shown). B, Ten lesionsrom the right and left face were excised and dressed open with ointment, nonadherent gauze, and tape. Permanent histology on all lesions ensued., Full-thickness groin and abdominal skin grafts covered all defects. D, Two months after diagnosed malignancies were removed, multipleremalignent AKs remain (left side shown). (Figure 4 continued on next page.)

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

Page 6: Actinic Keratosis: From the Skin to the Lip

mogtf1c

srAaiiAslpSm

paLaL

tcct

ctdtfrtppotl

baecnsc

Fr

M

MICHAEL F. ZIDE 1167

onths (usually 4 months) with occasional rest peri-ds due to intensity of inflammatory response. Re-ardless of the medical therapy chosen, patients wereold of the probable need to repeat the course in theuture. Some patients also were prescribed generic% hydrocortisone cream for application during theourse of therapy to reduce itching and burning.Medical methods to remove multiple AKs are occa-

ionally curative, often delineative, and may need to beepeated. Excoriating methods to eliminate multipleKs (5-FU or imiquimod, chemical or laser peel, derm-brasion or cryosurgical peeling, etc) reduce AKs signif-cantly, up to 75% in the short-term. Control results arenfluenced by patient history and depth of therapy.14,15

ll methods are best carried out during the colder sea-ons or with patient commitment to avoid direct sun-ight and to apply sunscreen. Deeper lesions that reap-ear around 3 months after therapy should be biopsied.tudies with 5-FU report 25% of patients needed retreat-ent within 2 years; 50% within 3 years.1

There are other medical preparations as well ashotodynamic light therapy that have been suggesteds therapeutic but are not available through the Facialesion Clinic. Costly but effective photodynamic ther-py involves administration of a photosensitizer (eg,

IGURE 4 (Cont’d). E, CO2 laser removal of surface AKs. Left foreesurfacing. F, Result 1 month later (left side). The deeper lesions will

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

evulan Kerastick; DUSA Pharmaceuticals, Wilming- b

on, MA) that selectively accumulates in cancerousells. After activated by light of a specific wavelength,ellular destruction occurs through generation ofoxic oxygen and other reactive species.

Removal of ear, eyelid, lips, and AKs in immuno-ompromised patients are indicated because the SCChat may occur in these areas are potentially moreeforming. In the case of immunocompromised pa-ients, SCC evidence occurs 10 years earlier (in theourth or fifth decade of life) and metastasizes moreeadily. In Norway,16 literature has shown that SCC ofhe lower lip occurs 20� more commonly in trans-lant patients than in the general population. Leuko-lakia occurs in 13% of transplant patients than 0.06%f controls. Additionally, in immunocompromised pa-ients, it is much more difficult to distinguish prema-ignant from malignant lesions.17

CO2 laser/chemical peel/dermabrasion have eacheen proposed for the patient with multiple AKs. Theyre equivalent to each other and to medical creams infficacy, but more rapid in execution and healing thanhemomedical creams. Just like the creams, they shouldot be carried out during sunny summer months whenunburn to raw new skin is a possibility. And just like thereams, those lesions that reappear after 3 months need

hown where some curettage (bleeding spots) were used before laserar at around 3 months for further therapy.

head sreappe

iopsy as suspicion should be raised as to the nature of

Page 7: Actinic Keratosis: From the Skin to the Lip

1168 ACTINIC KERATOSIS

FIGURE 5. A, Seventy-five year-old man Fitzpatrick type 1 skintype with multiple AKs. B, After 3-week skin regimen, a 35% TCApeel was performed under light sedation and facial regionalblockade. Acetone and light #10 blade scraping preceeded thepeel. C, At 3 months, most AKs have been cleared but deeperlesions are resurfacing and will be biopsied.

Michael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg2008.

Page 8: Actinic Keratosis: From the Skin to the Lip

tnrimi

mgocflmpmhhwr

ppitift

bbFbc

S

itlaw

cgbs

tmt

Fnnw

Fs

M

MICHAEL F. ZIDE 1169

he lesion. Finally, both the creams and abrasive tech-iques remove AK, but the reasons for their existenceemains, eg, skin type and sun exposure, etc. Hence, its necessary to install sun protection routines in patients’

inds. Reapplication of creams and procedures may bendicated every couple of years.

No single management strategy for AK is muchore effective than the other. It seems that fair to

ood results may be obtained with most clinical meth-ds. Patient compliance, length of use, and insuranceoverage must influence therapeutic choices. Routineollow-up is critical to prevention of SCC, which is aaudable goal. Practitioners who elect to treat AK

ight select a method that fits into their practiceatterns. Regardless, follow-up is critical because re-oval of any AK has never removed the patient’s sunistory, skin type, current occupation, or medicalistory from the ongoing equation. Care of the patientith AK is often a recurrent addition to the practice

ather than a single surgical event.These problems are especially problematic for the

rimary care physician, who sends the patient, with aathologically proved diagnosis of dysplastic AK or

nvasive SCC somewhere on the face. When the pa-ient arrives 2 to 3 weeks later, the area has healedmperceptibly. For this reason, we encourage all re-erring doctors and residents to annotate biopsy loca-ions via a clock face (Fig 8).

The author has found the family practitioner (FP) toe a most helpful ally in following the patient’s entireody with referral to the surgeon as needed. Currentacial Lesion Clinic follow-up patterns include referralack to the FP for uncomplicated AK at 6 months and

IGURE 6. SCC in situ, growing out of AK on an 80-year-old man’scalp. All in-situ lesions merit excision and other AK merit therapy.

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

omplex patients at 1 year. M

uggested Therapeutic Regimens

SINGLE LESIONS (�1 CM IN LOW RISK AREAS OFTHE HEAD AND NECK)

Areas of low risk include those that are easily mon-tored, such as the cheek or forehead. Areas behindhe ear or scalp, on the nose, lip, eyelid, or ear are notow risk nor are they monitored easily. Low risk areasre amenable to curettage and electrodesiccationith curetted material sent for biopsy.The surgeon should be aware that any palpable sub-

utaneous extension, poorly defined borders, lesionsreater than 1 cm, or those in high risk locations wouldest be biopsied as a primary choice. Lymph nodeshould be palpated in the expected drainage patterns.

Obviously, low risk areas treated by many derma-ologists include the arms or back. Often no speci-ens are examined histologically because liquid ni-

rogen is used.

IGURE 7. “Hypertrophic” AK horn, the base of which was diag-osed without SCC, which is surprising for its size. In view of dysplasiaoted histologically on the biopsy, conservative excision would bearranted.

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

Page 9: Actinic Keratosis: From the Skin to the Lip

sgpb

ttweLcddgfaihc

ampawwoJa

w

T

aacmfwrlblias1

sctpcfo

o

rp2ol

a

fl

Fswdl

M

1170 ACTINIC KERATOSIS

MULTIPLE LESIONS

Patients with multiple topographic areas of AKhould be treated in a plan that controls futurerowths that will, no doubt, occur. All multiple AKatients should be counseled regarding clothing, sun-lock, and monitoring.Patients with multiple AK are presented with options

o fit their financial abilities and lifestyles. Medical op-ions such as 5-FU or imiquimod encompass severaleeks of therapy. When shorter resolution time is ben-

ficial, laser resurfacing (Coherent UltraPulse laser;umenis Inc, New York, NY; 300 mJ, 60 W to ahamois-colored skin end point), 35% TCA peel andermabrasion are somewhat equivalent. We do notiffusely dermabrade anymore because of concern re-arding particulate effluvium in the room. Laser resur-acing entails a day surgery, with shortened healing timend the advantage of wrinkle effacement. Laser resurfac-ng (like dermabrasion) is especially effective on non-ypertrophic (vs the hyperkeratotic lesions that occur

IGURE 8. Drawing a clock face with the center on any fixed facialtructure will allow accurate description of the location of a lesion so itill not be “lost” after biopsy. For example, the lesions would beescribed as 12:00, 1:00, and 3:00 (plus the millimeters) from the left

ateral canthus.

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

ommonly in immunocompromised patients). w

The 35% TCA peel has the shortest recovery time ofll methods. Patients receive 2 to 4 weeks of pre-peeledications such as tretinoin or glycolic acid. De-ending on the evaluation of the depth of AK, moreggressive peels have been our norm. For example,e routinely defat the skin with acetone or scrapeith a #10 blade to remove skin oils or debris. Areasf concern may be rubbed with a coarse cautery pad.essner’s solution precedes the 35% TCA so that thectual TCA peel produces a solid white film.

CONCLUSION

Control of premalignant facial lesions is worth-hile management tool to prevent future cancers.

he Lip

Actinic cheilitis is solar keratosis of the lip second-ry to sun exposure. Dry, whitish gray scaly erosionsnd leukoplakia predominate. Leukoplakia is strictly alinical term and carries no therapeutic value. Squa-ous cell carcinoma has been known to develop in or

rom leukoplakia after many years but there is no realay to quantify when this will occur. Estimated occur-

ence of SCC is 89% on the lower lip, 3% on the upperip, and 8% on the oral commissures.18 It is known thatuccal leukoplakias are 96% benign; but floor of mouth

eukoplakias are around one third benign, one thirdn-situ carcinomas, and one third invasive SCC.19 Whenwedge SSC dissection is carried out on the lip and a lip

have concurrently on the leukoplakia, around 10% to2% with show evidence of cancer.For this reason, certain other factors should be con-

idered before random therapeutic laser ablation or ex-ision. These include past sun history (intermittent in-ense ultraviolet light B [UVB] exposure with sunburn),ast skin cancer history, skin type, and potential medicalompromise. Smoking history, which may contribute toormation of lip cancers,20 will definitely influence theutcome of surgical excisions.This section will review the surgical technique and

utcome of the last 15 patients referred for lip lesions.

METHODSFifteen men between the ages of 45 and 80 were

eferred to the Facial Lesion Clinic or the privateractice of the author between the years 2004 to006. All patients were referred for lip lesions andnly 2 came with a biopsy. Two were referred for

aser ablation of leukoplakia.Patients were followed up for a minimum of 6 months

nd all were sent back to primary care after 1 year.Biopsies of these patients included lichen planus,

at wart, and AK, but 10 had squamous cell cancer.Leukoplakic areas were removed concurrently

hen the cancer was removed.
Page 10: Actinic Keratosis: From the Skin to the Lip

R

sa

D

ttmanym

scppmt

mdhqtc3

MICHAEL F. ZIDE 1171

esults

Three patients had Mohs excision before the recon-truction (Figs 9, 10). The rest were done with frozennd permanent histologic sections.

iscussion

There is consensus that lip, eyelid, ear AK, andhose on immunocompromised patients (whose his-opathology is always severe dysplasia) should be re-oved because the SCC that may occur in these areas

re potentially more deforming. In the case of immu-ocompromised patients, SCC evidence occurs 10ears earlier (in the fourth or fifth decade of life) and

etastasizes more readily. In Norway,16 literature has t

hown that SCC of the lower lip occurs 20� moreommonly in transplant patients than in the generalopulation. Leukoplakia occurs in 13% of transplantatients than 0.06% of controls. Additionally, in im-unocompromised patients, it is much more difficult

o distinguish premalignant from malignant lesions.17

The lip corollary of skin AK is leukoplakia. Squa-ous cell carcinoma arising from actinic keratosis or

e novo on the skin rarely metastasize (0.5% to 3%);owever, vermilion border metastases have beenuoted up to 11%.19 The lip presents diagnostic andherapeutic dilemmas. Four considerations are criti-al: 1) correct diagnosis, biopsy; 2) choice of therapy;) amount of lip to be removed; and 4) timing of

GURE 9. Patient is a 65-year-old male nonsmoker. A, Lip shaveith wedge for SCC design. B, Closure of the 4-corners will healell in a nonsmoker. C, Closure at 1 month.

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

FIww

M

herapy.

Page 11: Actinic Keratosis: From the Skin to the Lip

ebdfhlf

ib

tkah

FlHt

M

1172 ACTINIC KERATOSIS

Assumption that all whitish lesions on the lip ben-fit from treatment is incorrect. In the past few years,iopsies of leukoplakic white lip lesions have yieldediagnoses of flat warts, nonspecific ulcer, fungal in-ection, lichen planus, benign hyperkeratosis, andigh-grade dysplasia. Therefore, the most exophytic

esion should be examined histologically before de-

IGURE 10. A, A 60-year-old male nonsmoking patient with heavyeukoplakia. B, Two small scabs on the right lip histologically were dealf the lower lip was removed as well as all the surface vermilion an

he labiomental crease and an Estlander flap. D, E, Result at 3 month

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

orming surgical therapy. After an initial consultation, t

t is certainly valid to wait 4 weeks if irritants haveeen eliminated on any non-growing lesion.The surgeon should not be overly concerned with

he histologic differential among the 5 types of actiniceratoses (hypertrophic and its lichenoid variant,trophic, bowenoid, acantholytic, and pigmented) ase is with the histologic and clinical description of

and sun history. Past CO2 laser did not eliminate the heavy whitishas SCC with invasion. Mohs was financially not a consideration. C,al leukoplakia. Closure design includes an advancement flap along

s good contour and a functional lip.

cigarscribedd interns show

he deep epithelial tissues. In instances where the

Page 12: Actinic Keratosis: From the Skin to the Lip

hdpobl

siflsamitttm

lpol

eo

se1Laatb

a2vIth

mlp

s

Fo

M

MICHAEL F. ZIDE 1173

istologic diagnoses are AK, but clinically are SCC,eeper biopsies or sections should be taken becauserogression from AK to SCC may have occurred inther areas and no sharp demarcating line occursetween the 2 conditions. The hypertrophic epithe-

ial horn will often be described this way.The surgeon may be further confused because

ome pathologists regard SCC as a lesion in whichrregular aggregates of atypical keratinocytes19 areound in the papillary dermis whereas others name allesions AK until they hit the reticular dermis. On thekin, both of these descriptions may be treated equiv-lently with a low metastatic rate. The descriptionay be critical on the lip because the concern with

ncreased metastasis will almost invariably knee-jerko a wedge resection when SCC is read out. Althoughhis progression might be argued as overkill to some,he classic 50% 5-year mortality when any SCC lesionetastasizes to the neck is a frightening concern.In-situ carcinoma, also referred to as precancerous

eukoplakia, may histologically be very similar to hy-ertrophic AK. Thus, the pathologist’s report of ple-morphism, atypical nuclei, dyskeratotic mid epithe-

ial cells, loss of polarity, downward proliferation of

IGURE 11. A, Excision of this off-center SCC cancer with Mohs microf the orbicularis muscle within the defect was excised and rejoined. B, Cl

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

pithelium, etc, may be read out as dysplastic AK byne pathologist and in-situ carcinoma by another.Topical agents (eg, 5-FU) to eradicate vermilion dry

cabs (AKs) are not prescribed because of the severexcoriation, but imiquimod 5% (Aldara; 2�/week �6 weeks) has been more acceptable to patients.iquid nitrogen is impossible to control. CO2 laserblation may diffusely vaporize surface vermilion, butny thickened hypertrophic leukoplakia will recur;herefore, permanent pathology should be evaluatedefore laser therapy.Biopsy-diagnosed (with histologic dysplasia) sun-dam-

ged lip leukoplakia (AK) should be excised. A 1- to-mm margin of the leukoplakia is suggested.21 Normalermilion is removed as the ellipse of closure demands.t is not necessary to carry out a complete lip shave backo the wet line in all cases, but symmetrical excision iselpful when esthetics are critical (Fig 11).Marx21 has stated that it is adviseable to remove theinor salivary glands on the advancing flap to prevent

umpiness. This was never done in this series and noatient noted any lumpiness.Timing of leukoplakia excision with an associated

kin cancer is controversial. I, personally, excise the

and the lip shaves outlined in a 70-year-old male nonsmoker. Two thirdsathology showed a small SCC in the left vermilion. C, Result at 3 months.

surgeryosure. P

Page 13: Actinic Keratosis: From the Skin to the Lip

ctnpuctfe

d

tnba9h

loBw

FUo

M

1174 ACTINIC KERATOSIS

ancer with the entire leukoplakia specimen for his-ological study. Others (personal communication)ever excise leukoplakia with the local lower lip cancer,referring to wait several weeks for leukoplakia re-eval-ation. Still others (personal communication), only ex-ise the cancer and refer the patient back to the derma-ologist for resolution of the leukoplakia (margins clearor cancer but AK noted at borders) found within thexcised mucosal margins.The rationale for this deferral may be the break-

own of the mucosa at the junction of the uniting 4

IGURE 12. A, Lip-shave with wedge in a 78-year-old male heavyndermining the lower lip for closure. C, Closure of the lower lip andf muscle. D, Breakdown 7 days later is evident at both sites. E, Sec

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

ips that always occurs in smokers (Fig 12) but not inonsmokers (Fig 13). Resolution of smoker’s tips maye considered by including the labial vessels in thedvancement flap,22 delaying the flaps with incisionsto 15 days before, or accepting secondary mucosal

ealing that often occurs with limited scar.The quandary over oral leukoplakias persists in lip

esions associated with smokeless tobacco. Brush bi-psy results supply questionable aid for the surgeon.iopsy of all white lesions, as suggested by Marx,21

ill only provide information concerning the level of

r. Additionally a basal cell Ca was removed from the upper lip. B,er lip with minimal undermining of the skin edge and a small excisionhealing 1.5 months later.

smokethe uppondary

Page 14: Actinic Keratosis: From the Skin to the Lip

d3s(ai

snn“etmp

FMC

ta

btoSig

R

Fidn

M

MICHAEL F. ZIDE 1175

ysplasia in 1 area, such as in Snuff dipping lesions. In0 plus years of practice, I have noted that virtually allnuff dipping cancers have been found by the patientbrought to a dentist’s attention and then referred, orssociated with a swollen neck lymph node), not byndiscriminate biopsy.

Historically, the patient who has voiced a desire totop dipping, will allow the doctor to prescribe aicotine substitute and the positive reinforcementeeded to arrest the habit. The negative warning,you may get cancer” has proved of no value whatso-ver to this author. It is the rare patient in this au-hor’s practice, who has ceased tobacco dipping for 3onths to allow resolution of a diffuse area of leuko-lakia so targeted biopsies may be harvested.

acial and Lip Lesions With Diagnosedalignant Potential Should Beonsidered for Removal

The oral and maxillofacial surgeon who treats ac-inic or cancerous changes to the lip should consider

IGURE 13. A, An 80-year-old Hispanic male farmer with 2 biopsy-pnvolved 6 mm margins around the cancers and 2 mm margin aroundone as well. No cancers were found in the additional lip excision. Bew pigmented BCC on his nose.

ichael F. Zide. Actinic Keratosis. J Oral Maxillofac Surg 2008.

dding facial lesions to his or her practice. Patient

enefit is significant because the number of AKs inhe general population is huge, and the potential riskf progression to cancer is high. Virtually every skinCC is preceeded by AK. Tissue handling skills arenherent in any surgical practice and the knowledgeained toward this endeavor may save lives.

eferences1. Helfand M, Gorman AK, Mahon S, et al: Actinic keratosis. Final

report submitted to Agency for Healthcare Research and Qual-ity under contract 290-97-0018, task order no. 6. May 19, 2001

2. Helfland M, Gorman AK, Mahon S, et al: Actinic keratosis.Healthcare report. Executive summary May, 2001

3. Lieblich LM: To perform a biopsy or excise suspected AK:Another view. Arch Dermatol 142:1363, 2006

4. Venna SS, Lee D, Stadecker MJ, et al: Clinical recognition ofactinic keratoses in a high risk population: How good are we ?Arch Dermatol 141:507, 2005

5. Hallock GG, Lutz DA: Prospective study of the accuracy of thesurgeon’s diagnosis in 2000 excised skin tumors. Plast ReconstrSurg 101:1255, 1998

6. Thai KE, Fergin P, Freeman M, et al: A prospective study of theuse of cryosurgery for the treatment of actinic keratoses. Int JDermatol 43:687, 2004

well-differentiated SCC and heavy hypertrophic leukoplakia. Excisionhave. Symmetrical removal of a small ellipse of the right lower lip wasdiate closure. C, Revisit at 18 months shows good lip healing and a

roventhe lip s, Imme

7. Goldmann G: The current status of curettage and electrodesic-cation. Dermatol Clin 20:569, 2002

Page 15: Actinic Keratosis: From the Skin to the Lip

1

1

1

1

1

1

1

1

1

1

2

2

2

1176 ACTINIC KERATOSIS

8. Cooley JE, Casy DL, Kauffman CL: Manual resurfacing and TCA forthe treatment of patients with widespread actinic damage. Clini-cal and histologic observations. Dermatol Surg 23:373, 1997

9. Cohn BA: From sunlight to actinic keratosis to squamous cellcarcinoma. J Am Acad Dermatol 42:143, 2000

0. Evans C, Cockerell CJ, Actinic keratosis, time to call a spade aspade. South Med J 93:734, 2000

1. Helfand M, Gorman AK, Mahon S, et al: Actinic keratosis. Finalreport submitted to Agency for Healthcare Research and Qualityunder contract 290-97-0018, task order no. 6. May 19, 2001, p 17

2. Ehrig T, Cockerell C, Piacquadio D, et al: Actinic keratosis andthe incidence of occult squamous cell carcinoma: A clinical-histopathologic correlation. Dermatol Surg 32:1261, 2006

3. Stockfleth E, Meyer T, Benninghoff B, et al: A randomizeddouble-blind vehicle-controlled study to assess imiquimodcream for the treatment of multiple actinic keratoses. ArchDermatol 138:1498, 2002

4. Fulton JE, Rahimi AD, Helton P, et al: Disappointing resultsfollowing resurfacing of facial skin with CO2 lasers for prophy-

laxis if keratoses and cancers. Dermatol Surg 25:729, 1999

5. Brodland DG, Roenigk RK: TCA chemexfoliation for extensivepremalignant actinic damage of the face and scalp. Mayo ClinProc 63:887, 1988

6. Jensen P, Hansen S, Moller B, et al: Skin cancer in kidney andheart transplant recipients and different long term immuno-suppressive therapy regimens. J Am Acad Dermatol 40:177,1999

7. Blessing K, McLaren KM, Benton EC, et al: Histopathology ofskin lesions in renal allograft recipients—An assessment of viralfeatures and dysplasia. Histopathology 14:129, 1989

8. Del Regato JA, Spjut HJ, Cox JD: Cancer of the respiratorysystem and upper digestive tract, in del Rogato JA, AckermanB (eds): Cancer. St Louis, CV Mosby, 1985, pp 248-272

9. Elder DE: Lever’s Histopathology of the Skin. Philadelphia,Lippincott Williams and Wilkins, 2005, pp 820-825

0. Weedon D: Skin Pathology. Edinburgh Churchill Livingstone,2002, p 762

1. Marx RE, Stern D: Oral and Maxillofacial Pathology. ChicagoQuintessence, 2003, p 355

2. Kolhe PS, Leonard AG: Reconstruction of the vermilion after

“lip-shave.” Br J Plast Surg 41:68, 1988