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Cryosurgical treatment of a gingival lichen planus: report of case
CLINICAL
14. H an sen , L.S., a n d B u ch n e r, A. C h a n g in g co n cepts o f th e ju n c tio n a l nevus a n d m elan o m a: review o f th e l i t e r a t u r e a n d r e p o r t o f c ase . J O r a l S u r g 39(12):961-965, 1981. 15. Sagebiel, R.W . H isto p ath o lo g y o f b o rd e rlin e a n d early m a lig n a n t m elan o m as. A m J S u rg Pathol 3(6):543-552, 1979. 16. C lark, W .H ., J r ., a n d o th e rs. T h e histogenesis a n d biologic b eh av io r o f p rim a ry h u m a n m alig n an t m elan o m as o f th e skin. C an cer Res 29(1):705-727,
1969. 17. M cG overn, V .J. T h e classification o f m elanom a a n d its r e l a t i o n s h i p w ith p r o g n o s is . P a th o lo g y 2(2):85-98, 1970. 18. C h au d h ry , A .R .; H a m p el, A.; a n d G orlin, B.J. P rim a ry m a lig n a n t m e la n o m a o f th e o ra l cavity. C an c e r 11:923-928, 1958. 19. W oods, J.E .; Soule, E .H .; a n d B orkow ski, J.J. E x p erien ce w ith m a lig n a n t m e la n o m a o f the h e ad and n eck. P last R eco n stru ct S u rg 61:64-69, 1978.
REPORTS
20. R eg e z i,J.A .; H ayw ood, J.P .; a n d Pickens, T .N . S uperficial m e la n o m as o f o ra l m ucous m em b ra n e s. O ral S u rg 45:73 0 -7 4 0 , 1978. 21. H a n se n , M .G ., a n d M cC arten , A .B . T u m o r thickness a n d lym phocytic in filtra tio n in m a lig n a n t m elan o m a o f th e h e ad a n d neck. A m J S u rg 12:557561, 1974. 22. B reslow , A . T u m o r thickness, level o f invasion a n d n o d e dissection in S tage I c u ta n eo u s m elanom a. A nn S u rg 18:572-575, 1975.
Cryosurgical treatment of a gingival lichen planus: report of case H aim Tal, DMD, PhD Barry Rifkin, DDS, PhD The treatm ent o f gin gival lichen planus, in vo lvin g cryosurgery, is discussed in a case report. A n overview o f the clinical and histological changes occurring after this treatm ent also is presented.
ichen planus is a relatively com mon inflammatory disorder of the skin and oral mucosa. Prevalence rates of 1.9% have been reported for the general population .1Approximately a third of the patients w ith oral lichen planus have cutaneous lesions.2 Andreasen 3 has described six clinical forms of oral lichen planus: reticular, papular, plaque, atro phic, erosive, and bullous. The reticular form is most common and usually asymp tomatic, whereas the erosive form tends to be the most painful. Desquamative gingi vitis is a common feature of the erosive form .4The oral lesions of lichen planus are found m ost com m only on the buccal mucosa and the tongue, followed by the lips, gingiva, floor of the m outh, and palate .5 Histological characterization of lichen planus includes hyperkeratosis, degenera tive changes in the basal area of the epithe lium, and infiltration of lymphocytes into the subepithelial connective tissue .6 Al though the cause of lichen planus remains unclear, the proximity of the lym phoid infiltrate to the damaged epithelium has suggested an imm une-mediated mecha nism. Furthermore, the clinical and histo logical findings in certain cases of graft versus host disease are virtually identical to those of lichen p lan u s .7'8 Studies have shown that the T-cell is the predom inant cell found within the lymphoid infiltrate,9“ 11 although there is considerable contro versy regarding the nature of T-cell sub
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type present .12 Some investigators have shown that there is a preponderance of helper/inducer cells ,13-14 whereas others claims that the majority of intraepithelial T-cells are of the cytotoxic/suppressor phe notype, im plicating cytotoxic T-cells as the principal cells responsible for keratinocyte destruction .12"15 Increases in epithe lial and dermal langerhans cells also have been reported .13'15Humoral immune events are apparently secondary in this disease. The current treatment for lichen planus is unsatisfactory, and the disease may per sist for years. Andreasen 3 has calculated that 41% of reticular lesions, 12% of atro phic, and 7% of plaquelike lesions heal spontaneously, whereas none of the erosive lesions heals spontaneously. Erosive lichen planus may respond to topical or intralesional steroids, but the disease is not cured by this mode of therapy. Further more, the potential for m alignant trans form ation 16-18 implies caution in the long term use of potent topical steroids. C ryotherapy, an effective m ethod of tissue destruction by freezing, has been used widely in the treatment of various oral lesions .19 Studies on oral cryosurgery have shown that after freezing of the diseased
F ig 1 ■ C lin ical view of p a rt of the p la q u e lik e lesion ex ten d in g from the m axillary rig h t central in ciso r to the second m olar. T h e lesion covers g in giva an d alveolar vestibular m ucosa.
oral mucosa, healing was uncomplicated and resulted in tissue regeneration .19-25 T his article reports the effects of cryother apy on a plaquelike form of lichen planus that had been nonresponsive to other modes of therapy, including topical ster oids. Report of case A 55-year-old female came to the department of oral medicine (New York) for evaluation of a large white lesion of the maxillary right gingiva and alveolar mucosa. T he m ain problem was the presence of the white, painless lesion for several years that “appeared to be extending toward the front of the m outh.” Because the lesion was eas ily noticed on the maxillary anterior right gin giva, the patient expressed concern regarding physical appearance. Furthermore, as the lesion appeared to be slowly enlarging, the patient was apprehensive about its possible m alignant na ture. T he patient appeared in good health and the medical history was noncontributory. No medications were being taken. Clinical examination showed a rough, plaque like lesion extending from the maxillary right central incisor to the right second molar (Fig 1). The lesion covered the gingiva, alveolar mucosa, and vestibule and extended onto the buccal mucosa. In addition, portions of the maxillary left gingiva and m andibular right and left gin giva showed evidence of mild desquamative gingivitis. Areas of both the right and left poste rior buccal mucosa appeared moderately atro phic. Fine, white striae, arranged in a lacelike pattern, were noted at the periphery of these atrophic areas. Cutaneous lesions were absent. The clinical features were consistent with a diagnosis of lichen planus. The diagnosis was confirmed by microscopic exam ination of an incisional biopsy specimen obtained from the large, white, plaquelike area. Histological exam ination of the biopsy specimen showed a subepithelial bandlike infiltration of lymphocytes,
Tal-Rifkin : CRYOSURGICAL TREATMENT OF LICHEN PLANUS ■ 629
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REPORTS
F ig 2 ■ M icro g rap h of the biopsy specim en shows su b ep ith elial b andlike in filtra tio n of lymphocytes and hyperkeratosis.
F ig 3 ■ Shortly after onset of th aw in g , the cryo surgical “ iceb all” s till covers m o st of the lesion on the alveolar m ucosa.
epithelial basal cell degeneration, and decided hyperorthokeratosis (Fig 2). Treatm ent of the oral lesions, particularly the plaquelike area, with topical fluocinide 0.05 in orabase, equal parts six times daily for several weeks, proved unrewarding. In spite of the plaquelike lesions being asymp tomatic and a biopsy specimen diagnosis of a nonm alignant lesion, the patient requested re moval of the lesion for cosmetic purposes, espe cially in the areas below the lipline. Given the size of the lesion and areas involved, it was decided that cryosurgical treatment of the keratotic epithelium and the underlying infiltrated superficial connective tissue m ight offer the best result. A gas expansion cryosurgical system was used (Model CT-73), operated with nitrous oxide at a pressure of 53 kg/cm. Treatm ent was initiated on the alveolar mucosa portion of the lesion apical to the maxillary right first premolar, canine, and lateral incisor. A single cryocycle of 1 minute freeze at -81 C followed by 1 minute thaw was selected, based on experience24 and other recommendations.26’27 Because the lesion was large, an oropharyngeal cryoprobe (probe 630 ■ JADA, Vol. 113, O ctober 1986
no. 7823) was selected for the alveolovesdbular part of the lesion. As the mucosa was moist, no water or water-soluble gel was needed to im prove contact between the firmly applied probe and the mucosa. The iceball stabilized after about 40 seconds. The probe was loosened shortly after onset of thawing and was w ith drawn (Fig 3). The iceball thawed spontane ously within 1 minute. Mild erythema developed during the first hour. Local swelling developed 24 hours later and became distinct after 3 days. One week later, superficial necrosis was appar ent, covering an area slightly larger than the active surface of the probe. The necrotic slough was separated from the underlying tissue, leav ing a clean, granulating surface, partially cov ered by epithelium (Fig 4). Epithelialization was completed after 2 to 3 weeks. At that time, swel ling subsided but slight paresthesia of the right side of the upper lip remained for an additional 4 weeks. One m onth after the first treatment, the gin gival portion of the lesion was frozen. This area, dry and irregular in shape, required the use of a water-soluble gel (k-y gel) to ensure good ther mal conductivity. Cycles of 30 seconds freeze and 1 m inute thaw per area were selected using a nasal probe (probe no. 2226) 4 mm in diameter and cooled to -81 C (Fig 5). Superficial necrotic slough could be removed after 5 days, leaving a clean, granulating surface (Fig 6). Epithelial ization was complete 10 days after freezing (Fig 7). Residual keratotic lesions located on the papillary gingiva were finally frozen by a micro probe (probe no. 7831) with a cryodose of -81 C X 10 seconds. H ealing was uncomplicated. A biopsy specimen from the vestibular area where the border of the treated area could be determined easily was obtained 4 months after treatment. The epithelium that initially was orthokeratinized and lacked glycogen, reverted to the parakeratinized or nonkeratinized form with normal distribution of glycogen (Fig 8). A 2-year follow-up examination showed that the treatment area on the alveolar mucosa remained clinically normal, and the gingival epithelium remained unchanged. However, the normal keratinization pattern of the keratinized gingiva had not been reestablished. The nontreated sites (buccal mucosa, mandibular gingiva) remained unchanged.
containing the diseased tissue. Previous observations have shown that cryosurgery of the oral and gingival m u cosa results in complete regeneration.29'3133 Regeneration of normal epithelium with normal distribution of glycogen also was expected in the present case, based on pre vious studies .24'25 Published reports 21-23 generally agree that after cryosurgery, oral lesions heal completely within B weeks, without scar formation. There is a remarkably low fre quency of secondary infection and hemor rhage after treatment with the cryoprobe .34 In view of the size and location of the pres ent lesion and the unique characteristics of cryotherapy, this proved to be the correct treatment. Several im portant questions still remain unanswered. Will the lesion recur? If it does, how rapidly will it recur and will it reappear in a clinical form similar to the previous lesion? Although the initial event in lichen planus remains elusive, the basal keratinocytes appear to be the primary site of im m unologic damage. Alterations in basal keratinocyte membranes in lichen planus have been suggested by diminished lectin binding to these cells compared with suprabasal cells that have normal bind ing .35 Thus, lichen planus lesions may develop in response to T-cell mediated response to altered basal keratinocytes.13 It is not known whether the regenerating epithelium will continue to contain altered
Fig 4 ■ O ne week after freezing, the necrotic
Discussion
slo u g h separated from the underlying tissue leav in g a clean, g ra n u la tin g surface (dotted).
Several factors influence the size and nature of the cryolesion (for example, the size of the probe, the depth of the tissue to be frozen, and the thermal conductivity and osmolality of the tissue and its cellular composition and vascularity ).28 Although most vital tissues freeze at approximately -2.2 C, for death to occur, the temperature must fall below -20 C .29 Larger cryodoses are recommended in the literature20' 30; how ever, given the nature of the current lesion, and based on experience ,24'31 a smaller dose was selected. This dose was sufficient to remove a superficial layer of oral mucosa
Fig 5 ■ Freezing of the gingival lesion. T h e lesion is covered w ith a w ater-soluble gel. G ingival seg m ents are frozen one at a time.
CLINICAL
basal keratinocytes after cryosurgical treat ment. Summary
Fig 6 ■ Five days after gingival cryosurgery. S uper ficial necrotic slo u g h is removed e x p o sin g a clean, g ra n u la tin g surface.
F ig 7 ■ T e n days after gingival freezing. Epithelialization is com plete. O nly a sm all resid u al keratotic lesion located o n the p a p illa ry g in g iv a distal to the rig h t canine is observed.
T his report provides an overview of the clinical and histological changes after cryo therapy of gingival lichen planus. The patient was a 55-year-old female who had a large keratotic lesion of the maxillary right gingiva and alveolar mucosa. The condi tion, which was diagnosed as lichen pla nus, did not respond to the conventional modes of therapy. Cryosurgical treatment was initiated on the alveolar mucosa and then on the gingiva. Finally, residual kera totic lesions on the papillary gingiva were treated. Operating temperature was -81 C; cryocycles varied between 10 seconds and 1 minute freeze, followed by up to 1 minute thaw. Frozen tissues (alveolar mucosa, gin giva) became necrotic and sloughed after 5 to 7 days, leaving clean, granulating sur faces. Epithelialization was complete 10 to 20 days after treatment. A 2-year clinical follow-up examination and biopsy specimens after 4 months sug gest that the treatment was successful and keratinized lesions did not reappear. The normal keratinization pattern of the kera tinized gingiva, however, had not been established during this period.
-------------------- Jk\OA\--------------------T h is study was su p p orted in p a rt by Frigitronics of Shelton, C T, Inc. Dr. T a l was associate professor, p eriodontics a n d oral m edicine, New York U niversity C ollege of D entistry, NY, an d is head, section of periodontology, School of D ental M edicine, Sackler Faculty of M edicine, T e l Aviv U niversity, T el Aviv, Israel. Dr. R ifkin is chairm an, dep artm en t of oral m edicine, New York U niversity C ol lege of D entistry, NY. Address requests for re p rin ts to Dr. T a l in Israel.
Fig 8 ■ T o p , m icro g rap h of a biopsy specim en from the border betw een treated (left) an d un treated (rig h t) m ucosa (H an d E stain). B ottom , th e ep ith e lium , w hich w as in itia lly o rthokeratinized and lacked glycogen (right), reverted to the parakeratinized or nonkeratinized form w ith n o rm a l dis trib u tio n of collagen (left). T h e tra n sitio n is a b ru p t (periodic acid-Schiff stain).
1. Axell, T . A prevalence study of oral m ucosal lesions in a d u lt Swedish p o p u la tio n (thesis). O d o ntol Rev 27:suppl 36, 1976. 2. H o lm stru p , P. C ellular hypersensibilitet m od oral lichen p la n u s affektioner in vitro. T hesis (in D anish), R oyal D ental College, C openhagen, 1975. 3. A ndreasen, J.O . O ral lichen p lan u s. A clinical evaluation of 115 cases. O ral Surg 25:31-42, 1968. 4. N isengard, R .J., and Neiders, M. D esquam ative lesions of the gingiva. J Periodontol 52:500-510, 1981. 5. Shklar, G., an d M cCarthy, P.L. T h e oral lesions of lichen p lan u s. O ral Surg 14:164-181, 1961. 6. A ndreasen, J.O . O ral lichen p lan u s. A histo lo g i cal evaluation of 97 cases. O ral S urg 25:158-166, 1968. 7. L am p ert, I. A., an d others. L y m phoid infiltrates in skin in g raft vs ho st disease. L ancet 11:1358, 1981. 8. R odu, B., an d G ockerm an, J.P . O ral m anifesta tions of th e g raft vs ho st reaction. JAM A 249:504-507, 1983. 9. W alker, D.M. Identification o f su b p o p u latio n s of lym phocytes a n d m acrophages in the infiltrate of lichen p la n u s lesions of skin an d oral m ucosa. Br J D erm atol 94:529-534, 1976. 10. Regezi, J.A.; Deegan, M.J.; and H ayw ard, J.R . L ichen p lan u s: im m u n ologic and m orphologic iden
REPORTS
tification of the subm ucosal infiltrate. O ral S urg 46:4452, 1978. 11. Dockrell, H .M ., a n d G reenspan, J.S. H istochem ical id e n tific a tio n of T -cells in oral lichen p lan u s. O ral S urg 48:42-46, 1979. 12. M atthew s, J.B .; Scully, C.M .; and P otts, A.J. O ral lichen planus: a n im m unoperoxidase study u sing m onoclonal a n tibodies to lym phocyte subsets. Br J D erm atol 111:587-595, 1984. 13. B han, A.K., and others. T -cell subsets in lichen p lanus: in situ characterization u sin g m onoclonal antibodies. Br J D erm atol 105:617-622, 1981. 14. M cM illan, E.M ., an d others. D em onstration in situ of “ T ” cells and “T ” cell subsets in lichen p lan u s u sin g m onoclonal antibodies. J C utan P ath o l 8:228234, 1981. 15. Becker, J., and others. O ral lichen p lanus: char acterization of im m u n o co m p eten t cells w ith hybridom a antibodies. J O ral P athol 12:117-123, 1983. 16. H o lm stru p , P ., an d P indborg, J.J. E rythroplakic lesions in re la tio n to o ral lichen plan u s. Acta Derm Venerol S uppl 59(85):77-84, 1984. 17. H akim , A.A., and Joseph, C.E. In vivo m a lig n a n t tran sfo rm atio n of cells from h u m a n oral lichen p lan u s lesions. N eoplasm 29:189-195, 1982. 18. G reenspan, J.S. Infectious and n o nneop lastic diseases of the o ral m ucosa. J O ral P ath o l 12:139-166, 1983. 19. T a l, H . O ral cryotherapy. C om p C o ntin Educ D ent IV(6):533-538, 1983. 20. Posw illo, D.E. A com parative study of the effects of electrosurgery and cryosurgery in the m anagem ent of b e nign oral lesions. Br J O ral Surg 9:1-7, 1971. 21. G oode, R ., and S pooner, T . Office cryotherapy an d o ral leuk o p lak ia. Am Acad O p h th a l O tolaryngol 75:963-973, 1971. 22. Sheperd, J.P ., an d Sussex, S. Effects of lowered tem peratures o n rat p u lp and gingiva. O ral Surg 42:387-394, 1976. 23. Sako, K.; M archetta, F.C.; a n d H ayes, R .L . Cryo therapy of in trao ral leukoplakia. Am J S urg 124:482484, 1972. 24. T a l, H .; C ohen, M.A.; a n d Lem m er, J. C linical a n d histological changes follow ing cryotherapy of a case w ith w idespread leukoplakia. In t J O ral Surg 11:64-68, 1982. 25. T a l, H . G lycogen co n te n t in regenerated e p ith e liu m follow ing cryosurgery of the oral m ucosa. J O ral Med 39:246-249, 1984. 26. L eopard, P .J., a n d Posw illo, D.E. Practical cryo surgery for oral lesions. Br D ent J 136:185-196, 1974. 27. Sokondi, I. C ryosurgery in stom ato-oncology. In t J O ral Surg 8:95-101, 1979. 28. G ill, W.; D eCosdta, J.; an d Fraser, J. T h e control an d p redictability of the cryolesion. C ryobiology 6:347353, 1970. 29. Fraser, J., and G ill, W. O bservations on u ltra frozen tissue. Br J Surg 54:770-776, 1967. 30. Z acharian, S.A., ed. C ryosurgery of tum ors of the skin and oral cavity, ed 1. S pringfield, IL , C harles C T h o m as, 1973. 31. T a l, H ., a n d A ltini, M. D ila n tin induced hyper plastic gingiva as a m odel for experim ental cryother apy. D iastem a 10:27-30, 1982. 32. H u rt, W .C.; N abers, C .L .; an d Rose, G .G . Some clinical and histological observations of gingiva treated by cryotherapy. J Periodontol 43:151-156, 1972. 33. B uch, B.; P ap ert, A.E.; a n d Shear, M. M icros copic changes in rat tongue follow ing experim ental cryosurgery. J O ral P ath o l 8:94-102, 1979. 34. Lloyd-W illiam s, K.; H ag, I.U .; and Elen, B. Cryodestruction of haem orrhoids. Br Med J 1:666-669, 1973. 35. H o lm stru p , P., and D abeistein, E. C hanges in carbohydrate expression of lichen p la n u s affected e p i thelial cell m em brane. J Invest D erm atol 73:364-367, 1979.
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14. H an sen , L.S., a n d B u ch n e r, A. C h a n g in g co n cepts o f th e ju n c tio n a l nevus a n d m elan o m a: review o f th e l i t e r a t u r e a n d r e p o r t o f c ase . J O r a l S u r g 39(12):961-965, 1981. 15. Sagebiel, R.W . H isto p ath o lo g y o f b o rd e rlin e a n d early m a lig n a n t m elan o m as. A m J S u rg Pathol 3(6):543-552, 1979. 16. C lark, W .H ., J r ., a n d o th e rs. T h e histogenesis a n d biologic b eh av io r o f p rim a ry h u m a n m alig n an t m elan o m as o f th e skin. C an cer Res 29(1):705-727,
1969. 17. M cG overn, V .J. T h e classification o f m elanom a a n d its r e l a t i o n s h i p w ith p r o g n o s is . P a th o lo g y 2(2):85-98, 1970. 18. C h au d h ry , A .R .; H a m p el, A.; a n d G orlin, B.J. P rim a ry m a lig n a n t m e la n o m a o f th e o ra l cavity. C an c e r 11:923-928, 1958. 19. W oods, J.E .; Soule, E .H .; a n d B orkow ski, J.J. E x p erien ce w ith m a lig n a n t m e la n o m a o f the h e ad and n eck. P last R eco n stru ct S u rg 61:64-69, 1978.
REPORTS
20. R eg e z i,J.A .; H ayw ood, J.P .; a n d Pickens, T .N . S uperficial m e la n o m as o f o ra l m ucous m em b ra n e s. O ral S u rg 45:73 0 -7 4 0 , 1978. 21. H a n se n , M .G ., a n d M cC arten , A .B . T u m o r thickness a n d lym phocytic in filtra tio n in m a lig n a n t m elan o m a o f th e h e ad a n d neck. A m J S u rg 12:557561, 1974. 22. B reslow , A . T u m o r thickness, level o f invasion a n d n o d e dissection in S tage I c u ta n eo u s m elanom a. A nn S u rg 18:572-575, 1975.
Cryosurgical treatment of a gingival lichen planus: report of case H aim Tal, DMD, PhD Barry Rifkin, DDS, PhD The treatm ent o f gin gival lichen planus, in vo lvin g cryosurgery, is discussed in a case report. A n overview o f the clinical and histological changes occurring after this treatm ent also is presented.
ichen planus is a relatively com mon inflammatory disorder of the skin and oral mucosa. Prevalence rates of 1.9% have been reported for the general population .1Approximately a third of the patients w ith oral lichen planus have cutaneous lesions.2 Andreasen 3 has described six clinical forms of oral lichen planus: reticular, papular, plaque, atro phic, erosive, and bullous. The reticular form is most common and usually asymp tomatic, whereas the erosive form tends to be the most painful. Desquamative gingi vitis is a common feature of the erosive form .4The oral lesions of lichen planus are found m ost com m only on the buccal mucosa and the tongue, followed by the lips, gingiva, floor of the m outh, and palate .5 Histological characterization of lichen planus includes hyperkeratosis, degenera tive changes in the basal area of the epithe lium, and infiltration of lymphocytes into the subepithelial connective tissue .6 Al though the cause of lichen planus remains unclear, the proximity of the lym phoid infiltrate to the damaged epithelium has suggested an imm une-mediated mecha nism. Furthermore, the clinical and histo logical findings in certain cases of graft versus host disease are virtually identical to those of lichen p lan u s .7'8 Studies have shown that the T-cell is the predom inant cell found within the lymphoid infiltrate,9“ 11 although there is considerable contro versy regarding the nature of T-cell sub
L
type present .12 Some investigators have shown that there is a preponderance of helper/inducer cells ,13-14 whereas others claims that the majority of intraepithelial T-cells are of the cytotoxic/suppressor phe notype, im plicating cytotoxic T-cells as the principal cells responsible for keratinocyte destruction .12"15 Increases in epithe lial and dermal langerhans cells also have been reported .13'15Humoral immune events are apparently secondary in this disease. The current treatment for lichen planus is unsatisfactory, and the disease may per sist for years. Andreasen 3 has calculated that 41% of reticular lesions, 12% of atro phic, and 7% of plaquelike lesions heal spontaneously, whereas none of the erosive lesions heals spontaneously. Erosive lichen planus may respond to topical or intralesional steroids, but the disease is not cured by this mode of therapy. Further more, the potential for m alignant trans form ation 16-18 implies caution in the long term use of potent topical steroids. C ryotherapy, an effective m ethod of tissue destruction by freezing, has been used widely in the treatment of various oral lesions .19 Studies on oral cryosurgery have shown that after freezing of the diseased
F ig 1 ■ C lin ical view of p a rt of the p la q u e lik e lesion ex ten d in g from the m axillary rig h t central in ciso r to the second m olar. T h e lesion covers g in giva an d alveolar vestibular m ucosa.
oral mucosa, healing was uncomplicated and resulted in tissue regeneration .19-25 T his article reports the effects of cryother apy on a plaquelike form of lichen planus that had been nonresponsive to other modes of therapy, including topical ster oids. Report of case A 55-year-old female came to the department of oral medicine (New York) for evaluation of a large white lesion of the maxillary right gingiva and alveolar mucosa. T he m ain problem was the presence of the white, painless lesion for several years that “appeared to be extending toward the front of the m outh.” Because the lesion was eas ily noticed on the maxillary anterior right gin giva, the patient expressed concern regarding physical appearance. Furthermore, as the lesion appeared to be slowly enlarging, the patient was apprehensive about its possible m alignant na ture. T he patient appeared in good health and the medical history was noncontributory. No medications were being taken. Clinical examination showed a rough, plaque like lesion extending from the maxillary right central incisor to the right second molar (Fig 1). The lesion covered the gingiva, alveolar mucosa, and vestibule and extended onto the buccal mucosa. In addition, portions of the maxillary left gingiva and m andibular right and left gin giva showed evidence of mild desquamative gingivitis. Areas of both the right and left poste rior buccal mucosa appeared moderately atro phic. Fine, white striae, arranged in a lacelike pattern, were noted at the periphery of these atrophic areas. Cutaneous lesions were absent. The clinical features were consistent with a diagnosis of lichen planus. The diagnosis was confirmed by microscopic exam ination of an incisional biopsy specimen obtained from the large, white, plaquelike area. Histological exam ination of the biopsy specimen showed a subepithelial bandlike infiltration of lymphocytes,
Tal-Rifkin : CRYOSURGICAL TREATMENT OF LICHEN PLANUS ■ 629
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F ig 2 ■ M icro g rap h of the biopsy specim en shows su b ep ith elial b andlike in filtra tio n of lymphocytes and hyperkeratosis.
F ig 3 ■ Shortly after onset of th aw in g , the cryo surgical “ iceb all” s till covers m o st of the lesion on the alveolar m ucosa.
epithelial basal cell degeneration, and decided hyperorthokeratosis (Fig 2). Treatm ent of the oral lesions, particularly the plaquelike area, with topical fluocinide 0.05 in orabase, equal parts six times daily for several weeks, proved unrewarding. In spite of the plaquelike lesions being asymp tomatic and a biopsy specimen diagnosis of a nonm alignant lesion, the patient requested re moval of the lesion for cosmetic purposes, espe cially in the areas below the lipline. Given the size of the lesion and areas involved, it was decided that cryosurgical treatment of the keratotic epithelium and the underlying infiltrated superficial connective tissue m ight offer the best result. A gas expansion cryosurgical system was used (Model CT-73), operated with nitrous oxide at a pressure of 53 kg/cm. Treatm ent was initiated on the alveolar mucosa portion of the lesion apical to the maxillary right first premolar, canine, and lateral incisor. A single cryocycle of 1 minute freeze at -81 C followed by 1 minute thaw was selected, based on experience24 and other recommendations.26’27 Because the lesion was large, an oropharyngeal cryoprobe (probe 630 ■ JADA, Vol. 113, O ctober 1986
no. 7823) was selected for the alveolovesdbular part of the lesion. As the mucosa was moist, no water or water-soluble gel was needed to im prove contact between the firmly applied probe and the mucosa. The iceball stabilized after about 40 seconds. The probe was loosened shortly after onset of thawing and was w ith drawn (Fig 3). The iceball thawed spontane ously within 1 minute. Mild erythema developed during the first hour. Local swelling developed 24 hours later and became distinct after 3 days. One week later, superficial necrosis was appar ent, covering an area slightly larger than the active surface of the probe. The necrotic slough was separated from the underlying tissue, leav ing a clean, granulating surface, partially cov ered by epithelium (Fig 4). Epithelialization was completed after 2 to 3 weeks. At that time, swel ling subsided but slight paresthesia of the right side of the upper lip remained for an additional 4 weeks. One m onth after the first treatment, the gin gival portion of the lesion was frozen. This area, dry and irregular in shape, required the use of a water-soluble gel (k-y gel) to ensure good ther mal conductivity. Cycles of 30 seconds freeze and 1 m inute thaw per area were selected using a nasal probe (probe no. 2226) 4 mm in diameter and cooled to -81 C (Fig 5). Superficial necrotic slough could be removed after 5 days, leaving a clean, granulating surface (Fig 6). Epithelial ization was complete 10 days after freezing (Fig 7). Residual keratotic lesions located on the papillary gingiva were finally frozen by a micro probe (probe no. 7831) with a cryodose of -81 C X 10 seconds. H ealing was uncomplicated. A biopsy specimen from the vestibular area where the border of the treated area could be determined easily was obtained 4 months after treatment. The epithelium that initially was orthokeratinized and lacked glycogen, reverted to the parakeratinized or nonkeratinized form with normal distribution of glycogen (Fig 8). A 2-year follow-up examination showed that the treatment area on the alveolar mucosa remained clinically normal, and the gingival epithelium remained unchanged. However, the normal keratinization pattern of the keratinized gingiva had not been reestablished. The nontreated sites (buccal mucosa, mandibular gingiva) remained unchanged.
containing the diseased tissue. Previous observations have shown that cryosurgery of the oral and gingival m u cosa results in complete regeneration.29'3133 Regeneration of normal epithelium with normal distribution of glycogen also was expected in the present case, based on pre vious studies .24'25 Published reports 21-23 generally agree that after cryosurgery, oral lesions heal completely within B weeks, without scar formation. There is a remarkably low fre quency of secondary infection and hemor rhage after treatment with the cryoprobe .34 In view of the size and location of the pres ent lesion and the unique characteristics of cryotherapy, this proved to be the correct treatment. Several im portant questions still remain unanswered. Will the lesion recur? If it does, how rapidly will it recur and will it reappear in a clinical form similar to the previous lesion? Although the initial event in lichen planus remains elusive, the basal keratinocytes appear to be the primary site of im m unologic damage. Alterations in basal keratinocyte membranes in lichen planus have been suggested by diminished lectin binding to these cells compared with suprabasal cells that have normal bind ing .35 Thus, lichen planus lesions may develop in response to T-cell mediated response to altered basal keratinocytes.13 It is not known whether the regenerating epithelium will continue to contain altered
Fig 4 ■ O ne week after freezing, the necrotic
Discussion
slo u g h separated from the underlying tissue leav in g a clean, g ra n u la tin g surface (dotted).
Several factors influence the size and nature of the cryolesion (for example, the size of the probe, the depth of the tissue to be frozen, and the thermal conductivity and osmolality of the tissue and its cellular composition and vascularity ).28 Although most vital tissues freeze at approximately -2.2 C, for death to occur, the temperature must fall below -20 C .29 Larger cryodoses are recommended in the literature20' 30; how ever, given the nature of the current lesion, and based on experience ,24'31 a smaller dose was selected. This dose was sufficient to remove a superficial layer of oral mucosa
Fig 5 ■ Freezing of the gingival lesion. T h e lesion is covered w ith a w ater-soluble gel. G ingival seg m ents are frozen one at a time.
CLINICAL
basal keratinocytes after cryosurgical treat ment. Summary
Fig 6 ■ Five days after gingival cryosurgery. S uper ficial necrotic slo u g h is removed e x p o sin g a clean, g ra n u la tin g surface.
F ig 7 ■ T e n days after gingival freezing. Epithelialization is com plete. O nly a sm all resid u al keratotic lesion located o n the p a p illa ry g in g iv a distal to the rig h t canine is observed.
T his report provides an overview of the clinical and histological changes after cryo therapy of gingival lichen planus. The patient was a 55-year-old female who had a large keratotic lesion of the maxillary right gingiva and alveolar mucosa. The condi tion, which was diagnosed as lichen pla nus, did not respond to the conventional modes of therapy. Cryosurgical treatment was initiated on the alveolar mucosa and then on the gingiva. Finally, residual kera totic lesions on the papillary gingiva were treated. Operating temperature was -81 C; cryocycles varied between 10 seconds and 1 minute freeze, followed by up to 1 minute thaw. Frozen tissues (alveolar mucosa, gin giva) became necrotic and sloughed after 5 to 7 days, leaving clean, granulating sur faces. Epithelialization was complete 10 to 20 days after treatment. A 2-year clinical follow-up examination and biopsy specimens after 4 months sug gest that the treatment was successful and keratinized lesions did not reappear. The normal keratinization pattern of the kera tinized gingiva, however, had not been established during this period.
-------------------- Jk\OA\--------------------T h is study was su p p orted in p a rt by Frigitronics of Shelton, C T, Inc. Dr. T a l was associate professor, p eriodontics a n d oral m edicine, New York U niversity C ollege of D entistry, NY, an d is head, section of periodontology, School of D ental M edicine, Sackler Faculty of M edicine, T e l Aviv U niversity, T el Aviv, Israel. Dr. R ifkin is chairm an, dep artm en t of oral m edicine, New York U niversity C ol lege of D entistry, NY. Address requests for re p rin ts to Dr. T a l in Israel.
Fig 8 ■ T o p , m icro g rap h of a biopsy specim en from the border betw een treated (left) an d un treated (rig h t) m ucosa (H an d E stain). B ottom , th e ep ith e lium , w hich w as in itia lly o rthokeratinized and lacked glycogen (right), reverted to the parakeratinized or nonkeratinized form w ith n o rm a l dis trib u tio n of collagen (left). T h e tra n sitio n is a b ru p t (periodic acid-Schiff stain).
1. Axell, T . A prevalence study of oral m ucosal lesions in a d u lt Swedish p o p u la tio n (thesis). O d o ntol Rev 27:suppl 36, 1976. 2. H o lm stru p , P. C ellular hypersensibilitet m od oral lichen p la n u s affektioner in vitro. T hesis (in D anish), R oyal D ental College, C openhagen, 1975. 3. A ndreasen, J.O . O ral lichen p lan u s. A clinical evaluation of 115 cases. O ral Surg 25:31-42, 1968. 4. N isengard, R .J., and Neiders, M. D esquam ative lesions of the gingiva. J Periodontol 52:500-510, 1981. 5. Shklar, G., an d M cCarthy, P.L. T h e oral lesions of lichen p lan u s. O ral Surg 14:164-181, 1961. 6. A ndreasen, J.O . O ral lichen p lan u s. A histo lo g i cal evaluation of 97 cases. O ral S urg 25:158-166, 1968. 7. L am p ert, I. A., an d others. L y m phoid infiltrates in skin in g raft vs ho st disease. L ancet 11:1358, 1981. 8. R odu, B., an d G ockerm an, J.P . O ral m anifesta tions of th e g raft vs ho st reaction. JAM A 249:504-507, 1983. 9. W alker, D.M. Identification o f su b p o p u latio n s of lym phocytes a n d m acrophages in the infiltrate of lichen p la n u s lesions of skin an d oral m ucosa. Br J D erm atol 94:529-534, 1976. 10. Regezi, J.A.; Deegan, M.J.; and H ayw ard, J.R . L ichen p lan u s: im m u n ologic and m orphologic iden
REPORTS
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