The lichenoid reaction Pattern M Ramaml, Asha Kubba'?

Sri Lanka lournal of Dermatology, 2002, 6,20-26

There is some confusion about the origin of the It is easier to bring these diverse conditions term lichen to describe skin diseases but it appears to together based on the histopathological appearance. characteristic of lichenoid have been a popular name for many conditions. An Histologically, the defining cell damage2-3. The damage impressive list of dermatoses that begin with the term tissue reactions is basal or liquefactive degeneration, Iichen or lichenoid could be colled from the index of a occurs by apoptosis processes that appear to be mediated by different major textbook (Table 1)1. It is difficult to conceive of a pathogenetic mechanisms. Apoptosis, a special type way to unify atl these conditions but there are some of single cell death, consists of the condensation features that some of these diseases share. These fea- of single cells followed by active budding and tures are also shared by diseases that do not have fragmentationa. Unlike necrosis, cell membranes and lichen in their names. Briefly, the common clinical organelles remain intact till late in the apoptosis. On denominator is the presence of small papules, purple light microscopy, apoPtotic keratinocytes appear as and histologically, damage to the or skin coloured, pink, shrunken globules (known as Civatte bodies) basal keratinocytes. which may show pyknotic nuclear remnants. The Civatte bodies may be phagocytosed by other keratinocytes and macrophages or may drop down into the papillary dermis as colloid bodies. Liquefac- Table 1. tive degeneration leads to keratinocyte damage by the Lichen amyloidosus accumulation of fluid within basal cells. On micros- aPpear swollen and vacu- Lichen aurcus copy, the keratinocytes olated. It appears that apoptosis is mediated by Lichen fibromdcinodosis cellular immunity and liquefactive degeneration by Lichen myxoedematosus humoral immunity. Other histological accompaniments of the Lichen nuchae lichenoid reaction are an infiltrate of lymphocytes and Lichen pigmentosus melanin incontinence. The lymphoeytes are present the Lichen planopilaris in the papillary dermis closely applied to undersurface of the epidermis and infiltrating the lower layers in some disorders. Apototic keratinocytes Lichen planus pemphigoides are sometimes found in close contact with lympho- Lichen planus pigmentosus cytes, an appearance referred to as satellite cell In some diseases, the infiltrate obscures the Lichen purpuricus necrosis. junction between the epidermis and dermis, an Lichen rubber moniliformis appearance that has been referred to as interface der- et atroPhicans matitis. Some accounts exclude this group of disor- Lichen scrofulosorum ders from the lichenoid reaction Pattern but we have chosen to use a broader definition. Other cells, chiefly Lichen simplex histiocytes, may be part of the infiltrate. Melanin in- Lichen simplex chronicus continence refers to the presence of melanin within Lichen spinulosus melanophages of the upper dermis. This results from unit by basal cell disruption of the epidermal-melanin damage. Once it occurs, melanin incontinence per- et reticularis Lichen verrucosus sists for long periods and in some situations may serve Lichenoid drug eruPtions as the only histological signpost of a lichenoid reac- Lichenoid melanodermatitis tion in the past,

t Associate professor, Department of Dermatology and Venereology, All lndia Institute of Medical Scietces, New Delhi 1L0 029, India, email: [email protected] 2 Consultant Dermatopathologist, Delhi Dermpath Lab. T-25, Green Park Main, New Delhi 11N16, lndia. The lichenoid reaction pattern 27

The sequence in which they appear and the On the scalp and at other hair-bearing sites, slightly pathogenetic significance of these histological findings purple, follicular papules are seen when lichen is unclear but they constitute a recognizable pattern. planus involves the hair follicles. These papules heal with follicular scarring and a blue-black pigmenta- The clinical features that correspond to these find- tion of the recently scarred area is a useful clue. Scar- ings are dependent on whether the lichenoid reaction ring is also a helpful diagnostic sign when the nails is acute or chronic. The prototype disease is lichen are affected.and a pterygium is highly suggestive of planus which represents the chronic type of lichenoid lichen planus. Other less specific signs include rough- reaction dnd is characterized by small, purple papules. ening of the surface of the nail plate, Iongitudinai In addition, skin coloured or shiny, minute papules ridging and thinning. may also occur and have exactly the same histo- pathological appearance. Occasionally, a lesion may H stologically, there is a dense upper dermal band show a combination of shiny papules and violaceous of lymphocytes that is closely applied to the epider- papules. ln such lesions, the shiny papules are aggre- mis but does not invade its. The basal keratinocytes gated closely together and show a purple coloration show evidence of injury as necrotic pink cells with a at the censer of the lesion while papules tend to remain pyknotic nucleus or as vacuolated ceils. The necrotic skin coloured and discrete at the periphery. We have cells drop down into the epidermis as colloid or Civatte also seen shiny macules that have the colour and sheen bodies. The basal cell damage may lead to the appear- of fine lichenoid papules. They may represent evolv- ance of a split between the epidermis and the dermis, ing or subsiding lesions, The, clinical appearance the so-called Max-]oseph space. The damage to basal is also modified by the site of the lesion; the character- keratinocytes of the rete ridges leads to a saw-tooth istic purple colour is hardly yisible at sites such as the appearance. Melanin is found within macrophages scalp and nail. Ii:r these locations, other clues such as in the upper dermis. There is compact orthokeratosis scarring alopecia and pterygium provide clues to a and hypergranulosis which is wedge shaped over the lichenoid process. acrotrichia and acrosyringia.

In acute lesions, the clinical appearance is domi- When lichen planus affects the hair follicles, oral nated by erythema. The brown-black colour of epider- mucosa or nail, the changes are essentially similar mal necrosis is often seen in erythema multiforme and but the appearance must be interpreted in the light of fixed . It is overshadowed by dermal the normal histology of the area. necrosis presenting as a necrotic crust in lichenoides et varioliformis acuta (PLEVA). The sub- In follicular lesions of lichen planus (ichen sidence of an acr$e lichenoid reaction is characteristi- planopilaris), the lymphocytic infiltrate is seen around cally followed by a persistent pigmentation which the hair follicle with damage to the basal cells of the represents the melanin incontinence that is prone to follicular epithelium. This may occur in isolation or occur in these dermatoses. in conjunction with involvement of non-follicular epidermis. Lichen planopilaris heals with scarring of An account of some of the major diseases that follicles and biopsies of late lesions show selerosed belong to this group and which are likely to be encoun- follicular units. tered in clinical practice follows. Lichen planus of the oral mucosa shows changes Lichen planus similar to cutaneous lesions. The finding of parak- eratosis is not compatible with a diagnosis of lichen Lichen planus is the prototype of a lichenoid tissue planus on the skin but it is a normal feature of oral reaction. The typical clinical lesion is an itchy, mucosa and is seen in oral lichen planus. Basal cell violaceous papule that shows whitish streaks known damage is less prominent than in cutaneous lesions, as Wickham striae. The papules occur on the legs, the wrists and the lower back but may develop at any site Lichen planus hypertrophicus demonstrates and can present.as a generalized eruption. At all these compact hyperkeratosis and acanthosis. The dermal sites, they retain their characteristic appearance. How- infiltrate of lymphocytes is not band-like and is local- ever, the presentation of the disease may be modified ized to the tips of the rete ridges with damage to the by the site. overlying basal keratinocytes. Papillary fibrosis is frequent. On the palms and soles, lichen planus is skin coloured and hyperkeratotic and diagnosis is diffi- Lichenoid drug eruptions cult when lesions are confined to this site. On the mucosa, there is a white or violaccous plague. White Itchy, violaceous papules that resemble idiopathic plaques may be lacy and reticular. Some white plaques lichen planus may develop following exposure to show violaceous discoloration. Erosions are frequent. certain drugs. Some drugs may cause oral lesions of

Vol. 5, 2002 E E

I I t i r 22 M Ra-tnam, Asha Kubba i

I i lichen planus, alone or in association with skin lesions. biopsies that showed features indistinguishable from i The list of drugs implicated is long and includes lichen nitidus and the diagnosis was established by : thiazide diuretics, i antimalarials, gold, streptomycin, the Mantoux test and response to therapy. i isoniazid, ethambutol and beta blockers among many othersT. a Oral lichenoid eruptions are induced by a Lichen striatus : smaller number of drugs8 including lithium carbonatee : and imatiniblo. (Histologically, lichenoid drug reac- Lichen striatus is much easier to diagnose ' tions may be indistinguishable from lichen planusll. clinically than on biopsy because its distinguishing Clues include the presence necrotic keratinocytes of characteristic of linearly arranged papules cannot be high in the epidermis along with parakeratosis and a appreciated under the microscope. The papuies are skin superficial and deep perivascular infiltrate. Eosino- coloured and shiny and often coalesce. The condition phils and plasma cells in the infiltrate are often used occurs mainly in children and spontaneous regres- as a diagnostic clue but this not a helpful finding sion is the rule. This may occur in one part of the lesion because it is uncommon in lichenoid drug eruptions while another shows papules. If a biopsy is performed, and occurs occasionally in lichen planus as well. The the latter area must be sampled. On brown skin, the diagnosis is documented by noting improvement in papules subside to leave a streaky hypopigmentation the eruption following withdrawal of the drug and that may persist for several months. If patients present confirmed by re-challenge. at this stage, a biopsy is iikely to show non-diagnosfic changes. Lichen nitidus Lichen striatus demonstrates a lichenoid pattern Lichen nitidus presents with minute, 1mm shiny, with a superficial and deep perivascular and skin coloured papules that are often grouped together periadnexal infiltratela. There is a patchy infiltrate of but tend to remain discrete. Slight umblication of the lymphocytes and histiocytes in the upper dermis with papules is evident. When located on the palms and overlying basal ceil necrosis and vacuolization. Mid soles, the papules demonstrate central keratotic plugs. spongiosis and exocytosis are usually associated. The Some papules may be located in a short, straight line infiltrate is also present around the vessels of the super- indicating Koebnerisation. Lesiom may deveiop ficiai and deep plexuses and around the sweat glands. anywhere but have a predilection for the tips of the Epithelioid histiocytes may be prominent in the fingers and the penis. infiltrate in some cases.

Histologically, lichen nitidus characteristically demonstrates a compact collection of epitheiioid Photosensitive histiocytes and lymphocytes enclosed within a single Photosensitive lichenoid eruption is the term that we papilla by inward bending rete ridgesl2. Ocassionally, use for a commonly encountered condition that does the infiltrate spans more than one papilia. The epi- not appear to have been described in detail. We ard dermis overlying the granuloma is thin and basal aware that others use different names for this condi- keratinocytes show necrosis and vacuolization. The tion including polymorphous light eruption, actinic stratum comeum is compact and orthokeratotic in lichen nitidus and summertime actinic lichenoid erup- some cases and parakeratotic in the remainder. tionls. The dermatosis occurs in young adults and many patients are aware of the relationship of their Lichen scrofulosorum eruption to sun exposure while some are not. The con- dition presents with grouped, shiny, 1-2 mm discrete Lichen scrofulosorum may cause diagnostic and coalescing papules on the extensor surfaces of confusion with lichen nitidus. Small, discrete skin the forearm, the dorsae of the hands and the nape and coloured papules are seen in small groups. A minute V of the neck. The face is usually not affected but may central crust is a feature of many papules. Subtle fea- show papules on the forehead. A purple colour often tures to differentiate them from lichen nitidus are the develops at the thicker central part of larger plaques lack of shininess, a predilection for the trunk a and that form from the coalescence of papules. The indi- waxing and waning course. Lichen scrofulosorum is vidual discrete papules resemble lichen nitidus but associated with a strongly positive Mantoux test the distribution on sun-exposed skin and the tendency and an extracutaneous focus of tuberculosis can be to coalesce and develop a violaceous hue serve to dis- detected in many patients. Treatment with antituber- tinguish the two. Photosensitive lichenoid eruption cular drugs is curative. Histologically, the classical reveals a rnild to moderately dense superficial perivas- appearance of lichen scrofulosorum with small epithe- cular infiltrate of lymphocytes with slight papillary lioid cell granulomas around sweat glands and hair edema. There are small foci of lichenoid change and follicles is diagnosticl3. However, we have seen some spongiosis. The circumscribed papillary granulomas

Sri Lanka lournal of Dermatology The lichenoil reaction pattern 23 of lichen nitidus are not a feature of photosensitive erythematosus and dermatomyositis lichenoid eruption. I-upus erythematosus may present with a variety of cutaneous lesions ranging from a blanchable Ashy dermatooie,.(lichen planus pigmentosus. mel- anodermatitis toxica, erythema dyschromicum erythema to indurated paques. The erythema of LE is easily recognizable when it occurs on the cheeks (but- perstans) terfly erythema) but may occur at other sites includ- This common but poorly understood dermatosis ing the trunk. Erythema is associated with acute flares suffers from an excess of inadequate slmonyms. The of disease and may be accompanied by evidence of characteristic lesion is an asymptomatic violaceous disease in other organ systems. On brown skin, the or ashy macule that often begins on the sun-exposed erythema subsides with a persistent brown-black pig- skin of the face and upper limbs. With time, the mentation which may obscure recurrences of active macules increase in size and coalesce into confluent disease. Slight indurated and scaly annular plaques areas of hyperpigmentation that may affect large parts are a feature of subacute lupus erythematosus. Discoid of the skin including non-exposed skin. lupus erythematosus presents as an indurated and atrophic scaly plague with adherent follicular scales. Biopsies demonstrate of ashy dermatosis changes The plaque is usually depigmented and has a rim of represent disease that appear to different stages of hyperpigmentation. Some lesions or parts of plaques activityl6. Early biopsies show a fairly dense band- may show a purple colour usually around the periph- like infiltrate lymphocytes with damage to the over- of ery. The plaques develop on sun-exposed skin; the lying basal keratinocytes associated with melanin in- concha is a characteristic site. On the scalp, DLE continence. Later biopsies show a moderately dense causes cicatricial alopecia. and patchy lichenoid infiltrate with melanin inconti- nence. Biopsies taken in the late stages of disease may Lupus erythematosus reveals a patchy lichenoid reveal only melanophages in the upper dermis with infilkate with a superficial and deep perivascular and no lichenoid infiltrate and a reconstituted basal layer. periadnexal infiltrate of lymphocytesl&1e. In established At this stage the histopathology is indistinguishable lesions of discoid lupus erythematosus, there is a from post-inflammatory pigmentation. Clinically, patchy infilhate of lymphocytes and vacuolization of however, it is not possible to recognize the different the overlying basal cells; nocrosis is less prominent. histopathological stages; the appearance of the The epidermis is thickened in parts and thin in others. macules is similar irrespective of the histological find- There are follicular plugs and patchy parakeratosis. ings. A biopsy from a recent lesion may be expected to Basement membrane thickening is a useful diagnostic provide the most useful information. feature but is present in a minority of cases. The der- mal infiltrate is present around vessels and adnexal Lichenoid secondaty syphilis structuresi Connective tissue mucin is seen in in- One of the protean manifestations of secondary creased quantities. Usually, it is easy to differentiate syphilis is violaccous papules. Lichenoid papules lichen planus from LE however, in some cases, the around the anogenital region should prompt a search histopathological appearance may be indistinguish- for syphilis but patients will often not mention these able and direct immunoflourescence to demonstrate a Iesions and only present papules on the limbs or trunk lupus band, scrological tests and clinicopathological for examination. These papules can resemble lichen correlation and follow up may be required to settle the planus very closely. Oral mucosal lesions typical of diagnosis. lichen planus do not occur. Hyperpigmented macules Dermatomyositis shows changes similar to those on the palms or condyoma lata, when present, may in early lupus erythematosus with a patchy lichonoid suggest the diagnosis. On biopsy, lichenoid second- infiltrate of lymphocytes, necrotic and vacuolated ary syphilis shows a combination of psoriasiform and keratinocytes, a thickened basement membrane and lichenoid changeslT. There is parakeratosis and increased. cortnective tissue mucin2o. acanthesis accompanied by basal cell damage and an upper dermal infiltrate of lymphocytes. The infiltrate Erythema also involves the deep dermis and may be centred multiforme around the adnexal structures. An ill-formed epithe- Erythema multiforme presents with erythematous lioid granuloma is observed in some biopsies. Plasma macules and plaques with a predilection for the hands cells are not numerous. This lack of concordance and feet though other areas including the oral mu- between the clinical and histological appearances cosa may be affected. Characteristically, the center of should arouse the suspicion of syphilis which is ihe plaque develops a circular brown-black discol- confirmed by serological testing. oration, which with its ring of erythema constitutes

Vol. 6, 2002 24 M Ramam, Asha Kubba the target lesion typical of this disease. Small vesicles malaise. The papules develop a necrotic crust at the may also develop within the plaque. The eruption is center which sloughs off and heals with a depressed self-limited and subsides in about 2 weeks. When scars. PLC is characterizedby asymptomatic, dully involvement is widespread and associated with erythematous papules with a central scale that can be extensive mucosal erosions and fever, it is known as peeled off in its entirety. Papules subside with a Stevens-Johnson syndrome. Histologically, erythema persistent, ill-defined hypopigmentation that often multiforme demonstrates necrotic keratinocytes in the worries the patient more than the papules. In both basal and upper layers of the epidermis, an uPPer varieties of disease, new papules continue to develop dermal infiltrate of lymphocytes that obscures the for a variable and unpredictable period though dermal-epidermal junction and a normal stratum PLEVA usually lasts a few months while PLC may corneum2l. A number of pink, necrotic keratinocytes continue for several years. Histologically, PLEVA are seen throughout the length and thickness of the demonstrates necrosis of keratinocytes accompanied epidermis. The acute nature of the process is borne by a superficial and deep infiltrate of lymphocytes. outby the normal appearance of the strafum comeum. The infiltrate is wedge shaped with the broad base of The infiltrate is composed predominantly of the wedge aligned along the epidermis. There is lymphocytes and is present within the lower layers extravasation of erythrocytes in the dermis. The of the epidermis and the papillary dermis. There is epidermal changes include parakeratosis and the presence the papillary edema that may be severe enough to form a of erythrocytes and lymphocytes within vesitle. Occasional eosinophils have been described epidermis and may be accompanied by epidermal the in the infiltrate but are uncommon. ulceration2a. In chronica, changes are similar but considerably less prominent2s. Fixed drug eruption Graft-versus-host disease Fixed drug eruption is an intriguing and distinctive drug reaction that manifests as circular areas of First described after bone marrow transplantation, erythema and edema which subside with a persistent graft versus host disease is now recognized to occur brown-black pigmentation. Re-exposure to the drug in other situations where a donor's lymphocytes are leads to the development of erythema at exactly the transferred to a host unable to inactivate them such as same locations; new lesions may also develop. In transfusion of non-irradiated blood and organ trans- severe reactions, a blister may develop within the plants. The acute disease presents usually in the erythematous plaque and generalized bullous erup- second week following bone marrow transplantation tions have been reported rarely. Fixed drug eruptions as an exanthem that begins on the hands, feet and on the genital and oral mucosa are usually eroded face and becomes generalized. The exanthem subsides and heal slowly. Histologically, fixed drug eruption with scaling. Toxic epidermal necrosis, bullae and shows several features in common with erythema ulcers have been described in severe cases. Bloody multiforme such as eosinophilic necrosis of diarrhoea and hepatitis usually accompany the versus host disease usually keratinocytes beneath a normal strafum corneum and eruption. Chronic graft an infiltrate that obscures the junction between the follows acute disease and develops as violaceous face, feet. epidermis and the dermis. Some additional features papules initially on the hands and Oral lesions lichen planus may also develop. Later, help to identify fixed drug eruption. The infiltrate is of there is resembling systemic present in both superficial and deep locations and binding down of the skin sclerosis associated with antinuclear autoantibodies. tends to be denser and contain more eosinophils than in erythema muitiforme. Melanin incontinence is a Histologically, acute graft versus host disease prominent featureu-ts. reveals a spectrum of epidermal changes range from a few necrotic and vacuolated keratinocytes to complete Pityriasis lichenoides epidermal necrosis. There is an accompanying sparse to morerate, superficial infiltrate of lymphocytes in Pityriasis lichenoides is a recurring, se*f-limited the papillary dermis. Lichenoid graft versus host eruption that varies in severity from necrotic lesions that disease may be histologically indislinguishable from heal with scarring (pityriasis lichenoides et varioliformis ordinary lichen planus. Early lichenoid GVHD acuta (PLEVA) to scaly papules that subside with demonstrates satellite cell necrosis. Sclerodermoid hypopigmentation (pityriasis lichenoides chronica). GVHD shows dermal sclerosis with an overlying In PLEVA, crops of erythematous, oedematous papules atrophic epidermis. At this stage, lichenoid changes are associated with a mild prodrome of fever and are absent26.

Sri Lanka lournal of Dermatology llte \icherLttid renction pottern 25

Figure 1. Lichenoid reaction. Bqsal cell damage, dense Figure 4. Lichen nitidus. Collection of histiocytes and upper dermal infiltrate of lymphocytes and melanin incon- lymphocytes expanding one papilla with damage to the tinence.@AExfi]). oaerlying basal keratinocytes. (H €t E x 400).

Figure 2. lnterface dernmtitis. Lymphocytes extend into Figure 5. Lichen scrofulosorum. Collection of lympho- the and the junction Eidermis obscure of the dermis and cytes and histiocytes in a superficial periaascular location epidermis. (H €i E x 400). extending into the papillary dermis. (H & E x 100).

Figure 3. Lichen planus. Band-like infiltrate of Figure 6. Lichen scrofulosorum-granulomas around the lymphocytes in close apposition to the epidermis with saw- hair follicle. (H €i E x 400). toothing of rete ridges (H €t E x 40).

Vol, 6, 2002 Ramam, Asha Kubba 26 M

Figure 7. Fhotosensitiae lichenoid etuption. trnfiltrate of Figure 8. Lichen planus pigmentlsus. Patchy infiltrate of incontinence. tymphocytes and histiocytes in the papillary dermis with lymphocytes, basal cell damage and melanin slight edema. (H €t E x 40). (H€iEx40A).

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Sri Lanka lournal of Dermatology