Clinicopathological study of lichenoid reactions: a retrospective analysis.
Histologically LTR are characterised by a inflammatory cell infiltrate obscuring the dermoepidermal junction (DEJ) in a band like fashion with associated vacuolar degeneration of basal layer. (2) LTR can also be referred as "interface dermatitis", (3) that refers to histological finding of inflammatory infiltrate that abuts dermoepidermal junction. (4) LTR can be subdivided into cell rich and cell poor categories on the basis of intensity of interface inflammation. Cell rich LTRs include lichen plaus with its variants and cell poor LTRs include conditions like autoimmune connective tissue disorders and erythema multiforme. (5)
This study focuses on the clinical and histopathological spectrum of various LTR as prompt diagnosis of these lesions can greatly influence the morbidity associated with the disease.
OBJECTIVES OF THE STUDY:
1. To find out the age & sex distribution of patients with LTR.
2. To review common histopathological findings in various LTR.
MATERIAL & METHODS: Retrospective analyses of the cases diagnosed with LTR clinically and histopathologically from June 2013 to July 2014 at Father Muller Medical College Hospital were included in the study. Clinical details were obtained from the case records and the histopathological features were studied again from the paraffin wax embedded tissue specimens. The data obtained was statistically analysed.
RESULTS: A total of 66 cases were studied, which were diagnosed as LTR clinically & histopathologically. Out of 66 cases, 51 cases were of lichen planus and its variants, 15 cases were of lichenoid eruptions.
(Table 1) Out of 66 cases, 35 were male and 31 were females. The oldest patient was of a 80 year male patient, and the youngest was a 11 year female patient. Male patients were more compared to female patients in our study. Most common age group was 4th decade followed by 2nd and 3rd decade. 11 patients were below 18 years of age (16.67%)
(Table 2) Most common site of lesions were lower limbs followed by upper limbs, trunk, oral lesions, face & neck, scalp and genital area in decreasing order of frequency.
(Table: 3) Among 51 cases of lichen planus type, classical lichen planus was the commonest presentation with 25 cases and 26 cases were morphological/ histopathological variants of lichen planus.
Table 4, enlists various epidermal histopathological features in LTR. The common epidermal changes were vacoular basal cell degeneration, hyperkeratosis, hypergranulosis, & acanthosis in decreasing order of frequency.
Table 5, showing in dermis most common histopathological feature dermis was melanin incontinence, followed by band like infiltrate over DEJ, infiltrate was predominantly composed of lymphocytes.
(Table 6) Based on the intensity of inflammation, LTR were subdivided into cell rich & cell poor Lichenoid tissue reaction/ interface dermatitis.
LP, Lichen planus pigmentosus, hypertrophic lichen planus were the main components of the cell rich LTR and Pityriasis lichenoides chronica, drug induced/ fixed drug eruption, lichen sclerosus et atrophicus were cell poor LTRs mainly, seen in this study.
Besides the classical LTR changes in the HPE following frequent/characteristic changes were noticed in different conditions:
Lichen planus pigmentosus showed thinned out epidermis (8 cases) and pigment incontinence (11 cases), in most of HPE. Characteristic claw clutching the ball appearance was noticed on HPE of lichen nitidus. Discoid lupus erythematosus specimen on examination showed follicular plugging in both samples & thickening of basement membrane with epidermal atrophy was noticed in systemic lupus erythematosus specimen. Pityriasis lichenoides chronica specimens showed spongiosis in all of its samples. Characteristic follicular plugging was noticed in follicular lichen planus specimen. Hypertrophic lichen planus showed hypertrophy in 12 cases most of specimen with irregular acanthosis (10 cases) as second most common finding. Sub epidermal bulla was noticed in bullous lichen planus specimen. Lichen sclerosus et atrophicus showed follicular plugging in both of the specimen. Parakeratosis was seen in oral lichen planus specimen.
DISCUSSION: LTR can be part of histological presentation of various diseases, lichen planus is the prototype of lichenoid reactions. As seen in this study 51 patients were of lichen planus and its variants. The term "lichenoid" refers to shiny, flat topped, polygonal papules of different sizes and occur in clusters creating a pattern resembling lichen growing on a rock. (6) In this study 25 cases were of classical lichen planus (37.87%), was the largest single group, followed by lichen planus pigmentosus 11 cases (16.66%), hypertrophic lichen planus 11 cases (16. 66%), pityriasis lichonides chronica 4 cases (6.06%), Lupus erythematosus 3 cases (4.54%), 2 cases (3.03%) each of oral lichen planus, lichen nitidus, & lichen sclerosus et atrophicus. One case (1.51%) each of drug induced lichenoid reaction, fixed drug eruption, follicular lichen planus, bullous lichen planus, lichen striatus, & lichenoid tattoo reaction.
Banushree et al, (7) showed the distribution of cases in their study as follows:
Classical lichen planus 73.3% cases was the most common diagnosis, which was followed by lichen planus pigmentosus 8.3% cases, follicular lichen planus 5% cases, lichen nitidus 3.3% cases, each of lichen planus hypertrophicus, lichen planus atrophicus, lichen planus actinicus, benign lichenoid keratosis, lichenoid eruption, and lichen striatus as 1.7% cases.
Mahesh kumar et al (8) in their study showed prevalence of different lichenoid tissue reactions with the following distribution: Classical lichen planus was 26. 66% of cases, as most frequent diagnosis. Followed by lupus erythematosus 10% cases, lichen sclerosus et atrophicus 7.77% cases, lichen planus pigmentosus 6.66% cases, each of follicular lichen planus, lichen nitidus, pityriasis lichenoides, and erythema multiforme had 5.55% cases, diagnosis of 4.44% cases were seen with lichen sclerosis and lichen striatus, 3.33% cases were of actinic lichen planus, drug induced lichenoid eruption, and poikiloderma, hypertropic lichen planus, eruptive lichen planus & lichen spinulosus each had 2.22% cases and lichen planus like keratosis as 1.11% cases.
The present study shows a slight predilection for males (53 %), when compared to females (47 %). Multiple studies Fordyce et al (9) White C J et al (10) Banushree et al, (7) Mahesh kumar et al (8) all have shown predilection for females. There also have been studies that have shown equal incidence in both the sexes Schmidt H. (11) In present study it showed that most of the cases were in the age group of 11-40 years of age, maximum in the 4th decade, similar to findings of Sehgal at al (12) (11-40years). (11) patients were below 18 years of age, comparable to Parihar A et al (13) Mahesh kumar et al (8) where most of the cases were in 1-30 years of age.
In our study, we found lower limbs (69.69%) were the most common site of presentation of lesions in the LTRs. Similar observation was found in study by Parihar et al, other sites in order of frequency were upper limbs, trunk, oral mucosa, face & neck and genital area. Oral mucosa was involved in 11 patients (16.66%).
Histopathological features of LTR are mainly attributed to its immunopathogenesis caused by T cell mediated autoimmune attack against the epidermal basal layer cells. (14) The damage and disorganisation of the cells in epidermal basal layer is the characteristic epidermal change in the LTR. (5) The basal layer degeneration is described as hydropic/liquefactive/vacuolar degeneration. (5)
Two types of cells are seen in the dermal layer in the lesions of lichen planus, attributed to the basal cell injury, that are melanophages and colloid bodies. Majority of inflammatory infiltrate cells in LTR are T lymphocytes, macrophages, dendritic cells.
For the diagnosis of LTR/ interface dermatitis, minimum of different combinations of leucocyte infiltration in dermis, vacuolar degeneration of the basal layer of epidermis, necrotic keratinocytes and accumulation of melanophages in papillary dermis must be present. (15) This study showed predominant lymphocyte infiltration in dermis in 48 cases (72.72%), & mixed inflammatory infiltrate in 18 cases (27.27%). Vacuolar degeneration of basal layer of epidermis was seen in 49 cases (74.24%). Necrotic keratinocytes (Civatte bodies) were seen in 17 cases (25.75%) and melanophages in papillary dermis were seen in 16 cases (24.24%).
In cases of lichen planus pigmentosus, most of our specimens showed thinned out epidermis with pigment incontinence, similar changes were noticed in study by Parihar A Et al. (13) Characteristic "Claw clutching the ball" appearance was noticed in the slides of lichen nitidus which has also been mentioned by various authors. (17,18,19) Discoid lupus erythematosus showed follicular plugging on examination as the most consistent finding which was also noticed in multiples studies. (20,21)
Thickening of basement membrane zone was observed in systemic lupus erythematosus specimen which was concurrent to findings of Alahlafi AM et al. (22) HPE of follicular lichen planus showed characteristic follicular plugging, similar findings were noticed by Wilk M et al (23) in fully developed lesions of follicular lichen planus. Subepidermal bulla noticed in the bullous lichen planus was a typical feature as reported by authours (24,25) in earlier reports and studies. Lichen sclerosus et atrophicus characteristic feature of follicular plugging was seen in both the specimen which has also been noticed by Kowalewski et al. (26) Parakeratosis was seen in oral lichen planus specimen. Parakeratosis was most consistent finding in specimen of oral lichen planus which was analogous to findings of Chatterjee K et al. in their study. (27)
CONCLUSION: Lichenoid reactions were more common among adults from the 2nd to 4th decade and can show a male preponderance, with the most frequent archetype being lichen planus. Thus this study emphasizes on the need of histological analysis in various clinically similar cases of lichenoid dermatoses in order to arrive at a definitive diagnosis which will help in specific treatment.
(1.) Pinkus MD. Lichenoid tissue reactions. A speculative review of the clinical spectrum of epidermal basal cell damage with special reference to erythema dyschromicum perstans. Arch Dermatol 1973; 107: 840-4.
(2.) Mobini N, Touissaint S, Kamino H. Non-infectious erythematous, popular, and squamous diseases. In Elder DE, Elenitsas R, Johnson BL, Murphy GF, editors. Lever's Histopathology of skin, 10th ed. Philadelphia: Lippincott Williams and Wilkins 2009; 185-90.
(3.) Hurwitz RM, Rivera HP, Gooch MH, Slama TG, Handt A, Weiss J (1982). Toxic shock syndrome or toxic epidermal necrolysis? Case reports showing clinical similarity and histologic separation. J Am Acad Dermatol 7: 246-54.
(4.) Crowson AN, Magro CM, Mihm M Jr. Interface dermatitis. Arch Pathol Lab Med 2008; 132: 652 66.
(5.) Sontheimer RD. Lichenoid tissue reaction/ Interface dermatitis: Clinical and histological perspectives. Journal of Investigative Dermatology 2009; 129: 1088-99.
(6.) Tilly JJ, Drolet BA, Esterly NB. Lichenoid eruptions in children. J Am Acad Dermatol 2004; 51: 606-24.
(7.) Banushree CS, Nagarajappa AH, Dayananda SB, Sacchidanand S. Clinico-Pathological Study of Lichenoid Eruptions of Skin. Journal of pharmaceutical and biomedical sciences (J Pharm Biomed Sci.) 2012, December; 25 (25); 226-230.
(8.) Kumar MU, Yelikar BR, Inamadar AC, Umesh S, Singhal A, Kushtagi AV. A clinico-pathological study of lichenoid tissue reactions--A tertiary care experience. Journal of Clinical and Diagnostic Research 2013; 7 (2): 312-16.
(9.) Fordyce JA, Mackee GM. Clinical types of lichen planus. J Cut Dis, 1919; 37: 671.
(10.) White CJ. Lichen planus-critical Analysis of 64 cases. J Cut Dis 1919; 37: 671.
(11.) Schmidt H. Frequency, duration and localisation of lichen planus. A study based on 181 patients. Acta Derm Venerol. 1961; 41: 164.
(12.) Sehgal VN, Rege V. Lichen planus: An appraisal of 147 cases. Ind J Dermat, 1974; 40 (3): 10407.
(13.) Parihar, A. et al., A clinicopathological study of cutaneous lichen planus. Journal of Dermatology& Dermatologic Surgery (2014), http://dx.doi.org/10. 1016/j. jssdds. 2013. 12. 003.
(14.) Shiohara T, Mizukawa Y (2005) The immunological basis of lichenoid tissue reaction. Autoimmun Rev 4: 236-41.
(15.) Horn TD. Interface dermatitis. In Raymond LB, Crowson AN (eds): Textbook of dermatopathology, 2nd ed, chapter 3. McGraw-Hill, 2002: 35-61.
(16.) Ellis Francis A. Histopathology of lichen planus based on analysis of one hundred biopsy specimen. J Invest dermatol, 1967; 48: 143-48.
(17.) Kawakami T, Soma Y. Generalized lichen nitidus appearing subsequent to lichen planus. J Dermatol. 1995 Jun; 22 (6): 434-7.
(18.) Metha V, Balachandran C. Generalized lichen nitidus in childhood. Indian J Dermatol 2008; 53: 221-2.
(19.) Weedon D. The Lichenoid Reaction Pattern. In: Weedon D, editor. Skin Pathology. 2 nd ed. New York: Churchill Livingstone; 2002. p. 31-74.
(20.) Jyothi AR, Shweta SJ, Sharmila PS, Dhaval P, Mahantachar V, T Rajaram. Lichenoid tissue reaction/ interface dermatitis: a histopathological study. INTERNATIONAL JOURNAL OF MEDICAL AND APPLIED SCIENCES. Volume 2 Issue 4 2013: 76-89.
(21.) Lopez-Tinos BO, Garcia-Hidalgo L, Orozco-Topete R. Dermoscopy in active discoid lupus. Arch Dermatol. 2009; 145: 358.
(22.) Alahlafi AM, Wordsworth P, Lakasing L, Davies D, Wojnarowska F. The basement membrane zone in patients with systemic lupus erythematosus: immunofluorescence studies in the skin, kidney and amniochorion. Lupus 2004; 13 (8): 594-600.
(23.) Wilk M, Zelger BG, Zelger B. Lichen Planopilaris-histologic Criteria & Clues in Vertical Sections. Hair Ther Transplant 2013; 3: 111.
(24.) Verma R, Vasudevan B, Kinra P, Vijendran P, Badad A, Singh V. Bullous lichen planus. Indian J Dermatol Venereol Leprol 2014; 80: 279.
(25.) Gawkrodger DJ, Stavropoulos PG, McLaren KM, Buxton PK. Bullous lichen planus and lichen planus pemphigoides--clinico-pathological comparisons. Clin Exp Dermatol. 1989; 14 (2): 150-3.
(26.) Kowalewski C, Kozlowska A, Gorska M, Wozniak K, Krajewski M, Blaszczyk M, et al. Alterations of basement membrane zone and cutaneous microvasculature in morphea and extragenital lichen sclerosus. Am J Dermatopathol 2005; 27: 489-96.
(27.) Chatterjee K, Bhattacharya S, Mukherjee CG, Mazumdar A. A retrospective study of oral lichen planus in paediatric population. J Oral Maxillofac Pathol. 2012; 16 (3): 363-7.
Figure 1: 4x view, showing hyperkeratosis, focal hypergranulosis, with irregular acanthosis and band like inflammatory infiltrate at dermo-epidermal junction.
Figure 2: 10x view showing basked weave hyperkeratosis, basal cell degeneration and max josephs space.
Figure 3: 10x view showing lichen nitidus--claw shaped elongation of epidermal rete ridges encircling well defined inflammatory infiltrate--claw clutching the ball appearance.
Figure 4: 40x view showing spongiosis with occasional basal cells degeneration, melanin incontinence and melanophages in the dermis.
Figure 5: 40x view showing lupus erythematosus-thickened basement membrane.
Figure 6: Bullous LP-multiple violaceous papules and plaques with bullae over dorsum of ankle and foot.
Figure 7: Discoid lupus erythematosus-multiple dusky red to violaceous plaques with erythematous margins over fore head, maxilla, cheeks and post auricular areas.
Figure 8: LICHEN PLANOPILARIS--multile grouped violaceous papules with irregular distribution and areas of cicatricial alopecia over occipital area of head.
Figure 9: LICHEN PLANUS--multiple skin coloured to erythematous, symmetrical, plane topped, polygonal papules over dorsum of hands.
Figure 10: ORAL LICHEN PLANUS--well defined violaceous plaque over buccal mucosa.
Ravikant Chauhan , Srinath M. K , Neema M. Ali , Ramesh M. Bhat , Sukumar D 
[1.] Ravikant Chauhan
[2.] Srinath M. K.
[3.] Neema M. Ali
[4.] Ramesh M. Bhat
[5.] Sukumar D.
PARTICULARS OF CONTRIBUTORS:
[1.] Post Graduate, Department of Dermatology, Father Muller Medical College, Mangalore.
[2.] Assistant Professor, Department of Dermatology, Father Muller Medical College, Mangalore.
[3.] Senior Resident, Department of Dermatology, Father Muller Medical College, Mangalore.
[4.] Professor & HOD, Department of Dermatology, Father Muller Medical College, Mangalore.
[5.] Professor, Department of Dermatology, Father Muller Medical College, Mangalore.
FINANCIAL OR OTHER COMPETING INTERESTS: None
NAME ADDRESS EMAIL ID OF THE CORRESPONDING AUTHOR:
Dr. Ravikant Chauhan, Department of Dermatology, Father Muller Medical College, Father Muller Road, Kankanady, Mangalore-575002.
Date of Submission: 20/03/2015.
Date of Peer Review: 23/03/2015.
Date of Acceptance: 08/04/2015.
Date of Publishing: 20/04/2015.
Table 1: Age and sex distribution of LTR Age in No. of No. of Total Percentage years males females cases (%) 1-9 0 0 0 0 10-19 5 6 11 16.6 20-29 5 5 10 15.15 30-39 9 7 16 24.24 40-49 3 5 8 12.12 50-59 4 2 6 9.09 60-69 5 4 9 13.63 70-79 3 2 5 7.57 >80 1 1 1.51 Total 35 31 66 100 Table 2: Distribution of lesions Site involved No. of patients Percentage (%) Upper limb 40 60.60 Lower limb 46 69.69 Trunk 19 28.78 Oral 11 16.66 Genital 2 3.03 Face & neck 8 12.12 Scalp 2 3.03 Table 3: Histopathological diagnosis of different lichenoid reactions Sl. No. of Percentage No. Diagnosis patients (%) Lichen planus & variants 1 Classical lichen planus 25 37.87 2 Lichen planus pigmentosus 11 16.66 3 Follicular lichen planus 1 1.51 4 Bullous lichen planus 1 1.51 5 Hypertrophic lichen planus 11 16.66 6 Oral lichen planus 2 3.03 Lichenoid eruptions 1 Lichenoid drug eruption 1 1.51 2 Fixed drug eruption 1 1.51 3 Lichen sclerosus et atrophicus 2 3.03 4 Lupus erythematosus (systemic/discoid) 3 4.54 5 Lichen nitidus 2 3.03 6 Lichen striatus 1 1.51 7 Pityriasis lichenoids chronica 4 6.06 8 Lichenoid tattoo reaction 1 1.51 Total 66 100 Table 4: Epidermal histopathological changes Sl. No Epidermis No. of Cases 1 Atrophy 14 2 Hyperkeratosis 47 3 Parakeratosis 11 4 Hypergranulosis 43 5 Acanthosis 40 6 Spongiosis 6 7 Papillomatosis 2 8 Elongated rete ridges (saw tooth) 4 9 Loss of rete ridges 2 10 Civatte bodies 17 11 Vacuolar basal cell degeneration 49 12 Max joseph space 2 13 Basement membrane thickening 2 14 Follicular plugging 5 Table 5: Dermal histopathological changes Sl. No Dermis No. of cases 1 Band like inflammatory infiltrate over DEJ 32 2 Melanin incontinence 42 3 Melanophages 16 4 Predominantly lymphocytic infiltrate 48 5 Mixed inflammatory infiltrate 18 6 Perivascular inflammatory infiltrate 40 7 Periadnexal inflammatory infiltrate 24 8 Subepidermal bulla 1 9 Plasma cells 3 10 Eosiniphils 3 Table 6: Classification of LTR based on the intensity of inflammatory infiltrate Sl. No Cell- rich LTR No. of cases 1 Lichen planus 25 2 Lichen planus pigmentosus 11 3 Hypertrophic lichen planus 11 4 Bullous lichen planus 1 5 Drug induced lichen planus 1 6 Discoid lupus erythematosus 2 7 Lichen striatus 1 8 Lichen nitidus 2 9 Lichenoid tattoo reaction 1 10 Oral lichen planus 2 Sl. No Cell- poor LTR No. of cases 1 Fixed drug eruption 1 2 Lichen sclerosus et atrophicus 2 3 Systemic lupus erythematosus 1 4 Pityriasis lichenoides chronica 4 5 Follicular lichen planus 1 Table 7: Comparative findings in this study and previous studies Present Banushree Features study et al, (7) 1. Atrophy 21.21% 8.33% 2. Hyperkeratosis 71.21% 80% 3. Parakeratosis 16.66% 5% 4. Hypergranulosis 65.15% 5. Acanthosis 60.60% 73.33% 6. Spongiosis 9.09% 70% 7. Papillomatosis 3.03% 16.66% 8. Elongated rete ridges (saw tooth) 6.06% 33.33% 9. Loss of rete ridges 3.03% 10. Civatte bodies 25.75% 80% 11. Vacuolar basal cell degeneration 74.24% 83% 12. Max Joseph space 3.03% 13.33% 13. Basement membrane thickening 3.03% 14. Follicular plugging 7.57% 5% 15. Band like inflammatory infiltrate over DEJ 48.48% 96.6% 16. Melanin incontinence 63.63% 93% 17. Melanophages 24.24% 18. Predominantly lymphocytic infiltrate 72.72% 100% 19. Mixed inflammatory infiltrate 27.27% 20. Perivascular inflammatory infiltrate 60.66% 21. Periadnexal inflammatory infiltrate 36.36% 22. Subepidermal bulla 1.51% 23. Plasma cells 4.54% 3.33% 24. Eosiniphils 4.54% 3.33% Mahesh kumar Features et al (8) 1. Atrophy 15.55% 2. Hyperkeratosis 93.33% 3. Parakeratosis 6..66% 4. Hypergranulosis 5. Acanthosis 83.33% 6. Spongiosis 67.77% 7. Papillomatosis 24.44% 8. Elongated rete ridges (saw tooth) 60% 9. Loss of rete ridges 10. Civatte bodies 21.11% 11. Vacuolar basal cell degeneration 96.66% 12. Max Joseph space 10% 13. Basement membrane thickening 14. Follicular plugging 13.33% 15. Band like inflammatory infiltrate over DEJ 93.33% 16. Melanin incontinence 93.33% 17. Melanophages 18. Predominantly lymphocytic infiltrate 100% 19. Mixed inflammatory infiltrate 20. Perivascular inflammatory infiltrate 21. Periadnexal inflammatory infiltrate 22. Subepidermal bulla 23. Plasma cells 8.88% 24. Eosiniphils 4.44% Ellis Francis Features (1965) (16) 1. Atrophy 47% 2. Hyperkeratosis 3. Parakeratosis 12% 4. Hypergranulosis 5. Acanthosis 23% 6. Spongiosis 7. Papillomatosis 8. Elongated rete ridges (saw tooth) 9. Loss of rete ridges 10. Civatte bodies 37% 11. Vacuolar basal cell degeneration 100% 12. Max Joseph space 17% 13. Basement membrane thickening 14. Follicular plugging 6% 15. Band like inflammatory infiltrate over DEJ 100% 16. Melanin incontinence 17. Melanophages 18. Predominantly lymphocytic infiltrate 100% 19. Mixed inflammatory infiltrate 20. Perivascular inflammatory infiltrate 21. Periadnexal inflammatory infiltrate 22. Subepidermal bulla 23. Plasma cells 3% 24. Eosiniphils
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|Author:||Chauhan, Ravikant; Srinath, M.K.; Ali, Neema M.; Bhat, Ramesh M.; Sukumar, D.|
|Publication:||Journal of Evolution of Medical and Dental Sciences|
|Date:||Apr 20, 2015|
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