INTRODUCTION Lichenoid dermatitis consists of various inflammatory skin disorders identified by a unique interface dermatitis histopathology, featuring basal cell damage and a band-like lymphocytic iltrate at the dermocpidermal junction, This condition is characterized clinically by flat- topped, red to violet polygonal papules and plaques often associated with pruritus (1). In clinical dermatology and dermatopathology, these disorders—neluding lichen planus and its variants, lichenoid drug eruptions, and graft-versus-host disease—present significant diagnostic and treatment challengs Accurate diagnosis and management of lichenoid dermatoses require comprehensive clinicopathological correlation due to the diverse aetiologies and clinical presentations despite their similar histological appearance (2). Numerous underlying diseases can result in the histopathological reaction pattern known as Jichenoid dermatitis. The most common cause is idiopathic lichen planus, an autoimmune condition causing distinctive skin and mucosal lesions due to cytotoxic T-cells attacking basal keratinocytes. Genetic predisposition, stress, and viral infections, especially hepatitis C, are linked to its development, even though the exact cause often remains unknown, Drug- induced lichenoid eruptions, triggered by specific medications such as gold salts, thiazide diuretics, antimalarials like chloroquine, antihypertensives like beta-blockers and ACE inhibitors, anticonvulsants like carbamazepine, and newer biologics and immune checkpoint inhibitors used in oncology, constitute another significant cause (3). Clinically and histotog eally, these drug-induced eruptions often resemble idiopathic lichen planus but may show subtle differences, such as deeper dermal infiltrates, eosinophil infiltration, and parakeratosis. Additionally, contact allergens, particularly in the oral mucosa, can cause persistent antigenic stimulation leading to lichenoid reactions. Theseallergens may be found in dental materials, cosmetics, and certain metals. Lichenoid tissue reactions can also indicate autoimmune disorders like lupus erythematosus, dermatomyositis. The variety of causes for lichenoid dermatitis underscores the need for careful clinicopathological correlation for accurate diagnosis and effective treatment (4). Lichenoid dermatitis can present with a wide range of symptoms, including mucosal involvement, annular or hypertrophic lesions, and pigmentary alterations, besides the classic violaceous, flat-topped papules and plaques. These variati is can lead to diagnostic challenges, as they might be mistaken for other dermatoses, especially when features overlap. A multidisciplinary approach to patient evaluation is necessary since some cases may be related to systemic disorders or medication use (5), Histopathologically, lichenoid tissue reactions are defined by a dense, band-like lymphocyte infiltration obscuring the dermogpidermal junction, basal cell degeneration, and colloid bodies, Minor variations in histological characteristies, such as the presence of eosinophils, parakeratosis, or deeper infiltrates, can hint at specific diagnoses within the lichenoid spectrum, An integrated interpretation requires the expertise of both pathologists and dermatologists (6,7) The comt ied_clinienpathologieal approach is essential when evaluating lichenoid dermatoses. Clinical correlation is necessary to distinguish between similar histological patterns caused by different etiological factors, which is part cularly important for determining management strategies that vary depending on whether the cause infectious, autoimmune, or drug-induced (8),Justification: A variety of clinically diverse inflammatory skin conditions with lichenoid hues and histopathologically derse lymphocytic infiltrates that obscure the dermoepidermal junction are collectively referred to as lichenoid dermatitis. Although Lchen planus serves as the model for lichenoid tissue reaction, many other lichenoid dermatoses with similar clinical and histological characteristics may also exhibit this type of reaction. Differentiating between various entities in lichenoid eruptions can be challenging for dermatologists and pathologists because “he majority of these en 'S present with similar clinical and histopathologic features, aside from a few differences and specif'e characteristies that aid in clinical diagnosis confirmation Clinicopathological correlation is therefore crucial in understanding the distinct histological entities in patients presenting with lichenoid dermatitis to ensure accurate clinical diagnosis and implement the most appropriate treatment methods currently available.AIM AND OBJECTIVE ‘To study and correlate the clinicopathological spectrum of tissue -eaction patterns in patients clinically presenting as lichenoid dermatitis during the study period.METHODOLOGY Study Design: ‘This study was conducted as a Hospital-based Cross-sectional Study in Coimbatore, Tamil Nadu Study place: ‘The current study was undertaken in the Department of Dermatology at Coimbatore Medical College and Hospital, Coimbatore Study duration: ‘The duration of the study was twelve months. Study popul ‘The study population ircluded Patients who were newly diagnosed with lichenoid dermatitis in the Dermatology OPD at Coimbatore Medical College and Hospital. Inclusion Criteria: 1. Patients of all age groups presenting with skin lesiors clinically suggestive of lichenoid dermatitis 2. Both male and “emale patients. 3. Patients willing to undergo skin biopsy for histopathological examination. 4. Patients who give informed written consent to participate in the study.Exclusion eriteria: Patients with a prior history of treatment for lichenoid cermatitis within the past 3 months. 2. Patients with coexisting dermatological conditions that may mimic or obscure histological fea:ures (e.g., psoriasis) 3. Patients unwilling or unable to provide informed consent 4, Immunocompromised individuals (eg. HIV-positive, on immunosuppressi therapy) ‘Sample si The total number of patients enrolled in our study is 100. Sampling Method: In our present study, the sample size was taken as 100 based Simple random Sampling method. Ethical consideration: Institutional Ethies Committee approval will be obtained before the commencement of the study. All patient data will be kept confidential and used solely for academic purposes. An explicit participant information document was created in both English and Tamil, the regional language, prior to data collection, Before giving their consent, the subjects were given this document, which explained every aspect of the investigation,Study procedure: Proper consent will be taken from the patient/guardian Detailed clinical history will be taken about the presenting complaints and and concomitant systemic illness if any and the current drug therapy if any. General examiration and systemic examination will be done. Investigations: complete blood count, bleeding time and slotting time, HIV testing. Allergy for locel anaesthetics is tested, Immunisation with Tetanus Diphtheria toxoid done wherever applicable. ‘The skin punch biopsies from the representative lesion were taken and dispatched in glass or plastic containers containing 10% formalin solution to the department of pathology The iopsy specimens were then fixed i formalin for 24 h and then processed by routine paraffin-seetion technique and stained with hematoxylin and eosin, All the slides were examined under light microscopy for epidermal and dermal changes Data collection: After Selecting the patients who are meeting inclusion criteria ard Exclusion criteria a brief introduction was given about our study. The doubts raised by the participants were cleared. ‘After getting informed consent the participants were enrolled in our study.Data Analysis: ‘+ The data will be entered into Microsoft Excel and analyzed using SPSS (version 27). Descriptive statistics will be used for baseline characteristics, ‘+The mean and standard deviation were used to display the quantitative data. ‘© Qualitative data are described in frequencies. ‘© A.95% CI of less than 0.05 is regarded as statistically significant Data entry: ‘The latest version of Microsoft Office Excel 2019 was used to gather and enter the data, Data presentation: Appropriate, tables and graphs were utilised to explain the findings.FLOWCHART OF OUR STUDY FORMULATION OF STUDY PROTOCOL J SELECTION OF PATIENTS WITH LICHENOID DERMATITIS AFTER INFORMED CONSENT , HISTORY, CLINICAL EXAMINATION & BASELINE INVESTIGATIONS | ‘SKIN PUNCH BIOPSY FROM REPIESENIALLVE LESION AND SEN 10. PATHOLOGY DEPARTMENT I HPE EXAMINATION OF EPIDERMAL AND DERMAL CHANGES q ‘CLINICOPATHOL OGICAT, CORRELATION OF ‘VARIOUS PRESENTATION OF LICHENOID DERMATITIS WITHITS SPECIFIC HISTOPATHOLOGICAL FEATURESREVIEW OF LITERATURE Lichenoid dermatitis represent a heterogeneous group of inflammatory skin conditions that resemble idiopathic Lichen Planus (LP) in terms of their clinical appearance and demonstrate lichenoid tissue reaction, The latter is a histologic pattern which is characterized by an epidermal basal cell damage that is intimately associated with a massive infiltration of mononuclear cells in the papillary dermis. Condit ns including lichen planus, lichenoid drug eruptions, graft-versus-host disease, and lupus erythematosus, among others, are the main causes of this reaction pattern. The word “lichenoid" refers to the histological cal similarity to the standard condition in this speetrum, Lichenoid Dermatitis: Despite the fact that "lichenoid dermatitis” and "interface dermatitis" are commonly used interchangeably in dermatopathology, there are some important distinctions between the two that must be recognis ed in order to properly diagnose and classify the condition. "Lichenoi dermatitis" describes a unique histopathological pattern that includes apoptotic keratinocytes (Civatte bodies), basal cell degeneration, and a dense, band-like lymphocytic infiltrate at the dermozpidermal junction. The prototypical disease lichen planus, wl prominently displays these characteristics, is the source of the term "lichenoid. (9,10)" This term is most appropriately used when the band-like infiltrate is well-formed, and the basal layer damage is prominent. It is often applied to: + Lichen planus and its variants + Lichenoid drug eruption w+ Lichen striatus * Lichen nitidus + Ashy dermatosis + Graft versus host disease + Lupus erythematosus + dermatomyositis Interface Dermatitis: “Interface dermatitis" isa general term that includes all in‘Tammatory skin conditions in which the dermoepidermal junction has inflammatory cell infiltration and damage to the epidermis basal layer, whether or not the infiltration is sparse or lichenoid. Crowson et al, have expanded the concept of interface dermatitis to include neutrophilic and Iymphohistiocytic forms, in addition to the traditional Lymphocytic type. ‘They also subdivide the lymphocytic type into a cell-poor type and @ cell-rich type. It is subclassified into two patterns: 1. Lichenoid type-dense, band-like infiltrate is predominant (as in lichen planus) 2. Vacuolar type —sparse infiltrate with predominant vacuolar degeneration of the basal keratinocytes (as seen in lupus erythematosus, dermatomyositis) ‘Thus, lichenoid dermatitis is considered a subset of interface dermatitis, specifically referring to those lesions with a band-like infiltrate (11,12,) nHistorical Background The term "lichenoid" is derived from the Greek word "lichen", meaning tree moss, describing the resemblance of lichen planus lesions to the growth pattem of lichen on tree bark (14). 1869: Erasmus Wilson first described lichen planus (LP) as a distinct clinical entity characterized by violazous papules with Wickham’s striae. 1900s: Brocq and Darier contributed to the histopathological characterization of lichen planus, noting liquefac:ive degeneration and interface inflammation (12). 1930s: The concept of lichenoid drug eruptions (LDE) emerged as clinicians observed LP- like eruptions triggeree by medications such as quinine (15). Development of Histopathological Classification Ackerman & Ragaz (1981) established the histological classification of lichenoid tissue reactions (LTRs), highlighting: Saw-tooth rete ridges Basal cell degeneration Band-like lymphocytic infiltrate (14). Weedon (2002) further refined these criteria, distinguishing, between primary lichenoid diseases and secondary lichenoid interface reactions (13). Shiohara et al. (2005) explored the immunopathogenesis of lichen planus, linking it to T- cell-mediated cytotoxicity against basal keratinocytes (14), 1Evolution of Diagnostic Criteria The differentiation of lichenoid dermatitis subtypes advanced with immunofluorescence studies and electron microscopy in the late 20th century. Ellis (1967): Established histopathological criteria for distingushing Lichen planus from Lupus erythematosus and Graft vs host disease. (15) Jacobs et al. (1983): Demonstrated that lichenoid drug eruptions (LDE) exhibit a deeper inflammatory infiltrate and cosinophils, differentiating them from idiopathic lichen planus (15). Saurat et al. (1975): Defined the histological spectrum of GVHD-associated lichenoid dermatitis, highlighting epidermal apoptosis and vacuolar interfece changes (14). By the 2st century, the role of immunopathology, cytokines, and molecular markers in lichenoid dermatitis became 4 key area of research, contributing to targeted therapies such ‘as JAK inhibitors and biologics (9,10), Nomenclature Usage and Diagnostic Importance When it comes to histopathological reporting, terminology is crucial: When the clinical diagnosis is still unknown, the term “interface dermatitis" is usually used in descriptive pathology reports. ‘The term "lichenoid dermatitis" can be used more precisely to indicate a diagnosis within the group of disorders that resemble lichen planus once the clinical context has been sziven ryThe correct categorisation of interface reactions according to the pattern (lichenoid vs. vacuolar) greatly facili-ates the reduction of differential diagnoses, according to a study by Ackerman (1997). Furthermore, being aware of the nomenclature helps prevent miselassification, particularly in cases of ambiguous or changing lesions, Pathogenesis and Immunological Mechanisms of Lichenoid Dermat Lichenoid dermatitis is a pattern of cutaneous reaction brought on by inflammation of the epidermis-dermis interface. Numerous illnesses, including lupus erythematosus, lichen planus, and lichenoid drug eruptions, exhibit this pattem, The underlying fed and involves intricate interactions between pathogenesis is mostly immune-me cytotoxic T lymphocytes, antigen-presenting cells, and keratinocytes (16). 1, Immunopathogenesis Overview The key immunological feature of lichenoid dermatitis is cell-mediated cytotoxicity directed against basal Keratinocytes. These keratinocytes express altered self-antigens or neoantigens, which trigger an immune response (16,17). 2, Role of T Cells + CD8+ cytotoxic T lymphocytes play a central role, They recognize antigens presented by MHC class I molecules on basal keratinocytes. + Upon activation, these T cells release perforin, granzyme B, and Fas ligand, leading to keratinocyte apoptosis. + CD4+ T-cells and Langerhans cells (antigen-presenting cells) also contribute to the initial activation and perpetuation of the immune response. 4+ Shiohara et al. (2005) demonstrated that CD8¥- cytotoxic T-cells and NK cells are abundant in lichenoid tissue reactions, confirming their role in keratinocyte apoptosis, + Massti et al. (2909) identified increased expression of granzyme B and perforin in lesional skin, providing further evidence of cytotoxic T-cell activity in lichen planus, and lichenoid drug eruptions 3. Basal Cell Apoptosis + Apoptotic basal keratinocytes (called Civatte bodies) area histological hallmark + Damage to the dermal-epidermal junction eauses separation and vacuolar degeneration of the basal layer: ‘Molecular Pathways Involved in Keratinocyte Apopte + Fas-FasL Mediated Apoptosis Fas receptor (C1D95) is expressed on keratinocytes, while Fas ligand (FasL) is expressed on activated T-cells, Binding of FasL. to Fas triggers caspase-dependent apoptosi leading to liquefactive degeneration of basal keratinocytes. © (TRAIL) tumor necrosis factor-related apoptosis-nducing ligand released by type I immune cells also result in cell death © Perforin-Granzyme Pathway Perforin forms pores in keratinocyte membranes, allowing granzyme B to enter and induce easpase-mediated apoptosis. 1sGranzyme B also induces DNA fragmentation and mitochondrial damage, leading to cell death (18). 4, Role of Cytokines and Chemokines Various pro-inflammatory cytokines are involved: + TEN. Produced by Thi cells and CD8+ T cells; enhances MHC expression on keratinocytes. + TNF-a: Promotes inflammation and apoptosis. « IL-2and IL-15: Promote T-cell proliferation and survival. CR3, CXCL9, CXCL10, and CXCLI1 are the Chemokines that recruit T cells to the skin, + In oral lichen planus, MMP-1 and MMP-3 may be principally associated with erosion development. + Also, the serum level of IL-17 has been shown to be increased in the atrophic and erosive oral lichen planus (18). 5, Role of Adhesion Molecules + ICAM-1 (Intercellular Adhesion Molecule-1) is upregulated on keratinocytes in response to cytokines like IFN-7. + Scrum levels of P-selectin are increased in lichen planus + This facilitates T-cell adhesion and migration across the dermoepidermal junction. + IKKB, a subunit of the IxB kinase complex, is required for activation 16of NF-«B, a protein that controls DNA transcription, + overexpression of IKK results in chronic inflammation with macrophages and CD45 + cells, interface dermatitis, and increased production of inflammatory cytokines by keratinocytes in animal model (19). 6. Triggering Factors Several factors may trigger or exacerbate the immune reaction: + Drugs: eg, NSAIDs, antihypertensives, antidepressants, metals, imatinib, etanercept, adalimumab, antimalarials (lichenoid drug eruptions) by acting as haptogens, leading to T-cell activation and autoimmunity + Viruses: hepatitis C (especially in oral lichen planus) , human papillomavirus (HPV -16), human hempesvirus 7 (HHV-7), varicella-zoster virus (VZV), and Epstein-Barr vins (EBV). + vaceination against hepatitis, influenza, or SARS-CoV-2. + Autoantigens or exogenous antigens can lead to cross-reactivity and autoimmune response. + Contact with dental amalgam and betel nut are also known triggers, especially for oral LP (190. Genetic Susceptibility HLA-DRI and HLA-D7 has been associated with nonfumilial and familial LP respectively nPolymorphisms in TNF-a and IFN-y genes are linked to chronic lichenoid inflammatory conditions (19), 7. Immune Dysregulation in Chronic Cases In chronic lichenoid disorders like lichen planus: + There's persistent antigenic stimulation. + Regulatory T-cell dysfunction may play a role in chronic inflammation and relapsing lesions (16). 8, Immunofluorescenee Findings + Direct immuno‘luorescence (DIF) often shows fibrin and globular IgM, IgG, or C3 deposits along the basement membrane or around necrotic keratinocytes (16). Direct Immunofluorescence (DIF) Findings LP: irregular fibrinogen deposition at the DEJ and necrotic keratinocytes stained by IgM. LE: Granular IgG, IgM, and C3 deposits along the basement membrane zone (BMZ) (lupus band test. Lichen Planus Per-phigoides-perilesional skin shows the presence of IgG and C3 in a linear arrangement along the basement membrane zone Indireet Immunofluorescence (IIF) Findings Usofial in lupus erythematosus where circulating anti-nuclear antibodies (ANA) or anti= dsDNA a odies may be detected 1s‘These findings support the immune-mediated nature of the disease and help differentiate it from lupus erythematosus or other dermatoses. A cytotoxic T-cell-mediated immune response is the primary cause of lichenoid dermatitis, which results in basal keratinocyte apoptosis and the distinctive inflammation of the interface. The disease is initiated and maintained by a variety of cytokines, adhesion ‘molecules, and environmental triggers. Immunohistochemistry (IHC) Markers Immunohistochemical analysis further refines the diagnosis by identifying immune cell subtypes and apoptotic pathways. CD8+ Tell predominance in LP and GVHD suggests cytotoxic T-cell-mediated apoptosis. ‘CD4+ infiltration in lupus erythematosus supports humoral auto:mmunity. Increased TL-17 in hypertrophic LP suggests a role in chronic inflammation (16,13) ‘Histopathological Features of Lichenoid Dermatitis A wide range of inflammatory skin diseases exhibits interface change with considerable overlap of histological features. A specific histological diagnosis can usually be made by attention to such factors as: + The nature and extent of the basal damage: + The nature, composition, and distribution of the inflammatory reaction; ‘+ The amount of melanin incontinence that results from the basal damage; + The coexistence of another tissue reaction + Other individual characteristies (16). y1. Epidermal Changes Hyperkeratosis: Thickening of the stratum cormeum, typically compact orthokeratosis in classical lichen planus. Parakeratosis may de seen in lichenoid drug eruptions (LDE), lichen striatus, and pityriasis lichenoides chronica Hypergranulosis: Increased thickness of the granular layer, often wedge-shaped in Lichen Planus. Wickham striae are believed to be caused by a focal increase in the thickness of the granular layer of the epidermis (13), Irregular acanthosis, which frequently gives the rete ridges a "saw-tooth" appearance The presence of apoptotic keratinocytes with homogenous eosinophilic cytoplasm (also called colloid bodies ar Civatte, hyaline, cytoid, or dyskeratotiz bodies) measuring about 20qm commonly found in lowermost layers of epidermis and papillary dermis, ‘The basal layer keratisocytes are not visible in early lesions because the dense dermal infiltrate obscures the dermal-epidermal junction with vacuolar alteration and necrosis of these cells, In fully developed lesions, basal layer keratinocytes appear as flattened squamous cells. Occasionally, disruption of the basal layer can result in the formation of tiny clefts at the dermoepidermal junction as a result of extensive basal cell damage (Max-Joseph spaces or Caspary joseph spaces) (14). 2.Dermal changes Dense, band-like infiltrate composed mainly of lymphocytes and macrophages, hugging the basal layer and sometimes obscuring the Dermoepidermal junction [6]. 20Plasma cells are rare to find but may be present in lichenoid drug eruptions, lichen planus like keratosis and mucosal Lichen planus. Eosinophils are mainly found in lichenoid drug eruptions (14,20). Melanin Incontinence and Pigmentary Changes ‘Melanin drop-off into the dermis due to basal cell damage, and ar: engulfed by macrophages in upper dermis to form melanophages. Itis more prominent in lichen planus pigmentosus (LPP), erythema dyschromicum perstans and chronic lichenoid reactions In older lesions, the cellular infiltrate decreases in density, but the number of melanophages increases, Post-inflammatory hyperpigmentation may be caused by melanin incontinence and pigment- Jaden macrophages in the upper dermis, In order to differentiate lichenoid drug eruptions from idiopathic lichen planus, eosinophils and plasma cells may also be observed (19). Satellite cell necrosis ~ damaged keratinocytes accompanied by two or more lymphocytes indicating lymphocyte-associated apoptosis is known as satellite cell necrosis. This is seen in conditions like Graft-versus-host disease, erythema multiforme, paraneoplastic pemphigus, regressing plane warts and drug reactions ‘These distinct histological and clinical characteristics set the foundation for identifying the various configurations and morphological variants of lichen plarus (19). aVariants of Lichen Planus: Based on configuration Annular Linear, Blaschkoid, and Zosteriform Lichen Planus Based on morphology Classical lichen planus Hypertrophic Atrophic Vesiculobullous Erosive and Uleerative Follicular Actinic Lichen Planus Pigmentosus Site of Involvement Palms, Soles, Mucous Membrane, Nails, Sealp, genitalia variants Lichen planus-like keratosis Keratosis lichenoides chronica Lichen nitidus Lichen planus pemphigoidesOther lichenoid disorders © Lichen striatus © Erythema dyschromicum perstans * Lichenoid drug eurptions ‘Pityriasis lichenoides chronica Lichen sclerosis © Lupus erythematosus ‘© Dermatomysoitis Graft versus host disease (13,19). CLINICAL FEATURES AND HISTOPATHOLOGICAL CHANGES OF LICHENOID DERMATOSES 1, Classic Cutaneous Lichen Planus Lichen planus the prototype of lichenoid dermatitis is Characterized by violaceous, flat- topped, polygonal papules and plaques, typically affecting the flexor aspects of the wrists, forearms, lower legs, and ankles. Lesions may show fine white lines on the surface (Wickham striae) Pruritus ranges from mild irritation to severe itching. Koehner’s phenomenon is commonly seen Typical papules of lichen planus show the following histopathological features : * Compact orthokeraosis # Wedge shaped hypergranulosis + Imegular acanthosis 2‘+ Pionted rete ridges -saw tooth appearance * Prominent civatte bodies * Clefts at the dermo epidermal junetion © Vacuolar Damage to basal cell layer + Band like dermal lymphocytic infiltrate hugging the epidermis + Pigment incontinence and melanophages This constellation of findings is sufficient to make a histological diagnosis of Lichen Planus rendered in more than 90% of the cases (21). 2. Hypertrophic Lichen Planus Presents as thickened, verrucous, hyperkeratotic plaques, most commonly on the shin , lower Jimbs especially around the ankles. It is often chronic and intensely prur post-inflammatory hyperpigmentation or central depigmentation. Cutaneous homs, keratoacanthoma, and squamous cell carcinoma may also develop in hypertrophic lichen planus, HPE-epidermis — hyperplasia overlying orthokeratosis acanthosis, papillomatosis Vacuolar changes are discrete and often limited to the tips of the rete ridges Dermis -Verti ly oriented collagen in papillary dermis 3. Atrophic Lichen Planus Atrophie Lichen Planas is seen as centrally thinned or depressed lesions, sometimes developing within pre-existing hypertrophic plaques. It is a less common variant and may ‘mimic other atrophic dermatoses. HPE- flat epidermis with loss of normal rete ridge pattern and less dense dermal infiltrates. 44, Annular Lichen Planus Annular lichen planus (ALP) is a rare clinical variant of lichen planus. It manifests as ring- shaped lesions varying from 0.5 to 2.5 em in diameter with central clearing and a raised violaceous border. It may be localized or generalized and commonly occur on the trunk , ectremities and the genitalia, HPE-superficial lichenpid reaction with massive apoptosis of keratinocytes at the tips of rete ridges. 5. Actinic Lichen Planus (Lichen Planus Actinicus) Other names—tichen planus tropicus, lichen planus subtropicus, lichenoid melanodermatitis, and summertime actinic lichenoid eruption (SALE). ‘Occurs in sun-exposed areas like the face, neck, and dorsal hanes, especially in individuals with darker skin, Lesions occur as well defined annular deeply hyperpigmented patches with surrounding hypopigmented zone .when erythematous often asscciated with oral erosive LP and chronic active hepatitis, HPE- The histological changes are similar to lichen planus with marked melanin incontinence and there may be focal spongiosis and parakeratosis 6. Linear Lichen Planus Lesions are arranged in a linear distribution, often following the lines of Blaschko, It can be mistaken for linear lichen striatus or linear epidermal nevi. Zosteriform variant is where lesions follow the dermatomes. 257. Lichen Planus Pigmentosus Lichen Planus Pigmentosus is characterized by diffuse , blotchy , perifollicular or reticulated hyperpigmented macules or patches, typically involving sun-exposed or flexural areas varying from slate gray to brownish black colour . More common in darker skin types and often asymptomatic. HPE- epidermal atroshy, a lymphocyte-poor lichenoid tissue reaction , prominent pigmentary incontinence with less prominent infiltrates. 8. Erythema dyschromicum perstans and ashy dermatosis Erythema dyschromicum perstans and ashy dermatosis are acquired hyperpigmentary inflammatory disorders characterized by asymptomatic, gradually progressive macules varying in size from 0.5 em to 2 em in different shades of grey. They usually begin on the trunk and then progress to involve the face and extremities with accentuation over photo- exposed sites and sparing of the neck creases, sealp, palms, soles, nails, and mucosa. The presence of a palpable erythematous border 12mm in width around the pigmented lesions in early stages differentiates erythema dyschromicum perstans fiom ashy dermatosis, HPE- The erythematous active borders show 1. 1.Foeal basal cell degeneration 2. Infiltrate is patchy and perivascular, not band like 3. Pronounced pigment incontinence 4. Active infiltrated border of the lesion shows the characteristic perivascular cuffing with lymphocytes 2%8. Follicular Lichen Planus (Lichen Planopilaris , Lichen Planus et Acuminatus Atrophicans) Lichen planopilaris_ manifests as violaceous plaques mainly involving the vertex of scalp , presenting with perifollicular erythema, scaling, and eventual scarring alopecia. It is a significant cause of lymphocytic cicatricial alopecia HPE-orthokeratosis, follicular plugging, and wedge-shaped hypergranulosis of the infundibulum are observed. Vacuolar changes of the basal layer of the outer root sheath and necrotic keratinocytes are often seen. Band-like infiltration is limited to hair follicle -at the level of isthmus. The interfollicular epidermis is often spared, but it can occasionally be involved. In more devoloped lesions, perifollicular fibrosis and epithelial atrophy at the level of the infundibulum and isthmus ere characteristic findings and give rise to an hourglass configuration. 9, Mucosal Lichen Planus Mucosal involvement of lichen planus can be seen in oral cavity , esophagus , genitals including the glans and labia © Oral Lichen planus ; frequently appears on the tongue, gingiva, or buccal mucosa as erosions, ulcers, with lacy reticular network of white coclescent patchess( Wickham striae), ‘© Other lesional patterns include plaque like , reticular , atrophic , papular , erosive and bullous 2‘+ Genital involvement: The glans penis or vulva may exhibit painful erosions, white patches, or plaques. + Diagnostic criteria for erosive vulvar lichen planus -Nine criteria were developed, at least three of waich should be present to allow a diagnosis = Well demarcated erosions or erythematous areas at the vaginal introitus ‘Presence of a hyperkeratotic lesional border or Wickham’s striae in surrounding skin ‘© Symptoms of pain or burning ‘Scarring or loss of normal architecture ‘© Presence of vaginal inflammation Involvement of other mucosal surfaces ‘© Presence of a well-defined inflammatory band involving the dermo-epidermal junction ‘+ Prosonce of a band-like inflammatory infiltrate consisting mainly of lymphocytes ‘Signs of basal layer degeneration (e.¢., Civatte bodies, abnormal keratinocytes) Associations - Castleman's tumor (giant or angio follicular lymph node hyperplasia) and malignant lymphoma, long-term therapy with hydroxyurea, and infection with hepatitis C HPE - atrophic epithelium, confluent parakeratosis. Plasma cells in addition to lymphocytes in the dermis band-like infiltrate may not be present 10, Nail Lichen Planus About 10% of cases involve nail, Finger nails are more involved than toe nail Features consist of: © Roughening, Fissuring and longitudinal ridging ‘+ Trachyonychia ‘twenty nail dystrophy 4‘© Brittleness and nail thinning The proximal nail fold adhering to the nail bed is known as dorsal pterygium formation whic’ is characteristic of lichen planus ‘© Ineextreme situations, onycholysis or anonychia 11. Lichen planus pemphigoides Lichen planus pemphigoides is Characterised by tense blisters located on extremities in patients with lichen planus over normal skin as well as lesional skin HPE- subepidermal bulla with mild perivascular infiltrates and eosinophilia Civatte bodies may be present at the margins of the blister Direct immunofluorescence usually demonstrate IgG and C3 deposition in the basement ‘membrane zone 12. Lichen nitidus Lichen nitidus is characterised clinically by asymptomatic discrete or grouped small pinpoint , dome sheped shiny papules found on forearms, penis and abdomen. ocbnerisation is not uncommon. HPE- focal parakeratosis, focal vacuolar alteration of basal cel! layer, focal subepidermal clefting with mixed dermal infiltrates containing lymphocytes, histiocytes and few Langerhans giant cells. The rete ridges are elongated and bent towards the infiltrate in claw clutching the ball appearance. 13. Lichen striatus Lichen striatus is a sel" limiting inflammatory dermatosis characterized by Small, discrete lichenoid papules in a linear distribution along the line of Blaschko commonly found in arms, leg, or neck. Association with atopy has been reported. Variants — parallel linear bands or zosteriform patterns have been reported 2»HPE-,focal parakeratosis, and dyskeratotic cells seen in all layers of epidermis mild spongiosis, focal basal degeneration, superficial perivascular inflammatory infiltrate of lymphoeytes mixed with histiocytes. lymphocyte exocytosis may be seen. Avery dis inctive feature is the presence of an inflammatory infiltrate in the reticular dermis, around hair follicles and ecerine glands. 14, Keratosis lichenoides chroniea -Nekams disease Nékams disease is a rare dermatosis characterised by violaceous, papular and nodular ons typically arranged in a linear and reticulate pattern most marked on the extremities, and buttocks, and accompanied by a seborrhoeic dermatitis-ike eruption on the face, palmoplantar hyperkeratosis, oral ulcers and thickened nails and warty hypertrophy of the periungual tissue HPE- ‘The lichenoid inflammatory infiltrate comprised of lymphocytes, histiocytes, and numerous plasma cells that obscures the dermal-epidermal junction with vacuolar alteration of the ‘basal cell layer and necrotic keratinocytes. The epidermis shows areas of acanthosis as well as atrophy covered by a hyperkeratotic cornified layer with focal parakeratosis and follicular plugging. Prominent dilated dermal capillaries are seen in cases with associated telangiectasias ichen planus like keratosis -benign lichenoid keratosis Lichen planus-like keratoses are usually solitary, discrete, slightly raised violaceous or pink les ins of short duration, measuring 3 to 10 mm in diameter with predilex yn to arms and presternal area 30HPE-lichenoid pattern with numerous apoptotic keratinocytes, eosinophils and plasma cells in addition to the lymphocytic infiltrate and a residual solar lentigo at the edge of the supports diagnosis of Lichen planus like keratosis 16, Lichenoid drug eruption Cutaneous reaction similar to lichen planus following ingestion of drug is called lichenoid drug eruption . manifests as localized or generalised erythematous to violaceous papules and plaques symmetrically distributed on the trunk and extremiti in association with drug ingestion, Wickham striae and mucosal involvement is rare, The latency ranges from months to more than a year .[mplicated agents most commonly include quinaerine, quinidine, and gold but also includs NSAIDs, antihypertensive medications (especially captopril), penicillamine, chloroquine, etanercept, imatinib, sildenafil, terazosin, infliximab, and hepatitis B vaccine HPE- parakeratosis , Numerous eosinophils, pigment incontinence and perivascular infiltratres around the mid and deep dermal plexuses may be seen in lichenoid drug ‘eruptions and are generally absent in lichen planus. 17.Pityriasis lichenoides chronica Pityriasis lichenoides chronica is a benign lymphoproliferative disorder characterized by recurrent crops of brown-red papules 4 to 10 mm in size, mainly on the trunk and extremities, that are covered with a thin adherent micaceous scale subsiding with hypopigmentation, HPE- focal parakeratosis Mild spongiosis 31Exocytesis of mononuclear cells Dermal perivascular mononuclear infiltrates Extravasation of RBCs 18.LICHEN SCLEROSIS. Lichen sclerosus is a differential diagnosis of atrophic lichen planus.It is a chronic inflammatory dermatoses with anogenital and extragenital manifestations, Charaterised by porcelain white atrophic papules coalescing into plaques with itching , erosions , and different degrees of sclarosis. ‘HPE- ‘Tri-layer appearance with compact orthohyperkeratosis and atrophic stratum malphigi (dark pink’red), hydropic degeneration of the basal layer, pronounced edema ard homogenization of collagen in dermis (White), inflammatory infiltrate in mid dermis (blue). Very early lesions may resemble lichen planus because of the apposition of the inflammatory infiltrate to the basal layer. And older lesions may resemble morphea. 19.Lupus erythematosus DISCOID LUPUS ERYTHEMATOS The lesions of discoid lupus erythematosus consist of well defined pigmented patches and plaques with adheren: scaling and follicular plugging, varying degrees of erythema 2‘commonly seen in the scalp, face, ears, and vermillion border of lips. Associated with central depigmentation and searring alopecia on the slp HPE- epidermis = hyperkeratosis, atrophy of malphigian layer, vacuolar basal degeneration with basement membrane thickening, scattered civatte bosies noted. multiple keratotic plugs over dilated follicular openings are seen. Dermis = dermal edema, dermal mucin deposition, mononuclear cell infiltration at the interface. deep and superficial peridanexal and perivascular infilirates may be seen CUTANEOUS LUPUS ERYTHEMATOSUS Lesions of subacute Iupus erythematosus and Systemic lupus erythematosus consist of erythematous macules and papules that evolve into annular, polycyclic plaques in the upper trunk, arms, and dorsa of hands. HPE — epidermal atrophy degeneration of basal layer severe enough to form subepidermal clefts apoptotic keratinocytes at all levels of epidermis Dermal edema Focal extravasation of erythrocytes and dermal fibrinoid deposits Pauci inflammatory infiltrates usually limited to periadnexal structures and blood vessels 20,DERMATOMYOSITIS Dermatomyositis is characterized by violaceous papules and plaques or macular violaceous cerythmea over various sites such as scalp, eyelids, malar eminence, V area of neck, Posterior neck o posterior shoulders (shaw! sign), Extensor surfaces of a-ms or forearms, overlying extensor tendons of dorsal hands, knuckles, Periungal skin and Lateral thighs or hips (holster sign). 33HPE- (On histopathological examination, dermatomyositis sometimes reveal only mild, non- specific inflammat i However, more commonly, the microscopic features closely resemble those of systemic lupus erythematosus (SLE). These include thinning of the epidermis, degeneration of the basement membrane, vacuolar change in the basal keratinocytes, a sparse lymphocytic infiltrate focused around blood vessels, and the presence ‘of mucin between collagen bundles in the dermis. Subepidermal deposits of fibrin may also bbe observed in some cases, 21.Graft versus host disease The lesions of chronic graft versus host disease include lichen planus like and sclerodermoid-like changes presenting as a combination of lichen-planus like violaceous papules (that can be folliculocentric), sclerodermatous and poikilodermatous change often along with deep fascial involvement that can lead to contractures. Also oral lichenoid changes and nail changes are seen HPE-basal vacuolation, lymphocytic infiltration of the dermis and scattered apoptotic keratinocytes with surrounding lymphocytes (satellite eell necrosis) may be scen (13,21,22) DERMASCOPY ~ Dermoscopy is « noninvasive diagnostic tool that provides valuable clues in the diagnosis of various dermatological condition based on the subtle surface changes. Dermoscopic findings of lichenoid dermatitis predominantly included radiating linear bands, white structures -wickham strize, brown dots, comedone-like lesions (hypertrophic lichen planus). ‘Targetoid bluish pigmentation in and around hair follicle is a clue to lichen plano pila lichen planus pigmen‘osus exhibited brownish black pigmentation with few of them 4showing hem like pattern, The less appreciated findings were the vascular features like red dots and globules (23,24) Articles related to our study: Maheshwari GR et al did a study by examining the patient's history, clinical examination, and histological details of the type and extent of epidermal, interface, and dermal changes as well as the distribution of different inflammatory cel! infiltrates, to obtain a clinicopathological co-relation in lichenoid interface dermatitis, which will aid in an accurate diagnosis. In their study, following a suitable case selection process based on the inclusion criteria, a biopsy was obtained and submitted for histological examination. For every patient, it was ‘examined and correlated, They found Lichen planus accounted for 108 of the 117 instances, followed by lichen striatus (8), lichenoid drug eruptions (2), and lichen nitidus (2). 70.94% of lichenoid interface dermatitis patients had a clinico-pathological connection, In 78% of lichen planus instances and 100% of lichen striatus cases, correlation was observed. They concluded that Melanin incontinence, band-like lymphocytic infiltrates, and basement ‘membrane degradation were the most recurring histological results in their investigation. It ‘was uncommon to see other abnormalities including civatte bodies and hypergranulosis. A prospective study was carried out in the Department of Pathology's Dermatopathology Section between January 2011 and June 2012 by Kumar M et al. The study covered every patient who presented with lichenoid tissue responses and visited the Dermatology ‘Outpatients/Inpatients Department, Clinical findings were recorded for the chosen patients, 35