Psoriasis is a chronic, relapsing, immune-mediated dermatosis with a recognized genetic predisposition and a global prevalence of roughly 2–3% [1]. Clinically, it most often presents as well-demarcated, erythematous plaques with adherent scale, commonly on extensor surfaces and the scalp; disease extent and flare periodicity vary widely between individuals [1]. On histopathology, classic features include regular acanthosis, parakeratosis with loss or attenuation of the granular layer, neutrophilic microabscesses within the stratum corneum (Munro microabscesses), spongiform pustules of Kogoj, elongated oedematous dermal papillae with dilated tortuous capillaries, and a mononuclear inflammatory infiltrate in the superficial dermis [2]. Environmental and host factors modulate disease expression. Infections, psychosocial stress, and several drugs and alcohol have been implicated as triggers in genetically susceptible persons [3]. Immunologically, psoriasis is characterized by dysregulated innate and adaptive responses with enhanced antigen presentation, expansion of Th1/Th17 pathways, cytokine overexpression, keratinocyte hyperproliferation, and angiogenesis [4]. Apoptosis-regulating proteins (e.g., Bcl-2 family, p53) have been studied mainly to understand epidermal turnover abnormalities, but their clinical utility for everyday diagnosis or grading remains uncertain and findings are heterogeneous across cohorts [5]. While descriptive clinico-pathological atlases are abundant, quantified clinicopathological correlation—linking clinical patterns (site, duration, signs) with specific histologic traits—remains under-reported from Indian centres, particularly North India, where phenotype distribution and healthcare-seeking patterns may differ from Western series [1–4]. Establishing such correlations can improve diagnostic confidence, refine differential diagnoses in overlapping papulosquamous disorders, and offer pragmatic anchors for clinical decision-making in resource-constrained settings [2–4]. This study aims to quantify clinicopathological correlation in biopsy-proven psoriasis by assessing associations between key clinical characteristics (age, sex, predominant site, disease duration, and cardinal signs) and predefined histopathological features in patients attending a tertiary centre in North India.

Study design and setting This cross-sectional study was conducted in 50 consecutive patients with biopsy-proven psoriasis attending the dermatology and pathology services of a tertiary care centre in North India. To avoid treatment-related histologic modification, all participants were systemically and topically untreated for ≥4 weeks before biopsy. The study adhered to the Declaration of Helsinki; institutional ethics approval was obtained (IEC approval number available on request). Written informed consent was taken from all participants (or guardians for minors). Participants Inclusion criteria. Any age or sex with (i) clinical diagnosis of psoriasis by a dermatologist and (ii) lesional skin biopsy confirming psoriasis on routine histopathology. Exclusion criteria. (i) Isolated nail psoriasis or psoriatic arthropathy without cutaneous lesions; (ii) concurrent cutaneous infection (bacterial, fungal, or viral) or eczematous superinfection; (iii) recent systemic corticosteroids, retinoids, methotrexate, cyclosporine, biologics, or phototherapy within 4 weeks; (iv) potent topical corticosteroids, vitamin D analogues, or keratolytics applied to the biopsy site within 4 weeks; (v) inadequate/artefactual biopsy precluding assessment. Clinical assessment and operational definitions A structured proforma captured demographics and predefined clinical variables prior to biopsy: • Age: categorized as 10–20, 21–30, 31–40, 41–50, and >50 years. • Sex: male/female. • Predominant site (based on the most representative active plaque sampled): extensor, flexor, palmar/plantar (recorded as palmar in our tables), scalp, erythrodermic (generalized erythema and scaling involving >90% BSA). • Duration of disease: <6, 6–11, 12–24, and >24 months (patient-reported onset corroborated by records when available). • Cardinal signs (present/absent at the sampled site): plaque morphology, silvery scale, Auspitz sign, grattage sign (multiple responses permitted). Biopsy site selection. When multiple sites were involved, we sampled a typical, untreated active plaque; scalp biopsies were taken only if clinically most representative and feasible. Lesions with overt excoriation/secondary infection were avoided. Specimen handling and histopathology A 4-mm punch was obtained including epidermis and superficial dermis, with a rim of perilesional skin when feasible (documented separately as perilesional sample). Specimens were formalin-fixed, paraffin-embedded, and sectioned at 4 µm. Slides were stained with hematoxylin & eosin using standard laboratory protocols. Lesional histopathology—features and scoring (binary). Presence/absence of: 1. Dilated vascular channels in dermal papillae/superficial plexus; 2. Regular acanthosis with elongated rete; 3. Hyperkeratosis; 4. Parakeratosis; 5. Hypogranulosis (reduction/absence of granular layer); 6. Munro microabscesses (neutrophils in stratum corneum); 7. Spongiform pustules of Kogoj (neutrophils in the upper spinous layer); 8. Clubbing of rete ridges; 9. Suprapapillary thinning; 10. Perivascular mononuclear dermal infiltrate. Perilesional histopathology—features (binary). Acanthosis, hyperkeratosis, parakeratosis, hypogranulosis, dermal mononuclear infiltrate, vascular dilatation. Rationale: This study prioritized a binary framework for clinicopathological correlation to reflect routine diagnostic practice and maximize inter-rater agreement. Blinding and observer agreement Two pathologists independently reviewed slides blinded to detailed clinical variables (beyond “psoriasis suspected”). Discrepancies were resolved by joint review; when needed, a third senior pathologist adjudicated. A 10% random subset was double-read to estimate agreement; Cohen’s κ (planned, not powered for primary inference) is available on request. Data management and quality control Data were double-entered into a password-protected spreadsheet and cross-checked against source forms. Range checks were applied (e.g., age bands, duration categories). Missingness was minimal; where a clinical sign was unrecorded, it was treated as missing (excluded from denominator for that variable) rather than imputed. Outcomes Primary outcome: proportion of histopathological features in lesional biopsies. Secondary outcomes: associations between clinical variables (age, sex, site, duration, signs) and histopathological features; description of perilesional changes by duration/site. Statistical analysis Data were analysed using SPSS version 13, employing both descriptive and inferential statistics, including means with standard deviations, frequency/percentage distributions, and chi-square tests.

Table 1: Cohort profile of the study subjects n = 50) Variable Category n % Age (years) 10–20 8 16.0 21–30 13 26.0 31–40 14 28.0 41–50 10 20.0 >50 5 10.0 Sex Male 32 64.0 Female 18 36.0 Predominant site Extensor 27 54.0 Flexor 9 18.0 Palmar 8 16.0 Scalp 3 6.0 Erythrodermic 3 6.0 Duration <6 months 16 32.0 6–11 months 7 14.0 12–24 months 11 22.0 >24 months 16 32.0 Clinical signs* Plaques 47 94.0 Silvery scales 41 80.0 Auspitz sign 41 80.0 Grattage sign 32 64.0 The cohort reflects a typical plaque-predominant psoriasis population: most patients were young–to–mid-adults with a peak in the 31–40-year band (28%) and a male preponderance (64%). Disease topography was characteristically extensor-dominant (54%), with smaller flexor (18%), palmar (16%), scalp (6%), and erythrodermic (6%) subsets—patterns that align with classic plaque psoriasis and provide internal validity for histopath comparisons. Duration showed a bimodal distribution (<6 months and >24 months each 32%), suggesting a mix of early presenters and chronic, long-standing cases likely to exhibit vascular ectasia and remodeling on histology. Clinically, nearly all had plaques (94%), and keratinization markers—silvery scales (80%) and Auspitz sign (80%)—were frequent, anticipating high rates of parakeratosis, hypogranulosis, suprapapillary thinning, and dilated tortuous capillaries in lesional biopsies and supporting robust clinicopathological concordance analyses. [Table 1] The lesional biopsies show a classic psoriatic pattern with epidermal remodeling and vascular change dominating: suprapapillary thinning and hypogranulosis in 92% each, alongside dilated papillary capillaries in 90%, indicate accelerated turnover with elongation of dermal papillae and reduced granular layer. High rates of hyperkeratosis and spongiform pustules of Kogoj (both 78%) further support active neutrophilic involvement and disordered keratinization. Mid-frequency findings—regular acanthosis, Munro microabscesses, and perivascular mononuclear infiltrates (≈40–42%)—suggest variable inflammatory activity across lesions, while parakeratosis and clubbing of rete at 40% likely reflect sampling of both early and chronic plaques. Overall, this distribution aligns with an extensor-predominant plaque cohort, and it anticipates strong clinico-path concordance for keratinization markers (scale, Auspitz) and vascular features in correlation analyses. Perilesional skin shows remodeling without the full lesional signature: hyperkeratosis is common (68%), while markers of vascular change (44%) and chronic inflammation (dermal mononuclear infiltrate, 36%) are moderate, and epidermal architectural shifts acanthosis (32%) and hypogranulosis (24%) are less frequent. The low parakeratosis (12%) indicates that abnormal keratinization is largely confined to the active plaque, with only a spillover of chronic-change features into adjacent skin. This gradient from higher keratin build-up to modest vascular and inflammatory changes supports the expectation that longer disease duration will correlate with perilesional hyperkeratosis/acanthosis (remodeling over time), whereas early disease should show minimal perilesional involvement.

In this single centre North Indian cohort of untreated, biopsy proven psoriasis, we observed an extensor predominant plaque phenotype with very high frequencies of suprapapillary thinning, hypogranulosis, and dilated papillary capillaries (90%), alongside common hyperkeratosis and spongiform pustules of Kogoj (78%). These features constitute a robust histologic signature of active plaque psoriasis and set clear anchors for clinicopathological correlation with site, duration, and clinical signs. The demographic pattern (male preponderance; peak in the 31–40 year band) and extensor dominance align with Indian clinical series from tertiary centres, supporting external validity for our setting [6,7]. The overall clinico morphological profile mirrors broader descriptions of plaque psoriasis summarized in global reviews and monographs [1,8]. Histologically, the very high prevalence of suprapapillary thinning, granular layer attenuation, and tortuous dilated capillaries is concordant with classic descriptions and teaching texts, which emphasize these as core diagnostic traits in conjunction with parakeratosis and neutrophilic microabscesses/pustules in the upper epidermis [2,12,13]. Our rates of Munro microabscesses (42%) and Kogoj pustules (78%) fall within the wide ranges reported historically, which vary with lesion chronicity, sampling plane, and pre biopsy therapy [9,10,13]. The scalp/erythrodermic subsets were small as is common in biopsy series where histologic overlap with seborrhoeic dermatitis on the scalp has been noted as a recurring diagnostic challenge [11]. The correlation templates we propose (site to keratinization/neutrophilic activity; duration to vascular ectasia/mononuclear infiltrate; signs to parakeratosis/hypogranulosis) are grounded in known pathobiology. Th1/Th17 skewed inflammation accelerates keratinocyte turnover and drives angiogenic remodeling, mechanistically linking scale/Auspitz to parakeratosis/hypogranulosis and vascular ectasia, respectively [1,4]. Extensor plaques, subject to friction and trauma, tend to show thicker orthokeratotic/parakeratotic caps and more frequent spongiform pustulation, which we expect to capture as stronger associations in χ² tests. Longer duration, conversely, should parallel vascular and stromal remodeling (ectatic papillary vessels, perivascular mononuclear infiltrates), reflecting chronicity rather than acute neutrophilic events [9,10,12,13]. Implications for practice and research Operationalizing standardized correlation panels in routine reports can improve clinico-path communication, particularly in papulosquamous differentials where clinical patterning (site, duration, signs) is pivotal. For research, these panels provide ready endpoints for phenotypic stratification in trials and enable harmonized datasets across centres in India, where disease burden and health-seeking behavior differ from Western cohorts [6–8].

Our data reaffirm a high-signal histologic triad of suprapapillary thinning, granular layer loss, and papillary vascular ectasia in extensor-predominant plaque psoriasis, closely matching Indian and classic descriptions. The proposed, ready-to-use correlation panels offer a pragmatic framework for quantifying clinico-pathological concordance in everyday practice and standardising reporting for research.

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