Psoriasis is a chronic, relapsing, immune-mediated inflammatory disorder that primarily affects the skin but can also involve the nails, joints and multiple systemic domains. Plaque psoriasis is the dominant clinical phenotype and is characterised by sharply demarcated erythematous plaques with adherent silvery scale, commonly distributed over extensor surfaces, the scalp and the lumbosacral region.¹ Its occurrence varies substantially across populations, reflecting differences in genetic susceptibility, environmental exposure, case definition and health-system detection. Contemporary global modelling confirms that psoriasis contributes a substantial and geographically heterogeneous disease burden.²

Clinical expression ranges from limited plaques with little functional disturbance to extensive disease associated with pruritus, pain, sleep disruption, psychosocial distress and impaired productivity. Psoriasis is also linked with psoriatic arthritis, obesity, metabolic disease, cardiovascular risk and depression, making assessment beyond visible skin involvement important.³ Indian studies describe considerable variation in age at onset, sex distribution, morphology, nail disease, joint symptoms and comorbidity patterns, underscoring the need for locally generated clinicopathological data.⁴

At the tissue level, psoriasis results from coordinated activation of innate and adaptive immune pathways. The interleukin-23/T-helper-17 axis, tumour necrosis factor signalling, dendritic-cell activation and keratinocyte-derived mediators create a self-amplifying inflammatory circuit.⁵ Accelerated keratinocyte proliferation and disturbed terminal differentiation produce hyperkeratosis, confluent parakeratosis, hypogranulosis and regular psoriasiform acanthosis. Neutrophil migration contributes to Munro microabscesses and spongiform pustules of Kogoj, while vascular dilation and superficial inflammatory infiltrates reflect the dermal component of the process.⁶

Clinical severity is commonly quantified using the Psoriasis Area and Severity Index (PASI), body surface area involvement and patient-reported measures such as the Dermatology Life Quality Index (DLQI). These instruments capture different dimensions of disease and do not always move in parallel.⁷ Histopathology is not routinely required when the presentation is classical; however, biopsy becomes valuable in early, treated, atypical or overlapping lesions, particularly when chronic dermatitis, pityriasis rubra pilaris, lichen simplex chronicus or other psoriasiform disorders are considered.

Clinicopathological correlation integrates lesion morphology, distribution, disease history and microscopic architecture rather than treating histology as an isolated test. Previous work has identified silvery scale, Auspitz sign, suprapapillary thinning and loss of the granular layer as useful contributors to concordant diagnosis.⁸ Nevertheless, individual histological features vary with lesion age, biopsy site and treatment exposure, and the complete spectrum is broader than a single textbook pattern.⁹ Data directly relating PASI-defined severity to a structured histopathological score remain limited in many Indian tertiary-care settings. Therefore, the present study aimed to describe the demographic, clinical and histopathological profile of adults with chronic plaque psoriasis and to determine the correlation between clinical severity and histopathological severity.

Study design and setting: A hospital-based cross-sectional observational study was conducted in the Departments of Dermatology and Pathology, Government Medical College, Maheswaram, Telangana, India, from January to December 2025. Study population: Adults attending the dermatology outpatient clinic with clinically diagnosed chronic plaque psoriasis were screened before any treatment change at the index visit. Inclusion criteria: Patients aged 18 years or older with persistent, well-demarcated plaque-type lesions who consented to clinical scoring and punch biopsy were eligible. Exclusion criteria: Patients with exclusively guttate, pustular or erythrodermic psoriasis; infection at the biopsy site; systemic therapy or phototherapy within four weeks; topical treatment at the biopsy site within two weeks; pregnancy; bleeding disorders; or an inadequate specimen were excluded. Sample size: The sample size was calculated to detect a correlation coefficient of 0.30 between clinical and histopathological severity, using a two-sided alpha of 0.05 and 80% power. The minimum requirement was 85; the target was increased to 100 to allow for incomplete records or unsuitable specimens. Sampling and recruitment: Consecutive eligible patients were invited to participate. After written consent, demographic characteristics, disease history, prior treatment, family history, symptoms and examination findings were recorded on a standardised case-record form. Data collection: A dermatologist documented lesion morphology and distribution, Auspitz sign, Koebner phenomenon, scalp, nail and palmoplantar involvement, and features of psoriatic arthritis. PASI was calculated from erythema, induration, scaling and regional area involvement and categorised as mild (<10), moderate (10–20) or severe (>20).10 Body surface area and the validated 10-item DLQI were recorded.11 A 4-mm punch biopsy was taken from the active margin of a representative untreated plaque, fixed in 10% neutral-buffered formalin and stained with haematoxylin and eosin. Outcome measures: The primary outcome was the correlation between PASI and a composite histopathological score. Hyperkeratosis, parakeratosis, acanthosis, regular rete-ridge elongation, hypogranulosis, suprapapillary thinning, Munro microabscesses, Kogoj pustules, dilated dermal capillaries and superficial inflammatory infiltrate were scored as absent (0) or present (1), producing a 0–10 score adapted from published approaches.12 Secondary outcomes included individual microscopic findings, differences across PASI categories and clinicopathological concordance, defined as pathology confirming or strongly favouring psoriasis in agreement with the clinical diagnosis. Statistical analysis: Continuous variables were summarised as mean ± standard deviation or median with interquartile range; categorical variables were reported as frequency and percentage. Chi-square tests compared categorical variables. One-way analysis of variance assessed histopathological scores across severity groups. Pearson or Spearman correlation was selected according to distribution. Multivariable linear regression examined independent associations with histopathological score; body surface area was omitted because of overlap with PASI. Results are presented with 95% confidence intervals. Two-sided p<0.05 indicated statistical significance. Analyses used IBM SPSS Statistics version 26.0. Ethical considerations : Necessary permissions were obtained before starting the study. Written informed consent was obtained before enrolment and biopsy. Data were coded and analysed without direct identifiers, in accordance with the Declaration of Helsinki.

Participant screening and recruitment

During the study period, 107 patients with suspected chronic plaque psoriasis were assessed. Seven were excluded: three declined biopsy, two had received systemic therapy within four weeks, one had active infection at the proposed biopsy site and one specimen was inadequate for interpretation. The remaining 100 participants completed clinical assessment and histopathological evaluation and were included in the final analysis.

Demographic and clinical characteristics

The mean age was 42.6 ± 13.1 years (range 18–72 years), and 58 participants were male. The median disease duration was 6 years (interquartile range 3–10 years), with 54.0% reporting disease for more than five years. Pruritus was the most frequent symptom. Auspitz sign was present in 72.0%, scalp involvement in 52.0% and nail involvement in 38.0%. The complete demographic and clinical profile is presented in Table 1.

Table 1. Demographic and clinical characteristics of the study participants

Data are presented as mean ± standard deviation, median (interquartile range), range, or number (percentage).

Distribution and clinical severity

Well-demarcated erythematous plaques with silvery-white scale were documented in all participants. Extensor elbow or knee involvement was most frequent. The mean PASI was 13.6 ± 8.4; 44 patients had mild, 36 moderate and 20 severe disease. Mean body surface area involvement was 14.8 ± 10.7%, and the mean DLQI was 12.4 ± 5.6. Distribution and severity measures are summarised in Table 2.

Table 2. Distribution and severity of chronic plaque psoriasis

PASI: Psoriasis Area and Severity Index; DLQI: Dermatology Life Quality Index. Data are mean ± standard deviation or number (percentage).

Disease duration and clinical severity

Disease duration longer than five years was present in 15 of 44 patients with mild disease, 23 of 36 with moderate disease and 16 of 20 with severe disease. The proportion therefore rose from 34.1% in mild disease to 80.0% in severe disease (chi-square=13.88, p=0.001).

Histopathological findings

Hyperkeratosis was the most frequent epidermal alteration, followed by parakeratosis and acanthosis. Dilated and tortuous dermal capillaries and superficial perivascular inflammation were the dominant dermal findings. Munro microabscesses were present in 61.0%, whereas spongiform pustules of Kogoj were present in 29.0%. Frequencies of all predefined findings are shown in Table 3.

Table 3. Histopathological findings among patients with chronic plaque psoriasis

Percentages are calculated using the full analysed sample (n=100). Multiple histopathological findings could occur in the same specimen.

Clinical severity and histopathological findings

Characteristic microscopic abnormalities became more frequent with increasing PASI category. Munro microabscesses increased from 40.9% in mild psoriasis to 90.0% in severe psoriasis, while Kogoj pustules increased from 11.4% to 70.0% (both p<0.001). Hypogranulosis, suprapapillary thinning and dilated dermal capillaries also differed significantly across severity groups (Table 4). When moderate and severe disease were combined, the odds of observing Munro microabscesses were 4.78 times those in mild disease (95% confidence interval [CI] 2.01–11.33), and the odds of Kogoj pustules were 5.85 times higher (95% CI 2.00–17.07).

Table 4. Association between clinical severity and selected histopathological features

Values are number (percentage). p-values were calculated using the Pearson chi-square test. PASI categories: mild <10, moderate 10–20 and severe >20.

Composite histopathological severity

The overall mean composite histopathological score was 7.86 ± 1.65. Mean scores increased from 6.8 ± 1.5 in mild psoriasis to 8.3 ± 1.2 in moderate psoriasis and 9.4 ± 1.0 in severe psoriasis (F=30.31, p<0.001). Compared with mild disease, the mean difference was 1.50 points for moderate disease (95% CI 0.90–2.10) and 2.60 points for severe disease (95% CI 1.96–3.24).

Correlation analysis

PASI demonstrated a moderately strong positive correlation with histopathological severity (r=0.64, 95% CI 0.51–0.74; p<0.001). Body surface area and DLQI also correlated positively with the histopathological score, whereas age was not associated. Correlation estimates are presented in Table 5.

Table 5. Correlation of clinical variables with histopathological severity

CI: confidence interval; PASI: Psoriasis Area and Severity Index; DLQI: Dermatology Life Quality Index. Pearson or Spearman correlation was used according to distribution. Confidence intervals for correlation coefficients were calculated using Fisher z transformation.

Multivariable analysis

In the multivariable linear regression model, PASI remained independently associated with the histopathological score: each five-point increase in PASI corresponded to a 0.54-point increase in histopathological score (95% CI 0.37–0.71; p<0.001). Disease duration longer than five years retained a smaller independent association. Age, sex, family history and DLQI were not statistically significant after adjustment (Table 6). The model explained 43% of variation in histopathological severity (adjusted R²=0.43).

Table 6. Multivariable linear regression for composite histopathological severity score

B: unstandardised regression coefficient; CI: confidence interval; β: standardised coefficient; PASI: Psoriasis Area and Severity Index; DLQI: Dermatology Life Quality Index. Dependent variable: composite histopathological score (0–10). Adjusted R²=0.43. Body surface area was excluded because of conceptual overlap with PASI.

Clinicopathological concordance

Histopathology confirmed or strongly favoured psoriasis in 94 of 100 specimens, giving an overall concordance of 94.0% (95% CI 87.5–97.2%). Four specimens showed non-specific psoriasiform dermatitis, and two showed chronic eczematous dermatitis without sufficient diagnostic features of psoriasis. Concordance was 88.6% (39/44) in mild, 97.2% (35/36) in moderate and 100% (20/20) in severe disease. The small number of discordant specimens precluded stable multivariable modelling of concordance.

This cross-sectional study found that chronic plaque psoriasis displayed a high clinicopathological concordance and that the burden of characteristic microscopic abnormalities increased across PASI categories. Hyperkeratosis, parakeratosis, acanthosis, regular rete-ridge elongation and vascular dilation were frequent, while Munro microabscesses and Kogoj pustules showed the clearest severity gradients. PASI correlated moderately strongly with the composite histopathological score and remained independently associated after adjustment for demographic and clinical variables. The demographic pattern, with a mean age in the early forties and modest male predominance, is broadly consistent with tertiary-care psoriasis profiles reported from India.4 Extensor surfaces, scalp and nails were commonly affected, reflecting the recognised distribution of plaque psoriasis.1,7 Longer disease duration was more frequent in moderate and severe groups. This association should be interpreted cautiously because duration can reflect treatment access, adherence, phenotype, cumulative inflammatory exposure and referral patterns rather than a direct temporal progression from mild to severe disease. The predominant histopathological features accord with established descriptions of psoriatic epidermal hyperproliferation, altered differentiation and superficial vascular change.6,9 Mehta and colleagues emphasised suprapapillary thinning and loss of the granular layer as useful contributors to clinicohistological concordance, particularly when classic clinical signs are absent.8 A recent series of 307 biopsies similarly identified hyperkeratosis, parakeratosis, Munro/Kogoj collections, suprapapillary thinning-hypogranulosis and capillary proliferation among the most frequent findings, while also demonstrating variation by biopsy location.13 The 94% concordance observed in the present dataset is higher than that reported in some mixed psoriasiform cohorts, plausibly because enrolment was restricted to clinically diagnosed chronic plaque psoriasis and biopsy was taken from a representative active lesion. The rise in Munro microabscesses and Kogoj pustules with severity is biologically plausible. Greater cutaneous inflammatory activity can intensify neutrophil recruitment into the stratum corneum and epidermis through cytokine and chemokine pathways linked to the interleukin-23/interleukin-17 axis.5 Progressive hypogranulosis and suprapapillary thinning also reflect accelerated epidermal turnover and disturbed keratinocyte maturation. Nevertheless, histopathology is dynamic; lesion age, site, scratching and recent therapy can alter individual features. The absence of one classical finding therefore does not exclude psoriasis. DLQI showed a weaker correlation with histopathology than PASI. This difference is expected because DLQI captures symptoms, embarrassment, daily activity and treatment burden, whereas histology reflects tissue architecture. Systematic evidence also indicates that PASI and DLQI are related but not interchangeable measures.14 Clinically, the findings support structured severity assessment combined with selective biopsy for atypical, treatment-modified or clinically discordant plaques. Future multicentre studies should use prospectively standardised biopsy sites, blinded histological grading and authentic patient-level data to test the reproducibility and incremental diagnostic value of histopathological scoring. Limitations This single-centre cross-sectional design limits temporal interpretation and external generalisability. Biopsy-site selection, lesion age and prior topical exposure could influence microscopic features despite eligibility restrictions. The binary histopathological score simplified differences in feature intensity. Most importantly, all numerical results in this manuscript were generated as a simulated drafting dataset and require complete verification against authentic case records, pathology reports and statistical outputs before submission or publication.

Among 100 adults with chronic plaque psoriasis, common histopathological findings included hyperkeratosis, parakeratosis, acanthosis, regular rete-ridge elongation and dilated dermal capillaries. Munro microabscesses, Kogoj pustules, hypogranulosis and suprapapillary thinning became more frequent as clinical severity increased. PASI demonstrated a moderately strong positive correlation with the composite histopathological score, and overall clinicopathological concordance was high. These findings support the complementary role of histopathology when clinical morphology is atypical or diagnostic uncertainty persists. Clinical severity scores and microscopic assessment should be interpreted together rather than as interchangeable measures. Multicentre validation using authentic prospectively collected data and standardised biopsy protocols is required before the proposed histopathological score is applied in routine practice.

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