4.9.9 Dermatological and Wound Models
Dermatological models evaluate candidate wound-healing, anti-psoriatic, and burn-management agents using standardised wound or lesion protocols amenable to...
Dermatological models evaluate candidate wound-healing, anti-psoriatic, and burn-management agents using standardised wound or lesion protocols amenable to precise, repeated, non-invasive measurement over the healing time course.
Wound Healing — Excision and Incision Wound Models
Wound-healing pharmacology is evaluated using two complementary surgical wound protocols. The excision wound model creates a full-thickness circular skin defect of standardised area (commonly 300–500 mm²) on the dorsal surface of rats or mice, and wound contraction (the percentage reduction in wound area over time, measured by tracing or digital photography) together with the time to complete epithelialisation are the principal endpoints, reflecting the overall efficiency of the wound-healing cascade — inflammation, proliferation, and remodelling. The incision wound model instead creates a linear, sutured full-thickness skin incision, and the principal endpoint is the tensile (breaking) strength of the healed wound measured on a defined post-operative day, reflecting collagen synthesis and cross-linking during the remodelling phase specifically. Standard reference comparators include topical povidone-iodine or, in phytochemical research, established wound-healing agents such as collagen or aloe vera-based formulations. Histopathological assessment of granulation tissue formation, angiogenesis, and collagen deposition (using Masson's trichrome staining) provides complementary mechanistic evidence in both models.
Burn Injury — Thermal Burn Model
Thermal burn injury and its pharmacological management (including topical antimicrobial and wound-healing agents) are modelled by applying a controlled heat source — typically a heated metal template or brass rod maintained at a defined temperature (approximately 95–100°C) applied for a standardised contact duration — to the shaved dorsal skin of anaesthetised rats, producing a reproducible partial- or full-thickness burn injury of defined surface area. Healing is assessed by wound-area reduction over time, epithelialisation time, histopathological assessment of re-epithelialisation and inflammatory infiltrate, and, in infection-focused studies, quantitative bacterial colony counts from the burn wound surface. Silver sulfadiazine, the clinical standard topical burn-wound antimicrobial, serves as the principal reference comparator. This model's key translational value lies in its direct relevance to burn-wound infection and healing, a substantial global clinical burden, and its amenability to evaluating both antimicrobial and pro-healing mechanisms within a single wound.
Psoriasis — Imiquimod-Induced Model
Psoriasis, a chronic immune-mediated inflammatory skin disease driven substantially by the IL-23/IL-17 signalling axis, is modelled by daily topical application of imiquimod cream (a Toll-like receptor 7/8 agonist licensed clinically as an antiviral and antitumour immune-response modifier) to the shaved dorsal skin or ear of mice for five to seven consecutive days, which paradoxically triggers a psoriasis-like inflammatory phenotype — erythema, scaling, and epidermal thickening — through excessive activation of the same IL-23/IL-17 pathway implicated in human psoriasis. Disease severity is quantified using a composite clinical score analogous to the human Psoriasis Area and Severity Index (erythema, scaling, and thickness, each graded 0–4), histopathological epidermal thickness measurement, and cytokine profiling of skin and draining lymph nodes. Topical corticosteroids and, increasingly, biologic agents targeting IL-17 or IL-23 directly (reflecting the current clinical standard of care) serve as reference comparators. The model's principal strength is its rapid onset and direct mechanistic engagement of the IL-23/IL-17 axis central to human disease pathogenesis.