Disorders of Epidermal Appendages --- 1. Acne Vulgaris Epidemiology - Nearly universal in middle-to-late teenage years - Affects both sexes; males tend to have
Disorders of Epidermal Appendages --- 1. Acne Vulgaris Epidemiology - Nearly universal in middle-to-late teenage years - Affects both sexes; males tend to have more severe disease - All races affected; milder in Asian descent - Hereditary component suggested by familial clustering Precipitating/Exacerbating Factors - Drugs: Corticosteroids, ACTH, testosterone, gonadotropins, contraceptives, trimethadione, iodides, bromides - Occupational: Cutting oils, chlorinated hydrocarbons, coal tars - Physical: Heavy clothing, cosmetics, tropical climates (favour sebaceous gland occlusion) --- Pathogenesis (4 Key Factors) 1. Keratinization of the lower follicular infundibulum → keratin plug → blocks sebum outflow 2. Sebaceous gland hypertrophy at puberty under androgen influence 3. Propionibacterium acnes colonizes upper/mid hair follicle → lipase activity converts sebum lipids → proinflammatory fatty acids 4. Secondary follicular inflammation Key facts: Castrated young males historically did not develop acne → confirmed androgen role. Isotretinoin (13-cis retinoic acid, synthetic Vit A) works via strong antisebaceous action . --- Types & Clinical Features Non-inflammatory Acne Type Features --- --- Open comedone (blackhead) Follicular papule + central black keratin plug (black = oxidised melanin, not dirt ) Closed comedone (whitehead) Follicular papule, no visible plug (trapped beneath epidermis); prone to rupture → inflammation Inflammatory Acne - Erythematous papules, nodules, pustules - Severe variant → Acne conglobata → sinus tract formation + dermal scarring - Follicle rupture → dermal abscesses → scarring --- Morphology (Histology) - Open comedones: large, patulous orifices - Closed comedones: orifices only visible microscopically - Variable lymphocyte & macrophage infiltrate around affected follicles - Extensive acute inflammation with follicle rupture - Dermal abscess formation → scarring --- Treatment Rationale Treatment Mechanism --- --- Antibiotics Eliminate P. acnes Isotretinoin (13-cis retinoic acid) Strong antisebaceous action; used in severe acne Androgens implicated Rationale for anti-androgen therapy --- --- 2. Rosacea Epidemiology - Common in middle age and beyond - Predilection for females - Primarily affects the central face Four Stages Stage Features --- --- 1 — Pre-rosacea Episodic flushing 2 Persistent erythema + telangiectasia 3 Pustules and papules 4 — Rhinophyma Permanent nasal skin thickening from confluent erythematous papules + prominent follicles Rhinophyma is the classic end-stage finding — bulbous, thickened nose, more common in males despite overall female predilection. --- Pathogenesis - High cutaneous levels of cathelicidin (antimicrobial peptide; key mediator of cutaneous innate immunity) - Cathelicidin peptides in rosacea patients are qualitatively distinct due to alternative processing by kallikrein 5 (stratum corneum tryptic enzyme) - Injection of these peptides into mice → cutaneous inflammation + vascular dilation (mimics rosacea) - TLR2 activation → upregulates kallikrein 5 in keratinocytes → suggests microbial triggers act via TLR2 - Several microbial triggers proposed (e.g., Demodex mites, H. pylori ) — none definitively proven --- Morphology (Histology) - Perifollicular lymphocytic infiltrate + dermal edema + telangiectasia - Pustular phase: neutrophils colonize follicles → follicle rupture → granulomatous dermal response - Rhinophyma: sebaceous gland hypertrophy + follicular plugging by keratotic debris --- Key Differences: Acne vs Rosacea Feature Acne Vulgaris Rosacea --- --- --- Age Teenagers Middle age+ Sex Males more severe Female predilection Comedones Yes No Flushing No Yes (early stage) Pathogen P. acnes No proven pathogen Key mediator Androgens Cathelicidin End-stage Scarring/conglobata Rhinophyma --- Exam tip: Rosacea has no comedones — this is the key clinical differentiator from acne. Always associate rhinophyma with rosacea stage 4.