Compression Therapy in Human Body Applications:An Overview from Principles to Practice

Introduction<br/>Compression therapy is widely used to manage diverse pathologies by applying controlled pressure to the body. However, as existing literature focuses on investigating compression therapy within individual pathologies, it limits cross-pathological synthesis and hampers translation of clinical findings into general design principles for compression devices.<br/><br/>Objective<br/>The aim is to identify cross-pathological insights from a tissue perspective that provide unified principles for compression device design by reviewing and synthesizing literature regarding three elements: biomechanical effects, theoretical models, and characteristics of compression for three representative pathologies, namely Chronic Venous Insufficiency (CVI), edema, and ligament injury. <br/><br/>Methods<br/>A systematic search of Scopus (1990-2025) using four search strings identified studies evaluating compression therapy for the selected pathologies. Search terms include “Compression therapy”, CVI, edema, ligament injury, etc. Inclusion criteria required quantitative characteristics of applied pressure and reported biomechanical outcomes, or identifying theoretical models directly describing tissue response to pressure. Studies were grouped by pathology and comparatively synthesized to extract shared mechanism and diverse pressure-response relationships.<br/><br/>Results<br/>Seventy-four studies were included (CVI: 9, edema: 18, ligament injury: 25, theoretical models: 21). In CVI, static compression between 15-70 mmHg, depending on venous type and body position, reduced venous diameter by 10-25%. Dynamic compression at 120 mmHg (4 impulses/min) achieved maximum venous pumping effect. In edema, 40-60 mmHg static compression promoted fluid drainage and reduced limb volume by 20%, while 120 mmHg dynamic compression reached up to 40% reduction. In ligament injury, 10-30 mmHg were generally used to improve proprioception and provide about 1.2 N/mm additional stiffness.<br/><br/>Conclusion<br/>Across pathologies, compression therapy operates through a shared biomechanical mechanism: external pressure regulates tissue pressure and stiffness. However, required pressure magnitude and mode (static or dynamic) depend on the therapeutic objective, such as improved venous return, fluid redistribution, or mechanical stabilization. These cross-pathological insights translate clinical goals into engineering design requirements for safe and adjustable compression devices.<br/>