Biomechanical factors related to clinical vs. structural progression of knee OA

Abstract

Purpose: The purpose of this presentation is to provide an overview of the in vivo human gait studies investigating biomechanical factors related to clinical (i.e. evidence of structural damage and symptoms) versus structural severity/progression in knee osteoarthritis (OA). Background: Biochemical responses, commonly triggered by biomechanical factors, are related to changes in the homeostatic balance of articular cartilage synthesis and degradation associated with OA. Historically, cartilage degradation has been the hallmark for OA; however, its effects on other structures such as muscles, ligaments, synovium and nerves are gaining recognition. The presence of symptoms is also fundamental in diagnosing OA (e.g. pain, stiffness, swelling, etc.), with pain as the most common symptom for seeking clinical care. Importantly, the level of pain and degree of structural damage are not well correlated in individuals with knee OA and suggest that each component may progress using different pathways. Much of our existing knowledge about OA mechanisms comes from fundamental in vitro or animal model studies that link biomechanical loading to biochemical responses related to OA processes (i.e. cartilage damage, inflammation and pain). In human models, gait (i.e. walking) studies have been the primary source of information for understanding knee joint-level loading in knee OA, and much of the work to date has examined joint moments from biomechanical models. Over the past 10 years an increasing number of studies have examined muscle activation patterns, including the contribution of muscles when modelling joint contact loads associated with OA processes. Summary: Differences in joint moment and muscle activation patterns have been associated with the level of structural severity, and evidence exists that associates specific pattern features with increased risk of structural progression defined using radiography and magnetic resonance imaging. Although fewer studies have focused on biomechanical and muscle activation patterns associated with clinical severity and risk of clinical progression, interesting trends are emerging and differ from features observed for structural outcomes. These gait studies provide information related to the magnitude, distribution, pattern and duration of joint loading. Features associated with the magnitude of joint moments are related to structural processes, whereas muscle function features and patterns of loading are linked with clinical outcomes such as joint replacement surgery. A critical evidence gap exists among these human studies related to the effect of loading frequency on OA progression. Aerobic exercise, particularly increasing walking frequency, is recommended across international non-surgical, non-pharmacological knee OA management guidelines based on pain relief, improved general health (i.e. cardiovascular outcomes), and the response of healthy cartilage to physical activity and exercise, but less on the effects on damaged tissue. The few human studies that link joint loading features during locomotion to biomarkers related to cartilage damage and pain processes in individuals with knee OA provide early evidence of a causal effect. Conclusions: Collectively, the work to date suggests that different biomechanical targets exist for structural versus clinical OA processes and should be considered when tailoring person-specific interventions.