Knee OA, biomechanics, and progression to TKA

Findings related to muscle activity during gait and progression to TKA may explain why interventions to improve joint stability can impact symptoms but not knee adduction moment (KAM).

By Cheryl Hubley-Kozey PhD, and Gillian Hatfield PT PhD, Lower Extremity Review September 2015

The frontal and sagittal plane gait biomechanics associated with progression to total joint replacement in patients with knee osteoarthritis, particularly variables related to sustained loading, may be promising new targets for conservative interventions.

Osteoarthritis (OA), the most prevalent type of arthritis, is characterized by damage to articular cartilage, a protective layer over the ends of bones, leading to changes in other joint structures (bones, ligaments, muscles, and nerves) that subsequently result in pain, stiffness, and functional disability in adults. OA is common at the knee joint, more so in the medial tibiofemoral compartment than the lateral compartment.

For people older than 65 years, knee OA results in more difficulties in performing activities of daily living, such as walking or climbing stairs, than any other medical condition. Currently, there is no cure for knee OA. Nonsurgical interventions have focused primarily on pain relief, and include pharmaceuticals, exercise, and various therapeutic modalities, with total knee arthroplasty (TKA) the main treatment for individuals with advanced OA.

Unfortunately, TKA rates are rising. In the US, the demand for primary TKA is projected to grow 673% between 2005 and 2030, to 3.48 million procedures, and five-year increases of 21.5% were reported for 2012 to 2013 in Canada. However, not all individuals with knee OA are suitable candidates for surgery, and not everyone is satisfied with the results of surgery.

Furthermore, residual functional deficits exist after TKA. While more than 35% of patients receiving TKA are aged between 65 and 74 years, the cohort aged 55 to 64 years had the largest five-year percentage increase from 2008 to 2009 (14% and 16.5% increases for men and women, respectively). This is concerning because knee implants have a lifespan of 15 to 20 years, so TKA is not an ideal solution for younger people as they will likely require at least one revision, and patient satisfaction and clinical outcomes diminish following revision surgery. Alternative interventions aimed to slow knee OA progression and ideally delay or even prevent the demand for TKA are crucial.

OA processes have two components: the disease (structural damage) component and the illness (symptom) component, described by Lane et al, and these two components are not always well-correlated. Thus, TKA offers an identifiable clinical endpoint, with surgical decisions based on both components, ie, patient complaints of pain and functional deficits as well as radiographic evidence of joint structural damage. Developing interventions to reduce rates of TKA requires an understanding of the factors responsible for more rapid progression to TKA in some patients with moderate OA, specifically modifiable factors.

Pharmaceutical interventions represent the most commonly used category of nonsurgical interventions and, though effective at reducing pain and improving functional deficits, most are not designed to slow structural damage. In fact, masking knee OA pain with medications might accelerate progression, as decreased pain intensity is associated with increased dynamic knee joint loading in patients with mild to moderate knee OA, a change that can create a negative mechanical environment on the joint.

Early research into disease-modifying osteoarthritis drugs that aim to inhibit destructive enzymes shows promise. However, OA is a mechanically induced disorder, so if the negative biomechanical environment is not addressed, any pharmaceutical treatment is unlikely to provide a long-lasting benefit.

Less used are conservative non-pharmacological interventions that target the biomechanical environment, such as braces, heel wedges, and exercise. Resistance to using these interventions has developed in part because the collective results of conservative interventional studies are equivocal for pain and symptom outcomes, which sometimes do not relate well with the biomechanical outcomes measured in these studies. Part of this disconnect can be explained by lack of correlation in the literature between structural damage and worsening of pain.

Perhaps another explanation is that studies so far have focused on one biomechanical factor, the peak external knee adduction moment (KAM). KAM is a surrogate measure for the ratio of the medial-to-lateral load on the knee joint, as it has been significantly correlated with medial compartment contact force and the ratio of medial compartment to total knee force as measured by an instrumented knee prosthesis. Peak KAM has been identified as the key biomechanical target and hence the main outcome in interventional studies of medial compartment knee OA, based primarily on cross-sectional studies of OA and gait, as well as one well-cited longitudinal study.

More recently it has been recognized that, to understand the loading environment, one needs to consider 3D loads and muscle forces. New evidence suggests that dynamic knee loading characteristics, including frontal and nonfrontal plane moments, during gait are linked to knee OA progression, predominantly structural progression. These findings are fundamental, as structural progression is a component of TKA clinical decision-making.

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