Knee OA and obesity: A cyclical clinical challenge

Obesity not only increases the risk of knee osteoarthritis but also makes it more difficult to treat, as typical exercise recommendations often are simply not practical. Gait researchers, however, are working to identify new potential therapeutic approaches.

by Elizabeth M. Russell, MS, and Joseph Hamill, PhD

Obesity rates are growing at epidemic proportions. Obesity can be categorized as  obesity 1 (body mass index (BMI) = 30-34.9 kgm-2), obesity 2 (BMI = 35-39.9 kgm-2), and obesity 3, or morbid obesity (BMI > 40 kg m-2).¹ In the last 15 years, obesity rates have increased twofold, morbid obesity rates of BMI values greater than 40 have increased fourfold, and morbid obesity rates of BMI values greater than 50 have increased fivefold.^2-4 As obesity rates rise, a number of associated health risks (such as coronary heart disease, diabetes mellitus, hypertension, and hyperlipidemia) are receiving mainstream attention.  Of particular interest to biomechanists are the loading forces the joints must sustain with each added kilogram of body weight.

Cartilage and other biological tissues were not constructed to effectively cushion the joints of obese and morbidly obese individuals during locomotion. The high-magnitude, repetitive loads that the knee sustains can lead to knee osteoarthritis (OA). The ability of cartilage to self-repair is poor and, over time, the degenerative process of cartilage deterioration exposes the subchondral bone and can lead to joint pain and osteoarthritis.  The pain and discomfort associated with knee OA brings the problem full-circle as these issues further limit mobility and the ability to exercise for weight loss, which further exacerbates the problem of obesity^5-7 (Figure 1). Although knee OA can occur in the medial, lateral and/or patellofemoral compartments, this review focuses on the biomechanical link between obesity and OA in the medial compartment of the knee, the most common site,⁸ and provides recommendations for decreasing risk factors for disease onset and progression during walking in obese individuals.

Linking obesity and OA

Knee OA incidence rates rose 22% from 1990 to 2005⁹ and are rising even faster than obesity rates.¹⁰ Although a vast number of research studies support a cross-sectional link between obesity and knee OA,^11-14 it was not initially clear whether obesity contributes to the disease development or results from inactivity due to joint pain.  Beginning in 1948, the Framingham Study sought to bring light to this chicken-and-egg conundrum.  Investigators followed the Framingham cohort over a period of 35 years to determine the risk of knee OA based on a person’s initial weight in 1948.¹⁵ They found that obese individuals at the beginning of the study, in particular obese women, had a four-fold higher incidence of knee OA than their healthy-weight counterparts.  With obesity starting at an earlier age than ever in previous history, the onset of knee OA is now present in younger aged men and women than ever before.¹⁶ Out of the world’s population, two-thirds are at risk for developing knee OA over the course of a lifetime, with increasing risk as body mass index rises.¹⁷

Biomechanics of obese gait

Many of the biomechanical risk factors for knee OA are already present in the gait of asymptomatic obese individuals, who display kinetics and kinematics that are remarkably similar to those of knee OA patients.  In individuals with knee OA, the peak external hip and knee adduction moments are significantly higher and the peak external knee flexion and hip extension moments and knee flexion angles are significantly lower than in their healthy counterparts.¹⁸ Characteristics of gait in obese individuals show similar results for the knee flexion angle and external knee adduction moment.^19,20 When comparing obese and non-obese individuals with knee OA, there are few differences in terms of ankle and hip kinematics, but higher BMI values are associated with lower peak knee flexion values, stride length and walking velocity.²¹ Obesity is the primary risk factor for knee OA progression and, as cartilage deterioration worsens, the distinguishing characteristics of gait become even more pronounced.  However, the clinical relevance of obesity on kinematic parameters of gait may be minor compared to the influence of knee OA.²¹

Predicting internal loading

The knee joint is exposed to high compressive and shear forces during weight bearing. Compressive loads can exceed three times body weight during walking and six times body weight during stair climbing²² in healthy-weight individuals. As body weight increases, the loads to which the knee joint is subjected also increase. This loading occurs disproportionately across the medial compartment of the tibial plateau^23-25 and, therefore, knee OA affects this area of the joint almost five times more frequently than the lateral compartment.²⁶ The external knee adduction moment (Figure 2) is the biomechanical variable most frequently studied with knee OA based on its correlation with medial loading and ability to distinguish the proportion of load borne by the medial compartment.^23,27-29

A number of studies support the finding that higher peak external knee adduction moments are present in individuals with medial compartment knee OA relative to asymptomatic, healthy populations.^30-36 The adduction moment is also correlated with disease severity.³⁶ In addition, this higher peak moment is one of the most consistently-found characteristics of the gait of obese individuals.³⁷ Thus, in obese individuals with knee OA, the peak values are disproportionately higher and the disease progresses faster. The magnitude of the peak external knee adduction moment is also influenced by the knee joint alignment, which can be compounded by obesity.^32,33,38

The role of knee alignment

When a varus, or bow-legged, joint alignment is present, the medial compartment is loaded substantially more than the lateral compartment³⁹ (Figure 3). A varus knee joint alignment is a mediating factor that may predispose a person to medial compartment knee OA.^40-44 In obese individuals with knee OA, the added body weight supported by the skeletal system can lead to a varus knee joint alignment and BMI is correlated with the severity of the malalignment in this population.⁴⁴ Up to 76% of obese individuals have an existing varus alignment at knee OA onset or will develop a varus alignment with disease progression.⁴⁵ Even after a period of only 18 months, individuals with varus-aligned knees experience significantly more disease progression and functional decline than knees with valgus alignments.⁴⁴ Moreover, obesity will exacerbate disease progression significantly faster in knee OA patients with varus alignments versus valgus alignments, the latter of which are better able to endure the loads.^40,46 This finding explains, in part, the disproportionately strong association between obesity and osteoarthritis of the knee versus osteoarthritis of other joints in the body.⁴⁷

Muscle strength limitations

Obese individuals exhibit lower levels of limb strength and power measures than non-obese individuals, per unit of body weight. Impaired strength, particularly of the quadriceps muscles, is a risk factor for the development of knee OA.^48,49 Studies investigating isometric and isokinetic knee extensor strength have found lower torque values in obese individuals, when normalized to body mass,^50-52 however, knee flexion strength is unchanged or lower compared to healthy-weight individuals.^50,51 Even though the overall strength of the knee extensor muscles has increased over time to adapt to the increased mass they must support and accelerate, obese individuals still avoid heavy reliance on them during gait. The adopted gait pattern limits knee flexion²⁰ to reduce the need for eccentric contraction of the quadriceps muscles during early stance, when they are most active in absorbing adverse loading on the joint.

This stiff-legged, “quadriceps avoidance” gait is also present in individuals with knee OA and is the most evident in obese individuals with knee OA.²¹ This gait limits the quadriceps’ control of knee flexion through eccentric contraction and results in significantly greater amounts of impact shock being transferred through the joint.⁵³ As the volume and thickness of cartilage deteriorates and the joint space narrows, the ligaments become more lax. Ligament laxity must be stabilized by the muscles spanning the knee joint, and weak quadriceps and hamstrings can result in loading rates 21% higher than in individuals with stronger muscles.⁵⁴

Not surprisingly, muscle strengthening through low-impact resistance exercise is often recommended in patients with knee OA,⁵⁵ particularly if they are obese. Obese individuals progress through knee OA sublevels faster than non-obese individuals and could benefit the most from increased quadriceps strengthening activities.

Exercise and weight loss

Although not all reports agree that weight loss provides benefits in obese individuals with knee OA,⁵⁶ there are many other studies that do show profound benefits of weight loss for preventing the onset of disease⁵⁷ and alleviating a number of the associated symptoms.^57-62 Thus, weight loss is strongly encouraged by the European League Against Rheumatism for obese patients with knee OA.⁶³

Weight loss is an effective way to reduce adverse joint loading,⁵⁸ relieve the pain experienced by the joints,⁵⁷ and improve function and mobility⁶² in obese and overweight individuals with knee OA. Reducing excess body fat, versus weight in general, may be the best way to improve knee OA symptoms.⁶⁴

Despite all these benefits, significant loss of weight and fat is still a difficult and daunting task. Physical activity and training may inadvertently have adverse effects on the knee joint,⁶⁵ accelerating joint destruction by increasing the wear and tear on the joint.  In addition, many patients with knee OA do not attempt weight loss programs,⁶⁶ and those who are obese may find even walking too exhausting to abide by a practitioner’s  activity recommendations.⁶⁷

A number of non-surgical strategies could be implemented to decrease knee joint loading in obese individuals with knee OA. One encouraged strategy is a toe-out gait pattern (Figure 4). The toe-out angle, formed by the long axis of the foot and the forward line of progression of the body, shifts the ground reaction force vector closer to the knee joint axis of rotation and decreases the moment arm of the externally-applied knee adduction moment.^38,68,69

A greater toe-out angle is associated with a lower likelihood of medial compartment knee OA progression in non-obese patients.⁷⁰ However, one recent in-vivo study found that, although the overall axial load decreases, the medial compartment load does not change relative to normal walking in a patient with knee OA.²⁹ Coincidently, obese individuals already tend to walk with a toed-out gait and also with wide step widths. Taking wide steps has a small impact on the overall compressive loading but actually increases the load on the medial compartment of the knee because it effectively reorients the frontal plane angulation of the tibia and femur such that the moment arm increases and the medial compartment becomes more compressed than the lateral compartment.⁷⁰ Therefore, fitness walking with an exaggerated toe-out gait may not be beneficial for obese individuals with knee OA.

A “medial-thrust” gait,^71-73 where the stance knee is brought toward the midline of the body by increasing knee flexion and hip internal rotation upon heel strike,⁷¹ or medial-lateral trunk sway^74,75 may also be used to reduce medial compartment loading.  These gaits are effective when patients with knee OA are asked to perform them in a laboratory setting, but it is unknown if these types of gait retraining have lasting effects or if they may prevent knee OA progression.

Obese individuals^37,76,77 and individuals with knee OA^78-80 walk slower than healthy-weight and asymptomatic individuals. Walking slower is accomplished, in part, by decreasing stride length, which has been shown to decrease the magnitude of the externally-applied moment in individuals with knee OA³⁴ and obese individuals.³⁷ However, slow walking is not recommended for weight loss. Our laboratory at the University of Massachusetts applied a gait strategy aimed at decreasing the external knee adduction while concurrently increasing the metabolic cost of activity.

During walking, speed can remain constant by increasing stride length while concurrently decreasing stride frequency (short, quick strides) or vice vesra (long, slow strides).  Both patterns have been shown to increase the metabolic cost of walking, ⁸¹ but a gait that uses short, quick steps has the benefit of reducing impact variables.^82,83 By walking with short, quick steps at a constant preferred walking speed, asymptomatic obese individuals were able to significantly increase the metabolic cost activity and decrease the angular impulse of the external adduction moment (which takes into account medial compartment loading over the course of a stride instead of at a discrete instant, as the peak moment does). Relative to healthy-weight individuals, the angular impulse of the adduction moment is higher in overweight and obese individuals with⁸⁴ and without⁷⁷ mild knee OA, even when peak moment values are not.

Conclusions

Adverse loading during locomotion may have be an initiator in the harmful cycle of obesity and knee OA, but current biomechanical strategies may be able to prevent further damage or disease progression. The results of these studies provide insight into potential mechanisms by which obese individuals can cope with knee OA, while still maintaining an active lifestyle or exercising for weight loss.

Elizabeth Russell, MS, is a doctoral student in the department of kinesiology at the University of Massachusetts in Amerst, MA, who researches injury prevention and weight loss in obese women. Joseph Hamill, PhD, is a professor in the same department whose research focuses on lower extremity injury prevention.

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