Obesity – There is considerable evidence indicating that the increased load on the knee joint due to an obese individual’s elevated body mass is a major risk factor of knee OA leading to antedated development of the disease, and causing an increased risk of radiographic knee OA progression (Cooper et al., 2000, Silman and Hochberg, 2001, Felson, 2004, Zhang and Jordan, 2010, Aaboe et al., 2011, Heather et al., 2012, Muraki et al., 2012, Johnson and Hunter, 2014, Murphy et al., 2016), with a single-limb stance phase of a normal gait cycle showing the force through the knee to increase by 2-3lbs for every 1lb increase in body weight (Felson et al., 2000). This can lead to cartilage breakdown, ligamentous malfunction and knee instability due to increased joint loading (Felson et al., 2000, Aaboe et al., 2011).
A study by Cicuttini et al., (1996) identified the risk of knee OA to increase by 9-13% for every 2 pound increment in body weight. Likewise, a meta-analysis by Jiang et al., (2012) identified a 35% increased risk of knee OA for every 5-unit increase in body mass index (BMI), additionally, Messier et al., (2005) identified that for each unit of weight loss, a four unit reduction in knee joint forces was observed during walking in overweight and obese individuals with knee OA, and with each 1kg of weight loss, a 1.4% reduction in the knee adduction moment was achieved, meaning a dose-response relationship can be identified between the risk of knee OA and obesity, particularly in females and weight loss resulting in a reduction of load exerted on the knee joint per step, accumulating each day gives a clinically meaningful reduction, and benefits to the individual (Messier et al., 2005).
Consequently, weight loss is advocated as an ideal first treatment for overweight and obese individuals with knee OA as it has been reported to yield clinically significant improvements
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in knee joint function and activity, and reductions in pain and inflammation, therefore reducing the disability of overweight and obese individuals with knee OA (Messier et al., 2000, Messier et al., 2004, Christen et al., 2005, Messier et al., 2005, Miller et al., 2006, Zhang et al., 2009, Messier et al., 2010, Richette et al., 2010, Aaboe et al., 2011, Heather et al., 2012).
Various methods of achieving weight loss and a subsequent reduction in the BMI of overweight and obese individuals with knee OA are available, with the most common methods involving combinations of energy deficit controlled diets, and exercise. Although, exercise can be difficult for individuals with knee OA due to pain, disability and reduced knee function, particularly if they are older and are of a higher BMI, and adherence to exercise and diet prescriptions can be difficult to control and ensure, a high number of studies have reported successful outcomes of trials using diet and exercise to reduce individuals weight for the treatment of knee OA (Messier et al., 2000, Messier et al., 2004, Christen et al., 2005, Messier et al., 2005, Miller et al., 2006, Zhang et al., 2009, Messier et al., 2010, Richette et al., 2010, Aaboe et al., 2011, Heather et al., 2012).
A study by Messier et al., (2010) examined weight loss in knee joint loads during walking in participants with knee OA, and reported that a 10% reduction in weight in overweight and obese participants led to a reduction in knee joint compressive forces during walking, compared to a non-weight loss group. The difference in knee joint compressive forces is mostly due to reductions in hamstring muscle co-contraction during early stance phase, similarly, an additional study by Messier et al., (2004) found that modest weight loss combined with moderate exercise led to better improvements in knee function, pain, and performance compared to either intervention alone.
Likewise, Christensen et al., (2005) also examined the effects of a diet induced 10% reduction in body weight and concluded the 10% reduction resulted in 28% improved function of the knee joint. A 16 week intensive combination treatment consisting of a hypo-energetic diet and nutritional education conducted by Aaboe et al., (2011) in overweight and obese individuals with knee OA aimed to reduce body mass by at least 10%. The average weight loss achieved by participants was 13.7kg from baseline weight. Weight loss was found to significantly reduce knee joint loads during walking, however as weight decreased walking speed increased which caused an interference in the reduction of joint loads. Each kilogram of weight loss reduced the peak knee joint load by 2.2kg (a reduction factor of 2.2), and the EKAM reduced by 12% (Aaboe et al., 2011).
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Miller et al., (2006) reported similar findings after conducting a trial involving intensive weight loss in older, obese and overweight individuals concluding that greater improvements were observed in those with the highest percentage of weight loss.
A reduction of two units of BMI in obese women with symptomatic knee OA was found to decrease the risk of developing knee OA by 50% (Felson et al., 1992). Similarly, the Framingham study states a weight loss of 5kg delivers a 50% reduction in the risk of developing knee OA (Felson et al., 1992).
Weight loss is therefore an excellent short term investment in terms of biomechanical joint loading, knee function and pain for patients with knee OA and obesity (Aaboe et al., 2011). Obesity is increasing in prevalence and therefore it is likely that a large number of individuals will be affected by knee OA in the future (Johnson and Hunter, 2014). Heather et al., (2012) advocates the screening of individuals who are at risk of developing knee OA at an early age, and the education of individuals and their family members, as weight loss and maintenance can reduce the exposure of load bearing joints to obesity induced stress to ensure successful long term disease prevention.
Joint Injury and Previous Lower Limb Injury – The knee joint is one of the most commonly injured joints, and those who have a history of knee injury have a moderate to strongly increased risk of knee OA symptoms, and radiographic symptoms (Silman and Hochberg, 2001, Zhang and Jordan, 2010, Muraki et al., 2012, Johnson and Hunter, 2014, Murphy et al., 2016). Previous lower limb injury, such as anterior cruciate ligament (ACL) rupture (often considered the most significant lower limb injury concerning knee OA) may cause synovitis and knee joint instability, and is often accompanied by damage to subchondral bone, articular cartilage, the menisci, and collateral ligaments (Slauterbeck et al., 2009). An injured and non- functional ACL causes alterations in the static and dynamic loading of the affected knee joint initiating changes in the joint cartilage and therefore impacting joint loading (Chaudhari et al., 2008).
An increased incidence of radiographic knee OA was identified in women who had experienced an ACL tear through sport injury (Lohmander, 1994). The tissue damage leading to knee OA is thought to be due to the large forces required to injure the ACL (Buckwalter, 2002). Unfortunately, most patients with ACL tears are aged 30 years or less, leading to an early onset of knee OA, usually between the ages of 30-50 years of age, which in turn leads to a reduced
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quality of life (Lohmander et al., 2007, Friel and Chu, 2013). Knee joint changes indicative of knee OA and functional disability can be identified as early as ten years after the initial injury to the knee joint (Lohmander et al., 2007, Slauterbeck et al., 2009).
Traumatic meniscal tears and articular cartilage damage as a result of injury are strongly correlated with the onset and development of knee OA (Johnson and Hunter, 2014), and therefore it can be stated that knee and other lower limb injuries often lead to an increased risk of early onset knee OA in individuals (Johnson et al., 2002, Friel and Chu, 2013).
Muscle Weakness – The quadriceps femoris works to decelerate the lower limbs during movement, provide dynamic joint stability, and absorb limb loading. Consequently, it has been hypothesised that quadriceps femoris weakness could play a role in the onset and progression of knee OA (Bennell et al., 2013, Johnson et al., 2014). Discrepancies in muscle strength, activation and proprioception of the quadriceps and gluteus medial muscles often occur as a result of knee OA and are continuously identified in individuals afflicted with knee OA within the literature, postulated to be due to pain avoidance disuse of the lower limbs (Slemenda et al., 1998, Lewek et al., 2004, Segal and Glass, 2011, Johnson et al., 2014,), thought to be due to the failure of voluntary activation of muscles, with knee OA patients demonstrating significantly lower quadriceps strength relative to body mass index (BMI) than a group of control subjects (Lewek et al., 2004).
A study by Slemenda et al., (1998) concluded that reduced quadriceps strength relative to body weight could possibly be a risk factor for knee OA in women. Likewise, Ikeda et al., (2005) identified significant reductions in the size of the quadriceps cross-sectional area in women with knee OA, compared with age and body mass matched healthy women. Muscle atrophy was identified in individuals with knee OA in a number of studies (Slemenda et al., 1997, Fink et al., (2007), Petterson et al., (2008) and therefore it can be assumed that muscle weakness associated with knee OA may be due to the loss in the muscle cross sectional area (Fink et al., 2007, Petterson et al., 2008).
Quadriceps muscle weakness has been reported as possibly causing the risk of structural damage to the lower limbs to increase, with a study by Slemenda et al., (1997) finding a 29% and 20% reduction in the risk of developing both symptomatic and radiographic knee OA for every 5kg increase in extensor strength respectively. Exercise is advocated as a means of improving muscle function, particularly strength, and has been reported to result in reduced pain and improved function in individuals with knee OA (Bennell et al., 2013). Exercise can
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be difficult to adhere to however, due to the symptoms experienced by individuals with knee OA and also due to the fact that those who suffer from knee OA are usually of an older age. Abnormal Lower Limb Biomechanics – Lower limb mal-alignment, joint laxity, reductions in proprioception (often due to old age), and increased load on the knee can lead to alteration of normal knee biomechanics (Miyazaki et al., 2002, Johnson and Hunter, 2014). Sharma et al., (2001) identified a strong association between varus and valgus mal-alignment of the lower limbs and knee joint and the increased risk of developing medial and lateral knee OA, leading to progression. Medial progression of knee OA was identified to be four times more likely in individuals with varus alignment, whereas lateral progression of knee OA was found to be five times more likely in individuals with valgus alignment (Cerejo et al., 2002, Johnson and Hunter, 2014). Although some subjects with healthy knees have displayed varus mal-alignment in their lower limbs, varus knee alignment is considered to be one of the most useful factors in determining a high knee adduction moment (Barrios et al., 2011). Varus malalignment can increase a person’s risk of developing knee OA (Moreland et al., 1987, Sharma et al., 2001), and no study to date has reported the slowing of knee OA disease progression when the malalignment is corrected (Johnson and Hunter, 2014).
Repetitive Joint Stress – Various activities involving continuous squatting, kneeling, and bending positions and the lifting of heavy loads can increase a person’s risk of development knee OA (Croft et al., 1992, Cooper et al., 1994, Messier et al., 2009). These activities are often related to occupation, or sports participation (for example skiing and football) (Kujala et al., 1995, Coggon et al., 2000, Gaudreault et al., 2012).
Hansen et al., (2012) states physical activity may be detrimental if it places excess load on the knee joint, despite the recognised benefits of conditioning and strengthening the periarticular muscles to aid joint stabilisation, leading to disease progression. The recent review by Hansen et al., (2012) acknowledged that no relationship existed between running, high volume running and knee OA in the general population, suggesting that without injury in the knee joint, there is no increased risk of developing knee OA due to running. In contrast, an association was found to exist between elite level athletes and knee OA development, due to the highly repetitive nature of certain sports, intense training demands, and the high impact on the knee joints, when compared to non-elite sports participants (Hunter and Eckstein, 2009). The elite athletes had a higher incidence of knee joint and lower limb injury, so it is unknown if the association is due to sports participation, or injury, with studies by Von Porat et al., (2004) and
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Lohmander et al., (2004) establishing the onset of knee OA in football players to be caused by knee injury, rather than due to repetitive stress caused by training loads.
These systemic and local biomechanical factors can result in a deleterious varus angulation deformity present in patients with medial compartment knee OA which increases or changes loading patterns on the medial compartment of the knee causing damage to the articular cartilage and subchondral bone (Fang et al., 2006). The progression of knee OA may also be exacerbated by previous injuries to the knee joint and ligaments, varus malalignment and proximal muscle weakness, all of which are considered to increase the force transmitted by the medial compartment of the knee (Shelburne et al., 2008). Knee OA poses a substantial burden on public health, and of the modifiable risk factors discussed above, to date, only obesity and the avoidance of knee joint injury are accompanied by sufficient evidence to support intervention (Johnson and Hunter, 2014). Therefore, there is a requirement for further epidemiological studies in order to prevent the onset and progression of knee OA, and also pain and function related to knee OA.