Biomechanical considerations in long-term management of Knee Osteoarthritis

Introduction to Knee Osteoarthritis[edit | edit source]

Knee Osteoarthritis (OA), according to Osteoarthritis Research Society International (OARSI), is a disease characterized by the degradation of extracellular matrix and cell stress arising from micro- and macro-injury that initiates an inappropriate repair process including pro-inflammatory pathways of innate immunity. The disease starts with abnormal joint tissue metabolism followed by anatomic, and/or physiologic changes (cartilage degradation, bone remodelling, osteophyte formation, joint inflammation and loss of normal joint function), that can result in joint disorder.[1] There is friction and increased bone on bone contact. The synovial joint of the knee is stabilized by ligaments and a fibrous capsule that contains synovial membrane encasing synovial fluid that assists with knee range of motion. The articular cartilage wears away over time and this joint space narrows, leading to increased friction resulting in pain.[2]

When standing or walking, ideally the knee should be aligned in the frontal plane. However, when there is medial space narrowing, it affects the frontal plane alignment. This shifts the alignment medially and produces abnormal gait. The medial and lateral sides can both be affected. Alignment that is medial to the knee joint centre is defined as varus (bow-leg), and valgus (knock-knee) if it passes laterally to the knee joint centre, with varus alignment appearing more commonly. This also results in individuals developing compensatory gait aka limping to alleviate the pain.[3] There is pain with day-to-day motion and exercises, there is joint stiffness and, in some cases, only alleviated by rest.[3][4]. There can be muscle wasting in some cases.[3] There is tenderness on joint palpation and reduced joint range of motion due to stiffness.[4]

There are primary and secondary classifications of Knee Osteoarthritis. Primary Knee Osteoarthritis is idiopathic and usually due to articular cartilage degeneration. Secondary Knee Osteoarthritis occurs when we are aware of a previous joint injury that predisposes an individual to develop knee OA.[5] Risk factors that make the individual more susceptible to developing knee OA include age, obesity, sex, genetics, ethnicity, diet, and bone metabolism. Factors that make the joint more susceptible are muscle weakness, sustaining a previous knee injury, joint malalignment, and physical activity with repetitive joint loading.[5][6] Females are also more likely to be affected by Knee Osteoarthritis.[5] This can be due to lack of calcium in post-menopausal women as well as predisposition in pelvic anatomy. Females have wider pubic arch and thus wider hips that can place increased mechanical stress on the lateral aspect of the knee akin to genu valgus (knock knees) as they are subject to a larger Q angle[7]. Other risk factors for knee osteoarthritis include external trauma and occupations that cause individuals to be exposed to repetitive squatting and kneeling.[5][6] [8] Obesity is related as increased joint loading adversely affects intra articular cartilage and body metabolic disturbances with adiposity leads to variation in development and remodeling of articular cartilage.[5][8]


Abnormal Biomechanics[edit | edit source]

Knee Osteoarthritis is a multifactor degenerative disease, these factors range from increased mechanical loading, breakdown of articular cartilage, bone development and muscle impairments.[3][6] [9] Varus alignment is associated with greater risk of developing tibiofemoral osteoarthritis and increased medial OA progression. [10]Due to this varus direction, the knee joint is subject to higher mechanical stress on the medial compartment.[9] [10] This also contributes to the degradation of the intra articular cartilage.

The majority of the patients with knee osteoarthritis have joint laxity, this is the loss of joint stabilization due to ligaments inability to counteract external mechanical forces [9]. Individuals with knee osteoarthritis have lower knee flexor/extensor muscle strength [11]. This is shown in gait studies where individuals with osteoarthritic knees have lesser knee flexion and higher knee adduction [9][10]. Knee extensor muscles are vital for knee stabilization during joint loading and consequent movement.[9] Abnormal joint mechanical stress causes the articular cartilage to degenerate faster, and weak extensor muscles further increase the symptoms of knee osteoarthritis.[8]. Recent research has shown there to be more medial varus laxity than lateral valgus laxity, where the knees are thrusted more medially than laterally in joint loading experiments.[3]. This affects malalignment of the knee and the foot also affecting pressure allocation and worsening symptoms of knee osteoarthritis.[3][9]. There is loss in joint proprioception, where proprioception is the conscious or unconscious joint space awareness. In an osteoarthritic knee, the degeneration of articular cartilage leads to faulty mechanoreceptors. This ties in with joint laxity, as weaker muscles have reduced muscle spindle sensitivity. This may lead to an overall reduction in knee proprioception accuracy.[12]

The knee joint has motions such as sliding, rolling, gliding and rotation[13]. The loss of cartilage and reduction in the meniscus changes the joint alignments and contributes to knee osteoarthritis. In the process of knee osteoarthritis, the knee articular cartilage can go metabolic disturbances where degenerative enzymes can be overexpressed. The chondrocytes release proteoglycans to balance the equilibrium and maintain the surface of the articular cartilage. External trauma faced near the knee joint can also cause intra articular fractures which may result in incongruent joint alignment.[5] This leads into an uneven load distribution and overall joint instability of the knee. Individuals with weaker quadriceps lead to increased lower limb loading in normal gait.[14] Individuals with occupations that lead to repetitive joint loading can lead to degeneration of the articular cartilage and chondrocytes increasing the progression of knee OA.[5][8] . Lastly, Individuals with damaged meniscus of the knee cartilage damage, and change in alignment via exercise can cause cartilage degeneration.[5]

Clinical understanding of patho-mechanisms[edit | edit source]

Knee ligaments are vital to joint stability. In this case, weak knee extensor muscles are known to contribute to knee OA. Due to ligament laxity, there are higher than normal shear forces. This also leads to knee misalignment (varus knees, bowlegged). As knee joint space is narrowed, weaker extensors such as vastus medialis, lateralis and intermedius will give out under load. As mentioned, medial laxity is common, and the medial aspect loses proprioception.[12][15]. The knee adduction moment is more harmful due to lack of muscle control.[13]

Under normal conditions the knee cartilage is maintained and balanced in terms of degeneration and regeneration of chondrocytes.[5][8]However, with increased loading, it produces stress on the articular cartilage and causes damage. The damage in the extracellular matrix due to overloading can contribute to joint remodelling. This is also where inflammation produces biochemical reactions (proinflammatory mediators) which work towards breaking down the collagen matrix and contributing to synovial inflammation.[5]

The combination of cartilage damage and increased joint loading along with reduced joint space contribute to bone damage.[10] The bone can be further misaligned if lead through bone envelope remodelling, as the narrower joint space regions will be prone to bone marrow lesions and leading to further bone marrow necrosis.[5][10]

Treatments and treatment efficacy[edit | edit source]

Conservative biomechanical treatment methods are more sought after than invasive surgical interventions to treat symptoms of knee OA. Some of these methods include modified footwear, knee braces, physical exercises that modify individual gait, knee muscle strengthening and weight loss. Physical exercises can include individuals walking barefoot to reduce knee adduction moments and alleviate symptoms of knee OA. In terms of gait modifications, affected individuals can involve toe out gait in their daily walking. Toe out gait causes an external rotation at the knee, which converts the knee adduction moment into a knee external flexion moment, thus minimizing abnormal joint loading. The force vector from the ground passes posteriorly causing increased knee flexion, while reducing knee adduction moment medially.[14]

Muscle Strengthening[edit | edit source]

Quadriceps strengthening exercises have been used to alleviate symptoms of knee OA. Individuals with knee pain have shown to be lacking complete activation of their quadriceps leading to lower joint stability. Isokinetic muscle strengthening at varying velocities can be used to strengthen the quadriceps, increase strength, and reduce pain. [16] Physical therapists can diagnose patients and include quadriceps strengthening exercises at designated velocities to reduce symptoms of knee OA. This will further assist in increased joint stability, increased range of motion of older adults. There is also enhanced force absorption lowering mechanical stress on the knee joint.[16][17] Strengthening hip abductors via land-based exercise is a sought-after treatment for individuals with knee OA. The strengthening of hamstrings combined with quadriceps improved overall medial joint stability [17][18] [19][20]. The increase in hip strength has led to reduced peak knee adduction moment because of reducing contra-lateral pelvic drop and stabilizing medial joint loading on the knee.[18]

Lateral wedge insoles[edit | edit source]

Lateral wedge insoles are another treatment method, where a laterally placed sole can reduce the pain in movement.[14] The lateral aspect of the foot is lifted at a 5-, 10- and 15-degree inclination, based on the thickness of the wedge.[14][21][22] This laterally displaces the centre of foot pressure.[14] This leads to an eversion of the ankle joint and reduction in the knee adduction moment.[14] [21]. It is an effective strategy for individuals with mild symptoms of knee OA, as these lateral wedge insoles can reduce the varus torque and provide comfort in walking.[22]. Individuals using such insoles are advised to maintain a constant step width with the help of a custom medial arch, as increased step width may increase ground reaction forces, increasing knee adduction moment and worsening knee OA symptoms.[14]

Shoes & Braces[edit | edit source]

A specialized shoe that simulates barefoot walking for the outdoors can be used to promote foot flexibility and lower knee adduction moments.[14] [23][21] Shoes with thinner soles reduce knee joint loads as the plantar surface of the foot is prone to joint loading.[14][24] Individuals with thinner soles or barefooted tend to take shorter strides. This effectively reduces knee extension and dorsiflexion on initial contact with the ground more akin to a mid-foot landing, significantly reducing peak knee adduction moments [14]. Valgus knee orthosis (braces) are another treatment method that can counterbalance the external adduction moment.[14] [25] This is done by applying pressure to elicit a valgus moment and reducing medial knee adduction moments in daily walking.[14] Ultimately, these interventions would be especially helpful in unloading excessive medial joint loading and creating medial tibiofemoral joint space, alleviating pain, and knee OA symptoms.[25]

Conclusion[edit | edit source]

Knee Osteoarthritis is a disease with no current cure to the condition. As summarized, knee OA is caused by a variety of factors ranging from overloading, mechanical stress, joint trauma, joint inflammation, biochemical reactions, and metabolic changes.[1] [5] The conservative biomechanical interventions prove to be a valid method to treat individuals suffering from knee OA symptoms. Future research should focus on looking at osteoarthritis knees in longitudinal studies, studying biomechanics and determining more interventions that can improve quality of life for individuals with knee OA.

References[edit | edit source]

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