Sample Paper on Osteoarthritis and Total Joint Replacement of Knee

Osteoarthritis and Total Joint Replacement of Knee

Abstract

Osteoarthritis (OA) is among the most prominent degenerative conditions and is of significant health concern to adults of 25 years of age and above. Prevalence is higher among women aged 50 years of age and above. Some of the leading risk factors for OA include: age, obesity, genetics, joint trauma, and injury. OA develops when matrix degradation of the cartilage is higher than matrix synthesis. Knee OA affects the kinematics and kinetics of the knee and hip joint owing to weight transfer, thereby causing an increase in knee adduction moment. While there is no cure for OA, biochemical treatment of knee OA aims to find a solution that will curb the deterioration of the condition. There are three levels of prevention of OA: primary, secondary, and tertiary. Primary prevention involves preventing the condition from occurring in the first place. Through weight control, sports injury and occupational injury prevention. Secondary prevention entails early diagnosis and prevention of OA but is limited by lack of effective diagnosis biomarkers. Tertiary prevention involves delaying or reducing the onset of disability and complications. Accordingly, we have various pharmaceutical, surgical, and therapeutic options that have been developed.

 

  1. Introduction

Osteoarthritis (OA) refers to a condition those results in a slow but progressive inflammation of the joints that could be as a result of cartilage degeneration. OA is a chronic arthropathy in which there is possible loss and disruption of joint cartilage and other changes to joints, such as osteophyte formation (bone hypertrophy). Whereas there are various forms of arthritis, OA is by far the most common, and the prevalent increases with an increase in age (Grayson & Decker S99). It has been reported that almost 27 million Americans of 25 years of age and above suffer from OA. It is also estimated that approximately 72 million Americans (about 20% of the population) will be aged 65 years and above by 2030, thereby increasing their risk of being diagnosed with OA (Bruyere et al. 257).  Below 45 years of age, the number of male patients with OA is greater than that of females. However, above 45 years of age, there are more women than men who are diagnosed with OA. Prevalence is also higher among overweight individuals, and individuals with stressful jobs.

According to Zenir, Axe and Snyder-Mackler, “arthritis is the leading cause of disability in the United States” (11). Lohmander (182) notes that hundreds of millions of individuals globally have been affected by OA, which is the cause of a huge burden of functional limitations, pain, and lost quality-adjusted life expectancy.  Zeni, Axe and Snyder-Mackler (86) have described OA is a degenerative diseases that has afflicted millions of US citizens. The authors further note that this degenerative condition mainly affects the knee, in effect making joint and knee OA as the main cause of functional limitations and disability among adults.  Approximately 13.9% of adults of 25 years of age and above are affected by OA (Centers for Disease Control and Prevention n.p.). Incidence of OA among individuals increase with an increase in age whereby 12.4 million adults of 65 years and above are estimated to suffer from OA. There is a dramatic rise in the incidence of OA among women after they attain 50 years of age. In addition, women when compared with men are highly likely to develop hip or knee OA (Centers for Disease Control and Prevention n.p.).

The significance of biomechanical factors has gained significance over the last few decades in regards to the pathogenesis of knee OA. Knee OA results in reduced neuromuscular control, weakness around the knee musculature, and knee joint instability (Lohmander 184). This results in an abnormal knee bracing in an attempt to maintain stability.

Path physiology

The balance between matrix degradation and matrix synthesis leads to a healthy cartilage. However, an imbalance between these two processes, in which matrix degradation gains supreme over matrix synthesis, leads to osteoarthritis. Two enzymes play a key role in matrix degradation in osteoarthritis. Matrix metalloproteinase’s helps to break down gelatin, collagen, and other proteinaceous elements of the matrix (DeGroot et al. 723). Aggrecanases helps to break down complex proteins known as aggrecans. Sustained breakdown of aggrecans is evident in the early stages of osteoarthritis where it plays a key role in loss of function and structure of the cartilage.

Age dependence osteoarthritis is linked to two mechanisms: Increased age causes advanced glycerin end products to accumulate. Consequently, it leads to reduced proteoglycans synthesis and a consequent in vitro degradation of human cartilage, matrix turnover reduction and, possibly, overall healing and repair capability (De Groot et al. 724). Chondrocyte senescence is the second mechanism in age dependence osteoarthritis. Several physiologic and metabolic changes are linked to aging in chondrocytes, including a change in the release of nitric oxide regulation; minimize proliferative capacity, declined response to IGF-1, as well as glycosaminoglycan production due to cytokines induction, reduced telomere length, and an increase in the production of ß-galactosidase (Barbero et al. 478).

At times, OA starts as a result of damaged tissue (such as torn meniscus) following mechanical injury, defects in cartilage metabolism, or even the movement of inflammatory mediators into the cartilage, from the synovium. Once the tissue has been damaged, the chondrocytes are stimulated in an attempt at repairing. Consequently, there is increased production of collagen and proteoglycans. On the other hand, attempt to repair the damaged tissues triggers the release of enzymes that in turn degrade cartilage (Barbero et al. 480). Inflammatory cytokines are also released. These inflammatory triggers also stimulate an inflammatory cycle that leads to further triggering of synovial lining cells and chondrocytes, as ultimately leading to a breakdown of the cartilage chondrocytes, ultimately leading to a breakdown of the cartilage. Chondrocytes are known to undergo apotosis (or programmed cell death). Following the destruction of the cartilage, the bone is exposed, and it becomes sclerotic and eburnated.

Under normal circumstances, joint use or movement normally stimulate a remodeling process of the cartilage (Centers for Disease Control and Prevention n.p.). However, in the case of OA, a combination of cellular, biochemical and mechanical processes, leading to not only an abnormal restitution, but also a rise in cartilage degradation (Ikeda et al. 123), normally change this process. OA is mainly distinguished by an ongoing cartilage loss, along with an increase in subchondral plate thickness, subchondral bone cysts, and ostephytes (Slemenda et al. 102). Vascular invasion also occurs, where the nearby articular cartilage could also develop calcification. As a result, the articular cartilage reduces in thickness and as time goes by, there could be increased cartilage deterioration and bone remodeling (Slemenda et al. 102) The ensuing inflammation basically entails the periarticular tissues.

There are a number of risk factors that are linked to osteoarthritis and include among others, joint trauma, age, obesity, or injury (Slemenda et al. 1954). With regard to age, persons aged 50 years and above are more likely to develop OA in comparison with those under the age of 50 years (Ikeda et al. 124). This is because as one ages, the process tends to affect the extracellular components and matrix structure of the cartilage. At the same time, the aging process has also been linked with a decline in the rate at which one responds to stimuli, and a declining chondrocyte function (Ikeda et al. 125). Joint over activity, trauma and joint injury, prolonged stress on an individual’s joint induced by strenuous occupation or sports activities have all been implicated with a rise in a person’s risk to developing OA, over time (Ikeda et al. 125). It is also important to note that obesity is also a risk factor to developing OA, especially in the individual’s weight-bearing joints. As the number of obese and overweight individuals rise, there is a corresponding rise in in not only the incidence of OA, but also the number of knee and hip replacements (Valderrabano et al. 2162). Another risk factor that has been attributed to the rising cases of OA is genetics (Slemenda et al. 102).

Biomechanical Considerations

Knee OA impacts on the kinematics and kinetics of the knee joint. The transfer of weight from an individual’s knee joint to hip joint further leads to biochemical changes on the hip joint (Heiden, Lloyd and Ackland 335). Such biomechanical changes are the main source of functional limitation and pain and as such, proper management of OA demands that their progression be prevented. This is because “the increase in knee joint loading causes further deterioration of the joint cartilage and worsens the symptoms of OA” (Rozen n.p.). In a normal knee joint without OA, the medial compartment carries nearly 70% of the body weight, with the rest of the weight being borne by the lateral compartment. Among patients with knee OA, there is a tremendous rise in knee adduction moment (Duffel et al. 1058) that is directly affiliated to loosening of the medial joint capsule, functional limitation, and joint space narrowing (Thorp et al. 3844).

In an attempt to prevail over the feeling joint instability, “the muscles surrounding the medial aspect of the knee adopt a bracing mechanism by which they contract as a whole to stabilize the medial aspect of the knee joint” (Rozen n.p.). Consequently, the medial compartment bears the additional load, and this hastens the degenerative changes experienced at the knee joint.

Treatment and Prevention

We now have well-established evidence as regards to the impact of biomechanical factors in knee OA. As a result, a lot of developmental and experimental effort has been directed at finding a sufficient biomechanical treatment for knee OA. The overall objective is prevention-oriented in that it aims at identifying a solution that will halt the deterioration of the diseases, with the likelihood of reversed pathogenesis. Current interventions are directed at minimizing knee adduction moment through muscle rehabilitation in the form of improved neuromuscular control and training (Fitzgerald 165). While biomechanical therapies have been shown to reverse the pathogenesis of knee OA, they have been characterized by limited clinical success. Some of the current biomechanical therapies being investigated today include orthotics, knee braces and walking aids. Other biomechanical therapies being investigated are exercise on sustainable surfaces with a view to improving neuromuscular control.

There are three levels of prevention of OA: primary, secondary, and tertiary. In primary prevention, the aim is to ensure that the condition does not occur, in the first place. There are only a limited number of primary prevention strategies that have thus far proven effective, including sports injury prevention, weight control, and occupational injury prevention. In terms of secondary prevention, this entails early diagnosis and prevention of OA (Hochberg and Dougados 584). This is however hard to undertake because we do not have effective biomarkers as regards the diagnossis of OA. On the other hand, tertiary prevention of OA is mainly focused on delaying or reducing the onset of disability and complications induced by OA. This is with a view to improving the quality of life of the individual (Hochberg and Dougados 585.

Tertiary prevention includes such strategies as cognitive behavioural interventions, self-management (including physical activity, weight control, and education) medical surgical treatments, and rehabilitation services.

Pharmaceutical treatment     

Pharmacological treatment of OA aims to control pain, improve quality of life and function, while reducing drug toxicity. However, a combination of exercise and pharmacological agents is usually recommended. Acetaminophen/paracetamol are recognized by the EULAR (European League Against Rheumatism Guidelines) and ACR (American College of Rheumatology) as first line agent in the management of OA. Others include NSAIDs (non-steroidal anti-inflammatory drugs) COX-2 (Cyclo-oxygenase-2) inhibitors (Skelly and Hawkez 302), and corticosteroids, among others.

 

 

Surgery          

Total knee arthroplasty (TKA) has over the years emerged as the most adopted surgical intervention for patients afflicted by end-stage knee OA.  In the United States alone, over 400,000 primary TKA surgeries are often conducted every year. In spite of this some of the individuals diagnosed with knee OA opt not to undergo this procedure (Valderrabano et al. 895; Valderrabano et al. 2161; Ikeda, Tsumura and Torisu 122). While there is yet to be developed criteria to be followed when determining who should not and who should not undergo TKA, some of the decisive factors that have been identified for consideration include elevated levels of disability, severe pain, and excessive cartilage degeneration (Slemenda et al. 101; Slemenda et al. 1953). Thus far, there have been no longitudinal studies that have been carried out to assess clinical impairments that trigger the application of TKA in individuals diagnosed with OA.

So far, priorities given to the decision to undertake TKA in persons with knee OA are mostly based on surveys carried out by orthopedic surgeons (Slemenda et al. 1954 ).  It is important to note that there is less likelihood of surgeons to advocate for total joint replacement if at all they have also been diagnosed with psychological or cardiovascular co-morbidities. Moreover, surgeons would be inclined to conduct total joint replacements on persons experiencing severe pain, “those with radiographic evidence of end-stage cartilage degeneration and for men” (Zeni et al. 86).

Surgery in OA is only considered after nonsurgical therapies have failed. There are four key surgical procedures that are recommended in OA: arthroscopy, osteotomy, arthroplasty, and arthrodesis. It is important however to note that all these four surgical procedures differ in terms of their variable benefits and the processes involved. Total joint replacement (arthroplasty) is the mainstay in OA surgical treatments as it is the most surgically advanced procedure out of the four (Brandt 119). In addition, it is also the most effective and highly successful operation. Moreover, it is cost-effective and eliminates disability and pain of end-stage OA. On the other hand, osteolysis and aseptic loosening are some of the common failures attributed to arthroplasty.

Exercise      

OA has no cure and as such, treatment mainly entails managing the symptoms associated with the condition. In this case, the main objective of therapy is to relieve pain, improve joint stability and function (Valderabano & Steiger 1). Studies carried out over the last several years offer data that support the presumption that muscle atrophy and muscle weakness play a key role in the progression of OA. For this reason, physiotherapy and rehabilitation were usually prescribed in order to increase mobility and alleviate pain. On the other hand, since exercise needs to be carried out regularly in an attempt to prevent muscle atrophy, it is usually recommended that people who have been diagnosed with degenerative joint diseases such as OA engage in continuous exercise programs. In this case, therapeutic exercise regime is mainly concerned with either aerobic activities or muscle stretching and strengthening.

One of the limitations of these exercises is that they do not permit biochemical alignment control in the knee. Consequently, they could lead to pain during exercise. When one exercises while in a state of pain, their proper motor learning is likely to be affected. It could as well result in poor compliance. In addition, stationary exercises are needed in motor learning and cannot be executed during activity. To overcome these limitations, there is need to conduct the neuromuscular training exercises under the right biomechanical alignment that has been shown to lead to no or reduced pain among patients (Haim et al. 3012).

 

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