Osteoarthritis (OA) continues to be one of the most difficult problems confronting the global health sector. The disorder is one of the top five causes of disabilities in the high-risk population, which includes those with a family history of arthritis, the elderly, and professional soccer players. OA affects more than 15% of the world's population. The United States spends more than $82.4 billion a year on OA therapies such as medications, non-pharmacological operations, and surgeries. Such costs are higher in third-world countries where members do not have access to disease statistics. As a result, studying the pathophysiology of OA is critical to reducing its negative effects. This paper discusses various aspects of OA focusing on its risk factors, pathogenesis, symptoms, diagnostic procedures, and most effective treatment strategies.
Table of Contents
HYPERLINK l "_Toc474329436" Abstract PAGEREF _Toc474329436 h 2
1.0. Introduction PAGEREF _Toc474329437 h 4
2.0. Literature Review PAGEREF _Toc474329438 h 6
2.1. Pathophysiology of OA PAGEREF _Toc474329439 h 6
2.2. OA effects on other Joint Tissues and Bones PAGEREF _Toc474329440 h 8
2.2.1. Subchondral Bone PAGEREF _Toc474329441 h 9
2.2.2. Bone Marrow Lesions PAGEREF _Toc474329442 h 9
2.3. Risk Factors PAGEREF _Toc474329443 h 10
2.3.1. Aging PAGEREF _Toc474329444 h 10
2.3.2. Abnormal Loading PAGEREF _Toc474329445 h 11
2.3.3. Genetic Factors PAGEREF _Toc474329446 h 11
2.3.4. Gender PAGEREF _Toc474329447 h 12
2.3.5. Lifestyle PAGEREF _Toc474329448 h 13
2.4. Impacts of Osteoarthritis PAGEREF _Toc474329449 h 13
3.0. Clinical Features of OA PAGEREF _Toc474329450 h 15
3.1. Diagnostic Procedures PAGEREF _Toc474329451 h 16
4.0. Treatment PAGEREF _Toc474329452 h 17
4.1. Nonpharmacologic Therapies PAGEREF _Toc474329453 h 17
4.2. Pharmacological Therapy PAGEREF _Toc474329454 h 19
4.3. Surgery PAGEREF _Toc474329455 h 20
5.0. Conclusion PAGEREF _Toc474329456 h 22
References PAGEREF _Toc474329457 h 23
Introduction
Osteoarthritis (OA) attacks the joint causing chronic pain, stiffness, and swelling. It often degenerate the entire the entire articular cartilage. This is a specialized connective tissue comprising collagen, water, chondrocytes and proteoglycans that provide a surface for smooth articulation as individual walks, runs or stretches (Leung, G., Rainsford & Kean, 2013). Normal joints move freely, the opposing articular surface does not create friction, and distribute the load evenly across the tissues. The proper joint functioning relies on its biomechanical properties. The joints have several composites such as subchondral bones, connective tissues, ligaments, cartilage surfaces, and capsule. The bone plates define the shape whereas the articular surface together with the synovial membrane, cells and capsules regulate the biological functions such as synthesis and absorption of enzymes and other chemicals during movements. The ligaments control the mechanical stability and flexibility while the synovial membrane secretes the enzymes (cytokines, growth factors), and hyaluronic acid (McAlindon, Bannuru, Sullivan, Arden, Berenbaum, Bierma-Zeinstra, & Kwoh, 2014).
On the other hand, Osteoarthritis destroys the cartilage in the main joints such as the hands, knees, spinal cord which in turn leads to pain and stiffness (Ganvir, & Zambare, 2013). OA ranks among the most prevalent musculoskeletal diseases accounting for 50% of disease burdens in this category. Researchers believe that the incidences of OA will increase significantly as and have greater effects on the society as the baby boomers are reaching middle age. Currently, 15% of the worlds population has OA. However, Osteoarthritiss prevalence varies worldwide. Centers of Disease Control and Preventions (CDC) statistics show that over 52.2 adults have arthritis globally. Osteoarthritis patients account for the highest percentage of these disadvantaged individuals. For example, the number of the United States citizens with this chronic type of arthritis increased from less than 21 million in 1990 to 27 million in 2005 (CDC, 2017).
Overall, 13.9% of adults aged between 25 and 64 years old and 33.6% (12.4 million) aged above 65 have Osteoarthritis (CDC, 2017). Similarly, between 10 and 15% of the United Kingdom citizens are OA patients while about 4 million Canadians have the condition. Therefore, OA places a heavy burden on the country health care system. Given that that OAs cure and cause are not known, the disease is one of the greatest concerns facing the global health system. CDC found that the US spends over $ 82.4 billion per year whereas Canada uses $ 18 billion in OA treatment and related expenditures (de Vrueh, Baekelandt, E & de Haan, 2015).
The chronic disease is not curable. However, the patients who comply with the recommended treatment and management plan record greater health outcomes than their counterparts that lack access to proper medical care. As such, the management procedures aim at reducing inflammation, pain; and slowing the degradation of cartilage. Pharmacological therapy such as non-steroidal anti-inflammatory drugs (NSAIDs) and viscosupplements-Hyaluronic acid help such patients in pain management (Man & Mologhianu, 2014; Allen & Golightly, 2016; Stack & McCarthy, 2016).
The chronic illness is also associated with regular hospitalizations and mortality. It contributes to over 47% of arthritis-related hospitalizations. For example, it led to the admission of the 3, 161,100 patients out of the 4,646,817 that were suffering from arthritis in 2011. The individuals incurred substantial expenses in related procedures such as hip and knee joint replacement procedures. The statics reveal that the knee replacement rose by over 217% between 1992 and 2011. Similarly, OA-related deaths are more than 1.6 times higher than those resulting from other causes (Silverwood, Blagojevic-Bucknall, Jinks, Jordan, Protheroe, & Jordan, 2015)..
Literature Review
Pathophysiology of OA
Several factors such as biomechanical, proteases and pro-inflammatory mediators influence the pathophysiology of osteoarthritis. In the past, researchers viewed OA in terms of cellular inflammation that resulted from the increase in leukocytes in the affected joint. The scholars categorized the condition with other rheumatoid arthritis that resulted whenever the number leukocytes exceeded 1000 cells per milliliter (Allen & Golightly, 2015). However, recent studies indicated that such synovial inflammation characterizes osteoarthritis, the inflammation in OA not only occur at the molecular level but are also caused by mediators such as chemokines and cytokines (Silverwood et al., 2015). The proinflammatory mediators trigger the manufacturing of the proteolytic enzymes that degrades the extracellular matrix. Mechanical factors, wear and tear, and excessive joint loading all play significant roles in the joint tissue destruction.
In simple terms, OA is a disease that attacks the cartilage, a viscoelastic tissue that controls movement and other functions of the joints. The cartilage has three components including the cellular, liquids and solid phase that account for 1-2%, 70% - 80%, and 20% - 30% respectively. The cellular constituents mainly include the chondrocytes while the solid phase contains substances such as collagen and proteoglycans. Stack & McCarthy (2016) argues that collagen has relatively slow turnover. On the other hand, proteoglycan records rapid turnover. Normal joints maintain this matrix as they balance the degradation and synthetic enzyme activities. The synovium is responsible for the remodeling by motivating the cells to synthesize the transforming growth factor ß (TGFß). Besides promoting the matrix synthesis, TGF ß minimizes the cartilage destruction by inhibiting the production of IL-1 and TIMP. OA cartilage also produces fibroblast and Insulin-like growth factor (b-FGF and IGF) to assist in the repair process (Fang, Xu, Li, & Zhao, 2016).
On the contrary, this is not the case in the OA patients as the matrix degradation exceeds the enzymes synthesis thereby resulting in a decrease in the loss of collagen and proteoglycans. Chondrocytes, in turn, synthesize more proteoglycan and collagen molecules so as to restore the equilibrium (Swift, 2012). However, the enhanced cartilage degradation often outmatches the attempts to achieve such a balance. Consequently, erosion, cracking and fibrillation occur at the cartilages superficial layer. As the degradation progress to the deeper layers, the patients condition worsens. This will also be evident through clinically noticeable symptoms such as swelling of the joints, and excessive pain during movements (Leung, Rainsford, & Kean, 2013).
OA begins with the destruction of the articular cartilage. This occurs when the body not only releases the catabolic enzymes but also decrease the production of chondrocytes that in turn breaks down the cartilage matrix. According to Garlanda, Dinarello, & Mantovani, (2013), inflammatory cytokines such as Interleukin-1 (IL-1), Interleukin-6 (IL-6), Interleukin-15 (IL-15), Interleukin-17 (IL-17), Interleukin-18 (IL-18), Interleukin-1(IL-1), and tumor necrosis factor (TNFα) are released during the matrix breakdown. These cytokines induce the synovial cells to synthesize the MMP and prostanoid and inhibits type II collagen and proteoglycans synthesis. For example, the IL-1 has been found not to stimulate cartilage destruction but also hinders the attempts to repair the damaged tissues (Garlanda et al., 2013).
Moreover, the cytokines produce Nitric oxide (NO) and NF-ĸB as well as promote chondrocyte apoptosis that further supports cartilage deterioration (Kashyap, Carter, Sauer, & Chen, 2013) In this case, NF-ĸBs are chemicals that regulate the production of matrix metalloproteases (MMPs). In other words, the chondrocytes often create MMPs that degrades the matrix during an injury. The synovial cells and chondrocytes produce such MMPs that are categorized into collagenases, gelatinases, and stromelysins. The joint synthesizes the substances as inactive enzymes and regulated or activated through a process known as enzymatic cleavage (Kashyap et al., 2013). Having been activated, the MMP lose the ability to resist against plasma-derived (alpha-2-macrglubulin) and tissue inhibitors (TIMPS). According to Man & Mologhianu (2014), OA enhances the MMPs synthesis to such a high levels that overwhelm the inhibitors thereby resulting in net degradation. Excess of deficiency in the cytokines supply is responsible for the damages to the joints.
OA effects on other Joint Tissues and Bones
Several recent studies have revealed that OA not only affects the cartilage but the entire joint. Martel-Pelletier, Teichtahl, Cicuttini, Abram, Wang, & Pelletier (2016) found that the articular cartilage degradation involves several cellular changes, biomechanical processes, bone remodeling, the formation of marrow lesions, and synthesis of enzymes by the synovium cells.
2.2.1. Subchondral Bone
This is the bone that surrounds the articular cartilage. It has a cortical bone and is joins the articular cartilage via a zone called calcified cartilage. Subchondral bone prevents diseases or conditions by reabsorbing excess secretions and forming new bones (Martel-Pelletier et al., 2016). However, the osteoarthritic process usually interferes with these functions. It can cause sclerosis and bone marrow lesions. The inflammation may also thicken the subchondral bone plate. The MMPs not only modifies the trabecular bone architecture but also inhibits the development of the new bones along the joint margins. Stack & McCarthy (2016) cite that OAs patients have high bone resorption indices that indicate the loss of the bone. The advanced stages of cartilage degeneration are often characterized by deposition thereby causing the swelling of the affected areas. The synovial fluids in such joints come into contact with the bone marrow that in turn causes the bone cysts. Stack & McCarthy (2016) further cites that the OA-affected subchondral bone produces type I collagen which stimulates abnormal mineralization. The normal bone α1 and α2 type I collagen chains ratio averages are 2.4:1 while affected bones ratio varies between 4:1 to 17:1. The abnormal mineralization pattern adversely affects the homeostatic processes.
2.2.2. Bone Marrow Lesions
The articular cartilage destruction is significantly associated with bone marrow abnormalities. The damage impacts negatively on the formation of the bone marrow as well as medical conditions such as the bone marrow necrosis and fibrosis. The abnormalities worsen the cartilage loss. Martel-Pelletier et al., (2016) found that the cartilage loss is always higher in joint areas with high bone marrow lesions. The defective bone marrow is also responsible for cysts that block the synovial fluids from synthesizing the enzymes.
Risk Factors
Aging
OA is more common among the elderly than the young people. In fact, the clinicians used to perceive osteoarthritis as an inevitable condition of old age. According to McAlindon et al., (2014) individuals initially thought that the frequent movements wear out the articular cartilage. In contrast, the recent studies indicated that regular use such as active physical exercises minimizes the chances of the cartilage degeneration. In other words, the older people who have not been using the articular cartilage adequately are at greater risk of OA than their physically active peers.
Researchers have also dedicated their time to finding the differences between the OA cartilages and aging joint tissues (Swift, 2012; Aftab, Siddiqui, Babur, & Memon, 2015). The studies reveal that there are denatured type II collagens in both the cartilages. However, these collagens are more predominant in OA than aging cartilages. Moreover, a significant difference exists in the liquid phase and chemical components such as the ratio of keratin sulfate to chondroitin sulfate. Möller, Gharbi, Serrano, Barbero, Milano & Henrotin (2016) found that the OA patients have about 846 chondroitin sulfate epitopes that can only be found in fetal and neonatal cartilages. This means that old age increases the chances of OA, but not all older adults have the disease.
Abnormal Loading
The joints can withstand normal physiologic loads. Occupations or diseases can increase the loading to higher levels than those that can be supported. For example, heavy manual labor, trauma, obesity and weight problems are leading risk factors of OA. Individuals in occupations that require such labor such as the coal mines and farmers experience higher rates of hip and knee osteoarthritis than the general population. Kerkhof, Bierma-Zeinstra, Arden, Metrustry, Castano-Betancourt, Hart, ... & Uitterlinden (2014) study also indicates that trauma such as microfracture can stimulate enzymatic activity or cause wear and tear consequently causing an imbalance between the degradation and repair of the cartilages.
The wear particles may alter the ability of the synovial cells to maintain homeostasis. For example, retired athletes, soccer, football and rugby players record high incidences of knee OA due to the numerous cruciate ligament injuries they suffered during the championships. The injuries cause subluxation of the joint as well as abnormal load distribution. In this case, subluxation refers to the altering of the collagen fibrils and ligaments. As a result, the tendons stiffen thereby decreasing the joint flexibility. Similarly, OA risks among obese people with a body mass index of between 30 and 35 are also four folds higher than other disadvantaged individuals (Aftab et al., 2015).
Genetic Factors
Family history plays a significant role in developing OA. The disease results from interactions of several genes such as those responsible for extracellular matrix proteins. Most OA patients have strong body build, wide geometrical bone measurement, and high bone mineral density (Kerkhof et al., 2014). This means that all young people who inherit these traits from their parents are at a significant disadvantage. In fact, genetic factors account for over 70% of all OA cases (Ganvir, & Zambare, 2013). All individuals from families with a history of other forms of arthritis such as lupus, ankylosing spondylitis, rheumatoid and psoriatic arthritis are at significantly higher risk of OA than the general population. Individuals with endocrine problems such as hemochromatosis and Wilson's disease also fall under the disadvantaged group. The conditions often affect the blood supply along the joints and trigger buildup of toxic materials around the articular cartilage (Allen & Golightly, 2015).
Gender
Gender also plays key roles in OAs prevalence. Several studies suggest that more senior women suffer from the disease than the males. Ganvir & Zambare (2013) found that the prevalence increases after the females reach menopause. The researcher attributes the rising cases to the loss of estrogen. That is, estrogen prevents cartilage inflammation. Therefore, the women lose this protection after menopause. Swift (2012) explains that different studies have produced compelling evidence on estrogen deficiencys effects on the joint. For example, estrogen often impairs the secretion of type II collagen. Leung et al., (2013) study confirm the findings as it indicated that OA prevalence rate was higher in men than women below 45 years old. However, OA incidence is significantly higher in females above 55 years than their male peers. The study showed that the women were 2.6 times more likely to develop hand OA after their 50th birthday than the men of the same age. The difference is attributed to the decline in estrogen levels. Therefore, hormonal therapy is effective for treating this group of senior women (Leung et al., 2013). At the same time, women have wider hips than their knees leading to higher rates of injuries than men. For example, researchers have observed that females playing soccer are three to four times more likely to experience joint problems as their male counterparts.
Lifestyle
Diet, the level of physical activity, smoking and drinking play key roles in developing and living with OA. Micronutrients such as vitamins C, D and K deficiency has been found to trigger arthritis. Leung et al., (2013) cite that lack of Vitamin C in a mice diet caused chondrocyte to degenerate at a faster rate than a mouse that ate all the vitamins. Similarly, humans who consume adequate Vitamin C and D achieve increases in bone density, which lowers the progression of osteoarthritis. Furthermore, Vitamin K supports the coagulation process that regulates cartilage mineralization.
Impacts of Osteoarthritis
OA have multiple and adverse social, financial and psychological impacts on the patients and their families. Since the pain is not predictable, OA restricts the patients from social activities. According to Swift (2012), virtually all people suffering from osteoarthritis complain of distress due to the loss of ability to control their lives. At first, the populations at risk of OA experience the physical challenges while participating in intense activities such as sports. Eventually, the individuals begin to experience more painful episodes during light movements. This, in turn, leads to sleep disturbance and distress. On the other hand, quality of sleep is positively correlated with the treatment outcomes. Swift (2012) study shown that the OA patients that sleep for at least eight hours cope better with the disease than their counterparts lacking adequate sleep. Those pursuing careers in sports or those that involve manual labor may lose their source of livelihood. The impacts are greater among the low-income families than the wealthy households. This is as a result of increased medical costs. However, most of these risky occupations are characterized by poor remuneration such as health insurance, social and retirement benefits. Consequently, the individuals psychological health deteriorates thereby exposing to other risks such as suicide and heart diseases.
The patients with low self-esteem suffer more harm as compared to their peers who quickly form and maintain social relationships. Phyomaung, Dubowitz, Cicuttini, Fernando, Wluka, Raaijmaakers, & Urquhart (2014) found that the pessimist individuals withdraw from recommended management procedures. For example, they do not like performing light exercises and healthy physical activities such as walking and yoga. Such cases lead to high pain prevalence and dissatisfaction with life. Swift (2012) argues that the stress severity increases with the intensity of pain, access to psychological needs and impacts of OA on the physical disability and financial stators. Overall, depression levels among the old patients range between 17% and 20%. Therefore, the caregivers should prioritize such disadvantaged patients psychological needs. Moreover, factors such as self-efficacy and catastrophization influence the stress levels. .Swift (2012) explains that OA patients experience catastrophization whenever they feel helpless or waits for the worse to happen. Over 31% people with OA experience anxiety. The rate rises to over 41% among the elderly patients.
However, the higher the negative emotions, the lower the ability to adhere to the appropriate treatment plans. Phyomaung et al., (2014) demonstrated that anxiety results to greater pain episodes than depression. This is attributable to the fact that anxiety reduces the quality of life both before and after undergoing surgery. On the other hand, self-efficacy is positively correlated with the coping strategies. The patients with high self-esteem gain the morale to stick to the dietary plans and honor all their doctors appointments. The people also perceive close relationships with the caregivers as an important step towards achieving better outcomes.
Clinical Features of OA
OA patients often suffer extreme pain accompanied with stiffness. The individuals discomfort increases during joint use and feel relieved while resting. However, advanced stages cause persistent pain at all times whether the patient is resting or not. According to Swift (2012), the loss of cartilage cushion results in friction between the bones and severe pain even during a period of inactivity. In other words, the pain cannot be linked to specific stimuli. Swift (2012) further cites that several studies that have explored the brain tissues during pain reveal that the discomfort does not necessarily result from movement, pressure or loading. However, it is believed that the pain may originate from the mechanical irritation of the synovial and capsular inflammation, bone sclerosis. As a result, the patient hardly gets enough sleep and struggle to engage in daily activities such as walking and climbing stairs.
The joints also become tender and may not move freely. This is not only because the muscles weaken but also due to the thickening of the synovial membrane. Such symptoms often vary. That is, some patients experience pain during as the weather changes while others record bad and good spells all year round. OA symptoms depend on the part of the body affected (Silverwood et al., 2015). For example, OA of the knees mostly occur due to obesity and repeated injuries. The excess upper body weight together with the progressive cartilage degeneration can deform the knees. A significant number of patients are forced to go for knee surgery as their conditions hardly respond to the medications.
OA of the fingers is associated with growth or spurs next to the joint. Thelier, Chevalier, Oppert, Poitou-Bernert & Katsahian (2013) cite that the patients may develop two types of bony enlargement, the Heberden and Bouchards node. That is, the growth that occurs at the end of the fingers was named after Dr. Herberden, a famous British physician, while the bony knob at the middle joint of the fingers got the name from Dr. Bouchard, a French doctor who made several discoveries about arthritis treatment in the 1800s. The fingers also swell and become tender. Similarly, the individuals that develop the osteoarthritis of the cervical spine suffer extreme pain in their necks and low back. The swelling prevents the normal functioning of the spinal nerves leading to numbness. The patients may not s also it upright.
At the same time, the pain intensity varies from a patient to the next. Swift (2012) found that the pain episodes are inconsistent. Therefore, the physicians cannot use a pain scale to determine whether an individual suffers greater pain than others. Moreover, the pain may come either every day or in episodes. Some patients describe the pain as intense and sharp while others say that it is dull.
Diagnostic Procedures
The diagnosis focuses on the symptoms. The physician should examine the affected joints for swelling, tenderness, pain and any other damage. He/she must supplement the physical examinations with imaging (x-rays and Magnetic Resonance Imaging (MRI) and laboratory tests (joint fluid analysis and blood tests). X-rays will not only reveal the cartilage loss but also show spurs and nodes around the joint. According to Leung et al., (2013) X-ray may indicate OA evidence before some patients develop severe symptoms. MRI also utilizes strong magnetic field and radio waves to depict finer details about the joint and the surrounding bone and soft tissues than X-ray.
Joint fluid analysis indicates whether there is inflammation while blood test helps to determine whether the joint discomfort results from other types of arthritis and other diseases. For example, the blood examination will indicate erythrocyte sedimentation or presence of antibodies and rheumatoid factors. The joint test also involves using a needle to withdraw fluids from the affected hip, knee, leg or spine (McAlindon, et al., 2014).
Treatment
Osteoarthritis treatment entails a mix of pharmacological, non-pharmacological, intra-articular and surgical procedures. The treatment begins with safe and cost friendly therapies before advancing to complex surgeries. The first treatment should include non-pharmacological activities such as education, exercise, nutrition, weight loss, and physical aids such as knee braces (Allen & Golightly, 2015). On the other hand, a patient should undergo the surgical procedures only if the pharmacologic and behavioral therapies do not yield positive results. 4.1.
4.1. Nonpharmacologic Therapies
These refer to creating physical exercise program and other behavioral therapies aimed at strengthening the joint muscles, easing pain and minimizing other risk factors such as weight problems. Aerobics, jogging, walking, swimming, cycling and other upper body exercise are effective in attaining healthy body weight. Clinical studies indicate that exercise presents some of the most significant intervention measures of living positively with OA. The individuals who exercise regularly also achieve appropriate weight loss that reduces pain and the risk of developing symptomatic osteoarthritis in women. According to Hawkeswood & Reebye (2010), losing at least 5% of the weight is adequate to reduce disability. At the same time, physical activities improve motion, joint flexibility, and muscle strength and endurance. Every loss of 1-kilogram body weight leads to a 4 kg in load per step and 4800 kg per each kilometer a patient walks (Hawkeswood & Reebye, 2010).
Behavioral therapy plays a critical role in managing OA. Effective education techniques such as individualized and group discussions equip the patient with adequate coping skills thereby making the learning processes 20% as effective as pharmacological strategies. Aftab et al., (2015) a sound management plan accounts for each patients expectations, the severity of the disease, occupation, social and psychological needs. For example, pessimistic patients require more counseling sessions than the individuals with high self-esteem. The therapies should be interactive so as to engage the patients in setting appropriate treatment goals.
Both the literature and evidenced based practices documents the benefits of patient-driven therapies over passive treatment procedures (Hawkeswood & Reebye, 2010. The patients adhere to the behavioral modifications more easily when they have unlimited access to the information than whenever the health professionals impose the procedures on them. Ideally, the first session should focus on informing the individuals about OA and outlining its treatment procedures. The second visit should concentrate on discussions about the standardized exercise procedures, healthy diets, and other weight loss activities. Leung et al., (2013) found that following such a program results in greater weight loss and pain relief than the traditional non-pharmacologic treatment. The patients also benefit from one-on-one interaction with experienced physical therapist and nutritionist. He/she can also access supportive devices such as canes and walkers.
Alternatively, the individual can use orthotic shoes that reduce stress on joints and splints to stabilize the affected areas. Furthermore, the new knowledge gathered to ensure the patient maintains low-energy food and increase Vitamins C, D, and K in their diets. The individuals with severe conditions can employ a transcutaneous electrical nerve stimulation device to manage the pain. This is equipment disrupts the transmission of the pain stimuli (Man & Mologhianu, 2014).
4.2. Pharmacological Therapy
Several medications help to minimize pain and improve the musculoskeletal functions. The drugs are categorized as pain management medications, nonsteroidal anti-inflammatory drugs (NSAIDS) and joint injections (Garlanda et al., 2013). For example, opioid and acetaminophen relieve mild pain. In contrast, narcotics are preferable for severe OA exacerbations. Like the analgesics, it is recommended to administer non-steroidal anti-inflammatory drugs (NSAIDs) to patients who are unresponsive to the nonpharmacologic measures because of their side effects. The drugs both reduce pain and minimize inflammation. Joint injections are effective for patients that are allergic to the NSAIDS. Injecting glucocorticoid into arthritic joint reduce OA symptoms. Similarly, cyclooxygenase-2 (COX-2) inhibitors and glucocorticoids are used in the management of knee arthritis to reduce inflammation of swollen joints. Viscosupplements such as hyaluronan and Hylan G-F 20 have similar effects (Martel-Pelletier et al., 2016).
However, these medications have several side effects. For example, non-steroidal anti-inflammatory drugs (NSAIDs) often lead to gastrointestinal and cardiovascular problems while steroid use may cause hypertension and psychological disorders (Slipman, 2008). As a result, physicians are increasingly using complementary and alternative supplements to diversify the health care and medication options for osteoarthritis patients. Stack & McCarthy (2016) argues that lack of cure from pharmacological therapies as well as the adverse effect on the patient has increased the interest on the part of patients to use complementary and alternative supplements. These mostly include natural herbs. According to Noureddin, Mato, & Lu (2015), S- Adenosylmethionine (SAMe) and capsaicin are some of the alternative supplements that help in treating osteoarthritis symptoms. The medication allows for improved healthcare outcomes by eliminating the adverse outcomes associated with the conventional treatment methods (the drugs side effects). SAMe contains dietary supplements derived from natural foods that are more effective than many analgesics. Similarly, capsaicin is herbal medicine made from chili peppers. It contains substance P that transmits the pain signals and stimulating inflammatory substances in the joints (Noureddin et al., 2015).
4.3. Surgery
Given the cost impacts and the risks associated with surgery, the joint operations are reserved for OA individuals that do not respond to the other treatment procedures. However, the patients should undergo surgery early enough before experiencing complications such as joint deformities and excessive muscle loss. The intervention entails replacing the affected joint, irrigation (arthroscopy), realignment and cartilage grafting (Martel-Pelletier et al., 2016). In joint replacement, the medical pr
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